Prana Biotech: PBT-2 - 500 Beiträge pro Seite

[Neoe]

Leider finde ich den alten Prana-Thread nicht mehr, daher eröffne ich einfach mal einen eigenen.

Ich spare mir vorerst Details, die Prana-Homepage gibt aber einigen Aufschluss für jene, denen dieses Unternehmen tatsächlich noch unbekannt ist.


New Alzheimer`s Drug Enters Development Track
Tuesday August 5, 9:25 am ET
Phase I Clinical Trials Scheduled for 2004


MELBOURNE, Australia, Aug. 5 /PRNewswire-FirstCall/ -- Neuro degenerative disease specialist Prana Biotechnology Ltd (Nasdaq: PRAN - News; ASX: PBT - News) has selected a new lead molecule for formal drug development that shows the best potential yet to effectively treat Alzheimer`s Disease.
ADVERTISEMENT


Prana`s scientists will develop the new proprietary compound called PBT-2. It is now a core business task and is based on the science established by the University of Melbourne and the Harvard Medical School at the Massachusetts General Hospital.

Prana Biotechnology completed the extension phase of its Phase II clinical trial on Clioquinol (PBT-1) earlier this year. PBT-1 is the initial drug compound which has established proof of concept of Prana`s approach and advanced to successful Phase II clinical trials. Prana`s proof of concept outlines the role of metal protein attenuating compounds in targeting the interaction between beta amyloid and oxidised metals in the brains of Alzheimer`s Disease patients.

"This step shows that Prana is bolstering its strong position to be the company behind an effective treatment for the highly debilitating Alzheimer`s Disease," said Dr Ross Murdoch, Prana`s Chief Operating Officer. "This is a major milestone and is the result of an impressive in house medicinal chemistry team effort."

"We have designed compounds that are superior to PBT-1. PBT-2 is a small molecular weight chemical entity that demonstrates a significant improvement on PBT-1. PBT-2 has characteristics appropriate for oral bioavailability and blood brain barrier permeability. PBT-2 exceeds PBT-1 in both pre-clinical in- vitro and in vivo-testing. The formal toxicology program will be initiated this year and the new drug is expected to enter into Phase I human clinical trials next year.

Addressing investors in New York, Prana`s Executive Chairman Geoffrey Kempler said "This is enormously encouraging for us as we have developed a whole library of proprietary metal protein attenuating compound designer molecules. These have applicability not only to Alzheimer`s Disease but other neurodegenerative diseases including Parkinson`s Disease".

Alzheimer`s Disease affects about 12 per cent of 65 year olds and about 50 per cent of 85 year olds. Existing Alzheimer`s treatments provide only short term relief from the onset of symptoms.

About Prana Biotechnology Limited

Based in Australia, incorporated in 1997 and listed on the Australian Stock Exchange in March 2000, Prana Biotechnology (Nasdaq: PRAN - News; ASX: PBT - News) was established to commercialize research into Alzheimer`s disease and other major age-related degenerative disorders. Its mission is to develop diagnostic and therapeutic drugs to treat the central disease pathways that cause degeneration of the brain as the aging process progresses. Prana`s technology has emerged from its researchers at prominent international institutions such as Massachusetts General Hospital at Harvard Medical School and the University of Melbourne. For further information, please visit our web site at www.pranabio.com.

[Neoe]

Das war wohl das Zeichen zum Abheben. Kein Wunder, immerhin reden wir vom größten Marktsegment in der Medikamentenbranche überhaupt.

Alleine das Alzheimer-Medikament hat ein Umsatzpotential von ca. 10 Milliarden Dollar .Und wir reden hier von einem Medikament, dass letzendlich keine Konkurrenz zu fürchten hat, da mittlerweile klar ist, dass Ashley Bush mit seiner Theorie, wie Alzheimer entsteht und geheilt werden kann, nichts anderes als den heiligen Gral entdeckt hat. Prana strebt eine Lizenzvereinbarung an, die (unter anderem von Salomon Smith Barney erwähnt) als sicher anzusehen ist und wohl nicht zuletzt von der gestrigen Pressemeldung abhängig war.

Vielleicht wird PBT-1 sogar völlig von PBT-2 ersetzt und kommt gar nicht mehr in Phase III.

Zu erwartende Lizenzeinnahmen: 500 Millionen bis 1 Milliarde jährlich (Anm.:Selbstangabe von Prana)


Mein Tip:

In 5 Jahren steht Prana da, wo sich marktkapitalisierungstechnisch heute Amgen befindet. Wird die Lizenzvereinbarung öffentlich gemacht, ist dieser Tip weit realer als so mancher beim jetzigen Durchlesen glauben möchte.

[Neoe]

Prima and Prana to develop Alzheimer`s vaccine

Biotechs Prima Biomed and Prana Biotechnology are combining with the Austin Research Institute and Melbourne University to develop the world`s first vaccine for Alzheimer`s disease. Prana`s research has linked metals in the brain to the development of Alzheimer`s disease and the company has conducted successful human trials testing metal protein attenuating compounds to treat the disease. Prima Biomed`s new vaccine technology, DCtag, will be used in conjunction with these compounds to help the body`s immune system recognise the protein or peptide extracts associated with Alzheimer`s disease. The research and development will be conducted by the Austin Research Institute and the Melbourne University.

[analle]

40 %usa

[analle]

bin seit heute drin, alte Beiträge unter 937103, allerdings
verstehe ich die unterschiedlichen WKNs nicht.Aber egal, ich bin in beiden drin.

ganz lange.

[Neoe]

Welcome [Sign In] To track stocks & more, Register
Financial News
Enter symbol(s) BasicDayWatchPerformanceReal-time MktDetailedChartResearchOptionsOrder Book Symbol Lookup







Press Release Source: PRIMABioMed Limited


PRIMABioMed`s Panvax Subsidiary Awarded Project to Develop Therapeutic Alzheimer`s Vaccine
Wednesday August 13, 12:19 pm ET


VICTORIA, Australia, Aug. 13 /PRNewswire-FirstCall/ -- PRIMABioMed Limited (ASX: PRR - News), the cancer and immunotherapy research and therapeutic development company, announced that its Panvax subsidiary has been awarded a project by Prana Biotechnology (Nasdaq: PRAN - News; ASX: PBT - News), one of Australia`s leading neurodegenerative disease companies, to collaboratively develop an effective therapeutic vaccine for Alzheimer`s disease. The project is also being supported by a $250,000 Biotechnology Innovation Fund (BIF) grant from the Commonwealth government.
Panvax has been developing its DCtag vaccine adjuvant, which induces high levels of antibodies and T-cell responses required for effective protection against a range of diseases. Panvax has previously reported that DCtag can both protect against and treat malaria and cancer.

Prana Biotechnology has identified protein fragments of the Beta Amyloid protein as potentially suitable and highly specific targets for Alzheimer antibody therapy. The Beta Amyloid protein accumulates in the brain tissue of Alzheimer`s patients and contributes to the disease, and these protein fragments could be used to vaccinate people against the disease.

By combining Prana`s protein fragments with the DCtag vaccine vehicle, the companies hope to generate an effective therapeutic vaccine, generating antibodies to the Beta Amyloid protein that will assist in the eradication of the protein from the brain tissue. Any antibodies generated will be further progressed towards the development of monoclonal antibody products for passive therapy. Both active (vaccination) and passive (antibody) treatment could improve outcomes for patients with the disease. Vaccination could further prove effective in protecting people against Alzheimer`s disease. Panvax researchers, located at The Austin Research Institute and Prana researchers at University of Melbourne will conduct the research and development program.

Annual sales of existing Alzheimer`s Disease treatments total more than $1 billion. Current treatments provide minimal alleviation of symptoms without addressing the underlying pathology of the disease.

Panvax and Prana Biotechnology will jointly share in the benefits of any intellectual property produced from the collaboration including milestone payments and royalties that may accrue as a consequence of producing a successful therapeutic vaccine therapy.

Marcus Clark, Prima Biomed Chief Executive Officer, stated, "We are pleased that Panvax`s DCtag technology has been recognized for its varied potential applications including infectious disease, cancer, and now neurodegenerative diseases.

"This project is a significant addition to Prima`s growing list of collaborative efforts with leading biotechnology companies and institutions around the world including Medarex Inc. in the United States and the Institute Pasteur in France."

Based in Melbourne, PRIMABioMed (ASX: PRR - News) is a biotechnology development and commercialization organization with first and last rights over technologies from the Austin Research Institute, a prestigious institution dedicated to medical research. Through its strongly incentivized management team and highly qualified scientific advisory board, including globally recognized researchers, PRIMABioMed specializes in immunology and cancer immunotherapy and adopts technology development that shows potential for commercial returns within three to four years. For more information, please visit PRIMABioMed`s website at www.primabiomed.com.au

[Neoe]

Leider wieder eine PDF-Datei, deswegen die News kurz mündlich und den Link dazu:

5 Millionen AUD wurden in die Kassen gespült und zwar durch ein Privete Placement von ca. 7 Millionen Aktien (der Preis lag exakt bei 0,7 AUD pro Aktie). Weitere interessante Details findet ihr in der ausführlichen News. Einfach den LInk anklicken.

http://www.asx.com.au/asxpdf/20030904/pdf/3hxnh4htv2hxg.pdf

[Neoe]

Offizielle Version von der Website:

5 September 2003

Prana Raises $5 million
4 September 2003 Melbourne: Prana Biotechnology Limited (ASX: PBT, NASDAQ : PRAN) is pleased to announce that it has reached agreement for the private placement of up to 7.15 million new shares in the capital of the Company at a subscription price of 70 cents per share. The securities have been placed to institutions and eligible sophisticated investors who are clients of Peregrine Corporate Limited (“PCL”) and the placement will raise up to $5 million before allowing for costs associated with the issue. Funds raised will be predominantly applied towards accelerating the Company’s development objectives, specifically the commencement of toxicology and clinical trials relating to Prana’s proprietary suite of metal protein attenuating compounds (“MPAC’s”) and for working capital purposes.

[Bullebio]

@ all

welche markt cap hat prana biotech??
oder wieviele aktien sind im umlauf??

danke

[Neoe]

Die Marktkapitalisierung liegt jetzt bei etwa 40-45 Millionen Euro, allerdings ist da schon die komplette Verwässerung miteinberechnet, also beeinhaltet alle ausstehenden Optionen.

Zur Info: Prana hat noch ein Optionsprogramm laufen, dass den Optionshaltern noch bis Dezember 2004 die Möglichkeit gibt diese zum Preis von 0,5 AUD in Aktien zu konvertieren. Ich weiss die genaue Zahl nicht mehr aber es dürfte sich um 12-20 Millionen Optionen handeln.

[Neoe]

Hier nochmal zur genaueren Info die Überschriften der News von 2003, besonders hervorzuheben ist die Einigung mit Schering:


5 September 2003
Prana Raises $5 million - Private Placement Of Shares To Institutional and Sophisticated Investors

5 August 2003
New Alzheimer`s Drug Enters Development Track
Phase I Clinical Trials scheduled for 2004



14 May 2003
Independent Industry Expert Recommends Prana


5 May 2003
Prana Awarded Australian Government Grant


14 April 2003
Prana investigators co-author Lancet article on "Novel findings in the eyes of alzheimer`s disease patients"


1 April 2003
Prana Executive Chairman Invited to Present at Salomon Smith Barney’s Forthcoming Micro Cap Conference


28 March 2003
DR. BUSH CO-AUTHORS ARTICLE ON ‘NOVEL THERAPY
FOR PARKINSON’S DISEASE’



18 March 2003
Prana Announces Commercial Collaboration with Schering A.G.
And Neuroscience Victoria on Diagnostics

Continuing Commercial Validation Initiative for 2003
18 March 2003

Prana Announces Commercial Collaboration with Schering A.G.
Melbourne, Australia – March 18, 2003 – Prana Biotechnology Limited (NASDAQ: PRAN; ASX: PBT), the Australian biotechnology company, announced that Schering A.G. (FSE: SCH, NYSE: SHR), Germany, will fund and license discoveries on new drug targets, especially in the area of diagnostics, in an agreement with Prana Biotechnology and Neuroscience Victoria. The commercial arrangements are subject to ongoing confidentiality, but will provide up to $7.5 million of funding for new discovery research over the life of the projects, with additional milestone payments and royalties from discoveries.

Dr. Ross Murdoch, Prana`s Chief Operating Officer, said, "Through Prana’s efforts in the area of neurological diseases we have identified multiple potential diagnostic and therapeutic targets which we believe worthy of exploration. Our commitment is to continually strengthen the technological base of the company through in-house and collaborative research; increasing the possibility of success and in turn lessening our reliance on any single technology. This collaboration with Schering A.G. is inline with our commitm ent and will allow funding of additional exciting technologies that although separate, complement our existing premier platform technology based on the Metal Protein Attenuating Compound ("MPAC") class of compounds. This collaboration will expand Prana’s project areas bringing significant additional funding and scientific expertise into the company’s laboratories.”

“In addition to this partnership with Schering A. G.,” Dr. Murdoch continued, “the company continues to be engaged in very positive, dialogue w ith a number of other global pharmaceutical companies regarding future collaborations around our MPAC platform technology. The success of our most recent Phase II human trials has fuelled excitement in the possibility that the MPAC class can provide novel Alzheimer’s disease therapies. The potential for this class to provide therapeutics outside AD is also looking increasingly promising.”

Commenting on the outlook for 2003, Executive Chairman Geoffrey Kempler said, "Today`s announcement with Schering is just the beginning of what we believe will be a series of announcements on collaborative and commercial deals to move our innovative and proprietary technologies closer to reality. Schering and our scientific management have a history of strong collaborative success, and we believe they are a logical partner to extend our reach into novel drug targets and innovative diagnostic technologies. We anticipate that the next collaboration to be announced by the company will be around developments arising from our most recent human clinical trials."

"In the last 12 months,” Mr. Kempler noted, “we have brought our MPAC technology to the point of commercialization, and now, in collaboration Schering A.G., we are going to extend our reach into the field of diagnostics and other drug targets. We are on track for 2003 benchmarks, and have as our top priority for the year "continuing commercial validation" of our neurodegenerative disease theory.”


N E W S R E L E A S E
NeuroSciences Victoria (NSV) is an organization of the Universities of Melbourne and Monash, established to promote commercialization of discoveries emanating from Victoria universities and medical research institutes. The CEO of NSV, Dr William Hart, said "The Schering collaboration is a major accomplishment, resulting in a deal which will have long term benefits for all the parties involved".

Prana`s current focus is the commercialization of its treatment for Alzheimer`s and other neurodegenerative disorders. The worldwide market for these products is approximately $5 billion. Prana’s scientists at Harvard Medical School and the University of Melbourne are pioneers in a global effort to develop treatments for these diseases. Prana has completed
Phase II clinical trials with its lead compound, PBT-1, and demonstrated proof of concept. Prana also recently announced that Dr. Ashley Bush, M.D., PhD, of Massachusetts General Hospital in Neurology and founding scientist to Prana has been elected by his peers in the American Academy of Neurology to be a recipient of this year’s Potamkin Award. This award recognizes major contribution to the understanding of the cause, prevention, treatment of and eventually the cure for Pick’s, Alzheimer’s disease and other related degenerative diseases.



14 March 2003
Prana Expands Collaboration with University of Melbourne


13 March 2003
Prana’s Chief Scientific Advisor Wins 2003 Potamkin Award for Alzheimer’s Disease Research


3 March 2003
Prana Announces Strong Demand for Options


11 February 2003
Prana Biotechnology Limited today announced that the management held a conference call yesterday to discuss the Company’s recent achievements and goals for 2003 and further progress since the AGM

[Neoe]

Der Jahresbericht:

http://www.asx.com.au/asxpdf/20030912/pdf/3j0hqggp5vqwx.pdf


Meiner Meinung nach hochinteressant. Wie herauszulesen ist hat man PBT-1 noch nicht abgeschrieben, aber es bestehen weiterhin Patentstreitigkeiten. Sollte man PBT-1 tatsächlich 2004 in die Phase III bringen, schaut sich Prana die Börsenwelt von oben an. Wenn nicht muss man auf PBT-2 warten und der Erfolg wird nur noch größer sein.

Noch einmal: Vermutlich das einzige tatsächliche Heilmittel gegen Alzheimer.

[Neoe]

Kleiner Auszug aus einem interessanten Artikel. Aus dem Text resultiert nichts anderes als die Tatsache, dass PRANA auf dem Radar der Pharamariesen in übergrösse erscheint:


GUEST COMMENTARY



Beyond the Blockbuster



.....But drug company executives, facing soaring costs and other hurdles, have pinned their growth strategies on new blockbuster drugs (meaning annual sales of $1 billion or more). Such drugs, increasingly rare, must be usable by large patient populations and be effective against widespread illnesses that require long-term medication, such as cancers or chronic degenerative diseases. .........



John Rhodes ([e-mail]) is the managing partner for Deloitte & Touche`s Life Sciences Practice

[Neoe]

Australian Government Supports Prana`s Drug, PBT-2, With AU$1.35 Million Start Grant
Wednesday February 18, 10:19 am ET


MELBOURNE, Australia, Feb. 18 /PRNewswire-FirstCall/ -- Drug development company, Prana Biotechnology Ltd (Nasdaq: PRAN - News; ASX: PBT - News) has been awarded a second R&D Start grant of AU$1.35m to take its second generation drug candidate for Alzheimer`s Disease, PBT-2, through safety testing and Phase I clinical trials.
ADVERTISEMENT


The competitive R&D Start grants, which are subject to close peer scrutiny, are made through the Australian Government`s business unit, AusIndustry, and the Industry Research and Development Board.

Prana will use the grant to fund ongoing formal toxicology testing program and early human trials of its promising new compound, PBT-2, for the treatment of Alzheimer`s Disease. Phase I clinical trials are scheduled to begin in late 2004.

Geoffrey Kempler, Executive Chairman of Prana Biotechnology said, "Alzheimer`s Disease is a terminal, malignant disorder with no cure. Not only does Alzheimer`s undermine the quality of life of patients and their families but it is also a substantial burden on our health system. This funding will enable Prana to accelerate the development of PBT-2 as a much-needed treatment for patients with this terrible disease."

"This is our second R&D Start grant. The first contributed to the design and synthesis of more than 200 new compounds, of which PBT-2 showed the most promise as a lead. Our first generation compounds provided us with initial clinical proof of concept and all findings with PBT-2 to date indicate that it has more desirable properties," Mr. Kempler said.

Prana`s pipeline of compounds targets neurodegenerative conditions in which metals bind to proteins. This binding leads to changes in structure of proteins, interfering with their function. In the case of Alzheimer`s Disease, much of the damage is associated with aberrant build-up of the protein, amyloid beta.

Prana`s compounds, called MPACs (metal protein attenuating compounds), bind specific metals such as copper, zinc and iron to decrease the interaction of these metals with proteins. Prana has shown with similar compounds to PBT-2 that MPACs have beneficial effects on amyloid beta formation, both in animal models of disease and in humans.

Prana`s progress in developing its pipeline received a boost late last year with the publication in the specialist journal Archives of Neurology of positive findings from the initial clinical trial of the company`s first generation MPAC for the treatment of mild to moderate Alzheimer`s Disease.

About Alzheimer`s Disease

Alzheimer`s Disease (AD) is the most common form of dementia, a brain disorder that seriously affects a person`s ability to carry out daily activities, among older people. AD involves the parts of the brain that control thought, memory, and language.

It is a malignant disease which, like malignant tumours, becomes progressively worse and results in death. Alzheimer`s usually begins after age 60 and risk goes up with age. It is uncommon for younger people to get AD. About 5 percent of men and women ages 65 to 74 have AD, and nearly half of those age 85 and older may have the disease. It is important to note, however, that AD is not a normal part of aging.

About Prana Biotechnology Limited

[Neoe]

In die Drugs.to-watch-Liste von Forbes aufgenommen worden:

http://www.forbes.com/sciencesandmedicine/2004/01/26/cx_mh_r…

[BrauchGeld]

Hi neoe

Hab mir die Aktie gekauft zu 4€ .Ich hoffe das ich nicht die falsche gekauft habe.
Jetzt meine frage warum gibt es dazu zwei wkn (753907) 3,5€
und (937103) 0,38 € ?
Und wie siehst Du das Chance/Risiko verhältnis ?

Vielen Dank

Grüsse
B.M.

[puhvogel]

Das ist die richtige Einstellung. Erst kaufen, dann fragen, wozu das gut ist.

Die Aktie hat eine Marktkapitalisierung von 34 Millionen $, da kaufst du pures Risiko, das im positiven Fall des Markteintritt extrem hohe Renditen erwirtschaftet, gerade bei solchen Blockbuster-Indikationen. Der Markt schätzt, gemessen an der Marktkapitalisierung, die Erfolgschancen scheinbar nicht hoch ein, aber der Markt irrt auch mal gerne.
Vergiss 937103, nimm die 753907, eine ADR, die 10 Aktien zusammenfasst und in New York gehandelt wird, d.h. Du kannst die Aktien im Notfall auch dort wieder loswerden.

[BrauchGeld]

PRAN

Name: Prana Biotechnology
Listed on: Nasdaq
Pick price: 4.60
Pick Date: March 30, 2004

2 month chart

Breaking out of base

Profile:

This week we bring you Prana Biotechnology. Prana develops therapeutic drugs designed to treat the underlying causes of brain and eye degeneration as a result of the aging process. The Company develops therapies for a broad spectrum of age-related diseases initially focused on Alzheimer`s disease. The Company`s initial product, PBT-1, is a therapeutic treatment for Alzheimer`s disease. In early August 2003, the Company announced a new lead metal protein attenuating compound (MPAC) molecule for Alzheimer`s disease designated as PBT-2 that had been selected to enter development. PBT-2 has undergone preclinical in-vitro and in-vivo testing and has been designed to have an improved safety and efficacy profile compared to PBT-1.

On March 26 th Prana Biotechnology was added Forbes Neurological Drug Watch List, highlighting the most promising experimental drugs to treat diseases of the brain and nervous system. On February 25 th , Professor Ashley Bush, MD, PhD, signed a 10 year consultancy agreement with Prana. The Forbes article described Professor Ashley Bush as a “provocative scientist”, whose approach to treating Alzheimer`s Disease is distinct from that of most big drug companies. Dr. Bush argues that copper and zinc interact with proteins in the brain (beta-amyloid) to make them toxic.

For the fiscal year ended 6/30/03 , Prana`s revenues rose from $448 thousand to $1.2 million. Net loss accord. to U.S. GAAP fell 31% to $2.2 million. Revenues reflect increased government grant and corporate partner revenue. Net loss was partially offset by increases in employee benefit costs and other expenses.

Prana`s recent chart action shows strong buying interest. On Thursday, Prana broke out of its $4 base area, followed by a two day shakeout. As of this morning, Prana gapped up, signaling that the shakeout may have ended, pushing Prana closer to the $5 resistance level. This positive action also acts as a follow through, and could signal the beginning of a longer-term upward trend. Another point of interest will be the $5.50 area, where Prana peaked in December, 2003.

The recent news releases confirm that Prana is proactively pursuing success in Biotechnology and is a great candidate for the iseegreen.com pick of the week.. Alzheimer drugs are still quite primitive in their effectiveness. If Prana can deliver a breakthrough in this field, it could open a door to billions in annual revenue, turning Prana into a major Biotech force.

Iseegreen.com`s stock profiles should not be used as the sole justification for a trading decision. Always do your own due diligence before investing in any stock. Please read our full disclaimer.

Iseegreen.com wishes you all the best success in your stock trading. Have a great week!

[Neoe]

Bis Dezember wird das Ding Probleme haben abzuheben, da noch 20 Millionen Optionen in Umlauf sind. Danach wird allerspätestens die Post abgehen.

Was aber für dieses Jahr keiner auf der Rechnung hat, ist die Zusammenarbeit mit SCHERING, die zu einer Diagnosemöglichkeit für Alzheimer führen soll. Ein Zwischenbericht ist bereits angekündigt worden. Sollte sich hier ein Durchbruch andeuten, wird Prana bereits früher gen Norden laufen als erwartet und zwar heftig.

[Neoe]

Nochmal für alle:

Nach Dezember werden zwischen 80 und 90 Millionen Aktien im Umlauf sein, je nachdem wieviele Optionen umgewandelt werden. Bei dem derzeitigen Kurststand würde dies eine Mkap. von ca. 35-40 Millionen Euro bedeuten.

Wer an PRANA-Aktien interessiert ist, sollte sie in Amerika ordern. Kürzel: PRAN (NASD-Smallcap-listing)

[BrauchGeld]

Hi Neoe

Hab ein paar fragen :

1.Wieviel cash besitzen die noch ?
2.Wie lange reicht cash aus?
3.Wie hoch ist die Chance das Medikament auf den Markt zu bringen ?

Vielen Dank

Gruss
B.M.

Ps:Was denkst Du über Biosante sollte man halten oder verkaufen sind nämlich nur noch am fallen ?

[Neoe]

brauchgeld:

Zu Biosante kann ich nur sagen mindestens halten, wer Geld hat unbedingt nachkaufen. Alles unter 4.20 $ ist ein Scherz. Hier sind ebenfalls Optionen fällig. Irgendwann im Mai. Kann also schon noch weiter runter gehen, wird aber die derzeitgen Levels zukünftig locker überflügeln.

Zu Prana:

1.Ohne nachzuschauen (sorry ist schon spät) würde ich sagen rund 6-7 Mio. AUD (+START-Grant von einer guten Million für PBT-2)Außerdem fließt von Schering Geld, jedes Jahr wohl so ca. 1,5 Mio AUD + potentielle Meilensteinzahlungen oder später Einnahmebeteiligungen.

Jedenfalls wird hier in Zukunft wohl noch anderes Geld gebraucht, teilweise wird das durch das Geld, das durch die Optionsumwandlungen reinkommt, geschehen.

2.Die obige Konstellation macht eine Vermutung schwer, Prana macht sich für 2005 zumindest öffentlich keine Sorgen. Scheint mir aber plausibel, das Prana 2005 locker durchhält ohne viel in die Wege zu leiten.

3.Wenn ich das nur wüsste. Ich gehe natürlich von guten Chancen aus. Da der Vorgänger von PBT-2 alle klinischen Hürden genommen hat, obwohl das Medikament bei weitem nicht so leistungsfähig und sicher ist, wie PBT-2 nach ersten Erkenntnissen sein soll, ist die Hoffnung berechtigt.
Anm.:PBT-1 wird/wurde?? aufgrund von Patentstreitigkeiten aufgegeben.

[puhvogel]

@Brauchegeld:
Der Ansatz ist auf jeden Fall kein Quatsch oder ein Dummpush, das kann man schon daran feststellen, dass die australische Regierung eine Art Anschubfinanzierung gegeben hat.

Über die Erfolgsaussichten kann man wenig sagen, da man noch zu wenig weiß wie genau Kupfer mit der Alzheimerentstehung zusammenhängt. Immerhin gab es im Januar im Lancet, eine der 5 wichtigsten medizinischen Journale der Welt, einen artikle über die Rolle von Kupfer bei Alzheimer.

Für meinen Geschmack hat die Aktie allerdings zur Zeit zu viel öffentliche Beachtung durch Forbes und Co., um sie gerade jetzt zu kaufen.

[BrauchGeld]

Als allererstes ein Dankeschön an Neoe.

Hi Puhvogel

Warum ist es ein schlechter Zeitpunkt für den Einstieg ?
Ist doch gerade mal ca.30% über 52w tief.
Und ausserdem kann beachtung der Aktie nur helfen oder nicht ?

Grüsse
B.M.

[puhvogel]

Ich mag nicht kaufen, wenn etwas in der Presse, und Forbes ist nun mal weitbeachtete Presse, gefeiert oder auch nur erwähnt wird. Das lockt nur ungeduldiges Kapital, das gerne bei Kursrücksetzern wieder bestens verkauft. Das ist alles und nur auf eigene Erfahrung beruhend.
Auf die langfristigen Perspektiven hat das natürlich keinen Einfluss!

[Neoe]

Die Prana hat ein derzeitiges Verlustrisiko bis ca. 0,45-0,5 AUD. Mehr nicht. Der Kurs ist Nicht HOCH, wegen Forbes und Co., sondern so NIEDRIG wegen den ausstehenden Optionen. Wer bei Prana länger dabei ist weiss das. Beim letzten Mal (März 2003) haben die Optionshalter den Kurs auch schon Monate vorher auf Richtung 0,5 AUD getrieben. So ist es auch dieses Mal, mit dem Unterschied, dass wir heute von 20 Millionen und nicht von 7 Millionen Optionen reden.

Ernsthafte Kursbewegungen werden nur durch sehr positive bzw. sehr negative News, die die Geschäftsgrundlage in Frage stellen, ausgelöst werden. Ansonsten wird Prana immer wieder auf ca. 0,50 AUD gehen.

[puhvogel]

Wo liegt denn der Strike der Optionen?
Auf der ASX-Seite steht nämlich nix über Warrants oder options...
Dito im Halbjahresbericht.
http://www.asx.com.au/asxpdf/20040225/pdf/3krn4sdbkl2gt.pdf
Der Kurs reagierte sehr wohl mit Kurs- und Volumensteigerungen auf die Forbes-Geschichte:

[Neoe]

Puhvogel:

Geh mal auf die Prana-Homepage und schau der die Jahresabschlüsse an, am besten den von 2001, dort wird alles sehr schön aufgelistet und übersichtlich präsentiert,insbesondere die Optionsfragen lassen sich so leicht klären.

Zu Kursbewegungen:
Der Kurs reagiert natürlich, aber in einer sehr engen Spanne, wenn man sich anschaut, welche bisher bleibenden Kursveränderungen manche Wertpapiere im letzten Jahr durchgemacht haben, viele ohne große News, sondern nur als Kurskorrektur, dann wird dir wohl am Prana-Chart spätestens was auffallen.
Und wohlgemerkt hatte Prana sogar einige gute News zu vermelden, die den Kurs hätten ebenso steigen lassen können, wie bei vielen anderen Papieren und keine wirklich schlechten (die Entscheidung PBT-1 nicht weiterzuentwickeln, ist?/war? abzusehen).

[puhvogel]

Wieso 2001? Wir haben das Jahr 2004!
Vielleicht sind die Optionen eingelöst, gelöscht oder umgewandelt, woher soll ich das wissen?

Der Kurs reagiert natürlich, aber in einer sehr engen Spanne, wenn man sich anschaut, welche bisher bleibenden Kursveränderungen manche Wertpapiere im letzten Jahr durchgemacht haben, viele ohne große News, sondern nur als Kurskorrektur, dann wird dir wohl am Prana-Chart spätestens was auffallen.

Na da kann ich dich aber mit Myriaden von Gegenbeispielen überschütten, gerade bei den Smallcaps.

Und wohlgemerkt hatte Prana sogar einige gute News zu vermelden, die den Kurs hätten ebenso steigen lassen können, wie bei vielen anderen Papieren und keine wirklich schlechten (die Entscheidung PBT-1 nicht weiterzuentwickeln, ist?/war? abzusehen).

Und wenn das führende Produkt fallen gelassen wird, ist das nie ein gute Nachricht! Und wieso hast du das im Vorfeld gewußt, wenn schon die Chefs von Prana im Vorfeld nicht wußten und weiter Geld in Studien über PBT-1 investierten?

[Neoe]

puhvogel:

Anscheinend hast du keinerlei Background-Infos, sonst wüßtest du, dass die Patentstreitigkeiten um Clioquinol (PBT-1) von Anfang an bekannt waren. Schon einige Zeit vor Bekanntgabe von PBT-2 wurde in diversen ResearchReports berichtet, das Clioquinol wahrscheinlich nur zum Proof-Of-Concept weiterentwickelt wird, was ja schließlich so war. Durch Die Studien PhaseIIb hat Prana schließlich das PeerReview in einem hochangesehenen Journal erreicht, unerlässlich um wissenschaftliche Anerkennung zu erlangen.
Im Übrigen soll Clioquinol durchaus weiterentwickelt werden, aber falls dies geschehen sollte wohl nur mit öffentlichen Einrichtungen, da es sich für Pharmakonzerne aufgrund der Rechtssituation /Sicherheitsrisiken nicht lohnen wird. Erhebliches Interesse öffentlicher Einrichtungen wird im Jahresbericht 2003 bestätigt

Bei den Kursveränderungen liegt die Feinheit darin, daß sie weder richtig steigt, noch wesentlich unter 0,50 AUD fällt und wenn nur kurzfristig. Aber eigentlich brauchen wir über den Kurs an sich nicht zu reden, Biotech bedeutet immer Langfristinvest, wenn man durch fundamentale Daten, nicht durch kurzfristige Hypes verdienen möchte.


Anscheinend hast du dir leider nicht ein einziges Mal die Mühe gemacht dich im Detail über eine Aktie zu informieren zu der du regelmäßig Dikussionbeiträge lieferst (die ich trotzdem gerne beantworte). Hättest du dir die Jahresberichte durchgelesen und vor allem den aktuellen von 2003, wüßtest du wie die Situation ist, z.B von PBT-1, aber auch von den OPTIONEN her. ES STEHEN NACH WIE VOR ÜBER 21 MILLIONEN ZUR AUSÜBUNG AUS, DAVON FAST EXAKT 20 MILLIONEN FÜR DEZ.2004

[Neoe]

Hier gleich der Link zum JA 2003:

http://www.pranabio.com/downloads/PBT_AR_2003.pdf

[puhvogel]

Na das ja schon mal ein Ansatz statt hier IMMER SO LAUT UND SINNLOS HERUMZUBRÜLLEN.
Den Hinweis, dass ich mich nicht informiert hätte ist eine Frechheit, weil du mit dem Hinschreiben einer simplen Zahl 0,5 AUS $ meinen Wissensdurst hättest befriedigen können. Wenn ich alles durchgelesen hätte, bräuchte ich auch nicht zu fragen, oder? "Ein weiß nicht, aber stand im letzten Jahresbericht" hätte vielleicht auch gereicht.

Stattdessen erzählst du lang und breit das wieder, was die 6 Leute auf ihrem Jahresrückblick alles so schreiben, ohne den Inhalt richtig zu verstehen. Sonst kämst du mir nicht mir einer 2001 Bilanz oder du würdest nicht vom "Peerreview- in einem hochangesehenen Journal erreichen" sprechen, das ist nämlich doppelt gemoppelt. Dieses Journal ist übrigens das "Archives of Neurology" mit einem impact factor von 4.

Wenn sich Prana mit einem Konkurrenten um die Patentrechte streitet, und diese Konkurrenz später die Patente bekommt, dann wäre das schlecht für Prana, dass sie mit ihrem Geld die Erforschung eines Konkurrenzproduktes finanziert haben. Solche Späße kosten immerhin Geld.
Für die näherer Zeit bleibt der Kurs wegen der Arbitrageverkäufe wohl gedrückt.

[BrauchGeld]

Puhvogel nun sei nicht so.
Ich finde Neoe macht sehr gute arbeit.
Seine Threads zu einigen Werten sind wirklich sehr Informativ.


Grüss
B.M.

[greenhorn1998]

Hallo zusammen!

Prana startet ja heute so richtig durch, zumindest in den USA. Hier die dazu passende Meldung:


"Journal of Neuroscience Paper Further Validates Prana Science
Wednesday April 7, 10:04 am ET

MELBOURNE, Australia, April 7 /PRNewswire-FirstCall/ -- Prana Biotechnology Ltd. (Nasdaq: PRAN - News; ASX: PBT - News), today announced the publication of a new paper in the current edition of Journal of Neuroscience. The results further support Prana`s theory that metals in the brain, rather than proteins on their own, are responsible for the pathology of Alzheimer`s Disease and that attenuating the action of these metals may hold the key to effective therapeutic intervention.
ADVERTISEMENT

It is known that zinc reacts with amyloid beta to cause the amyloid plaques around nerve endings in Alzheimer`s disease. The role of zinc in the formation of damaging amyloid plaques in blood vessels supplying the brain has, up to now, not been clear.

Amyloid deposits in arteries cause damage to the blood vessel wall resulting in impaired blood flow. If these deposits occur in arteries that supply blood to the brain then this may starve the brain tissue of oxygen compounding the dementia associated with Alzheimer`s Disease.

This Journal of Neuroscience article demonstrates that zinc plays a central role in the formation of amyloid plaques not only at the nerves but also in the blood vessels of the brains of people with Alzheimer`s Disease.

Prana`s scientific consultants produced a mouse model which lacked a protein from nerve endings that transports and mediates the levels of zinc in the nerves and surrounding tissue. They observed that not only did the blood vessel walls in the brains of these mice have lower levels of zinc, but with less zinc there is also significantly fewer amyloid deposits. These new results show that the same zinc responsible for toxic amyloid deposits around nerves is also responsible for causing amyloid deposits in blood vessels.

Dr. Ashley Bush, chief scientific consultant to Prana, and senior author on the publication explained; "These findings strongly support the suitability of Prana`s MPAC* class of drugs for targeting amyloid deposits in Alzheimer`s disease, both in the blood vessels in the brain and in the brain tissue around the nerve endings.

"It is yet another piece of evidence that attenuating the interaction of metals and amyloid protein could be beneficial in treating Alzheimer`s Disease," said Dr Bush.

Prana`s MPAC technology is designed to attenuate the interaction of zinc and amyloid protein in the brain of patients with Alzheimer`s Disease.

To view the abstract on the Journal of Neuroscience website please visit: http://www.jneurosci.org/cgi/content/abstract/24/13/3453

Background: Amyloid beta and amyloid plaques

Prana`s MPACs (metal protein attenuating compounds) are chemicals that bind zinc and copper, and have been shown by Prana to lower the levels of amyloid beta and the associated toxicity in the brains of transgenic mice used as a model of Alzheimer`s Disease. Prana`s scientists first described the metal-based structure of the beta amyloid
The brains of patients with Alzheimer`s Disease are affected by the chemical changes associated with the formation of `clumps` of amyloid beta (plaques) near and around nerve endings and in blood vessels, particularly in the areas used for memory and other cognitive functions. The normal form of amyloid beta is soluble, but in Alzheimer`s Disease, the protein comes out of solution to become a major component of insoluble amyloid plaques. Inappropriate accumulation of amyloid beta in the brain is intimately associated with the loss of neuronal function causing the dementia.

Metals, also a component of the brain, have chemical roles in the development and progression of plaque formation. Abnormal binding of zinc to amyloid beta leads to protein clumping. Abnormal binding of copper to amyloid beta can lead to the formation of hydrogen peroxide through oxidative reactions. Hydrogen peroxide is toxic to brain cells.

Experimentally, the amyloid can be dissolved by the use of metal-binding chemicals such as clioquinol that specifically reverse the copper and zinc interaction with amyloid beta.

About Prana:

Prana is a Melbourne-based biotechnology established in 1997 to commercialize research into Alzheimer`s disease and other major age-related degenerative disorders (Nasdaq: PRAN - News; ASX: PBT - News). Prana`s technology was discovered by the company`s researchers at prominent international institutions including Massachusetts General Hospital at Harvard Medical School, the University of Melbourne and the Mental Health Research Institute in Melbourne.

Source: Prana Biotechnology Ltd.

Ich bin nicht investiert, an solchen Tagen natürlich nicht so schön Bin gespannt, ob die Bewegung nachhaltig ist, oder ob es im Laufe der Wochen und Monate wieder konsolidiert. Habe mich noch nicht wirklich intensiv mit Prana beschäftigt, klingt aber sehr vielversprechend. Mal sehen, wie ich mich verhalte.

Gruß, greenhorn

[BrauchGeld]

Hurraaaaaaaaaaaaaaaaaaa es geht aufwärtsssssssssssssssssss


Neoe wann ungefähr dürfte bei Biosante die Zulassung erfolgen ?

Gruss
B.M.

[Neoe]

greenhorn:

Schön dich hier zu sehen, bist du bei Prana dabei oder verfolgst du die Aktie nur aus Interesse ?


puhvogel:

Hab keine Lust mich mit dir lange rumzustreiten, du hast bisher nix produktives beizutragen und diesem Stil scheinst du treu bleiben zu wollen.

[greenhorn1998]

Hi Neoe!

Ich verfolge die Aktie bislang nur aus Interesse und bin beim heutigen Anstieg leider nur als Zuschauer dabei. Naja, was will man machen. Dachte, ich hätte mit einem Investment noch ein bisschen Zeit, die ich nutzen könnte, um mich noch ein bisschen schlauer zu machen.

Bin durch deine Postings aufmerksam geworden und finde die Prana-Story sehr interessant. Was hälst du von dem heutigen Anstieg und wie schätzt du die Aktie mit der Meldung kurzfristig ein?

Sollte eine Erfolgsstory anstehen, sind diese Kurse langfristig sicher noch immer spotbillig. Ich weiß noch nicht, wie ich mich verhalten soll. Werde am Ball bleiben, vorerst wahrscheinlich noch an der Außenlinie. Vielleicht eine Konsolidierung abwarten?

Gruß, greenhorn

[BrauchGeld]

Wowwwwwwwwwwwwwwwwwwwwwwwwwwwwwwwwwwwwwwwwwwww
fast 100 % wahnsinnnnnnnnnnnnnnnnnnnnnnnnnnnnnn

Neoe soll man jetzt gewinne mitnehmen und eventuell später wieder einsteigen ?

Danke

Gruss

[Neoe]

Hab die Hälfte für 8,3 Dollar verkauft. So bin ich, wie auch immer es laufen sollte, auf der sicheren Seite. Ein (fast) 100%-Anstieg geht selten ohne größere Konsolidierung vor sich. Allerdings ist die NAchricht von heute nicht von schlechten Eltern. Werden Bushs Forschungsergebnisse,anstatt wie bisher als Schrott, als wertvoll eingestufft, könnt dies für den Pranakurs unabsehbare folgen haben. Niemand in der großen weiten Pharmawelt wäre auf diesen revolutionären Wandel in der Alzheimerforschung vorbereitet, außer Prana selbst eben: Mit ihren MPACs

[greenhorn1998]

Hi!

Ich gehe fest von einer Konsolidierung aus, auch wenn die News wirklich gut sind. Mal sehen, wie das Echo ist. Beruhigt sich die Nachrichtenlage, wer weiß, vielleicht sehen wir die "5" wieder vor dem Komma.

Wahrscheinlich nicht, aber ich habe etwas gegen fahrende Züge (erst recht mit dieser Geschwindigkeit) wenn ich nicht drinsitze. Aufspringen sehr gefährlich, lieber ein kleines abbremsen abwarten. Wie auch immer.

Gruß, greenhorn

[meislo]

Wall Street Journal Article Profiles Challenges for Alternative Alzheimer`s Researchers
Monday April 12, 10:28 am ET


MELBOURNE, Australia, April 12 /PRNewswire-FirstCall/ -- Australian drug development company Prana Biotechnology Limited (Nasdaq: PRAN - News; ASX: PBT - News) announced today that an important article appearing in the April 9th, 2004 edition of The Wall Street Journal has shed further light on the difficulties facing researchers of Alzheimer`s Disease that differ from the prevailing "amyloid hypothesis."
ADVERTISEMENT


The story serves as a follow-up to a feature profile of Prana Biotechnology`s Chief Scientist Professor Ashley I. Bush, M.D., Ph.D., of Harvard Medical School, which ran in The Wall Street Journal on December 26, 2003. In that article, Dr. Bush discussed his many challenges in gaining peer acceptance of his theories. His revolutionary work on brain zinc and copper interactions causing amyloid pathology was eventually recognized by his peers last year when he received the prestigious Potamkin Prize from the American Academy of Neurology. This work is the scientific platform behind Prana`s MPAC drug class, which showed benefit in a phase 2 clinical trial published last year.

The current article chronicles another Harvard Medical School team, that was able to shut down two mouse genes whose human forms have been linked to inherited forms of Alzheimer`s. Against the advice of the lead researcher`s mentor, the scientists submitted their findings to two leading journals, only to face a long list of criticisms that took months to address. "Powerful people in this field think that amyloid causes Alzheimer`s and won`t consider research that questions the amyloid hypothesis," said one of the Harvard scientists. In total, the publication of this potentially important paper was delayed nearly two years.

The difficulties such researchers face in introducing new theories to the Alzheimer`s debate has been gaining in recognition. In the article, Zaven Khachaturian, who ran research at the National Institute of Aging, said, "Whenever you have a field with limited funding, and a small number of people with big egos who have everything invested in one idea, you have the right chemistry for one theory to become so pervasive nothing else can flourish." Khachaturian added that the dominance of the amyloid hypothesis and the strangling of alternatives was "one of the most important issues in science today."

To obtain a copy of the story, contact The Anne McBride Company at 212-983-1702 ext. 212.

About Prana

Prana is a Melbourne-based biotechnology established in 1997 to commercialize research into Alzheimer`s disease and other major age-related degenerative disorders (Nasdaq: PRAN - News; ASX: PBT - News). Prana`s technology was discovered by the company`s researchers at prominent international institutions including Massachusetts General Hospital at Harvard Medical School, the University of Melbourne and the Mental Health Research Institute in Melbourne.

[Neoe]

Mal sehen, ob das auch mal zu weiteren Kooperationen für Prana führt.

Sollte Bush wirklich den richtigen Ansatz verfolgen (ich persönlich bin davon überzeugt), wäre das der heilige Gral der der Behandlung neuro-degenerativer Krankheiten.
Der Novartis-Chef hat ja Bush im Falle eines Falles schon als Nobelpreisträger im Visier.
Da die großen Pharmas also mit Sicherheit schon was von Prana gehört haben, muß doch mindestens mal einer darauf kommen, sich auf PBT-2 eine Option geben zu lassen. Das wäre das Mindeste. Wer kann sich in dr Pharmabranche erlauben ein Medikament, das ein Potential von 5 Milliarden Dollar jährlich hat, sich vielleicht wegschnappen zu lassen.

[BrauchGeld]

Hi Neoe

Weißt Du vielleicht wann etwa Phase 3 beginnt ?

Danke

Gruss
B.M.

[Neoe]

Ob und wann es zu einer Phase III von PBT-1 kommt, ist schwer zu sagen.
Wie ich aber schon mal sagte, wird es wohl keine Phase III
in Zusammenarbeit mit einem großen Pharmaunternehmen geben, sondern wenn dann mit einer öffentlichen Einrichtung und vielleicht mit der finanziellen Unterstützung eines Verbandes.

[BrauchGeld]

Danke Neoe

Wie auch immer ich wünsche allen investierten viel Glück mit der Aktie.

Grüsse
B.M.

Ps:Neoe welche Biotech Aktie kannst Du besonders empfehlen ? Danke

[Neoe]

BioSante und Antisoma . Es gibt zwar noch einge andere, die vielleicht sehr kurzfristig noch mehr Kurspotential haben, aber diese beiden Aktie werden in 2004 auf jeden Fall zu den Granaten gehören (oder natürlich zu den großen Verlierern, aber eher unwahrscheinlich). Jedenfalls weisen beide schon etwas Substanz vor, also nicht der ganz große Zock.

[Neoe]

Außerdem finde ich Theratech(aus Kanada) interessant. Bin schon seit ein paar Wochen dabei, da ich auf den Abschluss der PhaseII ihres wichtigsten Medikamentes wartete. Morgen kommen Ergebnisse.

Ich werde morgen aber einen Theratech-Thread eröffenen, dann mehr zu den enormen Chancen und zu den Risiken.

[BrauchGeld]

Gude Neoe

Scheinst denselben Geschmack zu haben.
Theratechnology hab ich auch vor paar Wochen gekauft .
Apropo Theratech wie wertest Du die Daten die gestern rauskamen ?

Grüsse
B.M.

[greenhorn1998]

Moin!

Mit Prana ging es in Australien heute weiter bergauf. Deutlich, auch wenn die größten Gewinne nicht gehalten werden konnten. Folgende News auf der Webseite:

16 April 2004

Prana’s Alzheimer’s drug shows continued promise in extended clinical trial
Melbourne, Australia – Friday April 16, 2004: Professor Colin Masters, a Director of Prana Biotechnology Limited (NASDAQ: PRAN, ASX: PBT) and Chairman of the Company`s Scientific Advisory Board, today will present data from the extended Phase II trial of Prana’s drug, PBT-1, at the 8th International Springfield/Montreal Symposium on Advances in Alzheimer`s Disease.
At a session devoted to novel treatments of Alzheimer’s disease, Professor Masters will report that the use of PBT-1 for 18 months markedly slowed the decline in cognitive function associated with Alzheimer`s disease compared with the predicted level of decline available from the scientific literature. In addition the longer term treatment was well tolerated.
The extension study was conducted over 48 weeks following the formal trial period of the trial of 36 weeks. Nine of the original 18 patients completed the extension.
Speaking from Montreal, Professor Masters stated that the outcome for patients in the extension study provided confirmatory and new evidence that MPACs such as PBT-1 may form the next generation of agents for the treatment of Alzheimer’s by slowing or stopping the disease rather than just dealing with the symptoms.
Dr Sam Gandy, Director of the Farber Institute for Neurosciences at Thomas Jefferson University, Philadelphia, commented: “This PBT-1 (clioquinol) extension study reaffirms the safety and possible efficacy of this new class of drug for Alzheimer`s disease. It will now be important to confirm the trend toward benefit in a larger trial with sufficient numbers of subjects to establish statistical significance.
“Overall, anti-amyloid, “plaque-busting” drugs such as PBT-1 (clioquinol) provide a powerful approach toward proof of principle regarding the relationship between amyloid and cognitive decline in Alzheimer`s disease," said Dr Gandy.
The biannual Symposium on Advances in Alzheimer`s Disease is organized by the Southern Illinois University (SIU) School of Medicine in Springfield, Illinois, the Department of Geriatrics at the Hopitaux Universitaires de Geneve, Switzerland, and the McGill University Faculty of Medicine in Montreal, Quebec.
Recently (March 26) Prana announced that Forbes.com had added PBT-1 to its list of “neurological drugs to watch”, highlighting the most promising experimental drugs to treat diseases of the brain and nervous system.
Prana also recently announced (7 April) that a publication in the Journal of Neuroscience added further support to Prana’s theory that metals in the brain, rather than proteins on their own, are responsible for the pathology of Alzheimer’s Disease and that attenuating the action of these metals, with drugs like PBT-1, may hold the key to effective therapeutic intervention.

About PBT-1
PBT-1, also called clioquinol, is an example of a Metal Protein Attenuating Compound or MPAC. It is a small molecule that binds metal ions. Due to its small size and solubility in lipid, PBT-1 is able to enter the brain from the bloodstream and bind to zinc. This action can remove the zinc already bound to amyloid beta and bind free zinc to prevent its association with amyloid beta protein.
About Prana
Prana is a Melbourne-based biotechnology established in 1997 to commercialize research into Alzheimer`s disease and other major age-related degenerative disorders (Nasdaq: PRAN; ASX: PBT). Prana`s technology was discovered by the company`s researchers at prominent international institutions including Massachusetts General Hospital at Harvard Medical School, the University of Melbourne and the Mental Health Research Institute in Melbourne. For more information about Prana, please visit www.pranabio.com

For more information contact:

Company
Geoffrey Kempler
Prana
[phone]
[e-mail]

Gruß, greenhorn

P.S.: Was haltet ihr denn von den vorgelegten Ergebnissen von Theratech? Dachte eigentlich, dass die ganz gut seien. Der Kurs hat sich aber gestern Abend wieder verabschiedet. Halte einiges von dem Unternehmen, gute Pipeline, zum Teil in weit fortgeschrittenen Stadien. Cash ist auch ersteinmal noch vorhanden, um weiterzumachen. Naja, aber das gehört ja auch nicht hierher.

[Neoe]

Bin gespannt, ob PBT-1 jetzt in die Phase III gehievt wird. Zumindest war das mehr als ein kleines Lebenszeichen, was da heut vermeldet wurde. Scheint mir als wären die öffentlichen Institutionen gefunden, die willens sind PBT-1 voranzutreiben. Immerhin kam der Kommentar, daß weitere klinische Studien erforderlich sind, von Dr. Gandy, der einer der Verantwortlichen der Jefferson University ist.

[meislo]

pran +16%

nicht schlecht

gruss meislo

[meislo]

mittlerweile + 24 % schade dass ich nur wenige aktien habe


gruss meilso

[meislo]

wird ja immer schöner, mittlerweile +36%

[meislo]

+ 50 %

[meislo]

9,99 dollar + 61%

dass geht ja schneller als man tippen kann

[Bullebio]

kurzzeitig war der kurs bei 10,30 $

schon über 120k stück gehandelt, wahnsinn!!!

[meislo]

NASDAQ GAINERLIST


http://finance.yahoo.com/mnpg?e=o

[meislo]

10:16AM Prana Biotech says drug slowed the decline in cognitive function associated with Alzheimer`s disease (PRAN) 8.30 +2.10: At a session devoted to novel treatments of Alzheimer`s disease, Professor Masters will report that the use of PBT-1 for 18 months markedly slowed the decline in cognitive function associated with Alzheimer`s disease compared with the predicted level of decline available from the scientific literature. In addition the longer term treatment was well tolerated

[meislo]

10,20 dollar + 64%



Prana stock soars on Alzheimer`s drug trial data
Friday April 16, 12:04 pm ET
By Toni Clarke


NEW YORK, April 16 (Reuters) - Shares of Prana Biotechnology Ltd (Australia:PBT.AX - News; NasdaqSC:PRAN - News) soared as much as 65 percent on Friday after it said data from a mid-stage clinical trial of its Alzheimer`s drug confirmed its safety and potential efficacy.
Data presented at a conference in Montreal showed that the drug, clioquinol, markedly slowed the decline in cognitive function associated with Alzheimer`s disease compared with levels of decline predicted in scientific literature, the company said.

Prana`s shares were up $2.68, or 43 percent, at $8.88 in midday trading on the Nasdaq, after reaching an all-time high of $10.25.

The study, conducted over 48 weeks, was a continuation of a previous study of 36 weeks. Nine of the original 18 patients completed the extension of the trial.

Colin Masters, chairman of Prana`s scientific advisory board, said the data provided new evidence that drugs such as clioquinol may form a new generation of Alzheimer`s treatments.

The trial was nowhere near large enough to establish statistical significance, nor to predict whether the results would be reproduced in a larger population. Nonetheless the compound is being closely watched in the scientific community.

The drug, introduced more than 30 years ago as an antibiotic, was taken off the market after several thousand people, mainly in Japan, developed vitamin B deficiencies that in some cases led to blindness.

Prana, which is based in Australia and holds the rights to clioquinol, has said it is no longer putting much money into its development. Instead it is trying to develop an analog that would not contain such side effects.

Researchers, however, are continuing to study the drug. So far there have been few side effects as patients are receiving vitamin B supplements.

The drug appears to work by lowering levels of a protein known as beta-amyloid that is thought to be implicated in the build-up of plaque. Most Alzheimer`s researchers believe that the cause of the disease is the formation of plaque in the brain, but that has yet to be proved.

The clioquinol researchers believe the plaque is created because the brain loses its ability to metabolize metals, particularly copper and zinc.

Clioquinol appears to work by inhibiting copper and zinc ions from binding to beta-amyloid, helping to dissolve the protein and preventing it from accumulating.

Excess copper produces hydrogen peroxide, which causes brain cells to rust and die. The cell death is caused by the rusting, not the plaque itself, they claim.

[meislo]

Durchbruch in der Alzheimer-Forschung
Ursache für Zerstörung der Gehirnzellen identifiziert

Washington (pte, 16. Apr 2004 09:15) - Ein internationales Wissenschaftlerteam hat erforscht, wie giftige Proteinablagerungen Nervenzellen in den Gehirnen von Alzheimerpatienten zerstören. Das Team um Wendy Lustbader hofft in Science, http://www.sciencemag.org dass dieser Durchbruch zur Entwicklung neuer Behandlungsansätze führen wird. Alzheimer wird mit der Bildung von Amyloid Plaquen in Verbindung gebracht. Die neue Studie hat nachgewiesen, dass diese Plaquen-Schäden durch die Interaktion mit einem Enzym verursacht werden, das in der Energieversorgung der Zellen gebildet wird. Werden diese Ergebnisse bestätigt, könnte dieses Enzym einen Ansatzpunkt für weitere Forschungen liefern.

Die Interaktion beschädigt laut BBC die Mitochondrien und führt dazu, dass toxische Substanzen in die restliche Zelle sickern. Es wird angenommen, dass das so verursachte Absterben von Zellen für die Beeinträchtigung des Gedächtnisses und andere Alzheimersymptome verantwortlich ist. Die aktuellen Forschungsergebnisse basieren auf der Analyse des Gehirngewebes von Patienten und gentechnisch veränderten Mäusen. Die Forscher hoffen, dass in Zukunft eine Blockierung oder Reduzierung der Interaktion zwischen den Amyloid-Plaquen und dem Enzym erreicht werden kann. (Ende

[karo1]

Hi, bin seit 4,15$ dabei und hatte zwischendurch ganz schön Muffesausen. Ich bin momentan aber mehr optimistisch.
Bin gespannt wo sich der nächste Boden einpendelt.

Auf gehts... Karo

[Bullebio]

die 9$ stellen einen massiven widerstand dar, auf dem weg zu 2stelligen kursen.

[Neoe]

Hi bullebio:

Der Kurs wird in Australien gemacht und pendelt sich spätestens nach zwei Handelstagen wieder ein.



http://www.asx.com Kürzel:PBT

[Neoe]

Bin im Moment nicht mehr dabei, aber trotzdem kleine Anmerkung:

Prana ist derzeit vom Handel ausgesetzt, mal sehen was rauskommt.

[Bullebio]

in australischen boards vermutet man eine kapitalerhöhung, ab mittwoch soll der wert wieder handelbar sein.

könnte vielleicht noch ein bischen nach unten gehen.

nach den news sollten vielleicht ein paar investoren interesse zeigen an dem wert!!

derzeitige market cap von ca. 43mio $

[Bullebio]

die news ist raus!!!!

Prana Biotechnology $US20m placement to US health funds


Sydney, Apr 28, 2004 (RWE via COMTEX) -- Prana Biotechnology Ltd has entered
definitive agreements with new American institutional investors for a $US20
million placement of 4 million ADRs at $US5 each.

The agreements also involved the acquisition by the investors of five-year
warrants to buy an additional 3 million ADRs at an exercise price of $US8 each,
which would raise a further $US24 million.

The transaction is to close upon shareholder approval, which is expected to be
obtained promptly.

Executive chairman Mr Geoffrey Kempler said, "These additional funds will allow
us to independently fund further trials of our MPAC technology, which has shown
early promise as a potential treatment for Alzheimer`s disease in clinical
trials.

"We intend to accelerate the development of PBT-2, our `second-generation`
product, into clinical trials planned for later this year."

Shares in Prana fell 18c to 82c today before improving to 93c.

The shares had risen from 48c last month to as high as $1.18 in April.


RWE Australian Business News


für mich ein klarer beweis, dass prana biotech ein top investment ist. die anzahl der shares erhöht sich jetzt natürlich um diese 4mio stück. die markt cap erhöht sich um 20mio$.

die gesamte markt cap beträgt nach meinem wissenstand derzeit dann ca. 63mio$. für einen blockbuster in der pipeline dürfte hier noch erheblich potential nach oben dasein.

die finanzielle zukunft und die forschungsarbeiten dürften gesichert sein.

bullebio

[meislo]

prana + 15% bei mittelmässigen umsätzen

Prana to Present at Citigroup Smith Barney Biotech Showcase
Thursday April 29, 8:30 am ET


MELBOURNE, Australia, April 29 /PRNewswire-FirstCall/ -- Prana Biotechnology Limited (Nasdaq: PRAN, ASX: PBT), today announced that the Company has been invited to present later today at Citigroup Smith Barney`s second biannual "Medtech and Biotech Bullring," in Sydney, Australia.
ADVERTISEMENT


Geoffrey Kempler, Prana`s Executive Chairman, will provide an update of Prana`s scientific and commercial milestones, including forthcoming clinical trials for its MPAC technology, which has shown early promise as a potential treatment for Alzheimer`s disease. Mr. Kempler will highlight recent data from an extended Phase II trial in patients with Alzheimer`s disease, which was presented earlier this month at the 8th International Springfield/Montreal Symposium on Advances in Alzheimer`s Disease.

About Prana

Prana is a Melbourne-based biotechnology established in 1997 to commercialize research into Alzheimer`s disease and other major age-related degenerative disorders (Nasdaq: PRAN - News; ASX: PBT - News). Prana`s technology was discovered by the company`s researchers at prominent international institutions including Massachusetts General Hospital at Harvard Medical School, the University of Melbourne and the Mental Health Research Institute in Melbourne. For more information about Prana, please visit www.pranabio.com

[Neoe]

Zum Wiedereinstieg steht Sie ca. 2-§ Dollar zu hoch, besonders gibt es da ein kleines Problem im Verhältnis ASX zu NASDAQ-Kurs. Ich hab eh keine Ahnung, wie das jetzt mit den ADRs und den Aktien in Australien läuft. Der US-Fond hat ADRs bekommen, was das bisherige Gleichgewicht aus der Angel hebt.

[meislo]

Welcome [Sign In] To track stocks & more, Register
Financial News
Enter symbol(s) BasicPerformanceReal-time MktDetailedChartResearchOptionsOrder Book Symbol Lookup







Press Release Source: Prana Biotechnology Limited


New Research Suggests Additional Role for Prana Technology Against Alzheimer`s Disease
Monday May 3, 10:06 am ET


MELBOURNE, Australia, May 3 /PRNewswire-FirstCall/ -- The Journal of Biological Chemistry has published findings by researchers for Prana Biotechnology Limited (Nasdaq: PRAN - News; ASX: PBT - News) suggesting an additional mechanism for the action of Prana`s technology in delaying the progress and severity of Alzheimer`s disease.
ADVERTISEMENT


Prana`s MPACs (metal protein attenuating compounds) have previously been shown to lower the levels of beta-amyloid in the brain -- the main component of amyloid plaques that are a feature of Alzheimer`s disease. The new research suggests that that these MPACs may also be effective in preventing beta-amyloid from attaching itself to and damaging COX-2, the key enzyme that mediates inflammation in the brain often associated with Alzheimer`s disease. Levels of beta amyloid/COX-2 complexes were found to be elevated significantly in the brains of patients with Alzheimer`s disease.

Professor Ashley Bush of Harvard Medical School and Chief Scientific Consultant to Prana was the senior author on the paper: "COX-2 has been implicated in Alzheimer`s disease, but studies of COX-2 inhibitors (anti- inflammatory drugs) have been disappointing. Our current findings explain how the interaction of beta-amyloid with brain copper corrupts the normal metabolism of COX-2 in Alzheimer`s disease. These findings further validate Prana`s MPAC drug approach, which targets the adverse metal interaction with amyloid. MPACs stop the beta-amyloid/metal complex from damaging COX-2. These findings also may explain why anti-inflammatory drugs would not be effective in Alzheimer`s disease."

An abstract of the article can be read online at

http://www.jbc.org/cgi/content/abstract/279/15/14673

[meislo]

Prana at the Rodman & Renshaw Techvest Global Healthcare Conference
Wednesday May 5, 10:28 am ET


MELBOURNE, Australia, May 5 /PRNewswire-FirstCall/ -- Executive Chairman of Prana Biotechnology Limited (Nasdaq: PRAN - News; ASX: PBT - News), Mr Geoffrey Kempler, has been invited to brief UK investors at the Rodman & Renshaw Techvest Global Healthcare Conference at Claridge`s Hotel in London on Wednesday May 12, 2004 at 8:40 AM local time.
ADVERTISEMENT


Prana is an Australian-based biotechnology company focusing on technology that has shown early promise as a potential treatment for Alzheimer`s disease and other age-related disorders. At the conference, Mr Kempler will provide an update of Prana`s scientific and commercial milestones, including forthcoming clinical trials for its MPAC technology.

Rodman & Renshaw, a leading investment bank dedicated to emerging growth companies, was recently agent for Prana Biotechnology`s US $20 million placement to US institutions and professional investors.

To arrange a one-on-one meeting with representatives of Prana Biotechnology during the conference, please contact Steven Silver at The Anne McBride Company, tel. [phone], ext 212, or [e-mail].

[meislo]

Neurological Drugs To Watch
Matthew Herper and Robert Langreth, 04.29.04, 2:00 PM ET

NEW YORK - The brain is a gold mine for drug companies. After all, some 20 million Americans suffer from depression alone. Our watch list of neurological drugs highlights the most promising experimental drugs to treat diseases of the brain and nervous system. Click on the drug names in the table below for more information, including sales forecasts and novelty ratings. Bookmark this page as it will be updated often.

http://www.forbes.com/sciencesandmedicine/2004/01/26/cx_mh_r…

[geldschneider]

Oh Mann neo, was erzählts du denn!

Wenn du nicht weißt was SDR´rs sind, dann lass, die finger von!!

ADRS, haben wir vile und sind ein Vielfaches meist der normalen aktienmenge, das können 10 , 3 , oder auch mal 100 sein.

Nun kannst Du dir das Mengen-Verhältniss selbst ausrechnen!
Kurs in US Dollar umrechnen, und ich glaube bei diesem Wert ist es mal 10! Nun ist es klar?

gruß
geldschneider


Ich weiß ja dass ihr alle nur merh onlinebroker habt, die keien Ahnung haben!

Wäre nicht schlecht, wenn man noch eine andere Bank hat wo man ein Depot führt, wo man mal fragen kann, bevor man so eien Unsinn verzapft!

Und sich selbst schadet!!
Meinst Du der Ami ist bekloppt??

Der ist teilweise mit Aktien cleverer als der Deutsche Anleger und so blöde Optionsscheine kann man auch bloss den Deutschen aufhängen!
die Amis kennen das gar nicht, haben nur Optionen!

[Neoe]

geldschneider:

Was hab ich den viel erzählt, außer das ich gesagt habe das ich keine genaue Ahnung habe was es mit den ADRs auf sich hat.

Das Verhältnis war bisher 10:1, das hat sich erheblich geändert. Normalerweise werden ADRs zu einem festen Verhältnis zur tatsächlichen Aktie ausgegeben. Liess dir bitte folgendes durch und sag mir dann bitte GENAU, wie die neue Aktienstruktur aussieht (NASDAQ und ASX):


American Depositary Receipts (ADR)
Als American Depositary Receipts werden auf Dollar lautende, von US-amerikanischen Depotbanken (depositary banks) in den USA ausgegebene Aktienzertifikate bezeichnet, die eine bestimmte Anzahl hinterlegter Aktien eines ausländischen Unternehmens verkörpern und an ihrer Stelle am US-Kapitalmarkt wie Aktien gehandelt werden. Ein ADR repräsentiert in der Regel einen Bruchteil einer Aktie, kann aber auch einer vollen Aktie entsprechen. Eine Übertragung von ADR erfolgt durch Indossament und Übergabe. Der jeweilige Inhaber eines ADR kann jederzeit gegen Rückübertragung des Zertifikats an die Depotbank die Herausgabe der bei einer ausländischen Hinterlegungsbank (custodian bank), in der Regel der Zweigstelle der Depotbank im Sitzstaat des ausländischen Unternehmens verwahrten Aktien bzw. deren Verkauf an der ausländischen Börse verlangen.

Ein wichtiger Grund für die Konstruktion von ADR-Programmen liegt darin, daß bestimmte amerikanische institutionelle Investoren, wie staatliche Pensionsfonds, Lebensversicherungsgesellschaften oder Kreditinstitute, Beschränkungen hinsichtlich deren Investment in ausländische Wertpapiere unterliegen. Da ADR wie amerikanische Aktien behandelt werden, kann so ohne die Emission von Aktien auf dem US-Kapitalmarkt dieser von ausländischen Unternehmen genutzt werden.

Eine Ausgabe von ADR kann grundsätzlich in der Form von unsponsored oder sponsored ADR-Programmen erfolgen. Bei unsponsored ADR-Programmen geht die Initiative allein von einer amerikanischen Depotbank oder einem Händler aus. Die Kosten für das ADR-Programm sind regelmäßig von den Investoren zu tragen. Darüber hinaus ist die Depotbank aufgrund des fehlenden Depotvertrages mit dem ausländischen Unternehmen nicht verpflichtet, Informationen des Unternehmens an die Investoren weiterzuleiten. Unsponsored ADR-Programme werden an vielen Börsen nicht zum Handel zugelassen, so daß nur geringe praktische Bedeutung zukommt.

Bei sponsored ADR-Programmen geht die Initiative vom Emittenten aus und wird von diesem in Zusammenarbeit mit der Depotbank realisiert. Dabei wird ein Depotvertrag (depositary agreement) geschlossen, der die Depotbank verpflichtet, die Ausgabe und Rücknahme von Zertifikaten, die Ausübung von Stimmrechten durch den US-Investor, die Weitergabe von Dividenden und Unternehmensinformationen und die Programmpflege zu übernehmen. Der Großteil der entstehenden Kosten bei sponsored ADR-Programmen wird von dem emittierenden Unternehmen getragen. Neben einer Privatplazierung gibt es drei verschiedene Ausprägungen für sponsored ADR-Programme:

Level I: Durch ein Level I-Programm kann für bereits existente Aktien eines Unternehmens ein Handel in den USA auf dem Over the Counter (OTC)-Markt initiiert werden. Hiermit kann jedoch weder neues Kapital aufgenommen noch das ADR an einer US-Börse notiert werden.
Ein Level I-Programm muß mit dem Formular Form F-6 bei der SEC gemäß den Bestimmungen des Securities Act (SA) angemeldet werden. Form F-6 verlangt nur Informationen über das ADR-Programm selbst, jedoch nicht über den dahinterstehenden ausländischen Emittenten. Eine Registrierung der hinterlegten Aktien nach dem Securities Exchange Act (SEA) ist aufgrund der Ausnahmeregelung der Rule 12g3-2(b) im Regelfall nicht erforderlich, da die ADR eines Level I-Programms weder an einer US-Börse noch im NASDAQ-System gehandelt werden sollen. Bei der SEC müssen die im Heimatmarkt des Unternehmens veröffentlichten Informationen in einer englischen Übersetzung eingereicht werden. Der bedeutende Vorteil eines Level I-Programms gegenüber höhergradigen Programmen liegt in der fehlenden Verpflichtung zur Rechnungslegung nach US-GAAP.

Level II: Für eine Notierung an einer US-amerikanischen Börse oder im NASDAQ ist mindestens ein Level II-ADR-Programm aufzulegen. Hierbei müssen neben der Form F-6 auch die zugrundeliegenden Aktien nach den Bestimmungen des SEA bei der SEC registriert und die Berichts- und Offenlegungsanforderungen der jeweiligen Börse beachtet werden. Eine Registrierung der Aktien erfolgt bei der SEC mit Form 20-F, das umfangreiche Angaben über den Emittenten verlangt. Es sind Abschlüsse nach US-GAAP vorzulegen, wesentliche Anteilsinhaber zu nennen und Angaben über die Vorstands- u. Aufsichtsratsmitglieder zu machen. Die Registrierung zieht allerdings eine mindestens jährliche Berichtspflicht in vergleichbarem Umfang nach sich.

Level III: Für die Aufnahme von Kapital durch die Emission neuer Aktien im Sitzstaat des Emittenten und den Handel der zugehörigen ADR an einer US-Börse ist ein Level III-Programm erforderlich. Neben den Formblättern Form F-6 und Form 20-F ist das Formblatt F-1 einzureichen; die dort geforderten Pflichten zur Offenlegung und Aufstellung von Jahresabschlüssen nach US-GAAP entsprechen weitgehend denen nach Form 20-F.

Neben den an die Öffentlichkeit gerichteten Level I- bis Level III-Programmen besteht die Möglichkeit einer Privatplazierung nach Rule 144 A, die sich an spezielle institutionelle Käufer (Qualified Institutional Buyers) richtet. Eine Privatplazierung hat den Vorteil, daß kein aufwendiges Registrierungsverfahren notwendig und kein Abschluß nach US-GAAP erforderlich ist.

Quellen:

Böckenhoff, J.; Ross, M., "American Depositary Receipts" – Strukturen und rechtliche Aspekte - , WM, 47. Jg. (1993), S. 1781-1786 u. 1825 - 1829.

Lendner, H., American Depositary Receipts – eine Zugangsmöglichkeit deutscher Unternehmen zum US-amerikanischen Eigenkapitalmarkt, WPg, 50. Jg. (1997), S. 596-608.

Rosen, R.; Prechtel, A., Zugang deutscher Unternehmen zum US-Kapitalmarkt, Die Bank, 36.Jg. (1996), S. 388-392 u. 478-482.

[geldschneider]

Hallo neo

mich würde mal interessieren , wo die Weisheit her- nimmst, dass der kurs in australien gemacht wird??

Prana wird in USA das 85ige mal mehr umgestzt als in Australien!!

Die Nachrichten, sicher, die kommen eher in Australien heraus, aber wie die Nachricht aufgenommen wird, entscheiden die Amis!!

Und glaube mir, ich stehe jede nacht auf und sehe nach, was der ASX Kurs macht und ich bin sicher wesentlich höher investiert als Du!

[geldschneider]

Die ADR´s sofern sie die gleiche Wertpapierkennung haben bzw. das gleiche Kürzel, haben die sich nicht geändert,
und ein Splitting gab es noch nicht!

Pass auf ich habe diese ADR´s PRAN, so, und die haben das Gleiche Verhältnis wie vorher.

Du meinst etwas ganz anderes, und das hat damit nichts zu tun!

[Neoe]

geldschneider:

Wo liegt eigentlich dein Problem ? Hab ich dich irgendwann mal beleidigt in der Vergangenheit oder warum bist du hier ständig im Attackemodus ?

Wenn du hier das Board mitverfolgt hast, weißt du, dass ich derzeit gar nicht investiert bin.

Außerdem würde mich brennend interessieren, was ich den in Bezug auf die ADRs meine. Ich würde mich wirklich gerne mal aufklären lassen, wo mein Denkfehler liegt. Das ist mein ernst


Nur meine bescheidene Ansicht:

Ich gehe davon aus, dass durch die 4 Millionen neue ADRs 40 Millionen neue Stammaktien repräsentiert werden.

Übrigens ist und bleibt die ASX die Heimatbörse von Prana, der Handel in den USA hat durch die neuen Investoren, aber tatsächlich eine neue Bedeutung bekommen. Da der Großteil der Forschungsaktivitäten von Bush (und damit die Aufmerksamkeit) als auch die Investoren-Präsentationen Pranas, die durch die neuen Teilhaber forciert werden, in den USA stattfinden, kann sich das Übergewicht vorerst an die NASDAQ verlagern.

[Neoe]

Erklärung bitte unter Rücksichtnahme auf diese PAssage des Textes zu ADRs, den ich reingesteelt hatte:

Als American Depositary Receipts werden auf Dollar lautende, von US-amerikanischen Depotbanken (depositary banks) in den USA ausgegebene Aktienzertifikate bezeichnet, die eine bestimmte Anzahl hinterlegter Aktien eines ausländischen Unternehmens verkörpern und an ihrer Stelle am US-Kapitalmarkt wie Aktien gehandelt werden. Ein ADR repräsentiert in der Regel einen Bruchteil einer Aktie, kann aber auch einer vollen Aktie entsprechen. Eine Übertragung von ADR erfolgt durch Indossament und Übergabe. Der jeweilige Inhaber eines ADR kann jederzeit gegen Rückübertragung des Zertifikats an die Depotbank die Herausgabe der bei einer ausländischen Hinterlegungsbank (custodian bank), in der Regel der Zweigstelle der Depotbank im Sitzstaat des ausländischen Unternehmens verwahrten Aktien bzw. deren Verkauf an der ausländischen Börse verlangen.

[geldschneider]

neo, tut mir leid, wenn es bei Dir so rüber kommt, einma slchreibst Du der Kurs wird in Australien gemacht, was nicht stimmt! Weil der Hanel an der Nasdaq das ca. 80 fache ist!
Ich verfolge jeden Tage den WErt!
dann hast Du gesagt, der Kurs wäre dir zu tuer, weil er an der Nasdaq zu hoch sei!

Und dabei hast Du das Mengenverhältnis nicht berücksichtigtr, der ADR´s

So und wo steht, dass neue Aktien ausgegeben wurden??
Bitte Quelle!

Ich weiß das ein Fond investiert hat oder investiert mit soundsoviel Mio. Das steht aber nicht, dass deswegen eine kapitalerhöung gemacht wird!!
Oder habe ich das überlesen?

Wenn ein fond investiert muß der die Aktien über die Börse kaufen, oder, wie es in dem Falle glaube ich war, zu einem bestimmtem Preis von Prana direkt.

Das andere habe ich schon erklärt.
#
Was auch immer Prana ist ein sehr interessanter WErt, der noch nicht so hoch wie andere Biotech Firmen bewertet ist, und somit noch Kurspotentioal hat!

gru´
gs

[geldschneider]

Ich konnte nichts finden, dass sich die Aktienanzahl vergrößert hat!

Verstehst du nun was ich meine? Neo?

MeinEnglisch ist auch nicht perfect, aber ichhabe nichts gelesen, dass neue Aktien herausgegeben werden!!

Das ist die aktuelle zahl und die war es schon vor der Nachricht über den Fond!!

Shares: PRAN has 5,000,000 shares of stock outstanding.

Market Capitalization: PRAN has a Market Capitalization of $33,000,000. Market Capitalization is calculated by multiplying price times shares outstanding.

Industry Group: PRAN has been assigned to the Drug (BiomedicalGenetic) Industry Group. VectorVest classifies stocks into over 200 Industry Groups and 40 Business Sectors.

Business Sector: PRAN has been assigned to the Drug Business Sector. VectorVest classifies stocks into over 200 Industry Groups and 40 Business Sectors.

The basic strategy of VectorVest is to buy Low risk, High reward stocks. We suggest that Prudent investors buy enough High Relative Value, High Relative Safety stocks to keep the overall RV and RS ratings of their portfolios above 1.00. As you do this, you`ll find that your risk will go down and your investment performance will improve.


Graph

Prana BiotchADR


Drug (BiomedicalGenetic)

[Neoe]

Geldschneider:

Das wirst du jetzt wohl kaum wirklich glauben was du da erzählst. Du solltest dich in korrekter Weise informieren. Die Anzahl an ausgegeben "Aktien" auf die du dich beziehst, sind die ADRs und deren Anzahl ist definitiv um 4 Millionen gestiegen.

Dein Gerede das keine Kapitalerhöhung stattgefunden hat ist also kompletter Nonsense. Sogar wenn man davon ausgeht, das in Australien keine neuen Aktien registriert werden (wovon ich persönlich aber ausgehe), wäre es sehr wohl eine Verwässerung für alle Investoren, die bereits vor der Kapitalerhöhung in Amerika investiert waren, da ihre ADRs dann nur 6,5 Aktien und nicht mehr 10 Aktien repräsentieren würden, da derzeit in Australien lediglich ca. 73 Millionen Aktien ausgeben sind. Lediglich die bisherigen australischen Investoren wären davon unberührt.

Folgt man deiner Interpretation sind ADRs in keiner Weise an die eigentlichen Stammaktien gekoppelt dies ist aber nicht der Fall, da die ADRs eben nichts anderes als Platzhalter sind. Das sieht man daran das sich das Volumen der ADRs mit der Anzahl der in Australien platzierten Aktien erhöht hat.
Derzeitige Marketcap ist entgegen deiner Angaben 41,52 Millionen (+ die 20 Millionen die durch den neuen Investor hinzukommen) bzw. 7,3 Millionen ADRs (+ die 4 Millionen ADRs, die noch hinzukommen)


Und auf was alles zurück ist diese Nachricht und hier wird das Verhältnis von ADRs zu Stammaktien klar definiert und zwar 10:1:

Prana Biotechnology Approved for Listing on Nasdaq
Prana Biotechnology Approved for Listing on Nasdaq

Move to improve access to US capital markets and continue commercialisation of Alzheimer’s Disease treatment


Melbourne– September 5, 2002 – Prana Biotechnology Limited (NASDAQ: PRAN; ASX: PBT), announced today that its common shares have been approved for listing on Nasdaq.

Prana’s shares will commence trading on Nasdaq effective September 5, 2002 at 9:30 AM American Eastern Time in the form of American Depository Receipts (ADRs) under the symbol PRAN. Each ADR will represent ten ordinary shares. The Bank of New York (NYSE: BK) is sponsoring the program.

“This enables all-important access to US capital markets and represents a solid base for the next growth phase for Prana Biotechology." stated Prana Biotechnology’s Executive Chairman Geoffrey Kempler.

"We have attracted substantial investment flows from US professional investors with the ability to trade via the ASX. Listing on Nasdaq means that US funds blocked from investing in non-US investments as well as retail investors will have a new ability to invest in Prana.

“In the last few months we have established a strong corporate infrastructure. We have appointed a Chief Operating Officer with over fifteen years experience in the global pharmaceutical industry and a Vice President of Intellectual Property and Licensing with a strong background in drug licensing.”

"Prana`s current focus is on the commercialisation of its treatment for Alzheimer`s Disease and other neurodegenerative disorders. The worldwide market for these products is approximately $5 billion,“ Prana’s scientists at Harvard Medical School and the University of Melbourne are pioneers in a global effort to develop treatments for these diseases. Prana has completed Phase II clinical trials with its lead compound, PBT-1, and demonstrated proof of concept.

“We are exploring how to best leverage the near-term commercial opportunities, which include expanded clinical studies for PBT-1, as well as strategic discussions with large pharmaceutical companies. The level of inquiry from pharmaceutical companies has been profound following previews of the human trial results at Alzheimer’s conferences in Geneva and Stockholm earlier this year. These developments, in conjunction with the listing, will solidify Prana’s position as a leader in the development of a treatment for Alzheimer’s Disease,” concluded Mr. Kempler.

Prana will conduct a listing ceremony on September 24, 2002 and will participate in a corresponding US roadshow with market makers, analysts, investors and brokers.

For more information contact:
Company Media
Geoffrey Kempler, Prana
[phone]
[e-mail]



Mal schauen, ob du die auch mal mehr als zwei Minuten für das Schreiben deines nächstes Postings gönnst.

[geldschneider]

http://www2.tradingroom.com.au/apps/qt/quote.ac?section=quot…

Das Mengenverhältnis der ADR´s kann sich nicht einfach durch eine Kapitalerhöung verändern!
Es können höchstens insgesamt mehr Aktien auf dem markt sein!

Es gibt 75.984.380 Aktien aktuell in Australien.


Das wären somit in ADR´s 7,6 Mio., bzw. die 76 Mio aktien beinhalten die ADR´s!

http://www2.tradingroom.com.au/apps/qt/quote.ac?code=PBT&sec…

außerdem hat der US Fond sich mit 20 Mio US $ beteiligt!
Insofern das eine Kaptialerhöung war, und dadurch neue Aktien herausgegeben werden oder wurden, stellt das keine Verwässerung dar, sondern eine echte Kaptialerhöung in Höhe von 20 MIo US $.

ADR:

American Depository Receipts. Von US-Banken emittierte Hinterlegungsscheine, die das Eigentum an Aktien verbriefen. Ein ADR kann sich auf eine oder mehrere Aktien beziehen, selten auch auf einen Aktienbruchteil, wie das an der NYSE gehandelte Daimler-ADR, das 1/10 einer Daimler Aktie verbrieft.
------------
Weiter möchte ich zu diesem Thema keine Ausführungen mehr machen!

Erkundige dich bei Prana, oder deiner Bank wegen dem ADR Verhältnis!


Es ist immer wieder erstaulich, wie lange um solche unnützen Dinge diskutiert wird in einer Art von Rechthaberei, anstatt sich Erkundigungen einzuholen, bei der Gesellschaft oder bei seiner Bank!!

[Neoe]

Geldschneider:

Apropos Rechthaberei:

Wenn mir jemand vorwirft Käse zu erzählen, dann versuche ich das richtig zu stellen, so wie dass jeder machen würde. Zumal es hier um ein Investment geht und damit Kohle.

Umso schöner das du eingesehen hast wie es läuft:

"....Es ist immer wieder erstaulich, wie lange um solche unnützen Dinge diskutiert wird in einer Art von Rechthaberei, anstatt sich Erkundigungen einzuholen, bei der Gesellschaft oder bei seiner Bank!!


Also Geldschneider, mit deinem letzten Posting haben sich unsere Ansichten ja überraschenderweise erheblich angenähert. Warum auch immer ??

An Sinnfragen wie "Kapitalerhöhung ?" oder "Verwässerung ?" werde ich mich jetzt auch nicht mehr aufhalten, da es letztlich ein Ausdruck für ein und dasselbe ist.

[geldschneider]

Es hat abolut keinen _Sinn , das habe ich gesehen, dir etwas zu erklären!

Wenn ich zu meinem Unternehmen 20 Mio bekomme, dann muß ich doch Aktien herausgeben, oder nicht? Anstatt 100 mio z.B. habe ich dann z.b. 120 mio

hatte ich cor 100 Aktien und ich bekomme 20 mio dazu??
dann wäre das eine Werterhöhung der aktien ohne herausgabe neuer, das gibt es aber nicht! alöso gebe ich 20 Teile dazu dan habe ich 120 Teile!
und 120 durch 120 ist das gleich wie 100 Teile durch 100 Teile!

Es ist keine Verwässerung, weil ich mehr Geld habe und dafür muß ich auch dem Investor seien Anteile dafür geben.

Aber streite dichmit deiner Frau und nicht mit mir!!

Ich kann nur das mit der Verwaässerunfg und mit der ADR aufteilung nicht sthen lassen, es gibt ja hier auch Leute an Board, die diesen Unsinn dann weiter erzählen!

Ich frage dich wieviel Jahre hast du Börsenerfahrung??

Und kannst du von Deinen Aktien leben?

Und nun bitte ich habe anderes zu tun, als mich mit dir zu streiten!



Ich habe diesen Unsinn nun wirklich satt.

[Neoe]

Geldschneider:

Was ist Verwässerung ?

Versuchen wir es doch mal so rum mit dir (find ich irgendwie witzig diese Diskussion, der Thread ist zwar am Arsch, aber dein enormes Wissen macht es für jeden Leser zu einer lehrreichen Erfahrung).


Erklärungen sind mir zu diesem Thema (bisher zumindest noch) zu blöd, obwohl ich für dich vielleicht noch zum Samariter werde. Schau mal in einer Bilanz nach, sogar dort wirst du denn Begriff finden, wenn du aufmerksam suchst.


Ach komm, ich spann dich nicht auf die Folter:

Lösung:

Es ist nicht die Entscheidung von Kapitalerhöhung oder Verwässerung, sondern aus einer Kapitalerhöhung resultiert ganz automatisch (und daran wird nicht mal ein Geldschneider etwas ändern können) die Verwässerung des Kapitals, aber vielleicht erfindest du ja das Rad bzw. das Aktienwesen in deinem nächsten Posting aufs Neue. Und bei Prana zehnmal, da die Kohle unmittelbar ge- und verbraucht wird.


So, jetzt hab ich dir ein buntes Posting mit vielen Bildchen geschrieben und jetzt geh schön raus spielen, so lange die Sonne noch scheint.

Nichts für ungut, dein Neoe

[geldschneider]

[Neoe]

Also die letzten 10 Postings bitte ausblenden, ich habe mich entschlossen trotz der unnötigen Diskussion keinen neuen Thread zu eröffnen:

Ich bin, wie angekündigt bei 5 Dollar wieder eingestiegen und erwarte in den nächsten 3-8 Wochen einiges an Aktivität.

1. Abschluss der toxikologischen Tests für PBT-2
2. Bekanntgabe einer Partnerschaft mit NIH oder NIAID und
einer britischen Behörde zur Durchführung von
Phase II/III Studie für Clioquinol(PBT-1)
3. Lösung des Patentstreits um PBT-1, der wohl zufrieden-
stellend gelöst werden kann
4. IND für PBT-2 wird bei der FDA eingereicht


Sollten diese Dinge wirklich alle in der von mir angegebenen Zeitspanne erfolgen, sehen wir kurzfristig nochmal alte Hochs.

Das dieser Zeitplan nicht aus der Luft gegriffen ist, sollte folgender Webcast vom 20.5. belegen, der unter folgendem Link zu erreichen ist:

http://www.veracast.com/webcasts/bas/healthcare-2004/id11211…

[greenhorn1998]

Hallo zusammen!

Tschuldigung, aber das wollte ich dann doch noch mal schreiben. Weiß auch nicht warum jetzt, aber ich habe gerade Lust dazu. Notfalls musst du doch noch einen neuen Thread aufmachen, Neoe. Wenn es gut läuft, könnten die nächsten Wochen ja auch durchaus Anlass geben.

Wenn neue Aktien ausgegeben werden, erhöht sich automatisch der Wert des Unternehmens, ob gerechtfertigt oder nicht.
Wenn das Unternehmen zufällig Gewinne macht (was ja hier nicht der Fall ist, aber nehmen wir das einfach mal an) tritt bei einer Kapitalerhöhung automatisch eine Verwässerung des Gewinns ein.

Sagen wir mal das Unternehmen X wird mit 1 Mio bewertet, verteilt auf 1 Mio Aktien.

Wert der Aktie: 1 Euro
Gewinn: 1 Mio, pro Aktie: 1 Euro, KGV: 1

Kapitalerhöhung: Es werden noch einmal 1 Mio Aktien zum Preis von einem Euro ausgegeben.
2 Millionen Aktien:
Wert des Unternehmens X auf einmal 2 Mio, Gewinn immer noch 1 Mio Euro.
pro Aktie, die einen Euro kostet: 50 Cent!!! KGV 2 !!!

VERWÄSSERUNG

Wer hat nun Recht???

Bin mal gespannt, ob die Aktie tatsächlich dreht. Jetzt bin ich wieder bei Prana. Dachte eigentlich, dass es gar nicht mehr soweit runter geht. Immerhin haben die neuen Investoren 5 USD pro ADR ausgegeben. Dachte, das sorgt für ein bisschen Stabilität. Naja, bin gespannt.

Gruß, greenhorn

[greenhorn1998]

Hi Neoe!

Ich habe mir mal gerade etwas Zeit genommen und mir Bushs Präsentation in Ruhe angehört. Sehr aufregend! Mehr kann ich nicht sagen, hast du ja schon - besten Dank!

Technische Frage: 96 Millionen USD Business Capitalization (fully diluted, bei einem ADR-Preis von 6 USD)? Soll heißen, dass alles inbegriffen ist, auch eventuelle Verwertung von Optionen?

Danke und noch schöne Pfingsten!

Gruß, greenhorn

[Neoe]

greenhorn:

Exakt. Durch die Optionen, die noch konvertiert werden können, können am Schluss bis zu 16 Millionen ADRs ausstehen bzw. 160 Millionen Stammaktien:

1. 20 Millionen Optionen können in Australien im Verhältnis 1:1 in Stammaktien zu 0.5 AUD konvertiert werden (=2 Millionen ADRs)

2. 3 Millionen Optionen können im Verhältnis 1:1 in Adrs konvertiert werden, zum Preis von 8 USD (= 30 Millionen neue Stammaktien)

daraus folgt:
Werden 1. und 2. voll konvertiert, fließt Prana neues Kapital in Höhe von 10 Millionen AUD und 24 Millionen USD zu.


Die derzeitige, unverwässerte Marktkap.(also exklusive Optionen) liegt bei 55 Millionen USD. Das heisst, da die Cashbestände und nicht-liquiden Mittel von Prana 34,5 Millionen Dollar ausmachen, werden die Forschungsergebnisse (immerhin oder gerade mal, je nachdem, wie man Prna gegenübersteht) mit 20 Millionen Dollar bewertet.

[Neoe]

Kapitalerhöhung, wie natürlich erwartet, beschlossen:

http://www.asx.com.au/asxpdf/20040601/pdf/3lr1s2nt3ynwf.pdf

[geldschneider]

Interessant!

die Umwandlung der Optionen erhöht das Aktienvolumen!
Noch so eine tolle Weisheit!

Einfach hoffnungslos!

Ebenso. wie man sehr leicht unter Kapitalerhöung nachlesen kann, das nicht jede Kapitalerhöhung eine Gewinnverwässerung ist!

Also ich habe von MAN eine Kaufoption und wenn ich die einlöse, wo kriege ich dann die Aktien wohl her??

Wenn ich Optionen herausgebe, als Stillhalter, dann muß ich auch damit rechnen, dass die eingelöst werden!

entwederich decke mcih vorher mit den Aktien ein, oder, wenn ich das nicht tue, dann muß ich sie eben über die Börse erwerben, um sie dann liefern zu können-

Im Normalfall, hat die Firma aber genügend Aktien!

good Trades
und nicht alles glauben, was hier geschrieben wird!

Gs

[goldmaie]

@Greenhorn

Geldschneider hat es doch schon erklärt!
Beispiel:

Habe ich 5 Mio Aktien zu 1 euro, habe ich 5Mio.

Kapitalerhöung: 1 Mio zu 1 Euro, Einzahlung 1 Mio

sind 6 Mio Euro, also fehlen noch 1 mio aktien!

Die werden für die Kapitalerhöhung neu herausgegeben.

Ich habe dann 6 Mio Aktien a 1 Euro!

Was hat sich dann im Verhältniss geändert?

Nichts!

Und das mit den Optionen ist noch ein dickerer Hammer von Neo!

Wo steht, dass Prana für die Optionen neue Aktien herausgeben wird??

Unglaublich was für Dummheiten in Wallstreet verfasst werden! War bisher nur stummer Mitleser!

Habe diesen Blödsinn von Noe nun langsam satt, und keiner ausser Geldschneider berichtigt ihn!


Greenhorn:
nicht der am meisten schreibt weiß mehr!

Aber frage nur weiter Noe und du bleibst ein Greenhorn!
Nicht böse sein! Sollte keine Beleidigung sein!

Geanauso wie sich das Verhältnis der ADR´s sich nicht durch die Kaptalerhöhung verändern darf. Es gibt aber insgesamt mehr ADR`s!
Eben wie es auch mehr Aktien gibt, im selben Verhältnis!!

Ich hoffe es hat nun jeder verstanden, ausser Noe, und der soll ruhig glauben was er sowieso besser weiß!

Schöne Grüße
Goldmarie

[Neoe]

Hi greenhorn:

Wenn wir Glück haben dürfte der Boden mit der heutigen News erreicht sein, bis zur nächsten News hoffe ich auf ein einpendeln bei ca. 4,5 bis 5 Dollar.

Dann sollte ein schneller Anstieg von dieser Basis möglich sein.

[Neoe]

PRANA BIOTECHNOLOGY LIMITED
ABN 37 080 699 065




INFORMATION MEMORANDUM




This Information Memorandum is dated 30 April 2004 and is provided to Members of Prana Biotechnology Ltd ("Prana" or "the
Company") in connection with a General Meeting of the Company to be held on 1 June 2004.




Proposed Placement




The Company has entered agreements with new institutional investors in respect of a proposed placement of 4 million
American Depository Receipts ("ADR`s") at US$5.00 per ADR together with 5 year warrants to purchase an additional 3
million ADR`s at an exercise price of US$8.00 per ADR ("the Placement"). The Placement would raise US$20 million before
costs. If exercised, the warrants would raise an additional US$24 million.




Funds raised by the issue will be used as working capital and for general corporate purposes to enable the Company to
independently fund further trials of its MPAC technology (Metal Protein Attenuating Compounds), including accelerating the
development of PBT-2 into clinical trials planned for later this year, and to pay the costs of the issue.




Each ADR represents 10 ordinary shares in the capital of the Company. Accordingly, the Placement involves the issue of 40
million ordinary shares and the issue of warrants in respect of 30 million ordinary shares. The subscribers under the
Placement are institutional and professional investors in the US named in the proposed Resolution set out in the Notice of
Meeting which this Explanatory Statement accompanies and forms part of. The institutional and professional investors were
led by OrbiMed Advisors and XMark Funds. Rodman & Renshaw, LLC acted as the placement agent for the offering. Pursuant to
Listing Rule 7.1 of the Listing Rules of Australian Stock Exchange Limited ("ASX"), shareholder approval is required to be
obtained before the shares and warrants are issued. The Resolution is proposed for this purpose.




The shares proposed to be issued are ordinary shares of the Company which will rank pari passu with the existing ordinary
shares of the Company. The shares will be represented by ADR`s. At the current Australian dollar / US dollar conversion
rate this represents a placement price of 69.93 cents per share Australian. The Company has previously issued ADR`s, and
the terms of the ADR`s will be the same as the Company`s existing ADR`s. ADR`s represent shares and are used for trading
on NASDAQ as part of the Company`s dual listing on that Exchange and the ASX. Prana`s ADRs trade on NASDAQ under the
symbol PRAN. Shares represented by ADR`s are issued to the Company`s Depository Service Provider, The Bank of New
York. Receipts representing 10 shares each are traded on NASDAQ.




The Company is also issuing warrants. Each warrant entitles the holder to acquire an ADR at an exercise price of US$8.00
each. At the current Australian dollar / US dollar conversion rate this represents a conversion price for the warrants of
$1.12 per share Australian. The warrants can be exercised at any time up to 5 years after their issue, and will expire on
the date which is 5 years after being issued following receiving shareholder approval for the Placement. The warrants will
not trade on any market.




Upon exercise of a warrant, the Company must create ADR`s by issuing shares to The Bank of New York. The terms of issue of
warrants provide that if there is a re-organisation of the Company`s capital the warrants are also re-organised. If the
Company proposes issuing any shares (other than shares subject to outstanding convertible securities or options) during
the eighteen months following the closing of the placement it must give the investors a right of first refusal. If the
Company determines to make a distribution to all holders of its ordinary shares of evidences of indebtedness or assets
(other than cash dividends or cash distributions payable out of consolidated earnings or earned surplus or dividends,
etc.), it must give each warrant holder 5 days notice of its intention to do so and if a majority of warrant holders
object to the distribution the Company must not proceed until








----------------------------------------------------------------------------------------------------------------------------





Prana Biotechnology Ltd. -- Information Memorandum Page 2




the consent of the warrant holders is obtained. Warrant holders may not withhold their consent unreasonably. The Company
is required to maintain a Registration Statement to enable the resale of ADR`s following the exercise of the warrants.




The shares and the warrants will be issued not later than three business days after the approval of the Proposal at the
meeting.




Directors` Recommendation




After having duly considered the terms of the proposed Placement each of the Directors recommend that shareholders vote in
favour of the resolution and approve the Placement and authorise the issue of shares and warrants to investors. The
raising which represents approximately $27 million in Australian dollars is a great achievement for a company of Prana`s
size and status. The quality and reputation of the U.S. institutions who have committed to subscribe for the securities
provides a strong endorsement of the Company`s science, the quality of its management and outlook for the future
development of its therapies.




None of the Directors of the Company have an interest in the subject matter of the Resolution or will receive a benefit
other than benefits the same as benefits would be received by all shareholders.




Each of the Directors intends to vote any shares he holds or controls and any undirected proxies in favour of the
Resolution.




Action To Be Taken




Members are requested to either attend personally at the forthcoming meeting at Suite 2, 1233 High Street, Armadale,
Victoria, at 10.30am,on Tuesday 1 June 2004 or to forward their proxy form duly completed to be received at the registered
office of the Company at Suite 2, 1233 High Street, Armadale, Victoria, Australia, 3143 (or by facsimile to [phone]
(international: [phone]), at least forty-eight (48) hours before the time for holding the meeting.








----------------------------------------------------------------------------------------------------------------------------





PRANA BIOTECHNOLOGY LIMITED
ABN 37 080 699 065




NOTICE OF GENERAL MEETING




Notice is given that a General Meeting of Prana Biotechnology Limited will be held at Suite 2, 1233 High Street, Armadale,
Victoria on Tuesday, 1 June 2004 at 10.30am.




AGENDA




ORDINARY BUSINESS




To consider and if thought fit, to pass the following as an ordinary resolution:




Resolution: Approval of Proposed Placement




"That Members approve the issue to the proposed recipients named below of the number of shares and warrants set out
against each proposed recipient`s name, at an issue price of US$0.50 per ordinary share and 3 for 4 attaching warrant:




Proposed recipient Number of Shares, represented by Number of Warrants,
American Depositary Receipts each to acquire 1 ADR
("ADRs") representing 10 shares
Albert Fried & Company, LLC 2,000,000 (200,000 ADRs) 150,000
Bristol Capital Advisors, LLC 2,000,000 (200,000 ADRs) 150,000
DKR Oasis Capital 2,000,000 (200,000 ADRs) 150,000
Highbridge Capital Management, LLC 6,000,000 (600,000 ADRs) 450,000
OrbiMed Advisors LLC 8,000,000 (800,000 ADRs) 600,000
Perceptive Lifesciences 2,000,000 (200,000 ADRs) 150,000
Ramius Capital Group, LLC 2,000,000 (200,000 ADRs) 150,000
Sands Brothers Venture Capital Funds 2,000,000 (200,000 ADRs) 150,000
SF Capital 2,000,000 (200,000 ADRs) 150,000
Treeline Capital 2,000,000 (200,000 ADRs) 150,000
Viking Global Investors 2,000,000 (200,000 ADRs) 150,000
William Harris 2,000,000 (200,000 ADRs) 150,000
Xmark Funds 6,000,000 (600,000 ADRs) 450,000
Total 40,000,000 (4,000,000 ADRs) 3,000,000




Dated: 30 April 2004




By the order of the Board




[sig]
Richard Revelins
Company Secretary

[Neoe]

Interessanter Artikel, zuerst sehr kritisch, aber letztendlich doch sehr positiv. Vor allem interessant, weil etwas näher auf die Studien eingegangen wird:


Biotech Tracker: Reformulation of Prana Compound May Be Required
December 18, 2003 A small phase II clinical trial published this week in the Archives of Neurology supports further investigation of metal-protein–attenuating compounds (MPACs) for the treatment of Alzheimer disease (AD). However, Prana’s (NASDAQ: PRAN) PBT-1 (clioquinol, iodochlorhydroxyquin), the MPAC used in this investigation, is unlikely to generate an appropriate risk-benefit ratio for use in the management of AD. Developmental data sets to date, including those from this program, suggest that PBT-1’s efficacy, safety, and pharmacological profiles are all suboptimal.
PBT-1 is a MPAC that inhibits zinc and copper ions from binding to amyloid constituents, thereby promoting amyloid dissolution and diminishing the formation of amyloid plaque associated with AD. Oral and topical clioquinol formulations were initially developed as antifungal and antibacterial medications, but were withdrawn from the market in 1970 because of an association with recipients developing a devastating condition known as subacute-myelo-optico-neuropathy (SMON), in turn associated with vitamin B12 deficiency.

Many over-the-counter and prescription formulations contain iodoquinol, a related compound, but they are not recommended for individuals over two years of age and not at risk for diaper dermatitis. Reports of both clioquinol and iodoquinol-related adverse effects still crop up: irreversible optic atrophy (wasting away of the optic nerve, which is primarily responsible for vision), peripheral neuropathy (non-brain or spinal cord nerve problems of various sorts), and other neurological insults.

Companies including Prana and the Gerolymatos Group in Greece are reformulating clioquinol to develop it as an AD treatment and minimize its adverse effects. Given to young mice engineered to develop Alzheimer-like deposits, clioquinol appeared to inhibit plaques from forming. In another study, clioquinol appeared to clear up plaques in mice old enough to have developed substantial deposits of amyloid.

The article published this week by Ritchie, et al describes a 36-week, randomized, double-blind, placebo-controlled study of 36 patients and their caregivers. Oral PBT-1 125mg twice daily was evaluated from weeks 0 to 12, 250mg twice daily from weeks 13 to 24, and 375mg twice daily from weeks 25 to 36. 32 patients generated per protocol data.

One PBT-1 recipient developed impaired visual acuity and color vision during weeks 31 to 36 of the trial, while she was receiving PBT-1 375mg twice daily. The subject’s symptoms resolved when PBT-1 was discontinued. Although only one other serious adversity was observed in the PBT-1 group, even the possibility that this represents SMON or a variant is of great concern, especially given its relationship with the highest dose of a dose range generating a poor efficacy profile.

PBT-1’s efficacy profile, in terms of cognitive ability preservation, was suboptimal, significant only for a modest magnitude of therapeutic effect for more severely affected participants. A statistically significant difference between the cognitive preservation capacity of PBT-1 and placebo was not observed at any week. Trends toward statistical significance were noted at weeks 4 and 24. A statistically significant difference between the cognitive preservation capacity of PBT-1 and placebo was not observed for less severely affected participants. A statistically significant difference favoring PBT-1 receipt was observed for more severely affected patients at weeks 4 and 24. But at week 36, this difference was relegated to a mere trend. It remains unclear whether the differences in mean change from baseline ADAS-cog score (the primary test of cognitive function) in the PBT-1 arm compared with the placebo arm at weeks 24 and 36 (7.37 [95% confidence interval, 1.51-13.24] and 6.36 [95% confidence interval, -0.50 to 13.23], respectively) bears clinical significance. As far as testing cognitive function with The Mini-Mental State Examination, similarly insignificant statistical differences, but favorable trends, were observed. Moreover, the non-cognitive ADAS and Clinician Interview-Based Impression of Change scores were neither significantly different between groups nor associated with favorable trends. Pharmacogenetic correlates of apolipoprotein E genotyping were also not observed, and are thus unavailable for study subject selection refinement.

Disappointing clinical results were associated with biochemical effects that support further development of MPAC compounds. Significant compound and/or protocol refinements will be required. For instance, plasma Aß42 (an amyloid fragment) levels declined significantly from baseline in the PBT-1-treated group from week 20 onward. During the same time, plasma Aß42 levels in the placebo group increased. Ironically, plasma Aß42 changes were evident only in the less severely affected group.

Data relevant to copper- and zinc-related parameters were sketchy, and certain assays were deemed invalid based upon technical issues during the conduct of the investigation. The zinc-related biochemical profile appears reassuring, though. Certain data also suggest that measurements of extracellular brain PBT-1 levels will be required, together with more refined plasma pharmacokinetics, before a more optimal dosing approach can be found and assessed. Vitamin B12 and folate metabolism also requires further assessment. The potential PBT-1-associated optic neuropathy suspected in the one study subject mentioned above is of considerable concern, although a direct causal link to PBT-1 remains uncertain. 27 subjects are participating in an open-label extension study. 10 subjects have received PBT-1 500 to 750mg/d for more than 18 months, and definite PBT-1-attributable adverse events have yet to be observed.

[Neoe]

Melbourne, Australia – 2 June, 2004: Shareholders in Prana Biotechnology Limited (NASDAQ: PRAN, ASX: PBT) have approved the issuing of securities worth US $20 million to institutional and professional investors, led by New York-based global healthcare fund managers, OrbiMed Advisors and XMark Funds. The transaction was originally announced on April 28, 2004.



Geoffrey Kempler, Executive Chairman of Prana commented: “This substantial support shown by leaders in the healthcare investment community reflects the progress and strength of Prana’s technology.

“With this offering, we have been able to enhance shareholder value by increasing our access and exposure to the vast US capital markets and broaden our base of US institutional investors, complementing our traditional Australian shareholder base.

“We continue to build on our already strong connection with the US and now have a board member, Dr Jon Alsenas, and our chief scientist (one of the inventors of our MPAC technology) Prof Ashley Bush, based there. This capital raising will provide the funds to progress PBT-2, our proprietary MPAC for Alzheimer’s disease, into clinical trials in Australia through 2005 and 2006,” said Mr Kempler.

Investors also purchased five-year warrants to purchase an additional 3 million ADR’s at an exercise price of US$8.00 per ADR. If exercised, this would raise an additional US$24 million for the Company. Investment bank, Rodman & Renshaw LLC acted as the placement agent for the transaction.

[Neoe]

Prana wird mittlerweile in einem Atemzug mit den Großen erwähnt:



Companies race for Alzheimer`s drug
Disease that afflicted Reagan for a decade has no cure
By Lisa Sanders, CBS.MarketWatch.com
Last Update: 1:00 PM ET June 10, 2004


DALLAS (CBS.MW) -- With millions of lives and billions of dollars at stake, companies are in fierce competition to cure the disease that killed former President Ronald Reagan.

Current drugs such as Pfizer`s (PFE: news, chart, profile) Aricept and Forest Labs` (FRX: news, chart, profile) Namenda treat some symptoms, but they can`t stop the fatal progression of Alzheimer`s disease, which affects 4.5 million Americans today -- including half of all people over 85 -- and could afflict 16 million by the middle of this century.

"Because of the large number of people that have it now, the increasing number in the future and a larger population at risk," said Bill Thies, a spokesman for the Alzheimer`s Association, "the company that finds the treatment that arrests progression ... will have a very large economic hit."

In Alzheimer`s patients, deposits build up in parts of the brain, stopping those brain cells from working. No one knows exactly why a person develops it, and getting old appears to be the greatest risk factor.

"If we figure out what the disease is, we might be able to cure it," said Dr. Myron Weiner, a geriatric psychiatrist at the University of Texas Southwestern Medical Center. "We know there is an abnormal substance deposited in the brain, and the stuff that forms the deposits is floating around in the brain. There also another change called neurofibrillary tangles ... and we don`t know what causes that to happen."

The drugs now in use are "not very impressive," Weiner said, adding that even a pill containing no medicine helps some patients. "The placebo response in this is just enormous," he said. "You wouldn`t think so, but giving somebody a pill ... they do better."

The Alzheimer`s Association says that even if new drugs don`t cure the disease, a treatment that delays the onset by five years would significantly reduce the number of victims. See the association`s Web site. The average lifetime cost to care for a person with the disease is $170,000.

Drugs under development

"The next wave of blockbuster drugs appear to (target) a lot of ailments of the brain," said Scott Henry, an analyst at Oppenheimer & Co. "The problem is the solution. The market opportunity is clearly there. It`s just figuring out how to get there."



One company with a possible solution is Axonyx (AXYX: news, chart, profile), a New York company that, based on its stock price, is already worth $250 million.

The company is developing a drug called Phenserine with what it hopes is a two-pronged effect: It would enhance memory, much like Aricept, but it would also inhibit the production of a protein called beta-amyloid.

That protein produces the deposits that form on brain cells in an Alzheimer`s patient. See an Anonyx video about how Alzheimer`s works.

Phenserine is undergoing trials in Europe "to prove whether our drug can intercept the bad beta-amyloid and decrease the production," said CEO Dr. Marvin Hausman. He is a former transplant surgeon, a scientist and the son of an Alzheimer`s patient.

"If memory gets better and the levels of beta-amyloid change consistent with memory, I think we`ve got a modifying drug," he said. Axonyx expects to know the results of the tests by the end of this year.

Though the Food and Drug Administration won`t confirm it, Thies said there are as many as 120 applications pending for trials of new Alzheimer`s drugs.

Henry said Merck (MRK: news, chart, profile) and Wyeth (WYE: news, chart, profile), among other big names, are working to find solutions.

Promising trial cancelled

Weiner said he`s most thrilled about the prospects of Elan`s (ELN: news, chart, profile) vaccine, which is designed to clear out the toxic beta-amyloid buildup in the brain. The Irish company started a second round of clinical trials late last year in collaboration with Wyeth. The first trials were halted in 2002 when 6 percent of 300 patients came down with encephalitis, or inflammation of the brain.

"But the attitude of the people is, `heal me or kill me,` so there`s no shortage of volunteers," Weiner said. In a later autopsy, one of the patients was found to have little sign of Alzheimer`s in her brain after being given the vaccine, he said.

"No one knows whether it was that way to begin with or it was the result of the drugs," Weiner said. "These plaques in the brain are ordinarily not very soluble, but, somehow, if you tag them with an antibody, the scavenger cells in the brain say: `Hey, I like this all of sudden` and start eating the stuff. So, the scavenger cells can pick up the plaque -- if the plaque is the problem. Some people think it`s not the plaque but what the plaque is formed of."

Dr. Ashley Bush, the founding scientist of Prana Biotechnology (PRAN: news, chart, profile) and a professor at Harvard Medical School, is sometimes called the "Metal Man." His work focuses on metals normally found in the brain, like copper and zinc.

As a person ages, Bush said, copper can cause amyloid to be released from its normal place in the brain. "It then drifts, carrying copper, in the microscopic spaces between brain cells, where it then reacts with high concentrations of zinc to form amyloid plaques," he said.

Noting that copper and iron concentrations in the brain increase with age, Prana says it`s working on drugs that would pluck metals out of the amyloid protein using a compound known as clioquinol, an antibiotic that is no longer used.

A study conducted by Bush and Dr. Robert Cherny and published in 2001 showed that mice given clioquinol showed a significant decrease in signs of Alzheimer`s within nine weeks. Beta-amyloid accumulation fell by 50 percent during that time.

The company is now in clinical trials of clioquinol and announced successful preliminary results in December. It`s also about to start testing new drugs that might have the same effect as clioquinol.

[Neoe]

Am 25.6. ist der nächste Verhandlungstermin mit Gerolymatos zwecks des Patents auf die Behandlung von Alzheimer mit Clioquinol.
Der Termin wurde bereits zweimal verschoben, vielleicht kommt es ja bis Ende Juni zu einer gütlichen Einigung. Das würde erhebliche Kursphantasie mit sich bringen.

[geldschneider]

sehr interessant der Artikel mit Kupfer und Zink im Gehirn.

Haben die Alzheimner Patienten nun zuviel, oder zuwenig Kupfer im Gehirn?

Auch bei shizophrenie hat man zuviel Kupfer im Körper nachgewiesen!

Zink dagegen ist ein Kupferantagonist.

Danke für Antwort.

und hier noch ein Link zu den herausgegebenen Mitarbeiter Optionen:

http://www2.tradingroom.com.au/news_research/index.jsp?secti…

Weiß allerdings nicht, ob es funktioniert, weil ich die Nachrichten nur über Password zugang erhielt!

Die Frage ist, wieviel Aktien hält Prana selbst,um die Optionen bedienen zu können.

Seltsam finde ich die Optionen für 0,5 austr. $.

die meisten sind jedoch bei 1,5 einzulösen bis zum Jahre 2005 im Juni oder Juli.

Heute wieder in Australien im Plus`!

Gruß
GS

[geldschneider]

Es ist mir gelungen, aus dem Text die Optionsbedingungen herauszukopieren.


9 Number and +class of all +securities not quoted on ASX (including the
securities in clause 2 if applicable)


19,750,000




897,167





10,000





200,000




412,000





3,000,000 Options exercisable at
$0.50 on or before 1
December 2004
(PBTAK)

Employee &
Consultant Options
exercisable at $0.50 on
or before 30 June 2005
(PBTAO)

Employee &
Consultant Options
exercisable at $1.50 on
or before 30 June 2005
(PBTAI)

Options exercisable at
$0.50 on or before 1
October 2005
(PBTAQ)

Consultant Options
exercisable at $0.50 on
or before 1 February
2007 (PBTAS)

Unlisted Warrants,
each Warrant
exercisable at
US$8.00 into 1
American Depository
Receipt (ADR)
(PRAN) on or before
4 June 2009. Each
ADR being equal to 10
Ordinary Fully Paid
Shares (PBT) 10 Dividend policy (in the case of a
trust, distribution policy) on the
increased capital (interests) Unchanged



die Zahlen haben sich leider übereinander und nicht nebeneinander dargestellt!

[Neoe]

Prana im australischen TV:

http://www.asx.com.au/asxpdf/20040617/pdf/3lwl8k7n2gd70.pdf

[greenhorn1998]

Hi zusammen!

Hier ein Transkript:

http://www.abc.net.au/catalyst/stories/s1134238.htm#transcri…


Full Program Transcript:
Narration:
Australia is facing an economic and social disaster.

As the population ages, the degenerative condition Alzheimer`s Disease will become much more common.

For almost a century it appeared to be a hopeless condition.

But this man has some good news.

Ashley Bush:
Well Alzheimer`s disease has been a hopeless diagnosis since it was first described in 1906 and this has been the first year where we`ve actually had a drug that`s capable at least in animals of stopping the disease and we`ve tried it out in humans with promising results so the future for the first time is looking a bit more rosy. It`s like the future for St Kilda Football Club here.

Narration:
A hopeless St Kilda supporter, Ashley Bush has always been a bit of a maverick and he has some radical ideas about Alzheimer`s disease.

But now he might have finally found a way, to not just arrest the development of Alzheimer`s disease, but possibly reverse some of it`s effects.

Marie has Alzheimer`s Disease. Diagnosed just 18 months ago, she`s only 57 years old. It`s a tragedy that effects both Marie and her husband Tom.

Tom:
Well one of the very early signs was that Marie has always been a meticulous organiser and manager things, left home to go to work and left the front door wide open.

Paul Willis, Reporter:
Did you notice this too Marie?

Marie:
Yes, because it was the garage door that was the killer. And you know, I would come back and think, oh god know I`ve done it again.

Narration:
More recently, as the effects of the disease have increased, Marie has lost her driving licence.

Tom:
And this time it was withdrawn, and of cause that has taken away a huge degree of independence for her.

Marie:
Nobody was telling me that I wasn`t driving properly, but it`s devastation, of not being able to go places, you know just takes so much away."

Narration:
There are 150,000 Australian`s like Marie, suffering from Alzheimer`s Disease.
And that number is rising rapidly.

This frightening statistic drives Ashley Bush toward finding a cure.

Ashley currently has two jobs, one here at the Mental Health Research Institute in Melbourne the other at Harvard University in Boston.

His year is split between the two where he focuses on the problems and potential cures for Alzheimer`s

Ashley Bush:
This is an image of a normal brain a normal adult brain which is enlarged and the normal size of a brain is about the same as a medium size cauliflower.

Paul Willis, Reporter:
Okay so this is the healthy brain, what`s wrong with this brain?

Ashley Bush:
Well this is a typical Alzheimer brain from an individual of the same age. What you see here is there is basically far less meat in it.

Paul Willis, Reporter:
So the brains just sort of shrunk?

Ashley Bush:
Effectively its shrunk and its lost weight, so the weight of this brain would be about one half of the weight of this brain.

Narration:
This disease was first diagnosed in 1906 by Dr Alois {AL-oys} Alzheimer. He conducted an autopsy on a patient and noted for the first time that the brain had shrunk. And under the microscope, he found something else.

Ashley Bush:
This is an image which would be typical of what Alzheimer himself saw down is microscope nearly a hundred years ago. What you see is that accumulating within the tissue are these brown spots and in Alzheimer`s disease typically the brain fills up with these deposits of this protein.

Paul Willis, Reporter:
Now are these symptoms of the problem or are they the problem themselves these plaques?

Ashley Bush:
Well that`s a very good question you would think with something that is so dramatic that you see down a microscope that this would be the cause of the problem but the further that we looked into it the more that we saw that in fact this is a signpost of the disease rather than the cause of the damage itself.

Narration:
The plaques turned out to be blobs of the protein beta amaloid.

It`s a normal protein found in every healthy person.

But in the brains of Alzheimer`s sufferers this protein formed abnormal blobs.

Most other researchers into Alzheimer`s disease thought that the blobs were the problem - the cause of the disease.

But Ashley thought they were just the symptoms of a deeper problem.

He and his team focussed on what`s inside the blobs; high doses of chemically active metals.

Ashley Bush:
This is a piece of metallic copper and we found that the amaloid plaques and Alzheimer`s disease typically are packed full of metals specifically copper zinc and iron. There`s actually about four or five hundred percent the normal concentration of metal that you see in healthy brain tissue.

Narration:
Ashley thinks that there`s a connection between beta amaloid and these chemically reactive metals. Normally beta amaloid stops these metals from causing corrosive reactions in the brain.

Ashley Bush:
Okay Paul well I`m doing this to show you how reactive copper is. Put it in this solution and we can watch it dissolve.

Paul Willis, Reporter:
Oh yeah it`s bubbling away there.

But Ashley thinks that, in the Alzheimer`s brain, beta amaloid is overloaded with metals and can`t stop them from corroding.

Ashley Bush:
And then when that happens it generates hydrogen peroxide as a product.

Paul Willis, Reporter:
Hydrogen peroxide that`s bleach!

Ashley Bush:
That`s right it`s bleach and what we knew for ages was that in Alzheimers disease it looks as if the brain has been soaked in hydrogen peroxide.

Narration:
If Ashley is right, each blob in the brain of an Alzheimer`s patient is a chemical factory that spews bleach throughout the living brain.

Could there be some way to stop the metals producing hydrogen peroxide?

He went searching for such a drug and found one called Clioquinol.

He then teamed up with Robert Cherney at the Mental Health Research Institute in Melbourne and together they put clioquinol {Clock-kwin-nol} to the test.

It was time for trials on mice, but these were no ordinary mice!

Paul Willis, Reporter:
So what`s so special about these mice?

Robert Cherney:
Well these little fellas are genetically engineered to producing in their brains the same amaloide deposits as are seen in the brains of human beings with Alzheimer`s disease.

Paul Willis, Reporter:
So they`re sort of preprogrammed to get Alzheimer`s!

Robert Cherney:
Yeah they`re sort of they get a mousy sort of Alzheimer`s disease.

Paul Willis, Reporter:
How do you spot a mouse with Alzheimer`s disease?

Robert Cherney:
They do have um memory deficits and we put them in a maze, a water maze which they have when they get older they have a little bit of trouble solving finding the cheese if you like.

Narration:
The experiment with the mice and clioquinol was conducted in Boston, but the brain samples were sent to the team in Melbourne for analysis.

Robert Cherney:
It was a classical double blind study. And when they sent the brains over to us they didn`t let us know which had the treatment which had not. We analysed the tissue we had a look to see how much of the amaloid was in there and then we sent the results back to them saying Mouse A had this amount, Mouse B had this amount and they went back to their list they opened up the envelope so to speak.

Narration:
And, when the results came through, they were stunning!

Robert Cherney:
I was about to go to bed and I got this phone call, and my wife said it`s actually from Harvard and I said what`s this all about. And he said, it worked! And I said what worked the clioquinol it worked and it was really really exciting time. I really didn`t sleep after that.

Ashley Bush:
This is some of the most important results that we ever achieved. This mouse that is treated with the placebo, so it`s received no active drug. And you see the brown spots are the typical amaloid that you see down microscope, and which is typical of Alzheimer`s disease. The upper panel is the same type of mouse that has been treated for only twelve weeks with this drug clioquinol and you see there is no brown spots what so ever.

Paul Willis, Reporter:
So is the reversal of the situation, or just prevented the situation from starting.

Ashley Bush:
This is a reversal, because at this age all of these animals have abundant brown spots in them.

If this compound is as effective in humans as it is in mice, we hope to stopped the deterioration associated with the disease, and then we give the brain a chance to repair itself.

Narration:
Limited human trials have, so far, produced promising results. But, as encouraging as the initial results of these trials appear to be, the fact is that most existing Alzheimer`s patients may have already lost too much.

Tom:
It`s a, it`s a gut retching experience. And because it is a slow and degenerative process, it`s takes a little bit away from you, everyday. Millimetre by millimetre, centimetre by centimetre, you can feel the grief come through you.

We are squeezing every good moment out of everyday that we can. We`re grateful for all the time we have together. We`re grateful for good sunny days, and fresh breeze. But we realise that the really really hard days, are yet to come.

Narration:
Ashley`s research offer`s some hope for the future, for people who have yet to develop Alzheimer`s disease.

However larger scale tests are needed before his unconventional ideas will be fully accepted by other medical researchers.

But it is a rare glimmer of hope for a future that otherwise looks very bleak.

Ashley Bush:
The number of people in Australia currently with Alzheimer`s disease is about a hundred and fifty thousand and so that`s about four times larger than the number of people who are currently at this stadium but by the year two thousand and fifty there will be half a million Australians with Alzheimer`s disease and that`s why we`ve got to get on top of it as soon as we can we can`t waste time about this because its going to come down on us like a social meteorite.


Gruß, greenhorn

[Neoe]

Leider war es wohl so, dass Prana in dem Zusammenhang aber nicht erwähnt wurde. Es wurden nur die wissenschaftlichen Ergebnisse, in neutraler Weise, vorgestellt.

Trotzdem gut für alle die Wissen, wer diese Ergebnisse in Therapien umsetzt. Wir gehören dazu.

[Neoe]

Alles was bei Prana Rang und Namen hat ist anwesend:


Prana Biotechnology`s Co-Founding Scientist Presenting at
The Elan Sponsored Satellite Symposium Dinner
and at The International Conference on Alzheimer`s Disease and Related Disorders
WHO: Ashley Bush, MD, PhD, Principal Fellow/Associate Professor, Departments of Pathology and Psychiatry, University of Melbourne, Director, Laboratory for Oxidation Biology at Massachusetts General Hospital, Associate Professor of Psychiatry at Harvard Medical School and Prana Biotechnology`s Co-founding Scientist

WHAT: Dr. Bush presenting at the Elan-Sponsored Satellite Symposium Dinner "Current Progress on Development of Therapeutic Strategies Based Upon the Amyloid Hypothesis."

In addition, Dr. Bush will also be giving a lecture at The International Conference on Alzheimer`s Disease and Related Disorders (July 17 - 22)

WHY: Topic of discussion at the Elan Symposium: `Clioquinol and the Metal-Protein Attenuating Compounds (MPACs) in the Treatment of Alzheimer`s disease`
Topic of discussion at the International Conference: Oxidation and Inflammation in Aging and Alzheimer`s Disease

WHERE: Elan-Sponsored Satellite Symposium Dinner
Pennsylvania Convention Center - Ballroom A/ B
Monday, July 19, 2004
5:30 PM - 9:00 PM

The International Conference on Alzheimer`s Disease and Related Disorders.
Pennsylvania Convention Center
Wednesday, July 21, 2004
10:30 AM - 12:30 PM



NOTE: Also in attendance:

Professor Colin Masters

Professor Rudolph Tanzi

Professor Konrad Beyreuther, M.D

Robert Cherney
Ross Murdoch, CFO of Prana Biotechnology



For more information contact:

Ivette Almeida

212-983-1702 ext. 209



About Prana

Prana is a Melbourne-based biotechnology established in 1997 to commercialize research into Alzheimer`s disease and other major age-related degenerative disorders (Nasdaq: PRAN; ASX: PBT). Prana`s technology was discovered by the company`s researchers at prominent international institutions including Massachusetts General Hospital at Harvard Medical School, the University of Melbourne and the Mental Health Research Institute in Melbourne. For more information about Prana, please visit www.pranabio.com



| | | | | Inbox

Get the latest updates from MSN
MSN Home | My MSN | Hotmail | Search | Shopping | Money | People & Chat
Feedback | Help
© 2004 Microsoft Corporation. All rights reserved. TERMS OF USE Advertise TRUSTe Approved Privacy Statement GetNetWise Anti-Spam Policy




Wäre natürlich nur zu schön, wenn am 25. Juni eine Beilegung des Rechtsstreits zwischen PRana und Gerolymatos bekanntgegeben wird, dass wäre natürlich ein Startschuss für eine Reihe von guten News.

[Neoe]

Auszeichnung für Dr. Bush:

http://www.asx.com.au/asxpdf/20040623/pdf/3lxy83vbts4mg.pdf

[BrauchGeld]

Hi Leute

Wollte nur mal unsere Prana wieder oben sehen .
Hoffentlich gibts bald News ,kurs scheint wie angewurzelt zu sein ,immer noch besser als in die Tiefe zu rauschen wie die meisten Biotechs.

Grüsse
B.M.

[BrauchGeld]

Endlich wieder neuigkeiten

Prana Biotechnology Presents at the 9th International Conference on Alzheimer`s Disease
Monday July 19, 11:31 am ET
Co-founding scientist to discuss new data on the interaction of cholesterol with beta-amyloid and brain metals


PHILADELPHIA, July 19 /PRNewswire-FirstCall/ -- Dr. Ashley Bush, chief scientific consultant and co-founder of Prana Biotechnology Limited (Nasdaq: PRAN - News; ASX: PBT - News) is scheduled to present a lecture tonight at the 9th International Conference on Alzheimer`s Disease and Related Disorders (ICAD), a specialist international symposium in Philadelphia at the Pennsylvania Convention Center, Ballroom A/B. The event will commence at 5:30 PM.
Dr. Bush intends to present a lecture entitled "Clioquinol and the Metal- Protein Attenuating Compounds (MPACs*) in the treatment of Alzheimer`s disease" at a session devoted to the development of therapeutic strategies. Based on the hypothesis that beta amyloid is a key player in the onset and progression of Alzheimer`s disease, Prana maintains that it is the inappropriate interaction of beta amyloid with brain metals copper and zinc that leads to the progression associated with the disease. As part of his remarks, Dr. Bush intends to discuss how clioquinol detects amyloid pathology in brain tissue and how the drug arrives at the appropriate biochemical target in living transgenic mice and in post-mortem tissue from patients with Alzheimer`s disease.

Dr. Bush and his co-workers at the University of Melbourne and Massachusetts General Hospital have developed this theory over 15 years of research. For much of this time, the research community has been sceptical toward what was a major departure from the more favoured theories. Invitations to present the MPAC approach at premier conferences such as ICAD demonstrate the increasing support for Prana`s technology in the Alzheimer`s community.

Co-founding Scientist of Prana, Dr. Rudolph E. Tanzi, Professor of Neurology at Harvard Medical School said, "This conference is regarded as an important event, not only for scientists and medical practitioners in the industry, but also for the millions of patients worldwide who have Alzheimer`s, This invitation to speak to international peers about the scientific basis for Prana`s MPAC technology is an indication that our theories have achieved considerable acceptance."

Also at ICAD, on Wednesday July 21, Dr. Bush is scheduled to give an invited lecture that will review the basic neuroscience describing the involvement of brain copper and zinc in Alzheimer pathology. New data is expected to be presented on the interaction of cholesterol with beta-amyloid and brain metals, which may play a key role in the sequence of events that leads to dementia. The possibility that beta-amyloid participates in the functional regulation of copper levels in health will be discussed.

(*MPACs, or Metal-Protein Attenuating Compounds are compounds that bind metals to prevent their interactions with proteins.)
International Conference on Alzheimer`s Disease (ICAD)

The ICAD is the world`s leading forum on dementia research, and provides the opportunity for more than 5,000 attending researchers to share knowledge and develop creative new approaches to increasing the understanding of Alzheimer`s.

[geldschneider]

gibts eine Erklärung warum der Kurs so runter rutscht??


Heute ja noch ein Termin:

The International Conference on Alzheimer`s Disease and Related Disorders.
Pennsylvania Convention Center
Wednesday, July 21, 2004
10:30 AM - 12:30 PM


Ist der Termin denn auf den 19. verschoben worden oder gibts heute nochmal eine Presentation?

[meislo]

Vollständiger Verlust des Ichs
Die Zahl der Alzheimerkranken in Deutschland wird sich bis 2015 verdoppeln. Wissenschaftler hoffen auf Kupfer. Es verhindert die Zersetzung der Nervenzellen
von Ingrid Kupczik

Sheldon Goldberg, Präsident der amerikanischen Alzheimer-Gesellschaft, macht sich keine Illusionen: "Wenn es uns nicht bald gelingt, Therapien zur Vorbeugung oder Heilung zu entwickeln, wird die Alzheimer-Krankheit unser ohnehin strapaziertes Gesundheitssystem aus den Angeln heben." Auf der 9. Internationalen Alzheimer-Konferenz diese Woche in Philadelphia zeigte Goldberg angesichts der "Flut viel versprechender Forschungsergebnisse" allerdings verhaltenen Optimismus. 2000 aktuelle Studien zu Krankheitsentstehung, Prävention und Therapie wurden den mehr als 4500 Experten präsentiert, darunter eine verblüffende Kupfer-Studie aus Deutschland sowie Erkenntnisse zu Risikofaktoren der häufigsten Demenzform.


Die Zeit dränge, so Goldberg, denn die Patientenzahlen explodieren, ebenso die Kosten. Für Medicare, eine Art öffentliches Krankenversicherungssystem der USA, werden sich die Ausgaben zur Behandlung von Alzheimer-Patienten in den kommenden zehn Jahren verdreifachen: auf jährlich 190 Milliarden Dollar.


In Deutschland leiden 850 000 Menschen an Alzheimer, bis 2015 rechnen die Experten mit einer Verdopplung der absoluten Krankheitszahlen - als Folge der gestiegenen Lebenserwartung, aber auch der Tatsache, dass die Babyboomer-Generation, jene geburtenstarken Jahrgänge zwischen 1945 bis 1965, langsam in die Jahre kommen. Das Alzheimer-Risiko steigt mit dem Alter exponentiell an: In der Gruppe der 65-Jährigen erkrankt jeder Zwanzigste, bei den 80-Jährigen jeder Fünfte, ab 90 jeder Zweite.


Der Entstehungsmechanismus der Alzheimer-Krankheit ist noch längst nicht geklärt. Nach der gängigen Amyloid-Hypothese spielt ein spezielles Protein, Beta-Amyloid, eine Schlüsselrolle beim schleichenden Untergang der Nervenzellen, der zu dem typischen Krankheitsbild mit kognitiven Störungen, einer veränderten Gefühlswelt und letztendlich dem vollständigen Verlust der Persönlichkeit führt. Das Beta-Amyloid verklumpt zu Plaques, die die Nervenzellen von außen zerstören, aber auch im Inneren das Zellgerüst zum Einsturz bringen.


Durch die Gabe von Kupfersalz lässt sich die Plaquebildung offenbar bremsen. Das konnten Professor Gerd Multhaup von der FU Berlin und Privatdozent Dr. Thomas Bayer, Universitätsklinik des Saarlandes in Homburg, in Versuchen mit Mäusen nachweisen. Mit ihrer Beobachtung liefern sie womöglich den Schlüssel für eine neue Behandlungsstrategie, die verhindert, dass die zerstörerische Kaskade im Gehirn in Gang kommt: Das Protein Beta-Amyloid ist Bestandteil eines großen, in der äußeren Zellmembran fast aller Körperzellen sitzenden "Amyloid-Vorläufer-Proteins" (APP), das im Gehirn unter anderem für Blutungsgerinnung und Nervenzellschutz sorgt. Bestimmte Enzyme, so genannte Sekretasen, zerschneiden APP in winzige Schnipsel. Das Enzym Alpha-Sekretase gilt als "gute" Schere, da es das Vorläuferprotein in unschädliche Bruchstücke zerteilt, von denen bisher allerdings niemand weiß, welche Funktion sie eigentlich besitzen.


Die beiden anderen enzymatischen Scheren (Beta- und Gamma-Sekretase) sind hingegen gefährlich, denn sie trennen aus dem APP das Beta-Amyloid heraus, lösen es aus der Zellmembran. Das macht zwar normalerweise nichts aus. Wenn aber durch einen "Fehler im System", zum Beispiel eine im Alter erworbene Genmutation, der Bauplan des Beta-Amyloids verändert wird, können sich Plaques bilden. In diesem Geschehen spielt Kupfer eine Doppelrolle: Ist Beta-Amyloid erst einmal aus dem APP herausgeschnitten, fördern Kupferionen außerhalb der Zelle offenbar die Plaquebildung. Einen Schritt zuvor jedoch sorgt das Metall für die entgegengesetzte, erwünschte Wirkung: Es lockt die "gute" Alpha-Sekretase, indem es ihr die passende Schnittstelle am APP präsentiert. Auf diese Weise verhindert Kupfer indirekt, dass die gefährlichen Bruchstücke entstehen können. Im Tierversuch beobachteten die deutschen Forscher genetisch veränderte Mäuse mit menschlichem APP-Gen. Diese produzierten sechs bis acht Mal mehr Beta-Amyloid als normale Mäuse. Nach spätestens neun Monaten hatten die meisten Mäuse massive Plaques entwickelt und starben im Verlauf der Studie. Transgene Mäuse, die täglich Kupfer in einer Zuckerlösung erhalten hatten, blieben hingegen gesund.

"Die Ergebnisse des Tierversuchs waren so überraschend positiv, dass wir uns entschlossen haben, Kupfer auch beim Menschen einzusetzen", sagt Privatdozent Dr. Frank-Gerald Pajonk von der Universitätsklinik für Psychiatrie in Homburg, wo kürzlich eine entsprechende Studie gestartet wurde. Rund 100 Patienten mit milder Demenz, dem Frühstadium der Krankheit, erhalten täglich eine Kapsel mit acht Milligramm Kupferorotat. Parallel nehmen sie das Standardmedikament Donepezil ein. Die Kontrollgruppe erhält dieses Medikament sowie ein Placebo. "Sollte sich die Wirkung wie erhofft einstellen, stünde endlich eine kausale Therapie zur Verfügung, die zudem leicht verfügbar und kostengünstig ist", sagt Prüfleiter Dr. Pajonk.


Bisher ist die Alzheimer-Krankheit unheilbar, und die Möglichkeiten, den Zelluntergang wenigstens zu bremsen, sind dürftig. Der Standardwirkstoff Donepezil (Handelsname "Aricept") habe nur "bescheidene und zeitlich eingeschränkte Wirkung", sagte Professor Donald Petersen in Philadelphia. Das Fortschreiten der Krankheit lasse sich um durchschnittlich 18 Monate verzögern. Anschließend geht der massenhafte Untergang der Hirnzellen trotz Einnahme des Medikaments ungehemmt weiter.


Große Fortschritte macht die Suche nach einer Impfung. Durch die Gabe von Amyloid-Ablagerungen soll das Immunsystem angeregt werden, Antikörper gegen die Plaques zu bilden und diese abzuräumen. Eine erste weltweite Impfstudie am Menschen lieferte viel versprechende Ergebnisse, wurde aber gestoppt, nachdem einige Probanden eine Gehirnentzündung entwickelt hatten. Der renommierte Züricher Alzheimer-Experte Professor Roger Nitsch, der federführend an der Studie beteiligt war, hat für Ende dieses Jahres "eine neue Impfung, möglichst ohne Nebenwirkungen" angekündigt.


Unterdessen verdichten sich die Hinweise, dass ein ungesunder Lebensstil Alzheimer begünstigt. Einer finnischen Studie zufolge verdoppelt Übergewicht im mittleren Lebensalter das Alzheimer-Risiko. Wer mit 45 zudem einen chronisch erhöhten Cholesterinspiegel und Bluthochdruck hat, muss mit einem sechsfachen Demenzrisiko rechnen. Ob die Statine, Wirkstoffe zur Senkung des Cholesterinspiegels, auch zur Alzheimer-Prophylaxe taugen, ist nicht geklärt. Die in Philadelphia vorgestellten Untersuchungen liefern dazu widersprüchliche Ergebnisse.


Dagegen scheint eine aktive Freizeitgestaltung, die soziale, intellektuelle und körperliche Anforderungen stellt, einen gewissen Schutz vor der gefürchteten Demenz zu bieten. Darauf weist eine Studie am Karolinska-Institut in Stockholm hin. Entscheidend sei, so Dr. Laura Fratiglioni, dass man sich bis ins hohe Alter eine Vielfalt verschiedener Aktivitäten erhalte. Dadurch, so eine Theorie, bildet das Hirn eine Reserve aus neuronalen Verknüpfungen, sodass ein krankhafter Schwund an Nervenzellen viel länger kompensiert werden kann. Der aktuelle Slogan der amerikanischen Alzheimer-Gesellschaft lautet entsprechend: "Maintain your brain" - erhalte dir dein Gehirn.


Artikel erschienen am 25. Juli 2004

[meislo]

Alzheimerimpfstoff im Entwicklungsstadium
Plaques und Tangles erfolgreich entfernt

Irvine (pte, 05. Aug 2004 09:15) - Wissenschaftler der University of California http://www.uci.edu arbeiten an der Entwicklung eines Impfstoffes gegen Alzheimer. Es hat sich gezeigt, dass das Injizieren von Antikörpern bei Mäusen den Aufbau der charakteristischen Plaques verhindert. Zusätzlich stellte sich heraus, dass auch die Bildung der Tangles eines anderen Proteins innerhalb der Gehirnzellen gestoppt werden kann. Bei einer Alzheimererkrankung bilden sich Ablagerungen des Proteins Beta-Amyloid (Ab) im Gehirn. Theorien gehen davon aus, dass dadurch in der Folge Tangles des Proteins Tau entstehen, die Gehirnzellen von innen zerstören.

Für die aktuelle Studie wurden gentechnisch veränderte Mäuse eingesetzt, die über menschliche Gene verfügten und so Plaques ausbilden konnten. Die Forscher brachten Anti-Beta-Amyloid Antikörper in den Hippokampus ein. Die Plaquen verschwanden innerhalb von drei Tagen. Die Tau Tangles konnten zwei Tage nach der Zerstörung der Plaques nicht mehr nachgewiesen werden. Als die Tiere 30 Tage nach der Behandlung zum dritten Mal untersucht wurden, hatten sich wieder Plaques aber keine Tangles gebildet. Das legt nahe, dass sie in einem späteren Stadium des Prozesses gebildet werden.

Für die Überprüfung dieser Annahme wurde den Mäusen ein Medikament verabreicht, das die Aktivität eines Enzyms blockiert, das für die Produktion von Beta-Amyloid entscheidend ist. Dieses Vorgehen führte ebenfalls zu einem Verschwinden des Tau. Das Team um Frank LaFerla schreibt im Fachmagazin Neuron, http://www.neuron.org dass diese Ergebnisse nahe legten, dass eine Immunisierung für Plaques und Tangles sinnvoll sei, vorausgesetzt, dass sie bereits früh erfolge. Derzeit wird laut BBC erforscht, ob eine kombinierte Behandlungsform, die auf Plaques und Tangles getrennt abzielt, am meisten Aussicht auf Erfolg hat.
(Ende)

[geldschneider]

Der Kurs in Australien war heute 0,46 zu US $ sind das 0,43.
Plus 5,7 %

für die ADR´s wären das 4,3 der Kurs geht heute aber abwärts!
aktuell 3,60.


Sollte sich heute noczh ausgleichen sonst haben wir schlechte Karten

gruß
gs

[BrauchGeld]

Hi

News

Melbourne, Australia – August 9, 2004: Prana Biotechnology Limited (NASDAQ: PRAN, ASX: PBT) today announced that Prana and Massachusetts General Hospital have agreed to settle all outstanding litigation with P.N Gerolymatos S.A. (P.N.G.) regarding the exploitation rights to certain patents relating to pharmaceutical compositions and uses of clioquinol (also known as PBT-1). Accordingly, all patent oppositions in Europe and Australia are being withdrawn and the law suits pending before the U.S. District Court for the District of Columbia and the Court of Athens in Greece are being dismissed.



As a result of the settlement, Prana and P.N.G. have agreed to recognize the rights of each other to develop clioquinol in their respective territories. Prana will hold the rights to clioquinol in the United States and Japan, while P.N.G. will hold the rights for European and other territories. Prana has agreed to allot 1.35 million shares which will be held in escrow for twelve months and pay a royalty to P.N.G. on sales in the USA and Japan, Prana will receive a percentage of PNG’s income for the other territories.



Mr. Geoffrey Kempler, Executive Chairman of Prana commented, “Prana now holds issued patents in the US on clioquinol (PBT-1), a drug which has already demonstrated that it can slow down the progression of the disease in a group of moderate to severe Alzheimer’s disease patients. In December 2003, promising Phase II clinical trial results evaluating clioquinol in Alzheimer’s disease were published in the Archives of Neurology. This settlement heralds a very important opportunity for Prana, its an important part of our drug pipeline and allows Prana to undertake further clinical development of clioquinol.”



“


Commenting on the settlement, Mr. Panayotis Gerolymatos, President and Chief Executive Officer of P.N. Gerolymatos S.A. stated: “We are pleased to put this litigation behind us. The amicable settlement makes possible the further development of clioquinol and we look forward to working jointly with Prana in this regard.”



Unlike current approved Alzheimer’s therapies that largely treat the symptoms of the disease, clioquinol, PBT-2 and Prana’s other MPAC’s (Metal Protein Attenuating Compound) hold promise to help prevent the progression of the disease.



of Melbourne and Massachusetts General Hospital as a teaching hospital of Harvard Medical School discovered Prana’s technology.

This press release contains “forward looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995 regarding the Company’s business strategy and future plans of operation. Forward-looking statements involve known and unknown risks and uncertainties; both general and specific to the matters discussed in this press release. These and other important factors, including those mentioned in various Securities and Exchange Commission filings made by the Company, may cause the Company’s actual results and performance to differ materially from the future results and performance expressed in or implied by such forward-looking statements. The forward-looking statements contained in this press release speak only as of the date hereof and the Company expressly disclaims any obligation to provide public updates, revisions or amendments to any forward-looking statements made herein to reflect changes in the Company’s expectations or future events.

[geldschneider]

Ich sehe schon, dass hier noch ein paar News fehlen.

Prana Biotech ist auf den 10 biotech Aktien von Forbes zur Beobachtung gelandet!

siehe die Beiträge in Ariva: ab 10.8.04

http://www.ariva.de/board/193617/thread.m?backurl=index.m&a=…

gruß

gs

Charttehcnisch gings schon seit ein paar Tagen auch aufwärts, und ich habe nochmal kräftig nachgelegt.

[geldschneider]

chart hat , bzw. bildet ein W, wird ca. bis 3,6 runtergehen, und dann wieder hoch.

Wahrscheinlich sind wieder ein paar sl ausgelöst worden, oder jemand muzß zwangsverkaufen, was momentan bei der Börse kein Wunder ist!

gruß
gs

[goldmaie]

Test

[goldmaie]

Tagchen,

schon mal aufgefallen dass jemand auf den Kurs drückt?
Wo habt Ihr denn den Wert gekauft? Und über welche Bank?

Irgend etwas stinkt hier sehr!

Mein Empfehlung nicht über CD oder Commerzbank kaufen! sofern es derselbe Marketmaker ist.
Sonst könnt ihr euer Geld auch gleich verbrennen.

Mehr kann ich dazu hier nicht sagen.Näheres nur über Mail zu erfahren, und nur wenn CD Kunde.

Markets Quote Level II Charts News Filings Streamer

Get Quote: MarketsDetailed QuoteLevel II Quote Charts News FilingsStreamer Symbol Lookup powered by
quotemedia.com


Market Depth For Prana Biotechnology Ltd Ads Delayed: Sep 10 1:34 AM EDT

MMD Bid Bid Size
NITE 3.470 43
WIEN 3.460 1
BAMM 3.430 1
MLCO 3.400 1
GSCO 3.380 1
JEFF 3.380 1
SCHB 3.380 1
EKNS 3.260 2
CRWN 3.260 1
TDCM 3.260 1
HILL 3.000 1
SUSQ 3.000 1
SKYC 2.970 1
AFCO 2.000 1
GVRC 1.090 1
NQMO 0.000 0
SIZE 0.000 0
NOCI 0.000 0
ADFN 0.000 0
BRUT 0.000 0
BTRD 0.000 0
TRAC 0.000 0



MMD Ask Ask Size
WIEN 3.540 1
SCHB 3.550 50
NITE 3.600 10
GSCO 3.600 1
SIZE 3.760 20
TDCM 3.800 1
MLCO 3.900 1
EKNS 3.990 5
SKYC 4.500 10
CRWN 4.890 1
BAMM 4.900 1
SUSQ 5.000 1
JEFF 5.340 1
HILL 6.000 1
GVRC 6.620 1
AFCO 10.000 1
NQMO 0.000 0
NOCI 0.000 0
ADFN 0.000 0
BRUT 0.000 0
BTRD 0.000 0
TRAC 0.000 0



Price Qty Time
3.500 330 09/09/04
3.500 380 09/09/04
↑ 3.500 500 09/09/04
3.470 2650 09/09/04
3.470 1900 09/09/04
3.470 100 09/09/04
3.470 3000 09/09/04
3.470 100 09/09/04
↓ 3.470 400 09/09/04
3.500 500 09/09/04
↑ 3.500 500 09/09/04
↑ 3.471 100 09/09/04
↓ 3.460 500 09/09/04
3.500 200 09/09/04
3.500 180 09/09/04
3.500 500 09/09/04
3.500 1500 09/09/04
3.500 300 09/09/04
3.500 500 09/09/04
3.500 320 09/09/04
3.500 680 09/09/04
3.500 320 09/09/04
↓ 3.500 500 09/09/04
3.510 1200 09/09/04
↑ 3.510 200 09/09/04





Copyright © 2004 QuoteMedia. All rights reserved. Terms of Use.
Data delayed 15-20 min. EPS & PE Ratio are based on rolling 12 month figures.
Provided by QuoteMedia, Market Data by NAQ.

[Neoe]

Hier stinkt überhaupt nichts. Im Dezember sind 20 Millionen Optionen in Aktien zu 0.5 AUD konvertierbar. Bis dahin wird sich der Kurs immer wieder diesem Niveau annähern, Anstiege sind vorher nochmal bei der Bekanntgabe des IND-Filings für PBT-2, des Beginns der Phase I und einer eventuellen Phase II/III für PBT-1 zu erwarten.

[Neoe]

Ist zwar auf jeden Fall 6-12 Monate alt, trotzdem ist mir die Nachricht aber noch nie aufgefallen:


Trial Success For Alzheimer`s

By David Welsh, London Press Service

A CLINICAL trial has shown that a treatment for Alzheimer`s disease slowed the progression of cognitive decline in a group of patients with moderate-to-severe symptoms.

The findings of the trials into the effectiveness of the drug Clioquinol for treating Alzheimer`s disease (AD) was carried out by University College London`s (UCL) Department of Psychiatry and Behavioural Sciences in collaboration with Australian drug company Prana Biotechnology. The results were published in the Archives of Neurology.

The study enrolled 36 patients who were assessed for indicators of cognitive performance such as memory, orientation, language, attention and reasoning. The results were assessed using a cognitive score on the Alzheimer`s assessment scale known as ADAS-cog.

Scores range from zero to 70, with lower scores indicating a healthy adult. As dementia progresses, the score increases. Eighteen of the patients were assigned to placebo and 18 received Prana`s Alzheimer`s disease drug, PBT-1 (Clioquinol) the first of Prana`s metal protein attenuating compounds to be developed for Alzheimer`s.

PBT-1 is a chemical that binds zinc and copper, and has been shown to lower levels of antibodies and hence toxicity in the brains of transgenic mice used as a model of AD.

The more-affected patients entering Prana`s pilot clinical trial (those with higher ADAS-cog scores) showed an average change in score at 24 weeks of about 1.5 points on PBT-1 and about 8.9 on placebo, a difference of 7.4 (website: www.pranabio.com).

Generally, untreated patients with mild to moderate AD could be expected to gain 6 to 12 points in their ADAS-cog score over 12 months. A panel convened by the Food & Drug Administration in the US declared an improvement of four points would be clinically significant.

"The results of this trial have been very encouraging to a clinician," said Dr Craig Ritchie of UCL who led the study, adding: "Our findings have led to the development by Prana Biotechnology of new, possibly, more effective drugs which hit the same target as Clioquinol. UCL plans to be involved in further testing of the principal using Clioquinol in a larger, UK multi-centre study which is seeking public funding."

Dr Susanne Sorensen, head of research at the Alzheimer`s Society, says: "The society welcomes this research as the results indicate that there may be a novel use for this already existing drug in the treatment of Alzheimer`s disease. The trial presented here is limited in its scale and the Alzheimer`s Society believes it would be valuable to see a larger-scale trial.

"The potential for new drugs that may interfere with or revert the progression of Alzheimer`s gives hope to people with dementia and their carers. There are currently only limited and expensive treatment options available for Alzheimer`s disease and none that revert the disease for more than a short period."

University College London, Gower Street, London, United Kingdom, WC1E 6BT. Contact: Heidi Foden, Press Office. Telephone: [phone]. Fax: [phone].

[Neoe]

Hier nochmal ein Press Release, dass direkt von der UCL stammt, ist auch mit Datum:


16 December 2003

Clinical trial of Alzheimer’s disease drug shows clear reductions in AD development.
A new clinical trial has shown that a treatment for Alzheimer’s disease slowed the progression of cognitive decline in a group of patients with moderate to severe symptoms. The findings of the trials into the effectiveness of the drug Clioquinol on the treatment of AD, carried out by UCL’s Department of Psychiatry and Behavioural Sciences and Prana Biotechnology Limited, are set out in the new edition of the Archives of Neurology, published on Monday 15th December.

The study enrolled 36 patients who were assessed for indicators of cognitive performance such as memory, orientation, language, attention and reasoning. The results were assessed using a cognitive score on the Alzheimer’s disease Assessment Scale, the so-called ADAS-cog score. The scores range from 0 to 70, with lower scores indicating a healthy adult. As dementia progresses, the score increases. Eighteen of the patients were assigned to placebo and 18 received Prana’s Alzheimer’s disease drug, PBT-1 (Clioquinol) (the first of Prana’s metal protein attenuating compounds (MPACs) to be developed for Alzheimer’s disease). PBT-1 is a chemical that binds zinc and copper, and has been shown to lower the levels of Ab and the associated toxicity in the brains of Transgenic mice used as a model of Alzheimer’s Disease.

The more affected patients entering Prana’s pilot clinical trial (i.e. those with higher ADAS-cog scores) showed an average change in score at 24 weeks of about 1.5 points on PBT-1 and about 8.9 on placebo, a difference of 7.4. Generally, untreated patients with mild to moderate disease could be expected to gain six to 12 points in their ADAS-cog score over 12 months. A panel convened by the Food and Drug Administration in the US deemed an improvement of four points would be clinically significant.

“The results of this trial have been very encouraging to a clinician,” said Dr Craig Ritchie of UCL, who led the study. “Our findings have led to the development by Prana Biotechnology of new, possibly more effective drugs which hit the same target as Clioquinol. UCL plans to be involved in further testing of the principal using Clioquinol in a larger, UK multi-centre study which is seeking public funding.”

Dr Susanne Sorensen, Head of Research at the Alzheimer`s Society says: “The Alzheimer`s Society welcomes this research as the results indicate that there may be a novel use for this already existing drug in the treatment of Alzheimer`s disease. The trial presented here is limited in its scale and the Alzheimer`s Society believes it would be valuable to see a larger scale trial. The potential for new drugs that may interfere with or revert the progression of Alzheimer`s disease gives hope to people with dementia and their carers. There are currently only limited and expensive treatment options available for Alzheimer`s disease and none that revert the disease for more than a short period.”

[Neoe]

Der Jahresabschluss. Persönlich fand ich vor allem, die (wenn auch knappen) Informationen zur Schering-Kooperation interessant, hier tut sich einiges. Eine klinische Pilot-Studie läuft bald an(zwecks Alzheimerdiagnose) und 2004 gab es 1,4 Millionen AUD von den insgesamt möglichen 7,3 Millionen, die im Laufe der Zeit von Schering transferiert werden. Die Allianz ist also in höchstem Maße aktiv.
Zum träumen regt auch die Tatsache an, daß explizit erwähnt wird, dass Neuroscience Victoria, der dritte Partner in dieser Kooperation (und entscheidendes Bindeglied) auch aktiv mit Eli Lilly zusammenarbeitet. Vielleicht wurde dieses Detail nicht umsonst im Jahresabschluss von Prana dokumentiert....


http://www.asx.com.au/asxpdf/20040914/pdf/3mtwpf3xt8mf9.pdf

[Erbse1]

Hallo Prana Fans. Hab nen interessanten Artikel gefunden.

Körpereigene Demenz-Heilung
Zustände von Alzheimer-Patienten, die im Test mit einem Antikörper-Impfstoff behandelt wurden, verbesserten sich

http://derstandard.at/?url=/?id=1794928

Schönen Tag noch
Erbse1

[greenhorn1998]

Hallo zusamen!

Ein Artikel aus der Time.

Lest They Forget
As more people succumb to Alzheimer`s, the search gathers pace for ways to treat or avert the disease
BY DANIEL WILLIAMS

Tuesday, Sep. 14, 2004
An attribute tom valenta once admired in his wife was the methodical way she went about things. "Say we were setting up a piece of kitchen equipment," he says. "She`d have read the instructions and made it work while I was still scratching my head trying to figure out step one." In her 30s, with the couple`s three children all at school, Marie Valenta went to university to study primary school teaching, finishing each year in the top 1% of her class. More recently, she learned bookkeeping to make herself useful in the family`s public relations business. She was clever? "Marie`s a great believer in Edison`s line that genius is 99% perspiration," says Valenta. "She was a super-organized person." Which is why he was quick to notice when she began behaving oddly a few years ago - leaving the front door open when she left the house, "vagueing out" during conversation, struggling with basic instructions. In January last year, at the age of 54, she was diagnosed with Alzheimer`s disease, which doctors predict will end her life within six years unless there`s a breakthrough in treatment.
It`s only her relatively young age that makes Marie`s case unusual: she`s one of 170,000 Australians with dementia, of which Alzheimer`s is the most common type. The incidence of dementia is set to soar in wealthy countries as their populations age. The number of Australians 65 and over is projected to more than double, to 5.7 million, by 2041. Within 20 years, over-85s - of whom roughly a quarter have dementia - are expected to comprise 2% of the population, twice the present figure. But the problem isn`t simply that there`ll be more oldies. A recent report by British researchers suggests that, compared to 30 years ago, brain diseases such as Alzheimer`s strike a higher proportion of people in developed countries, a trend attributed to worsening pollution and greater exposure to harmful chemicals.
Australian authorities are counterattacking. A team of health experts, assembled by the national advocacy group Alzheimer`s Australia and spearheaded by American dementia expert Zaven Khachaturian, will on Sept. 20 in Sydney present a "Vision Statement" that argues "there is no time to lose" and outlines a four-point plan for delaying the onset of dementia. If that goal sounds modest, there`s cause to hope for more. "This is the best of times for Alzheimer`s research," says group member Colin Masters, professor of pathology at the University of Melbourne, who says drugs that could stop or reverse the disease may not be far off. Alzheimer`s inexorably strips people of their memory, personality and eventually all cognitive function. Characterized by the spread of sticky plaques and clumps of tangled fiber that disrupt communication between brain cells, Alzheimer`s typically kills within 5 to 10 years of onset. Partly because the majority of patients spend the last stages of the illness in government-subsidized aged-care homes, Alzheimer`s is extremely costly: an Access Economics report, also to be released next week, estimates that in 2004 the disease will drain more than $A3 billion from the public purse. The thrust of the report is that any measures that can delay the onset of dementia by a few years - or at least delay the need for institutionalized care - will save billions of dollars over coming decades.

The expert group wants the Australian government to fund a dementia research program that tackles the disease from all angles, including drug development. Like remedies for colds and `flu, the four drugs being marketed for the treatment of Alzheimer`s do no more than ameliorate the symptoms. Researchers like Melbourne University`s Masters are involved in developing drugs that they hope will break down the plaques and tangles in patients` brains. "We`ve learned in the last five years that there`s a handful of major therapeutic targets - enzymes that make the protein that accumulates in the brain - that if addressed properly might have a major effect on the disease," says Masters, a director of Melbourne biotech firm Prana, whose Alzheimer`s drug, clioquinol, showed encouraging results last year in a small-scale human trial. "The best-case scenario" for clioquinol and other similar drugs being developed elsewhere, says Masters, "is that they could stop the disease in its tracks." Then, perhaps, the body`s repair mechanism would kick in and clean up some of the damage.
Through a public awareness campaign, the group wants to ram home the message that some people may be able to reduce their risk of dementia. Researchers believe vascular disease increases vulnerability not only to vascular dementia - the second most common type of dementia - but also to Alzheimer`s, presumably because it decreases blood flow to the brain. Doctors want word to spread that things known to be good for the heart - eating well, not smoking, exercising regularly - may also give some protection from dementia. As for the value of mental exercise, the jury is still out.
Masters says there`s no evidence from "solid" trials that doing crosswords and the like does a spot of good. Alzheimer`s Australia leans toward a different position: "Mental stimulation," says national executive director Glenn Rees, "may do some good and certainly does no harm."
The expert group also wants to stress the importance of early diagnosis. Prompt clinical intervention can delay the need for institutionalization and give families extra time to plan for that stage. The same logic applies to the group`s final point: the need for better care of people with Alzheimer`s, and more support for the family members who look after them.
In that area things are moving. On the second Monday of every month, Bob Clarke lunches with up to 14 other men at the Southern Cross Yacht Club on the shores of Canberra`s Lake Burley Griffin. Mostly in their 60s, they form one of Australia`s few all-male Alzheimer`s support groups - the husbands of women in various stages of decline. "You can talk or you can listen, but I`m sure the lunches help," says Clarke, whose wife, Bonnie, 74, was diagnosed in the early 1990s and entered a nursing home two years ago after Clarke had a heart attack. Those who know describe caring for a loved one with Alzheimer`s as one of the most exhausting and distressing jobs, and say governments must do more to help those who take it on. Citing international research, a soon-to-be-released Alzheimer`s Australia paper says "psychosocial interventions for carers have been shown to delay . . . the person with dementia`s admission to a nursing home."
Tom Valenta wants to keep his wife at home "for as long as humanly possible." His feeling is that clioquinol is still three or four years away from the market (others say it could be much longer) - too late to help Marie. So he`s trying to enroll her in the drug`s next trial. Since there`s evidence that Alzheimer`s runs in families, it`s also with thoughts of his children that Valenta longs for speedy progress toward preventing and treating this awful disease.


Gruß, greenhorn

[Erbse1]

Noch ein Ansatz bei Alzheimer.

Grüße
Erbse1

Ceregene Begins Phase I Clinical Trial Of Novel Gene Therapy Product For Patients With Alzheimer`s Disease

http://news.biocompare.com/newsstory.asp?id=51170

[geldschneider]

Steigende Umsätze,
und Kaufsignal

[karo1]

PRANA BIOTECHNOLOGY LTD ADR
Other Search Views: Institutional Ownership View Mutual Fund Ownership View


Displaying North American Holders


N Holder Name Position Pos Change $ Mkt Val % Port % O/S Rpt Date
1 OrbiMed Advisors, Inc. 800,000 800,000 3,600,000 0.08 6.90 06-30-04
2 Highbridge Capital Management LLC 600,000 600,000 2,700,000 0.09 5.17 06-30-04
3 William Harris Investors, Inc. 200,000 200,000 900,000 0.17 1.72 06-30-04
4 Perceptive Advisors LLC 200,000 200,000 900,000 0.33 1.72 06-30-04
5 DKR Capital Partners LP 200,000 200,000 900,000 0.03 1.72 06-30-04
6 Viking Global Investors LP 200,000 200,000 900,000 0.04 1.72 06-30-04
7 Neuberger Berman LLC 10,500 0 47,250 0.00 0.09 06-30-04
8 Marketocracy Capital Management LLC 8,230 8,230 37,035 0.05 0.07 06-30-04
9 Deutsche Bank Securities, Inc. 7,654 7,654 34,443 0.00 0.07 06-30-04


BIOTECHNOLOGY LTD ADR
Other Search Views: Mutual Fund Ownership View Institutional Ownership View


Displaying North American Holders


N Holder Name Position Pos Change $ Mkt Val % Port % O/S Rpt Date
1 UBS Eucalyptus Fund 243,000 243,000 1,093,500 0.40 2.09 06-30-04
2 Marketocracy Masters 100 Fund 8,230 8,230 37,035 0.05 0.07 06-30-04

[Neoe]

Prana`s Open Label Extension Study of PBT-1 Reinforces Positive Phase II Results
Tuesday October 12, 8:31 am ET
- PBT-1 Slows Alzheimer`s Disease Progression and Well Tolerated by Patients -


MELBOURNE, Australia, Oct. 12 /PRNewswire-FirstCall/ -- Prana Biotechnology Limited (Nasdaq: PRAN, ASX: PBT), today announced the results of the open label 84-week "Extension Study" of its Phase II clinical trial of PBT-1 (clioquinol) study, also known as the CQAD study. The data from the formal treatment phase of the study was published in the December 2003 issue of Archives of Neurology.
ADVERTISEMENT


All participants from the original 36-week blinded and placebo-controlled portion of the Phase II trial were offered the opportunity to continue the PBT-1 treatment on an open label basis for an additional 48 weeks. 18 (66.7%) out of 27 patients elected to start the CQADEX extension study. Nine patients completed the full 84-week study.

"The Extension Study data demonstrates that PBT-1 treatment for Alzheimer`s appears to slow the expected disease progression by about half," said Jon Alsenas, DVM, chief executive officer of Prana Biotechnology Limited. "The rate of decline in PBT-1 treated patients, compared to the predicted rate of decline, suggests that the drug has a disease-modifying treatment effect, not simply a cognition enhancement effect. Moreover, the results show that PBT-1 is well tolerated by patients and has no increased adverse effects over those to be expected in untreated patients suffering from Alzheimer`s disease."

Data from the Extension Study data revealed that Alzheimer`s patients with ADAS-cog scores similar to those in the CQAD and the CQADEX would have been expected to decline by an average of 18 points over the treatment period. The results showed an average decline of approximately eight points for a difference of 10 points from that predicted without treatment in the nine patients on PBT-1 for 84 weeks. Results from the MMSE (Mini Mental State Examination) were also encouraging, as, when compared to baseline, the patients on 84 weeks of PBT-1 demonstrated no statistically significant decline.

"PBT-1 represents a novel approach to Alzheimer`s: namely, a disease-modifier. In other words, PBT-1 targets a key feature of the underlying process that appears to cause the destruction of nerve cells," said Sam Gandy, MD, PhD, Professor of Neurology and Director of the Farber Institute at Thomas Jefferson University. "Alzheimer`s is believed to begin as long as 10 years or more before clinical memory loss is manifested. Accordingly, disease-modifying drugs may need to be administered for many years. Along this line, it is extremely encouraging to see evidence that PBT-1 is well-tolerated for extended periods."

The full publication on the data from the extension study is available on Prana`s website http://www.pranabio.com.

Prana is currently evaluating the next potential steps in continued PBT-1 clinical development and anticipates being able to announce its plans in the near future.

Company Management is hosting an Analyst Day at The Four Seasons, Salon A&B, in New York City, on Monday, October 18, 2004. Featured speakers will include Dr. Bush, Professor Rudolph Tanzi, Neurology, Harvard Medical School, Massachusetts General Hospital, Dr. Craig William Ritchie, Psychiatry, Royal Free Campus, University College London, UK and Medical Director, Clinical Trials Centre, UCL Biomedica, University College London, UK, as well as Dr. Jon Alsenas, CEO and Dr. Ross Murdoch, COO of Prana.

[geldschneider]

http://www.ariva.de/board/193617/thread.m?backurl=board_hot.…

Hier gibts noch weitere News!

[karo1]

Ups
Da fehlte doch der Link zu #125
http://www.lionshares.com/details.cfm?SEARCH=symbol&CUSIP=73…

[BrauchGeld]

Hallo !

Melbourne, Australia – October 15, 2004: Prana Biotechnology Limited (NASDAQ: PRAN, ASX: PBT), today announced that the Journal of Biological Chemistry has published a new paper in its September 30 edition called ‘Clioquinol Mediates Copper Uptake and Counteracts Cu Efflux Activities of the Amyloid Precursor Protein of Alzheimer’s Disease.’ The paper further supports Prana’s theory that PBT-1 (clioquinol) slows down the progression of Alzheimer’s disease.



Based on the hypothesis that beta amyloid is a key player in the onset and progression of Alzheimer’s disease, Prana maintains that it is the inappropriate interaction of beta amyloid with brain metals, copper and zinc, that leads to the progression associated with the disease. Unlike current approved Alzheimer’s therapies that largely treat the symptoms of the disease, PBT-1, PBT-2 and Prana’s additional MPACs (Metal Protein Attenuating Compounds) hold promise to help prevent the progression of the disease.



The newly published paper helps clarify the normal role of Amyloid Precursor Protein (APP), the precursor of amyloid beta protein that is the primary constituent of the senile plaques that are characteristically found in Alzheimer’s disease brains. APP appears to be a critical regulator of intracellular Cu homeostasis. The authors also show that oral treatment of transgenic mice with clioquinol (also known as PBT-1) does not result in a depletion of Cu and Zn systemically suggesting that PBT-1 does not act as a metal chelator, but instead may be redistributing these metals from the amyloid plaques back to cells.



Rudolph E. Tanzi, Ph.D., Director, Genetics and Aging Research Unit, Massachusetts General Hospital, Professor of Neurology, Harvard Medical School and co-founding scientist of Prana Biotechnology, commented, "The new findings showing that PBT-1 can act therapeutically by facilitating copper uptake into cells could be clinically very beneficial for treating Alzheimer’s disease when taken together with it`s ability to clear senile plaques."

Gruss
B.M.

[BrauchGeld]

Guten Morgen

PRANA PLANS TO INITIATE PHASE II/III ALZHEIMER’S DISEASE STUDY
Study Enables Company to Move
from Pre-Clinical to Late Stage Clinical
Melbourne, Australia – October 18, 2004: Prana Biotechnology Limited (NASDAQ:
PRAN, ASX: PBT), today announced that it plans to initiate a Phase II/III study to
examine the effect of PBT-1 in moderate to severe Alzheimer’s disease patients in the
late first quarter or the second quarter of 2005.
The Phase II/III study on PBT-1 will be known as the PLACQUE (Progression Limiting
in Alzheimer’s: ClioQUinol’s Efficacy study) and will be conducted under the overall
direction of Dr. Craig Ritchie of the Royal Free Campus, University College London.
“The results from the recently released CQADEX study have provided supportive
evidence for the conclusions of our double -blind Phase II trial,” said Dr. Ritchie. “It is
with some optimism that we look forward to further testing of this drug in a much larger
study. Of the third generation drugs for Alzheimer’s disease, clioquinol appears to be
one of the lead candidates to make it into the clinic and to have a significant impact on
both clinical symptoms and disease progression.”
Plans for the study include enrollment of 435 patients in the United Kingdom, Australia,
and the Republic of South Africa under double blind conditions. Patients will be treated
for 52 weeks, and randomized into placebo and two treatment arms (125 mg and 250
mg BID). Prana currently anticipates that the results will be available no sooner than
late 2006 but expects to be able to provide updates as the trial progresses.
“The initiation of the study allows us to make a substantial leap forward of two to three
years in terms of the amount of time it will take to achieve potentially pivotal results with
our core MPAC platform,” said Dr. Jon Alsenas, CEO of Prana Biotechnology. “In
addition, securing the patent of PBT-1 in August enables us to leap from being an early
stage, pre-clinical company to a late stage company with a drug in advanced clinical
trials.”
Prana’s decision to advance PBT-1 into advanced clinical trials was strongly influenced
by the promising proof-of-principle Phase II results published in the December 2003
Archives of Neurology, as well as the extension phase results from that study that was
released on October 12, 2004, demonstrating the deterioration of Alzheimer’s disease
patients was significantly slowed when compared to their predicted rate of decline. The
differences in the rates of predicted decline and the actual decline suggest that PBT-1
has a disease-modifying treatment effect, not simply a cognition enhancing effect.
Dr. Alsenas concluded, “Prana will soon have two very promising drugs in the clinic with
PBT-2, our other clinical candidate, which is expected to start a Phase I clinical trial in
early 2005.”

Gruss
B.M.

[BrauchGeld]

Hi

Prana Biotechnology Receives Clinical Trials Authorization in UK to Initiate PLACQUE Phase II/III Study
Tuesday January 4, 8:31 am ET
-- Enrollment of 435 Alzheimer`s Patients to Begin in Q2 2005 --


MELBOURNE, Australia, Jan. 4 /PRNewswire-FirstCall/ -- Prana Biotechnology Limited (Nasdaq: PRAN, ASX: PBT), today announced it has received a Clinical Trials Authorization (CTA) from the Medicines and Healthcare Products Regulatory Agency (MHRA) of the United Kingdom to initiate the potentially pivotal PLACQUE (Progression Limitation in Alzheimer`s: ClioQUinol`s Efficacy) Phase II/III clinical trial.
-- CTA approval enables company to move forward

-- Study enables Prana to progress to late stage development company

-- Prana meets milestone outlined at Analyst Day

-- PBT-1 may be first drug to modify the progression of Alzheimer`s
disease


Study Specifics

The PLACQUE trial will be conducted over 52-weeks and will enroll 435 patients in the United Kingdom, Australia and the Republic of South Africa. The purpose of the study is to assess the efficacy of two dose levels of PBT-1 (clioquinol) when added to the current therapy of patients with moderate Alzheimer`s disease. The trial will be randomized, double blind and placebo-controlled. The primary endpoint of the study will be to demonstrate a reduction in the progression of Alzheimer`s as measured by the Alzheimer`s Disease Assessment Scale-cognition (ADAS-cog).

Significant Milestone

"Receiving CTA approval is a significant milestone for Prana," said Jon Alsenas, CEO of Prana. "When 2004 began, the future of PBT-1 was uncertain due in large part to patent litigation and other concerns. Now as we begin 2005, the patent litigation with P.N. Gerolymatos, S.A. is behind us and we are on the cusp of transforming Prana from an early stage development company to a late stage development company with the initiation of the potentially pivotal PLACQUE trial. The CTA approval allows us to clear the first regulatory hurdle to establishing PBT-1 as the first truly effective therapy for Alzheimer`s sufferers.

"We are extremely hopeful that PBT-1 will be the first drug to target what is believed to be the root cause of Alzheimer`s disease -- the accumulation of amyloid plaques in the neocortex of the brain," continued Dr. Alsenas. "Clioquinol appears to be one of the lead candidates to have a significant impact on both clinical symptoms and disease progression."

Outlook for 2005

Prana expects to have two promising Alzheimer`s drugs in the clinic, with the PBT-1 Phase II/III PLACQUE study initiating in the second quarter and the PBT-2 Phase I clinical trial also commencing in early 2005. Moreover, Prana continues to focus upon developing a pipeline of drugs for the treatment of other disorders where inappropriate protein aggregation plays a key role, such as in Parkinson`s disease.

"The Metal Theory"

The prize-winning science behind PBT-1 is based upon what is known as "the metal theory" of Alzheimer`s disease. The theory is based on the premise that key metals, such as zinc and copper, are required for the inappropriate aggregation of amyloid beta to form the amyloid plaques. These plaques are then thought to cause the neurodegeneration associated with Alzheimer`s disease. PBT-1 is the first of Prana`s Metal-Protein Attenuating Compounds (MPACs) to be studied in a potentially pivotal trial. The metal-mediated aggregation of proteins is also thought to be a key contributor to the development of a variety of other degenerative disorders.

Gruss
B.M.

[Neoe]

Prana ist mein persoenlicher Favorit fuer 2005. Sollte die Boerse nicht abstuerzen, gehe ich fuer Mitte des Jahres von 8 Dollar aus (AMEX:Pran).

Sollte Axonyx erfolgreich sein mit Phenserine und Prana zeitgleich die Phase I fuer PBT-2 und die Phase II/III fuer PBT-1 einleiten, wird das nicht spurlos am Aktienpreis vorbeigehen. Der Hype steht vor der Tuer.

[BrauchGeld]

Hi

Prana Biotechnology initiated with "market outperform"

Wednesday, January 26, 2005 10:10:11 AM ET
Rodman & Renshaw


NEW YORK, January 26 (newratings.com) - Analysts at Rodman & Renshaw initiate coverage of Prana Biotechnology (ticker: PRAN) with a "market outperform" rating. The target price is set to $12.


Gruss
B.M.

[goldmaie]

" target="_blank" rel="nofollow ugc noopener">http://www.ariva.de/board/board_hot.m

[BrauchGeld]

Hi

Schlechte news von Axonyx, einer weniger im Spiel.


Axonyx Announces That Phenserine Did Not Achieve Significant Efficacy in Phase III Alzheimer`s Disease Trial
Monday February 7, 12:15 am ET


NEW YORK--(BUSINESS WIRE)--Feb. 7, 2005--Axonyx Inc. (NASDAQ:AXYX - News) announced today that the top line outcome of its first Phase III clinical trial with Phenserine, in development for mild to moderate Alzheimer`s disease (AD), showed that although there were encouraging trends with both Phenserine 10mg and 15mg twice daily, overall these did not result in a statistically significant improvement over placebo for the protocol`s primary endpoints following 26 weeks of treatment. While Phenserine-treated patients performed better in the ADAS-cog and CIBIC assessments, the study`s primary endpoints at almost all time points, the outcome was potentially confounded by a better than expected ADAS-cog response in the placebo-treated patients. A preliminary review of the adverse events has revealed no safety or tolerability concerns associated with Phenserine treatment. Axonyx is continuing to further analyze the data and will use this valuable information to optimise the trial designs in the currently planned program.
ADVERTISEMENT


The Phase III trial recruited 384 mild to moderate Alzheimer`s patients from 16 clinical sites in Spain, United Kingdom, Croatia, and Austria. Patients, after being diagnosed as having probable AD, were randomized to receive placebo, Phenserine 10mg twice daily or 15mg twice daily for a period of 6 months. Throughout the treatment period patients were regularly assessed using standard cognition and memory assessments.

Phenserine is currently undergoing testing in a Phase IIB trial to evaluate its anticipated ability to lower levels of beta-amyloid precursor protein ((beta)-APP) and beta-amyloid (A(beta)) in the plasma and cerebrospinal fluid (CSF), which may lead to a slowing of disease progression. The results of the Phase III trial will not impact the interim analysis planned of the available CSF and plasma samples for (beta)-APP and A(beta), and these results are expected before the end of March.

Phenserine is a highly selective acetylcholinesterase (AChE) inhibitor that breaks down a neurotransmitter in the brain important in memory and cognition. Unlike other AChE inhibitors, which only suppress the activity of the enzyme, Phenserine has been shown to have two mechanisms of action: (1) the inhibition of the AChE enzyme, and (2) in preclinical studies, the inhibition of the synthesis of A(beta), the protein in the brain that is thought to be a cause of brain cell death in Alzheimer`s disease.

Gruss
B.M.

[derschweizer]

@all

Wow, Axonyx bricht vorbörslich -63,5% auf 1,72 US$ ein

[Neoe]

Also kein Phenserine-Hype, aber mal wieder eine Bestaetigung, dass PRANA das goldene Kalb im Stall stehen haben koennte.

In drei Jahren steht der Prana-Kurs bei minimum 40 Dollar.

[BrauchGeld]

Hi

Prana Biotechnology Maintains Position On Forbes `Neurological Drugs to Watch` List
Monday February 14, 8:30 am ET


MELBOURNE, Australia, Feb. 14 /PRNewswire-FirstCall/ -- Prana Biotechnology Limited (Nasdaq: PRAN, ASX: PBT), today announced that Forbes.com continues to list PBT1 (Clioquinol) on its list of "Neurological Drugs to Watch", which highlights the most promising experimental drugs to treat diseases of the brain and nervous system.
For more information on Forbes "Neurological Drugs to Watch", visit:
www.forbes.com/sciencesandmedicine/2004/01/26/cx_mh_rl_neuro…

Gruss
B.M.

[BrauchGeld]

Moin

Prana Biotechnology Commences Phase I Clinical Trial of PBT2
Monday March 14, 8:30 am ET
- Second MPAC Enters Human Clinical Studies -


MELBOURNE, Australia, March 14 /PRNewswire-FirstCall/ -- Prana Biotechnology Limited (Nasdaq: PRAN, ASX: PBT), announced today that it has commenced the Phase I clinical trial of PBT2 with the dosing of its first subject at a facility associated with the Utrecht University Hospital in Utrecht, The Netherlands. The Phase I clinical trial is the first of a planned series of studies examining the safety and pharmacokinetics of PBT2 in normal human volunteers.
ADVERTISEMENT


PBT2 is the first completely Prana-discovered compound, and is the successor to PBT1 for the treatment of Alzheimer`s disease. PBT2 is designed to have an improved safety and efficacy profile compared to PBT1. The compound has demonstrated significantly greater effectiveness in lowering plaque in the transgenic mouse model in both pre-clinical in-vitro and in-vivo testing. Moreover, it appears to be better than PBT1 at decreasing the toxicity of plaques through improved peroxide inhibition, and appears to have better pharmaceutical characteristics, such as improved solubility.

"We are extremely excited to be taking the first exclusively Prana-developed compound into the clinic," said Dr. Jon Alsenas, CEO of Prana. "I am extremely proud of Prana`s staff for achieving this important milestone. The Phase I clinical trial of PBT2 marks a second significant milestone for our Company in the past three months. The other was the previously announced approval in the United Kingdom of a CTA (Clinical Trials Authorization) for the initiation of the potentially pivotal Phase II/III PLACQUE study of our lead compound PBT1 for Alzheimer`s disease. PLACQUE is on track to begin enrollment in the first half of 2005. The PBT1 and PBT2 clinical programs demonstrate our commitment to developing Metal-Protein Attenuating Compounds (MPACs) for the treatment of Alzheimer`s disease."

Alzheimer`s currently affects 4.5 million individuals in the US and 14 million individuals worldwide, and the rate of incidence is expected to increase with aging demographics

"The Metal Theory"

The prize-winning science behind PBT2 is based upon what is known as "the metal theory" of Alzheimer`s disease. The theory is based on the premise that key metals, such as zinc and copper, are required for the inappropriate aggregation of amyloid beta to form the amyloid plaques. These plaques are then thought to cause the neurodegeneration associated with Alzheimer`s disease. The metal-mediated aggregation of proteins is also thought to be a key contributor to the development of a variety of other degenerative disorders.

[Neoe]

Ich hoffe dieses Jahr auch noch was von der Kooperation mit Schering zu hoeren zwecks Alzheimer-Diagnose.

Ausserdem steckt da noch einiges in der Roehre im Zusammenhang mit der PhaseII/III in England. Eigentlich sollte hier noch die finanzielle Unterstuetzung durch einen Verband bekanntgegeben werden. Zudem eine weitere Einigung mit PN Gerolymatos eingegangen werden, um die Studie zur Zulassung in Europa verwenden zu koennen, wo ja PNG die Rechte hat.

[greenhorn1998]

Hallo zusammen!

ABC-News:
Last Update: Friday, April 1, 2005. 12:00pm (AEST)
Companies given $47m R&D funding

The Federal Government has given $47 million to seven Australian pharmaceutical and biotechnology companies.

Federal Industry Minister Ian Macfarlane says the funding is part of a five-year initiative to encourage high-quality research and development.

" There is a tremendous breadth in the successful projects - from research and development in cancer treatments to HIV/AIDS, cardiovascular and central nervous system problems and age-related neurodegenerative conditions," Mr Macfarlane said.

" They are importantly all projects with the potential to improve our lives, just as much as they will build on company bottom lines and this investment will make sure our home-grown research is commercialised in Australia."
Companies

Starpharma has been offered $5.6 million to develop products to fight cancer, HIV and respiratory diseases.

CBio Queensland has been given $6 million to commercialise its treatments for inflammatory and auto-immune disorders.

Prana Biotechnology in Victoria has been given $10 million for research and development of age-related, neurodegenerative disease.

Peplin in Queensland has been given $5.6 million to build on its treatment for non-melanoma skin cancer.

Pfizer Australia has been given $10 million for work in areas including cardiovascular, oncology, the central nervous system and infectious and inflammatory diseases.

Alphapharm in Queensland has been given $1.9 million to further develop their range of more than 550 generic medicines.

Alchemia in Queensland has also been given $7.8 million to develop carbohydrate-based therapeutics for the global market.

Gruß, greenhorn

[greenhorn1998]

Hallo zusammen!

Es ist ziemlich ruhig geworden. Und der Kurs findet momentan keinen Halt. Zu meiner völligen Überraschung. Mittlerweile haben wir ein Niveau nahe Cash erreicht, es kann mir doch keiner erzählen, dass die Arbeit, die Prana bisher geleistet hat, nichts wert sein soll?

Wie geht es weiter? (Gute Frage ich weiß.)

Gruß, greenhorn

[Neoe]

Hi greenhorn,

lange nicht gesprochen. Nach einem boesen, boesen Maerz bin ich ebenfalls wieder zu Prana zureuckgekehrt.

Mit den 10 Millionen AUD der Regierung und den Non-Cash-Assets wird Pranas wissenschaftliche Leistung momentan tatsaechlich mit 0,0 Euro bewertet.
Ich habe es zu einem Gross-Einstieg genutzt. Die ersten zehn bis 20 Prozent sind dann schon drin, wenn allein nur endlich mal die Regierungs-News auf den Weg gebracht wird.
IR-technisch sind sie leider immer noch in der Amateur-Klasse.

Ein Problem ist definitv, dass die Aktien in Australien und den USA gehandelt werden, sie ausserdem die USA alles ihren Zielmarkt angeben, aber leider PBT-1 in Europa weiterentwickeln, wo sie leider keine rechte zur Kommerzialisierung haben.
Hier geht mir der Sinn ab, obwohl ich hoffe, dass ich den noch entdecke und vor allem hoffe, dass mehr dahintersteckt als wir gerade wissen.

Hier mal einige Theorien, nur so zum Spass:

1.Gerolymatos wird nach positiven Studien auf Basis der Prana-Ergebnisse die Kommerzialisierung in Europa beginnen. Vielleicht zu verbesserten Konditionen fuer Prana, da Gerolymatos ja selbst anscheinend keinen Finger ruehrt, um hier was vorwaerts zu bringen. Vielleicht kauft Prana die Rechte auch zurueck und zahlt Gerolymatos dafuer hinterher Royalties.

2.Prana bringt PBT-1 durch die Muehlen der Englischen Behoerden und vertreibt hinterher PBT-1 hinterher in den Commonwealth-Staaten. Das scheint mir nicht unlogisch, da die Trials in Australien, Suedafrika und England stattfinden.
Dies allerdings unter der Voraussetzung, dass diese Studien ausreichend sind/anerkannt werden, um in diesen Laendern zur Zulassung einzureichen. Davon gehe ich mit grosser Sicherheit aus.
Viel wichtiger ist, wie wurden die Maerkte zwischen Gerolymatos und Prana aufgeteilt. Bisher habe ich nichts genaueres gelesen, ausser:
Europa and other territories?? (Gerolymatos)
USA and Japan (Prana)


Wer weiss mehr ???

[goldmaie]

Ich sags mal rundheraus, meines Erachtens nach undmeiner Beobachtung nach, wird der Kurs von einem Makler ganz stark manipuli9ert. Dieser Makler hat mir schon eine Menge Geld gekostet und ihr solltet ihn mal auf die Watch Liste nehmen. Unglücklicherweise habe ich vorher Konto bei Commerzbank, bzw. Comdirect gehabt, die haben mir dann wegen meiner Reklamation wegen dieses maklers gekündigt und 9ich habe durch den Kursverlaust nicht nur bei Prana sondern insgesamt durch den Zwanzusverkauf bei Codei, alles was ich verdient habe verloren. Trotz Erkrankung, erhielt ich keinen qaufschub um ein e bank zu finden, die mir die gleichen Konmditonen wie codi gewährt. Kurz die haen noch einen Zewangsverkauf gemacht mit Vivacon, war eine große Menge, habe immer einen Teil auf Kredti daich Vieltrader bin, , Vivacon war meine Altersversurgung. Kurs Vivacon machte danch in weniger 1000 %, Der Verlust lä´ßt sich nciht ermessen. einschl. Prana.


Jedesmal, wenn ich bei Codi, und jetzt auch bei dem neuen Makler drer neuen Bank den Wert in großen Mengen zum Verkauf reingestellt habe, weil bei Codi, gab es damals ja hohe Gebühren bei Streiungen, also ließ ich alles aufträge drin, malte sich der Makler aus, dass hier jemand das ist, der 5000 Aktion verkaufen wrd, wenn er nur tief genug den Kurs drückt.

Tagesumsatz ist Q 10 TSD, dann kann man sich vorstellen was passiert, wenn einer mit meinen aktien sozusagen Short geht.

Der Makler heißt SCHB. Und ist auch für Cortal Consors tätig, ermqacht nun das gleiche Spiel schon wieder, weil ich eben Verkäufe overnight stehen ließ, weil ich nun mal auch welche Kaufe um sie wieder zu verkaufen. Da es bei Prana oft so ist, dass der Höschtkurs, wie gestern wieder immer in der ersten Stud. erreicht wird und wenn das verpasst wurde ist es wieder vorbei, lass ich die Order eben stehen. Genau das ist bei den beiden Banken, aber tödlich, weil dieser SCHB also z.B., sah,
1200 Stück zu 4,44
Dann ging der Kurs runter ich ließ die Orsder stelle rein
zusätzlich jeweils imjmer zu verstehen:
1000 Stück zu 4,38
danach:
1500 zu 4,22
bis es am schluss genau 4500 gesamt an Aktien gab zum Verkauf von Prana oder 4800, läßt sich alles belegen.
Rest zu 4,15
5000 ist aber nur ein Teil was ihc von Prana gesamt habe.

Kursz ich merkte, dass der Makler, der für meine Bank handelte auf einmal zu 3, 70 5000 reinstellte, was den Preis rapide nach unten drückte. Er verkaufte leer.
Da bin ich mir ganz sicher. Auf der Bid Seite stand er schon auf der Lauer und kaufte jeweils noch günstiger ein.
Er rechnete dann damit, dass ich meine 4500 Aktien bald für unter 4, 70 einstellen würde zum Verkauf. Ganu das tat ich nicht, ich strich alle meine Orders, jedenfalls bei diesem Makler.

von dan an ging der kurs langsam aber stetig wieder nach oben.
Und Der Makler hatte wohr erst mal Probleme wieder rauszukommen, aus dem Markt, da er sich eindeckenmußte.
Leider treibt er das Spiel schon

nur dass er diesmal vrosichtiger ist, ich habe nämlich diesmal die Börsen Sec. in USA verständigt, und reduziert die Mengen mit denen er den Kurs drückt aber dennoch immer in großen Mengen zum kleinen Kurs.

ich bin bald pleite, weil lange kann man so ein Spiel iund soclhe Verlauste nicht mehr machen, weil der kUrs nun wieder künstlich gedrückt wurde, trotz guter News.

eine Zeitlagn habe ich durch traden eien Teil meiner Verluste auch mit diesem Wert wieder wettgemacht, aber der Handel ist edie letzen Wochen einfach immer weinger geworden, und wie gesagt, leider geht der Makler " SchB" bzw. ging in grußen Mengen short.

Es ist sicher verbvoten short zu gehen mit Aktien unter 5 $ und bei dieser geringen Hadelsmenge, aber wo klien Kläger , ist keien Richter. und ich hatte noch nicht dei Zeit, und die Nervben alles zusmamenzustellen was leztes Jahr geschah, als der Makler den Kurs so massiv drückte.


Deshalb Warnung:

Wer mit dem Makler SCHB zu tun hat und Prana verkaufen will oder auch kaufen, der Makler manpuliert den Kurs. Leider wurden z.B. damals auch nicht die aktien zu den WErten verkauft, die zwar mehrmals am Tage erreicht wurden mit diesem Kurs, weil der Makler meines ERachtens nach den Wert nicht anbot. Damals hatte ich das Lebvel II nur verzögert, so dass ich nich lückenlos, beweisen konnte, dass der Makler Fehlerhaft gehandelt hat, Bzw. die Comdirekt hat meine berechtigte Reklamation nicht anerkannt.

Bei einem anderem Wert den ich dort handelte, ein OTC Wert, ging der Makler an manchen Tagen mit dem Wert erst gar nicht an die Börse, genau an den Tagen, an dem aber massiv gehandelt wurde, an macnhen Tagen gerade mal eine Std. am Tag.,

Aufgrund eben dieser Reklamationen wurde mir gekündigt. und ich kam vom Regen in die Traufe. Habe zwar nun Level II Zugang, aber Kulanz ist dort ein Fremdwort.

Trotz richtiger Eingabe, von VK Prana zu 4,15, hättt ich angeblich 3,15 3ingegeben, und es wurde dann zu 3,85 natürlich der VK ausfgeführt. Was für ein Verlust und löäste natülich wieder einen Kursrutsch bei diesem Wert aus.

Lange Geschichte.?

Fazit ist, wer gester, oder heute noch einsteigt, es sollte charttechnisch wieder nach oben gehen, wenn nicht wieder der Makler shortet, bzw. wenn ich nicht unvorsichterweise übernacht, Prana zum Verkauf stehen lasse. Weil mir das zum Verhängnis wird. Aber es nervt natürlich sowas, weiil ich keine Lust habe, und Zeit mich nur noch auf Pran zu konzentireren und am liebsten würde ich nach USAfliegen und
mir den Makler vorknöpfen.

Es ist zum Weinen! Der SchB dürfte auch für Penson, Cortal consors tätig sein.
Fazit, Prana bei Commerzbank und Co, Penson und Cortal Consors nur vorsichtig handeln und nie über Nacht , und nie volle Mengen dem Makler aufzeigen was da ist , insbesondere beim VK, weil er dann sofort shorten geht.



Bis vorgestern hat der Maler SCHB wieder zu Dumpingpreisen
3 Tsd angeboten, und prompt fiel der Kurs, die ganzen letzten Tage.

Im bid lauerte der Makler aber jedesmal wieder und kaufte billig ein. ich hängte mich mal dazu., aber leider verfiel der Kurs weiter, Kauf zu 3, 50, mittlerweile bis zu 3, 11 gestern im low.


Aber wie gesagt, Kaufgelegenheit heute, weil es geht heute hoch, zumindest nach der Candlelight analsyse. Stand gestern auf buy-if, heute noch nicht aktualiesiert.

Habe keinen Verkauf bei SCHB overnight dirn, es sollte wieder hoch gehen.

[Neoe]

goldmaie:

Obwohl dies natuerlich theoretisch immer moeglich ist, lass uns bitte davon absehen, da diese Spekulationen nirgendwo hinfuehren und es keine geeigntete Stelle gibt, die dir dass unter Umstaenden jemals bestaetigen koennte.

Nutze es fuer einen Einstieg/Zukauf und freu dich spaeter.
PRAN heute schon 5 Prozent im Plus und News sind kurzfristig zu erwarten.

1. 10 Millione AUD von der australischen Regierung

2. Praeklinische Daten auf einer der kommenden Konferenzen. Vielleicht schon dieses Wochende ?

3. Phase II/III in England

Alles noch dieses Quartal und dass bei PPS at asset level.
Wo soll es hingehen ausser nach oben????

[goldmaie]

Es ist wie es ist, es ist lächerlicxh der Kursanstieg heute.

Der makler hängt schon wieder im bid vorher mit 1000, bei 3, 20, jetzt mit 3,30 drin, diesmal eine kleine Menge.

Nachweisbar versucht er mit großen Mengen sowohl beim Kauf, als auch beim VK auf den kurs zu drücken. Dei Rechnung geht bei ihm auf.

Nachweisen läßt sich das schon über das SEC Office, weil er dann beweisen muß, ob er Aufträge hatte, oder ob er selbst so gehandlet, spricht Akteine leer verkauft hat, die er nicht hatte.

Bei einem bisherigen Verlust von zig tausend Euro, bruache ich mich über so kleine Kursanstiege nicht beunruhigen, sprich freuen.

Ich sagte doch, dass es charttechnisch auf Plus steht!!


Durch meine Verluste kann ich nicht nachkaufen, schon gar keine Pennystocks, weil die nicht beleihbar sind. Habe sovieso zu viel von Prana. Werde sie jedoch nicht verschleudern zu dumpingpreisen.

die Aktie machte insgesamt 30 % Minus seit diesen Manipulationen.
Die Aktie notierte gestern oder vorgestern fast zum Allzeittief, wenn das nichts ausssagt.Und das ohne schlechte news!

Deshalb keine VErköufe und Käufe über Nacht stehen lassen, insbes. wenn es eine der Banken ist, die mit dem SCHB Makler arbeiten!

[goldmaie]

Sorry< jetzt habe ich vorhin vergessen den Screenshoot, alleredings verzögert reinzustellen. Der Makler SCH steht
als einziger mit einer Riesenmenge und einen Riesen- Niederen Kurs, Dumping Kurs drin, nämlcih 1000 zu 3,10.
Damit drückt er natrülich auch den Kurs, da er zwar eine größere Menge, aber doch zu keinem vernünftigen Kurs signalisiert. Alles zufall? Ich glaube nicht daran, dass der Makler nicht für sich selbst bei deiesem Wert tätig ist, weil er weiß, das jemand da ist, z.B. ich, der große Mengen hat, von seinen Auftraggebern. Damit kann er mich in die Knie zwingen. Er hat das ja anfangs, als ich es noch nicht wußrte auch sgeschafft. Und die anderen wissen es ja nicht, und verkafen und verkaufen zu den dumping Kursen.

Manipulation kann man leider bei Werten machen, wie man sieht, wenn der Handel gering ist. Tagesvolumen 10 TSd Stück heute, 12000, das ist nicht viel, ich war heute nur mit 1000 Stück VK dabei.

Allerdings habe ich diese Stücke vor 2 Tagen billiger gekauft und natürlich gleich den kleinen Anstieg ausgenutzt.

Sorry< meiner Tippfehler, ich tippe blind und haue in die Tasten rein.

Time MMID Size Bid
13:29 BRUT 2 3.28 ↓
10:07 ETRD 2 3.26
14:33 NITE 4 3.20
13:29 GSCO 1 3.19 ↓
14:28 TDCM 1 3.14 ↓
13:43 SCHB 10 3.10 ↓
07:30 EKNS 5 3.10
07:30 HDSN 1 3.10
07:30 JEFF 1 3.06
07:30 HILL 1 3.00
07:30 RODM 1 3.00
08:04 MLCO 1 3.00
08:47 SKYC 1 3.00 ↓
07:30 SUSQ 1 2.55
07:30 AFCO 1 2.00
09:25 PUGS 1 0.010 ↑
07:30 ADFN 0 0.000
07:30 BTRD 0 0.000
07:30 NOCI 0 0.000
07:30 NQMO 0 0.000
13:29 SIZE 0 0.000 ↓
14:33 TRAC 0 0.000









Ask Size MMID Time
↓ 3.31 10 NITE 14:33
↑ 3.45 1 TRAC 14:33
3.46 1 GSCO 13:29
3.65 1 MLCO 08:04
3.65 1 TDCM 14:28
3.90 1 SKYC 08:47
4.00 5 EKNS 07:30
4.10 1 HDSN 07:30
4.15 7 SCHB 13:43
4.42 1 SUSQ 07:30
5.00 1 HILL 07:30
5.00 1 JEFF 07:30
5.00 1 RODM 07:30
6.00 3 ETRD 10:07
10.00 4 BRUT 13:29
10.00 1 AFCO 07:30
↑ 2,000.00 1 PUGS 09:25

[Neoe]

@goldmaie:

Du solltest in diesem Zusammenhang vielleicht einen neuen Thread aufmachen. Wie gesagt KANN sein, allerdings hat es mit dem Unternehmen wenig zu schaffen. Ob du deinen Einstiegskurs wieder siehst hat doch eher was mit der Unternehmensqualitaet zu tun als mit irgendeinem Makler, zumal Prana derzeit auch kein Kapital aufnehmen muss.

[Neoe]

Hier nochmal potentieller Sprengstoff, hab ich glaube ich schon irgendwann gepostet, heute aber interessanter denn je:


Clinical Trial of Alzheimer`s Disease Drug Shows Clear Reductions in AD Development
alzheimersupport.com

12-22-2003

A new clinical trial has shown that a treatment for Alzheimer`s disease slowed the progression of cognitive decline in a group of patients with moderate to severe symptoms. The findings of the trials into the effectiveness of the drug Clioquinol on the treatment of AD, carried out by UCL`s Department of Psychiatry and Behavioural Sciences and Prana Biotechnology Limited, are set out in the new edition of the Archives of Neurology, published on Monday 15th December.
The study enrolled 36 patients who were assessed for indicators of cognitive performance such as memory, orientation, language, attention and reasoning. The results were assessed using a cognitive score on the Alzheimer`s disease Assessment Scale, the so-called ADAS-cog score. The scores range from 0 to 70, with lower scores indicating a healthy adult. As dementia progresses, the score increases.

Eighteen of the patients were assigned to placebo and 18 received Prana`s Alzheimer`s disease drug, PBT-1 (Clioquinol) (the first of Prana`s metal protein attenuating compounds (MPACs) to be developed for Alzheimer`s disease). PBT-1 is a chemical that binds zinc and copper, and has been shown to lower the levels of A and the associated toxicity in the brains of Transgenic mice used as a model of Alzheimer`s Disease.

The more affected patients entering Prana`s pilot clinical trial (i.e. those with higher ADAS-cog scores) showed an average change in score at 24 weeks of about 1.5 points on PBT-1 and about 8.9 on placebo, a difference of 7.4. Generally, untreated patients with mild to moderate disease could be expected to gain six to 12 points in their ADAS-cog score over 12 months. A panel convened by the Food and Drug Administration in the US deemed an improvement of four points would be clinically significant.

"The results of this trial have been very encouraging to a clinician," said Dr Ritchie of UCL who led the study, adding; "Our findings have led to the development by Prana Biotechnology of new, possibly more effective drugs which hit the same target as Clioquinol. UCL plans to be involved in further testing of the principal using Clioquinol in a larger, UK multi-centre study which is seeking public funding."

Dr Susanne Sorensen, Head of Research at the Alzheimer`s Society says: "The Alzheimer`s Society welcomes this research as the results indicate that there may be a novel use for this already existing drug in the treatment of Alzheimer`s disease.

The trial presented here is limited in its scale and the Alzheimer`s Society believes it would be valuable to see a larger scale trial. The potential for new drugs that may interfere with or revert the progression of Alzheimer`s disease gives hope to people with dementia and their carers. There are currently only limited and expensive treatment options available for Alzheimer`s disease and none that revert the disease for more than a short period."

[goldmaie]

@neo bei Pran ist das sehr wichtig, weil der Wert nun aml eine sehr geringe Handelsmenge aufweist. Und da wir alle daran interssiert sind, dass der Kurs nicht durch eine Axt , der fürhende Makler kaputt gemacht wird, sollte es jeder wissen.

ein eigener Thread ist sicher nicht schlecht, aber fehlt die zeit und später geht es wieder unter.

Fazit:
prana hat Tieftskurse nun ereicht Chart ähnlich wie BKHM, Langfristchart mal ansehen.

Hat gestern stark nach oben gedreht mit 24 % Plus ca.

Leider läßt sich bei meinem Browser der Chart nicht reinkopieren. Bookham Inc.

und seit dem Tiefstpunkt von 1, 50 steht der Kurs dort auf 3,50 das sind über 100 %. Das wäre toll wenn es bei prana auch passieren würde! Höchstkurs war bei pran bei 10,50.

Der widerstand leigt bei 5 $.

Es ollte in diesem Jahr möglich sein, dei 5 $ zu erreichen und bei günstigen News natrülich weider zum Hoch von 10, das wären dann, 200 %.

Deshalb Pran zukaufen und halten, Verkaufen auf keinen Fall jetzt, das wäre Dummheit.

[BrauchGeld]

Hallo

Für mich war es keine dummheit zu verkaufen nachdem prana unter die 0,50A$ gefallen war .
Ich kann nur aufatmen das ich nicht mehr dabei bin,heute gehts nämlich um knapp 32% in den keller.

11 April 2005

PRANA BIOTECHNOLOGY CANCELS PLANS FOR PLACQUE CLINICAL STUDY
Melbourne, Australia – April 11, 2005 – Prana Biotechnology Limited (NASDAQ: PRAN, ASX: PBT), announced today that it will not proceed with supporting the initiation of the PLACQUE study evaluating PBT1 (clioquinol) for Alzheimer’s disease and has re-evaluated any further work on the PBT1 program.
As part of the effort to manufacture GMP grade PBT1 clinical trial material, Prana has characterised the various impurities that occur in the synthetic process and found unacceptably high levels of a di-iodo (toxic) form of PBT1. After further investigation, Prana now believes it is possible that the di-iodo impurity that occurs during PBT1 synthesis could be responsible for an increased risk of side–effects and mutagenicity. While Prana has considered methods to reduce the levels of the di-iodo impurity, it has come to the conclusion that attempts to reduce the impurity to safe levels are not likely to be successful in a timely manner and that further development of PBT1 is not warranted.
PBT2 is a backup compound for Alzheimer’s disease that is currently in Phase I clinical testing in Utrecht, the Netherlands. PBT2 has a structure that does not contain iodine and is therefore not capable of forming the di-iodo impurity that has been associated with mutagenicity.

After successfully settling the PBT1 patent litigation with P.N. Gerolymatos, S.A., in the third quarter of 2004, and after successfully achieving a Clinical Trials Authorization (CTA) in the U.K. in the fourth quarter of 2004, Prana made the decision to advance PBT1 into the potentially pivotal Phase II/III PLACQUE trial and attempt to accelerate the development timelines of its MPACs.

As a result of these events, Prana is conducting a strategic review of its development programs.

Gruss
B.M.

[goldmaie]

Ja da wäre ich auch froh, aber es macht dem Kurs in Deutschland gar nichst aus, heute nach den aqmi Vorgaben in
Berlin allerdings bei 0 Umsätzen, 2,58 %.

außerdem ist der Handel in Australien ausgestzt worden, zumindest bei Beginn., sollte nach PBT eigentlich bis zum 13.April geschehen, aber schint nicht der Fall gewesen zu sein.

Aber Prana hat ja noch ein Medkament das PBT 2 ist in Phase1, klinische Tests in Utrecht, Niederlande, und hat kein IOdine.

Mal sehen was die Amis heute machen.

[goldmaie]

http://www2.tradingroom.com.au/apps/qt/quote.ac?section=char…

bis 14 Uhr war der Kurs ausgesetzt, danach gings dann bergab.

Es haben sich aber schon wieder welche eingedeckt, der Kurs ging am Schluß wieder etwas hoch.

[Erbse1]

Prana Biotechnology Cancels Plans for PLACQUE Clinical Study
http://biz.yahoo.com/prnews/050411/nym100.html?.v=5

[goldmaie]

Erbse danke, Nachricht hatten wir schon heute ganz früh bekommenb.

an der Nasdaq ist heute ein Riesenumsatz bis jetzt 350TSD,
sonst nur 10000 Durchschnitt.

Eröffnung bei 1, 70 , da vorbörslich leider der Kurs schon in den Keller ging zu Dumpingpreisen.

[goldmaie]

Umsatz 600TSD an der nasdaq, und das bei ADR, also mal 100 im Vergleich zu dem Austr. Markt.

[goldmaie]

wird zwar niemand trösten, weil der Vergleich hinkt, aber wenn ich mir den Chart von Pfizer ansehe, mit dem ging es auch bergab Mitte Dezember als sie ein Medikamant vom Markt genommen haben. Allerdings hat Pfizer eine breit aufgestellte Pallette und sitzt sattelfest am Markt mit vielen Produkten.

http://www.wallstreet-online.de/index.php

Chart läßt sich bei dem Mistbrowser nicht reinkopieren.


Was wird prana nun mit dem PBT 2 machen?

[goldmaie]

Zufall?

der Makler, von dem ich shcon geschireben habe,die sogenannte Axt, schlägt wieder zu.

Er kauft in Riesenstückzahlen shcon wieder ein 9900 zu 1, 43,
auch andere Makler greifen zu, allerdings max. in 5 Tsd Stücken.

Gleich wird er bedient. Leider kann ich mit meiner Sotware nicht sehen, welche Makler sich gut eingedeckt haben heute.

Das gibt es nämlich auch, bei einigen Amibanken.

[goldmaie]

Die Pakete werden zwischen den maklern nur hin und hergeschoben.

die Makler versuchen Gewinne zu machen, indem Sie in riesigen mengen billig einkaufen und versuchen wieder günstiger auszusteigen. Wasd anders läuft hier teilweis nicht und das drückt natürlich wieder auf den Kurs.

ein heißes Spiel für starke nerven.

Habe ich auch schon mal gemacht, habe ich aber nicht die Nerven und das Geld für!

Ich bin nicht mehr rausgekommen und sehe jezt auch keinen Grund mehr zu dem übertrieben nierigen Kurs auszusteigen. Wegschmeißen kann ich sie immer noch.




1,211 Mio Umsatz bis jetzt!

[goldmaie]

Leider versuchen die Makler die Kurse dermaßen zu drücken ,auch der Makler der xx Bank, sieht, dass große Stückmengenn zum Verkauf liegen, z.b. meine und er steht im bid mit einer größeren Stückzahl. Das ist der Size.

Hält sich aber im Rahmen.

Bei der anderen Bank, hae ich über ARca und Inet gemacht, das ist unauffälliger.

[Neoe]

Harter Tobak, aber Ende des Monats wieder ueber 2.5 Dollar.

[Neoe]

goldmaie:

Bitte ausverkaufen und neuen Verschwoerungs-Thread aufmachen. Wenn ein bisschen Ahnung haettest, wuerdest du heute nachkaufen anstatt zu verkaufen.

Prana hat sich heute von PBT-1 getrennt, einer 70 Jahre alten Pille fuer die sie in England Millionen von Dollarn ausgegeben haette und hinterher NICHT EINMAL Royalties kassiert haette.

Ich habe schon lange geraetselt, was Prana servieren wuerde, um dieses Vorgehen zu rechtfertigen.
Jetzt hat sich die Raetselei erledigt und PRana hat 30 Millionen US Dollar in der Kasse um PBT-2 voranzubringen und das bei einer laecherlichen Marketcap von sage und schreibe 16 Millionen Dollar. Dazu muss man nichts mehr sagen. PBT-2 weisst in der chemischen Zusammensetzung NICHT die Probleme auf die PBT-1 zu sehen waren.

[goldmaie]

Ich bin Tader und kein Anleger.
Auf Aktien mit unter 5 $ gibt es keine Beleihung, du Großspuriger Redner. Nicht in USA
Weißt du überhaupt wieviel ich in Prana angelegt habe und verloren habe?

Sicher mehr als jeder hier.Und morgen muß ich Geld auftreiben weil die Konten im Minus sind, du Oberschlauberger.

Und hätte ich nicht dummerweise soviel gehabt und auch nicht nachgekauft, wäre ich längst draußen, weil man mit großen Mengen nicht leicht rauskommt! Jedenfalls nicht bei dem Umsatz, den die Aktie normalerweise macht.

Es war ein Fehler mich nicht früher zu trennen.

Das die noch PBT2 haben ist mir auch aufgefallen.

Deshalb denke ich , dass morgen eine Gegenbewegung kommt, vielleicht geben die ja auch nochmal heute nacht eine Meldung raus!

[Neoe]

goldmaie:

Immerhin habe ich mir bisher nicht die Muehe gemacht diesen Thread zuzumuellen...

[geldschneider]

Commences Phase 1 Clinical Trial of PBT2

Announced by: PBT
Announced on: 15/03/2005 09:13:58
Words: 1136
Status: Not market sensitive (N)
View original PDF

PRANA BIOTECHNOLOGY COMMENCES PHASE I CLINICAL TRIAL OF PBT2
- Second MPAC Enters Human Clinical Studies -
Melbourne, Australia ­ March 15, 2005 ­ Prana Biotechnology Limited (NASDAQ: PRAN,
ASX: PBT), announced today that it has commenced the Phase I clinical trial of PBT2 with the
dosing of its first subject at a facility associated with the Utrecht University Hospital in Utrecht,
The Netherlands. The Phase I clinical trial is the first of a planned series of studies examining
the safety and pharmacokinetics of PBT2 in normal human volunteers.

PBT2 is the first completely Prana-discovered compound, and is the successor to PBT1 for the
treatment of Alzheimer`s disease. PBT2 is designed to have an improved safety and efficacy
profile compared to PBT1. The compound has demonstrated significantly greater effectiveness
in lowering plaque in the transgenic mouse model in both pre-clinical in-vitro and in-vivo testing.
Moreover, it appears to be better than PBT1 at decreasing the toxicity of plaques through
improved peroxide inhibition, and appears to have better pharmaceutical characteristics, such
as improved solubility.

"We are extremely excited to be taking the first exclusively Prana-developed compound into the
clinic," said Dr. Jon Alsenas, CEO of Prana. "I am extremely proud of Prana`s staff for achieving
this important milestone. The Phase I clinical trial of PBT2 marks a second significant milestone
for our Company in the past three months. The other was the previously announced approval in
the United Kingdom of a CTA (Clinical Trials Authorisation) for the initiation of the potentially
pivotal Phase II/III PLACQUE study of our lead compound PBT1 for Alzheimer`s disease.
PLACQUE is on track to begin enrolment in the first half of 2005. The PBT1 and PBT2 clinical
programs demonstrate our commitment to developing Metal-Protein Attenuating Compounds
(MPACs) for the treatment of Alzheimer`s disease."
Alzheimer`s currently affects 4.5 million individuals in the US and 14 million individuals
worldwide, and the rate of incidence is expected to increase with aging demographics.
"The Metal Theory"
The prize-winning science behind PBT2 is based upon what is known as "the metal theory" of
Alzheimer`s disease. The theory is based on the premise that key metals, such as zinc and
copper, are required for the inappropriate aggregation of amyloid beta to form the amyloid
plaques. These plaques are then thought to cause the neurodegeneration associated with
Alzheimer`s disease. The metal-mediated aggregation of proteins is also thought to be a key
contributor to the development of a variety of other degenerative disorders.


About Prana Biotechnology Limited
Prana Biotechnology was established to commercialise research into Alzheimer`s disease and
other major age-related degenerative disorders. The company was incorporated in 1997 and
listed on the Australian Stock Exchange in March 2000 and listed on NASDAQ in September
2002. Researchers at prominent international institutions including the University of Melbourne
and Massachusetts General Hospital, a teaching hospital of Harvard Medical School,
discovered Prana`s technology.

For further information, please visit our web site at www.pranabio.com.
###
Forward Looking Statements ­ This press release contains "forward-looking statements" within the meaning of section 27A of the
Securities Act of 1933 and section 21E of the Securities Exchange Act of 1934. The Company has tried to identify such forward-
looking statements by use of such words as "expects," "intends," "hopes," "anticipates," "believes," "could," "may," "evidences" and
"estimates," and other similar expressions, but these words are not the exclusive means of identifying such statements. Such
statements include, but are not limited to any statements relating to the Company`s drug development program, including, but not
limited to the initiation, progress and outcomes of clinical trials of the Company`s drug development program, including, but not
limited to, PBT-1 and PBT-2, and any other statements that are not historical facts. Such statements involve risks and uncertainties,
including, but not limited to, those risks and uncertainties relating to the difficulties or delays in financing, development, testing,
regulatory approval, production and marketing of the Company`s drug components, including, but not limited to, PBT-1 and PBT-2,
the ability of the Company to procure additional future sources of financing, unexpected adverse side effects or inadequate
therapeutic efficacy of the Company`s drug compounds, including, but not limited to, PBT-1 and PBT-2, that could slow or prevent
products coming to market, the uncertainty of patent protection for the Company`s intellectual property or trade secrets, including,
but not limited to, the intellectual property relating to PBT-1 and PBT-2, and other risks detailed from time to time in the filings the
Company makes with Securities and Exchange Commission including its annual reports on From 20-F and its reports on Form 6-K.
Such statements are based on management`s current expectations, but actual results may differ materially due to various factions
including those risks and uncertainties mentioned or referred to in this press release. Accordingly, you should not rely on those
forward-looking statements as a prediction of actual future results.
.


Contacts:
Media and investor relations
Rebecca Piercy
Buchan Consulting
Ph: + 61 3 9866 4722



Advertise with Us | Fairfax Digital Network Privacy Policy | Conditions of Use | Member Agreement
Help | Contact Us

Copyright © 2002. Any unauthorised use or copying prohibited.

[geldschneider]

Wer hier keine Ahnung hat, bist lediglich du Noe.

Manche machen einfach die Augen zu. Du hast keine Ahnung wie in Amerika die Kurse gemacht werden! Sonst würdest du nicht so dumm daher reden.

Wahrscheinlich weißt du auchnicht was eine "AXT" ist, das ist ein Fachausdruck. Und in Amerika, dürfen marketmaker selber handeln , da gelten ganz andre Gesetze du "Oberschlaumi".

Und was golmaie uns wahrscheinlich damit sagen wollte, ist, wenn die sogeannte Axt, sich dick eindeckt, dann erwartet er Kurssteigerungen. Weil er irgendwann die Aktien wieder verkaufen will, die er billiger eingekauft hat. _

In Australien ist es heute nochmal 30 % runtergegeangen, das heißt so wie es gestern in USA endete, mit 60 % Minus.

Es könnte heute eine Gegenreaktion kommen.

Über 2 Mill. Umsatz gestern.
Goldmaie hat recht, gestern wurden nur Pakete hin und hergeschoben.
So kann man auch bei fallenden Kursen Geld verdienen. Die Marketmaker jedenfalls machen es so.

Auch die Instis. Ein Mistspiel war das gestern.

Hättest du Level II Kurse , dann wüßest du wer die AXT ist, und wer den Kurs macht! Es gibt Tage, da handelt nur die AXT, weil keine Käufer da sind., bzw. der Market Maker macht den Preis!

Empfehle dir mal das Buch: "Beherrsche den Markt", dann weißt du vielleicht mehr.

[Neoe]

geldschneider:

Vai tomar no cú, imbecíl. Filho dum piranha...Agora estamos no mesmo nivel, não é ?
Mas eu posso maldizer você e ainda você é tonto demais para dar-me uma resposta apropriada...que carapato na pele duma pessoa honesta você é.

[goldmaie]

Zum Thema Kursmanipulation durch Marketmaker.

Heute habe ich im TV Bloomberg gehört, dass wegen Betrugs über insgesamt 4 Jahre, mehrere Marketmaker in USA verurteilt wurden. Und zwar weil sie nicht im Interesse ihrer Kunden handelten, sondern nur an ihren eigenen Vorteil dachten, und für sich handelten! Dadurch haben sie Kurse manpluliert.

Na passt doch wunderbar, zu meinen "Verschwörungstheorien " ala Mr. Noe.

Habe Anfrage an Prana gestellt was weiter geschehen soll, bzw. Ausblick wäre schön wenn es andere auch machen würden. Habe leider noch keine Antwort erhalten.

[Neoe]

goldmaie:

Ich fuehle mich geehrt hier mit 007 das Prana-Board zu teilen. Weiter so, ich glaube so langsam fuerchten sich die MMs und Institutionellen...Ich rate dir aber, dich damit abzufinden, dass es definitv immer staerkere Kraefte im Markt gibt als deine Zwei-Mark-Fuenfzig.


Fuer alle Normalsterblichen:

Zur Erinnerung: Prana hat PBT-1 freiwillig aufgegeben. Eine Bearbeitung der Komponente waere (unter Zeitaufwand) moeglich gewesen. Ein Grund (und auch der Wichtigste) ist im folgenden Ausschnitt eines Research-Berichts gut nachzuvollziehen:


The ‘son of clioquinol’ trial

Prana announced in August 2003 that it intended to take the best volume in its MPAC molecule library, a compound
called PBT-2, into a formal clinical trial setting. By eight different accounts studies both in vitro and in vivo have shown PBT-2 to be better than PBT-1. Probably the most important measures are ‘brain amyloid solubility’, which shows PBT-2 to be 2.5 times better at reducing amyloid plaques than PBT-1, and ‘inhibition of peroxide’, where PBT-2 is 1.6 times better at holding back H202 production than its predecessor compound. These two measures indicate that PBT-2 works against ‘mechanistic targets’, that is, targets at work in what Prana believes is the
underlying mechanism of action in Alzheimer’s Disease. In terms of its ability as a drug to treat a central nervous
system disorder, PBT-2 also scores more highly than PBT-1. The new drug is over ten times more soluble than PBT-
1, which makes it a much easier drug to work with. PBT-2 has four times the ‘neuroprotective’ ability of PBT-1,
meaning that the amyloid beta killed markedly fewer neurons when PBT-2 was used. The ability of PBT-2 to get
through the blood-brain barrier is much higher than PBT-1. And finally, in transgenic mice that had been engineered
to suffer Alzheimer’s there was a 29% reduction in insoluble amyloid beta still in the brain and a 37% fall in soluble
amyloid beta in the brain as a result of PBT-2. By contrast PBT-1 could cut insoluble amyloid levels by nearly half
but make no dent in soluble amyloid still in the brain. In short, PBT-2 is a more powerful drug.
It probably won’t be until October 2004 that the formal clinical trial of PBT-2 begins. Toxicology studies are
currently being undertaken and the drug will have to be produced ahead of the start of the trial. However if the
results of Phase I yield some good results like the proof of concept trial, Prana should be a more appreciated stock as
we approach Christmas 2005 and if all goes to plan the drug could be approaching approval by around Christmas
2008. As we’ll see below, PBT-2 alone can be responsible for some serious shareholder value well in excess of the
current share price.

[geldschneider]

nie gab es soviel Umsatz, wie seit dem Kurseinbruch!

Heute 254TSD, ist aber noch nicht das Ende des Tages.

Gestern waren es soweit ich im Kopf habe ca. 600000 Umsatz.

Heute wurden große Pakete eingekauft für 1,24, und weitere 110 TSD stehen im Bid für 1,22.

Ob die Insider wohl einkaufen?

Man wird es erst später erfahren.

[Marktinsider]

Prana ist jetzt für mich interessant geworden und kommt auf die watch list. Ich beobachte die Aktie mal weiter. Es gefällt mir nicht, dass Prana einen Tag nach dem massiven Kurssturz nochmals um 3% gefallen ist. Wenn nicht einmal eine technische Gegenreaktion zu sehen ist, stinkt diese Sache. Offenbar besteht sehr geringes Interesse.

Prana könnte sich ähnlich entwickeln wie La Jolla. La Jolla fiel Mitte März von 1.20 USD auf 0.70 USD. Und seither gab es eine langsame Talfahrt. Nun notiert LJPC bei 0.57 USD. Vielleicht könnte Prana auch einen "langsamen Tod" erleiden. Die Charttechnik sieht katastrophal aus. Bei Kursen um 0.95 bis 1.00 EUR schau ich mir aber Prana nochmals an und überlege mir einen Einstieg.

[Neoe]

Comment by: Ashley Bush, Rudy Tanzi
Submitted 14 April 2005
Posted 14 April 2005



Prana`s decision to cancel the phase II/III "PLACQUE" clinical trial of PBT1 is, of course, disappointing. PBT1 (clioquinol or "CQ") is an old drug that required redevelopment of its synthetic route to meet today`s GMP standards. As was highlighted in Prana`s press release, during large-scale synthesis, unacceptably high levels of a mutagenic impurity were found. The levels of this di-iodo derivative in the batch made for the PLACQUE trial exceeded new international impurity guidelines, and therefore this batch could not be used in the clinical trial. The trial thus could not proceed.
So why not try to purify or resynthesize CQ? While it may be theoretically possible after additional work to satisfactorily reduce or even eliminate the levels of the di-iodo impurity (either by new synthetic chemistry or by new purification techniques), this investment in time and money may not be the best option for several reasons, the first being that Prana has a pipeline of new, custom-designed drug candidates which have already passed testing in the same preclinical models for Alzheimer [...continued] disease where CQ showed efficacy: The most advanced of these, PBT2, has already entered phase I clinical trials. In addition, the remanufacturing of PBT1 would require considerable time, quite possibly putting its testing behind PBT2, anyway. Finally, as Prana explained, the di-iodo contaminant cannot form with PBT2 because its structure does not contain any iodine.

Speaking on behalf of our research teams working on the metallochemistry of Aβ, we want to point out that the trial cancellation is neither because of problems with the underlying science, nor because of new concerns about the efficacy of the drug or its class (Metal Protein Attenuating Compounds, MPACs). We believe that the underlying science remains strong and can be used to screen for and test new drug candidates. Clioquinol established the principles that are involved in targeting abnormal metal-Aβ interactions to identify new orally bioavailable MPACs as drug candidates for Alzheimer disease.

In summary, being mindful that Prana has PBT2 and other candidate compounds in its development pipeline, it would seem prudent to shift emphasis to the testing of PBT2 and the newer drug candidates.

We hope this clarification is helpful.

Disclosure: Dr Ashley Bush and Dr Rudolph Tanzi disclose that they are shareholders and paid consultants for Prana.

[geldschneider]

Aufgrund der Newes heute deutlich im Plus
PRANA BIOTECHNOLOGY LTD - Nasdaq SmallCap Market: PRAN
Real-time ECN Quote*
Last Change (%) After Hours Chg (%)** Trade Time Bid Ask
1.11 0 (0.00) N/A 15:58 1.12 (1) 1.17 (1)
New flat rate: $7 online market AND limit orders at Scottrade. Get Info!
Exchange Quote
Last Change (%) Trade Time Bid (size) Ask (size)
1.19 0.08 (7.21) 10:06 1.13 (1) 1.19 (27)
Latest Ticks Prev Close Open Low High
=+=+ 1.11 1.14 1.14 1.19
Day Volume Avg Day Vol VWAP 52 Wk Low 52 Wk High
13,300 249,400 1.1656 0.98 6.60
# of Trades Last Size Avg Trade Size P/E Ratio Market Cap (mil)
9 1,250 1,478 0 20
10:27:37 AM EDT - Thursday, May 5, 2005- Exchange quote is delayed at least 15 minutes.

$7 TRADES!

Prana Biotechnology to Present at Rodman & Renshaw Techvest 2nd Annual Global Healthcare Conference

MELBOURNE, Australia, May 4, 2005 /PRNewswire-FirstCall via COMTEX/ -- Prana
Biotechnology Limited (Nasdaq: PRAN, ASX: PBT), today announced that its
founding scientist, Professor Ashley Bush of Harvard Medical School, will
present at the Rodman & Renshaw Techvest 2nd Annual Global Healthcare Conference
at the InterContinental Hotel in Paris on Thursday, May 5, 2005, at 12:40 PM
CET.

Professor Bush`s presentation will contain a scientific review of the MPAC
(Metal-Protein Attenuating Compounds) theory. A live web cast and replay of the
presentation will be available on the Prana Biotechnology web site:
http://www.pranabio.com.

To arrange a one-on-one meeting with Professor Bush during the conference,
please contact Kathy Price at The Anne McBride Company, tel. [phone], ext
212, or [e-mail].

The founding scientists`, Professors Rudolph Tanzi and Ashley Bush, theories
concerning the interaction between metals and the protein beta-amyloid in the
brain are the basis of Prana`s treatments for Alzheimer`s and other
neurodegenerative diseases.

About Prana Biotechnology Limited

Prana Biotechnology was established to commercialize research into Alzheimer`s
disease and other major age-related degenerative disorders. The company was
incorporated in 1997 and listed on the Australian Stock Exchange in March 2000
and listed on NASDAQ in September 2002. Researchers at prominent international
institutions including the University of Melbourne and Massachusetts General
Hospital, a teaching hospital of Harvard Medical School, discovered Prana`s
technology.



For further information, please visit our web site at

http://www.pranabio.com.



Contacts:

Investor Relations Media Relations

Kathy Price Ivette Almeida

T: 212-983-1702 ext. 212 T: 212-983-1702 ext. 209

E: [e-mail] E: [e-mail]

SOURCE Prana Biotechnology Limited



CONTACT: Investor Relations - Kathy Price, [phone] ext. 212, [e-mail],

or Media Relations - Ivette Almeida, [phone] ext. 209,

[e-mail], both for Prana Biotechnology Limited



URL: http://www.prnewswire.com

http://www.pranabio.com

www.prnewswire.com


Copyright (C) 2005 PR Newswire. All rights reserved.





KEYWORD: Australia

INDUSTRY KEYWORD: HEA

BIO

MTC

SUBJECT CODE: TDS

CCA

[DerKartoffelsack]

nach den interessanten ausführungen von goldmaie weiss ich nun, dass
1. die welt böse
2. eine breite depotstreuung dagegen tendenziell eher gut ist

aus letzterm grund habe ich mir einige wenige Prana-Aktien gekauft. wenn man sich die daten zu pbt2 im vergleich zu pbt2 anschaut, ist die reaktion vom April eigentlich in keiner weise nachzuvollziehen. ich tue mir ja eigentlich grundsätzlich schwer, den aussagen von Biotech-Unternehmen zu vertrauen, im Fall von Prana glaube ich aber vorbehaltlos daran, dass uns hier die wahrheit gesagt wird (also nur eine suboptimale lösung zugunsten einer besseren eingestellt wurde).
ein viel größeres Risiko, als der Kauf eines 17-Mann Biotech Unternehmens kann man ja eigentlich fast nicht eingehen, aber eine MK von 14Mio bei Barreserven von 21Mio und einem vielversprechenden Forschungsprojekt lassen eigentlich keine andere Möglichkeit zu (auch wenn man eigntlich eher risikoavers ist....).
der eigentliche grund für dieses posting ist aber folgender: Prana wäre ja, wenn sie den nicht vollkommen im trüben forschen, ein idealer übernahmekandidat. für hinweise, ob es diesbezüglich irgendwelche bewegungen gibt, wäre ich sehr dankbar. klasse wäre auch, wenn mir jemand eine quelle nennen könnte, wo ich die insiderkäufe/verkäufe in diesem wert nachvollziehen könnte.
ich habe mich bislang weniger mit dem Wert beschäftigt, als ich es für gewöhnlich tue, bevor ich einkaufe. aber da ich zum einen nur sehr wenige aktien, zum anderen auch wenig Zeit habe, ging´s leider nicht anders....

ich wünsche euch (und vorallem mir!!!!) das die hoffnungen, die wir in diesen wert setzen, berechtigt sind und Prana nicht im biotech-orcus der vergessenheit entschwindet (allein für dieses poetische wortkonstrukt hätte ich ein kursplus von 20% verdient).

[geldschneider]

leider schriebt hier keiner mehr was rein, noe ist abgewandert, schrieb mal eine Zeitlang bei den Amis mit.

in Ariva gibts Neues.

http://www.ariva.de/board/193617

[geldschneider]

leider schriebt hier keiner mehr was rein, noe ist abgewandert, schrieb mal eine Zeitlang bei den Amis mit.

in Ariva gibts Neues.

http://www.ariva.de/board/193617

[MODzart]

Dieser Thread ist wieder geöffnet.

Habe die Ehre,
MODzart

[Fruehrentner]

Antwort auf Beitrag Nr.: 32.927.364 von MODzart am 03.01.08 16:15:58

Danke

2008/2009 werden entscheidende Jahre sein für PRANA.

Und es gibt schon News zum Alzheimer-Kandidaten (Kurs stieg schon eine zeit lang vorher):

Prana Announces Completion of Phase IIa Trial of PBT2 in Alzheimer's Disease Patients

02 Jan 2008

Prana Biotechnology Limited today announced it has completed its Phase IIa clinical trial of PBT2 in patients with early Alzheimer's disease

MELBOURNE, Australia | January 2, 2008 | Prana Biotechnology Limited (NASDAQ: PRAN / ASX: PBT), a biopharmaceutical company focused on the research and development of treatments for neurodegenerative disorders, today announced it has completed its Phase IIa clinical trial of PBT2 in patients with early Alzheimer's disease.

All patients have completed their final clinical assessment. The data are being analysed, and results will be delivered in the first quarter of 2008.

Geoffrey Kempler, Chairman and CEO of Prana Biotechnology, said, “The completion of the Phase IIa trial for PBT2 represents a significant milestone in the development of Prana's innovative therapeutic platform for Alzheimer's Disease, and other neurodegenerative diseases.”

This Phase IIa trial is a double blind, placebo-controlled study exploring the safety and tolerability of PBT2, Prana’s proprietary lead compound. The trial also measured PBT2’s effects on the mechanism and progression of the disease, by investigating biomarkers of Alzheimer's Disease, as well as measures of cognition.

About Prana Biotechnology Limited

Prana Biotechnology was established to commercialise research into Alzheimer's disease and other major age-related neurodegenerative disorders. The company was incorporated in 1997 and listed on the Australian Stock Exchange in March 2000 and listed on NASDAQ in September 2002. Researchers at prominent international institutions including the University of Melbourne, the Mental Health Research Institute (Melbourne) and Massachusetts General Hospital, a teaching hospital of Harvard Medical School, discovered Prana’s technology.

For further information, please visit our web site at www.pranabio.com.

Forward Looking Statements

This press release contains "forward-looking statements" within the meaning of section 27A of the Securities Act of 1933 and section 21E of the Securities Exchange Act of 1934. The Company has tried to identify such forward-looking statements by use of such words as "expects," "intends," "hopes," "anticipates," "believes," "could," "may," "evidences" and "estimates," and other similar expressions, but these words are not the exclusive means of identifying such statements. Such statements include, but are not limited to any statements relating to the Company's drug development program, including, but not limited to the initiation, progress and outcomes of clinical trials of the Company's drug development program, including, but not limited to, PBT2, and any other statements that are not historical facts. Such statements involve risks and uncertainties, including, but not limited to, those risks and uncertainties relating to the difficulties or delays in financing, development, testing, regulatory approval, production and marketing of the Company's drug components, including, but not limited to, PBT2, the ability of the Company to procure additional future sources of financing, unexpected adverse side effects or inadequate therapeutic efficacy of the Company's drug compounds, including, but not limited to, PBT2, that could slow or prevent products coming to market, the uncertainty of patent protection for the Company's intellectual property or trade secrets, including, but not limited to, the intellectual property relating to PBT2, and other risks detailed from time to time in the filings the Company makes with Securities and Exchange Commission including its annual reports on From 20-F and its reports on Form 6-K. Such statements are based on management’s current expectations, but actual results may differ materially due to various factions including those risks and uncertainties mentioned or referred to in this press release. Accordingly, you should not rely on those forward-looking statements as a prediction of actual future results.

SOURCE: Prana Biotechnology Limited

[Fruehrentner]

[Fruehrentner]

Deutscher Chart

Jetzt schon weiter hoch? Wäre aber auch nicht das erste mal, das der Kurs eines Biotechwerts schon länmgere Zeit vor den nächsten News zur klin. Entwicklung weiter ansteigt und positive Ergebnisse vorwegnimmt bzw. einpreist.

Also jetzt schon Positionen aufbauen oder besser auf Rücksetzer warten? Schwere Entscheidung...

[Fruehrentner]

Antwort auf Beitrag Nr.: 33.003.610 von Fruehrentner am 10.01.08 10:56:46

Wow!

Das Teil schiesst weiter hoch!!

Eins steht fest: Die Indikation "Alzheimer" ist eine absolute Blockbusteranwendung!!

Bei Erfolg würde PRANA durch die Decke gehen bzw. im Vorfeld weiterer positiver Daten schon anziehen.

Eine Übernahme ist ebenfalls wahrscheinlich. Vielleicht wird das Szenario einer Übernahme ja jetzt schon und in nächster Zeit (teilweise) eingepreist. PRANA wäre doch wohl jetzt noch spottbillig!

Wäre schön, wenn sich ein Mediziner oder gar Alzheimerexperte hier im thread beteiligen würde.

[Fruehrentner]

schöner Überblick vom März 2007 über Alzheimer und mögliche pharmakologische Ansätze:

http://www.alzheimer-bw.de/cms/_data/Vortrag_Bey_maerz2007_T…

Prana Bioscience wird darin erwähnt.

Ebenso Myriad Genetics, die sogar schon in Phase III sind! Schau ich mir mal näher an. Ich glaube da ist ebenfalls ein neuer thread fällig. Kursentwicklung bei Myriad ebenfalls beeindruckend.

[Fruehrentner]

PRANA heute in USA schön im plus - und das bei dem schwachen Marktumfeld.

[Fruehrentner]

Antwort auf Beitrag Nr.: 32.927.620 von Fruehrentner am 03.01.08 16:29:50

Im April sollen übrigens die Ergebnisse der klin. Phase IIa mit PBT2 bekannt gegeben werden - alles wie von Prana avisiert.

Die Phase IIa liegt damit voll im Zeitplan, es kam zu keinen Verzögerungen bei der Durchführung dieser Phase.

Offenbar antizipiert der Kurs gute Nachrichten im April und steigt schon im Vorfeld der Bekanntgabe der Ergbnisse.

[Fruehrentner]

18 January 2008

Prana Announces Publication in Neurobiology of Aging Journal

MELBOURNE, Australia – January 18, 2008

Prana Biotechnology Limited (NASDAQ: PRAN / ASX: PBT), a biopharmaceutical company focused on the research and development of treatments for neurodegenerative disorders, today announced that the current online addition of Neurobiology of Aging Journal, has published a paper entitled, “Zinc and Copper Modulate Alzheimer A-beta Levels in Human Cerebrospinal Fluid,” which further supports Prana’s scientific approach in the treatment of Alzheimer’s Disease.

Results of the NIH study, conducted by Dorothea Strozyk, M.D. at The Albert Einstein College of Medicine in New York, and collaborators in the USA, Sweden and Australia, found that the removal of A-beta from the brain may be dependent upon maintaining normal levels of metals in the brain. The authors hypothesized that a breakdown in normal metal metabolism, accompanied by the accumulation of metals within the amyloid plaques, deprives metal dependent enzymes of the copper and zinc they need to drive the removal of A-beta from the brain.

Compounds synthesized by Prana chemists (MPACs) are expected to restore brain metals to normal levels by redistributing metals from A-beta plaques back to normal cells, rather than merely depleting brain tissue of metals. As a consequence, MPACs have been shown to restore normal function to A-beta impaired synapses and improve cognitive performance in mouse models of Alzheimer’s Disease. Unlike current approved Alzheimer’s therapies that only treat the symptoms of the disease, Prana’s lead MPAC compound, PBT2, targets the underlying cause of the disease.

Professor Ashley Bush senior author of the study from the Mental Health Research Institute of Victoria and Prana’s senior scientific consultant commented that, “Understanding that certain metal dependent enzymes degrade A-beta, these results show that the clearance of A-beta, which is damaged in Alzheimer’s Disease, could be influenced by metal levels in the CSF. As part of their mechanism of action, MPACs stop A-beta oligomers from trapping essential metals and return the metals to these clearance enzymes. This normalizes the removal of A-Beta, which we believe is key to a disease-modifying drug for Alzheimer's Disease.”


About Neurobiology of Aging Journal
Neurobiology of Aging Journal publishes the results of studies in behavior, biochemistry, cell biology, endocrinology, molecular biology, morphology, neurology, neuropathology, pharmacology, physiology and protein chemistry in which the primary emphasis involves mechanisms of nervous system changes with age or diseases associated with age.


About Prana Biotechnology Limited
Prana Biotechnology was established to commercialise research into Alzheimer's disease and other major age-related neurodegenerative disorders. The Company was incorporated in 1997 and listed on the Australian Stock Exchange in March 2000 and listed on NASDAQ in September 2002. Researchers at prominent international institutions including The University of Melbourne, The Mental Health Research Institute (Melbourne) and Massachusetts General Hospital, a teaching hospital of Harvard Medical School, contributed to the discovery of Prana’s technology.

For further information, please visit the Company’s web site at www.pranabio.com.

[Fruehrentner]

Prana Bio hält sich - wenn auch volatil - im aktuell schwachen unsicheren Marktumfeld ganz gut auf dem erhöhten Kursniveau seit dem jüngsten Kursausbruch im letzten Dezember.

Mal weiter beobachten. Im Laufe des 1. Quartals 2008 sind weitere News zur Phase II Studienergebnissen von PBT-2 angekündigt.

Ob dies eher im Febr. o. März sein wird, habe ich bei Prana angefragt. Mal sehen, wie schnell die antworten.

[Fruehrentner]

Prana hält sich im weiterhin schwachen Börsenumfeld ausgezeichnet.

Im Januar wurde angekündigt, dass die Ergebnisse zu PBT-2 noch im 1. Quartal veröffentlicht werden, also bis spätestens Ende März.

Das wird spannend.



2 January 2008

Prana Announces Completion of Phase IIa Trial of PBT2 in Alzheimer's Disease Patients

MELBOURNE, Australia – January 2, 2008 – Prana Biotechnology Limited (NASDAQ: PRAN / ASX: PBT), a biopharmaceutical company focused on the research and development of treatments for neurodegenerative disorders, today announced it has completed its Phase IIa clinical trial of PBT2 in patients with early Alzheimer's disease.

All patients have completed their final clinical assessment. The data are being analysed, and results will be delivered in the first quarter of 2008.
Geoffrey Kempler, Chairman and CEO of Prana Biotechnology, said, “The completion of the Phase IIa trial for PBT2 represents a significant milestone in the development of Prana's innovative therapeutic platform for Alzheimer's Disease, and other neurodegenerative diseases.”

This Phase IIa trial is a double blind, placebo-controlled study exploring the safety and tolerability of PBT2, Prana’s proprietary lead compound. The trial also measured PBT2’s effects on the mechanism and progression of the disease, by investigating biomarkers of Alzheimer's Disease, as well as measures of cognition.



For further information, please visit our web site at www.pranabio.com.

[Fruehrentner]

Da ist was im Busch!

[Fruehrentner]

Die News sind raus!!!


MELBOURNE, Australia – February 26, 2008: Prana Biotechnology Limited (NASDAQ: PRAN / ASX: PBT), a biopharmaceutical company focused on the research and development of treatments for neurodegenerative disorders, today announced that PBT2 has demonstrated safety and tolerability and reduced Abeta 42, in a Phase IIa study of PBT2 in patients with early Alzheimer’s Disease. PBT2 also improved Executive Function performance in select cognitive tests.

“This is a very exciting and important milestone for the company, particularly because PBT2, a drug known to inhibit the toxic oligomers of Abeta that cause the functional damage in Alzheimer’s Disease, was able to show such a clear effect in a short trial,” commented Geoffrey Kempler, Prana’s Chairman and CEO.

In this double blind multi-centre clinical trial, 78 patients in Sweden and Australia were randomized to receive either a placebo, PBT2 50mg or PBT2 250mg capsule once per day for 12 weeks.

Analysis of the trial data demonstrated that the safety and tolerability profile of PBT2 at both doses was indistinguishable from that of placebo. There were no study withdrawals related to adverse events. There was no serious adverse event (SAE) in any PBT2 treated patient.

The study also demonstrated the impact of PBT2 on reducing Abeta 42 in the cerebrospinal fluid (CSF) that surrounds the brain and spinal cord, considered a key biomarker for Alzheimer’s Disease. Specifically, PBT2 at the 250mg dose showed a highly significant reduction in CSF Abeta 42 compared to placebo (p=0.006). The effect of PBT2 was dose related (p=0.02).

Professor Jeffrey Cummings, Director of the Easton Centre for Alzheimer’s Disease at UCLA, and Head of Prana’s Research and Development Advisory Board, commented that “PBT2 has hit what we consider to be the critical target for Alzheimer’s Disease, as evidenced by the significant reduction in Abeta 42.”

Encouraging signs of cognitive improvement, as measured by the Neuropsychological Test Battery (NTB), were also observed. Statistically significant improvement was evident in two of the four Executive Function NTB tests: the Category Fluency Test (p=0.028) and the Trail Making Test part B (p=0.005), both after 12 weeks of treatment at the 250mg dose compared to placebo. PBT2, in this study of early disease progression, had no effect on ADAS-cog, a test of cognition not designed to measure Executive Function changes. The NTB is a test of cognition that is more sensitive to the changes in Executive Function that are seen in the early stage of Alzheimer’s Disease.

“The impact of this drug on Executive Function is very encouraging as this is likely to predict an improvement in the day to day functioning in the lives of people with Alzheimer’s Disease. The ability to plan and execute everyday activities, even more so than memory, offers great practical and clinical benefit to patients” added Professor Cummings.

These results build on earlier observations using PBT2 in transgenic mouse models of Alzheimer’s Disease, where PBT2: reduced toxic oligomers of Abeta, reversed the Abeta-induced loss of neurotransmission and improved cognition.

Prana now plans to further progress PBT2 into larger and longer clinical trials to investigate its potential as a disease modifying drug.

“We are very hopeful that PBT2 will continue to perform as well as it has in this trial and progress through the development pathway, eventually to bring true benefit to patients with Alzheimer’s Disease. PBT2 is one of many Metal Protein Attenuating Compounds (MPACs) within the Prana pipeline, which we are enthusiastic to develop for a range of neurodegenerative diseases,” concluded Mr. Kempler.

Please refer to the Appendix below which is included in, and forms part of, this announcement.


Conference call details:

The company will hold a conference call to discuss the above results and welcomes participation from interested parties.

Australia

Wednesday, February 27, 2008
9.00am(Eastern Summer Time)

Dial in number:

1800-002-971

USA

Tuesday, February 26, 2008
5.00pm (US Eastern time)

Dial in number:
888-713-4218 from the US or Canada (toll-free)
or [phone] from other locations
Dial in at least 10 minutes prior to commencement to access call

Reference Prana or conference ID # 64631038
The call will be webcast and available on the Prana website www.pranabio.com

REPLAY OF TELECONFERENCE
A replay of the call will be available 2 hours later until 11.59pm (US eastern time) on March 3, 2008.

Dial + 1 888-286-8010 from the US or Canada (toll – free) or [phone] from other locations.To enter conference dial ID # 16766828

About Prana Biotechnology Limited
Prana Biotechnology was established to commercialize research into Alzheimer's Disease and other major age-related neurodegenerative disorders. The Company was incorporated in 1997 and listed on the Australian Stock Exchange in March 2000 and listed on NASDAQ in September 2002. Researchers at prominent international institutions including The University of Melbourne, The Mental Health Research Institute (Melbourne) and Massachusetts GeneralHospital, a teaching hospital of HarvardMedicalSchool, contributed to the discovery of Prana’s technology.

For further information, please visit the Company’s web site at www.pranabio.com



Forward Looking Statements
This press release contains "forward-looking statements" within the meaning of section 27A of the Securities Act of 1933 and section 21E of the Securities Exchange Act of 1934. The Company has tried to identify such forward-looking statements by use of such words as "expects," "intends," "hopes," "anticipates," "believes," "could," "may," "evidences" and "estimates," and other similar expressions, but these words are not the exclusive means of identifying such statements. Such statements include, but are not limited to any statements relating to the Company's drug development program, including, but not limited to the initiation, progress and outcomes of clinical trials of the Company's drug development program, including, but not limited to, PBT2, and any other statements that are not historical facts. Such statements involve risks and uncertainties, including, but not limited to, those risks and uncertainties relating to the difficulties or delays in financing, development, testing, regulatory approval, production and marketing of the Company’s drug components, including, but not limited to, PBT2, the ability of the Company to procure additional future sources of financing, unexpected adverse side effects or inadequate therapeutic efficacy of the Company's drug compounds, including, but not limited to, PBT2, that could slow or prevent products coming to market, the uncertainty of patent protection for the Company's intellectual property or trade secrets, including, but not limited to, the intellectual property relating to PBT2, and other risks detailed from time to time in the filings the Company makes with Securities and Exchange Commission including its annual reports on From 20-F and its reports on Form 6-K. Such statements are based on management’s current expectations, but actual results may differ materially due to various factions including those risks and uncertainties mentioned or referred to in this press release. Accordingly, you should not rely on those forward-looking statements as a prediction of actual future results.






Contacts:



USA:





Investor Relations Media Relations

Leslie Wolf-Creutzfeldt Ivette Almeida



T: 646-284-9472 T: 646-284-9455



E: [e-mail] E: [e-mail]

[Fruehrentner]

Kursplus heute in Australien: knapp 55 % !!!

http://www.asx.com.au/asx/research/CompanyInfoSearchResults.…

[Fruehrentner]

Antwort auf Beitrag Nr.: 33.474.347 von Fruehrentner am 26.02.08 08:44:34

hier nochmal übersichtlich die news vom 26.02.2008 als pdf-file:

http://www.pranabio.com/pdf/Success%20in%20Phase%20IIa%20Cli…

[Fruehrentner]

Antwort auf Beitrag Nr.: 33.474.392 von Fruehrentner am 26.02.08 08:50:19

Hervorragende Ergebnisse

[Fruehrentner]

Und wie nach den heutigen news aus Australien erwartet, Kursabflug in USA, wo Prana ebenfalls gelistet ist (Heimatbörse ist Australien, ASX).

Der Zug rollt ...

[StaatsKnecht]

....der zug wird nicht lange rollen denn die haben nicht genug cash.

[Fruehrentner]

Antwort auf Beitrag Nr.: 33.482.132 von StaatsKnecht am 26.02.08 19:20:10

Wichtiger Hnweis. Danke. Das hab ich bis jetzt ausgeblendet. Ist eine Frage an Prana wert, wie es mit dem cash weiter gehen soll und möglicher Verpartnerung/Auslizenzierung.

Das Ende ist eswegen momentan keinesfalls besiegelt, gerade mit den heutigen Zwischenergebnissen werden sich nach meiner Auffassung Geldgeber finden und evtl. kauft sogar ein grösserer die Bude für'n Apel und'n Ei.

Ich glaube schon, dass PRANA mit den jetzign Zwischenergebnissn auf dem Radarschirm so mancher Pharmafirma und von Investoren auftauchen wird. Bisher flogen die doch quasi völlig unter'm Radar.

Ich halte den wissenschaftlich-pharmakologischen Ansatz von Prana/PBT-2 für aussichtsreich. Dieser ist völlig andersartig von allen anderen Second-Generation Alzheimer-Entwicklungskandidaten, die sich gegenwärtig in den Entwicklungslabors der Welt befinden.

[Fruehrentner]

Und ich Depp hab den Wert bisher nur auf der watch list seit ca. Mitte letzten Jahres

.

[Fruehrentner]

Prana Biotech releases sound clinical trial results

27/02/2008 By: Nicholas Clydsdale

Prana Biotechnology Limited (PBT), rose 54% yesterday on the back of positive news regarding its research and development of treatments for eurodegenerative disorders. It announced that PBT2 demonstrated safety and tolerability and reduced Abeta 42, in a Phase IIa study of PBT2 in patients with early Alzheimer’s Disease.
Advertisement
PBT2 also improved Executive Function performance in select cognitive tests.

CEO Geoffrey Kempler said it was an exciting and important milestone for the company, particularly because PBT2, a drug known to inhibit the toxic oligomers of Abeta that cause the functional damage in Alzheimer’s Disease, was able to show such a clear effect in a short trial.

In the double blind multi-centre clinical trial, 78 patients in Sweden and Australia were randomized to receive either a placebo, PBT2 50mg or PBT2 250mg capsule once per day for 12 weeks.

The biotech said that the analysis of the trial data demonstrated that the safety and tolerability profile of PBT2 at both doses was indistinguishable from that of placebo.

The company said that the study also demonstrated the impact of PBT2 on reducing Abeta 42 in the cerebrospinal fluid (CSF) that surrounds the brain and spinal cord, considered a key biomarker for Alzheimer’s Disease.

Specifically, PBT2 at the 250mg dose showed a highly significant reduction in CSF Abeta 42 compared to placebo (p=0.006). The effect of PBT2 was dose related (p=0.02).

Professor Jeffrey Cummings, deirector of the Easton Centre for Alzheimer’s Disease at UCLA, and head of Prana’s Research and Development Advisory Board, said that PBT2 has hit what is considered to be the critical target for Alzheimer’s Disease, as evidenced by the significant reduction in Abeta 42.

The company said the results build on earlier observations using PBT2 in transgenic mouse models of Alzheimer’s Disease, where PBT2: reduced toxic oligomers of Abeta, reversed the Abeta-induced loss of neurotransmission and improved cognition.

Prana said it now plans to further progress PBT2 into larger and longer clinical trials to investigate its potential as a disease modifying drug.

Shares in Prana Biotechnology were down 16c or 23% to 53.5c.

[Fruehrentner]

weitere Reaktionen auf die gestrigen news:

Prana Biotechnology: Why I Wanted To Do Their Story

Posted By:Mike Huckman
Topics:Stock Market | Medicine | Corporate News | Pharmaceuticals
Sectors:Health Care Equipment and Services | Health Care | Pharmaceuticals
Companies:Prana Biotechnology Ltd

I often get pitched by PR people who want me to do a story on their micro-cap biotech company. And I almost always turn them down. I know that most of the sector toils in the five- and six-digit market value space and that there's a bit of a Catch-22 at work. I mean, how can a micro-cap get any bigger if they aren't given more attention and a higher profile when they've got news? I get it.

But there's not much I can do about it. There's a limited amount of airtime on CNBC and whether it's biotech or any other sector, management draws the line on the market cap of companies that we'll highlight. But there are exceptions to the rule. And today there's an example.

Prana started out the trading day in the U.S. with a market value of about $75 million. On relatively heavy volume--as I write this--it's crossed the $100 million threshold. Typically not a company I'd be permitted to spend any time covering. But here's why I was able to "sell" what in TV-news lingo we call a "hit" (approximately one minute or the equivalent of maybe two inches of copy in a newspaper) to the producers of "Squawk on the Street" this morning: (You can watch it in the video clip.)

A. It's Alzheimer's Disease, a burgeoning epidemic that affects a lot of viewers.

B. The mostly positive results are from a mid-stage test. That increases the likelihood in today's environment that a pipeline-poor, cash-rich big drug company might come along and partner with or take out the company which doesn't have the money to pay for a large, late-stage clinical trial.

To PR folks who might be reading this, please don't interpret the coverage as setting any kind of precedent and start flooding my inbox or voicemail with a bunch of micro-cap pitches. This was a one-and-done report. In other words, I'm not doing the story on any other CNBC shows today with the exception, of course, of writing about it on this blog. And editorial decisions are made on a case by case basis.

Prana is sanskrit for life force. Namaste.

http://www.cnbc.com/id/23352893

[Fruehrentner]

Es geht los!!!

Über die Anschlussfinanzierung für die weiteren klin. Studien für PBT-2 brauch sich PRANA wohl keine Sorgen zu machen.


Prana confirms talks with pharmaceutical companies
Tuesday, March 04, 2008; Posted: 01:32 AM

Sydney, Mar 04, 2008 (RWE via COMTEX) -- PRAN | news | PowerRating | PR Charts -- (RWE Australian Business News) Prana Biotechnology Ltd (ASX: PBT) today confirmed it had entered confidentiality arrangements with "several large pharmaceutical companies" and was in various stages of discussion in respect of the licencing of its lead compound PBT2.

"The company wishes to emphasise that neither Prana nor any other party is obliged to conclude a transaction," directors said.

They said Prana made this announcement after becoming aware of certain comments appearing in today's press which followed on from the release of February 26 when Prana announced the successful outcome of its Phase IIa Clinical Trial of PBT2 in Early Alzheimer's Disease.

"The comments relate to a visit to Prana by pharmaceutical company executives and expressed the belief that Prana was engaged in confidential commercial discussions to fund further trials of PBT2," the directors said.

"The company is delighted with the outcome of the recent clinical trial as it demonstrated the safety and tolerability of PBT2 in the 12-week trial.

"The trial also demonstrated significant reductions in Abeta 42 in patients with early Alzheimer's Disease and significant improvements in Executive Function performance in select cognitive tests.

"The positive outcomes from the trial were viewed as a pre-requisite to advancing negotiations with a number of interested parties, as well as attracting the interest of new parties," they said.

rweabn.com.au

http://www.tradingmarkets.com/.site/news/Stock%20News/116204…

[Fruehrentner]

Antwort auf Beitrag Nr.: 33.541.004 von Fruehrentner am 04.03.08 08:45:34

aktuelle Kursreaktion in USA auf diese Meldung: + 15 %

Bin auf die australische Kursreaktion morgen gespannt.

Fakt ist: PRANA ist wie von mir avisiert jetzt plötzlich auf dem Radarschirm von (Big) Pharmafirmen!

[Fruehrentner]

Antwort auf Beitrag Nr.: 33.546.820 von Fruehrentner am 04.03.08 17:00:05

auch in AUS ca. 15 Kursplus in Folge der Gespräche mit Pharmafirmen.

[Fruehrentner]

Mar 04, 2008 10:10 ET

Prana Responds to Press Comments on Visits by Pharmaceutical Executives

MELBOURNE, AUSTRALIA--(Marketwire - March 4, 2008) - Prana Biotechnology Limited (NASDAQ: PRAN) (ASX: PBT), has become aware of certain comments which appeared in today's press which have followed on from the release of 26 February 2008 when Prana announced the successful outcome of its Phase IIa Clinical Trial of PBT2 in Early Alzheimer's Disease. The comments relate to a visit to Prana by pharmaceutical company executives and expressed the belief that Prana was engaged in confidential commercial discussions to fund further trials of PBT2.

The Directors of Prana have received legal advice that under the Listing Rules of the Australian Stock Exchange the Company is obliged to clarify the situation with this press release.

The Company confirms that it has entered into confidentiality arrangements with several large pharmaceutical companies and is in various stages of discussion in respect of the licensing of its lead compound PBT2. The Company wishes to emphasize that neither Prana nor any other party is obliged to conclude a transaction.

The Company is delighted with the outcome of the recent clinical trial as it demonstrated the safety and tolerability of PBT2 in the 12-week trial. The trial also demonstrated significant reductions in Abeta 42 in patients with early Alzheimer's Disease and significant improvements in Executive Function performance in select cognitive tests. The positive outcomes from the trial were viewed as a pre-requisite to advancing negotiations with a number of interested parties as well as attracting the interest of new parties.

About Prana Biotechnology Limited

Prana Biotechnology was established to commercialize research into Alzheimer's Disease and other major age-related neurodegenerative disorders. The Company was incorporated in 1997 and listed on the Australian Stock Exchange in March 2000 and listed on NASDAQ in September 2002. Researchers at prominent international institutions including The University of Melbourne, The Mental Health Research Institute (Melbourne) and Massachusetts General Hospital, a teaching hospital of Harvard Medical School, contributed to the discovery of Prana's technology.

For further information, please visit the Company's web site at www.pranabio.com

Forward Looking Statements

This press release contains "forward-looking statements" within the meaning of section 27A of the Securities Act of 1933 and section 21E of the Securities Exchange Act of 1934. The Company has tried to identify such forward-looking statements by use of such words as "expects," "intends," "hopes," "anticipates," "believes," "could," "may," "evidences" and "estimates," and other similar expressions, but these words are not the exclusive means of identifying such statements. Such statements include, but are not limited to any statements relating to the Company's drug development program, including, but not limited to the initiation, progress and outcomes of clinical trials of the Company's drug development program, including, but not limited to, PBT2, and any other statements that are not historical facts. Such statements involve risks and uncertainties, including, but not limited to, those risks and uncertainties relating to the difficulties or delays in financing, development, testing, regulatory approval, production and marketing of the Company's drug components, including, but not limited to, PBT2, the ability of the Company to procure additional future sources of financing, unexpected adverse side effects or inadequate therapeutic efficacy of the Company's drug compounds, including, but not limited to, PBT2, that could slow or prevent products coming to market, the uncertainty of patent protection for the Company's intellectual property or trade secrets, including, but not limited to, the intellectual property relating to PBT2, and other risks detailed from time to time in the filings the Company makes with Securities and Exchange Commission including its annual reports on From 20-F and its reports on Form 6-K. Such statements are based on management's current expectations, but actual results may differ materially due to various factions including those risks and uncertainties mentioned or referred to in this press release. Accordingly, you should not rely on those forward-looking statements as a prediction of actual future results.

http://www.marketwire.com/mw/release.do?id=828433

[Fruehrentner]

Prana Announces Updated Investor Presentation Available on Prana Website

Datum: Fri, 14. Mar 2008 15:24:36 +1100

ELBOURNE, Australia - March 14, 2008: Prana Biotechnology Limited
(NASDAQ: PRAN / ASX: PBT), today announced that the Company has posted a
new investor presentation' which includes further details regarding the
results of PBT2's Phase IIa clinical trial, on the Company's website.
The presentation highlights the outcome of the recent clinical trial
demonstrated the safety and tolerability of PBT2 in the 12 week trial.
The trial also demonstrated significant reductions in Abeta 42 in
patients with early Alzheimer's Disease and significant improvements in
Executive Function performance in select cognitive tests. The positive
outcomes from the trial were viewed as a pre-requisite to advancing
negotiations with a number of interested parties as well as attracting
the interest of new parties.

Prana will be utilizing the new presentation in meetings with
institutional investors. For more information, or to view the most
current presentation, please visit the Company website at
www.pranabio.com
---------------------------------------------


PRANA hält sich hervoragend im aktuell schwachen Marktumfeld. Bleibt spannend!

[Fruehrentner]

nochmal zum wissenschaftlichen Hintergrund des Wirkstoffkandidaten PBT-2 und dessen Ansatzpunkt:

14 August 2007
Prana Announces Independent Studies of Metal Ion-Binding Suggest Broad Implications for Effect of Metal Ions in Alzheimer’s Disease

MELBOURNE, Australia – 14 August 2007: Prana Biotechnology Limited (NASDAQ: PRAN / ASX: PBT) announced that reporting in today’s edition of the journal, Proceedings of the National Academy of Sciences, the multi-institutional team led by Professor David Lynn showed how interactions between beta-amyloid (ABeta) with the biological metals copper and zinc can induce conformational alterations to the Abeta protein causing it to adopt a multitude of toxic forms.

In their article entitled, "Engineering metal ion coordination to regulate amyloid fibril assembly and toxicity" the authors note that subtle variations in the chemical environment of the brain can radically influence the binding of copper to a specific sequence of Abeta to generate both fibrillar and non fibrillar (or ‘oligomers’) forms of the protein. The oligomeric forms of Abeta in particular, are currently the subject of great interest in the Alzheimer's research community as the best validated therapeutic target in Alzheimer’s Disease. The authors also emphasize that their findings have relevance to other neurodegenerative conditions including Parkinson's Disease, where metal binding is believed to modulate or induce the pathological aggregation of proteins.

Prana scientists, whose work is often cited in this publication, have promoted the concept that changes in brain chemistry associated with the aging process cause subtle fluctuations in the regulation of copper, zinc and iron, permitting toxic interactions with the Abeta protein. Prana's therapeutic approach uses Metal Protein Attenuating Compound (MPAC) technology comprising orally bio-available small molecules which specifically target such pathological interactions.

PBT2, the company's lead compound, was designed to inhibit the formation of toxic oligomers of Abeta resulting from interactions with copper and zinc. PBT2, is currently undergoing a 80 patients double-blinded Phase IIa Alzheimer’s Disease clinical trial due to be completed by the end of 2007, and leads from the 400 strong MPAC library are currently being validated for clinical development in other neurodegenerative disorders.

Prana CEO Geoffrey Kempler remarked "This report from an authoritative independent research group lends further endorsement to the Prana therapeutic approach in neurodegeneration, which is to intercede in the metal dependent process of target protein aggregation".

http://www.pranabio.com/company_profile/press_releases_item.…

[Fruehrentner]

Prana Reports Increase in Percent of Major Shareholder Ownership

March 17, 2008: 11:49 AM EST

Prana Biotechnology Limited (NASDAQ: PRAN) (ASX: PBT) today announced that Balyasny Asset Management L.P. (BAM), an institutional investment firm, has purchased additional shares resulting in ownership of over five percent of Prana's publicly traded stock.

Balyasny Asset Management stated in an Australian Stock Exchange (ASX) filing dated March 7, 2008, that it now holds 9.26 million Prana shares. BAM is a global investment firm, headquartered in New York, with over 60 investment professionals across multiple investment disciplines.

Geoffrey Kempler, Chairman and CEO of Prana Biotechnology, said, "We are pleased that a firm like Balyasny Asset Management has demonstrated this strong level of confidence in Prana's science and future growth potential."


About Prana Biotechnology Limited

Prana Biotechnology was established to commercialize research into Alzheimer's Disease and other major age-related neurodegenerative disorders. The Company was incorporated in 1997 and listed on the Australian Stock Exchange in March 2000 and listed on NASDAQ in September 2002. Researchers at prominent international institutions including The University of Melbourne, The Mental Health Research Institute (Melbourne) and Massachusetts General Hospital, a teaching hospital of Harvard Medical School, contributed to the discovery of Prana's technology.

For further information, please visit the Company's web site at www.pranabio.com

http://money.cnn.com/news/newsfeeds/articles/marketwire/0375…

[Fruehrentner]

Prana Announces Updated Investor Presentation

Prana Biotechnology Limited (NASDAQ: PRAN) (ASX: PBT) today announced that the Company has posted a new investor presentation which includes further details regarding the results of PBT2's Phase IIa clinical trial, on the Company's website.
The presentation highlights the outcome of the recent clinical trial demonstrated the safety and tolerability of PBT2 in the 12 week trial. The trial also demonstrated significant reductions in Abeta 42 in patients with early Alzheimer's Disease and significant improvements in Executive Function performance in select cognitive tests. The positive outcomes from the trial were viewed as a pre-requisite to advancing negotiations with a number of interested parties as well as attracting the interest of new parties.

Prana will be utilizing the new presentation in meetings with institutional investors. For more information, or to view the most current presentation, please visit the Company website at www.pranabio.com.

[Bullebio]

hallo frührentner,

wieviel ausstehende aktien hat prana biotech ??

und darausfogend

wie hoch ist die aktuelle marktkapitalisierung ??

danke,
und ein schönes osterfest an alle investierten.

ich will ja nächste woche nochmal zulagreifen.

[Fruehrentner]

Antwort auf Beitrag Nr.: 33.705.579 von Bullebio am 21.03.08 17:17:12

Hallo Bullebio,

genau das frag ich mich auch gerade

Seit wann bist du investiert?

Ich hab's aus Zeitgründen noch nicht recherchiert. Vielleicht kann uns hier mal jemand unterstützen hinsichtlich Aktienzahl und MK?

[Bullebio]

hallo,

ich bin schon über einige jahre investiert. jedoch mit einer kleinen stückzahl von 300. ich habe pran auch ewigkeiten nicht mehr beachtet, da ich diese schon mehr oder weniger abgeschrieben hatte.
ich kann mich daran erinnern, dass ich diese zu 5 $ gekauft hatte. dies ist bestimmt schon 3-4 jahre her.

habe gerade bei yahoo-finanzen reingeschaut, die geben eine market-cap von 83 mio $ an. da hätten wir noch nicht einmal 20 mio aktien ausstehend.

wenn ich zeit habe, schaue ich mir mal die ganzen jahresberichte von pran an.

bis später

rico

[Erbse1]

Antwort auf Beitrag Nr.: 33.705.890 von Fruehrentner am 21.03.08 18:36:47

Aktienanzahl und Kapitalisierung PRAN

http://www.nasdaq.com/quote.dll?mode=stock&page=multi&symbol…

Weiß aber nicht ob die Einträge aktuell sind.

Grüße
Erbse

[Fruehrentner]

Antwort auf Beitrag Nr.: 33.706.036 von Erbse1 am 21.03.08 19:29:41

danke Erbse1.

Mal angenommen, die Zahlen zur MK sind (halbwegs) aktuell.

Was kann man aktuell daraus ableiten, sofern PBT-2 erfolgreich die Zulassung schaffen würde?

Hab's nicht sooo mit Zahlen und BWL-Wissen ...

[Erbse1]

Antwort auf Beitrag Nr.: 33.706.110 von Fruehrentner am 21.03.08 19:48:23

Ich will dich nicht entmutigen. Das war erst mal eine 2a Studie. Habe PRANA nicht recherchiert. Aus der Kapitalisierung kann man jetzt noch gar nichts ablesen. Das dauert bestimmt noch 4-5 Jahre bis hier überhaupt was spruchreif ist. Selbst dann ist ein Scheitern nicht ausgeschloßen. Die Zahl der Shorties ist auch etwas angestiegen. Es glauben also nicht alle an einen Erfolg. Sicher benötigt PRAN in der Zwischenzeit noch viel Geld und es stehen noch einige Kapitlmaßnahmen an. Es liegt an deiner Strategie, ob du so lange in PRANA investieren willst. Die Konkurrenz auf dem Gebiet der Alzheimer Forschung ist riesig. Sollte PRANA allerdings mit seinem Wirkstoff Erfolg haben, dürften sie um ein vielfaches höher stehen. Es dauert sehr lange und es ist sehr risikoreich. Ich kann dir leider nicht so sehr helfen. Ich glaube aber, daß PRANA nach einem Partner sucht, der die Finanzierung und Entwicklung übernimmt. Dann dürfte PRAN ca 12-15% vom Ertrag erhalten und eine Vorabzahlung. Das sind die üblichen Konditionen nach einer erfolgreichen 2a Studie.

Grüße
Erbse

[Fruehrentner]

Antwort auf Beitrag Nr.: 33.706.209 von Erbse1 am 21.03.08 20:16:38

Viele Dank für deine Ersteinschätzung. Das hilft einem erst mal, wider etwas auf den Boden der Tatsachen zurückzukommen.
Phase IIa ist in der Ta noch recht früh, dessen sollte sich jeder bewusst sein. Habe Prana bisher auch nur auf der watch list und werde weiter beobachten.

Nach den Phase-IIa News hält sich Prana aber zumindest auf dem erhöhten Kursniveau ganz gut und knickt (noch) nicht ein auf das Ausbruchsniveau - trotz des äusserst angespannten Marktumfelds.

An neuen Alzheimermitteln mit neuem Wirkmechanismen arbeiten ne Menge Firmen, das ist richtig. Aber Prana's Ansatz der Metallchalitisierung ist m W. einzigartig und so wie ich denke auch sehr vielversprechend und findet offenbar auch besondere Beachtung in der Fachwelt. Ist aber nur meine persönl. Einschätzung, bin kein Alzheimer-Fachmann, dazu müsste man sich tief in die Alzheimerforschung einarbeiten.

[Fruehrentner]

auch bei einem der Big Pharma, hier Eli Lilly, tut sich was beim Alzheimer Entwicklungskandidaten:

Lilly Launches Its First Phase III Trial for Treatment of Alzheimer's Disease

March 31, 2008

Late-stage IDENTITY study of once-daily, oral agent is now enrolling patients

INDIANAPOLIS, March 31, 2008 /PRNewswire-FirstCall via COMTEX News Network/ -- Eli Lilly and Company (NYSE: LLY) has announced today the start of a Phase III clinical trial studying LY450139, an investigational gamma secretase inhibitor for the treatment of mild to moderate Alzheimer's disease.

LY450139 is being tested to see if it can slow the progression associated with Alzheimer's disease by inhibiting gamma-secretase, an enzyme that can create a sticky protein called amyloid beta. Current Alzheimer's disease theory is that subtypes of amyloid beta clump together into plaques that eventually kill off brain cells. By blocking gamma secretase, there is less amyloid beta formed, potentially slowing brain-cell death.

Slowing the rate of disease progression could preserve independent functioning and quality of life for Alzheimer's patients in the milder stages of the disease, potentially delaying the onset of the severe stages of the disease. Currently available treatments for Alzheimer's disease have no documented effect on amyloid beta. They provide modest improvements in symptoms but do not slow the underlying disease process.

The IDENTITY Trial - Interrupting Alzheimer's Dementia by EvaluatiNg Treatment of AmyloId PaThologY

IDENTITY is a randomized, double-blind, placebo-controlled trial that will be conducted in the U.S. and 21 additional countries. As part of IDENTITY, 1,500 patients will be studied for 21 months, and an open-label extension will be available to all participants completing the study. Patients who are taking currently available symptomatic treatments for Alzheimer's disease can continue treatment during their participation in IDENTITY. Because the IDENTITY study also incorporates a "randomized delayed start" design, even those subjects initially assigned to the placebo arm of the study will be started on active LY450139 treatment sometime before the end of the 21-month study period. Both the subjects and investigators will be blinded to the exact timing of this delayed start of study drug administration.

"Alzheimer's is a devastating disease that destroys brain cells, affecting everything from a patient's memory to their work and social life. Currently available medications treat the symptoms of Alzheimer's disease but have not been shown to change its underlying progression, creating an urgent unmet medical need. Today, we are proud to announce the start of the IDENTITY clinical trial and hold hope that LY450139 will represent an advance in the attempt to slow the progression of this fatal disease. We encourage patients or their caregivers to review the enrollment criteria for IDENTITY to see if they are eligible to participate," said Eric Siemers M.D., Medical Director, Alzheimer's disease research for Eli Lilly and Company.

Alzheimer's disease is a progressive neurodegenerative condition that is the most common cause of dementia in patients over 65 years of age. Estimates show that 6-8% of people over age 65 are affected by Alzheimer's disease(1), totaling approximately 5 million people in the United States alone(2). Every 72 seconds, an American is developing Alzheimer's disease(3), and it is the seventh-leading cause of death in the United States(4). The direct and indirect health care costs associated with Alzheimer's disease in the U.S. are estimated to be about $150 billion(5). In 2005, the total cost worldwide was estimated at $315.4 billion(6).

Given the aging population, without the availability of medicines that delay or prevent the onset of Alzheimer's disease, the number of affected people is expected to at least triple by the year 2050 in developed nations(7). The average duration between onset of symptoms and death due to complications of Alzheimer's disease is about 8-10 years(8). The burden to caregivers and health care costs can increase dramatically in the late stages of Alzheimer's disease, when patients cannot maintain independent function and are frequently bedridden.

To more completely characterize the disease-modifying effects of LY450139, a number of optional biomarker sub-studies will be available to patients. These optional sub-studies will utilize new brain-scanning techniques to determine the amount of amyloid beta plaque in the brain, employ other, more established scanning techniques to examine brain structure and function, and evaluate a number of additional biochemical measures of Alzheimer's disease. By determining the effect of LY450139 on these objective biomarkers, a more complete understanding of the effect of LY450139 on underlying Alzheimer's disease pathology is possible.

Additional information regarding the IDENTITY trial, including global recruitment sites, may be found by visiting www.clinicaltrials.gov or www.lillytrials.com, or by calling 1-877-CTLilly (1-877-285-4559).

About LY450139

LY450139 inhibits gamma secretase, an enzyme that cuts a protein, creating a shorter, sticky protein called amyloid beta. Alzheimer's disease theory suggests that some subtypes of amyloid beta clump together into plaques that eventually kill off brain cells. Clinical studies have examined the effect of LY450139 on amyloid beta in blood and cerebrospinal fluid. The most frequently occurring side effects experienced in earlier clinical studies with LY450139 include diarrhea, upset stomach, and fatigue. For a more complete listing of potential side effects, prospective clinical trial participants should refer to the informed consent document.

-------------------------------------------
About Lilly

Lilly, a leading innovation-driven corporation, is developing a growing portfolio of first-in-class and best-in-class pharmaceutical products by applying the latest research from its own worldwide laboratories and from collaborations with eminent scientific organizations. Headquartered in Indianapolis, Ind., Lilly provides answers - through medicines and information - for some of the world's most urgent medical needs. Additional information about Lilly is available at www.lilly.com. P-LLY

This press release contains forward-looking statements about the potential of the investigational compound LY450139 and reflects Lilly's current beliefs.

http://newsroom.lilly.com/releaseDetail.cfm?ReleaseID=302104

[Fruehrentner]

Antwort auf Beitrag Nr.: 33.706.247 von Fruehrentner am 21.03.08 20:30:38

das sollte Metallchelatisierung heissen, und nicht Metallchalitisierung

[Erbse1]

Zur Information. Aus einem anderen Board kopiert.
Grüße
Erbse

Samaritan Alzheimer's Drug Selected
for 2008 ''100 Greatest Investigational Drugs'' by R&D Directions MagazineT
uesday April 15, 10:24 am ET

-Caprospinol Shows Promise to Delay or Halt Alzheimer's

-In Animal Studies, Caprospinol Restores Memory, Maintains Neuronal Cell Energy Levels and Protects Against Future Neuronal Damage in Brain

-Samaritan Readying Drug for Phase I Clinical Trial


LAS VEGAS--(BUSINESS WIRE)--Alzheimer’s drug Caprospinol (SP-233), from Samaritan Pharmaceuticals, Inc., (OTCBB:SPHC) (http://www.samaritanpharma.com), a biopharmaceutical company committed to commercializing new innovative therapeutic drugs, was cited by R&D Directions’ magazine’s seventh-annual list of 100 greatest investigational drugs in development by large and small companies throughout the world. According to R&D Directions, compounds on this list distinguish themselves as "innovative, first-in-class or clearly advanced compared with those on the market."


Six drugs for Alzheimer’s disease, some also targeting other cognitive disorders, were chosen, including candidates from Wyeth (NYSE:WYE - News), GlaxoSmithKline (NYSE:GSK - News), and AstraZeneca (NYSE:AZN - News).

Caprospinol (SP-233) is a novel Alzheimer’s drug candidate that has shown numerous properties to indicate it as a promising direct treatment for Alzheimer’s disease. Caprospinol clears beta-amyloid plaques from the brain and protect the brain against Beta-Amyloid induced cell death. Caprospinol binds to the Beta-Amyloid peptide, preventing its aggregation into more neurotoxic entities and entry into neurons, as well as protecting neuronal mitochondria from Beta-Amyloid induced damage, and maintaining neuronal cell energy levels.

“Unlike drugs currently used to treat Alzheimer’s that simply alleviate symptoms, Caprospinol has the potential be a viable treatment for the disease itself,” said Dr. Janet Greeson, Chief Executive Officer of Samaritan. “There are more than five million Americans who suffer with this mind robbing disease and the current market is over $4 billion a year, and expected to grow dramatically, with the aging of the baby boomers.”

[Fruehrentner]

Neues aus der Alzheimer-Forschung:

25.04.2008 08:30:00

Neuartiger Ansatz zur Behandlung von Alzheimer und anderen Krankheiten durch Abzielen auf Zellmembran-RAFTS

DRESDEN, Deutschland, April 25 /PRNewswire/ --

- Kooperierende Wissenschaftler und Mitarbeiter von JADO Technologies veröffentlichen Studie in Science

Die JADO Technologies GmbH, das führende Unternehmen in der Entwicklung von RAFT-Therapeutika, hat heute die Veröffentlichung einer Studie in Science bekannt gegeben, die eine potentielle neuartige Strategie für die therapeutische Intervention bei Alzheimer und anderen Erkrankungen darstellt, indem sie eigenständige funktionale Domänen in der Zellmembran (RAFTS) beeinflusst. Die von Wissenschaftlern von JADO zusammen mit mehreren Kollegen aus dem akademischen Bereich durchgeführte Studie wird in der Ausgabe der Zeitschrift vom 25. April 2008 erscheinen.

Unter dem Titel "Efficient inhibition of the Alzheimer's disease Beta-secretase by membrane targeting" beschreibt der Artikel, wie Beta-Sekretase, das entscheidende Enzym bei der Produktion des mit Alzheimer in Verbindung stehenden Beta-Amyloid-Peptids, durch die Verwendung von in den Zellmembran-RAFTS verankerten Substanzen effektiv gehemmt werden kann. Anders als bestehende Ansätze zur Hemmung von Beta-Sekretase, die den intrazellulären Aufenthaltsort des Zielproteins oder die unterschiedliche Gestalt, die das Protein in diesem Zusammenhang annehmen kann, nicht berücksichtigen, werden diese Hemmstoffe durch die RAFT-Verankerung direkt an den Ort gebracht, an dem die Beta-Sekretase ihre neurotoxische Aktivität ausübt.

"Unsere Daten bilden den Proof-of-Principle für einen neuen Ansatz, bei dem niedermolekulare Hemmstoffe zu den RAFT-Zielen in den Zellmembranen geleitet werden, die die Krankheit verursachen. In diesem Fall verfügt der Ansatz durch die Ausrichtung der Hemmung auf die funktionale Zellmembran-Domäne, in der das Enzym aktiv ist, über Potential zur Nutzung bei der Entwicklung von wirkungsvolleren Beta-Sekretase-Hemmern zur Behandlung von Alzheimer", erklärte Professor Kai Simons vom Max-Planck-Institut für Molekulare Zellbiologie und Genetik und Mitgründer von JADO. "Wir glauben, dass diese neuartige Strategie auch bei der Entwicklung von Therapeutika gegen andere RAFT-Ziele bei einer Vielzahl von anderen Krankheiten eingesetzt werden kann."

Beta-Sekretase wird aus der Zellmembran in intrazelluläre Kompartments (Endosome) internalisiert, wo es sein Substrat, das Amyloid-Precursor-Protein (APP), spaltet. Die meisten löslichen Hemmer von Beta-Sekretase erhalten keinen Zugang zu diesem internen Aufenthaltsort. Die Forscher untersuchten deshalb zunächst, ob die Verankerung eines solchen Beta-Sekretase-Hemmstoffs an der Membran diesem eine höhere Wirkung verleiht, indem er zum richtigen Kompartment gebracht wird. Ein Beta-Sekretase Peptidinhibitor, der die lösliche Beta-Sekretase hemmte, ohne allerdings das Enzym im zellulären Assay zu blockieren, wurde mit einem Sterol-Ankermolekül verbunden. Mit diesem RAFT-verankerten Wirkstoff konnte eine starke Hemmung der Beta-Sekretase-Aktivität nachgewiesen werden, wobei Konzentrationen von nur 100 nM ausreichend waren, um das Auftreten des Amyloid-Peptids vollständig zu blockieren. Im Tiermodell von Alzheimer hat der gleiche Sterol-verankerte Hemmstoff die Bildung von Beta-Amyloid im Gehirn über 4 Stunden um 50% reduziert, wogegen der freie Inhibitor wirkungslos war.

Die Forscher erklärten, dass der Vorteil der Verwendung eines Sterol-Ankers darin bestand, auf die Konzentration des Inhibitors in den sterolreichen RAFT-Domänen, in denen die Beta-Sekretase APP spaltet, abzuzielen und diese zu erhöhen. Überdies wurde auch nachgewiesen, dass der RAFT-Anker nicht durch einen anderen Lipidtyp ersetzt werden kann und dass Kenntnisse der RAFT-Chemie von entscheidender Bedeutung sind.

"Dieser bahnbrechende Artikel bildet den Höhepunkt vieler Jahre wegbereitender Forschung durch dieses Team auf dem aufstrebenden Gebiet der RAFT Interventionstherapeutika. Bei JADO haben wir diesen Ansatz nun auf die nächste Stufe gebracht und entwickeln eine Reihe von Präparaten, die zur Behandlung von Allergieerkrankungen und Infektionskrankheiten auf RAFTS abzielen. Die Alzheimer-Erkrankung war bereits früher ein Forschungsgebiet der Gründer unseres Unternehmens. Die vorliegenden Daten unterstützen unsere Überzeugung, dass der RAFT Ansatz auch über Potential für eine groBetae Anzahl von Indikationen verfügt", so Charl van Zyl, CEO von JADO.

Der Artikel wurde verfasst von: Lawrence Rajendran(1), Anja Schneider(4), Georg Schlechtingen(2,6), Sebastian Weidlich(2), Jonas Ries(3), Tobias Braxmeier(2,6), Petra Schwille(3), Jörg B. Schulz(5), Cornelia Schroeder(6), Mikael Simons(4), Gary Jennings(6), Hans-Joachim Knölker(2,6), Kai Simons(1,7)

(1)Max-Planck-Institut für Molekulare Zellbiologie und Genetik, Pfotenhauerstr. 108, 01307, Dresden, Deutschland;

(2)Fachrichtung Chemie, Technische Universität Dresden, Bergstr. 66, 01069 Dresden, Deutschland;

(3)Biotec, Biotechnologisches Zentrum, Tatzberg 47/49, Dresden, 01307 Deutschland;

(4)Max-Planck-Institut für experimentelle Medizin, 37075, Göttingen, Deutschland;

(5)Zentrum für Neurologische Medizin, Waldweg 33, 37073 Göttingen

(6)JADO Technologies GmbH, Tatzberg 47-51, 01307 Dresden, Deutschland.

(7)Korrespondenz sollte an K.S. ([e-mail]) adressiert werden.

Über RAFTS

RAFTS sind eigenständige funktionale Domänen in der Lipidmembran von Zellen, die eine zentrale Rolle in komplexen physiologischen Prozessen wie der Immunreaktion oder in vielen pathologischen Situationen spielen. Durch das Hemmen dieser Prozesse verfolgt JADO die Entwicklung neuartiger Therapeutika mit einem neuen Wirkmechanismus.

Über JADO Technologies

JADO ist führend auf dem aufstrebenden Gebiet der RAFT Therapeutika. Das Konzept der RAFT Therapeutika leitet zugleich einen Paradigmenwechsel in der Medikamentenentwicklung ein und birgt groBetaes Potential für das Herangehen an viele bisher nicht erfüllte medizinische Anforderungen, insbesondere bei allergischen und infektiösen Krankheiten, Alzheimer und Krebs.

Geschützt durch eine starke Patentposition bietet die RAFT Intervention Technology(R) der Firma eine einmalige Plattform für neuartige Medikamentenentwicklung. JADO hat diese Technologie zur Erzeugung verschiedener niedermolekularer Arzneimittelkandidaten, mit dem Schwerpunkt auf klinische Studien für Allergieindikationen, wirksam eingesetzt. Die Firma wird von einem globalen Netzwerk klinischer und akademischer Experten unterstützt, darunter den Gründern von JADO, Prof. Kai Simons, Prof. Marino Zerial, Dr. Teymuras Kurzchalia (Max-Planck-Institut für Molekulare Zellbiologie und Genetik, Dresden) und Prof. Hans-Joachim Knölker (Technische Universität Dresden). Der Hauptgeschäftssitz von JADO befindet sich in Dresden, Deutschland und das Unternehmen hat eine Tochtergesellschaft in Bethlehem, Pennsylvania (USA). Nähere Informationen finden Sie auf unserer Website: http://www.jado-tech.com.

Kontaktpersonen:

JADO Technologies Halsin Partners
Charl van Zyl, CEO Mike Sinclair, Direktor
[phone] [phone]
Quelle:PR NEWSWIRE

[Erbse1]

Hallo Fruehrentner,
dein letzter Bericht klingt sehr interessant. Werde diese JADO GmbH mal im Auge behalten. Sind bisher leider noch nicht börsennotiert.
Grüße
Erbse

[Fruehrentner]

Prana Biotechnology has discovered novel drug candidates for use in Parkinson's disease

Published: Tuesday, 6-May-2008

Prana Biotechnology Limited has announced that it has identified novel therapeutic drug candidates from its Parkinson's disease program. Already, a lead candidate drug has demonstrated positive effects in pre-clinical studies, protecting the brain from damage to the substantia nigra, the area of the brain affected in Parkinson's disease.

Prana's drug candidates are being tested on two widely used mouse models for Parkinson's disease, which employ either the 6-hydroxy-dopamine (6-OHDA) or MPTP toxins. These models mimic the disease by using these toxins to destroy the substantia nigra cells over time, leading to motor function loss. Already a candidate lead drug has been shown to protect and preserve the substantia nigra cells from the damage of 6-OHDA and was also able to increase motor function in those animals treated with Prana's drug. In addition, the same lead candidate drug showed benefit in the MPTP animal model and protected the substantia nigra cells from the toxic damage of MPTP.

Prana's drug design is based on the understanding of the relationship between metals, particularly Iron, and the oxidative damage to the substantia nigra. This damage results in progressive neurodegeneration leading to the characteristic symptoms of the disease, notably a gradual loss of motor function over several years and a loss of cognitive function in the later stage of the disease. The compounds being tested in the program are novel compounds selected from Prana's proprietary MPAC (metal-protein-attenuating compounds) library for their selective suitability for Parkinson's research.

"Prana's drug candidates for Parkinson's disease are designed to target the underlying cause of the disease by protecting the brain from neuronal loss with the aim of minimising the actual disease in patients, in contrast to providing temporary symptomatic relief," stated Geoffrey Kempler, Chairman and CEO of Prana. "We are optimistic for the potential of our Parkinson's disease program to deliver an effective treatment to help patients. This will be a valuable addition to our expanding pipeline of drug opportunities arising from our MPAC library. To date, Prana's lead Alzheimer's Disease MPAC, PBT2, has successfully completed a Phase IIa clinical trial in Alzheimer's Disease and the company is looking to partnership strategies as one way to accelerate its development into larger trials. Prana's MPAC's are also being studied in other neurodegenerative diseases such as Huntington's Disease as well as in various cancers".

Individuals affected with Parkinson's disease in 15 of the world's most populous nations are estimated to double over the next generation. By 2030, the number is anticipated to reach between 8.7 million and 9.3 million worldwide.[1] In the US alone, an estimated one million Americans currently suffer from Parkinson's disease.

The data will be presented at the Australian Society for Neurology meeting in Brisbane on May 19 and the International Movement Disorders Meeting in Chicago on June 22

http://www.news-medical.net/?id=38080

[Fruehrentner]

MELBOURNE, Australia – May 13, 2008:

Prana Biotechnology Limited (NASDAQ: PRAN / ASX: PBT), a biopharmaceutical company focused on the research and development of treatments for neurodegenerative disorders, today announced a publication in the Proceedings of the National Academy of Sciences (PNAS) journal,1 describing a completely new class of amyloid inhibiting drugs.

The reported drugs are directed against the amyloid present in Alzheimer’s Disease, composed of the Abeta protein. By specifically targeting and blocking the metal binding site on the Abeta protein, these drugs change the intrinsic structural properties of Abeta and its oligomers, stopping neuronal toxicity and the subsequent formation of ABeta fibrils.

The PNAS paper highlights several key characteristics of these amyloid inhibitors, which upon binding to Abeta change the protein’s structural properties and consequent behaviour including:

· Ability to stop Abeta aggregation progressing into amyloid fibrils.

· Shut down of toxic free radical production by Abeta.

· Rescue of synapses from Abeta-induced toxicity, as measured by long term potentiation (LTP), a measure of synaptic strength which is commonly viewed as a biochemical measure of memory.


Prana’s chemistry program is building upon the structural template provided by these proof-of-concept compounds to create a library of novel drugs that are orally available. To date, Prana’s lead anti-amyloid compound has been designed to penetrate the brain, and is able to reduce both Abeta and tau protein biomarkers in the brain of Alzheimer’s disease transgenic mouse models.

Notably, the lead compound has demonstrated the ability to arrest the formation of covalently cross-linked oligomers of Abeta, a type of oligomeric Abeta that is a key Alzheimer’s disease target.

Prana’s drug development program has now resulted in two complimentary drug development platforms. First MPAC’ s (metal protein attenuating compounds), which compete with Abeta by directly binding metal ions such as copper and zinc, and now these new anti-amyloid compounds which bind and block the actual metal binding site on Abeta.

Geoffrey Kempler, Chairman and CEO of Prana, stated, “This is a major advance for the Company and confirms our confidence in targeting metal protein interactions. Not only does this increase confidence in the value of PBT2, our lead Alzheimer’s Disease MPAC drug, this new class of drugs reported in PNAS also opens future commercial opportunities to expand our drug pipeline. Prana hopes to employ this anti-amyloid strategy in the treatment of other amyloid indications.”

1. Platinum-based inhibitors of amyloid- as therapeutic agents for Alzheimer’s disease Kevin J. Barnham et al PNAS May 13, 2008 vol. 105 no. 19 6813–6818.

[Fruehrentner]

MELBOURNE, Australia - May 21, 2008 - Prana Biotechnology Limited
(NASDAQ: PRAN / ASX: PBT), a biopharmaceutical company focused on the
research and development of treatments for neurodegenerative disorders,
today announced it has raised in a private placement transaction over
A$7 million (Australian) dollars from existing investors at a price of
$0.40 (AUS) a share. Investors include both US and Australian
professional and sophisticated investors.

Geoffrey Kempler, Chairman and CEO of Prana Biotechnology, stated, "The
funds will allow us to boost our R&D activities. We are particularly
gratified by the increased confidence shown by these investors, who
previously invested approx. six months ago at a value almost 50 percent
below today's level. Since then we have achieved key milestones,
including a successful Phase 2a clinical trial of PBT2 and commencement
of commercial discussions, as well as the widening of our pipeline
opportunities into different indications."

Funds will be used for the development of the Company's pipeline in
treatments for Alzheimer's and other neurodegenerative diseases, such as
Parkinson's and Huntington's disease.

"We are progressing discussions with potential pharmaceutical partners
and are confident that PBT2, our lead drug for Alzheimer's disease,
offers a very attractive opportunity. A strategic partnership is one way
that we can achieve our central goal of advancing the commercialization
of PBT2," Mr. Kempler concluded.

[Fruehrentner]

Und wieder einer in Phase III gescheitert mit einem Alzheimer-Kandidaten, diesmal MYRIAD:

Myriad's Phase III Alzheimer's study fails end point

30th June 2008 - By Staff Writer

Myriad Genetics has announced results of the Act-Earli-AD trial, an 18-month Phase III study of Flurizan in patients with mild Alzheimer's disease.
The study did not achieve statistical significance on either of its primary endpoints - cognition and activities of daily living.

Peter Meldrum, president and CEO of Myriad Genetics, said: "We are disappointed that Flurizan failed to achieve significance in this study, and we will now discontinue development of this compound. The discontinuation of Flurizan will reduce our pharmaceutical development spend substantially and should enable Myriad to achieve profitability next year, ending June 30, 2009."

http://www.pharmaceutical-business-review.com/article_news.a…

[Fruehrentner]

Press Release 8 July 2008 - Prana Co-Founding Scientist Professor Rudolph Tanzi, Addressed U.S. Senate Special Committee on Aging

Comments on Prana Developments and Future Prospects for Therapeutic Approaches for Alzheimer’s Disease

MELBOURNE, Australia – July 8, 2008 – Rudolph E. Tanzi, Ph.D., Co-Founding Scientist of Prana Biotechnology Limited (NASDAQ: PRAN / ASX: PBT), a biopharmaceutical company focused on the research and development of treatments for neurodegenerative disorders, was invited this past May to testify in front of the U.S. Senate Special Committee on Aging on the Future of Alzheimer's: Breakthroughs and Challenges. The hearing, lead by Senator Herb Kohl (D-WI) and Senator Gordon H. Smith (R-OR), discussed Alzheimer’s Disease as a growing crisis and how the United States can accelerate its efforts against the disease. Additional participants included Sandra Day O'Connor, Former Supreme Court Justice, Member of the Alzheimer's Study Group, Newt Gingrich, Former Speaker of the House of Representatives, Member of the Alzheimer's Study Group, Charles Jackson, Alzheimer's patient and Suzanne Carabone, Alzheimer's patient caregiver.

The recent failed clinical studies of what were once-promising Alzheimer’s drugs have now attracted much attention to Prana and the future of therapeutic treatments to Alzheimer’s disease. In response Dr. Tanzi, an internationally recognized authority on Alzheimer’s disease who has co-discovered three of the four known genes that cause Alzheimer's disease, presented information to the U.S. Senate on the differing Abeta-targeted therapeutic approaches, and commented upon the ongoing clinical trials in Alzheimer’s disease.

Key material from the testimonial included:

· Future prospects for immunotherapy and gamma-secretase therapeutic approaches;

· Approaches to targeting and regulating Abeta production; and,

· Recent developments regarding drugs aimed at treating and preventing Alzheimer’s disease.

Prana’s theories concerning the interaction between metals and the protein Abeta in the brain are the basis of the company’s treatments for Alzheimer's and other neurodegenerative diseases. Prana’s proprietary lead compound, PBT2, recently concluded a Phase IIa trial in early Alzheimer’s disease, which demonstrated safety and tolerability, and significant reductions in Abeta 42 and improvement in Executive Function performance in cognitive tests. Prana will be presenting this data at the International Conference on Alzheimer’s Disease (ICAD) in July.

Dr Tanzi stated, “Unlike other approaches, Prana’s PBT2 appears to neutralize the neurotoxicity of Abeta and facilitates it's clearance from the brain. Prana’s latest clinical trial results were highly encouraging, by significantly lowering Abeta 42 in the cerebrospinal fluid, and improving cognition in the executive function of patients over a 12-week period. I testified to the U.S. Senate that therapies targeted against the amyloid beta protein offer the best chance at slowing down the progression of Alzheimer's disease. It is my strong belief that PBT2 is among the very best therapies available for achieving this goal."

About Dr. Rudolph Tanzi

Dr. Rudolph Tanzi is a Professor of Neurology (and Neuroscience) at Harvard University, and serves as the Director of the Genetics and Aging Research Unit consisting of eight laboratories in the MassGeneral Institute for Neurodegenerative Diseases at MGH. Since 1982, Dr. Tanzi has focused his studies on Alzheimer's disease (AD). He isolated the first familial Alzheimer's disease (FAD) gene, known as the amyloid β-protein (A4) precursor (APP) in 1987, and another in 1995, called presenilin 2.

Dr. Tanzi is also a co-founder of the “Metal hypothesis of Alzheimer’s disease”. His laboratory first discovered that the metals zinc and copper are necessary for the formation of neurotoxic assemblies of the AD-associated peptide, Aβ, the main component of β-amyloid deposits in brains of AD patients. These studies have led to ongoing clinical trials for treating and preventing AD by targeting Aβ-metal interactions.
Dr. Tanzi has co-authored over 320 research articles and reviews, including three of the top ten most cited papers in AD research over the last decade over which time he was the 5th most cited scientist in the field of AD research. He is also a co-author of a popular trade book on Alzheimer’s disease entitled “Decoding Darkness: The Search for the Genetic Causes of Alzheimer’s Disease”. Dr. Tanzi has received several awards for his work including the two highest awards for Alzheimer’s disease research: The Metropolitan Life Foundation Award and The Potamkin Prize.


About Prana Biotechnology Limited

Prana Biotechnology was established to commercialize research into Alzheimer's disease and other major age-related neurodegenerative disorders. The company was incorporated in 1997 and listed on the Australian Stock Exchange in March 2000 and listed on NASDAQ in September 2002. Researchers at prominent international institutions including The University of Melbourne, The Mental Health Research Institute (Melbourne) and Massachusetts GeneralHospital, a teaching hospital of HarvardMedicalSchool, contributed to the discovery of Prana’s technology.

For further information, please visit our web site at www.pranabio.com.

[Fruehrentner]

10 July 2008

Neuron to Publish Prana’s PBT2 preclinical research

Melbourne, Australia – July 10, 2008 – Prana Biotechnology Ltd (NASDAQ: PRAN, ASX: PBT) announced the publication of key research findings with its lead Alzheimer's Disease drug, PBT2.

The article titled “Rapid restoration of cognition in Alzheimer's transgenic mice with 8-hydroxyquinoline analogs" is associated with decreased interstitial Abeta” appears in the current edition of the prestigious scientific journal Neuron, and can be viewed online.

The key findings reported are:

- PBT2 profoundly and rapidly improved cognition in transgenic mice.
- PBT2 prevented the formation of soluble Abeta oligomers, the form of Abeta believed to be the most toxic.
- PBT2 substantially reduced the amount of all forms of Abeta in the transgenic mouse brain, over a nine week period.
- PBT2, within hours of oral administration, significantly lowered soluble (interstitial) Abeta in the brain, sampled using in vivo microdialysis.
- Using a well established model for memory formation, PBT2 protected neurons in living brain tissue from the toxic effects of Abeta which impairs the signaling between neurons in Alzheimer’s disease.

"The Alzheimer's field is eagerly awaiting the results of several clinical trials of therapies aimed at the toxic amyloid beta protein. Prana's PBT2 is uniquely positioned as an oral drug that neutralizes the toxicity of the amyloid beta protein and clears it from the brain. The positive findings in Alzheimer's mouse models along with the encouraging results from the phase II clinical trial of PBT2 greatly strengthen my belief that this drug will ultimately be shown to slow down disease progress in Alzheimer's patients," commented Dr. Rudolph Tanzi, Professor of Neurology at Harvard University, and Director of the Genetics and Aging Research Unit at MassGeneral Institute for Neurodegenerative Diseases.

In their discussion, the authors explain that healthy brain function is dependent upon the tightly regulated movement of metals within and between neurons. They speculate that with aging this restraint may be loosened, rendering the brain vulnerable to oxidative stress and the pernicious effects of Abeta accumulation. In the article, multiple modes of action for PBT2 are proposed based on the drug’s intrinsic ability to capture and transport metals in the brain. This property explains how PBT2:

• inhibits the production of toxic free radicals and the formation of toxic “oligomeric” aggregates .
• promotes the solubilization and detoxification of Abeta aggregates and plaques
• transports metals into depleted neurons and thereby enhances the production of enzymes which break down Abeta, reducing its concentration in the brain.

The beneficial effects upon cognition are thus a net effect of the disaggregation of plaques, the detoxification of Abeta and enhanced removal of Abeta from the brain.

Associate Professor Robert Cherny, PhD, of the Mental Health Research Institute of Victoria (Australia), Head of Research of Prana Biotechnology Limited and a co-author on the paper, said “using in vivo microdialysis, we can monitor the effects of a drug on brain Abeta in real time in the conscious, freely-moving transgenic mouse. We can literally see the drug altering brain chemistry. The publication emphasises that the dramatic improvements in memory in mice seen with PBT2 are associated with reduction in this soluble (interstitial) Abeta.”

Geoffrey Kempler, Chairman and CEO of Prana, noted that: “we are pleased that the research has been reported in Neuron, a highly regarded peer reviewed journal. Given this, together with the data from our recently completed Phase IIa trial (in press), we are very confident that our drug has the potential to be marketed as a treatment for Alzheimer’s disease. Prana’s approach is different to others because PBT2 targets toxic metal interactions in the brain.”

The data will be presented at the 11th International Conference on Alzheimer’s Disease (ICAD) in Chicago on July 29, 2008 by Associate Professor Robert Cherny describing key preclinical findings of PBT2 in a lecture entitled, “The 8-hydroxyquinoline analog PBT2 rapidly restores cognition and reduces soluble Abeta in Alzheimer’s transgenic mice”.

For access to the full journal article visit the company website at www.pranabio.com

[Fruehrentner]

Prana Selected for "Hot Topics" and Alzheimer's Association Press Briefing at ICAD

MELBOURNE, Australia – July 17, 2008

Prana Biotechnology Limited (NASDAQ: PRAN / ASX: PBT), a biopharmaceutical company focused on the research and development of treatments for neurodegenerative disorders, today announced that Dr. Jeffrey Cummings, the Chairman of Prana’s Research and Development Advisory Board has been invited to present findings from the company’s Phase IIa clinical trial during the “Hot Topics” session at the 2008 International Conference on Alzheimer’s Disease (ICAD) to be held in Chicago, Illinois.

Dr. Cummings will be presenting a talk entitled “Targeting Abeta as a Modifying Therapy of Alzheimer’s Disease: Safety, Efficacy and Biomarker Findings of a Phase IIa Randomised, Double-Blind Placebo-Controlled trial of PBT2” on July 30 at 11:15am.

Part of the Alzheimer’s Association research program, ICAD is the world's leading forum on dementia research. The conference brings together more than 5,000 researchers, physicians and care providers from 60 different countries. The “Hot Topics” session is devoted to exciting advances in Alzheimer’s therapy. Prana’s drug, PBT2, is a novel and very promising approach to the treatment of Alzheimer’s disease.

During the presentation Dr. Cummings will present data from Prana’s latest clinical trial. In the 12 week study in mild Alzheimer’s disease patients, PBT2 demonstrated safety and tolerability, reduced Abeta 42 in the cerebrospinal fluid, and improved Executive Function performance in select cognitive tests.

“In 2006 the Alzheimer’s Association selected Prana’s PBT2 pre-clinical data to be highlighted at ICAD’s “Hot Topics” session. Now, two years later, we are excited to be selected again, this time to discuss our clinical trial results,” said Geoffrey Kempler, Prana’s Executive Chairman. “This continued interest in PBT2 is very encouraging”.

“We know that Abeta requires metals in order to become toxic in the brain and PBT2 protects the brain from this interaction. So we are increasingly optimistic about the prospects of PBT2 as a therapy for Alzheimer’s disease, and our inclusion in Hot Topics and the associated Alzheimer’s Association Press Briefing at ICAD is indeed very gratifying”, concluded Mr. Kempler.

In addition to Dr. Cummings, five of Prana’s scientists and consultants have also been invited to present their research at ICAD and will discuss PBT2:

-- Rudy Tanzi, PhD. July 27 at 10:50am
Professor, Department of Neurology, Harvard Medical School, USA
Genetic association studies in Alzheimer's disease -- Genetics can be
used to guide drug discovery and development in AD.

-- Kaj Blennow, PhD. July 28 at 10:30am
Professor, Neurochemistry Lab, Sahlgrenska University Hospital,
Gothenburg, Sweden
Overview of Biomarkers -- Cerebrospinal fluid biomarkers reflect the
central pathogenic processes in AD, including the deposition of Abeta
in plaques (the 42 amino acid form of Abeta, Abeta42). PBT2 has been
shown to reduce Abeta42 in patients with mild AD after 12 weeks of
treatment.

-- Colin Masters, MD. July 28 at 11:30am
Executive Director, Mental Health Research Institute, Victoria,
Australia
Rational therapeutic strategies for modifying Alzheimer's disease:
Abeta oligomers as the validated target

-- Robert Cherny, PhD. July 29 at 3:45pm
Associate Professor, Mental Health Research Institute, Victoria,
Australia
The 8-hydroxyquinoline analog PBT2 rapidly restores cognition and
reduces soluble Abeta in Alzheimer's transgenic mice

-- Kevin Barnham, PhD. July 30 at 3:00pm *Hot Topics Session*
Associate Professor, Department of Pathology, University of Melbourne,
Victoria, Australia
Therapeutic inhibition of GSK3beta decreases Abeta oligomers, decreases
tau phosphorylation, and improves cognition in a mouse model of AD.

-- Further investigations into the mechanism by which Metal Protein
Attenuating Compounds (MPACs), such as PBT2, can manipulate metals in
the AD brain.

-- July 28 at 12:30pm (Poster)
Second generation MPAC PBT2 inhibits Tau phosphorylation and promotes
Abeta degradation

[Fruehrentner]

PRANA hat das neuerliche High zurückerobert. Die news wurden offenbar sehr gut aufgenommen

[Fruehrentner]

Antwort auf Beitrag Nr.: 34.556.075 von Fruehrentner am 21.07.08 23:00:08

Durchbruch nach oben?

[Fruehrentner]

23 July 2008

Prana Biotechnology Announces Conference Call Following ICAD Presentations

MELBOURNE, Australia – July 23, 2008: Prana Biotechnology Limited (NASDAQ: PRAN / ASX: PBT), a biopharmaceutical company focused on the research and development of treatments for neurodegenerative disorders, announced today that the Company will be hosting a conference call with Geoffrey Kempler, Chairman and CEO, and Dr. Jeffrey Cummings, Chairman of Prana’s Research and Development Advisory Board, on July 31, 2008 at noon EDT (USA time).

The Company will provide a discussion of recent preclinical and clinical trial highlights and an overview of the ICAD presentations. Members of Prana’s Scientific and Management team will be on the call.

The call will simultaneously be Webcast on Thursday, July 31, 2008 at noon p.m. EDT (USA time). A question-and-answer session will follow management's presentation. Interested parties may participate in the conference call by dialing the following numbers approximately five to ten minutes before the call start time:

[phone] from the US or Canada (toll-free)
[phone] (International)

A live Webcast of the conference call will be available on the Prana Web site at www.pranabio.com

A replay of the call will be available starting on Thursday, July 31, 2008, at 3:30 p.m. EDT (USA time) until August 7, 2008 at 11:59 p.m. EDT (USA time). An archived Webcast of the conference call will be available on the Prana Web site at www.pranabio.com. Interested parties may access the replay by dialing the following numbers and entering the account number and conference ID number below:

[phone] (North America)
[phone] (International)
Account #: 286
Conference ID #: 291849


About Prana Biotechnology Limited
Prana Biotechnology was established to commercialize research into Alzheimer's disease and other major age-related neurodegenerative disorders. The company was incorporated in 1997 and listed on the Australian Stock Exchange in March 2000 and listed on NASDAQ in September 2002. Researchers at prominent international institutions including the University of Melbourne, the Mental Health Research Institute (Melbourne) and Massachusetts General Hospital, a teaching hospital of Harvard Medical School, discovered Prana’s technology.

For further information, please visit our web site at www.pranabio.com.

[Erbse1]

Neues in Sachen Alzheimer aber ohne Prana

Grüße
Erbse

Alzheimer's Drug Showdown

Robert Langreth, 07.29.08, 2:39 PM ET

Chicago - Big drug firms like Wyeth, Elan and Eli Lilly have spent years pursuing drugs based on the theory of what causes Alzheimer's disease. At a conference of Alzheimer's disease specialists in Chicago this week, neurologists are looking eagerly to get some of the first good clues on whether they are right.

At center stage at the conference is Elan (nyse: ELN - news - people ), which will present detailed data late Tuesday from a second-stage trial of its amyloid-busting drug, bapineuzumab. The drug is now in final tests with partner Wyeth, and Wall Street is eagerly trying to assess its odds of success.

Eli Lilly (nyse: LLY - news - people ), meanwhile, is touting data from its two amyloid drugs, including a pill drug that dramatically lowers levels of amyloid in the cerebral spinal fluid. Not to be outdone, Pfizer (nyse: PFE - news - people ) even held an analysts' meeting at the W Hotel during the conference to tout its two amyloid-busting entries in early human trials.

The drugs aim to remove aberrant protein clumps called amyloid plaques from the brains of Alzheimer's patients. The question is whether this will also stave off dementia.

Neurologists fiercely debate whether the amyloid clumps are the cause of the disease--or merely a consequence.

Amyloid proponents have held the upper hand for years. But now "we are at a historic point where some new ideas are being able to question the orthodoxy of the amyloid hypothesis," says Zaven Khachaturian, president of Keep Memory Alive in Las Vegas and former head of Alzheimer's research at the National Institutes of Health. He says targeting amyloid is still a reasonable idea, but "maybe it is not the panacea that the orthodoxy is leading us to believe."

In June, Myriad Genetics (nasdaq: MYGN - news - people ) said its Flurizan anti-amyloid drug was totally ineffective in a final-stage trial. And just a couple weeks ago, British researchers reported autopsy data from nine patients in a trial of an anti-amyloid vaccine that was abandoned years ago because of safety issues. Some of the patients had no amyloid in their brain, indicating that the vaccine removed amyloid as expected. Yet they still died from severe dementia. Says Khachaturian: "We are beginning to find out that when you eliminate the amyloid some people still have the dementia."

The amyloid theory "is in a meltdown," says Claude Wischik of the University of Aberdeen, founder of the biotech TauRx Therapeutics. He argues that the amount of amyloid in patient brains doesn't correlate much with dementia, and blocking tau, a second protein that accumulates in the brain cells of demented patients, as his company is doing is a much better way to go. "I could never understand why people were so persuaded by the amyloid theory. It is more about sociology with science," he says.

But Pfizer neurologist Larry Altstiel counters the amyloid theory "is alive and well. It is pretty hard to explain away." He and others point to lab data showing that amyloid can be toxic to brain cells. They note that rare inherited gene mutations that seem to cause Alzheimer's disease by raising amyloid levels. "The evidence for amyloid is still pretty impressive," adds Ronald Petersen of the Mayo Clinic.

One worry is that Alzheimer's takes years to develop, and doctors may not have a way to identify patients in time. Even if amyloid does trigger the disease process, by the time symptoms become obvious "the disease becomes independent of amyloid so it progresses even if the amyloid is removed," says Scott Turner of Georgetown University.

Meanwhile, researchers are beginning to focus on alternative targets to amyloid. At the conference, the Alzheimer's Association International Conference on Alzheimer's Disease, two companies, TauRx Therapeutics from Singapore and Allon Therapeutics of Vancouver, presented human trial data for drugs that target tau. Another non-amyloid drug showing intriguing results is Dimebon from Medivation (nasdaq: MDVN - news - people ). This drug, an antihistamine used in Russia, emerged from nowhere a couple years ago when Medivation reported that the drug slowed Alzheimer's progression in a big trial in Russia.

In a second-stage trial presented at the conference, one of the doses of the TauRx drug that was tested was able to dramatically slow the progression of the disease; the effect was almost twice as big as typically seen with existing drugs, Wischik says. "We have stopped the progression of AD for 19 months," he claimed. The drug tested is an old chemical that previously has been used for a variety of purposes, including treating urinary tract infections.

Muddling matters is the fact that another higher dose was inactive, a problem that Wischik attributed to formulation problems. Meanwhile, the Allon Therapeutics drug helped improve some measures of short-term memory in patients with mild cognitive impairment, a condition that often leads to Alzheimer's disease.

"For the first time we are actually starting to see tau therapeutics results, which is something we have never seen before," enthuses neurologist Scott Turner of Georgetown University. While the data for the tau drugs "aren't definitive at this point," says the Mayo Clinic's Ronald Petersen, they do provide researchers enough of a signal to continue forward in larger trials that may provide more definitive results.

[Fruehrentner]

Antwort auf Beitrag Nr.: 34.611.118 von Erbse1 am 30.07.08 05:54:16

@Erbse

sehr interessanter Artikel. War mir nicht klar, dass die Amyloid-Theorie und der Angriff auf das Amyloid nicht das nonplusultra ist.

Dies zeigt das komplexe Geschehen bei Alzheimer. Womöglich existieren mehrere Ursachen u. Formen der Krankheit.

[Fruehrentner]

news!

Prana Press Release: The Lancet Neurology Publishes Clinical Results of PBT2 in Alzheimer's Disease Patients
Datum: 30.07.2008 02:45:43

- Phase 2a study of PBT2 demonstrates positive biomarker and cognitive effects -

MELBOURNE, Australia – July 30, 2008 –

Prana Biotechnology Limited (NASDAQ: PRAN / ASX: PBT), a biopharmaceutical company focused on the research and development of treatments for neurodegenerative disorders, announced today the publication of the results of its Phase 2a clinical trial on Alzheimer’s disease patients in The Lancet Neurology journal.

PBT2, Prana’s lead Alzheimer’s drug, improved executive function, an important aspect of cognitive performance, in patients with early stage Alzheimer's disease. Further, PBT2 reduced the levels of Abeta in the spinal fluid of patients. Abeta is a key protein associated with Alzheimer’s disease.

Dr Craig Ritchie, the senior author of the publication and Prana’s Chief European Clinical Advisor, commented that “The published clinical data is very encouraging, especially when coupled with PBT2’s strong preclinical efficacy data, as recently published in Neuron.” The PBT2 preclinical research findings demonstrated that PBT2 reduced Abeta in Alzheimer’s disease animal models, with a corresponding cognitive improvement.

“The observed reduction of Abeta levels in the spinal fluid and improvement in signals of Executive Function in the clinical trial has similarities to the pattern of improvement observed in the animal models,” concluded Dr. Ritchie. Prana’s scientists have proposed that in the aged brain, Abeta interacts with abnormally distributed levels of zinc and copper, making the Abeta toxic. PBT2 prevents this interaction, restoring copper and zinc to normal levels in the brain.

Geoffrey Kempler, Prana’s Chairman and CEO commented: “It is very pleasing that The Lancet Neurology, a prestigious peer reviewed journal, has published this clinical data. We have very high hopes for PBT2, and are delighted with its progress to date. We believe that PBT2 offers a unique mechanistic strategy for the treatment of Alzheimer’s disease, and is well positioned to enter larger clinical trials and advance towards commercialization.”

Study Overview:

Seventy-eight early stage Alzheimer's disease patients took either PBT2 (50mg or 250mg) or placebo once daily for 12 weeks, in a randomized, double-blind clinical trial. The safety and tolerability profile of PBT2 was similar to that of placebo. There were no study withdrawals related to adverse events, nor any serious adverse events (SAE) in PBT2-treated patients.

PBT2 250mg produced a highly significant reduction in Abeta 42 of 13% in the spinal fluid, compared to placebo (p=0.006). The effect of PBT2 was dose related (p=0.023).

In the cognitive tests, patients on PBT2 250mg performed significantly better than placebo in two tests of executive function. In the “Trail Making Part B” test, patients completed the task in an average of 42 seconds faster than they had at the beginning of the trial. In contrast, the placebo group was an average of 6 seconds slower. This difference between PBT2 250mg and placebo was statistically significant (p=0.009) and the effect of PBT2 was dose-related (p=0.031). In the “Category Fluency test”, patients improved their word generation response in 60 seconds by an average of 2.4 more words than at the beginning of the trial. This compared with a decrease of 0.3 words in the placebo group. This difference between PBT2 250mg and placebo was statistically significant (p=0.041).

For further information, please visit our web site at www.pranabio.com.

[Fruehrentner]

Antwort auf Beitrag Nr.: 34.612.649 von Fruehrentner am 30.07.08 10:44:45

zur Erklärung:

"Abeta" ist "Amyloid beta"

http://en.wikipedia.org/wiki/Amyloid_beta

[Fruehrentner]

Heute schwere Rückschläge bei anderen Alzheimer-Kandidaten

Wyeth verloren 11,90 Prozent auf 39,74 Dollar. Händler verwiesen auf Analystenaussagen, denen zufolge negative Studiendaten die Wahrscheinlichkeit für eine Markteinführung des Medikamenten-Kandidaten Bapineuzumab verringerten.
Das Mittel soll gegen Alzheimer helfen. Aktien von Elan Corp stürzten sogar um 41,84 Prozent auf 19,63 Dollar ab. Bapineuzumab wurde von Wyeth und Elan entwickelt.


Auch Eli Lilly hat heute P-II Ergebnisse zu einem Alzheimermittel gemeldet.

[Erbse1]

Antwort auf Beitrag Nr.: 34.619.132 von Fruehrentner am 30.07.08 22:47:22

Hallo Frührentner.
hier noch der Kommentar des NeuroInvestor zu den letzten Alzheimer Meldungen.
Grüße
Erbse

Commentary(last updated 7/30/08)

The Search for Intelligent Life in Alzheimer's Trial Design and Analysis

Bapineuzumab did not hit its endpoints for cognition, and from the point of view of a prospective study, it was an abject failure. However, given that Elan/Wyeth announced many months ago that they were going to initate a 4100pt Phase III trial, the companies conducted a intensive posthoc slicing and dicing of the data which has now produced a hodgepodge of contradictory findings. Their main conclusion was that there was a bifurcation amongst study patients based on whether or not they were 'carriers' of the pathognomonic APOE4 gene. The 65% of the patient population studied who were carriers showed no significant benefit from bapineuzumab, though if one only counted completers, they appeared to have a slightly (2.6 ADAS-cog points) better outcome than the placebo group. The non-carriers showed a difference of 5 ADAS-cog points, which did reach significance. However, this was in comparison to a placebo group whose rate of decline was essentially the same as the drug group until they reached the final third of the 18 month trial, and their late nosedive took them towards the extreme end of the expectable range for the slope of cognitive decline over the 18 month timespan. No dose-response pattern was seen, further adding to the impression that these data represented a 'random walk' which could only be made to look coherent via posthoc data manipulation in extreme form, and a disregard for the seemingly distinct possibility that the contrast was an artifact of the placebo group, not a result of drug effect.

There was also a safety signal of note: the incidence of vasogenic edema which appeared related to high doses of the antibody in conjunction with the APOE4 genotype--though 25% of those with vasogenic edema were not APOE4 carriers. On the one hand, most of the patients were asymptomatic, the VE was only detected via MRI. A few patients were symptomatic and required treatment with steroids. It may well be true that asymptomatic VE is not in itself dangerous--but in a real world population of Alzheimer's patients, how reliably can they be monitored to be sure that what was asymptomatic is not worsening? The notion of hundreds of thousands of elderly patients receiving MRI's because of ambiguity around the VE diagnosis seems fiscally untenable. Elan/Wyeth have responded with a plan to give APOE4 patients only a low dose of bapineuzumab, a solution that may lack something in the eyes of a safety-conscious FDA.

But no matter: two trials of 'carriers' and two trials of 'noncarriers', totalling 4100 patients, are still planned. This data, even when spun to the max, has gaping holes in terms of patient selection, efficacy, and dosing. It is data that cries out for a Phase IIb trial to answer these questions, not a premature $300 million expenditure on pivotal studies.


Given the substantive questions about bapineuzumab, and the wisdom of moving from a very confused Phase II dataset to Phase III, Lilly's handling of Phase II data for its own monoclonal antibody, LY2062430, was surprising, to say the least. This was only a 12 week trial involving 52 patients, and Lilly dealt with those vexing efficacy issues by declaring that they neither expected nor found any cognitive effects in this shortterm study. They stated that this Phase II was intended only to show safety and tolerability, and has done so. That is an interesting twist on the usual nomenclature, given that safety trials in a patient population are generally called 'Phase Ib', Phase II generally implies some interest in efficacy signals, and not just biomarkers. What was even more striking, indeed shocking, was that, based on the biomarkers of beta-amyloid levels in blood and CSF, Lilly declared this antibody is ready for pivotal Phase III testing, to begin in 2009.


This is mind-boggling. Having seen Myriad Genetics, Neurochem, Medivation, and now Elan/Wyeth move into Phase III without solid Phase II efficacy data, the first two crashing and burning in tragic style, one might think Lilly would have taken the hint and reconsidered this strategy. But instead, Lilly is dispensing with functional efficacy testing altogether in their haste to reach Phase III with this antibody. We are aware of the pressures upon small companies like Neuorchem and Medivation, pressing them to push the clinical envelope as they try to stretch limited resources and attract more funding. Elan and Wyeth are also making a mistake, but at least they tried to assess efficacy over an eighteen month timespan, even if they have tied themselves into knots trying to spin the data into something positive. But what is Lilly's excuse? It's like watching two teenage drivers who are playing a game of 'chicken': one car zooms off the cliff and bursts into flames, the second driver decides 'that looks pretty cool', and drives off the cliff as well. This pretty much puts to rest the whole concept of Intelligent Design, because there's none to be found here.

[Fruehrentner]

Prana Alzheimer's Drug Safe, Improves Brain Function in Study

By Simeon Bennett

July 29 (Bloomberg) -- Prana Biotechnology Ltd.'s experimental Alzheimer's disease drug was safe and improved brain function in a study, furthering research into the most advanced approach to treat a suspected cause of the illness.

Patients taking the medicine performed better at word association and visual tests than those on a dummy pill, researchers said in a study in the journal Lancet Neurology that was presented at the U.S. Alzheimer's Association meeting in Chicago. Melbourne-based Prana said the improvements were triggered by the drug's ability to prevent the buildup of a toxic protein in patients' brains.

The findings support a contested theory that suggests Alzheimer's develops when the protein, beta amyloid, accumulates in the brain, killing some cells and preventing others from working. The hypothesis has been disputed after anti-amyloid drugs developed by Myriad Genetics Inc. and Neurochem Inc. failed in trials the past year.

`This rather inventive approach to anti-amyloid beta therapy might hold promise for the treatment of Alzheimer's disease,'' Norman Relkin, director of the memory disorders program at Cornell University, said in a commentary accompanying the study. Larger, longer studies are needed to confirm the drug works, Relkin wrote. He wasn't involved in the trial.

The medicine, PBT2, works by preventing amyloid-beta from interacting with zinc and copper in the brain, helping reduce the build up of plaques linked to Alzheimer's.

Better Brain Function

Researchers in Sweden and Australia studied PBT2 in 78 patients over 12 weeks, and observed no serious side effects. Those who took the highest dose completed a test asking them to link letters to corresponding numbers an average 42 seconds faster than before they started treatment. Patients who took a placebo were more than six seconds slower. Treated patients also did better in a word association test after 12 weeks, while those on a placebo did worse.

The medicine reduced one type of amyloid-beta by 13 percent in patients on the highest dose of PBT2, suggesting that preventing the protein from forming plaques in the brain is more effective than cleaning them off later, said Geoffrey Kempler, Prana's chief executive officer.

``If you're knocking it out further downstream you're locking the stable door after the horse has bolted,'' Kempler said in a telephone interview today. ``Even if you've got rid of a lot of the amyloid, you haven't got rid of the damage.''

Prana, which has nine employees and has never made a profit, is racing larger competitors including Wyeth, Elan Corp. and Eli Lilly & Co. to develop the first drugs that delay Alzheimer's instead of treating its symptoms.

Final Stage

The company is planning the third and final stage of trials usually needed for a drug's regulatory approval, and expects to license the drug to a larger pharmaceutical partner to complete its development, Kempler said.

The number of people with Alzheimer's will almost double to 34 million in 2025, according to the World Health Organization. The disease affects 18 million people around the world, making it the most common form of dementia. Current drugs temporarily ease symptoms of the mind-robbing disease without slowing it.

To contact the reporter on this story: Simeon Bennett in Singapore at [e-mail]

Last Updated: July 29, 2008 14:30 EDT

http://www.bloomberg.com/apps/news?pid=20601081&sid=aFjMBCHA…

[Fruehrentner]

Ebenfalls von der Alzheimer Konferenz in Chicago:

TauRx Therapeutics Ltd & University of Aberdeen - New treatment halts progress of Alzheimer's disease

30 Jul 2008

A major breakthrough in the treatment of Alzheimer's disease is revealed today (July 29) by scientists at the Alzheimer's Association International Conference on Alzheimer's Disease (ICAD 2008) in Chicago, Illinois

Aberdeen, UK | July 30, 2008 |

A major breakthrough in the treatment of Alzheimer's disease is revealed today (July 29) by scientists at the Alzheimer's Association International Conference on Alzheimer's Disease (ICAD 2008) in Chicago, Illinois. Their pioneering research points to a new treatment that appears to slow the progress of the disorder by 81% over a year, and could offer hope to millions worldwide. The product - remberTM - is the first drug to act on the tangles discovered by Alois Alzheimer over a century ago.

The team at the University of Aberdeen (UK), working with TauRx Therapeutics - a Singapore-based company spun out of the University - developed a novel treatment based on an entirely new approach which targets the tangles, aggregates of abnormal fibres of tau protein forming inside nerve cells in the brain. These aggregates first destroy nerve cells critical for memory and then destroy neurons in other parts of the brain as the disease progresses.

Patients receiving the study treatment experienced an 81% reduction in cognitive decline over one year, and did not experience a significant decline in their mental function over 19 months. The TauRx brain imaging data also showed that the drug had its biggest effect in the memory critical parts of the brain where the tangle density is highest.

Professor Claude Wischik, Chairman of TauRx Therapeutics and Professor of Psychiatric Geratology and Old Age Psychiatry at the University of Aberdeen's Institute of Medical Sciences, who led the research, said: "This is an unprecedented result in the treatment of Alzheimer's disease. We have demonstrated for the first time that it may possible to arrest the progression of this disease by targeting the tangles which are highly correlated with the disease."

"This is the most significant development in the treatment of the tangles since Alois Alzheimer discovered them in 1907."

Alzheimer's disease is a degenerative and terminal brain disorder which affects millions of people around the world and a major and growing burden on health services in all countries with an ageing population. During the course of its progress there is a build up in the brain of lesions called plaques and tangles.

Following these results from the largest Phase 2 clinical trial of a disease modifying treatment conducted to date, TauRx is now planning a Phase 3 trial which should begin next year. If the Phase 3 trial confirms the Phase 2 findings, the drug could be available by 2012.

The results of the Phase 2 study of TauRx's new treatment strongly suggest that it is possible to halt progression in mild and moderate Alzheimer's. TauRx is continuing to refine its treatment and hopes that restoration may be possible at least at the earlier stages with improved versions of its drug. Tangles are already destroying nerve cells in parts of the brain critical for memory in people in their fifties and upwards. The ultimate goal is to develop a product that is convenient for patients that could be widely used at the very earliest stages of the disease, long before patients experience the first symptoms of Alzheimer's.

"With the world population ageing globally and the enormous burden on health services and economies worldwide, we urgently need to confirm our findings in a larger trial with a view to making this treatment available as soon as possible," commented Professor Wischik. "World Health Organisation (WHO) figures indicate that there will be more than one billion people aged 65 and over by 2050, of whom we calculate about half will have tau tangles in their brains. This makes it particularly important to develop new treatments to halt and prevent tangles forming in the brain." Professor Wischik and his team have spent 24 years investigating the structure and role of the tangles in the development of the disease. This builds on their discovery 20 years ago that the tangles are made up of a protein called tau and later that its aggregation or clumping is highly correlated with the progression of Alzheimer's. They found that plaque development, which has been the main focus of research so far, is more a feature of normal ageing and is poorly correlated with dementia.

The team then looked for a drug with the ability to dissolve the tau protein fibres of the tangle and developed remberTM - a novel form of a chemical with a long history of use in the treatment of other conditions. They found that the drug works in a range of laboratory test systems which they pioneered. TauRx has patented the medical use of remberTM for the treatment and prevention of Alzheimer's.

TauRx tested the drug in the Phase 2 clinical trial involving 321 patients with mild and moderate Alzheimer's disease in the UK and Singapore. The decline seen in patients treated with remberTM was not significantly different from their starting score to the assessment at one year and at their final assessment at 19 months. In addition to cognitive testing, patients had repeat brain scans at the start of the study and after 25 weeks. These showed that the treatment effect was greatest in the memory-critical brain regions where the density of Alzheimer tangles is greatest. In the control group, there was a significant decline from the starting score in cognitive testing and on brain scans. There were statistically significant differences between the patients receiving the study drug remberTM and the controls at 24 and 50 weeks.

Revealing the University of Aberdeen and TauRx's findings to the the 2008 Alzheimer's Association International Conference on Alzheimer's Disease (ICAD 2008) in Chicago, United States, Professor Wischik added, "I am delighted with these results. This is the first trial of an Alzheimer's disease modifying drug which actually hit its primary pre-specified efficacy target."

Professor Stephen Logan, Senior Vice Principal of the University and TauRx board member, added: "This is a fantastic breakthrough and is an example of an important collaboration between our spinout company TauRx and the University of Aberdeen. There is no doubt that this close relationship has been crucial in providing an ideal platform for a major medical advance. The University of Aberdeen is extremely well placed to lead this research due to our first class imaging facilities, in partnership with NHS Grampian, and our expertise in medicinal chemistry and medical sciences. This is further evidence for Aberdeen's growing reputation as a centre of excellence in life sciences."

TauRx Therapeutics LogoTauRx Therapeutics was established in Singapore in 2002 with the aim of developing new treatments and diagnostics for a range of neurodegenerative diseases based on its technology platform which it is also reporting for the first time at ICAD 2008. As well as Aberdeen, it has operations in Warsaw, Berlin, France and China. Professor Wischik commented: "This result now validates our pipeline capability for development of second and third generation disease modifying treatments in this space." In addition to the imminent Phase 3 trial in Alzheimer's, TauRx is planning a trial in Parkinson's as remberTM also has activity on the synuclein fibres which accumulate in the brains of these patients. TauRx is also developing substances which it hopes to test in brain scans to measure the build up of tangles so they can be diagnosed early and treatment can be started before they cause permanent damage.

SOURCE: TauRx Therapeutics

http://www.pipelinereview.com/content/view/21260/113/

[Fruehrentner]

Weitere Meldungen von der Alzheimer Konferenz in Chicago:

Allon Therapeutics presents AL-108 human efficacy data at world’s leading Alzheimer’s disease conference

29 Jul 2008

A potential new treatment for Alzheimer’s disease that reduces the classic Alzheimer’s “tangle” pathology in mice has also improved specific memory function in humans with amnestic mild cognitive impairment (aMCI)

CHICAGO, IL, USA | July 28, 2008

A potential new treatment for Alzheimer’s disease that reduces the classic Alzheimer’s “tangle” pathology in mice has also improved specific memory function in humans with amnestic mild cognitive impairment (aMCI), a precursor to Alzheimer’s disease, according to a presentation today at a news conference hosted by the Alzheimer’s Association at their International Conference on Alzheimer’s Disease and Related Disorders (ICAD 2008).

Dr. Donald E. Schmechel, a Duke University geriatrics professor and the principal investigator of the clinical trial that evaluated drug candidate AL-108 in 144 aMCI patients, said the trial’s results increase the importance of “tangles” in the search for treatments that modify the course of Alzheimer’s disease.

“The cause and effect of classic Alzheimer’s hallmarks, beta amyloid ‘plaques’ and neurofibrillary ‘tangles’, is the subject of much investigation, but the preponderance of drug development has so far focused on ‘plaques’, ” said Dr. Schmechel. “This new data suggests that ‘tangles’ may be as important — or perhaps more important — than ‘plaques’.”

“This positive aMCI clinical trial makes AL-108 the first drug to validate in humans the potential of the ‘tangle’ pathway in memory disorders present in Alzheimer’s disease,” Dr. Schmechel said.

In addition to today’s briefing to the news conference, perspectives of AL-108 are being presented to four scientific sessions at ICAD 2008. Dr. Schmechel is presenting additional details of the aMCI clinical trial data at a poster session today featuring new therapies and at Wednesday’s Hot Topics session. Additional data examining AL-108’s mechanism of action that halts and reverses “tangles” pathology and increases cognition in animals will also be presented at two sessions on Wednesday.

AL-108 is being developed by Allon Therapeutics (TSX: NPC), a Canadian biotechnology company located in Vancouver. The drug was discovered by Professor Illana Gozes of the Sackler Faculty of Medicine at Tel Aviv University.

Prof. Gozes also heads up research activities at Allon Therapeutics. Collaborative research led by Prof. Gozes has been supported by Tel Aviv University and the U.S. National Institutes of Health.

Clinical trial in aMCI patients

The Phase IIa trial was a double-blind, randomized, placebo-controlled, multiple-dose study to evaluate the safety, tolerability and effect on cognitive function of AL-108 after 12 weeks of intranasal administration in patients with aMCI. Clinically, patients with aMCI demonstrate memory impairment with otherwise normal cognition. Several aspects of cognitive function were evaluated. The trial was conducted at 17 sites in the United States in 144 patients aged 55 to 85 years and evenly divided between genders.

The trial demonstrated statistically significant, dose-dependent and durable improvements on key endpoints that measure short-term recall and working memory — two types of memory that are clinically relevant in Alzheimer’s disease. Successfully impacting these specific memory domains indicates AL-108 is active in the regions of the brain responsible for their function — primarily the medial temporal lobe, hippocampus and prefrontal cortex. AL-108 did not affect measures of cognitive functions that are not clinically impaired in patients with aMCI.

In this trial AL-108 was safe and well tolerated by patients. The most commonly reported side effects in subjects treated with AL-108 were headache and nasal congestion or irritation.

Trial results

Cognitive function was measured in the aMCI patients by tests that are widely-used and validated in clinical trials evaluating patients with mild cognitive impairment and Alzheimer’s disease.

Prior to receiving drug or placebo, the cognitive function of each patient was measured with these tests. These results became the baseline for each patient’s performance during the trial.

Patients were treated for 12 weeks and tested at weeks four, eight, 12 and 16. Each patient’s test results were compared with his or her baseline performance and to other treatment groups.

A significant, dose-dependent and durable improvement was seen in two tests that measure short-term recall and working memory — delayed-match-to-sample and digit span. The high dose (15 mg twice daily) group showed a 62.4% improvement from baseline (p=0.038, versus placebo) in the delayed-match- to-sample 12-second delay test by the end of the trial.
Similarly, the high dose group showed a 17.2% increase from baseline (p=0.028, versus placebo) in the digit span forward test.

The primary end-point for the trial was a composite of several cognitive tests (composite cognitive memory score, or CCMS) that measured memory and executive function. Patients treated with AL-108 showed statistically significant improvement on tests that measured short-term recall and working memory, but no improvement on tests that involved executive functions, such as planning, cognitive flexibility and abstract thinking.

This divergence in results explains why the composite primary endpoint was trending toward, but did not achieve, statistical significance.

This data suggests that patients with aMCI have significant memory impairment but no significant impairment of executive function. Thus, AL-108 appears to have an impact on regions of the brain that are impaired in aMCI such as those that are known to control memory (medial temporal lobe, hippocampus and prefrontal cortex). However, no measurable effect of AL-108 on executive function was seen in this population since they were not impaired on tests that involve executive function such as Paired Associates Learning, Spatial Working Memory and One-Touch Stockings of Cambridge.

AL-108 was safe and well tolerated in this study. Overall, the incidence of adverse events between the placebo group and the AL-108 group was similar with most adverse events being mild to moderate. Headache (13%), nasopharyngitis (8%), and nasal discomfort (4%) were the most common adverse events reported in subjects receiving AL-108 and were more frequent in subjects receiving AL-108 than those receiving placebo. The rates of discontinuations for adverse events were low and similar between the placebo and AL-109 groups.

About aMCI and Alzheimer’s Hallmarks

There is increasing evidence that some forms of cognitive impairment are precursors to Alzheimer’s disease. Amnestic mild cognitive impairment (aMCI) is a subset of MCI in which only the memory components of an individual’s function are affected.

Scientists agree that the brains of Alzheimer’s patients are characterized by two classic hallmarks of the disease: amyloid beta plaque accumulation outside neurons and neurofibrillary tangles inside neurons. No drug on the market today has any impact on these plaques and tangles.

Scientific studies have shown that the pathology of aMCI and Alzheimer’s is similar. For example, amyloid beta plaques and neurofibrillary tangles occur in both. Allon’s extensive animal data show that AL-108 dramatically reduces neurofibrillary tangles, reduces plaques, and that treated animals have significantly improved cognition. AL-108 is the first drug in development to have shown reduction of both neurofibrillary tangles and amyloid beta plaques in animal studies.

Neurofibrillary tangles are the result of degeneration of microtubules, key components of the communication and transport pathways inside brain cells. Tangles occur when tau protein, which normally acts to hold microtubules together, converts from a soluble to an insoluble form, a process known as hyperphosphorylation.

AL-108 is derived from an eight amino acid peptide (NAPVSIPQ: “NAP”) synthesized from a naturally occurring neuroprotective brain protein known as activity dependent neuroprotective protein (ADNP).

About ICAD 2008

The International Conference on Alzheimer’s Disease and Related Disorders (ICAD 2008) is being held in Chicago July 26-30. ICAD 2008 is organized by the Alzheimer’s Association, the leading U.S. voluntary health organization in Alzheimer’s care, support and research. The conference is bringing together more than 5,000 researchers, physicians and care providers from 60 countries – the largest group of international leaders in Alzheimer research and care ever convened.

About Allon’s neuroprotective platforms

Allon’s two neuroprotective technology platforms are based on two naturally occurring proteins secreted by the brain in response to a range of insults. The platforms are activity-dependent neuroprotective protein (ADNP) and activity-dependent neurotrophic factor (ADNF). Because the two platforms are based on different proteins, the drugs from each are different molecules with different therapeutic mechanisms and distinct commercial opportunities. Clinical-stage drugs AL-108 and AL-208 are derived from ADNP, while preclinical stage drug AL-309 is derived from ADNF.

About Allon

Allon Therapeutics Inc. is a clinical-stage biotechnology company developing treatments for major neurodegenerative conditions. In Q1 2008, Allon’s drug AL-108 demonstrated human efficacy in amnestic mild cognitive impairment, a precursor to Alzheimer’s disease. Allon has Phase II human efficacy programs pursuing three large underserved markets: Alzheimer's disease, stroke and schizophrenia-related cognitive impairment. The Company is listed on the Toronto Stock Exchange under the trading symbol "NPC" (Neuro Protection CompanyTM) and based in Vancouver. For additional information please visit the Company's website: www.allontherapeutics.com.

SOURCE: Allon Therapeutics Inc.

http://www.pipelinereview.com/content/view/21231/109/

[Fruehrentner]

PRANAS Alzheimer Kandidat wird sogar in einem Artikel zur Alzheimer Konferenz in Chicago in der Ärztezeitung genannt!!


Ärzte Zeitung, 31.07.2008

Neue Ansätze gegen Alzheimer mit Antibiotika und Farbstoffen

Ermutigende Phase-II-Studien mit Therapien gegen β-Amyloid und Tau-Fibrillen

CHICAGO (mut). Zwei neue Studien wecken die Hoffnung auf Alzheimer-Medikamente, die direkt in den Krankheitsprozess eingreifen. In der einen Studie wurden Exekutivfunktionen wie Sprachflüssigkeit von Patienten verbessert, in der anderen ließ sich der Zustand der Patienten 19 Monate lang stabilisieren.

Beide Studien wurden jetzt auf einem Alzheimer-Kongress in Chicago in den USA vorgestellt. Das Team von Professor Lars Lannfelt aus Uppsala in Schweden zielte mit einer neuen Strategie auf das β-Amyloid-Protein, dessen Verklumpung als eine der Ursachen für Alzheimer gilt. Die Forscher verwendeten in einer Phase-II-Studie bei 78 Patienten mit leichter Alzheimer-Erkrankung einen Abkömmling des topischen Antibiotikums Clioquinol. Die Substanz mit der Bezeichnung PBT2 verhindert Interaktionen zwischen β-Amyloid und Metallionen wie Kupfer und Zink. (PRANA's PBT2!!!)

Während der zwölf Wochen dauernden Studie wurde bei den Patienten eine deutliche Reduktion von löslichem Amyloid im Liquor beobachtet. Zwar war mit PBT2 das Gedächtnis insgesamt nicht besser als mit Placebo, jedoch konnten die Patienten bei Wortflüssigkeits-Tests mehr Wörter wieder geben als zu Beginn, mit Placebo waren es weniger. Bei solchen Tests werden die Patienten etwa gebeten, in einer bestimmten Zeit möglichst viele Tiernamen zu nennen.

Auch konnten die Patienten in anderen Tests manche Aufgaben wieder schneller erledigen, mit Placebo brauchten sie dagegen mehr Zeit. Die Ergebnisse wurden zeitgleich mit dem Kongress in "Lancet Neurology" online veröffentlicht. Sie müssen jetzt allerdings in größeren Studien bestätigt werden, zumal andere Studien die Amyloid-Hypothese infrage stellen.

In einer vergangene Woche publizierten Post-mortem-Analyse bei Patienten mit einer Amyloid-Impfung ließ sich die Krankheitsprogression selbst durch eine fast komplette Amyloid-Entfernung nicht aufhalten (The Lancet 372, 2008, 216).

Einen anderen Ansatz verfolgen schottische Forscher aus Aberdeen. Sie behaupten, mit dem Farbstoff Methylenblau in einer Studie bei über 300 Alzheimer-Patienten den Verlauf um 19 Monate verzögert zu haben. Die Substanz wurde früher gegen Harnwegsinfektionen verwendet, und soll sich gegen die bei Alzheimer typischen Tau-Fibrillen im Gehirn richten. Nach 24 Wochen war der ADAS-cog-Wert (maximal 70 Punkte) mit Methylenblau um 5,5 Punkte besser als mit Placebo, nach 50 Wochen sogar um 6,8 Punkte.

http://www.aerztezeitung.de/medizin/?sid=506431

[Erbse1]

Ergänzend noch ein Beitrag zu dem Themengebiet Alzheimer aus der Äztezeitung.
Quelle: http://www.aerztezeitung.de/medizin/krankheiten/demenz/?sid=…

Dämpfer für Amyloid-Hypothese

Eine Impfstudie bei Alzheimer-Patienten bringt die Amyloid-Hypothese ins Wanken: Obwohl bei einigen Patienten durch die Therapie das Amyloid fast komplett aus dem Gehirn entfernt wurde, schritt die Krankheit ungebremst voran.

Inzwischen weiß man, woraus die Amyloid-Plaques in den Gehirnen von Alzheimer-Kranken bestehen. Man weiß sogar genau, wie sich die β-Amyloid-Proteine bilden, wie sie molekular aufgebaut sind, welche Gene ihre Produktion steuern. Doch man weiß immer noch nicht richtig, weshalb sie gerade bei Alzheimer- Kranken so zahlreich entstehen und im Gehirn verklumpen.

Und diese Wissenslücke könnte der Grund dafür sein, weshalb einige Unternehmen mit der Entwicklung von Medikamenten gegen β-Amyloid vielleicht gerade Milliarden Euro in den Sand setzen. Denn neue klinische Studien lassen Zweifel an der Hypothese aufkommen, dass die Amyloidklumpen tatsächlich die Ursache für den geistigen Abbau bei Alzheimer sind. So ließen sich die Plaques durch eine Impfung bei zwei Patienten komplett entfernen.

Genützt hat es ihnen jedoch nichts: Die Krankheit schritt unaufhaltsam voran, bis die Patienten daran starben. Die Wahrheit über Amyloid ist offenbar komplizierter als angenommen.

Das Grundproblem mit den Plaques ist noch ungelöst: Bislang ist nicht ganz sicher, ob sie den Tod von unzähligen Hirnzellen bei Alzheimer auslösen oder sich nur als Folge der zellulären Katastrophe bilden, vielleicht sogar als ein verzweifelter Versuch, die Zellen zu retten. Für Amyloid als Auslöser einer Demenz spricht zwar einiges, etwa, dass bei erblich bedingten Alzheimer-Formen oft Gene für die Amyloid-Synthese oder -Verarbeitung verändert sind, oder dass man in transgenen Tiermodellen durch übermäßige Amyloid-Produktion ebenfalls eine Demenz auslösen kann. Ob diese Prozesse jedoch dem Verlauf bei der Alzheimer-Krankheit entsprechen, ist weiterhin fraglich.

Einen Dämpfer erhielten die Vertreter der Amyloid-Hypothese jetzt durch eine Publikation britischer Forscher (The Lancet 372, 2008, 216). Sie hatten in einer Post-mortem- Analyse die Gehirne von acht Patienten untersucht, die mit dem Impfstoff AN1792 gegen β-Amyloid immunisiert worden waren und etwa fünf Jahre später an Alzheimer starben.

Zur Erinnerung: Eine große Studie mit dem Impfstoff war 2002 gestoppt worden, nachdem einige der Patienten eine aseptische Meningoenzephalitis entwickelt hatten. Insgesamt hatte die Immunisierung nach einem Jahr keinen signifikanten Einfluss auf die Kognition, wenngleich sich bei einigen Patienten mit sehr hohen Antikörpertitern die geistigen Fähigkeiten etwas stabilisiert hatten.

Die Forscher um Professor Clive Holmes aus Southampton haben in ihrer Analyse jetzt festgestellt, dass der mangelnde Erfolg nicht auf ein Scheitern der Immunisierung zurückzuführen ist - diese hat offenbar sehr gut funktioniert und ihr Ziel erreicht: Der β-Amyloidgehalt in den Gehirnen der Geimpften war deutlich niedriger als bei ungeimpften Alzheimerkranken (2,1 versus 5,1 Prozent), und er war am niedrigsten bei den beiden Patienten mit den höchsten Antikörpertitern gegen β-Amyloid: Bei ihnen lag der Amyloidgehalt nur noch bei 0,35 und 0,12 Prozent. Die angeblich toxischen Proteine waren also praktisch fast völlig aus dem Gehirn verschwunden.

Auf den klinischen Verlauf hatte das zumindest bei diesen beiden Patienten keinen Einfluss: Sie hatten genau so schnell eine schwere Demenz entwickelt wie ungeimpfte Alzheimerkranke und waren auch genau so schnell an Alzheimer gestorben. Bei Patienten mit hohen Antikörpertitern schien der Verfall sogar noch etwas schneller zu gehen.

Allein durch einen Abbau des Amyloids lässt sich Krankheitsprozess offenbar nicht aufhalten, folgern Holmes und seine Mitarbeiter aus den Daten. Möglicherweise kommt die Immunisierung zu spät - einmal durch Amyloid in Gang gesetzt, läuft der Prozess vielleicht auch ohne das Protein weiter - dann müsste man früher impfen, spekuliert Holmes. Vielleicht ist aber auch nicht das verklumpte β-Amyloid das Problem, sondern das lösliche.

Die Verklumpung wäre dann vielleicht sogar eine Schutzreaktion und die Impfung gegen Amyloidklumpen mitunter schädlich. Allerdings müssten für stichhaltige Aussage noch weitere Gehirne analysiert werden. Daran dürfte es künftig nicht mangeln: Studien mit neuen Amyloid-Impfstoffen sind geplant oder laufen bereits.

Schlechte Nachrichten gibt es auch zu einem anderen Ansatz gegen β-Amyloid: Mit Sekretase-Hemmern versucht man die Bildung des Proteins zu verhindern. Mit diesem Ansatz würde auch die Menge an löslichem β-Amyloid reduziert. Der γ-Sekretase-Hemmer Tarenflurbil konnte in einer Phase-II-Studie zumindest bei Patienten mit frühem Alzheimer die Progression etwas verzögern. Eine Phase-III-Studie dazu wurde jetzt jedoch abgebrochen worden - aufgrund mangelnder Wirksamkeit.

Tot ist die Amyloid-Hypothese damit aber noch lange nicht. Ein Therapie-Ansatz, der sich ebenfalls auch gegen lösliches β-Amyloid richtet, lässt aufhorchen. Wie bereits berichtet, wurde in der Zeitschrift Lancet Neurology online eine Phase-II-Studie mit einem Derivat des topischen Antibiotikums Clioquinol publiziert. Die Substanz mit der Bezeichnung PBT2 verhindert Interaktionen zwischen β-Amyloid und Metallionen wie Kupfer und Zink - sie sind offenbar für die Verklumpung von Amyloid nötig.

In Tierversuchen ließ sich damit auch die Konzentration von löslichem β-Amyloid drastisch senken. In der klinischen Studie mit der Substanz bei 78 Patienten wurde eine deutliche Reduktion von löslichem β-Amyloid im Liquor beobachtet.

Zwar waren nach zwölf Wochen Therapie die kognitiven Fähigkeiten insgesamt nicht besser als mit Placebo, jedoch war die Exekutivfunktion bei Patienten mit PBT2 deutlich besser als mit Placebo: Die Patienten konnten bei Aufzählungen mehr Wörter flüssig wiedergeben als zu Beginn, mit Placebo waren es weniger. Auch konnten sie nach 12 Wochen manche Aufgaben wieder schneller erledigen, mit Placebo brauchten die Patienten dagegen mehr Zeit als zu Beginn. Doch auch hier müssen erst größere und längere Studien die Wirksamkeit bestätigen

[Fruehrentner]

Antwort auf Beitrag Nr.: 34.651.384 von Erbse1 am 05.08.08 15:00:16

@Erbse,

danke für den Artikel in deutsch. Spätestens nach der ALzheimer Konferenz in Chicago muss man wirklich über die Amyloid-Hypothese ernsthaft nachdenken. Dies wird nun Gegenstand zahlreicher wissenschaftl. Fachdiskussionnen von Alzh.-Experten in der Welt sein und es wird spannend, das zu verfolgen und welche Ergebnisse da noch kommen werden.

Das lässt mich nun auch bei PRANA und allen anderen Kandidaten zweifeln, die es allein auf den Plaque und dessen Auflösung bzw. Verhinderung abgesehen haben.

Steht hier ein Paradigmenwechsel bevor? Vielleicht ist es aber auch eine Kombination aus Plaque und anderen Mechanismen, oder es gibt verschiedene Alzheimner-Formen: eine, die durch Plaques entsteht und andere eben nicht.

[Fruehrentner]

Meldung aus der Alzheimer-Forschng bzw. Wettbewerb: hier PROTEO TECH


07.08.2008 21:02:00

ProteoTechs Exebryl-1(R) zur Behandlung der Alzheimer-Krankheit tritt in die Phase der klinischen Studien am Menschen ein

KIRKLAND, Washington, August 7 /PRNewswire/ --

ProteoTech Inc. (ProteoTech) gab heute bekannt, dass es alle aufsichtsbehördlichen Anforderungen im Rahmen des IND (Investigational New Drug)-Antrags erfüllt und von der FDA die Genehmigung erhalten hat, seine klinisches Studie der Phase 1 am Menschen zu Exebryl-1(R) zu beginnen. Bei Exebryl-1(R) handelt es sich um ein neuartiges, kleinmolekulares Arzneimittel, das bei der Behandlung der Alzheimer-Krankheit auf die toxische Akkumulation von Beta-Amyloid-Protein abzielt. ProteoTech begann mit seiner Phase-1-Studie am Menschen am 29. Juli 2008.

Auf der 2008 International Conference on Alzheimer's disease, die letzte Woche in Chicago stattfand, stellte ProteoTech bemerkenswerte Ergebnisse zur Wirksamkeit von Exebryl-1(R) bei transgenen Mäusen mit Alzheimer-Krankheit vor, bei denen die Belastung des Gehirns mit dem Beta-Amyloid-Protein um mehr als 30-50% gesenkt wurde, was mit einer deutlichen Verbesserung der Gedächtnisleistungen dieser Tiere korrelierte. Man nimmt an, dass die Ansammlung von toxischem und unlöslichem Beta-Amyloid-Protein eine wichtige Rolle bei der bei allen Alzheimer-Patienten beobachteten Krankheitsprogression und Gedächtnisbeeinträchtigung spielt. Auch wurden Ergebnisse vorgestellt, die die orale Bioverfügbarkeit von Exebryl-1(R) und dessen Fähigkeit zur Überwindung der Blut-Hirn-Schranke aufzeigen.

Bei Exebryl-1(R) handelt es sich um ein neuartiges, kleinmolekulares Arzneimittel, das bei ProteoTech aus dessen einzigartiger Bibliothek kleiner Moleküle, die für den Einsatz bei bestimmten Amyloidosen konzipiert sind, entwickelt wurde. Mehr als sechs Jahre präklinischer In-vitro- und In-vivo-Forschung führten zur Entwicklung von Exebryl-1(R), von dem man annimmt, dass es die Bildung, Ablagerung und Ansammlung des Beta-Amyloid-Proteins in allen Stadien der Krankheitsprogression verhindert. Weiterhin trägt Exebryl-1(R) auch zu einer Verringerung und Beseitigung von bereits im Gehirn entstandenen Beta-Amyloid-Ablagerungen bei. Dies zeigt sich an der signifikanten, ausgeprägten Verringerung der Amyloidplaques im Gehirn von älteren transgenen Mäusen mit Alzheimer-Krankheit.

Erste Untersuchungen legen nah, dass Exebryl-1(R) möglicherweise auch eine wichtige zweifache Wirkung im Sinne einer Blockierung und Reduzierung der Bildung von gepaarten helikalen Filamenten durch Tau-Protein - ein Prozess der bei der neurofibrillären Knäuelbildung wichtig ist - ausübt. Das Vorliegen von neurofibrillären Knäuel, die Tau-Protein enthalten, im Gehirn ist ein wichtiges pathologisches Kennzeichen der Alzheimer-Krankheit. Zurzeit laufen weitere Studien, um diese hochinteressanten Ergebnisse zu bestätigen. So ist es möglich, dass Exebryl-1(R) das erste oral bioverfügbare, kleinmolekulare Arzneimittel sein könnte, dass auf die Ansammlung von Amyloidplaque und neurofibrillären Knäuel, den beiden wichtigen und für die Alzheimer-Krankheit charakteristischen pathologischen Veränderungen, einwirkt.

Informationen zu ProteoTech: ProteoTech ist ein Arzneimittelentwicklungsunternehmen in privater Hand, das 1996 gegründet wurde und weltweit führend in der Therapie und Diagnostik von Amyloidosen ist. Zum geistigen Eigentum von ProteoTech gehören über 165 Patente, und das Unternehmen führt derzeit klinische Studien am Menschen zur Prüfung seines oral wirksamen, kleinmolekularen Arzneimittels Exebryl-1(R) bei der Behandlung von leichter bis mässiger Alzheimer-Krankheit durch. ProteoTech hat mit Synuclere(TM) zur Behandlung der Parkinson-Krankheit und Systebryl(TM) zur Behandlung der systemischen Amyloidose die späte Phase der präklinischen Entwicklung erreicht. Das Unternehmen befindet sich ebenfalls in der späten Phase der präklinischen Entwicklung mit einem neuartigen kleinen Peptid, das unter dem Namen PeptiClere(TM) geführt und als Nasenspray zur Behandlung der Alzheimer-Krankheit geprüft wird. Schliesslich entwickelt ProteoTech noch eine neuartige kleinmolekulare Verbindung zur Behandlung der mit Typ-2-Diabetes assoziierten Amyloidose. Weitergehende Informationen finden Sie unter http://www.proteotech.com, oder wenden Sie sich an Steve Runnels, CEO, unter [e-mail].

Website: http://www.proteotech.com

Quelle: PR NEWSWIRE

[Fruehrentner]

Paradigmenwechsel in der Alzheimer-Bekämpfung?

Attention shifts from beta-amyloid to tau in the hunt for an Alzheimer's disease therapy
01 Sep 2008

In years to come, scientists and pharmaceutical companies may look at the 2008 International Conference on Alzheimer's disease (ICAD) as a water-shed in the development of truly effective disease modifying treatments. As beta-amyloid focused treatments continue to produce disappointing results, approaches focused on tau tangles have now emerged as the most promising candidates.

In 1906 Dr Alzheimer described "miliary foci" (beta-amyloid plaques) and "dense bundles of fibrils" (tau neurofibrillary tangles) when first classifying Alzheimer's disease in a postmortem examination. Over the last 20 years researchers have focused predominantly on beta-amyloid as the primary Alzheimer's disease drug and research target. However, there was a small group of Alzheimer's disease researchers who believed that tau tangle formation was a more prominent feature in Alzheimer's disease pathology, supported by a closer correlation between dementia pre-mortem and tau tangle density post-mortem than that seen with beta-amyloid plaques.

Results presented at the ICAD conference this week suggest that the tau protein may well be the more viable target for clinical benefit in Alzheimer's disease. Trials of two beta-amyloid focused treatments found disappointing results, whereas developers of two tau focused treatments presented surprising and very promising positive results.

TauRx Therapeutics' tau focused treatment Rember (methylthioninium chloride) has captured the mass media's attention following announcement at the conference of the most promising Alzheimer's disease clinical trial results so far. TauRx tested the drug in a Phase II clinical trial involving 321 patients with mild and moderate Alzheimer's disease. The decline seen in patients treated with Rember was not significantly different from their starting score to the assessment at one year or 19 months, indicating a complete halting of disease progression.

Earlier in the week a 144 patient Phase IIa clinical trial of Allon Therapeutics' AL-108, an experimental therapy designed to combat tau neurofibrillary tangles in amnestic mild cognitive impairment patients (a condition believed to represent early Alzheimer's disease), showed a 62% improvement from baseline on short-term memory recall (statistically significant improvement over placebo).

Meanwhile, further analysis of Phase II results from Wyeth/Elan's anti-amyloid focused therapy bapineuzumab (AAB-001), previously thought to be the most promising pipeline candidate, have led to concern over the drug's safety. As a result of this, and the additional competition from emerging Phase II candidates, the share price of both companies has declined significantly in recent days. In addition, full results from a Phase III trial of Myriad's Flurizan (tarenflurbil), another anti-amyloid therapy, have confirmed that the drug failed to achieve significant effect on its primary endpoints.

A lot is at stake for pharmaceutical companies interested in the Alzheimer's disease market. With a high prevalence, aging population, and high unmet need, a disease modifying Alzheimer's treatment could gain in excess of $10 billion annual revenues. The tau focused treatments now look best placed to gain access to this considerable market opportunity.

http://www.pipelinereview.com/content/view/21744/309/

[Fruehrentner]

Rodman and Renshaw Upgrades Prana Biotechnology (PRAN) to Market Outperform

September 9, 2008 7:34 AM EDT

Rodman and Renshaw upgrades Prana Biotechnology (Nasdaq: PRAN) from Market Perform to Market Outperform. Price target $8.

Rodman analyst says, "Following recent partnering activity in the Alzheimer's disease space, we believe Prana's lead molecule PBT2 represents a significant asset and could attract a lucrative partnership in the near-term."

Prana Biotechnology Limited (Prana), is a development stage enterprise, which is at an early stage in the development of its pharmaceutical products that are designed to treat the underlying causes of degeneration of the brain and the eye as aging progresses.

http://www.streetinsider.com/Upgrades/Rodman+and+Renshaw+Upg…

[Erbse1]

Leipziger Forscher beweisen Wirksamkeit von Enzym-Hemmer gegen Alzheimersche Krankheit

Von Sandra Hasse

Informationsdienst Wissenschaft

Wissenschaftlern des Paul-Flechsig-Instituts für Hirnforschung an der Universität Leipzig ist gemeinsam mit Forschern von Partnereinrichtungen ein entscheidender Schritt für die Entwicklung eines Medikamentes gegen die Alzheimersche Krankheit gelungen. "Wir konnten anhand von Versuchen mit Mäusen erstmals nachweisen, dass die Hemmung eines bestimmten Enzyms die Bildung Alzheimer-typischer Ablagerungen, sog. Plaques, im Gehirn reduziert und dadurch die Auswirkungen der Krankheit deutlich gemildert werden", erläutert PD Dr. Steffen Roßner, Mitarbeiter des Instituts. Die Erkenntnisse wurden jetzt in der renommierten Fachzeitschrift Nature Medicine veröffentlicht.

Die für die Erkrankung typischen Amyloid-Plaques im Hirngewebe von Patienten wurden bereits Anfang des letzten Jahrhunderts vom Entdecker der Krankheit, Alois Alzheimer, beschrieben. "Aber erst seit reichlich zehn Jahren ist bekannt, dass sich eine bestimmte Form von kurzkettigen Eiweißen im Hirn von Alzheimer-Patienten bevorzugt ablagert", so der Hirnforscher. Bei diesenAmyloid-Eiweißen ist die randständige Aminosäure Glutamat zu einem ringförmigen pyro-Glutamat umgewandelt. "Damit sind die Eiweiße praktisch versiegelt und schwerer abbaubar", erklärt Roßner weiter. Dies führe dazu, dass sie sich im Gehirn Betroffener anreichern, verklumpen und so genannte Fibrillen oder Oligomere bilden. Diese wiederum schädigen Nervenzellen und können im fortgeschrittenen Stadium der Erkrankung zum Verlust ganzer Neuronengruppen führen.

"Darüber hinaus haben die pyro-Glutamat-modifizierten Amyloid-Eiweiße die unangenehme Eigenschaft, die eigentlich leicht abbaubaren, unveränderten Amyloid-Eiweiße gleich mit zu verklumpen und diese damit dem in der gesunden Nervenzelle fortwährend stattfindenden Abbau zu entziehen." Vergleichbar sei dies mit einem stark verdichteten Schneeball, der einen verschneiten Hang hinabrollt und dabei größer und größer wird. Während der auf dem Hang liegende Schnee bei Sonneneinstrahlung schnell abtaut, widersetzt sich die große Schneekugel sehr lange der Schmelze. Die pyro-Glutamat-modifizierten Amyloid-Eiweiße im Gehirn von Alzheimer-Patienten sind in diesem Sinne durchaus mit dem verdichteten Schneeball vergleichbar.

Bisher war allerdings unbekannt, wie es zu dieser Veränderung der Amyloid-Eiweiße kommt. In der jetzt publizierten Studie konnte nachgewiesen werden, dass das Enzym Glutaminyl-Zyklase (QC) für die krankheitsfördernde Umwandlung der Amyloid-Eiweiße verantwortlich ist.

Nach dieser Entdeckung lag nun die experimentelle Strategie auf der Hand die QC zu hemmen, um so die Plaque-Bildung im Gehirn zu reduzieren und im Idealfall zu verhindern. "Dies konnten wir im Tierversuch eindeutig nachweisen", so Roßner. Transgene Mäuse, die eine menschliche Erbanlage tragen, welche eine vererbbare Form der Alzheimerschen Krankheit auslöst, bekamen mit dem Futter QC-Hemmer verabreicht. Dabei wurden drei Versuchgruppen gebildet: Eine bekam normales Futter, die zweite Gruppe eine geringe und die dritte Versuchsgruppe schließlich eine höhere Dosis des QC-Hemmers. Bei den Mäusen, die keine Hemmer bekommen hatten, ließen sich die Eiweiß-Verklumpungen in großer Zahl feststellen. Die Tiere, die den QC-Hemmer mit dem Futter aufgenommen hatten, zeigten wesentlich weniger Eiweißablagerungen, wobei bei den Mäusen, die mit der höheren Dosis behandelt worden waren, auch tatsächlich eine stärkere Wirkung zu verzeichnen war.

"Und außerdem konnten wir einen weiteren interessanten Effekt beobachten", sagt Roßner. Die Forscher stellten nämlich fest, dass bei den behandelten Mäusen mit dem Umfang der Ablagerungen auch die Zahl der aktivierten Immunzellen im Hirn abnahm. "Dies ist eine höchst erwünschte Begleiterscheinung, denn es ist bekannt, dass die Aktivierung von Immunzellen im Hirn Entzündungsreaktionen auslöst, die wiederum zum weiteren Absterben von Nervenzellen beitragen können", umreißt der Wissenschaftler die Bedeutung dieser Beobachtung.

Die Forscher des Paul-Flechsig-Instituts arbeiten bei ihren Untersuchungen eng mit verschiedenen weiteren Institutionen zusammen. So hatten Wissenschaftler der Probiodrug AG aus Halle (Saale) den Mechanismus der pyro-Glutamat Amyloid-Bildung als erste entschlüsselt und das Enzym QC als ausschlaggebend für die Bildung von Eiweiß-Ablagerungen im Gehirn von Alzheimer-Patienten identifiziert. Probiodrug hält 27 Patente für therapeutische Anwendungen und hat das Forschungsfeld auf diesem Gebiet in den letzten 5 Jahren revolutioniert. Unter Federführung von Probiodrug wurde schließlich ein Konsortium von akademischen Partnern rekrutiert, das alle erforderlichen Expertisen zur systematischen Untersuchung der zu Grunde liegenden Mechanismen bündelte. Außer der Leipziger Arbeitsgruppe testeten auch Forscher aus dem österreichischen Graz im Mäuseversuch die Wirkungen des QC-Hemmers und konnten feststellen, dass die mit den Hemmern behandelten transgenen Tiere deutlich bessere Lern- und Gedächtnisleistungen zeigten als ihre unbehandelten Artgenossen. Andere Wissenschaftler aus Halle (Saale) untersuchten menschliches Hirngewebe beziehungsweise bestätigten die Ergebnisse in einem weiteren experimentellen Modellsystem, der Fruchtfliege Drosophila melanogaster.

Wie Roßner berichtet, beginnt nun eine weitere Phase der Erforschung der QC-Hemmer, bei der seine Arbeitsgruppe am Paul-Flechsig-Institut für Hirnforschung vom Bundesministerium für Bildung und Forschung über einen Zeitraum von drei Jahren mit 300.000 Euro gefördert wird. Unter anderem sollen neue, von der Probiodrug AG entwickelte QC-Hemmer im Tiermodell getestet werden, um Wirkstoffkandidaten für sich anschließende Klinische Studien auszuwählen.

Die aktuelle Publikation "Glutaminyl cyclase inhibition attenuates pyroglutamate Abold beta and Alzheimer's disease-like pathology" kann online abgerufen werden.

Jörg Aberger weitere Informationen:

PD Dr. Steffen Roßner Telefon: [phone] E-Mail: [e-mail] Weitere Informationen:

http://www.uni-leipzig.de/~pfi

[Erbse1]

Antwort auf Beitrag Nr.: 35.326.165 von Erbse1 am 29.09.08 13:54:42

Ergänzend zu dem vorherigen Artikel noch eine andere Ausführung. Sollte man mal im Auge behalten. Wäre toll, wenn es klappen würde.


Neue Methode könnte Alzheimer stoppen

Von Holger Dambeck

Gibt es bald eine Therapie gegen Alzheimer? Das glaubt zumindest ein deutsch-österreichisches Forscherteam. Im Tierversuch habe ein neuer Wirkstoff die typischen Ablagerungen in den Gehirnzellen fast vollständig verhindert. Ein Medikament für Menschen ist indes noch weit entfernt.

Bislang sind Mediziner weitgehend machtlos, wenn sie die Diagnose Alzheimer gestellt haben. Eine wirksame Therapie für die Demenzkrankheit existiert nicht - trotz intensiver Forschungsarbeit in den vergangenen Jahrzehnten. Für die nächsten Jahre rechnen Wissenschaftler vielmehr mit einer rasanten Zunahme neurologischer Erkrankungen wie Alzheimer und Parkinson.

Neues Paradigma für die Behandlung?
Deutsche und österreichische Wissenschaftler haben nun einen neuen Ansatz zur Alzheimer-Behandlung entwickelt. "Wir sind überzeugt, dass sich mit unseren Erkenntnissen eine einzigartige Möglichkeit bietet, die Zerstörung von Nervenzellen und die Bildung von Ablagerungen zu stoppen oder zu verhindern", sagte Hans-Ulrich Demuth, einer der beteiligten Forscher der "Mitteldeutschen Zeitung". Es werde aber noch einige Zeit dauern, ehe ein marktreifes Medikament zur Verfügung stehe, erklärte der Wissenschaftler. Grund seien die aufwendigen klinischen Tests. "Frühestens in sieben Jahren können diese abgeschlossen sein."

Die beteiligten Forscher sprechen von einem "neuen Paradigma" in der Alzheimer-Behandlung. Man habe einen ursächlichen Mechanismus entdeckt, "der die Zerstörung und den Abbau von Nervenzellen im Hirn von Alzheimer-Patienten erklärt und damit eine einzigartige Möglichkeit bietet, die Zerstörung von Nervenzellen und die Bildung von Plaques zu stoppen oder von vornherein zu verhindern", heißt es in einer Pressemitteilung des Pharma-Unternehmens Probiodrug, das an der Studie maßgeblich beteiligt war.

Das Team von Demuth blockierte in Versuchen mit Mäusen das Enzym Glutaminylzyklase (QC) und stellte dabei fest, dass sich so die Demenzerkrankung womöglich therapieren lässt. Im Gehirn von Alzheimer-Patienten werde mehr QC gebildet als im Gehirn gleichaltriger, nicht dementer Menschen, schreiben die Forscher im Fachblatt "Nature Medicine". QC wiederum sei für die Bildung einer bestimmten, für Nervenzellen schädlichen Variante des Amyloid-b-Peptids verantwortlich, welche die Bildung der für Alzheimer typischen Plaques anrege.

Neuer Ansatz besitzt Potential

In Tierversuchen seien die gefährlichen Ablagerungen bis zu 80 Prozent reduziert worden. Damit sei es gelungen, den Verlauf der Krankheit extrem zu verlangsamen oder zu stoppen. Nach Angaben der Forscher habe der Wirkstoff im Tierversuch keine Nebenwirkungen gezeigt. Im Gegenteil: Die orale Gabe des Wirkstoffs, der die Bildung von QC blockiert, hat bei Nagetieren sogar zu einer deutlichen Verbesserung der Gedächtnisleitung geführt.

"Das ist eine neue Möglichkeit, die sollte man austesten", sagte Kai Simons, Alzheimer-Experte am Max-Planck-Institut für molekulare Zellbiologie und Genetik Dresden, der an der Untersuchung nicht beteiligt war. Von einem Durchbruch will der aus Finnland stammende Forscher aber erst sprechen, wenn sich die Methode auch in einer sogenannten Phase-III-Studie bewährt hat, also in einer klinischen Studie mit zahlreichen Teilnehmern, die mehrere Monate oder Jahre dauert. Der neue Ansatz besitze Potential, aber zum jetzigen Zeitpunkt könne man nicht sagen, wie erfolgreich er sein werde, sagte Simons. Alzheimer entwickle sich sehr langsam, und nicht zuletzt deshalb gebe es viele mögliche Ansätze einer Behandlung.

In den vergangenen Jahren hatten Forscherteams weltweit wiederholt über erfolgversprechende Tierversuche berichtet. Simons' Team gelang es kürzlich, einen bislang wenig effektiven Alzheimer-Hemmer aufzurüsten. Anstatt die Wirkstoffe gegen die Bildung der Proteinplaques wie bis dahin üblich frei im Gehirn herumschwimmen zu lassen, statteten die Forscher eine der Substanzen mit einem speziell konstruierten Anker aus. So konnte sich der Wirkstoff in den Hüllen der Hirnzellen festhaken und genau dorthin gelangen, wo ein entscheidender Schritt der Plaquebildung stattfindet. Klinische Studien könnten nach Aussage der Dresdner Forscher etwa in zwei Jahren beginnen, eine mögliche Therapie sei frühestens in zehn Jahren zu erwarten.

Welche Methode auch immer den Durchbruch schafft, ein wirksames Alzheimer-Medikament verspricht angesichts der immer älteren Bevölkerung hohe Gewinne. So haben die an der neuen Alzheimer-Tierstudie beteiligten Forscher, die unter anderem von den Universitäten Leipzig und Halle-Wittenberg kommen, über die Firma Probiodrug bereits mehr als 27 Patente angemeldet, um ihre Methode zu schützen. 8 der 19 Autoren sind bei Probiodrug beschäftigt, ein weiterer hält Aktienanteile an dem Unternehmen. Die 1997 in Halle gegründete Firma hat bereits ein Verfahren zur Behandlung von Diabetes Typ 2 entwickelt, auf dessen Basis seit Ende 2006 Medikamente angeboten werden.

[Fruehrentner]

MELBOURNE, Australia - September 29, 2008

Prana Biotechnology Limited (NASDAQ: PRAN / ASX: PBT), a biopharmaceutical company focused on the research and development of treatments for neurodegenerative disorders, today announced that it has filed its annual report containing audited consolidated financial statements for the year ended June 30, 2008, with the U.S. Securities and Exchange Commission.

The annual report is available on Prana's website (www.pranabio.com). Shareholders may receive a hard copy of the annual report free of charge upon request.

About Prana Biotechnology Limited:

Prana Biotechnology was established to commercialize research into Alzheimer's disease and other major age-related neurodegenerative disorders. The company was incorporated in 1997 and listed on the Australian Stock Exchange in March 2000 and listed on NASDAQ in September 2002. Researchers at prominent international institutions including The University of Melbourne, The Mental Health Research Institute (Melbourne) and Massachusetts General Hospital, a teaching hospital of Harvard Medical School, contributed to the discovery of Prana's technology.

For further information, please visit our web site at www.pranabio.com.

[Fruehrentner]

Pranma hat übrigens eine neu gestaltete Internetseite.

[Fruehrentner]

Der Kurs hält sich angesichts der dramatischen Marktlage relativ gut.

[Fruehrentner]

MELBOURNE, AUSTRALIA - Oct 30, 2008

Prana Biotechnology Limited (Nasdaq: PRAN /ASX: PBT), a biopharmaceutical company focused on the
research and development of treatments for neurodegenerative disorders,
today announced that the Company is scheduled to present at the Rodman &
Renshaw 10th Annual Global Healthcare Conference, on November 10, in New
York City.

Dr. Rudolph Tanzi, co-founding scientist of Prana, will give a
presentation on November 10, at 9:55 a.m. EST on the Company's lead
product, PBT2, which has completed its Phase IIa clinical trial for
Alzheimer's disease. Dr. Tanzi will also provide update on the Company's
pipeline development.

The Conference will feature innovative growth companies and investors
interested in such companies, will focus on firms within the Life
Science, Energy, and Natural Resources sectors, as well as firms based
in promising Emerging Markets. Last year's conference, which focused on
Life Science firms, attracted more than 2,500 investors and industry
attendees and included presentations by more than 350 companies.

[Fruehrentner]

Company's MPACs for the Treatment of Alzheimer's Disease Shown to Prevent Neural Cell Death and the Production of Amyloid-Beta Protein

MELBOURNE, Australia - November 18, 2008:

Prana Biotechnology Limited (NASDAQ: PRAN / ASX: PBT), a biopharmaceutical company focused on the research and development of treatments for neurodegenerative disorders, today announced that a recent independent study conducted by Massachusetts General Hospital (MGH) has demonstrated that the Company's Metal-Protein Attenuating Compounds (MPACs) could halt Alzheimer's pathology.

The study published in the November edition of Annals of Neurology shows that the administration of the anesthetic gas isoflurane can spur the production of amyloid-beta protein, which causes plaques in the brains of Alzheimer's patients. A group of mice in the study treated with clioquinol, also known as PBT1 and the predecessor of Prana's compound PBT2, prior to receiving the isoflurance, had significant lower levels of the enzyme that leads to amyloid-beta production.

Geoffrey Kempler, Chairman and CEO of Prana, said, "Although PBT1 has now been superseded by PBT2 and is no longer being developed, we are happy that once again our underlying technology has demonstrated strong benefits in the fight against Alzheimer's."

Rudolph E. Tanzi, the study's senior author, Director of the Genetics and Aging Research Unit at Mass. General, and Prana's Co-Founding Scientist, said, "The new findings suggest that post-operative cognitive dysfunction and delirium may be related to increased amyloid beta protein levels driven by the commonly-used anesthetic, isoflurane. The fact that pretreatment with PBT1, which blocks amyloid beta protein accumulation, helped reduce the extent of neuronal cell death in the isoflurane-treated animals suggests that this class of drugs, which includes PBT2, might be considered as a prophylactic for mitigating the potential adverse effects of isoflurane during surgery. It must be emphasized, however, that all of these results have thus far been derived from mice studies and would therefore have to be first validated in humans."

PBT2 is designed to have an improved safety and efficacy profile and has demonstrated significantly greater effectiveness in lowering plaque in Alzheimer patients.

"Studies conducted by noteworthy institutions such as MGH reaffirms our commitment to commercialize and develop the second generation of MPACs for the treatment of Alzheimer's disease," added Kempler.

The study was also featured in the Boston Globe on November 12th.

For further information, please visit the Company's web site at www.pranabio.com

[Erbse1]

Antwort auf Beitrag Nr.: 35.986.594 von Fruehrentner am 18.11.08 09:16:45

Hallo Fruehrentner,
hier noch ein neuer Lösungsansatz. Mittlerweile habe ich den Überblick verloren. Ich verfolge die Alzheimer Wirkstoffe nur noch am Rande. Mein Wissen reicht leider nicht aus, die wirklichen guten Lösungsansätze raus zu filtern. Wünsche dir viel Glück mit deinem PRANA Invest.
Grüße
Erbse

Peptid löst Alzheimer-Plaques auf
Forscher mit neuem Weg zu einer Alzheimer-Therapie

Eine neue Substanz kann die Alzheimersche Krankheit wirksam bekämpfen - zumindest im Tierversuch. Dies bestätigt jetzt eine Studie Düsseldorfer und Jülicher Forscher. Danach vermindert eine Therapie mit dem Peptid „D3“ die Anzahl der gefährlichen Alzheimer-Plaques deutlich.

Die Alzheimersche Demenz (AD) ist eine chronische, neurodegenerative Erkrankung, von der mittlerweile weltweit mehr als 20 Millionen Menschen betroffen sind, davon alleine eine Million in Deutschland. Bisher ist AD nicht heilbar, es können lediglich die Symptome bekämpft werden.

Gefährliche Protein-Ablagerungen
Eine entscheidende Rolle bei der Entstehung und Entwicklung der AD spielt das Amyloid-beta-Peptid (Abeta). Im Gehirn von Alzheimer Patienten sind Protein-Ablagerungen nachzuweisen, die als Amyloid- oder Alzheimer-Plaques bezeichnet werden.

Alzheimer-Plaques sind diffus in die Hirnrinde und verschiedene andere Gehirnregionen eingestreute, außerhalb der Zellen liegende „Proteinverklumpungen“, deren Hauptbestandteil das Abeta ist. Viel wäre deshalb gewonnen, wenn es Wissenschaftlern gelänge, die Anhäufung von Abeta im Gehirn zu unterbinden.

Neues Peptid entwickelt
Die Forscher um Professor Dr. Dieter Willbold, Leiter des Instituts für Physikalische Biologie der Universität Düsseldorf und Direktor am Institut für Neurowissenschaften und Biophysik des Forschungszentrum Jülich haben nun ein Peptid entwickelt, das an Abeta bindet. Es besteht aus D-enantiomeren Aminosäuren, also Spiegelbildern der natürlich in Eiweißen vorkommenden Aminosäuren, gilt als besonders stabil im Körper und ruft in der Regel keine schädliche Immunantwort hervor.

Versuche im Reagenzglas zeigten, dass das Peptid „D3“ die Aggregation von Abeta aufhalten und sogar rückgängig machen kann. In Zellkulturen kann das Peptid die schädlichen Auswirkungen von Abeta unterbinden.

Weniger Plaques im Tierversuch
In bestimmten Mäusestämmen, die die Alzheimersche Demenz entwickeln, konnte die deutschen Forscher in enger Kooperation mit amerikanischen Kollegen von der Universität von Alabama in Birmingham zeigen, dass eine Behandlung mit D3 die Zahl der Alzheimer-Plaques in den Gehirnen der Mäuse erheblich reduziert. Dabei werden interessanterweise auch entzündliche Prozesse im Gehirn deutlich herabgesetzt.

Die beteiligten Wissenschaftler wollen nun möglichst schnell belegen, dass sich die kognitiven Leistungen der behandelten Mäuse selbst nach oraler Aufnahme des Peptids verbessern. Erste Versuche geben nach Angaben der Forscher allen Anlass zur Hoffnung. Anschließend soll das neue Peptid „D3“ möglichst schnell auf seine Anwendbarkeit beim Menschen geprüft werden.



(idw - Universität Düsseldorf - 21.11.2008)

[Fruehrentner]

€rbse,

danke für den Artikel, hatte ich auch von gelesen.

Aus Zeitmangel kann auch ich mich nicht in Details einarbeiten. Es gibt mittlerweile zuviele neue Ansätze. Welcher von den vielen Erfolg verspricht? Keine Ahnung

PRANA hab ich nur auf der watch list, bin nicht investiert. Der Kurs kommt ja enorm unter die Räder.

Aber spannend es weiter von der SEitenlinie aus zu verfolgen ist es allemal.

[Fruehrentner]

MELBOURNE, Australia - November 28, 2008 - Prana Biotechnology Limited (NASDAQ: PRAN / ASX: PBT), today provided an update of highlights of current and future activities of the Company at the Annual General Meeting.

PBT2 for Alzheimer's Disease

Chairman and CEO, Geoffrey Kempler, discussed the success of Prana's Phase IIa clinical trial of PBT2 in early Alzheimer's Disease and affirmed that the Company plans to enter larger clinical trials and advance towards commercialization.

Earlier this year the Company announced preliminary trial results and that the primary endpoints of safety and tolerability were met. In addition, PBT2 showed improvement in executive function, an important aspect of cognitive performance, and reduced the levels of abeta in the spinal fluid of patients. Abeta is a key protein associated with Alzheimer's Disease."

In July, the trial results were published in The Lancet Neurology journal and presented at this year's International Conference on Alzheimer's Disease. The publication of the results has attracted a great deal of attention from industry.

Mr. Kempler confirmed that the Company has entered into confidentiality arrangements with several large pharmaceutical companies and is in various stages of discussion in respect of the licensing of its lead compound PBT2; noting that the positive outcomes from the trial were viewed as a pre-requisite for advancing negotiations with a number of existing parties as well as attracting the interest of new parties.


Second Indication for PBT2 - Huntington Disease

Prana has received a commissioned report from independent US based clinical researchers entitled, "The suitability and recommendations for the clinical development of PBT2 in Huntington Disease". In the report, the researchers concluded that PBT2 was a suitable candidate for investigation in Huntington Disease clinical trials.

Huntington Disease is a genetically inherited degenerative brain disease causing uncontrolled movements, loss of intellectual faculties and emotional disturbance.

Professor Jeffrey Cummings, Chairman of Prana's R&D Advisory Board, commenting on the report, said that "the recommendation of this report is a real plus for PBT2. There are currently no drugs available to patients which prevent or delay Huntington Disease. PBT2 has the potential to affect the disease process and therefore to treat the disease."

Both Huntington and Alzheimer's Disease involve the toxic interaction of metals and specific protein aggregates in the brain (huntingtin protein in Huntington Disease and abeta protein in Alzheimer's Disease) that lead to nerve damage. PBT2, a Metal Protein Attenuating Compound (MPAC), exerts its activity by reducing this metal protein association thereby reducing the damage to nerve tissue. Very importantly, PBT2 has a neuroprotective effect.


The authors of the report concluded that "On the basis of a relevant mechanism of action, supportive non-clinical proof-of-concept studies in Huntington Disease models, preliminary evidence of clinical safety and tolerability, and promising clinical and biomarker outcomes in Alzheimer's patients, PBT2 is recommended to proceed to clinical trials in Huntington Disease research participants".


Ultimately PBT2 may be used to treat both Huntington and Alzheimer's patients.


Candidates for Use in Parkinson's Disease

Mr. Kempler discussed the Company's novel therapeutic drug candidates from its Parkinson's disease program. Prana's drug design is based on the understanding of the relationship between metals, particularly iron, and the metal induced oxidation of dopamine, believed to be involved in damage to the substantia nigra, the area of the brain affected in Parkinson's Disease.
"Already, a lead candidate drug, PBT427, has demonstrated positive effects in pre-clinical in vivo studies, protecting against damage to the substantia nigra".

These results have been presented and very well received at the prestigious Society for Neuroscience Conference, held last week in Washington D.C. In addition, a recent cover story of Science-Business eXchange, a weekly publication distributed by the publishers of BioCentury and nature was dedicated to a description of Prana's work on Parkinson's Disease.

[Erbse1]

Eine Frage der Durchblutung
Ursache für Alzheimer entdeckt

Wissenschaftlern in den USA ist offenbar ein Durchbruch bei der Suche nach den Ursachen und nach Behandlungsmöglichkeiten für Alzheimer gelungen. Die Forscher des Instituts für Medizin der Northwestern University in Chicago fanden heraus, dass eine zu geringe Durchblutung des Gehirns die wesentliche Ursache für Alzheimer sein könnte, wie sie in der jüngsten Ausgabe der US-Fachzeitschrift "Neuron" erläutern. Durch eine gezielte Verbesserung der Durchblutung sowie durch das Blockieren entscheidender Proteine könnte die Krankheit demnach behandelt oder ganz verhindert werden. Bislang war bekannt, welche Mechanismen zu Alzheimer führen, nicht aber, welche genaue Ursache dahinter steckt.

Laut den Forschern um Studienleiter Robert Vassar setzt eine unzureichende Zufuhr von Glucose, die mit dem Blut transportiert wird, eine biochemische Kettenreaktion in Gang. Dadurch kommt es zu einer Anhäufung von Proteinen, welche die Nerven angreifen. Die gezielte Verbesserung der Durchblutung des Gehirns - durch Sport, die Verringerung der Cholesterinzufuhr und die Behandlung von Bluthochdruck - könnte dabei helfen, dem Gehirn mehr Sauerstoff und Glucose zuzuführen.

In ihren Experimenten an Menschen und Mäusen fanden die Forscher heraus, dass eine geringe Durchblutung das Protein elF2alpha verändert. In seiner abgewandelten Form stößt das Protein verstärkt das Enzym aus, das die Produktion von Amyloid-Beta-Proteinen anregt. Diese Proteine siedeln sich auf Nervenzellen an und behindern deren Fähigkeiten, Botschaften zu senden. Vassar war bereits vor zehn Jahren auf die entscheidende Rolle des Enzyms BACE1 bei der Entstehung von Alzheimer gestoßen. Die Erkenntnisse der neuen Studie könnten den Autoren zufolge bei der Entwicklung eines Medikaments helfen, welches das Protein elF2alpha blockt und somit den biochemischen Entstehungsprozess von Alzheimer behindert.

Wie ein langsamer Hirnschlag

Die Forscher stellten zudem die Vermutung auf, dass Alzheimer durch dieselbe Art von Energiemangel entsteht wie ein Hirnschlag. Anstatt abzusterben, reagieren die Gehirnzellen mit einer Verstärkung der Produktion des BACE1-Enzyms, was kurzfristig hilft, aber langfristige Schäden verursacht. "Ein Hirnschlag ist eine Blockade, die in einem akuten, dramatischen Ereignis die Durchblutung verhindert und Zellen absterben lässt", sagte Vassar. Bei Alzheimer hingegen geschehe dasselbe über Jahre hinweg in einem "langsamen, hinterhältigen Prozess". "Es ist so sanft, sie merken es nicht einmal, aber es hat langfristige Auswirkungen, weil es eine chronische Verringerung der Durchblutung auslöst."

Bei Alzheimer sterben schrittweise Nervenzellen im Gehirn ab. Die Krankheit äußert sich in Vergesslichkeit bis hin zur Demenz. Meist tritt Alzheimer bei alten Menschen auf. Nach Schätzungen der Weltgesundheitsorganisation (WHO) könnte die Zahl der Alzheimer-Kranken von heute 24 Millionen weltweit auf 42 Millionen im Jahr 2020 und 81 Millionen im Jahr 2040 steigen

[Erbse1]

Schutzmechanismen für Alzheimer-Erkrankung: Enzymaktivität nimmt Schlüsselfunktion ein

Von Petra Giegerich

Informationsdienst Wissenschaft

Journal of Alzheimer's Disease (JAD) veröffentlicht neue Erkenntnisse über die Schutzwirkung des Enzyms Alpha-Sekretase (Mainz, 16. Februar 2009, lei) In einer institutsübergreifenden Kooperation ist es Wissenschaftlern der Johannes Gutenberg-Universität Mainz gelungen, weitere Einsichten in die körpereigenen Schutzmechanismen gegen die Alzheimer-Erkrankung zu gewinnen. Dabei zeigte sich, dass die enzymatische Aktivität der Alpha-Sekretase maßgeblich für die protektive Wirkung verantwortlich ist. "Wir haben früher schon festgestellt, dass das Enzym Alpha-Sekretase dazu beiträgt, die typischen Plaques-Ablagerungen im Gehirn zu verhindern und die Gehirnleistungen wie das Lern- und Erinnerungsvermögen zu verbessern", teilte Univ.-Prof. i.R. Dr. Falk Fahrenholz vom Institut für Biochemie mit. Seine Arbeitsgruppe ist vor diesem Hintergrund zusammen mit der Klinik für Psychiatrie und Psychotherapie der Universitätsmedizin sowie der Zentralen Versuchstiereinrichtung ZVTE den Ursachen für diese günstigen Eigenschaften der Alpha-Sekretase nachgegangen. Das Fachjournal Journal of Alzheimer's Disease (JAD) stellt die Ergebnisse in seiner neuen Ausgabe vom Februar 2009 vor.

Alpha-Sekretase ist ein körpereigenes Enzym, das im Gehirn in den Nervenzellen vorkommt und dort einen bestimmten Eiweißstoff spaltet. Dabei entsteht ein lösliches Protein-Fragment, das das Wachstum von Nervenzellen fördert und so der Gehirn-Erkrankung vorbeugt. Wird dagegen das Enzym Beta-Sekretase aktiv, dann nimmt eine Reaktionskette ihren Lauf, die schließlich zu der Alzheimer-Erkrankung mit dem meist vollständigen Gedächtnisverlust führt. "Die Alpha-Sekretase ist sozusagen das schützende Enzym, die Beta-Sekretase das schlechte", so Fahrenholz. "Und wir wollen nun herausfinden, wie wir das 'gute' Enzym aktivieren oder sein Vorkommen im Gehirn erhöhen können, um diese Erkrankung zu bekämpfen." Zu diesem Zweck haben die Kooperationspartner untersucht, ob der positive Effekt der Alpha-Sekretase auf seiner enzymatischen Aktivität beruht oder ob andere Eigenschaften des Enzyms für die Schutzwirkung verantwortlich sind. Enzyme oder Fermente spielen im gesamten Stoffwechsel eine wichtige Rolle, weil sie zahlreiche biochemische Vorgänge steuern, regulieren oder beschleunigen. "Die Alpha-Sekretase ist ein sehr komplexes Enzym mit vielen anderen Funktionen. Es übermittelt beispielsweise auch Signale aus dem Zellzwischenraum in die Zelle hinein und interagiert mit Molekülen auf anderen Zellen." Fahrenholz und seine Kollegen haben bei ihren Untersuchungen an transgenen Mäusen nun festgestellt, dass allein die enzymatische Aktivität die Schutzfunktionen garantiert. Wird diese Aktivität abgeschaltet, zeigen die Labor-Mäuse genau die Defizite, die für die Alzheimer-Krankheit so typisch sind: verminderte Lernfähigkeit, schlechte Gedächtnisleistung und Ablagerung von Plaques. Die enzymatische Aktivität der Alpha-Sekretase könnte also ein Ansatzpunkt für künftige Therapien darstellen.

Gleichzeitig konnten die Wissenschaftler in ihren Experimenten bestätigen, dass nicht die Plaques-Ablagerungen selbst für die nachlassende Gedächtnisleistung verantwortlich sind. In den Plaques sammeln sich nur die zellschädigenden Stoffe, die in Lösung die Synapsen der Nervenzellen zerstören. "Es ist wichtig, dass man nicht nur die Plaques im Auge hat, sondern vor allem ihre Vorstufen genau betrachtet, die die eigentlichen Verursacher der Krankheit sind", so Fahrenholz.

Originalveröffentlichung:

Anja Schroeder, Falk Fahrenholz, Ulrich Schmitt Effect of a dominant-negative form of ADAM10 in a mouse model of Alzheimers' Disease Journal of Alzheimer's Disease, Februar 2009, Volume 16:2 Kontakt und Informationen:

Univ.-Prof. i.R. Dr. Falk Fahrenholz Institut für Biochemie Johannes Gutenberg-Universität Mainz Tel. [phone]; Fax [phone] E-Mail: [e-mail] Dr. Anja Schröder Zentrale Versuchstiereinrichtung ZVTE Johannes Gutenberg-Universität Mainz Tel. [phone] E-Mail: [e-mail] PD Dr. rer. nat. Ulrich Schmitt Klinik für Psychiatrie und Psychotherapie Universitätsmedizin der Johannes Gutenberg-Universität Mainz Tel. [phone]; Fax [phone] E-Mail: [e-mail] Weitere Informationen:

http://www.bio.chemie.uni-mainz.de/ http://www.klinik.uni-mainz.de/psychiatrie http://www.j-alz.com http://www.j-alz.com/issues/16/vol16-2.html (Abstract)

[Fruehrentner]

Galapagos reveals key drug target for Alzheimer’s disease

13 Feb 2009

Starting point for potential breakthrough treatment

MECHELEN, Belgium | February 13, 2009 | Galapagos NV (Euronext: GLPG) announces the discovery of a human drug target that plays a key role in Alzheimer’s disease. This breakthrough was published today in Science, one of the world’s most prestigious scientific journals. The data presented in Science are a result of the collaboration between Galapagos and the academic group of Professor Bart De Strooper at the Flanders Institute for Biotechnology VIB and the KU Leuven in Belgium. The U.S. patent office has granted Galapagos a patent on this discovery.

“GPR3 is a promising drug target for developing a treatment for Alzheimer’s. There is a lack of drug targets in this field, and it is gratifying that Galapagos discovered GPR3,” commented Onno van de Stolpe, CEO of Galapagos. “Through this collaboration with Professor Bart De Strooper, one of the leading experts in the Alzheimer’s field, we have been able to prove the key role of GPR3 in Alzheimer’s and are excited that we can now share these data with the scientific community. Galapagos is now starting drug discovery with the aim to deliver a candidate drug to treat Alzheimer’s disease.”

Crucial role of drug target
The Science article describes how GPR3 was identified in human cells using Galapagos’ platform. The article further describes the role of GPR3 in Alzheimer’s disease. Inhibition of GPR3 prevented the accumulation of beta-amyloid, a protein in the brains of Alzheimer’s patients that is believed to cause the disease. The article also shows that GPR3 levels are higher in the areas of the brain that are affected in Alzheimer’s patients. The activity of GPR3 can likely be inhibited with a small molecule drug. Taken together, GPR3 is a promising drug target for development of a treatment for Alzheimer’s disease.

Galapagos has recently been awarded U.S. patent 7,429,459 for the use of GPR3 in screening for Alzheimer’s drugs. Similar patent applications are pending in Europe and other major territories. Galapagos made its Alzheimer's discovery in the same way as its novel, patent-protected targets in bone & joint disease were identified.

The article entitled “The orphan G protein–coupled receptor 3 modulates amyloid-beta peptide generation in neurons” is available today through the Science website at www.sciencemag.org and is published in the 13 February printed edition of the journal.

About Alzheimer’s disease

Alzheimer’s disease is a terminal, degenerative illness that causes problems with memory, thinking and behavior. In 2006 there were an estimated 27 million patients worldwide with Alzheimer; this is expected to quadruple by 2050. There is no cure available for Alzheimer; current therapies address only symptoms of the disease.

About Galapagos’ Alzheimer’s disease program

Galapagos identified novel targets in Alzheimer’s disease using its proprietary adenoviral based discovery platform. This work was supported by a €1.4 million grant from the Flemish IWT. A number of novel targets were identified, including GPR3, and patent applications were filed on the role of these targets in Alzheimer’s disease. In January 2006, Galapagos made the strategic decision to focus its internal drug discovery on the bone and joint diseases, but continued working on the Alzheimer’s disease program through a collaboration with Professor Bart De Strooper of the VIB and KU Leuven (Belgium). Galapagos plans to enter into discussions with potential pharmaceutical partners while progressing GPR3 into drug discovery.

About Galapagos

Galapagos (Euronext: GLPG; OTC: GLPYY) is a drug discovery and development company with small molecule programs in bone and joint diseases, bone metastasis, cachexia, anti-infectives and metabolic diseases. It has established risk sharing alliances with GSK, Janssen Pharmaceutica, Eli Lilly and Merck. Through an alliance with MorphoSys, Galapagos is also developing new antibody therapies in bone and joint diseases. Its division BioFocus DPI offers a full suite of target-to-drug discovery products and services to pharmaceutical and biotech companies and to patient foundations, encompassing target discovery and validation, screening and drug discovery through to delivery of pre-clinical candidates. Galapagos currently employs 470 people and operates facilities in six countries, with global headquarters in Mechelen, Belgium. More info at: www.glpg.com.

VIB

VIB, the Flanders Institute for Biotechnology, is a non-profit research institute in the life sciences. Some 1,100 scientists and technicians conduct strategic basic research on the molecular mechanisms that control the functioning of the human body, plants, and micro-organisms. Through a close partnership with four Flemish universities - Ghent University, the Katholieke Universiteit Leuven, the University of Antwerp, and the Vrije Universiteit Brussel - and a solid investment program, VIB unites the forces of 65 research groups in a single institute. Their research aims at fundamentally extending the frontiers of our knowledge. Through its technology transfer activities, VIB strives to convert the research results into products for the benefit of consumers and patients. VIB also develops and distributes a broad range of scientifically substantiated information about all aspects of biotechnology. More info at: www.vib.be.

K.U. Leuven

The University of Leuven is Belgium’s largest university and one of the oldest universities in Europe, founded in 1425. It is a comprehensive university with 14 faculties, with a long tradition of high-quality interdisciplinary research and teaching. The University of Leuven has over 33,000 students (12 percent international) and over 17,000 staff members (8,600 in the various university departments and 8,700 at UZ Leuven, the university hospital). More info at: www.kuleuven.be.

Center for Human Genetics

The Center for Human Genetics provides research, education and services in the fields of genetics, cell biology and developmental biology. With the aid of genetics, the Center strives to increase our understanding of human diseases. It conducts leading research in molecular genetics and provides a platform for genetic technologies to support clinical and fundamental research in Belgium and abroad. The Center places its clinical and scientific expertise at the service of society in the form of advice, diagnosis and treatment. Attention is also directed to the social, ethical and psychological implications of new insights and clinical practices in human genetics on the individual and on society. More info at: http://med.kuleuven.be/dme.

This release may contain forward-looking statements, including, without limitation, statements containing the words “believes,” “anticipates,” “expects,” “intends,” “plans,” “seeks,” “estimates,” “may,” “will,” “could,” “stands to,” and “continues,” as well as similar expressions. Such forward-looking statements may involve known and unknown risks, uncertainties and other factors which might cause the actual results, financial condition, performance or achievements of Galapagos, or industry results, to be materially different from any historic or future results, financial conditions, performance or achievements expressed or implied by such forward-looking statements. Given these uncertainties, the reader is advised not to place any undue reliance on such forward-looking statements. These forward-looking statements speak only as of the date of publication of this document. Galapagos expressly disclaims any obligation to update any such forward-looking statements in this document to reflect any change in its expectations with regard thereto or any change in events, conditions or circumstances on which any such statement is based, unless required by law or regulation.

SOURCE: Galapagos NV

[Fruehrentner]

ExonHit Therapeutics Reports Advancements in the Clinical Development of EHT 0202, its Phase II Drug for Alzheimer's Disease

26 Feb 2009

Successful Completion of Patient Enrolment for Phase IIa Study Study Results Available in Q4 2009 Preclinical Data Suggest EHT 0202 Could Modify Disease Evolution

PARIS, FRANCE | February 26, 2009 | ExonHit Therapeutics (Alternext: ALEHT) is pleased to announce that clinical testing of EHT 0202, its lead compound in Alzheimer's disease, is progressing well. Patient enrolment for the Phase IIa trial assessing EHT 0202 in patients with Alzheimer's disease is completed.

"The successful completion of patient enrolment for the Phase IIa represents an important milestone in the development of EHT 0202, and provides a clear timeline for the release of results," stated Dr. Loic Maurel, President of the Management Board of ExonHit Therapeutics. "Our strategy is to bring EHT 0202 up to the end of the ongoing study and then to look for a partner to move EHT 0202 through further clinical development. We have already met with several pharmaceutical companies that are looking forward to the Phase IIa results."

The trial is conducted under the supervision of Professor Bruno Vellas, Head of Alzheimer's Disease Clinical Research Center and Gerontopole, Toulouse University Hospital, France.

"EHT 0202 has an original mechanism of action: it stimulates the alpha-secretase pathway. If the neuroprotective and symptomatic effects of EHT 0202 demonstrated in animal models are confirmed in humans, it could change the treatment paradigm for Alzheimer's disease," stated Professor Vellas. "Current available drugs are symptomatic only and their clinical efficacy is limited over time, after which the evolution of the degenerative process starts progressing again. EHT 0202 is an interesting approach to potentially slow the evolution of the disease."

The Phase IIa trial is a multicenter, randomized, double-blind, placebo-controlled study primarily investigating the safety and tolerability of EHT 0202 in approximately 150 patients with Alzheimer's disease. The effect of two different doses of EHT 0202 as adjunctive therapy to an acetylcholinesterase inhibitor will be evaluated in comparison to placebo. Ambulatory patients suffering from mild to moderate Alzheimer's disease are randomized and receive oral treatment, twice a day, of either 40 or 80 mg of EHT 0202, or placebo over a three-month period. The study design will also allow for the collection of preliminary data related to many clinical efficacy parameters of EHT 0202, notably including a battery of cognitive assessments (ADAS-Cog, NTB, MMSE) but also assessment of patients' daily living activities, global assessment and behaviour.

Study results will be available in Q4 2009.


About EHT 0202

EHT 0202 has a novel mechanism of action when compared to existing Alzheimer's disease therapeutics: it stimulates the alpha-secretase pathway, thus enhancing the production of the procognitive and neuroprotective sAPPalpha fragment of APP (Amyloid Precursor Protein). The stimulation of the alpha-secretase pathway being to the detriment of Abeta amyloid peptide production, EHT 0202 potentially reduces toxic Abeta plaque formation [1].

Phase I studies demonstrated good tolerability of EHT 0202 in both young and aged healthy volunteers; importantly, no sedation or emesis were observed clinically.

Preclinical studies have shown that EHT 0202 protects cortical neurons against Abeta42-induced stress and that this neuroprotection is associated with sAPPalpha induction. EHT 0202 has also demonstrated pro-cognitive properties in several animal models: age-related memory impairment and scopolamine-induced amnesia [2].

About Alzheimer's disease

Alzheimer's disease is the most frequent cause of dementia in the aging population. The World Health Organization estimated in 2001 that 18 million people around the world were suffering from Alzheimer's disease and that this figure could nearly double by 2025 to 34 million [3].

About ExonHit Therapeutics

ExonHit Therapeutics is the world's leader in the analysis of alternative RNA splicing, a process which when deregulated plays a key role in the onset of various diseases.

ExonHit Therapeutics has a multi-component commercial strategy to capture the maximum value from its leadership in alternative splicing. The Company is already generating revenues from a new generation of microarrays, SpliceArray(TM) family of products that enable life science researchers to detect crucial disease-associated information. These products are marketed worldwide in conjunction with Agilent and Affymetrix. In the field of diagnostics, ExonHit Therapeutics has a major collaboration with bioMerieux to develop completely novel predictive blood-based cancer diagnostics, which could play a key role in improving the treatment of breast cancer and other major cancers.

In parallel, ExonHit Therapeutics is developing its own therapeutic pipeline in the field of neurodegenerative diseases and cancer. The Company has advanced drug candidates into clinical trials and is evaluating several promising preclinical compounds. ExonHit Therapeutics also has a strategic partnership with Allergan, to discover and develop new therapeutics in the areas of pain, neurological diseases and ophthalmology. This collaboration provides ongoing research funding to ExonHit.

Founded in 1997, ExonHit is headquartered in Paris, France and has a U.S. facility in Gaithersburg, Maryland. The Company is listed on Alternext of Euronext Paris (ISIN: FR0004054427; ticker: ALEHT) since November 17, 2005. For more information, please visit http://www.exonhit.com.

References

[1] Marcade M, Bourdin J, Loiseau N, Peillon H, Rayer A, Drouin D, Schweighoffer F, Desire L. Etazolate, a neuroprotective drug linking GABAA receptor pharmacology to amyloid precursor protein processing. Journal of Neurochemistry. 2008; 106: 392-404
[2] Pando M, Marcade M, Peillon H, Rayer A, Drouin D, Desire L. An alpha-secretase stimulator drug for cognitive disorders associated with neurodegeneration. Presented at the 12th congress of the European Federation of Neurological Societies; 23-26 August, 2008; Madrid, Spain
[3] WHO 2001. Azheimer's disease: The Brain Killer.

SOURCE: ExonHit Therapeutics

[Erbse1]

Alzheimer: Plaque-Folgen komplexer als gedacht.
Neues Ziel für Medikamentenentwicklung in Aussicht

Charlestown (pte/27.02.2009/10:00) - Die klebrigen Amyloid-Plaquen, die bei Alzheimer auftreten, dürften weitreichendere Auswirkungen auf das Gehirn haben als bisher angenommen. Die Ablagerungen sind dafür bekannt, dass sie die Neuronen beschädigen, jene Zellen, die für die Signalübertragung zuständig sind. Jetzt hat Kishore Kuchibhotla vom MassGeneral Institute for Neurodegenerative Disease http://www.mghmind.org nachgewiesen, dass auch die Astrozyten, die eine entscheidende unterstützende Rolle spielen, betroffen sind. Die in Science veröffentlichte Studie legt nahe, dass die Auswirkungen der Plaquen viel komplexer sind als bisher angenommen. Damit könnte auch ein neues Ziel für die Entwicklung von Medikamenten gefunden worden sein.

Astrozyten kommen im Gehirn reichlich vor. Sie machen bis zur Hälfte des Gesamtvolumens aus. Bis vor kurzem nahmen die Wissenschaftler an, dass die Astrozyten eine passive Rolle bei der Unterstützung der Neuronen spielen. Jetzt wird davon ausgegangen, dass sie eigene chemische Signale abgeben, die große Distanzen im Gehirn überwinden können. Die aktuelle Studie ergab, dass die Plaquen die Astrozyten scheinbar aktiver werden lassen. Davon sind jedoch nicht nur die Zellen in ihrer unmittelbaren Umgebung betroffen. Bisher wurde gedacht, dass die Plaquen nur die nahe liegenden Neuronen beeinträchtigen, berichtet BBC Online. Nun scheint es, als ob einzelne Plaquen ihren negativen Einfluss viel weiter ausbreiten könnten.

Laut Kuchibhotla spielen diese Plaquen wahrscheinlich eine komplexere Rolle bei der Veränderung der Gehirnfunktion als gedacht. "Wir bekommen erst eine Ahnung davon, wie die Ablagerungen die Funktion der Astrozyten beeinflussen." Die entscheidende Frage werde sein, wie ihre verstärkte Signalwirkung die Funktion der Neuronen verändert. Eine weitere sei, ob diese Aktivität die Ablagerung der Plaquen einschränkt oder verstärkt. Das Team markierte Astrozyten mit einer Farbe, die aufleuchtet, wenn die Zelle aktiv ist. Zur allgemeinen Überraschung waren sie bei entsprechend gezüchteten Mäusen viel aktiver als angenommen. Diese Aktivität schien synchron zu laufen und wellenförmig an entfernte Bereiche des Gehirns gerichtet zu sein. Die Blockierung der Neuronenaktivität hatte keine Auswirkung auf die Aktivität der Astrozyten. Damit liegt nahe, dass die Auswirkungen auf die Zellen voneinander unabhängig sind. (Ende)

[Fruehrentner]

MELBOURNE, Australia -March 11, 2009- Prana Biotechnology Limited (NASDAQ: PRAN / ASX: PBT), today announced that its lead compound for the treatment of Alzheimer's Disease, PBT2, in addition to previously reported benefits, also prevents the loss of synapses (the space) between neurons that underlies the process of neurodegeneration in Alzheimer's Disease.

Ordinarily, transgenic Alzheimer's Disease mice suffer a loss of synapses, which leads to cognitive impairment because nerve cells can no longer communicate with each other. The new data shows that in mouse models of AD, PBT2 can reverse the effect of Abeta protein toxicity on nerve cell synapse loss.

Professor Colin Masters, Director of the Mental Health Research Institute and Laureate Professor, University of Melbourne, commented "this confirms that our preclinical and clinical findings of PBT2 opens the pathway for PBT2 to prevent the damage caused by Abeta in the brain of a person with Alzheimer's Disease and to improve cognitive function".

The effects of PBT2 in a Phase IIa clinical trial in early Alzheimer's Disease were published in the journal Lancet Neurology and were presented at the 2008 International Conference on Alzheimer's Disease.

The new data will be presented by Professor Masters at 9th International Conference on Alzheimer's and Parkinson's Disease in Prague on 14 March 2009 at 3.50pm. In addition, the data will be presented by Dr Paul Adlard and Associate Professor David Finklestein at the conference in a poster entitled "8-hydroxy quinoline effects on neuronal plasticity".

Geoffrey Kempler, Chairman of Prana, said, "These findings are very exciting for us. We already knew that PBT2 could reduce the toxic effects of Abeta oligomer protein on Alzheimer Disease patients, but this new data demonstrates that PBT2 can, in a mouse model, reverse the actual loss of nerve tissue that is believed to underlie Alzheimer's Disease. Given the lack of a disease-modifying drug available to patients, we are further encouraged by the enormous potential of PBT2. We are continuing our discussions with potential partners to accelerate its further development."

[Erbse1]

Alzheimer künftig heilbar?

Von Kristina Gronwald

Informationsdienst Wissenschaft

Neuer Ansatz für die Behandlung von Alzheimer gefunden - Molekül "Aph 1B" für Plaquebildung verantwortlich -
Absterben von Gehirnzellen stoppen Erstmals gibt es begründete Hoffnung, dass die Alzheimer-Erkrankung zukünftig doch gestoppt werden könnte. Wissenschaftler aus Belgien, Deutschland, Amerika und England - darunter auch Essener Forscher der Uni-Klinik für Psychiatrie und Psychotherapie am LVR-Klinikum Essen - fanden ein Molekül, das die Basis für die Entwicklung neuer Medikamente bilden könnte. Die Ergebnisse ihrer Untersuchungen veröffentlichten die Wissenschaftler jetzt in der renommierten Fachpublikation "Science". "Mit der neuen Erkenntnis haben wir erstmals einen Ansatz gefunden, wie wir das Absterben von Gehirnzellen stoppen können. Dies gelingt hier ohne die bekannten problematischen Nebenwirkungen vergleichbarer Ansätze auf Nervenzellen des Gehirns", erklärt Prof. Dr. Jens Wiltfang, Professor für Psychiatrie und Psychotherapie an der Universität Duisburg-Essen. Allerdings würden noch mindestens 15 Jahre vergehen, bis die ersten Patienten hiervon profitieren könnten, dämpft er allzu hohe Erwartungen für die nähere Zukunft.

Charakteristisch für die Gehirne von Alzheimer-Patienten sind Eiweißablagerungen, so genannte Plaque, die starken Einfluss auf das Absterben der Gehirnzellen haben. Schon seit längerem ist bekannt, dass eine Gruppe von Proteinen, der so genannte Gamma-Sekretase-Komplex, eine wesentliche Rolle bei der Bildung dieser Plaque spielt. Potentielle Medikamente, die den gesamten Komplex angreifen würden, haben auf der Basis der bisherigen Wirkmechanismen tödliche Nebenwirkungen. Aktuell haben die Wissenschaftler nun ein ganz spezielles Molekül des Komplexes identifiziert: "Aph1B". In Versuchen mit Mäusen schalteten die Forscher unter der Federführung von Prof. Bart de Strooper aus Belgien genau dieses Molekül aus und konnten zeigen, dass sich der Zustand der Tiere besserte - ohne dass gravierende Nebenwirkungen auftraten.

"Unsere Forschungen zeigen, wo wir effektiv in der Behandlung der Alzheimer-Erkrankung ansetzen können - ohne dass zu große Nebenwirkungen entstehen", fasst Prof. Wiltfang zusammen. Einer der nächsten Schritte würde sein, gezielt nach einer Substanz zu forschen, die die Aktivität von Aph 1B-Molekülen im menschlichen Gehirn verringert und damit die Plaquebildung stoppen kann.

Alzheimer ist mittlerweile die bedeutendste Demenzerkrankung in der westlichen Welt; Tendenz steigend. Schätzungen sprechen allein in Europa von voraussichtlich rund sieben Millionen Betroffenen im Jahre 2020. Bisher ist die Erkrankung unheilbar. Die Patienten verlieren innerhalb weniger Jahre mehr und mehr ihre Persönlichkeit. Heutige Medikamente erhalten die Gedächnisfunktion nur in den ersten Phasen der Erkrankung. Das Absterben der Gehirnzellen verhindern sie bisher aber nicht.

Nähere Informationen:

Prof. Dr. med. Jens Wiltfang, Direktor der Uni-Klinik für Psychiatrie und Psychotherapie des LVR-Klinikums Essen, Kliniken und Institut der Universität Duisburg-Essen, Tel.: [phone], [e-mail]

[Fruehrentner]

MELBOURNE, Australia - April 2, 2009: Prana Biotechnology

(ASX:PBT; NASDAQ:PRAN) today announced that an independent study conducted by researchers at the University of California, Irvine, validates Prana's fundamental drug strategy for Alzheimer's Disease in blocking the toxic interaction between Abeta and brain metals, such as zinc, that damages synapses and cause cognitive loss.

The study, published in the Journal of Neuroscience showed that the release of zinc from synapses is critical for Abeta to form oligomers and to aggregate. Dr Glabe an author of the paper noted, "These results are very exciting news for understanding the mechanism of Alzheimer pathogenesis. They help elucidate the fundamental role of metal ions like zinc in causing the formation of Abeta oligomers which damage synapses".

Prana's lead Alzheimer's Disease compound, PBT2, targets a toxic form of the Abeta protein in the synapses of the brain by inhibiting the interaction between Abeta and zinc. The findings provide an explanation as to how PBT2 has demonstrated the ability to restore normal function to Abeta-impaired synapses and so reverse cognitive loss in animal models of AD. PBT2 has completed a Phase IIa study in Alzheimer's Disease patients, demonstrating a lowering of Abeta levels in the CSF and signs of cognitive improvement within three months.

Commenting on the significance of these findings Dr Jeffrey Cummings of UCLA, and Chair of Prana's Scientific Advisory Board, noted that, "the role of Abeta oligomers in damaging synapses resulting in cognitive impairment is well established in the literature. What has been less clear is why oligomers congregate at the synapse. The work by Dr. Glabe and his colleagues provides an explanation, showing that synaptic activity stimulates the release of Abeta and zinc leading to the build up of toxic Abeta oligomers at the synapse. Previous studies demonstrating that PBT2, can disperse Abeta oligomers attracted by synaptic zinc, suggest that the benefit of PBT2 seen in the recent clinical trial may reflect this synaptic effect".

Professor Colin Masters, Director of the Mental Health Research Institute and Laureate Professor of Medicine at the University of Melbourne, said "these findings provide independent validation that this therapeutic approach is likely to benefit Alzheimer's Disease patients by slowing down or delaying the onset of the illness".

The study titled "A role for Synaptic Zinc in Activity-Dependent Aβ Oligomer Formation and Accumulation at Excitatory Synapses" published in the April issue of the Journal of Neuroscience


1Deshpande A, Kawai H, Metherate R, Glabe CG, and Busciglio J. J. Neurosci 2009; 29 (13)


Contact:
Prana Biotechnology Ltd
[phone]
If you wish to be taken off of this distribution list, please reply with the word "UNSUBSCRIBE" in the subject line.

[Fruehrentner]

MELBOURNE, Australia - July 10, 2009: Prana Biotechnology

(ASX: PBT; NASDAQ: PRAN) today announced that Dr. Craig Ritchie of Imperial College, London will present an update on the clinical efficacy of Prana's PBT2 drug for the treatment of Alzheimer's Disease at the 2009 International Conference on Alzheimer's Disease (ICAD) in Vienna, Austria. Dr. Ritchie will be presenting a paper on "PBT2 for Alzheimer's Disease: An Update on Clinical Development" as part of the Featured Research Symposium, "New Horizons: From Discovery to Successful Clinical Trials" on Sunday, July 12th at 11:10 am.

Key findings from our Phase IIa clinical trial, first published in Lancet Neurology in July 2008, as well as additional analysis of the efficacy findings which further support the potential of PBT2 to help Alzheimer's Disease sufferers, will be presented.

The Lancet Neurology paper documented that patients on Prana's PBT2 showed significant improvement in two measures of Executive Function after only 12 weeks of treatment. Dr Ritchie will present new results showing that there was a statistically significant improvement in the overall Executive Function z-score component of the NTB (Neuropsychological Test Battery) in patients receiving 250mg PBT2 compared with placebo.

Dr Ritchie will report on the results of a post-hoc analysis of the Phase IIa trial data. An analysis of the responses of individual patients in the trial, showed 41% of those receiving PBT2 demonstrated substantial cognitive improvement compared to only 4% of those on placebo.

"Patients on PBT2 very clearly benefited from the drug and their overall cognitive function, especially Executive Function, improved. The results would be reflected in an improvement in day to day functioning in the lives of people with Alzheimer's Disease and confirms the importance for PBT2 to be further developed as a therapy for patients afflicted with the disease" noted Dr. Ritchie.

Geoffrey Kempler, Prana's CEO, said that "planning is currently underway for a Phase IIb clinical trial of PBT2. Comprehensive analysis of our existing data suggests that in this trial, the longer treatment period using a much larger number of patients will confirm PBT2's ability to provide even greater cognitive benefit".

[Fruehrentner]

Lead Compound, PBT2, improves cognition in both Alzheimer's disease Transgenic and normal Aged cognitively impaired mice

. New data indicates PBT2 benefits not only Alzheimer's disease patients, but also could treat the cognitive loss commonly associated with the normal ageing process.

. PBT2 lowers amyloid burden in the brain and also corrects metal imbalances that occur in the aged brain.

MELBOURNE, Australia - July 16th, 2009

Prana Biotechnology Limited (NASDAQ: PRAN / ASX: PBT), today announced that its Head of Research, Assoc. Prof. Robert Cherny, presented new data on PBT2, the Company's lead compound in development for Alzheimer's disease, during the Hot Topics 2 session at the International Conference of Alzheimer's Disease (ICAD) in Vienna, Austria. The presentation was entitled "PBT2 ameliorates cognitive impairment in Alzheimer's disease transgenic and aged mice: Evidence for a common mechanism of action."

Age related cognitive loss and Alzheimer's disease are both characterized by alterations in the normal distribution of metals in the brain. Assoc. Prof. Cherny presented evidence that the beta amyloid protein, which lies at the center of Alzheimer's disease pathology, exacerbates metal imbalance in the brain.

PBT2 has already been shown to rapidly improve cognition in transgenic Alzheimer's disease mice; the new data show that PBT2 is equally effective in restoring function to normal mice that are cognitively impaired as a consequence of ordinary aging. In both cases, the brains of mice treated with PBT2 showed benefits in the area of the brain associated with learning and memory*. PBT2 restored synaptic spine density, a physical measure of improved neuronal health, to normal levels. This structural change was accompanied by restoration of neurotransmitter receptors and other markers of neuronal health to the levels seen in healthy young mice**.

Jeffrey Cummings, MD., Chair of Prana's scientific advisory board said "The effect of PBT2 on synapses indicates that this agent is affecting the fundamental process regarded as central to the cognitive deficits of Alzheimer's disease".

"Coupled with our Phase IIa clinical trial data, this new evidence of the positive effects of PBT2 on normal aged mice is very exciting. Imbalances in brain metals, such as zinc and copper, may affect cognition in Alzheimer's disease patients even before dementia is present. PBT2 appears to not only lower amyloid burden in the brain, but also correct metal imbalances that occur in the aged brain and particularly in Alzheimer's where the condition is exacerbated by beta amyloid deposition," commented Geoffrey Kempler, Prana's CEO.

____________________________________________________________________________
* 20 month old C57B6 Normal mice were treated for 11 days oral PBT2 30 mg/kg (n=15), and tested on the Morris Water Maze. Placebo-treated old mice (n=20) were significantly impaired in performance in the maze compared to younger (12 month old, n=8) placebo-treated mice. PBT2 treatment restored the animals after 6 days treatment to a level of performance equivalent to that of the 12 month old animals (p< 0.001).

** In the brains of the PBT2 treated mice, there is a significant (p<0.01) normalization of neuronal spine density in the hippocampal region of old mice. Major biochemical components of memory function in the hippocampus that are decreased in the old mice, CREB, PSD95, NMDAR2a, AMPAR, were normalized to the levels in younger animals within 11 days of PBT2 treatment.

[Fruehrentner]

MELBOURNE, Australia - August 5, 2009:

Prana Biotechnology (ASX: PBT; NASDAQ: PRAN) today announced that it has secured a key patent protecting its clinical drug asset PBT2, with the European Patent Office issuing a notice of Decision to Grant in Europe.

The patent entitled '8-Hydroxyquinoline derivatives' covers the composition of matter of selected families of 8-Hydroxyquinoline compounds, including PBT2 and the uses of such compounds for the treatment of neurological diseases, including Alzheimer's Disease and Huntington's Disease.

The European patent has a twenty year term expiring on 16 July 2023, with a possible extension of term of up to 5 years under supplementary protection provisions.

Prana's lead Alzheimer's Disease compound, PBT2, has already completed a Phase IIa study in early Alzheimer's Disease patients and has demonstrated safety and tolerability. In addition, PBT2 showed improvement in executive function, an important aspect of cognitive performance, and reduced the levels of Abeta in the spinal fluid of patients. Abeta is a key protein associated with Alzheimer's Disease.

The trial results were published in The Lancet Neurology journal as well as presented at this year's International Conference on Alzheimer's Disease.

PBT2 has been designed to be a disease modifying drug that prevents the formation of toxic forms of the Abeta protein in the synapses of the brain and to improve neurotransmission, resulting in improved cognition.

Geoffrey Kempler, Prana's CEO, said "The decision of the European Office to grant this patent further protects Prana's valuable clinical asset PBT2, and well positions us to enter larger clinical trials and advance towards commercialization with the aim of having the first disease modifying drug and provide hope to millions of Alzheimer's sufferers and their families."

[Fruehrentner]

Prana Allowed Key Patent for PBT2 in the United States

. Related patents also granted in Russia, Singapore, South Africa, New Zealand, Accepted in Australia.

MELBOURNE, Australia - August 12, 2009:

Prana Biotechnology (ASX: PBT; NASDAQ: PRAN) today announced that it has received a Notice of Allowance from the United States Patent and Trade Mark Office (USPTO), protecting its clinical asset, PBT2, in the USA. The patent entitled, '8-Hydroxyquinoline derivatives' covers the composition of matter of selected families of 8-Hydroxyquinoline compounds, including PBT2 and pharmaceutical compositions containing these compounds.

The USA patent is expected to formally proceed to Grant by December 2009, following payment of official fees. Prana has also secured the Grant of related patents in Russia, Singapore, South Africa, New Zealand and has a Notice of Acceptance in Australia. Previously Prana has announced receiving a notice of Decision to Grant in Europe.

Each of the granted patents have a twenty year term expiring on July 16, 2023, with extensions of term possible under the legal provisions of some of these countries, including USA and Europe.

Geoffrey Kempler, Prana's CEO, said "The Notice of Allowance from the USPTO and the grant of patents in other key jurisdictions gives Prana exclusive rights to develop and market PBT2, Prana's lead Alzheimer's Disease drug, with the aim of PBT2 becoming the first disease modifying drug for the treatment of Alzheimer's Disease."

PBT2 has already completed a Phase IIa study in early Alzheimer's Disease patients and has demonstrated safety and tolerability. In addition, PBT2 showed improvement in executive function, an important aspect of cognitive performance, and reduced the levels of Abeta in the spinal fluid of patients. Abeta is a key protein associated with Alzheimer's Disease.

The trial results were published in The Lancet Neurology journal as well as presented at this year's International Conference on Alzheimer's Disease.

PBT2 has been designed to be a disease modifying drug that prevents the formation of toxic forms of the Abeta protein and restores metal homeostasis in the synapses of the aged brain. This results in improved neurotransmission and cognition.

Mr. Kempler concluded, "We believe that the granting of these key patents enhances the value of investing in Prana as our intellectual property is now firmly protected".

[Fruehrentner]

Melbourne, Australia - September 2, 2009

Prana Biotechnology (ASX:PBT; NASDAQ:PRAN) today announced that Geoffrey Kempler, Chairman and Chief Executive Officer, and Dr. Rudy Tanzi, Chief Scientific Officer, will present at the Rodman & Renshaw (NASDAQ: RODM) Annual Global Investment Conference in New York City on Wednesday, September 9, 2009 at the New York Palace Hotel.

Mr. Kempler, will give a presentation on Wednesday, September 9th at 3:15 p.m. in the Garrison Salon of the NY Palace Hotel. Mr. Kempler will provide an overview of the Company's drug development program and class leading library of compounds with a focus on treating Alzheimer's Disease and other major age related neurological disorders. In addition, Mr. Kempler and Dr. Tanzi will be available during the conference for investor one on one meetings.

A pre-recorded video of Prana's presentation will be available on the Rodman & Renshaw website shortly after the conference. For more information about the Rodman & Renshaw 11th Annual Global Healthcare Conference, please visit Rodman & Renshaw's website at www.rodmanandrenshaw.com.

About Prana Biotechnology Limited:

Prana Biotechnology was established to commercialise research into Alzheimer's Disease and other major age-related neurodegenerative disorders. The Company was incorporated in 1997 and listed on the Australian Stock Exchange in March 2000 and listed on NASDAQ in September 2002. Researchers at prominent international institutions including The University of Melbourne, The Mental Health Research Institute (Melbourne) and Massachusetts General Hospital, a teaching hospital of Harvard Medical School, contributed to the discovery of Prana's technology.

For further information please visit the Company's web site at www.pranabio.com.

[Fruehrentner]

MELBOURNE, Australia - 9th September 2009 :

Prana Biotechnology (ASX: PBT; NASDAQ: PRAN) today announced that it has reached agreement to raise $6 million (Australian) to support its R&D programs, to promote its drug development pipeline and to maintain corporate activities.

The funds come from an existing shareholder committed to Prana's strategy to become a leader in the development of drugs to treat age related neurodegenerative diseases. Under the terms of the funding, Prana will issue 30 million ordinary shares ranking equally with the existing ASX listed ordinary shares (equivalent to 3 million ADR's on NASDAQ) at a price of 20 cents (Australian currency) per share. These shares which are subject to limited price protection, will be issued without shareholder approval pursuant to the Company's allowance under ASX Listing Rule 7.1.

The investor will also receive, subject to shareholder approval, 10 million free attaching options each to acquire 1 ordinary share at an exercise price of 30 cents and expiring 4 years from the date of issue of the abovementioned shares. The Company will receive $5.7 million (Australian) net of all fees.

Geoffrey Kempler, Prana's CEO, said, "We are always appreciative of the continuing support we receive from existing shareholders. The new funds will allow Prana to continue to build its development pipeline by providing the financial flexibility to choose to advance PBT2 into the next Alzheimer's Disease clinical trial supported by either a pharmaceutical company or by investors. The funds will also enable Prana to promote our other clinical opportunities, especially around Parkinson's Disease, and we hope soon to announce that we have selected a lead compound for development."

Prana's lead Alzheimer's Disease compound, PBT2, has already completed a Phase IIa study in early Alzheimer's Disease patients and has demonstrated safety and tolerability. In addition, PBT2 showed significant improvement in Executive Function, an important aspect of cognitive performance, and reduced the levels of Abeta in the spinal fluid of patients. Abeta is a key protein associated with Alzheimer's Disease.

Rodman & Renshaw, LLC, a wholly-owned subsidiary of Rodman & Renshaw Capital Group, Inc. (Nasdaq: RODM - News) and Peregrine Corporate (Melbourne) were advisors on the transaction.


About Prana Biotechnology Limited
Prana Biotechnology was established to commercialise research into Alzheimer's Disease and other major age-related neurodegenerative disorders. The Company was incorporated in 1997 and listed on the Australian Stock Exchange in March 2000 and listed on NASDAQ in September 2002. Researchers at prominent international institutions including The University of Melbourne, The Mental Health Research Institute (Melbourne) and Massachusetts General Hospital, a teaching hospital of Harvard Medical School, contributed to the discovery of Prana's technology.

For further information please visit the Company's web site at www.pranabio.com.


About the Placement

The Placement of the shares and options is subject to limited price protection in the event of potential registration delays that may arise in converting the 30 million ordinary shares to tradable American Depository Receipts (ADR's) on the NASDAQ market. The limited price protection compensates the subscriber should the closing price of Prana shares on the ASX fall below A$0.19 (19 cents) provided that protection is limited to a maximum of down to A$0.17 (17 cents) from the date of issue of the Placement Shares until 5 days after the registration of the ADR's on NASDAQ. The subscriber will be entitled at no further consideration to such number of additional shares as may be required so that the average subscription price of the shares is equivalent to the relevant closing price between the issuance of the shares and 5 days after the filing of a registration statement with the Securities and Exchange Commission, with a maximum protection down to A$0.17 (17 cents) per ordinary share.

[orange99]

Wie ist eure Einschätzung zu prana... wie seht ihr das unternehmen und wo in 1 Jahr, 5 Jahren?

[orange99]

Da kommt Geld ins Spiel:

September 11, 2009 (FinancialWire) -- Prana Biotechnology (ASX: PBT) (NASDAQ: PRAN | Quote | Chart | News | PowerRating) has reached an agreement to raise $6 million (Australian) to support its R&D programs, to promote its drug development pipeline and to maintain corporate activities.

The funds come from an existing shareholder committed to Prana's strategy to become a leader in the development of drugs to treat age related neurodegenerative diseases. Under the terms of the funding, Prana will issue 30 million ordinary shares ranking equally with the existing ASX listed ordinary shares (equivalent to 3 million ADRs on NASDAQ) at a price of 20 cents (Australian currency) per share. These shares, which are subject to limited price protection, will be issued without shareholder approval pursuant to the company's allowance under ASX Listing Rule 7.1. The investor will also receive, subject to shareholder approval, 10 million free attaching options each to acquire 1 ordinary share at an exercise price of 30 cents and expiring 4 years from the date of issue of the abovementioned shares. The company will receive $5.7 million (Australian) net of all fees.

Prana's lead Alzheimer's Disease compound, PBT2, has already completed a Phase IIa study in early Alzheimer's Disease patients and has demonstrated safety and tolerability. In addition, PBT2 showed significant improvement in Executive Function, an important aspect of cognitive performance, and reduced the levels of Abeta in the spinal fluid of patients. Abeta is a key protein associated with Alzheimer's Disease.

Rodman & Renshaw, LLC, a wholly-owned subsidiary of Rodman & Renshaw Capital Group, Inc. (NASDAQ: RODM), and Peregrine Corporate (Melbourne) were advisors on the transaction.

[Fruehrentner]

Prana Selected to Present at Windhover's Therapeutic Area Partnerships Conference by Independent Expert

PBT2 Selected as Top 10 Most Interesting Neuroscience Projects in Development

Melbourne, Australia - November 12, 2009 : Prana Biotechnology (ASX:PBT; NASDAQ:PRAN) today announced that Dr. Rudy Tanzi, Scientific Advisory Board, will present at the 2009 Windhover's Therapeutic Area Partnerships Conference being held November 18 at 3:30 PM at the Westin Copley Place Hotel in Boston, Massachusetts.

Prana's lead Alzheimer's disease compound, PBT2, has been chosen by Windhover Information and independent expert, Harry Tracy, as one of the top 10 most interesting neuroscience projects in development available for strategic partnering.

About Windhover
Windhover Information Inc (www.windhover.com), an Elsevier company, has led the field in providing analysis of the healthcare industry to decision-makers at all levels since the founding of its flagship publication, IN VIVO, the Business & Medicine Report, in 1983. Windhover provides its information and analysis in many formats, including print, electronic databases, international conferences and webinars.

About Prana Biotechnology Limited
Prana Biotechnology was established to commercialise research into Alzheimer's Disease and other major age-related neurodegenerative disorders. The Company was incorporated in 1997 and listed on the Australian Stock Exchange in March 2000 and listed on NASDAQ in September 2002. Researchers at prominent international institutions including The University of Melbourne, The Mental Health Research Institute (Melbourne) and Massachusetts General Hospital, a teaching hospital of Harvard Medical School, contributed to the discovery of Prana's technology.

For further information please visit the Company's web site at www.pranabio.com.

Contact:
Prana Biotechnology Limited
[phone]

In US:
Leslie Wolf-Creutzfeldt
Grayling
[phone]
[e-mail]

[orange99]

Aber so richtig läuft hier auch noch nichts? Sollte die Phase 3 nicht dies Jahr noch abgeschlossen werden? Weiß irgendwer was?

[orange99]

Antwort auf Beitrag Nr.: 38.551.526 von orange99 am 11.12.09 14:40:27

Hat irgendwer hier news?

[orange99]

Wow --- was ist denn da gerade los? Laut meinem Aktienwidget hatten wir gestern über 12 % und heute 15% ? Passiert da was?

[orange99]

Irgendwie kein großes Interesse an Prana mehr?

[Fruehrentner]

Antwort auf Beitrag Nr.: 38.925.614 von orange99 am 11.02.10 13:47:20

ist auf watch list

[Neoe]

Warte auch schon Ewigkeiten auf den Einstieg. Hab es leider vor einigen Monaten verpasst bei 1 USD zuzuschlagen. Aber man muss schon sagen, eine echte Schande auf so einem Kandidaten zu sitzen und in nicht in die Klinik zu bekommen.

Auf was warten die eigentlich noch?

Bin sonst aber immer noch überzeugt, dass Prana den besten Ansatz bei Alzheimer verfolgt.

[Fruehrentner]

Prana to commence Phase IIb trial on PBT2

- 525 Alzheimer's disease patients to be treated for 12 months -

Melbourne - 20 April 2010: Prana Biotechnology (NASDAQ:PRAN; ASX:PBT) today announced that it is finalising plans to commence a definitive Phase IIb trial of its lead Alzheimer's disease drug, PBT2, before the end of this year.

The Phase IIb trial will involve 525 patients with mild to moderate Alzheimer's disease. Treatment will be over a period of 12 months, with the key performance measure being cognition (including ADAS Cog* and Executive Function tests from the NTB*). The trial, a double blind placebo controlled study, will test the efficacy of 2 doses of PBT2 (250mg and 100mg). "We are excited by this protocol because we already know how patients benefited from a 250mg dose of PBT2 in just 12 weeks, so we are confident the benefit will be even stronger and more pronounced over a 12 month trial" said Mr. Kempler. "This trial is all about cognition and helping patients".

"Over recent years most drug companies have made late stage drug development decisions based on secondary biomarkers and imaging. Certainly, many have seen amyloid signals, but not necessarily robust cognition outcomes. PBT2 has shown both positive cognitive and biomarker changes, which is why we are so optimistic in the ability of PBT2 to really help sufferers of Alzheimer's disease".

The Company has prepared an explanation of its understanding of how PBT2 works in the brains of patients with Alzheimer's disease and in particular how PBT2 is uniquely different to other approaches for treating the disease. The explanation, in the form of a Mechanism of Action Position Statement will be available on the Prana website next week.

"The landscape has changed. Patients need and deserve a therapeutic solution based on strong science as well as clinical trials that translate the science into real benefits for patients. We believe that PBT2 will achieve this" concluded Mr. Kempler.

Discussions with potential sources of finance for the upcoming trial, both with investors and pharmaceutical partners, are progressing well and we will keep our shareholders updated.


* ADAS-Cog (Alzheimer's Disease Assessment Scale - cognitive subset) and NTB (Neuropsychological Test Battery) are tests given to Alzheimer's disease patients to measure changes in memory and Executive Function.



About Prana Biotechnology Limited
Prana Biotechnology was established to commercialise research into Alzheimer's Disease and other major age-related neurodegenerative disorders. The Company was incorporated in 1997 and listed on the Australian Stock Exchange in March 2000 and listed on NASDAQ in September 2002. Researchers at prominent international institutions including The University of Melbourne, The Mental Health Research Institute (Melbourne) and Massachusetts General Hospital, a teaching hospital of Harvard Medical School, contributed to the discovery of Prana's technology.

For further information please visit the Company's web site at www.pranabio.com.

[Fruehrentner]

New analysis of Prana’s Clinical Trial is published in the Journal
of Alzheimer’s Disease

PBT2 Rapidly Improves Cognitive Performance in Alzheimer’s Disease
Melbourne – 19 April 2010: Prana Biotechnology (NASDAQ:PRAN; ASX:PBT) today announced that the authoritative scientific journal, Journal of Alzheimer's Disease published an article on April 19 about Prana’s lead drug candidate for Alzheimer's disease, PBT2, providing new analysis that it is effective in reversing dementia symptoms. The analysis conducted by Professor Ashley Bush, of The Mental Health Research Institute and The University of Melbourne, Australia, is based on tracking and ranking the responses of each individual patient, rather than only groups of patients, in Prana’s PBT2’s Phase IIa Alzheimer’s disease clinical trial.
The results of the Phase IIa clinical trial, previously reported in The Lancet Neurology (July 2008 and an erratum in July 2009), showed that patients with mild Alzheimer’s Disease treated with 250mg of PBT2, experienced an overall statistically significant improvement in Executive Function on a Neuropsychological Test Battery (NTB) within 12 weeks of treatment.
“Improvements in Executive Function is strongly related to improvement in daily function and to the quality of the daily life of patients,” noted Dr Jeffrey Cummings, Director, Alzheimer Disease Research Center, UCLA, and Chairman of Prana’s Scientific Advisory Board.
"Very few drugs in clinical development have been able to bring these benefits to Alzheimer’s Disease patients. I am very encouraged by these findings,” concluded Dr Cummings.
The Journal of Alzheimer's Disease paper reports the results of a post-unblinding analysis of the cognitive data that was not included in the original paper. The objective of the analysis was to see how individual patients who were receiving PBT2 responded compared to the individual patients who only received placebo. Importantly, even placebo patients showed some improvement in the tests because of a ‘learning effect’ of repeated testing. This new analysis has adjusted for this and demonstrated that:
• 81% of patients on the 250mg dose of PBT2 responded better on the Executive Factor NTB score than the best performing patient on placebo.
• 41% of patients on the 250mg dose of PBT2 responded better on the overall Composite NTB score than the best performing patient on placebo (of which Executive Function is one of 2 parts).
Asking the specific question, ‘What is the probability that any patient who showed cognitive improvement was receiving PBT2?’, the paper reports there was a significant probability that:
• Patients who improved in Executive Function were probably receiving 250mg of PBT2 (p=1.3 x 10-9)
• Patients who improved their Composite NTB were probably receiving 250mg of PBT2(p=.0007)
Improvement in ADAS-Cog, a measure of memory and cognition, almost achieved a statistically significant level in the 12 week trial. Patients who improved their ADAS-Cog score were probably receiving 250mg of PBT2 (p=.056).
Professor Colin Masters of the Mental Health Research Institute and internationally acknowledged leader in Alzheimer’s Disease research, commented that: “These results are very exciting given that they were achieved in mild Alzheimer’s Disease sufferers in a relatively short period of time. Based on clinical trial outcomes to date, Prana’s therapeutic strategy stands up as one of the safest and most effective means of treating the disease.”
PBT2 targets the pathological interaction between A-beta and synaptic metal ions to prevent downstream toxic A-beta oligomer formation. PBT2 can also transfer metal ions otherwise trapped by A-beta oligomers into neurons, helping to promote normal memory function.

[bombastik]

Antwort auf Beitrag Nr.: 39.365.296 von Fruehrentner am 20.04.10 09:13:40

http://www.pranabio.com/downloads/Media%20Releases/Prana%20t…

[bombastik]

Prana Biotechnology soars on Alzheimer's trial data. Cadence re-submits NDA. After the bell, Array BioPharma flys on Novartis agreement
Written by BioMedReports.com Staff
Monday, 19 April 2010 16:26
Below is a list of the companies that made news in the healthcare sector on Monday, April 19, 2010.

Prana Biotechnology (NASDAQ:PRAN) (ASX:PBT) soared today after the company announced that the authoritative scientific journal, Journal of Alzheimer's Disease, published an article on April 19 about Prana's lead drug candidate for Alzheimer's disease, PBT2, providing new analysis that it is effective in reversing dementia symptoms. The analysis, conducted by Professor Ashley Bush of The Mental Health Research Institute and The University of Melbourne, Australia, is based on tracking and ranking the responses of each individual patient, rather than only groups of patients, in Prana's PBT2's Phase IIa Alzheimer's disease clinical trial.

The results of the Phase IIa clinical trial, previously reported in The Lancet Neurology (July 2008 and an erratum in July 2009), showed that patients with mild Alzheimer's Disease treated with 250mg of PBT2, experienced an overall statistically significant improvement in Executive Function on a Neuropsychological Test Battery (NTB) within 12 weeks of treatment.

"Improvements in Executive Function is strongly related to improvement in daily function and to the quality of the daily life of patients," noted Dr. Jeffrey Cummings, Director, Alzheimer Disease Research Center, UCLA, and Chairman of Prana's Scientific Advisory Board.

"Very few drugs in clinical development have been able to bring these benefits to Alzheimer's Disease patients. I am very encouraged by these findings," concluded Dr. Cummings.

The Journal of Alzheimer's Disease paper reports the results of a post-unblinding analysis of the cognitive data that was not included in the original paper. The objective of the analysis was to see how individual patients who were receiving PBT2 responded compared to the individual patients who only received placebo. Importantly, even placebo patients showed some improvement in the tests because of a 'learning effect' of repeated testing. This new analysis has adjusted for this and demonstrated that: 1) 81% of patients on the 250mg dose of PBT2 responded better on the Executive Factor NTB score than the best performing patient on placebo. 2) 41% of patients on the 250mg dose of PBT2 responded better on the overall Composite NTB score than the best performing patient on placebo.

Shares of Prana raced higher, surging $1.06 or 78.52%, closing the day at $2.41.
http://biomedreports.com/articles/most-popular/36492-rxnews-…

[Fruehrentner]

Melbourne, Australia - June 1, 2010:

Prana to Present Findings at the American Aging Association's 39th Annual Meeting in June 2010

Prana Biotechnology (ASX PBT NASDAQ PRAN) today announced that Professor Ashley Bush, Prana's co-founder and a member of the Company's R&D Advisory Board, will present at the 39th Annual Meeting of the American Aging Association (AGE) in Portland, Oregon on Monday, June 7th at 10:15 (PT) regarding the effects of PBT2 on Alzheimer's Disease sufferers as well as potential benefits for cognitive impaired aged individuals. The American Aging Association is a national not-for-profit organization whose aims are to promote biomedical aging studies directed towards increasing the functional life span of humans and to keep the public informed of progress of aging research.

According to Prof. Bush, "Based on our studies, we believe the PBT2 can be effective in reversing age-related cognitive decline in mice by restoring zinc flow in the synapse. Alzheimer's Disease exaggerates the loss of synaptic zinc homeostasis that occurs in age-related cognitive decline. Our data show that PBT2 can positively impact both conditions - Alzheimer's as well normal age-related cognitive decline - by a similar mechanism."

Based on clinical and laboratory studies, results have shown that PBT2 can transfer metal ions otherwise trapped by A-beta oligomers into neurons, helping to restore normal memory function. PBT2 also targets the pathological interaction between A-beta and synaptic metal ions to prevent toxic A-beta oligomer formation. Results of the Phase IIa clinical trial, previously reported in The Lancet Neurology (July 2008 and an erratum in July 2009) as well as the current edition of the Journal of Alzheimer's Disease, showed that patients with mild Alzheimer's Disease treated with 250mg of PBT2, experienced an overall statistically significant improvement in Executive Function on a Neuropsychological Test Battery (NTB), as well as a near-significant (p=0.056) improvement in ADAS-cog, within 12 weeks of treatment.

Unlike other approaches, Prana's PBT2 appears to both neutralize the neurotoxicity of A-beta while also facilitating its clearance from the brain. In addition, PBT2 helps to restore the balance of synaptic metals (copper and zinc) that are essential for normal neuronal function in the brain. An updated mechanism of action paper for PBT2 is available on Prana's website (www.pranabio.com).

Mr. Geoffrey Kempler, CEO of Prana, said, "We are pleased that Prof. Bush will be presenting our science and clinical data at the American Aging Association Conference. We believe that PBT2 has a unique mechanism of action among potential Alzheimer therapeutics, and we now are confident that this approach could be a potential therapeutic for patients with age-related cognitive impairment, a very common condition."

[Fruehrentner]

Melbourne - 21 June 2010:

Prana Biotechnology (ASX: PBT; NASDAQ: PRAN) today announced that Professor Ashley Bush, Prana's co-founding scientist and a member of the Company's R&D Advisory Board, has co-authored an article which was published in the online edition of Progress in Neurobiology.

Professor Bush, who is based at The Mental Health Research Institute of The University of Melbourne, Australia, said "This publication provides a comprehensive review of the literature and science on the role of metals in the pathogenesis of Alzheimer's Disease."

Progress in Neurobiology is an authoritative, peer-reviewed scientific journal, designed to help individuals keep abreast of advances in knowledge in the broad field of neurosciences through the publication of global scientific reviews by leading researchers.

The article is entitled, "Biological metals and Alzheimer¹s disease: Implications for therapeutics and diagnostics.", and the reference is Prog. Neurobiol. (2010), doi:10.1016/j.pneurobio.2010.04.003, by Duce, J.A., Bush, A.I.

The review describes the importance of biochemically relevant transition metals in the brain; zinc, copper and iron and the observed changes in the distribution of these metals in the ageing brain and the brains of Alzheimer's Disease (AD) patients. The review documents the many roles of altered metal distribution or homeostasis in the AD brain including A-beta degradation, production of toxic species of A-beta and phosphorylation of tau and drug strategies targeting these metals.

Mr. Geoffrey Kempler, CEO of Prana, said, "Professor Bush's article synthesizes 20 years of published data in the field and provides an important review of the role of metals in Alzheimer's Disease for anyone wanting to better understand the potential of Prana's MPACs (Metal Protein Attenuating Compounds). This publication complements the Mechanism of Action of PBT2 Position Statement that is available on Prana's website (www.pranabio.com) to provide an understanding of the scientific basis for disease-modifying MPAC's such as Prana's PBT2, under development to treat Alzheimer's Disease


#####

About Prana Biotechnology Limited
Prana Biotechnology was established to commercialise research into Alzheimer's Disease and other major age-related neurodegenerative disorders. The Company was incorporated in 1997 and listed on the Australian Stock Exchange in March 2000 and listed on NASDAQ in September 2002. Researchers at prominent international institutions including The University of Melbourne, The Mental Health Research Institute (Melbourne) and Massachusetts General Hospital, a teaching hospital of Harvard Medical School, contributed to the discovery of Prana's technology.

For further information please visit the Company's web site at www.pranabio.com.

Contacts:
Prana Biotechnology Limited
[phone]

[Fruehrentner]

Ein Wettbewerber gibt auf:

Eli Lilly to stop Alzheimer drug semagacestat development
Published: 18-Aug-2010

Eli Lilly and Company is set to stop semagacestat development as preliminary results from two ongoing long-term Phase III studies showed it did not slow Alzheimer's progression.

According to Eli Lilly, semagacestat, a gamma secretase inhibitor being studied as a potential treatment for Alzheimer's disease, was also associated with worsening of clinical measures of cognition and the ability to perform activities of daily living.

Semagacestat Phase III trials compared the drug with placebo in patients with mild-to-moderate Alzheimer's disease.

Eli Lilly has now reviewed data from a pre-planned interim analysis of semagacestat studies which demonstrated that cognition and the ability to complete activities of daily living of placebo-treated patients worsened.

Eli Lilly, as part of safety measures, is instructing clinical trial investigators for all Semagacestat studies to contact study participants as soon as possible and tell them to immediately stop taking the study drug they have received.

Although dosing with Semagacestat is being stopped, Eli Lilly said that it plans to continue collecting safety data, including cognitive scores, for at least six months through regularly scheduled follow-up visits with study physicians and modifications of the existing Phase III protocols.

[Fruehrentner]

New evidence strongly supports Prana's therapeutic strategy to regulate brain metals

Melbourne - September 3, 2010: Prana Biotechnology (NASDAQ: PRAN; ASX: PBT) today announced that Professor Ashley Bush, a co-founding scientist of Prana and a member of the Company's R&D Advisory Board, has in conjunction with the University of Melbourne, Australia, and Harvard Medical School, Boston, published an article that appears online today entitled: "Iron-export ferroxidase activity of beta-amyloid precursor protein is inhibited by zinc in Alzheimer's Disease" scheduled for the September 17 edition of Cell, the prestigious peer-reviewed, international biological research journal.

Prana's therapeutic strategy is to restore normal metal levels and distribution in the brain, such as zinc, which typically changes with aging and is exacerbated in Alzheimer's Disease, resulting in (i) reduced synaptic function and (ii) beta-amyloid reacting with the metals to form toxic oligomers that impair cognition.

The Cell publication now adds a third metal-dependent event, iron accumulation, which if left untreated, contributes to neuronal death in the Alzheimer's brain.

Sam Gandy, M.D Ph.D, Mount Sinai School of Medicine, New York, described this report, as "providing a major advance in deciphering the underlying causes of Alzheimer's Disease while at the same time pointing us toward a new and exciting strategy for treating or preventing the disease with a drug such as PBT2, which affects brain metals."

The evidence published in Cell shows that the source of beta-amyloid, the beta- amyloid precursor protein (APP), plays a hitherto unknown critical role in exporting iron out of neurons. If APP fails to carry out this role, iron builds up in the neurons contributing to oxidative stress, neurofibrillary tangle formation and ultimately neuronal cell death. Importantly, Prana scientists have demonstrated that synaptic zinc can prevent APP from performing its normal iron transporting role. Synaptic zinc levels and distribution changes in the Alzheimer's diseased brain, because zinc released into the synaptic space is drawn into the beta-amyloid that forms plaques in the synapse. This is problematic for the brain because neurons are deprived of the zinc required for neurotransmission and the zinc induces toxic beta-amyloid oligomer formation. Moreover, as now indicated by the Cell publication, the zinc caught up in the beta-amyloid can be exchanged or transported to the APP, impeding its ability to prevent iron buildup in neurons. Accordingly, the maintenance of correct zinc levels in the brain is vital for neuronal function and ultimately cognition.

Prana's lead Alzheimer's drug, PBT2 acts as a zinc chaperone that transports zinc from the brain beta-amyloid deposits and returns it to neurons to facilitate normal neurotransmission. PBT2 has also recently been shown to have important neuroprotective and neurotrophic properties, consistent with its ability to prevent zinc from impairing the ability of APP to prevent iron overload.

Dr Rudolph Tanzi of Harvard Medical School, a Prana co-founding scientist and co-author of the Cell paper commented that "these findings are timely in distinguishing PBT2's unique mechanism of action from the recent clinical trial failures that target amyloid but did not address the need to restore synaptic metal homeostasis". PBT2 has completed a Phase 2a clinical trial where it significantly increased the cognitive performance of patients with Alzheimer's Disease after only 12 weeks of treatment.

Mr. Geoffrey Kempler, Executive Chairman of Prana, said, "The report is the most comprehensive validation to date of the importance of brain metals, which are the key therapeutic target of PBT2, in treating Alzheimer's Disease. These new findings strengthen the expectation that PBT2 will reverse brain damage in Alzheimer's Disease, and raise hopes that it will achieve further success in the next stage of clinical trials".

###


About Prana Biotechnology Limited
Prana Biotechnology was established to commercialise research into Alzheimer's Disease, Huntington's Disease and other major age-related neurodegenerative disorders. The Company was incorporated in 1997 and listed on the Australian Stock Exchange in March 2000 and listed on NASDAQ in September 2002. Researchers at prominent international institutions including The University of Melbourne, The Mental Health Research Institute (Melbourne) and Massachusetts General Hospital, a teaching hospital of Harvard Medical School, contributed to the discovery of Prana's technology.

For further information please visit the Company's web site at www.pranabio.com.

About CELL

Cell publishes high impact papers that have come to form the foundation of contemporary life science research. Cell is at the forefront of exciting developments in biology, continually redefining the important areas of science with cutting edge papers.
For further information visit the Cell website at www.cell.com


Forward Looking Statements
This press release contains "forward-looking statements" within the meaning of section 27A of the Securities Act of 1933 and section 21E of the Securities Exchange Act of 1934. The Company has tried to identify such forward-looking statements by use of such words as "expects," "intends," "hopes," "anticipates," "believes," "could," "may," "evidences" and "estimates," and other similar expressions, but these words are not the exclusive means of identifying such statements. Such statements include, but are not limited to any statements relating to the Company's drug development program, including, but not limited to the initiation, progress and outcomes of clinical trials of the Company's drug development program, including, but not limited to, PBT2, and any other statements that are not historical facts. Such statements involve risks and uncertainties, including, but not limited to, those risks and uncertainties relating to the difficulties or delays in financing, development, testing, regulatory approval, production and marketing of the Company's drug components, including, but not limited to, PBT2, the ability of the Company to procure additional future sources of financing, unexpected adverse side effects or inadequate therapeutic efficacy of the Company's drug compounds, including, but not limited to, PBT2, that could slow or prevent products coming to market, the uncertainty of patent protection for the Company's intellectual property or trade secrets, including, but not limited to, the intellectual property relating to PBT2, and other risks detailed from time to time in the filings the Company makes with Securities and Exchange Commission including its annual reports on Form 20-F and its reports on Form 6-K. Such statements are based on management's current expectations, but actual results may differ materially due to various factions including those risks and uncertainties mentioned or referred to in this press release. Accordingly, you should not rely on those forward-looking statements as a prediction of actual future results.


Contacts:

Prana Biotechnology Limited
[phone]

Kyahn Williamson
Buchan Consulting
[phone]
[e-mail]

[Fruehrentner]

Melbourne, Australia - 8 November 2010:

Prana Biotechnology has today announced it has received confirmation that a re-elected Victorian Labor Government would commit $15 million to the Mental Health Research Institute (MHRI) as crucial funding toward the commencement of a large scale trial of PBT2. MHRI is Prana Biotechnology's long standing partner in Alzheimer's research and PBT2 is its lead compound for the treatment of Alzheimer's and Huntington's Disease.

The grant would go towards the further development of PBT2 by Prana, including a clinical trial involving 525 patients with mild to moderate Alzheimer's Disease, treated for twelve months. The study is aimed to confirm the results received in an earlier trial. The company is seeking further funding to run the trial. PBT2 has already demonstrated very promising results in an earlier Phase IIa trial, which in just 12 weeks showed significant improvement in cognitive tests that measure executive function in Alzheimer's patients.

"At a time when so many Alzheimer's drug candidates have failed, PBT2 has delivered positive results and has generated a great deal of interest in the global scientific community. The funding will come at a very important time for Prana and it is another vote of confidence in the promise of this drug," said Mr. Geoffrey Kempler, CEO of Prana Biotechnology.

"This grant money would be used in a crucial stage of the development of PBT2. It would enable Prana to proceed with the planned Phase IIb trial in a larger clinical setting. We hope to build on the positive clinical results we've already achieved and take us one step closer to delivering a new treatment for Alzheimer's. This will be welcome news for the many people touched by the disease."

PBT2 is a novel and exciting treatment for Alzheimer's Disease, a degenerative disease that is the fourth largest killer of adult Australians. PBT2 works by correcting an imbalance of metals in the ageing brain. Scientists believe this imbalance is one of the underlying causes of Alzheimer's Disease and other neurodegenerative conditions. PBT2 offers a unique therapeutic strategy in the treatment and ultimate modification of the disease process. Prana's research has won strong praise from leading scientists including Sir Gustav Nossal, a world renowned research biologist and former winner of the Albert Einstein World Award for Science, who describes Prana's research as "one of the iconic discoveries in Australian medical and health research".

The $15 million grant, conditional on the re-election of the Brumby Government, is significant to a biotechnology company such as Prana and represents a strong endorsement of the world-leading work being undertaken by Prana. The company's deep pipeline includes Alzheimer's Disease, Huntington's Disease, Parkinson's Disease, and brain cancer, all of which have the potential to produce new treatments based on Prana's world leading technology. It also ensures that the pioneering work of Prana will remain in Victoria.

International scientists have applauded the Brumby Government's commitment to this research, saying it will put Victoria at the forefront of development in this area. Rudolph E. Tanzi, Ph.D., the Joseph P. and Rose F. Kennedy Professor of Neurology, at Harvard Medical School said: "The combined preclinical and clinical data on PBT2 leads me to believe that PBT2 has the best chance of all currently available potential competitors to be the first effective disease modifying treatment for Alzheimer's Disease. The Victorian Premier deserves congratulations for pledging this funding".

[Fruehrentner]

$4 million (AUD) grant to study the mechanism of MPACs including PBT2

Melbourne - March 4, 2011 :

Prana Biotechnology (NASDAQ: PRAN; ASX: PBT) today announced that Professor Ashley Bush, Prana's Co-Founding Scientist, has been awarded a National Health and Medical Research Council (NHMRC) Australia Fellowship. The $4 million (AUD) award was announced by Australia's Federal Minister for Mental Health and Ageing, The Hon Mark Butler MP. The Australia Fellowships are Australia's most prestigious award for excellence in the fields of health and medical research and recognise those researchers with the vision and application to tackle some of the biggest health issues facing society today.

Prana's Executive Chairman, Geoffrey Kempler, said, "We are thrilled for Professor Bush and congratulate him on this award. His work was peer reviewed at the highest level and this government recognition underscores the effort by Prana to develop a library of MPACs (Metal Protein Attenuating Compounds) like PBT2 to treat neurodegenerative diseases."

Professor Bush said, "The $4 million grant will allow us to extend our understanding of the underlying causes of neurodegenerative disease including how MPACs could work as therapies for diseases such as Alzheimer's and Huntington's, as well as the cognitive decline that can accompany the ageing process. I am honoured and greatly encouraged by this grant."

About Prana Biotechnology Limited
Prana Biotechnology was established to commercialise research into age-related neurodegenerative disorders. The Company was incorporated in 1997 and listed on the Australian Securities Exchange in March 2000 and listed on NASDAQ in September 2002. Researchers at prominent international institutions including The University of Melbourne, The Mental Health Research Institute (Melbourne) and Massachusetts General Hospital, a teaching hospital of Harvard Medical School, contributed to the discovery of Prana's technology.

For further information please visit the Company's web site at www.pranabio.com.

[Fruehrentner]

Melbourne - March 9, 2011

Prana Biotechnology (NASDAQ: PRAN; ASX: PBT) today announced that the Company is scheduled to present at the Cowen and Company Health Care Conference in Boston taking place from March 7th through March 9th, 2011

Executive Chairman Geoffrey Kempler will give a presentation discussing corporate developments and the current status of Prana's clinical trials. The presentation will begin at 11:00 a.m. (EST) on Wednesday, March 9th, 2011 followed by a question and answer session. A copy of the Prana presentation can be viewed on Prana's website www.pranbio.com

For further information please visit the Company's web site at www.pranabio.com.

[Fruehrentner]

MELBOURNE, Australia - March 15, 2011

Prana Biotechnology Limited (NASDAQ: PRAN / ASX: PBT), announced that its Head of Research, Assoc. Prof. Robert Cherny, is presented new data on PBT434, the Company's lead compound in pre-clinical development for Parkinson's Disease on March 12th at the 10th International Conference on Alzheimer's and Parkinson's Diseases in Barcelona. The oral presentation is entitled, "PBT434: A Novel Neuroprotective Drug for PD". The presentation will be available later today on Prana's website www.pranabio.com

Prana previously announced the election of PBT434 as its lead drug candidate in September 2010, when the first efficacy data with the drug was published at the World Parkinson's Congress. Importantly, unlike most other PD drugs on the market or in development today, PBT434 does not artificially manipulate levels of the neurotransmitter dopamine. Dopamine controls motor function, and when the cells that produce dopamine, the substantia nigra, die motor control and function are diminished. Instead, PBT434 works upstream by preventing the initial cascade of substantia nigral cell loss, and the subsequent loss of motor function. The presentation included data from three different animal models supporting the disease modification therapeutic strategy of the drug.

PBT434 is derived from Prana's 600 strong library of Metal Protein Attenuating Compounds (MPACs) that have been developed as neurologically active, brain penetrant, orally available compounds targeting neurodegeneration.

Geoffrey Kempler, Prana's Executive Chairman commented, "What is so exciting about the development of PBT4343 for Parkinson's Disease is that we hope the drug will treat patients from early diagnosis and minimize dependence on dopamine supplementation which becomes difficult to manage and often ineffective as the disease advances."

[Fruehrentner]

PLoS ONE publication on PBT2 consolidates the underlying mechanisms for the preclinical and clinical benefits of PBT2 in Alzheimer's Disease

Melbourne - 21 March, 2010

Prana Biotechnology (NASDAQ:PRAN; ASX:PBT) today announced the publication of new data on the ability of PBT2 to repair the damage in an Alzheimer's affected brain thereby facilitating the restoration of cognition in Alzheimer's Disease (AD).

The findings help to explain the rapid improvement in cognition previously reported in transgenic Alzheimer's mice* and in patients in a Phase IIa clinical trial with PBT2**. The article published in the science journal PLoS ONE is entitled "Metal Ionophore Treatment Restores Dendritic Spine Density and Synaptic Protein Levels in a Mouse Model of Alzheimer's Disease".

The authors led by Dr Paul Adlard, Head of The Synaptic Neurobiology Laboratory at The Mental Health Research Institute, describe the biochemical and anatomical changes occurring in the brains of transgenic*** Alzheimer's mice treated with PBT2.

After 11 days of treatment, the brains of the Alzheimer's mice showed a statistically significant increase in the numbers of spines on the branches (or dendrites) of neurons in the hippocampus, a memory centre specifically affected in AD. Increasing the number of spines is important as this permits many more neurons to interconnect with any particular neuron thereby increasing the brain's capacity to carry out learning and memory functions.

Importantly, these anatomical changes to the hippocampus were also accompanied by increased levels in key proteins**** involved in learning, memory and neuronal growth. The levels of many of these proteins were restored to the levels seen in healthy, cognitively normal animals.

"The ability of PBT2 to promote the forming and reforming of connections between neurons is fundamental to the repair of brain tissue damaged by AD, and the expression of key neuronal receptors and signaling proteins indicates that the repaired tissue is functional" noted Prana's Head of Research, Associate Professor Robert Cherny.

In a series of parallel experiments, the authors also administered PBT2 to cultured neurons. In these in vitro experiments, PBT2 was able to elicit elongation of 'arm like' projections from the immature developing neurons called neurites. These projections can ultimately mature into either axons or dendrites of an adult neuron. Significantly, the changes observed in the in vitro experiments were strictly dependent on the presence of copper or zinc in the growth medium, confirming that the restorative effect of PBT2 is due to its ability to deliver these metals to deficient neurons.

It has previously been shown that PBT2 neutralises the toxicity of the Alzheimer's Abeta protein by preventing the formation of toxic aggregates or oligomers*. These new results further explain how PBT2 can achieve such rapid improvements in cognition: by liberating copper and zinc trapped in amyloid deposits and returning those essential metals to neurons, where they are needed for normal function.

"These findings further demonstrate the unique combination of detoxification and neuronal restoration provided by PBT2 that underlie cognitive improvement in the clinic," concluded Dr Cherny.

* Adlard et al. Neuron (2008) vol. 59, pp. 43-55
**Lannfelt et al. Lancet Neurology (2008) vol. 7, pp. 779-86; Lannfelt et al. Lancet Neurology (2009) vol. 8, pp. 981.
*** The AD transgenic mouse model is the Tg2576
**** These proteins include different subtypes of NMDA receptors, which are known to be depleted in AD, the signaling protein CamKII, and TrkB, and the receptor for Brain Derived Neurotrophic Factor.


About Prana Biotechnology Limited
Prana Biotechnology was established to commercialize research into age-related neurodegenerative disorders. The Company was incorporated in 1997 and listed on the Australian Securities Exchange in March 2000 and listed on NASDAQ in September 2002. Researchers at prominent international institutions including The University of Melbourne, The Mental Health Research Institute (Melbourne) and Massachusetts General Hospital, a teaching hospital of Harvard Medical School, contributed to the discovery of Prana's technology.

For further information please visit the Company's web site at www.pranabio.com.

[Fruehrentner]

Melbourne, Australia - 23 March 2011:

Prana Biotechnology Limited (NASDAQ: PRAN / ASX: PBT), today announced that it entered into a definitive agreement on 23 March 2011, to sell securities to institutional investors in a private placement for aggregate gross proceeds of approximately A$6,120,000 (US$6,190,992). The closing of the offering is expected to occur on or about 25 March, 2011 and is subject to the satisfaction of customary closing conditions.

The Company intends to use the proceeds of the private placement for ongoing and future research programs into the development of the Company's proprietary compounds, including its lead compound PBT2, and for working capital purposes.
Under the terms of the offering, the Company will sell an aggregate of approximately 27,200,000 ordinary shares (equivalent to 2,720,000 ADRs) at a price of A$0.225 per share (A$2.25 per ADR). The Company also agreed to grant to the investors options to purchase up to an aggregate of approximately 6,800,000 ordinary shares (equivalent to 680,000 ADRs) at an exercise price of A$$0.225 per share (A$2.25 per ADR). The options are exercisable for a term of four years, and the exercise price is subject to future adjustment for various events, such as stock splits or dividend distributions. The securities offered and sold in the private placement have not been registered under the Securities Act of 1933, as amended, or any state securities laws, and may not be offered or sold in the United States absent registration, or an applicable exemption from registration under the Securities Act and applicable state securities laws.
Rodman & Renshaw, LLC (NASDAQ:RODM), a wholly-owned subsidiary of Rodman & Renshaw Capital Group, Inc., acted as the exclusive placement agent for the offering.
This press release shall not constitute an offer to sell or the solicitation of an offer to buy securities.

[ikarusfly]

wie blöd ist den das management????? ein pp zu 2,25$ ausgeben wenn man auch locker 3$ bekommen hätte.. vorallem stand der kurs zu der zeit bei 3,75

biotechunternehmen sind schon risikoreich....aber mit einem unfähigem management dazu , keine überlebenschance

[Fruehrentner]

Wird schon seine Gründe haben, denke ich.

[Fruehrentner]

Prana's PBT2 Phase II trial receives funding from Alzheimer's Drug Discovery Foundation

31.03.2011 02:28:23

Melbourne - 31 March, 2010: The New York based Alzheimer's Drug Discovery Foundation (ADDF) and Prana Biotechnology (NASDAQ: PRAN; ASX: PBT) today jointly announced that the ADDF will provide Prana with a mission-related investment of US$700,000 over two years to conduct a clinical trial investigating the potential of PBT2 to reduce the accumulation of beta-amyloid in the brain of people with Alzheimer's Disease (AD). Beta-amyloid is thought to be a cause of brain cell death and dementia in Alzheimer's Disease. The Phase II study will enroll 40 patients with mild AD for 12 months, with Positron Emission Tomography (PET) amyloid neuroimaging and other biomarkers as the primary outcome measures.

Howard Fillit, MD, the ADDF's Executive Director commented that "PBT2 stands out as one of the few orally available agents with clinical trial evidence of cognitive benefit for Alzheimer's patients. If this Phase II trial is successful, it will further demonstrate target engagement by PBT2 in the brain of people with Alzheimer's Disease. It is hoped that these additional data will accelerate the clinical development of PBT2 to patients".

Previously PBT2 demonstrated a significant decrease in beta-amyloid in the cerebrospinal fluid and significantly improved executive function in mild Alzheimer's Disease patients within three months of treatment*. The ADDF funded Phase II study will ask the question, 'what is happening to the amyloid burden of these patients using the same dose that previously resulted in cognitive improvements, and is this change sustainable?' Since the number of patients in the study is relatively small, cognitive function will be included as a secondary outcome measure.

"We are honored to be selected for funding by the ADDF, an organization that is internationally recognized as supporting some of the most ground breaking drug discovery and development research today in Alzheimer's Disease," said Mr. Geoffrey Kempler, Prana's Executive Chairman. "The trial will advance our understanding of PBT2's potential mechanism of action for disease modification in humans, a critical step forward that complements our strategic plan to advance PBT2 through clinical trials for the treatment of both Alzheimer's and Huntington's Disease."

The Phase II trial is planned to commence in Australia in the second half of 2011. It will recruit patients with mild Alzheimer's Disease who have demonstrated evidence of amyloid burden in the brain by PET-amyloid imaging.
*Lannfelt et al. Lancet Neurology (2008) vol. 7, pp. 779-86; Lannfelt et al. Lancet
Neurology (2009) vol. 8, pp. 981.

About the Alzheimer's Drug Discovery Foundation (ADDF)
The ADDF (www.alzdiscovery.org) is the only public charity whose sole mission is to accelerate the discovery and development of drugs to prevent, treat and cure Alzheimer's Disease, related dementias and cognitive aging. Since 1998, the ADDF has granted more than $45 million to fund over 325 Alzheimer's drug discovery programs in academic centers and biotechnology companies in 17 countries.
For more information about the ADDF or to speak with Dr. Fillit, please contact Filomena Machleder at 212-901-8004 or [e-mail].

[Fruehrentner]

MELBOURNE, Australia - April 11th, 2011:

Prana Biotechnology (ASX: PBT; NASDAQ: PRAN) today announced that it has secured a key PBT2 patent in Japan. The Japanese Patent Office has granted a composition of matter patent for Prana'slead clinical asset, PBT2 and other selected 8-Hydroxyquinoline compounds in Japan. The patent entitled '8-Hydroxyquinoline derivatives' also covers pharmaceutical compositions containing PBT2 and selected 8-hydroxyquinoline compounds and the use of the compounds for the treatment of Alzheimer's Disease.

Geoffrey Kempler, Prana's Executive Chairman, said "This decision by the Japanese Officeto grant a claim to PBT2 completes a suite of core patent rights protecting this asset in key markets including the United States, Europe, Japan and Australia, further bolstering our commercialization plans in both Huntington's and Alzheimer's Disease".

The Japanese patent has a twenty year term expiring on 16 July 2023, with a possible extension of term of up to 5 years under pharmaceutical protectionprovisions. Importantly there is no post-grant opposition process in Japan whereby third parties can register objections following this decision. In 2010, the company announced the grant of similar claims in Europe and the decision of the United States Patent Office to extend the term of the patent granted in the United States**.

PBT2 was selected from Prana's Metal Protein Attenuating Compound (MPAC) library as its lead development compound in Alzheimer's Disease in 2004 and has since successfully completed Phase I and Phase IIa* trials. The MPAC library has expanded and matured to generate over 600 novel, neurologically active compounds with leads in Parkinson's Disease, brain cancer and other potential neurological indications. Geoffrey Kempler noted, "Generating patentable and differentiated MPACs is the foundation of Prana's therapeutic pipeline".

*Lannfeltet al. Lancet Neurology (2008) vol. 7, pp. 779-86; Lannfeltet al. Lancet Neurology (2009) vol. 8, pp. 981.
** Patent term in the United States is calculated as 21 December 2025 which may be extended by the application of pharmaceutical extension of term provisions. In Europe the patent term, as for Japan, is to 16 July 2023 with possible extension of term of up to 5 yearsunder pharmaceutical extension provisions.

[Fruehrentner]

Melbourne - 20 April 2011:

Prana Biotechnology (NASDAQ: PRAN; ASX: PBT) today announced its business strategy to accelerate development of its lead asset, PBT2. The strategy, that now includes Huntington's Disease, should enable Prana to target market approval for PBT2 several years sooner than previously planned and at considerably less cost.

The company has designed a Phase II placebo controlled double blind study in 100 mild Huntington's Disease (HD) patients, in Australia and the US, treated over 6 months. This trial will be conducted in parallel, to the previously announced 12 month Phase II brain imaging study in 40 mild Alzheimer's Disease (AD) patients, in Australia, supported by the US based Alzheimer's Drug Discovery Foundation. Recruitment for both trials is planned to commence in the second half of the year.

"We are excited by this strategy because from a commercial perspective these diseases are very complimentary. From our earlier Alzheimer's trial we showed that PBT2 significantly improves cognitive executive function. This is very relevant to Huntington's Disease given that these patients also suffer cognitive decline, for which there is no marketed treatment available. Success in the trial that we have announced today will position PBT2 as a frontrunner in the treatment of Huntington's Disease. We believe that PBT2 can bring the same cognitive benefits to Huntington's Disease patients that it did to Alzheimer's Disease patients" commented Mr Geoffrey Kempler, Prana's Executive Chairman.

"Because Huntington's Disease is a relatively uncommon disease, it is classed as an 'orphan indication' by regulators, a status that typically confers accelerated regulatory review by authorities and faster approval to market. That also means the cost will be considerably less" added Mr Kempler.

The Huntington's Disease Market

HD is a genetically inherited neurodegenerative disease resulting in severe motor dysfunction and cognitive decline. It affects 30,000 people in the US and about 70,000 worldwide. The only treatment currently approved for the disease only targets some of the motor loss symptoms and sells approx. $250 million pa. There are no drugs in development that have established clinical evidence for treating cognitive decline. Prana aims, in this trial, to demonstrate the same cognitive benefits for HD patients that it has already demonstrated in AD patients treated with PBT2. A treatment for HD that addresses the underlying progression of the disease could generate sales of 750 million to $1 billion pa.

What benefits has PBT2 already shown

In a Phase IIa trial of PBT2 in mild Alzheimer's Disease*, cognitive executive function was significantly improved in patients. Recently the company published that PBT2 was able to directly restore neurons critical to cognition in mouse models. In particular it was demonstrated that PBT2 increased the number of spines on the branches (or dendrites) of neurons, an important means of permitting many more neurons to interconnect with any particular neuron thereby increasing the brain's capacity to carry out learning and memory functions.

These findings pointing to the ability of PBT2 to restore cognition in degenerative conditions, together with positive data achieved with PBT2 in mouse models of Huntington's Disease** provide confidence that PBT2 will be able to confer cognitive benefit to patients with HD and AD.

What Alzheimer's and Huntington's diseases have in common

Mechanistically, both AD and HD appear to involve a protein that combines with brain metals to become toxic. In Alzheimer's, Prana scientists believe that the formation of toxic A-beta protein oligomers leading to impaired synaptic function, is a metal dependent event. In Huntington's recent publications*** indicate that copper is critical in the formation of toxic oligomers of the Huntington's Disease protein, huntingtin, that causes the brain degeneration in HD patients.

"The demonstration that PBT2, a Metal Protein Attenuating Compound (MPAC) can redress metal imbalances in the brain and intercede in toxic oligomer formation offers a very promising therapeutic strategy to tackle Huntington's Disease" commented Dr Robert Cherny, Prana's Head of Research.

* Lannfelt et al. Lancet Neurology (2008) vol. 7, pp. 779-86; Lannfelt et al. Lancet Neurology (2009) vol. 8,
pp. 981.
*Faux et al. J. Alzheimer's Disease 20 (2010) pp. 509-516
**Presented at the International Conference on Alzheimer's Disease, Honolulu Hawaii, 2010.
*** Fox et al. J. Bio. Chem. published as manuscript M110.199448 http://www.jbc.org./cgi/doi/10.1074/jbc.M110.199448

[Fruehrentner]

Prana's Founding Scientists Present Findings at World Pharma Congress

Professor Rudy Tanzi and Professor Ashley Bush highlight promise of Prana's Drugs for Alzheimer's, Huntington's, and Parkinson Diseases

Melbourne - June 8, 2011: Prana Biotechnology (NASDAQ: PRAN; ASX: PBT) today announced that Co-Founding Prana Scientists, Rudolph Tanzi and Ashley Bush will discuss the latest information and insights about Prana's drug therapies for Alzheimer's, Huntington's and Parkinson's Diseases at the World Pharma Congress taking place in Philadelphia this week.

Rudy Tanzi, Joseph P. and Rose F. Kennedy Professor of Neurology, Harvard University, presented on Tuesday, June 7, a summary of recent findings regarding the genes that influence risk for Alzheimer's disease and the biological systems they implicate for drug discovery. Prof. Tanzi discussed why he believes that clearing excess amyloid beta protein from the brain is the best way forward for treating and preventing Alzheimer's disease and that Prana's PBT2 provides the most promising solution to safely and efficaciously clear amyloid beta protein from the brain while also correcting harmful metal imbalances caused by the deposition of excess beta-amyloid in the brain.

Professor Ashley Bush, the Australian Research Council Federation Fellow at the Mental Health Research Institute of Victoria (Australia), will speak about Prana's therapeutic approach to neurodegenerative disease. On Wednesday June 8th, Professor Bush will discuss the subject of "Synaptic Zinc as a Pharmacological Target in Alzheimer's Disease". In this talk he will describe the therapeutic value of PBT2 in Alzheimer's disease and Huntington's disease, disorders linked by deposits of aggregated protein and brain metal imbalance. On June 9th at the same venue, he will describe the actions of Prana's lead Parkinson's drug PBT434 in a talk entitled "Tau and DJ-1: Insights into the Mechanism of Action of PBT434 in Parkinson's Disease Mouse Models".

For more information, see: http://www.worldpharmacongress.com

[Fruehrentner]

Prana's PBT2 presented at the Huntington's Disease Society of America National Convention

Melbourne - June 28, 2011: Prana Biotechnology (NASDAQ: PRAN; ASX: PBT) today announced that information on PBT2 for the treatment of HD was presented at the HDSA annual National Convention held in Minneapolis, Minnesota over the weekend. Dr Steve Hersch, Associate Professor of Neurology at MGH and Harvard Medical School, and Director of the Huntington's Disease Center of Excellence and the Laboratory of Neurodegeneration and Neurotherapeutics presented* scientific and clinical information on PBT2 and Prana's development plans in Huntington's Disease (HD).

"We are delighted to have the opportunity to introduce Prana and the scientific strategy behind PBT2 to the broader HD community" commented Geoffrey Kempler, Prana's Executive Chairman, "We are hopeful that PBT2 can bring the same cognitive benefits to HD patients that it did to Alzheimer's Disease (AD) patients in a Phase IIa trial."

What benefits has PBT2 already shown

In a Phase IIa trial** of PBT2 in mild AD, cognitive executive function was significantly improved in patients. Recently the company published that PBT2 was able to directly restore neurons critical to cognition in mouse models. In particular it was demonstrated that PBT2 increased the number of spines on the branches (or dendrites) of neurons, an important means of permitting many more neurons to interconnect with any particular neuron thereby increasing the brain's capacity to carry out learning and memory functions.

These findings pointing to the ability of PBT2 to restore cognition in degenerative conditions, together with positive data achieved with PBT2 in mouse models of HD***
provide confidence that PBT2 will be able to confer cognitive benefit to patients with HD and AD.

Plans for a Phase II study in HD patients.

Prana is progressing its plans for a Phase II placebo controlled double blind study in 100 mild HD patients, in Australia and the US, treated over 6 months this year. The study will investigate a number of key parameters including cognitive, motor and functional changes over the study duration. In parallel, as previously announced, Prana is progressing plans for a 12 month Phase II brain imaging study in 40 mild AD patients in Australia.

* The HDSA presentation will be posted on Prana's website by the end of this week, www.pranabio.com.
** Lannfelt et al. Lancet Neurology (2008) vol. 7, pp. 779-86; Lannfelt et al. Lancet Neurology (2009) vol. 8,
pp. 981. Faux et al. J. Alzheimer's Disease 20 (2010) pp. 509-516
***Presented at the International Conference on Alzheimer's Disease, Honolulu Hawaii, 2010.

[Fruehrentner]

Melbourne - June 30th, 2011:

Prana Biotechnology Limited (NASDAQ : PRAN; ASX: PBT) announced today that leading global clinical research provider Quintiles will purchase shares in Prana for a total subscription of US$1,000,000. The funding will be used in support of Prana's recently announced business strategy to accelerate the clinical development of PBT2 through Phase II trials of Huntington's Disease and Alzheimer's Disease to be initiated this year.

Investment by Quintiles

Quintiles has been closely involved with Prana for a number of years and acted as the clinical research partner for Prana's last successful clinical trial. To date, the activities of Prana have been supported by Quintiles via:

1) The acquisition of US$1 million of ordinary Prana shares in June 2010 at an issue price of AU$0.1624 (16.24 cents per share) raising AU$1.15 million.

2) Today's announced purchase of US$1 million of new ordinary Prana shares at an issue price of AU$0.225 (22.5 cents per share). Quintiles will also receive an option to purchase a fully paid share at an exercise price of AU$0.225 for every four ordinary shares received by Quintiles under the placement.

"Prana is delighted to have the continued support of Quintiles as a significant shareholder and supporter of Prana's therapeutic goals. Their endorsement means a great deal to us," said Mr. Geoffrey Kempler, Prana's Executive Chairman.

[Fruehrentner]

Melbourne - July 14, 2011

Prana Biotechnology Limited (NASDAQ : PRAN; ASX: PBT) today announced that it has filed a prospectus supplement to sell up to an aggregate 50,000,000 ordinary shares, represented by 5,000,000 American Depositary Shares (ADSs) through an "at-the-market" (ATM) offering. If utilized, the ADSs would be offered through McNicoll, Lewis & Vlak LLC (MLV) as sales agent who, at Prana's discretion and instruction, will use its commercially reasonable efforts to sell the ADSs at market prices from time to time, including sales made by means of ordinary brokers' transactions on the NASDAQ Capital Market.

Prana currently intends to use the proceeds from any sales related to the ATM offering primarily for ongoing and future research programs into the development of its proprietary compounds, including its lead compound PBT2, and for working capital purposes. Prana intends to commence a Phase II imaging trial for PBT2 in Alzheimer's disease patients and a Phase II trial for PBT2 in Huntington's disease patients later this year.

Sales in the ATM offering, if any, would be made pursuant to the prospectus supplement dated July 13, 2011, which supplements the company's prospectus dated May 31, 2011, filed as part of the effective shelf registration statement that Prana filed with the Securities and Exchange Commission (SEC) on May 17, 2011.
For more complete information about Prana and the ATM offering, you are encouraged to read the prospectus in Prana's May shelf registration statement, the prospectus supplement, and other documents Prana has filed with the SEC. You may obtain these documents on the SEC's website at www.sec.gov.

This press release does not constitute an offer to sell or a solicitation of an offer to buy, nor may there be any sale of Prana's common stock in any state or jurisdiction in which such an offer, solicitation or sale would be unlawful prior to registration or qualification under the securities law of any state or jurisdiction.

[Fruehrentner]

PBT2’s ‘mechanism of action’ presented in a Plenary Lecture at
International Conference on Alzheimer’s Disease (ICAD) on July 21 in Paris

Positions PBT2 as a leading therapeutic strategy targeting the underlying causes of
neurodegenerative disease

MELBOURNE, Australia – July 21, 2011 – Prana Biotechnology Limited (NASDAQ: PRAN /
ASX: PBT), announced that Professor Ashley Bush, Prana’s Co-Founding Scientist, will give a
Plenary Lecture on July 21st entitled, “Tau and Presenilin: The Metal Ion Regulatory Proteins of
Alzheimer’s Disease.” The talk draws on 20 years of medical research into the role of metals in
neurodegenerative diseases.
Geoffrey Kempler, Prana’s Executive Chairman, said, “This is the first time that the importance
of metals in neurodegenerative diseases has been given such a prestigious platform and focus
at ICAD. Changes in the metal status in the neuron may in fact be the trigger that sets off
Alzheimer’s Disease (AD). Professor Bush’s Plenary Lecture highlights a very promising and
different approach to treating AD which distinguishes Prana’s PBT2 from other drugs in
development. PBT2 prevents Abeta from becoming toxic to synapses, promotes neuronal
transmission and directly restores neurons critical to cognition. Alongside the rapid improvement
in cognition in the Phase II clinical trial of PBT2 for Alzheimer’s Disease, this Plenary Lecture
endorses our approach as a competitive and leading therapeutic strategy to treat
neurodegenerative disease”.
“In my opinion, PBT2 directly addresses the pathological mechanism of the amyloid beta protein
and, thus, has the greatest chance to stop the progress of this devastating disease” said
Professor Rudolph E.Tanzi, Joseph P. and Rose F. Kennedy Professor of Neurology, Harvard
Medical School, and Co-Founding Scientist at Prana
"It is important for the greater Alzheimer's community to recognize the fact that, beta-amyloid is
associated with metal imbalances in the brains of Alzheimer's patients. In addition to blocking
the aggregation of Abeta and dissolving Abeta deposits and oligomers, PBT2 also redistributes
metals that were previously trapped in the brain by Abeta deposits. In this way, PBT2 uniquely
addresses a pathogenic mechanism of Abeta deposition involving the sequestration of metals
like zinc and copper, which are essential for neural health”, explained Professor Tanzi.
The Plenary Lecture
Focusing on the function of APP, the precursor protein that gives rise to Abeta (the target
protein in AD) in ensuring that iron is able to move out of neurons, Professor Bush described
how both the disease and age-related changes to the pathways responsible for the trafficking of
brain metals (copper, zinc, iron) give rise to the various pathological features seen in AD.
Each feature of AD pathology - amyloid plaques, neurodegeneration, tau accumulation and
phosphorylation, the presence of metals in plaques, and the cognitive impairment experienced
by patients – can be explained by alterations to the pathways that are responsible for the
trafficking of metals in the brain.
Drawing on extensive studies in transgenic animal models, in vitro cell based studies and
human brain tissue, Professor Bush showed how the major proteins, which are strongly
implicated in the disease pathways in AD – APP, Abeta, tau and presenilin –are responsive to
the uptake and turnover of neuronal zinc, copper and iron. PBT2 influences the interaction of
metals with these key disease proteins.
Professor Bush’s Plenary Lecture will soon be available on Prana’s website.

http://www.pranabio.com/downloads/Media%20Releases/Media%20R…

[Fruehrentner]

MELBOURNE, Australia - August 8, 2011 -

Prana Biotechnology Limited (NASDAQ: PRAN / ASX: PBT), today announced that Lawrence Gozlan, a leading biotechnology investor and advisor, has joined the Company's Board of Directors. Mr. Gozlan is the Chief Investment Officer and Founder of Scientia Capital, a specialised global investment fund focused exclusively in life sciences. The Company was founded to provide high level expertise and to manage investments for high net worth individuals, family offices and institutional investors wanting exposure to the biotechnology industry.

Prior to this, Mr. Gozlan was responsible for the largest biotechnology investment portfolio in Australia as the institutional biotechnology analyst at QIC ("the Queensland Investment Corporation"), an investment fund with over AU$60 billion under management. He previously worked as the senior biotechnology analyst in the equities team at Foster Stockbroking, and gained senior corporate finance experience advising life science companies at Deloitte.

Mr. Gozlan is an investment advisor to several companies in the biotechnology industry, presented at numerous international healthcare conferences, and has been featured in various published media as an expert on investing in life sciences. He holds a Bachelor of Science with Honours in microbiology and immunology from the University of Melbourne specializing in neurodegenerative diseases.

Geoffrey Kempler, Prana's Executive Chairman, said, "It is with great pleasure that we welcome Lawrence to our Board of Directors. Lawrence's in-depth experience in biotechnology and finance will be invaluable as we move to the next stage of drug development at Prana. We look forward to his active involvement as a Director as we advance Prana's technologies into commercialization for a number of illnesses including Alzheimer's, Huntington's and Parkinson's Diseases.

Commenting on his appointment, Mr. Gozlan said, "Prana has shown very promising data and is advancing its research and development aggressively into clinical trials. It is an exciting time to be joining the Board and I look forward to assisting the Company in the successful clinical development and commercialization of their technology

[Fruehrentner]

MELBOURNE, Australia - August 22, 2011

Prana Biotechnology Limited (NASDAQ: PRAN / ASX: PBT), announced today that the company has received a grant from The Michael J. Fox Foundation (MJFF) to support the initiation of pre-clinical studies which precede human trials of a novel treatment for Parkinson's disease known as PBT434. Prana, a leading Australian biotechnology company, is developing a range of highly unique treatments for neurodegenerative diseases. The funding was awarded by the well-known foundation after a highly competitive, international, peer-reviewed process. The support comes from the MJFF's 2011 Pipeline Program to support its Therapeutic Development Initiative.

"It is our hope that PBT434 will provide treatment from very early diagnosis to prevent the damage to the part of brain (the substantia nigra) which is responsible for normal movement, thus preventing the loss of physical coordination and control experienced by Parkinson's disease patients," said Geoffrey Kempler, Prana's Executive Chairman.

PBT34 appears to be able to to impede the iron-induced oxidative damage and neurotoxic cascade that kills neurons. "There is evidence to show that the onset of Parkinson's disease is associated with an increase in iron in the cells of the substantia nigra, the part of the brain that is progressively destroyed in Parkinson's disease," said Associate Professor Robert Cherny, Prana's Head of Research . "We are particularly encouraged by data that suggests that the neuroprotective effects of PBT434 are accompanied by a significant decrease in the toxic accumulation of the alpha synuclein protein, a hallmark of Parkinson's disease pathology. Collectively, the neuroprotective properties of PBT434 indicate that there may be potential to develop the drug as a disease modifying agent".

"We are very pleased to receive this award that will help us move PBT434 closer to the clinic. In addition to Phase 2 trials in Alzheimer's disease and Huntington's disease with PBT2 planned for later this year, the advancement of PBT434 for Parkinson's disease reinforces our commitment to building shareholder value through product and disease diversification," said Mr Kempler.

The MJFF grant marks the transition from basic preclinical research for Prana's PBT434, the company's lead Parkinson's disease compound from its 700 strong MPAC compound library into the drug development pipeline. The initial grant of approximately $200,000 will be used to initiate the preclinical toxicology program needed before human testing.

Parkinson's disease is a devastating illness which can result in not only the loss of muscle control, speech, balance and digestive functions; it may also impair a patient's psychiatric and cognitive function. With 4 million people affected worldwide, Parkinson's disease is the second most common neurological indication behind Alzheimer's disease. The current market size for drugs to treat Parkinson's disease is approx. $4 billion per year; however most currently available drugs primarily treat the symptoms and do not actually prevent the ongoing destruction of the substantia nigra in the brain and progression of the disease.
*Refer to company announcements dated Sept 29, 2010 and March 15, 2011.

[Fruehrentner]

MELBOURNE, Australia - September 14, 2011

Prana Biotechnology Limited (NASDAQ: PRAN / ASX: PBT), has presented research on its planned PBT2 trial to leading scientists at the World Congress on Huntington's Disease, being held this year in Melbourne. One of Prana's scientific collaborators, Laureate Professor Colin Masters, provided the Congress with details of the similarities between Alzheimer's (AD) and Huntington's (HD) disease with a particular focus on the analogy between the pathologic mechanisms underlying both diseases. Prana is developing a new drug therapy, PBT2, which the company hopes will treat both disorders.

Prof. Masters, who is the director of the Mental Health Research Institute, provided an overview to the Congress on the role of Beta Amyloid in AD and its interaction with metals and provided a comparison to how the Huntington's Htt protein may become toxic through its interaction with metals. Prof. Masters told the Congress that PBT2 showed promise as one of the few disease modifying drugs in development for both Huntington's and Alzheimer's.

"PBT2 presents a novel and important approach to intervening in the toxic cascade of cellular degeneration that occurs in both diseases," says Prof. Colin Masters. "This is exciting, because developing therapies for this area has been quite challenging given the complexity of these diseases."

Geoffrey Kempler, Prana's Executive Chairman, said: "Prana's PBT2 is being increasingly recognised and accepted by those in both the Alzheimer's and Huntington's communities as a very promising potential therapy. Prof. Masters' presentation further reinforces our understanding of the links between the two diseases and the fact that patients with Huntington's Disease could receive significant benefit from PBT2. This is a very exciting time for the company."

PBT2
In a Phase IIa trial of PBT2 in mild Alzheimer's Disease, cognitive executive function was significantly improved in patients. At the conference, details showing PBT2 was able to directly restore neurons critical to cognition in mouse models were also presented. In particular it was demonstrated that PBT2 increased the number of spines on the branches (or dendrites) of neurons. Dendrites provide an important means of permitting many more neurons to interconnect with any particular neuron thereby increasing the brain's capacity to carry out learning and memory functions. In addition, positive new data with PBT2 in mouse models was presented at the conference.

"The available evidence points to PBT2 being able to restore cognition in degenerative conditions, holding promise that PBT2 will be able to confer cognitive benefit to patients with HD and AD", said Prof. Colin Masters.

[Fruehrentner]

Prana's Planned Huntington's Trial Receives Strong Interest from Patients and Researchers

MELBOURNE, Australia - September 16, 2011

Prana Biotechnology Limited (NASDAQ: PRAN / ASX: PBT), received a very positive reaction from international patient groups and researchers at this week's World Congress on Huntington's Disease in Melbourne. The company had a major presence at the Congress and the Prana team has held numerous meetings and conversations with patient groups and researchers.

"It has been very heart-warming to be so well received by the Huntington's community," says Prana Executive Chairman, Geoffrey Kempler. "Prana and our collaborators at major research institutions have been conducting extensive research into neurodegenerative diseases for more than a decade, including our efforts to learn more about Huntington's. Since we decided to conduct a Phase IIa trial of our experimental drug PBT2 in Huntington's patients, the Huntington's community has been very quick to support our research program."

Patient groups in Australia and the United States have welcomed the news of the planned trial. Shiralee Judge, chair of Australian Huntington's Disease Association, says, "it's very exciting and positive that an Australian company is conducting such extensive research to help us learn more about this disease and to identify a potential treatment to help patients. Huntington's is a very challenging disease, currently without an effective treatment or cure. Patients are very interested in new clinical research and we are looking forward to assisting Prana and their team of researchers with their investigation of PBT2."

The clinical trial will be conducted in conjunction with clinical experts and researchers at US based schools, including Harvard's Massachusetts General Hospital and Johns Hopkins University. This research is receiving strong interest from the world's largest Huntington's group, the Huntington's Disease Society of America. The organisation's CEO, Louise Vetter, says, "we are hopeful and encouraged by Prana's commitment and look forward to the start of recruitment. Patients and families have always been involved in research which fosters a better understanding of this disease and will undoubtedly embrace this new opportunity. We are anxiously awaiting more information on Prana's trial."

Prana's earlier Alzheimer's trial showed that PBT2 significantly improves cognitive Executive Function in patients. This is relevant to Huntington's Disease given these patients also suffer cognitive decline. Prana researchers believe PBT2 can bring the same cognitive benefits to Huntington's Disease patients that it did to Alzheimer's Disease patients. Prana will need to recruit approximately 100 people with early stages of the disease across Australia and the United States, at 14-16 sites. Patients will be followed over 6 months. Researchers will assess safety, tolerability and efficacy of PBT2. Final results are expected late in 2013.

In addition to the Huntington's trial, Prana continues to expand research and clinical development programs in Alzheimer's and Parkinson's. The company will also conduct a Phase II brain imaging trial for Alzheimer's at the end of this year and recently received a research grant for its Parkinson's program from the prestigious Michael J. Fox Foundation for Parkinson's Research.

[Fruehrentner]

PBT2 Directly Restores Neurons Critical to Cognition

Important Further Demonstration of Mechanism of Action

Journal of Neurochemistry publication on biochemical effects of PBT2 explains the preclinical and clinical benefits of PBT2 in Alzheimer's Disease


Melbourne - 19 September, 2011:

Prana Biotechnology (NASDAQ: PRAN; ASX: PBT) today announced that The Journal Of Neurochemistry has published an update on the mechanism of action of PBT2 in the treatment of Alzheimer's Disease (AD). The study explains how PBT2 is able to restore cognition in AD sufferers through repair of affected Alzheimer's brains.

The findings further explain the rapid improvement in cognition previously reported in transgenic Alzheimer's mice and in patients in a Phase IIa clinical trial with PBT2*.

The article published in the peer-reviewed Journal of Neurochemistry** is entitled "The Alzheimer's therapeutic PBT2 promotes amyloid-B degradation and GSK phosphorylation via a metal chaperone activity".

"The data published adds significantly to the information published in PLoS ONE and announced on 21 March 2011. The March article described what PBT2 does in the brain - it directly restores neurons. This new article details how the mechanism of action works and brings cognitive improvement" commented Mr. Geoffrey Kempler, Prana's Executive Chairman.

The study findings are particularly timely as Prana is about to start two clinical studies, one in AD and one in Huntington's Disease.

According to Prana's Head of Research, Associate Professor Robert Cherny, PBT2 provides a unique combination of detoxification and neuronal restoration to bring about the cognitive improvement observed in patients. It prevents Abeta oligomer formation, and delivers neurologically active metals (copper and zinc) into neurons damaged in AD.

This new data shows that delivery of these metals triggers intracellular molecular pathways which lead to improved cognition and increased expression of neuronal markers.

"Our findings indicate that PBT2 causes phosphorylation of the key cellular kinase, GSK3 by inhibiting the activity of the phosphatase, calcineurin, and refine our understanding of the mechanism of action of PBT2. Both GSK3 and calcineurin are viewed as important targets for AD therapies," Dr. Cherny stated.

Activation of this pathway also explains how PBT2 caused the large decrease in hyperphosphorylated tau, a brain protein associated with AD. ***

These new results further explain how PBT2 can achieve rapid improvements in cognition: by liberation of copper and zinc trapped in amyloid deposits and returning those essential metals to neurons, where they are needed for normal function.


*Lannfelt et al. Lancet Neurology (2008) vol. 7, pp. 779-86; Lannfelt et al. Lancet Neurology (2009) vol. 8, pp. 981.
**Crouch et al. Journal of Neurochemistry (2011) vol. 119, pp.220-230
***Adlard et al. Neuron (2008) vol. 59, pp. 43-55

[Finee]

MLV Capital Analysts Now Covering Prana Biotechnology (PRAN) Stock
October 4th, 2011 by ABMN Staff.
Equities research analysts at MLV Capital initiated coverage on shares of Prana Biotechnology (NASDAQ: PRAN) in a research note issued to investors on Tuesday. They set a “buy” rating and a $6.00 price target on the stock.
Prana Biotechnology Limited (Prana) is an Australia-based company engaged in drug development and research. The focus of the Company is to develop disease modifying therapeutics for the treatment of common neurological disorders, with a focus upon Alzheimer’s, Parkinson’s and Huntington’s diseases, specific cancers and age-related macular degeneration. It has developed a platform technology in association with internationally scientists and academic institutions, including The University of Melbourne, Massachusetts General Hospital and The Mental Health Research Institute of Victoria; and its research collaborators are The Buck Institute for Age Research, University of California and University College, London. As of June 30, 2010, the Company held interest in two subsidiaries: Prana Biotechnology Inc and Prana Biotechnology UK Ltd, and Prana’s majority shareholder was National Limited.

Shares of Prana Biotechnology traded up 3.57% during mid-day trading on Tuesday, hitting $1.45. Prana Biotechnology has a 52 week low of $1.13 and a 52 week high of $4.50. The stock’s 50-day moving average is $1.67 and its 200-day moving average is $1.99. The company has a market cap of $40.7 million.

Stay on top of analysts' coverage with American Banking & Market News' daily email newsletter that provides a concise list of analysts' upgrades, analysts' downgrades and analysts' price target changes for each day.

[Fruehrentner]

Antwort auf Beitrag Nr.: 42.168.676 von Finee am 04.10.11 18:41:57

Die Jungs von MLV lesen wohl meine postings hier


Danke fürs Reinstellen

[Finee]

Government grant to study effects of PBT2 in the ageing brain
Australian Federal Government Grant to Study effect of PBT2 in the ageing brain
Dr Paul Adlard awarded funding to investigate prevention of age-related cognitive decline.

Melbourne – 20 October, 2011:
Prana Biotechnology (NASDAQ:PRAN; ASX:PBT) today announced Dr Paul Adlard, Head of The Synaptic Neurobiology Laboratory at The Mental Health Research Institute and Prana research scientist, has been awarded an NHMRC (National Health and Medical Research Council) Project Grant to study the benefits of PBT2 and other compounds in age-related cognitive impairment. The grant is entitled "The role of metals in healthy brain ageing: identification of novel compounds to prevent age-related cognitive decline". PBT2 is Prana’s lead drug in development for Alzheimer’s and Huntington’s Diseases.
“This highly competitive grant from the Australian Federal Government will fund the study of compounds including PBT2, researching effects on brain anatomy and biochemistry, and also cognition and behaviour”, commented Geoffrey Kempler, Prana’s Executive Chairman. “Earlier this year, Dr Adlard published a landmark paper in the science journal PLoS One**, describing how PBT2 restores healthy function to neurons damaged in an animal model of Alzheimer’s Disease. I congratulate Dr. Adlard on his success”.

[Fruehrentner]

Antwort auf Beitrag Nr.: 42.235.062 von Finee am 20.10.11 08:22:51

hier die vollständige Meldung:


Melbourne - 20 October, 2011:

Prana Biotechnology (NASDAQ: PRAN; ASX: PBT) today announced Dr Paul Adlard, Head of The Synaptic Neurobiology Laboratory at The Mental Health Research Institute and Prana research scientist, has been awarded an NHMRC* Project Grant to study the benefits of PBT2 and other compounds in age-related cognitive impairment.

The grant is entitled "The role of metals in healthy brain ageing: identification of novel compounds to prevent age-related cognitive decline". PBT2 is Prana's lead drug in development for Alzheimer's and Huntington's Diseases.

"This highly competitive grant from the Australian Federal Government will fund the study of compounds including PBT2, researching effects on brain anatomy and biochemistry, and also cognition and behaviour", commented Geoffrey Kempler, Prana's Executive Chairman. "Earlier this year, Dr Adlard published a landmark paper in the science journal PLoS One**, describing how PBT2 restores healthy function to neurons damaged in an animal model of Alzheimer's Disease. I congratulate Dr. Adlard on his success".

Prana has previously reported that in older normal mice, that is mice that were not genetically bred to develop Alzheimer's, the cognitive decline normally associated with the ageing process was significantly improved or reversed by PBT2. This grant for $762,975 will allow Dr Adlard to extend the evidence for the role of the biological metals targeted by PBT2, in both Alzheimer's Disease as well as normal age-related cognitive loss.***
The normal ageing process, together with age-related disorders such as Alzheimer's Disease (AD), are characterised by a progressive decline in many cognitive processes, with memory impairment representing one of the most debilitating features of both "normal" and "pathological" ageing. There are currently no effective long-term treatments, or even a defined understanding of how these deficits occur. "With this grant we will develop our hypotheses as to the cause and potential treatments of memory impairments, specifically linking synaptic zinc dyshomeostasis as a causative factor, and indeed as a therapeutic target, of this dysfunction. PBT2, already shown to bring cognitive benefit to Alzheimer's Disease patients may also improve the cognitive decline associated with normal ageing"' commented Dr Adlard.

*National Health and Medical Research Council
** Press release July 16 2009
***Adlard et al (2011). "Metal Ionophore Treatment Restores Dendritic Spine Density and Synaptic Protein Levels in a Mouse Model of Alzheimer's Disease". PLoS ONE 6(3): e17669.doi:10.1371/

[Finee]

MELBOURNE, AUSTRALIA--(Marketwire -10/27/11)- Prana Biotechnology (NASDAQ: PRAN - News) (ASX: PBT.AX - News) today announced Associate Professor Kevin Barnham, Principal Research Fellow at The Mental Health Research Institute and Prana scientist, has been awarded an NHMRC* Project Grant to study the benefits of PBT2 and other compounds in preventing excitotoxicity. The grant is entitled "Modulating Cellular Copper Levels To Prevent The Effects Of Excitotoxicity In Neurodegenerative Diseases." Associate Professor Barnham is one of the co-inventors of PBT2, Prana's lead drug in development for Alzheimer's and Huntington's diseases.

"This grant from the Australian Federal Government will fund scientific work to further explain how PBT2 can improve cognition in patients," commented Geoffrey Kempler, Prana's Executive Chairman. "We have evidence to show that excitotoxicity, a destructive phenomenon arising from excessive stimulation of brain cells, is inhibited by PBT2. Dr. Barnham's work will expand our understanding of the molecular pathways by which PBT2 achieves its neuroprotective effects. I congratulate Dr. Barnham on his success."

Excitotoxicity is a common feature of the brains of people affected by a variety of neurological and neurodegenerative conditions, particularly Alzheimer's and Huntington's diseases. It results from excessive stimulation of NMDA receptors in glutamatergic synapses by the neurotransmitter glutamate. To prevent glutamate excitotoxicity, drugs which inhibit NMDA receptor activity have been developed for use in both Alzheimer's and Huntington's diseases. However these drugs are indiscriminate and can have numerous side effects. In contrast, PBT2 is very specific because its interaction with biological metals in the brain, allows it to provide the metals (copper) that NMDA receptors require for healthy function to allow normal neurotransmission across synapses and healthy cognition.

This grant for roughly $419,000 will allow Dr. Barnham to extend beyond the data presented at ICAD in 2010 which showed that PBT2 is an effective inhibitor of glutamate excitotoxicity. "Given that we have already seen PBT2's cognitive benefits in the clinic, we are pleased to receive this grant to further our understanding of PBT2's mechanism of action," commented Dr. Barnham. "I believe that PBT2's action suggests it will be a very useful therapy for Alzheimer's and Huntington's disease patients," he added.

http://finance.yahoo.com/news/Australian-Federal-Government-…

[Finee]

Prana Biotechnology’s PBT2 shows potential to reverse effects of Alzheimer’s and Huntington’s

Monday, November 14, 2011 by Angela Kean
Prana Biotechnology’s (ASX: PBT) PBT2, which is in development for the treatment of both Alzheimer’s and Huntington’s Disease, has demonstrated an improvement in synaptic activity in neurons needed for memory.
Both Alzheimer’s and Huntington’s affect a patient’s memory and ability to plan and execute tasks. Pathologically, both diseases are associated with the formation of toxic oligomers of a protein.

Scientists from Merz Pharmaceuticals and the Max Planck Institute presented data showing that PBT2 was able to prevent synapatic toxicity or loss of signal conductivity, caused by the formation of toxic Aβ oligomers.
The data indicates that it may be most beneficial for neuroprotective agents such as PBT2, that can interrupt Aβ self-assembly into aggregates, to be administered to early stage patients to best maintain synaptic plasticity and function as an effective treatment for Alzheimer’s Disease.
Importantly, this independent data helps Prana understand how PBT2 can help the brain create new memories by preventing the formation and toxicity of soluble β-amyloid oligomers.
PBT2 resulted in significant cognitive improvement in a clinical trial with Alzheimer’s Disease patients.

http://www.proactiveinvestors.com.au/companies/news/21999/pr…
http://www.pranabio.com/downloads/Media%20Releases/Media%20R…

[Fruehrentner]

Melbourne - 14 November, 2011:

Prana Biotechnology (NASDAQ: PRAN; ASX: PBT) today announced that scientists from Merz Pharmaceuticals GmbH and the Max Planck Institute presented data showing that Prana's PBT2 improves synaptic activity in neurons needed for memory. The scientists presented their data at The Society for Neuroscience meeting in Washington D.C. in a poster titled "Aggregation inhibitors reverse β-amyloid (Aβ)-induced inhibition of long term potentiation (LTP) in murine hippocampal slices".

The experiments reported that PBT2 was able to prevent synapatic toxicity or loss of signal conductivity, caused by the formation of toxic Aβ oligomers. The data indicates that it may be most beneficial for neuroprotective agents such as PBT2, that can interrupt Aβ self-assembly into aggregates, to be administered to early stage patients to best maintain synaptic plasticity and function as an effective treatment for Alzheimer's Disease (AD).

Associate Professor Robert Cherny, Prana's Head of Research noted that "these independent data help us to understand how PBT2 can help the brain create new memories by preventing the formation and toxicity of soluble β-amyloid oligomers. Whilst these findings confirm our belief that Alzheimer's Disease patients will most benefit from early intervention in the disease process, we believe that PBT2's benefits will include but not be limited to helping early patients."

PBT2 is in development for the treatment of both Alzheimer's and Huntington's Disease, both of which affect a patient's memory and ability to plan and execute tasks. Pathologically, both diseases are associated with the formation of toxic oligomers of a protein. PBT2 is able to prevent these oligomers from forming and can also disaggregate many existing oligomers. PBT2 resulted in significant cognitive improvement in a clinical trial with Alzheimer's Disease patients. The next PBT2 trials, in both Alzheimer's and Huntington's Diseases, will further advance PBT2's potential as a therapy for these diseases.

For further information please visit the Company's web site at www.pranabio.com.

####



Aha interessant; die deutsche Merz GmbH, die derzeit ein Mittel gegen Alzheimer auf dem Markt hat (Memantin) und dessen Patentschutz bald abläuft, haben offenbar PRANA auf dem Radarschirm. Scheint so, als ob größere Pharmafirmen nun auf PRANA aufmerksam werden. Ob es vielleicht zu einem license deal oder gar Übernahme kommt in absehbarer Zeit?

Es bleibt spannend!

[Finee]

Prana Biotechnology to start 12 month trial of Alzheimer’s treatment

Tuesday, 22 November 2011

Prana Biotechnology (ASX: PBT NASDAQ: PRAN) has received approval to begin a 12 month Phase II Imaging trial to test the company’s Alzheimer’s Disease treatment.

The trial, approved by the Austin Health Research Ethics Committee, will measure the physical changes in the brains of participants tested with Prana’s PBT2 drug for 12 months.

This Phase II trial will also build on an earlier 12 week Phase IIa clinical trial, gathering longer term evidence of the positive effects of PBT2 on patients’ cognition.

It aims to demonstrate PBT2’s potential as an effective disease-modifying treatment.

PBT2 has already been shown to significantly change Abeta levels in spinal fluid and improve the cognition of Alzheimer’s Disease patients in the 12 week trial.

A 12 month trial will provide a much greater amount of safety and efficacy data.

If successful, this trial could accelerate the clinical development of PBT2.

The Phase II trial has received funding from the Alzheimer’s Drug Discovery Foundation.

http://www.onenewspage.com.au/n/Business/74mxa1p4p/Prana-Bio…

[Finee]

Hier die Einzeheiten:
http://hotcopper.com.au/asx_announcements.asp?id=368073

[Finee]

Der Kommentar dazu:

Prana Biotechnology receives approval and funding for Alzheimer’s trial
By Motley Fool Staff - Tuesday, November 22nd, 2011

Prana Biotechnology Ltd. (ASX:PBT) jumped 19.4% on Tuesday to close at $0.185. The Melbourne based micro-cap biotechnology company primarily focuses on cures for Alzheimer’s, Parkinson’s, and Huntington’s diseases.
The share price rise was on the back of Prana receiving approval from the Austin Health Research Ethics Committee to commence a 12 month Phase II Imaging trial testing PBT2, the company’s drug for Alzheimer’s Disease (AD).
This trial continues Prana’s incredibly slow progress in the multi-billion race to find a cure for Alzheimer’s Disease. Investors must be hoping that this tortoise will win the race. More importantly, AD sufferers and their families will be happy to see some progress for Prana’s promising drug.
Investors were relieved that the trial will receive funding from the Alzheimer’s Drug Discovery Foundation (ADDF), as Prana continues to be short of cash.

Howard Fillit, MD, the ADDF’s Executive Director commented that
PBT2 stands out as one of the few remaining orally available agents with clinical trial evidence of cognitive benefit for Alzheimer’s patients. Success in this trial will demonstrate target engagement by PBT2 in the brain of people with Alzheimer’s Disease, and accelerate the clinical development of PBT2 to patients.

[Fruehrentner]

Klingt ja gut

Es liegt aber noch ein langer Weg vor PBT-2.

[Finee]

Prana secures key patent for Parkinson's drug PBT434 in the United States
MELBOURNE, Australia - November 28, 2011:
Prana Biotechnology (ASX:PBT; NASDAQ:PRAN) today announced that the United States Patent and Trademark Office (USPTO) has issued a Notice of Allowance for a composition of matter patent for selected 8-hydroxy quinazolinone compounds, including its lead Parkinson's Disease (PD) drug candidate, PBT434, in the United States. The patent entitled 'Neurologically Active Compounds' also covers pharmaceutical compositions containing PBT434 and selected 8-hydroxy quinazolinone compounds.
Once granted, the United States patent has a twenty year term expiring June 7, 2026. This expiry date may in the future be further extended by the application of pharmaceutical extension of term provisions of up to five years in the United States.
Geoffrey Kempler, Prana's CEO, said "securing granted rights to our lead PD drug candidate furthers our commercialization plans for PBT434 for which Prana was recently awarded a grant from The Michael J. Fox Foundation to undertake preclinical development studies to enable human clinical trials".
PBT434 has been designed to prevent or slow the loss of the neurons of the substantia nigra that produce the chemical dopamine, the neurotransmitter that controls motor function in the brain. As a neuroprotective agent, PBT434 preserves critical interneuronal connections between the substantia nigra and the striatum (neurons which have dopamine receptors and transmit the signals to coordinate movement pathways and a variety of cognitive processes involving executive function). Experiments in two animal models of PD have shown that; in animals treated with PBT434, motor coordination and performance were significantly improved compared to untreated control animals, the characteristic accumulation of the disease associated protein alpha synuclein in the brains of PD animal models was reduced and that expression of a key genetic susceptibility factor, the antioxidant protein, DJ-1, was elevated in substantia nigra neurons.
http://www.4-traders.com/news/Prana-secures-key-patent-for-P…

[Fruehrentner]

Prana Commences Alzheimer's Trial Recruitment

15.12.2011 05:38:08

12 month Phase II Imaging study with PBT2 in early Alzheimer's patients

Melbourne - 15 November, 2011: Prana Biotechnology (NASDAQ:PRAN; ASX:PBT) today announced that it has commenced recruitment and screening of patients for a 12 month Phase II Imaging trial testing PBT2, the Company's drug in development for Alzheimer's Disease.

Screening of patients began last week with psychological tests to measure cognition1. This week, the first patient was tested for evidence of significant levels of Abeta deposits in the brain2.

Professor Colin Masters, Director of the Mental Health Research Institute, explained that "we are selecting patients with established Alzheimer's Disease, as well as targeting those very early in the disease process. We are using the most modern techniques available for measuring PBT2's disease modifying effects to establish cognitive, functional and physical changes in the brain. By disease modifying, I mean modifying the rate of progress of Alzheimer's, slowing it down and delaying onset. We are using PiB-PET imaging to measure the drug's effects on the insoluble form of Abeta, and we are using a recently developed blood test to measure levels of the soluble oligomers of Abeta3. This week we have been taking pre-drug dosing measures of eligible patients to compare with measures that will be taken throughout the trial. Per protocol, each patient qualifying for entry to the trial will receive the first dose of drug or placebo on their second visit to the clinic."

"In my opinion PBT2 has the best and highest chance of all drugs currently in development to have a major impact on the disease process, and help avoid the global epidemic of Alzheimer's which, left untreated, is poised to become unmanageable. This trial that is now in progress will establish for the first time not only that PBT2 can improve cognition, as already shown, but that it can actually modify the course of the disease. It will be a major step forward if the drug demonstrates, as I think it will, its ability to affect both soluble and insoluble Abeta levels", concluded Professor Masters.

1Cognition Tests

NTB
The NTB is a battery of commonly used and validated neuropsychological tests which
includes tests of both amnestic and executive impairment.

ADCS-ADL-23
The ADCS-ADL-23 consists of a comprehensive battery of ADL questions used to measure the functional capabilities of Patients. Each ADL item is rated from the highest level of independent performance to complete loss.

MMSE
The MMSE is a brief test of cognitive function including orientation, immediate recall, delayed recall, constructional ability and language.

2Brain Imaging techniques

PiB PET SUVR (measuring placques or insoluble Abeta)

PET is a sensitive molecular imaging technique that allows in vivo quantification of radiotracer concentrations. PET radiotracers are typically designed to bind a substrate known to be involved in the biological process being evaluated. This interaction allows the in vivo assessment of the molecular processes at their sites of action, permitting detection of disease at asymptomatic stages, when there is no evidence of anatomic changes on CT and MRI.

PiB is a PET radio tracer used to image in vivo, amyloid plaques which are one of the major histopathological hallmarks of AD. Quantitative analysis of C-PiB retention requires normalisation of the C-PiB uptake values, to allow inter- and intra- subject comparisons. The SUVR normalises the uptake values to the mean uptake value within a region containing nonspecific binding, the cerebellar grey matter in the case of Screening. For inclusion in the trial patients need a C-PiB PET neocortical retention ratio relative to the cerebellum (neocortical Standardised Uptake Value Ratios (SUVR)) of > 1.7.

F-FDG PET (measuring energy usage and brain activity)

F-FDG PET is a glucose analogue and PET radio tracer that is used to measure metabolic activity non-invasively. F-FDG uptake thus reflects the regional consumption of glucose. In the brain, this regional metabolic activity is mainly related to neuronal/synaptic function.

MRI (measuring brain volume)

MRI measures the volume of specific parts of the brain involved in cognition (cortical grey matter volume, hippocampal volume, and ventricular volume).

3Blood test for soluble Abeta levels

This test utilises mass spectrometry to detect a variety of forms of soluble Abeta, the levels of which correlate with cognitive performance and brain amyloid in the Alzheimer's human brain. Villemagna et al. J Neurosci [2010] 30:6315-6322.

For further information please visit the Company's web site at www.pranabio.com.


About the Alzheimer's Drug Discovery Foundation
The Alzheimer's Drug Discovery Foundation (ADDF) is the only non-profit organization whose sole mission is to accelerate the discovery and development of drugs to prevent, treat and cure Alzheimer's Disease, related dementias and cognitive aging. Since 1998, the ADDF has granted more than $50 million to fund over 325 Alzheimer's drug discovery programs in academic centers and biotechnology companies in 18 countries. For more information about the Foundation, please visit www.AlzDiscovery.org.

[Fruehrentner]

Landmark Publication Endorses Prana`s Strategy

16.12.2011 04:53:02

Melbourne - 16 December, 2011: Prana Biotechnology (NASDAQ:PRAN; ASX:PBT) today announced that the Journal of Biological Chemistry* has published research that provides strong validation of Prana's strategy to treat neurodegenerative diseases.

The authors, led by Professor Susan Lindquist, Professor of Biology at Massachusetts Institute of Technology, discussed the broad therapeutic potential of 8-hydroxyquinolines (8-OHQ), which were identified as being protective against the neurotoxic proteins that cause disease in disorders such as Alzheimer's, Huntington's, Parkinson's and other neurodegenerative disorders. PBT2, Prana's lead Phase II drug is a specific type of 8-OHQ designed and selected for enhanced efficacy and tolerability as a therapeutic intervention. The authors cite the positive therapeutic results of PBT2.

The paper, entitled "Different 8-OHQ's Protect Models of TDP-43, synuclein, and Polyglutamine Proteotoxicity through Distinct Mechanisms" describes the identification of selected 8-OHQ compounds, from 200,000 compounds tested, as protective against neurodegeneration due to their influence on metal homeostasis in the brain. The authors noted that the "ability of different 8-OHQ's to impinge on diverse proteotoxicities (neurotoxicity caused by overabundant mutant or misfolded proteins) further links metal homeostasis to neurodegenerative diseases including Alzheimer's, Parkinson's and Huntington's diseases".

Importantly, the authors make the point that subtle changes to the chemical backbone of this class of drug can permit rational drug design for different disease indications. PBT2 was selected on the basis of unique chemical modifications designed to confer subtle but effective redistribution of metals in the brain, ability to prevent amyloid induced neurotoxicity and neuro-regenerative effects. To date, Prana's 800 strong novel compound library has yielded a Phase II candidate for Alzheimer's and Huntington's with PBT2, Parkinson's' with PBT434 and brain cancer with PBT519.

"This is a landmark paper supporting Prana's therapeutic strategy", commented Prana's Head of Research, Assoc. Professor Robert Cherny. "The findings by the authors that precise chemical modifications to the 8-OHQ compounds altered metal binding and metal transport properties resulting in various mechanisms of action supports findings by Prana scientists that the therapeutic benefits of selected members of this class of compound arise from a unique combination of metal recovery and redistribution", concluded Dr Cherny.

The paper can be accessed online here

Prana has commenced a 12 month clinical trial of PBT2 Alzheimer's Disease (see company announcements dated 22 November 2011 and 15 December 2011). Mr Geoffrey Kempler, Prana's Executive Chairman, commented that "the findings in this publication further fuel the momentum building toward the acceptance and success of our strategy for treating neurodegenerative diseases".


*Daniel F. Tardiff, Michelle L. Tucci, Kim A. Caldwell, Guy A. Caldwell and Susan Lindquist, December 6, 2011, doi:10.1074/jbc.M111.308668

http://www.jbc.org/cgi/doi/10.1074/jbc.M111.308668

[Fruehrentner]

Antwort auf Beitrag Nr.: 42.489.455 von Fruehrentner am 16.12.11 09:19:02

http://www.jbc.org/cgi/doi/10.1074/jbc.M111.308668

[Finee]

Prana Biotechnology given the green light to begin Huntington’s Disease clinical trial in the U.S.
Wednesday, January 04, 2012 by Angela Kean

Prana Biotechnology (ASX:PBT) has received approval from the United States Food and Drug Administration to begin recruiting patients for the company's first clinical trial using PBT2 in patients with Huntington’s Disease.
Huntington’s Disease is a complex and severely debilitating genetic, neurodegenerative disease, for which there is no cure.
The disease often affects young adults and, while associated with severe physical movement symptoms, progressively impacts the mind and emotions as well. The disease causes incapacitation and death about 15-25 years after onset.
The disease affects 30,000 people in the U.S. and about 70,000 worldwide. According to Prana, there are currently no drugs in development that have established clinical evidence for treating cognitive decline.
Prana is developing PBT2 for the treatment of both Alzheimer’s and Huntington’s Disease. Previous research by the company has shown that PBT2 can improve synaptic activity in neurons needed for memory.
The randomised, double-blind, placebo-controlled trial will enrol 100 patients with early to mid-stage Huntington’s Disease at clinical sites in the U.S. and Australia.
The aim of this trial is to demonstrate safety, motor benefits and the same cognitive benefits for Huntington’s patients that it has already demonstrated in Alzheimer’s patients treated with PBT2.

http://www.proactiveinvestors.com.au/companies/news/23774/pr…

[Finee]

Noch einmal etwas ausführlicher

FDA Approval to Commence Huntington's Disease Clinical Trial Using Prana's PBT2
Huntington Study Group Appointed to Coordinate the Trial and Start Recruitment

MELBOURNE, AUSTRALIA--(Marketwire -01/04/12)- Prana Biotechnology (NASDAQ: PRAN - News) (ASX: PBT.AX - News) today announced that it has received approval from the United States Food and Drug Administration (FDA) to start recruiting patients for the company's first clinical trial using PBT2 in patients with Huntington's Disease (HD).
Prana's Investigational New Drug Application (IND) is now open. "The opening of this IND for a Phase 2 study follows an extensive review of PBT2 data by the FDA and reflects a favourable analysis from the FDA to support the study of PBT2 in Huntington's Disease patients", commented Geoffrey Kempler, Prana's Executive Chairman.
Huntington's Disease is a complex and severely debilitating genetic, neurodegenerative disease, for which there is no cure. The disease often affects young adults and, whilst associated with severe physical movement symptoms, progressively impacts the mind and emotions as well. The disease causes incapacitation and death about 15-25 years after onset.
The Company has appointed the Huntington Study Group (HSG) to coordinate the trial. HSG will commence recruitment of patients for the trial, named "Reach2HD, at clinical sites across USA and in Australia. The randomised, double-blind, placebo-controlled trial will enrol 100 patients with early to mid-stage Huntington's Disease. The Principal Investigator on the study is Dr. Raymond Dorsey of Johns Hopkins University Medical Center. The protocol synopsis appears below in Appendix 1.
Professor Ira Shoulson, Professor of Neurology, Pharmacology and Human Science at Georgetown University (Washington DC) and the Chair of the Executive Committee of the Huntington Study Group said "PBT2 attracted our attention as an experimental drug with the potential to bring real benefit to Huntington's Disease patients who suffer from a range of motor, behavioural and cognitive symptoms. The favourable signals from the PBT2 trial in Alzheimer's Disease are particularly promising".
The disease affects 30,000 people in the US and about 70,000 worldwide. There are no drugs in development that have established clinical evidence for treating cognitive decline. Prana aims, in this trial, to demonstrate safety, motor benefits and the same cognitive benefits for Huntington's patients that it has already demonstrated in Alzheimer's patients treated with PBT2.
Appendix 1 - Protocol synopsis
A randomised, double-blind, placebo-controlled study to assess the safety and tolerability, and efficacy of PBT2 in patients with early to mid-stage Huntington's disease (HD)
Study Number PBT2-204
Study Name/Acronym Reach2HD
Study Design
Randomised, double-blind, placebo-controlled, parallel group, multi-centre, Phase 2a study.
Objectives
Primary objective:
To evaluate the safety and tolerability of two dose levels of PBT2 when administered orally once daily over 26 weeks in patients with HD.
Secondary objectives:
Determine the effect of PBT2 after 26 weeks in patients with HD on:
1. Cognition
2. Motor function
3. Behaviour
4. Functional abilities
5. Global function
6. Plasma and urine biomarkers
7. Brain volumes and function (imaging), and
8. To evaluate the Pharmacokinetics of PBT2 in patients with HD.
Number of Patients
It is planned that 100 patients will be randomised in to the study.
Key Patient Criteria
Men and women with Total Functional Capacity (TFC) 6-13, inclusive, and a CAG repeat number of ≥ 36
Montreal Cognitive Assessment (MoCA) score ≥ 12
Doses
Placebo (0mg PBT2), 100mg PBT2 and 250mg PBT2, once daily capsules.
Per Patient Duration
34 weeks: Four week Screening period, 6 months (26 weeks) treatment period and Follow-up 4 weeks post treatment.
Endpoints
Primary
Safety and Tolerability assessments.
Secondary
Cognition Tests: Cognitive Test Battery (consisting of Category Fluency Test, Trail Making Test parts A and B, Map Search, Symbol Digit Modalities Test and Unified Huntington Disease Rating Scale (UHDRS) Stroop Word Reading). MoCA.
Motor Function Tests: UHDRS '99 Motor component; Speeded Tapping Task.
Behaviour: UHDRS Behavioural component.
Functional Abilities: Total Functional Capacity and Independence Scale from UHDRS '99; Schwab & England Activities of Daily Living Scale (SEADL).
Subject and investigator global assessments: Patient Reported Outcomes; Clinical Global Impression - Severity Scale.
Biomarkers: small molecule markers of metabolic and oxidative stress in blood and urine; blood levels of total and mutant huntingtin; gene expression markers of HD progression; plasma selenium.
Brain Imaging: volumetric and functional measures.
Pharmacokinetics: sparse sampling.
Trial Locations
Australia,USA
Trial Standard
Study will be conducted according to ICH GCP

http://finance.yahoo.com/news/FDA-Approval-Commence-iw-35760…

[Finee]

Professor Rudy Tanzi Appointed Prana´s Chief Scientific Advisor

http://www.asx.com.au/asxpdf/20120111/pdf/423pzxxpfk7qxz.pdf

[Fruehrentner]

Und wieder ein Wettbewerber, der in Phase III scheitert:


Dimebon drug trial fails to meet primary endpoint: Medivation, Pfizer report

18. Jan. 2012

Medivation, a biopharmaceutical company, and Pfizer have reported results from the Phase 3 Concert trial, which assessed dimebon (latrepirdine) to treat Alzheimer's disease when added to ongoing treatment with donepezil HCL tablets.

The data demonstrated that Dimebon did not achieve statistically significant results for either of the two co-primary endpoints including the Alzheimer's Disease Assessment Scale and the Alzheimer's Disease Cooperative Study.

The Alzheimer's Disease Assessment Scale comprises cognitive subscale (ADAS-cog), which measures cognitive ability while the Alzheimer's Disease Cooperative Study includes Activities of Daily Living (ADCS-ADL), which measures self care and daily function.

Dimebon was, however, well tolerated in the study.

The 12-month global randomized, double-blind, placebo-controlled trial enrolled 1,003 patients with Alzheimer's disease.

Patients on a stable dose of donepezil for at least four months were randomized to one of three treatment groups: dimebon 20 mg three times per day, dimebon 5 mg three times per day or placebo.

[Finee]

Prana Doses First Patient in the “IMAGINE” Phase II Alzheimer’s
Disease Trial...
http://www.pranabio.com/downloads/Media%20Releases/Media%20R…

[Fruehrentner]

Melbourne - 26 March, 2012: Prana Biotechnology (NASDAQ: PRAN; ASX: PBT) today announced the publication in the journal PLoS ONE, of an article that strongly endorses PBT2's potential to treat Alzheimer's Disease.

The paper, entitled "The Zinc Dyshomeostasis Hypothesis of Alzheimer's Disease"1 presents an integrated explanation of the major pathological features of Alzheimer's Disease, based upon a combination of new experimental data and mathematical modeling.

The senior author on the paper is Professor Rudy Tanzi, the Joseph P. and Rose F. Kennedy Professor of Neurology at Harvard University and Prana's Chief Scientific Advisor.

Dr. Tanzi explained that "the hallmark pathological features of Alzheimer's Disease are the amyloid plaques, composed of the Abeta protein, and neurofibrilliary tangles (NFTs), composed of Tau protein. Everything we have learned from the genetics of Alzheimer's Disease indicates that the disease is caused by excessive accumulation of the Abeta protein in the brain. We also know that hyperphosphorylation of the Tau protein which forms NFTs is the feature of the disease which correlates with neuronal damage and cognitive loss. Prana's drug PBT2 reduces levels of both Abeta and hyperphosphorylated tau in animal studies4 and improved cognition and lowered Abeta in a Phase 2a clinical trial of Alzheimer's Disease patients2,3.

"So, Alzheimer's Disease can be defined as an amyloid-induced tauopathy. The big question is this - how does amyloid aggregation lead to NFTs? In this paper we propose that at least part of the answer to that question is zinc dyshomeostasis, that is to say, abnormal distribution of zinc in the brains of Alzheimer's Disease sufferers. The drug PBT2 directly addresses this problem by binding zinc and normalising its distribution. This bodes very well for the current PBT2 clinical trial that is in progress" concluded Dr. Tanzi.

This paper builds on Prana's previously published findings that as we age our ability to maintain normal zinc distribution deteriorates. Abeta forms amyloid by capturing and holding zinc, which in turn further reduces our ability to maintain normal zinc distribution. "This is a vicious pathological cycle. PBT2 interrupts this cycle, re-distributing zinc needed for healthy brain function", commented Prana's Head of Research, Associate Professor Robert Cherny.

Supporting this, the Journal of Alzheimer's5 Disease recently published data from an independent laboratory showing the ability of the brain to move zinc in and out of neurons deteriorates with the progression of Alzheimer's Disease. These two papers are the latest of a number of high profile scientific articles that have been published on the role of metals in neurodegenerative diseases, supporting Prana's therapeutic strategy to treat these disorders.

Prana has recently commenced clinical trials for Alzheimer's Disease and Huntington's Disease, both using the drug PBT2.

Synopsis of PLoS ONE paper
In the paper the authors propose that sequestration of zinc by Abeta-amyloid deposits (Abeta oligomers and plaques) not only drives Abeta aggregation, but also disrupts zinc homeostasis in zinc-enriched brain regions important for memory and vulnerable to Alzheimer's Disease pathology, resulting in intra-neuronal zinc levels, which are either too low, or excessively high. Moreover, they carry out modeling to suggest that this can lead microtubule instability and the abnormal tau pathology, including neurofibrillary tangles (NFT).

To evaluate this hypothesis, the authors:

1) used molecular modeling of zinc binding to the microtubule component protein tubulin, identifying specific, high-affinity zinc binding sites that influence side-to-side tubulin interaction, the sensitive link in microtubule polymerization and stability.

2) performed kinetic modeling showing zinc distribution in extra-neuronal Abeta deposits can reduce intra-neuronal zinc binding to microtubules, destabilizing microtubules.

3) used metallomic imaging mass spectrometry (MIMS) to show anatomically-localized and age-dependent zinc dyshomeostasis in specific brain regions of Tg2576 transgenic, mice, a model for Alzheimer's Disease. We found excess zinc in brain regions associated with memory processing and NFT pathology.

They present a theoretical framework and support for a theory of Alzheimer's Disease linking extra-neuronal Abeta amyloid to intra-neuronal NFTs and cognitive dysfunction.

The connection, they propose, is based on beta-amyloid-induced alterations in zinc ion concentration inside neurons affecting stability of polymerized microtubules, their binding to MAP-tau, and molecular dynamics involved in cognition.

This theory supports novel Alzheimer's Disease therapeutic strategies targeting intra-neuronal zinc homeostasis and microtubule dynamics to prevent neurodegeneration and cognitive decline, such as PBT2.

1 Craddock TJA et al The Zinc Dyshomeostasis Hypothesis of Alzheimer's Disease. PLoS ONE (2012) 7(3): e33552. doi:10.1371/journal.pone.0033552

2 Lannfelt et al. "Safety, Efficacy, and biomarker findings of PBT2 in targeting Abeta modifying therapy for Alzheimer's Disease: a controlled phase IIa, double-blind, randomized, placebo-controlled trial", Lancet Neurology (2008) 7: 779-86.

3Lannfelt et al. Errata: Lancet Neurology (2009) 8: 981.

4Adlard PA et al Rapid Restoration of Cognition in Alzheimer'sTransgenic Mice with 8-Hydroxy Quinoline Analogs Is Associated with Decreased Interstitial A. Neuron (2008) 49: 43-55

5 Beyer, N et al Zinc Transporter mRNA Levels in Alzheimer's Disease Postmortem Brain. J Alz Dis (2012), 28: 1-11

[Finee]

Prana enrolls 1st patient in Reach2HD Phase II Huntington Disease trial

Prana Biotechnology announced that the first patient has been dosed in the "Reach2HD Trial" - a 6 month Phase IIa clinical trial testing PBT2, the company's drug in development for Huntington disease. Reach2HD, a double blind placebo controlled study, is enrolling 100 patients with early to mid-stage Huntington Disease. The Principal Investigator on the study is Dr. Ray Dorsey of Johns Hopkins University. The trial will be conducted in approximately 20 sites across the U.S. and Australia.
http://finance.yahoo.com/news/prana-enrolls-first-patient-re…

[Finee]

Prana Comments on Archives of Neurology Publication Which
Highlights Critical Role of Brain Metals in Huntington Disease
Progression
MGH team publishes data that supports the use of PBT2 in Huntington disease
Melbourne – 1 May 2012: Prana Biotechnology (NASDAQ:PRAN; ASX:PBT) today commented on the publication of new data of relevance to the current clinical trial, testing Prana’s PBT2 as a treatment for Huntington disease.
The authors of the publication are led by Professor Diana Rosas of the Center for Neuroimaging of Aging and Neurodegenerative disease at Massachusetts General Hospital (MGH) in Boston. The paper, entitled “Alterations in Brain Transition Metals in HD”, published in the Archives of Neurology* describes how the rise in levels of Iron in the brains of people carrying the mutant gene which causes Huntington disease,correlates with the severity of symptoms and also predicts the time of disease onset. The
article concluded that “an important and early role of altered metal homeostasis is suggested in the pathogenesis of Huntington disease” and this points to “metals as potential therapeutic targets”. Selected patients in the current Reach2HD trial, testing PBT2, will be monitored using the imaging technology described in the publication.
According to Professor Rudy Tanzi, Prana’s Chief Scientific Advisor and the Joseph P. and Rose F. Kennedy Professor of Neurology at Harvard University, "The new findings serve to further support the role of brain metal imbalances in the pathology of neurodegenerative diseases such as Alzheimer's disease and Huntington disease. It is becoming increasingly clear that PBT2 and Prana's other metal chaperone drugs could have broad utility as powerful modifiers of disease progress in a growing number of
neurodegenerative diseases caused by misfolded proteins."
Ira Shoulson MD, Professor of Neurology, Pharmacology and Human Science at
Georgetown University (Washington DC) and the Chair of the Executive committee of the Huntington Study Group said “The data from the Harvard group are very encouraging and timely. The Reach2HD trial is underway and intended to characterize the safety and dosing parameters of PBT2, an experimental drug aimed at restoring function to neurons damaged by the pathological interaction between the mutant Huntingtin protein and transition metals. PBT2 has signaled some cognitive benefit in
patients with Alzheimer disease that may also involve a pathological interaction between a protein and transition metals.”
Huntington disease is a complex and severely debilitating genetic, neurodegenerative disease, for which there is no cure. It is caused by an abnormally high number of repeats of a DNA sequence (CAG) which encodes for the amino acid glutamine. The disease often affects young adults and, whilst associated with severe physical movement symptoms, progressively impacts the mind and emotions as well. The disease causes incapacitation and death about 15-25 years after onset. The disease affects 30,000
people in the US and about 70,000 worldwide.

http://hotcopper.com.au/announcements.asp?id=424792

[Finee]

Professor Rudy Tanzi to Discuss PBT2 Trial on Thursdey, May 10

http://www.asx.com.au/asxpdf/20120509/pdf/42656s0mb1611w.pdf

[Fruehrentner]

http://www.spiegel.de/wissenschaft/medizin/alzheimer-demenz-…

[Finee]

Prana's PBT2 Presented at the Huntington's Disease Society of America National Convention
Prana's 'Reach2HD' Phase II Trial on Track
MELBOURNE, AUSTRALIA--(Marketwire -06/13/12)- Prana Biotechnology (PRAN) (PBT.AX) today announced that an update on Prana's Phase 2 clinical trial in Huntington disease (HD) was presented at the HDSA annual National Convention held in Las Vegas, Nevada over the weekend. Professor Ira Shoulson, Professor of Neurology, Pharmacology and Human Science and Director, Program for Regulatory Science & Medicine at Georgetown University spoke to the 'Reach2HD' trial objectives and potential future of PBT2 as a novel therapeutic strategy for the treatment of HD.
"We are hopeful that PBT2 can bring the same cognitive benefits to HD patients that it did to Alzheimer's disease (AD) patients in a Phase IIa trial," commented Geoffrey Kempler, Prana's Executive Chairman. Mr Kempler also commented that "the Reach2HD study has been initiated and enrollment commenced on time and it is pleasing that the trial has been so enthusiastically embraced by the HD community."
Phase II Reach2HD clinical trial
Prana has commenced an FDA approved Phase II placebo controlled double blind study in 100 early to mid-stage HD patients, in Australia and the US. The study, named 'Reach2HD,' is a 6 month clinical trial testing PBT2, the Company's drug in development for HD. The Principal Investigator on the study is Dr. Ray Dorsey of The Johns Hopkins University in Baltimore. For further information visit the Huntington Study Group website www.huntington-study-group.org
http://finance.yahoo.com/news/pranas-pbt2-presented-huntingt…

[Finee]

Kaufempfehlung für Prana!!!
http://www.pranabio.com/downloads/analyst_reviews/MLV%2012-0…

[Finee]

MLV VALUATION
Based on our long-term revenue and expense projections, and if
development of PBT2 and other drug candidates in Prana's pipeline
proceeds without any significant delays, unfavorable trial results, or
other negative surprises, we think Prana could become profitable in
2016 based on regulatory approvals and launch of PBT2 for
Huntington’s Disease in the US and EU, both in 2016. We use a
discounted P/E model applied to our projected 2016 EPS to arrive at
our current value of $4.50 per share and one-year price target of
$6.00 per share. In our view, a 45% discount rate is appropriate for
current uncertainties regarding the timing and outcome of ongoing
clinical trials. We believe a 25x P/E multiple is appropriate for our
projection of the company's growth.

[Fruehrentner]

Antwort auf Beitrag Nr.: 43.494.718 von Finee am 15.08.12 09:40:13

15.08.2012

New Analyst Report Recommends Prana

Prana Biotechnology receives a BUY Recommendation from MLV & Co. Equity Research.
Senior Biotech Analyst George Zavoico, Ph.D. says, "There is mounting evidence that compounds that can restore metal homeostasis in the neuron can stop and even reverse cognitive decline associated with neurodegenerative diseases. We think Prana's PBT2 could be such a compound."

To access the entire report, click here:

http://www.pranabio.com/downloads/analyst_reviews/MLV%2012-0…

[Finee]

Mega-Blockbuster Potential That’s Ready to Run

Prana Biotechnology (ASX: PBT) is a small Melbourne based biotechnology company in search of a cure for one of the few remaining unmet medical needs with mega-blockbuster potential, Alzheimer’s Disease. A cure for this neurodegenerative disorder would be a massive relief for AD sufferers, their families, and society, as the worldwide annual cost of AD is reported to be $600 billion per year. It would also be hugely rewarding for shareholders of the company that wins the AD development race. And there’s a chance that could be Prana!
A cure for AD is estimated to be worth around $25 billion in annual sales. Consequently it is an area that has attracted significant research. Unfortunately neurological trials are the graveyard of clinical development. Trials have an expensive and difficult development path as highlighted by a number of AD Phase III failures; including Eli Lilly’s Semagacestat in 2010 and Pfizer’s Dimebon in 2012. So far the front runners have all fallen at the final post.

A Quick History

Prana was founded in 1997 to commercialise research into Alzheimer’s Disease and other major age-related neurodegenerative disorders. It listed on the ASX in March 2000 with the ticker PBT and a Nasdaq listing followed in September 2002, ticker PRAN. More interestingly, Prana is Sanskrit for “vital life”, it is the notion of a vital, life-sustaining force of living beings. Yes, I did award bonus marks for a totally cool name!
Prana’s key compound, PBT2, recently commenced a Phase IIb clinical trial for the treatment of AD and a Phase IIa trial for Huntington’s disease. Flipping back to the past, PBT2 successfully completed PIIa trials in February 2008. Investors were expecting a partnering deal to be announced soon after, and rumours about a deal surfaced on message boards towards the end of 2008.
However, it’s now 4 years since the Phase IIa trial, and not only did no deal eventuate, but it took Prana until the end of 2011 to commence recruitment for its next trial.

Looking Forward

Prana commenced recruitment for its 12 month PBT2 Phase II imaging trial, called IMAGINE, in November 2011. This double blind, placebo-controlled trial will enrol 40 patients with early or mild Alzheimer’s Disease in Melbourne. The first patient was dosed in early March 2012.
Due to limited capital, Prana is developing its pipeline at a snail’s pace. So let’s take a closer look at its funds. The company had $5.64 million in cash at the end of June 2012 and $5.45 million in net current assets at 31 December 2011. Operations consumed $3.9 million in the second half of last year, but that was without major trials. Cash burn will skyrocket this year, and while the IMAGINE trial has received funding from the Alzheimer’s Drug Discovery Foundation (ADDF), Prana’s funding position is unclear.
Massive Market Potential

Alzheimer’s Disease is a massive unmet market. Recent reports suggest that there are now over 26 million Alzheimer’s sufferers worldwide.
Current AD drugs provide little more than symptomatic relief. They neither cure AD nor meaningfully improve cognition. Yet, those drugs still ring up around $6 billion in annual sales. So the race is on to find a disease modifying drug.
The market size for AD drugs that do improve cognition has been estimated at $25 billion annually. It is one of the few remaining potential mega-blockbusters and big pharma would dearly love to be first to market with a cure.
PBT2 is well protected by patents, and supported by solid science. Its Phase IIa study was published in The Lancet Neurology journal and there are numerous peer reviewed papers by leading AD scientists demonstrating that Prana’s approach to finding a cure for Alzheimer’s is sound. PBT2 has been designed to be a disease modifying drug that prevents the formation of toxic forms of the Abeta protein in the synapses of the brain and to improve neurotransmission, resulting in improved cognition.
It’s All in the Pipeline

The Phase IIa results in early 2008 demonstrated that PBT2 was safe and tolerable, and able to modify the course of Alzheimer’s disease by reducing the patient’s levels of amyloid beta, a protein understood to be a significant factor in Alzheimer’s. It demonstrated an improvement in executive function, an important aspect of cognitive performance, and reduced the levels of Abeta in the spinal fluid of patients.

Source: Prana’s website 14 August 2012
To date, Prana’s 800 strong novel compound library has yielded a phase II candidate for Alzheimer’s and Huntington’s with PBT2, Parkinson’s with PBT434 and brain cancer with PBT519.
Prana announced in early January that it has received approval from the United States Food and Drug Administration (FDA) to start recruiting patients for the company’s first clinical trial using PBT2 in patients with Huntington’s Disease (HD). Enrolment of the planned 100 patients in the 34 week, double-blind, placebo-controlled study has recently commenced. HD affects 30,000 people in the US and about 70,000 worldwide.
In August 2011 Prana announced it at had received a grant from The Michael J. Fox Foundation to support the initiation of pre-clinical studies for PBT434.

Competition

As we live longer the number of people suffering with AD is growing. This already large un-met medical problem continues to grow, and with baby boomers now approaching the age of AD onset, a cure becomes all the more important. The potential market is huge and growing.
So it’s no surprise that big pharmaceutical companies are lining up to take a shot on the AD goal. For the sake of sufferers I desperately hope someone scores a goal soon. If it’s Prana all the better!
Competitors include a ‘who’s who’ of large pharmaceutical companies, but it is rumoured there is not a lot of promise among their compounds. Recent research has highlighted that many of the current compounds including Pfizer’s bapineuzumab, which is in phase 3 trials, may be aiming at the wrong target. As Prana’s Chairman and CEO, Geoffrey Kempler, said in the 2011 annual report, “PBT2 is strongly placed to avoid many of the issues that have emerged, as it works in a unique way that is very different to these failed approaches.”
AstraZeneca has one drug in phase 2 and three in phase 1. Roche’s pipeline is more advanced, it has three compounds in phase two trials and a fourth in phase one.
Despite Dimebon’s failure, Pfizer still has bapineuzumab, a beta amyloid inhibitor, in phase 3 trials along with three other drugs and a vaccine in early clinical trials. GSK also have a drug in phase 2 trials.

[Finee]

Nachtrag:

With significant news flow expected over the next year Prana will gain more attention. There will be trial updates, publications and possibly more patents. The news flow should underpin the share price and attract the attention of more investors.
As a valuation benchmark, Pfizer paid an industry high US$225 million upfront with up to $500 million in milestones, for the rights to Medivation’s Dimebon. Prana is unlikely to get such an incredible deal for PBT2 rights, but with a market cap under $50 million any deal should deliver massive upside.
PBT2 is a good asset that has shown promise in trials. The current IMAGINE trial should trigger fresh interest by large pharmaceutical companies. If the trial confirms that PBT2 can improve cognition, this speculative punt should be highly rewarding.

[Finee]

Prana Biotechnology ( PBT) Stock Price
Australian Stock Exchange
http://au.advfn.com/p.php?pid=qkquote&symbol=PBT&s_ok=OK&btn…

[Fruehrentner]

Prana Provides Clinical Trials Update

22.08.2012

Melbourne - 22 August, 2012; Prana Biotechnology (NASDAQ:PRAN; ASX:PBT) today reported on its progress in its Phase II clinical trials with its lead development asset PBT2. PBT2 has a unique therapeutic action that can benefit people suffering neurodegenerative disease because of its specialized ability to prevent the toxic relationship between disease proteins and biological metals in the brain.

Prana's world leading work in neurodegenerative diseases is capturing significant international recognition, particularly at a time when other potential treatments are failing.

"There is mounting evidence that compounds that can restore metal homeostasis in the neuron can stop and even reverse cognitive decline associated with neurodegenerative diseases. We think Prana's PBT2 could be such a compound," said New York based MLV & Co. Equity Research, Senior Biotech Analyst George Zavoico, Ph.D. The full report is available at www.pranabio.com.


Alzheimer's disease Trial Update - the "IMAGINE" trial

In an earlier 12 week trial PBT2 both significantly changed amyloid levels in spinal fluid and improved the cognition of patients with Alzheimer's disease.1,2 The IMAGINE trial, with 12 months of treatment, aims to establish PBT2 as a safe and effective treatment for Alzheimer's disease. The following provides an update on the trial:

. 100% of sites approved and open for recruitment;
. 40% of patients in dosing;
. Recruitment On Track to report 2H13;
. 3 patients have reached 24 weeks of dosing - doubling the previous longest exposure to PBT2;
. No serious adverse events reported; and
. First Data Safety Monitoring Board meeting in September 2012, reporting on safety and tolerability.

The randomized, double-blind, placebo controlled trial is enrolling 40 patients with prodromal or mild Alzheimer's disease in five sites in Melbourne, Australia. Brain Imaging is being used to measure PBT2's effect on amyloid deposits in the brain (using PiB-PET scanning) and effects on increasing brain activity (FDG PET). Cognition effects are being measured by the Neuropsychological Test Battery (NTB).


"The results of the IMAGINE trial will be closely watched by the Alzheimer's community, given the recent failure of several late-stage therapeutic candidates. We believe that PBT2's mechanism of action explains the clinical benefits that the drug has already shown, and we anticipate positive results from this trial," said Chief Executive Officer, Mr Geoffrey Kempler.

The trial has received funding from the Alzheimer's Drug Discovery Foundation (ADDF).

Howard Fillit, MD, the ADDF's Executive Director commented, "PBT2 stands out as one of the few orally available agents with clinical trial evidence of cognitive benefit for Alzheimer's patients. Success in this trial will demonstrate target engagement by PBT2 in the brain of people with Alzheimer's disease, and accelerate the clinical development of PBT2 to patients."

The protocol for the IMAGINE trial is available by clicking here.


Huntington Disease Trial Update - the "Reach2HD" trial

The Reach2HD trial is a 6 month trial in 100 patients with early to mid-stage Huntington disease. An IND was opened to conduct the trial across sites in the USA and Australia. The following provides an update on the trial:

. 70% of sites approved and open for recruitment;
. 14% patients in dosing;
. Recruitment On Track to report 2H13;
. No serious adverse events reported; and
. First Data Safety Monitoring Board meeting in October 2012, reporting on safety and tolerability.

Professor Ira Shoulson, Professor of Neurology, Pharmacology and Human Science at Georgetown University (Washington DC) and the Chair of the Executive Committee of the Huntington Study Group said: "PBT2 attracted our attention as an experimental drug with the potential to bring real benefit to Huntington disease patients who suffer from a range of motor, behavioural and cognitive symptoms. The favourable signals from the PBT2 trial in Alzheimer's disease are particularly promising."

Only one drug is marketed for Huntington disease and that is only for the relief of the severe motor or chorea symptoms. There are no approved treatments for the significant cognitive and behavioural components of the disease, which typically manifest before motor problems.

"The trial objective is to demonstrate safety, motor and behavioural benefits and the same cognitive benefits for Huntington's patients that it has already demonstrated in Alzheimer's patients treated with PBT2," said Mr Kempler.

The protocol and site updates for the Reach2HD trial can be accessed by clicking here.

References
1. Lannfelt et al. Lancet Neurology (2008) vol. 7, pp. 779-86;
2. Lannfelt et al. Erratum: Lancet Neurology (2009) vol. 8, pp. 981.

About Prana Biotechnology Limited
Prana Biotechnology was established to commercialize research into age-related neurodegenerative disorders. The Company was incorporated in 1997 and listed on the Australian Securities Exchange in March 2000 and listed on NASDAQ in September 2002. Researchers at prominent international institutions including The University of Melbourne, The Mental Health Research Institute (Melbourne) and Massachusetts General Hospital, a teaching hospital of Harvard Medical School, contributed to the discovery of Prana's technology.

For further information please visit the Company's web site at www.pranabio.com.

About Huntington disease
Huntington disease is a complex and severely debilitating genetic, neurodegenerative disease, for which there is no cure. The disease often affects young adults and, whilst associated with severe physical movement symptoms, progressively impacts the mind and emotions as well. The disease causes incapacitation and death about 15-25 years after onset. The disease affects 30,000 people in the US and about 70,000 worldwide. There are no drugs in development that have established clinical evidence for treating cognitive decline.

About the Alzheimer's Drug Discovery Foundation
The Alzheimer's Drug Discovery Foundation (ADDF) is the only non-profit organization whose sole mission is to accelerate the discovery and development of drugs to prevent, treat and cure Alzheimer's disease, related dementias and cognitive aging. Since 1998, the ADDF has granted more than $50 million to fund over 325 Alzheimer's drug discovery programs in academic centers and biotechnology companies in 18 countries. For more information about the Foundation, please visit www.AlzDiscovery.org.

[Fruehrentner]

ABC Radio Program Features Prana's Alzheimer's Trial

22.08.2012

Melbourne - 22 August, 2012: Prana Biotechnology (NASDAQ:PRAN; ASX:PBT) today advised that Professor Michael Woodward, the National Study Coordinator for the Company's Alzheimer's disease IMAGINE trial, will be interviewed by ABC Radio commentator Jon Faine.

Prof. Woodward has been invited on to the program to discuss the IMAGINE trial. The interview will take place on ABC 774 Melbourne at 9.35am (Australian EST) Thursday 23rd August.

The IMAGINE trial, with 12 months of treatment, aims to establish PBT2 as a safe and effective treatment for Alzheimer's disease. People aged 55 plus with mild Alzheimer's disease are participating in the trial. The company has announced that this trial is progressing well with 100% of sites approved and actively recruiting. Already 40% of patients are in dosing with PBT2 and importantly no serious adverse events have been reported.

Currently, all available treatments for Alzheimer's disease provide some degree of symptomatic relief; however, none change the course of the disease, or the eventual decline in a patient's cognition and health. An extensive body of research suggests that PBT2 could do just that; disrupt the progression of Alzheimer's disease and potentially stop the onset of the disease. Notably, this study has huge relevance for people who are experiencing the first stages of memory loss.

Prof. Woodward is one of the world's leading experts in neurodegenerative disease and geriatrician.

To register your interest in the trial please call 1800 837 683.

[Fruehrentner]

24.08.2012

Demenz-Medikament: Pharmakonzerne scheitern reihenweise an Alzheimer-Arzneien

http://www.spiegel.de/wissenschaft/medizin/alzheimer-medikam…

[Finee]

Prana's Parkinson's Drug Meets Michael J. Fox Foundation Development Milestone
MELBOURNE, AUSTRALIA--(Marketwire -08/29/12)- Prana Biotechnology Limited (PRAN) (PBT.AX) announced today that its lead compound in development for Parkinson's disease (PD), PBT434, had progressed successfully though a series of preclinical development studies used to assess the suitability of a candidate compound for human clinical studies. The studies were funded by The Michael J. Fox Foundation (MJFF) 2011 Pipeline Program to support its 'Therapeutic Development Initiative.' The MJFF Program grant is milestone based. PBT434 achieved all of its milestones in preclinical toxicology studies, genotoxicity and safety pharmacology -- allowing the compound to be positioned for larger scale animal toxicology studies prior to commencing clinical trials.
PBT434 is a novel, orally available compound that easily crosses into the brain and is able to exert potent neuroprotective properties. Most particularly, it preserves the brain tissue in PD that degenerates over time, the substantia nigra. By preserving this tissue, Prana's scientists have demonstrated significant restoration of motor coordination and strength in animal models. PBT434 has been shown that it is able to impede the iron-induced oxidative damage and neurotoxic cascade that kills the substantia nigra. As such, PBT434's mechanism of action offers a novel disease modifying therapeutic strategy in contrast to the currently marketed symptomatic agents that, at best, serve to reduce the side effects of the disease rather than alter its course.
"Based on these efficacy studies and now the completion of this suite of preclinical development assessments, Prana will look to move PBT434 into longer term toxicology studies in parallel to our scale up manufacturing plans for PBT434. All being well, we could file an IND by the end of next year and commence clinical trials in 2014," said Mr. Geoffrey Kempler, Prana's Executive Chairman. "PBT434 also marks another product pipeline milestone for Prana to complement our two ongoing trials with PBT2 in Alzheimer's disease and Huntington disease," commented Mr. Kempler.
Parkinson's disease is a devastating illness which can result in not only the loss of muscle control, speech, balance and digestive functions; it may also impair a patient's psychiatric and cognitive function. With 4 million people affected worldwide, Parkinson's disease is the second most common neurological indication behind Alzheimer's disease. The current market size for drugs to treat Parkinson's disease is approximately $4 billion per year; however most currently available drugs primarily treat the symptoms and do not actually prevent the ongoing destruction of the substantia nigra in the brain and progression of the disease.
* The program grant title is 'PBT434, a novel neuroprotective drug for Parkinson's Disease; completion of pre-clinical studies to enable human clinical trials.'
http://finance.yahoo.com/news/pranas-parkinsons-drug-meets-m…

[Finee]

BUY RECOMMENDATIONS

Prana Biotechnology (PBT)

Development of its PBT 2 drug for treating Alzheimer’s and Huntington’s diseases has provided encouraging responses during clinical phase 2 trials. This company has the potential to tap into a multi-billion dollar pharmaceutical market if the trials prove successful. A speculative buy.
http://www.thebull.com.au/premium/a/31077-18-share-tips---3-…

[Fruehrentner]

Antwort auf Beitrag Nr.: 43.565.358 von Finee am 04.09.12 09:18:16

Weitere werden bestimmt folgen

Dennoch: High Risk - wie bei allen Biotechs

[Finee]

Prana Shows Significant Promise in the Fight Against Alzheimer's Disease, According to Experts at Celebration of Science Conference
MELBOURNE, AUSTRALIA--(Marketwire - Sep 10, 2012) - Prana Biotechnology ( NASDAQ : PRAN ) ( ASX : PBT ) today provided highlights and excerpts from the panel discussion, entitled 'Alzheimer's and Other Issues of Aging,' which took place on Sunday, September 9th at the Celebration of Science Conference in Washington, D.C. Freda Lewis-Hall, Executive Vice President and Chief Medical Officer of Pfizer, moderated the panel. The Celebration of Science gathered over 1,000 leaders from the scientific, government, industry, philanthropic and academic communities to honor the tremendous accomplishments of science and to discuss promising possibilities for future breakthroughs.
Professor Jeffrey Cummings, Director of the Cleveland Clinic Lou Ruvo Center for Brain Health in Las Vegas, and Chairman of Prana's Scientific Advisory Board, discussed the rising Alzheimer's epidemic among the aging US population and the need to find drugs that can reverse the disease. According to Dr. Cummings, "Patients with Alzheimer's Disease urgently need new therapies. While recent late stage clinical drug failures are disappointing, there is a promising pipeline of emerging therapies including PBT2, Prana's metal-protein attenuating compound."
Dr. Rudy Tanzi, Joseph P. and Rose F. Kennedy Professor of Neurology, Harvard Medical School and Prana's Chief Scientific Advisor, reviewed why he felt that the late-stage therapeutic candidates had failed and said that there is mounting evidence that compounds like PBT2 that can simultaneously prevent amyloid beta protein from accumulating, neutralize its toxicity, and restore metal homeostasis in the neuron can stop and perhaps even reverse the neurodegenerative process of Alzheimer's Disease. According to Professor Tanzi, "Prana's PBT2 may prove to be the winning technology, based on not only a large and growing literature of scientific research but also on Phase II trial data. PBT2 has a unique therapeutic action that can benefit people suffering neurodegenerative disease because of its specialized ability to prevent the toxic relationship between disease proteins and the metals, zinc and copper, in the brain. In a 12 week trial PBT2 both significantly lowered beta-amyloid levels in spinal fluid and improved the cognition of patients with Alzheimer's Disease."
The currently ongoing IMAGINE trial, with 12 months of treatment, aims to establish PBT2 as a safe and effective treatment for Alzheimer's Disease. The double blind placebo controlled trial is enrolling 40 patients with prodromal or mild Alzheimer's Disease in five sites in Melbourne, Australia. Brain Imaging is being used to measure PBT2's effect on amyloid deposits in the brain (using PiB-PET scanning) and effects on increasing brain activity (FDG PET). Cognition effects are being measured by the Neuropsychological Test Battery (NTB).
Prana is also conducting a 6 month trial in 100 patients with early to mid-stage Huntington's Disease and the company believes that PBT2 has the potential to bring real benefit to Huntington's Disease patients who suffer from a range of motor, behavioural and cognitive symptoms. The trial objective is to demonstrate safety, motor and behavioural benefits and the same cognitive benefits for Huntington's patients that it has already demonstrated in Alzheimer's patients treated with PBT2.
The Celebration of Science gathered over 1,000 leaders from the scientific, government, industry, philanthropic and academic communities to honor the tremendous accomplishments of science so far and to imagine what's possible for the future.

[Finee]

Prana Biotechnology gets green light for Alzheimer’s clinical trial
Wednesday, September 12, 2012 by Angela Kean
Prana Biotechnology (ASX: PBT, NASDAQ: PRAN) has received a recommendation from the Data Safety Monitoring Board that its clinical trial of PBT2 to treat Alzheimer’s disease continue as planned following an initial review of clinical data. The 12-month IMAGINE trial aims to establish PBT2 as a safe and effective treatment for Alzheimer’s disease. The double blind placebo controlled trial is enrolling 40 patients with prodromal or mild Alzheimer’s disease in five sites in Melbourne. Brain imaging is being used to measure PBT2’s effect on amyloid deposits in the brain and effects on increasing brain activity.
In the current trial, all of the sites have been approved and are open for recruitment with 45% of patients already in dosing. Three patients have reached 28 weeks of dosing, over double the previous longest exposure to PBT2, with no serious adverse events reported.
In an earlier 12 week trial, PBT2 both significantly changed amyloid levels in spinal fluid and improved the cognition of patients with Alzheimer’s disease. PBT2 has a unique therapeutic action that can benefit people suffering neurodegenerative disease because of its specialised ability to prevent the toxic relationship between disease proteins and the metals, zinc and copper in the brain. Scientific experts have described it as a promising emerging therapy.
Continued success in the development of PBT2 has piqued investor interest, with shares gaining over 71% in the past four months.
Shares hit an intra-day high of A$0.24 yesterday following positive comments on PBT2 from scientific leaders at the recent Celebration of Science Conference in Washington D.C., up from a low of $0.14 in mid-May.
http://www.proactiveinvestors.com.au/companies/news/33366/pr…

[Fruehrentner]

[Fruehrentner]

Therapy Trends: Alzheimer’s Disease
Beta-amyloid light fades to leave development hole

An incisive, dynamic analytical report that uses insight from the most influential key opinion leaders (KOLs) in Alzheimer’s disease (AD) to map the current treatment landscape and identify future trends.

Alzheimer’s Disease: Beta-amyloid light fades to leave development hole
By the end of 2012, the Alzheimer’s disease market will reach a pivotal stage with the release of Phase III results of disease-modifying therapies, and new research into biomarkers to aid early AD diagnosis. If positive, these results will validate the beta amyloid approach, but if negative, it will represent a huge blow to Alzheimer’s research. Recent trends in the AD market also represent a clear shift in researchers’ approaches to detecting, treating and preventing AD.

‘Therapy Trends: Alzheimer’s Disease’ is compiled from exclusive, in-depth interviews with the world’s leading KOLs in AD. It identifies and analyses the major factors, advances and trends currently influencing the AD treatment landscape. The report focuses on late-stage pipeline products, and how these could modify future AD management.

http://www.firstwordplus.com/therapy_trends_alzheimers_disea…






Es wird spannend ...

[Fruehrentner]

Prana's PBT2 Clinical Trials Cited as Most Advanced in Addressing Neurodegeneration from the Metal Equilibrium Perspective

20.09.2012

Melbourne - September 20, 2012

Prana Biotechnology (NASDAQ: PRAN; ASX: PBT) today reported that it had been cited in an interview in The Life Sciences Report with George Zavoico, Ph.D., senior equity analyst and managing director with MLV & Co., as the only drug company to address in clinical trials the control of transition metal levels in neuronal synapses, a key event in age-related dysfunction of the brain. The Report citing Prana is titled, "Seven Innovative Biotechs That Could Soar By Year-End".

In the published interview, Dr. Zavoico spoke about an emerging hypothesis addressing the formation of beta amyloid plaques, and how another neuronal protein, tau, is hyperphosphorylated, enabling it to form neurofibrillary tangles. These are recognized by experts in the field as key events in age-related brain dysfunction and cognitive loss. The basis for what has been called the "Metals Dyshomeostasis Hypothesis" is the abnormal distribution and loss in the control of transition metal levels in neuronal synapses. Dr. Zavoico said, "Metals like zinc, copper and iron have a number of important biologic functions, most notably in the function of numerous enzymes and receptors. Zinc, in particular, binds to beta amyloid, leading to its aggregation and, ultimately, plaque formation".

Moreover, studies have shown that abnormal distribution of transition metals driven partly by beta amyloid plaque formation affects the function of tau, an intracellular protein essential for normal neuronal function. Tau becomes hyperphosphorylated and forms neurofibrillary tangles, which is thought to cause neuronal cell death.

Prana is evaluating the potential clinical benefit of PBT2 in two Phase II trials in two different neurodegenerative diseases. In Alzheimer's disease, the IMAGINE trial, a double-blind placebo controlled trial enrolling 40 patients with prodromal or mild Alzheimer's disease, being treated for 12 months will test cognition and use brain imaging to measure the effects of PBT2 on beta-amyloid deposits in the brain and effects on increasing brain activity.

In the interview, Dr. Zavoico added: "In preclinical studies, Prana's lead drug candidate, PBT2, has been shown to redistribute zinc and other transition metals, preventing beta amyloid aggregation and even inducing its disaggregation. Sequestration of zinc in beta amyloid plaques reduces zinc levels inside the neuron, which can lead to its [tau protein's] hyperphosphorylation. The metals hypothesis appears to unify the pathology underlying both amyloid plaque and neurofibrillary tangle formation, which makes this approach so compelling, in my mind".

Notably, Huntington's disease is also characterized by misfolding and aggregation of proteins, but of Huntingtin protein, not beta amyloid. Like Alzheimer's, studies indicate that the pathology underlying Huntington's disease is also due to abnormal distribution of certain transition metals. The Reach2HD trial, enrolling 100 patients with early to mid-stage Huntington's disease, being treated for 6 months, aims to demonstrate safety, motor and behavioural benefits and the same cognitive benefits for Huntington's patients that it has already demonstrated in Alzheimer's patients treated with PBT2. Results of Prana's clinical trials are expected in the second half of next year.

Prana's CEO, Geoffrey Kempler, commented that "it is very encouraging that the strength of our science and the clinical potential of PBT2 is being recognized by industry experts and analysts, particularly at a time when so many competing drug candidates to treat Alzheimer's have failed to meet their clinical endpoints. As some researchers are losing hope that Alzheimer's can even be treated, we remain very confident in the potential of PBT2 to help patients".

*The Life Sciences Report, A Streetwise Report, September 13, 2012.

[Fruehrentner]

Study Shows Stem Cells May Prevent And Cure Alzheimer's

27 Sep 2012

Revolutionary Findings in Study by Seoul National University & RNL Bio Stem Cell Technology Institute Suggest the First Real Breakthrough toward Preventing Alzheimer's and Helping Millions of Patients and Families by Relieving its Symptoms

SEOUL, South Korea I September 26, 2012 I In the first study of its kind, researchers at Korea's leading university and the RNL Bio Stem Cell Technology Institute announced this week the results of a study that suggests an astounding possibility: adult stem cells may not only have a positive effect on those suffering from Alzheimer's disease, they can prevent the disease. Using fat-derived adult stem cells from humans [scientific term: adMSCs, or human, adipose-derived mesenchymal stem cells], researchers were able to cause Alzheimer's disease brains in animal models to regenerate. The researchers, for the first time in history, used stem cells to identify the mechanism that is key to treatment of Alzheimer's disease, and demonstrated how to achieve efficacy as well as prevention of the symptoms of Alzheimer's with adult stem cells, a "holy grail" of biomedical scientists for decades.

Alzheimer's disease, the most common form of dementia (loss of brain function), is the 6th leading cause of death, and affects 1 in 8 people -- more than breast cancer. As of 2010, there were 35.6 million people with Alzheimer's disease in the world, but this number is expected to double every 20 years. It is estimated that the total cost of Alzheimer's is US $604 billion worldwide, with 70% of this cost in the US and Europe. To put that in perspective, Alzheimer's care costs more than the revenues of Wal-Mart (US$414 billion) and Exxon Mobil (US$311 billion), according to the British World Alzheimer's Report of ADI. The cost of Alzheimer's is at the top of health economists' list of the disorders of aging that could topple nations' entire economies, and that regularly ruin not only the lives of patients but of their relatives.

According to the results of this first major study, Alzheimer's may soon be a preventable disease, or even a thing of the past. Equally important, the safety human administration of the kind of adult stem cells used in this experiment has been established in multiple articles and government-approved clinical trials.

THE RESEARCH:

The study was jointly led by Seoul National University Professor Yoo-Hun Suh and RNL Bio Stem Cell Technology Institute (SCTI) director Dr. Jeong-Chan Ra.

The researchers and their teams injected stem cells into mice genetically designed to have the core symptoms and physiology of Alzheimer's disease. They were able to identify that these human stem cells, derived from adipose tissue, behave in a very special way when injected into the tail vein of mice subjects. The cells migrated through the blood brain barrier, thought by many to be impossible for adult stem cells to cross, and went into the brain. In fact, fluorescent labeled cells were monitored for distribution in subjects and the team identified that the infused cells migrated throughout the bodies including brain except the olfactory organ, and therefore confirmed that IV infused stem cell can reach to the brain across the blood brain barrier.

The team infused human adipose stem cells intravenously in Alzheimer model mice multiple times two weeks apart from three month to 10 month. Once there, the mice who received cells improved in every relevant way: ability to learn, ability to remember, and neuropathological signs. More important, for the first time ever, Alzheimer model mice showed the mediation of IL-10, which is known for anti-inflammation and neurological protection.

The team also found that stem cell restored special learning ability from Alzheimer model subjects with great reduction of neuropathy lesions. This was found using tests used for Alzheimer's disease: behavioral assessment. In assessment it was found, amazingly, that stem cells' therapeutic effect on Alzheimer's disease was tremendous. This was also found in pathological analysis. The key though was prevention: the scientists showed that stem cells, when infused into Alzheimer's mice, decreased beta amyloid and APP-CT, known to cause brain cell destruction, leading to dementia and Alzheimer's disease. In the lab it was clear that stem cells increased neprilysin, which hydrolyzes toxic proteins. No other compound or treatment has ever suggested so strongly the potential to prevent, as well as stop, this epidemic of incurable dementia sweeping across suffering patients and their families.

Stopping Alzheimer's disease, let alone preventing it, is the focus of thousands of researchers worldwide. Speaking of their breakthrough discovery, Professor Yoo-Hun Suh, who led the study, said, "It is a ground breaking discovery that such a simple method as IV injection of the safest autologous adipose stem cells, without causing any immune rejection, or any ethical issues, opened a new door to conquering Alzheimer's disease, one of the most horrible, expensive and incurable diseases of our time." Joining him, leader of the RNL Bio Stem Cell Technology Institute Dr. Jeong-Chan Ra said, "It has never been more clear that it is an ethical imperative for governments to provide patients with incurable diseases with their right to participate not only in studies like this but in therapies with such obvious potential, once they have been tested as many times for safety as has our technology." Both scientists stressed that the real breakthrough in their complex research is the prevention of the onset of symptoms.

Specifically, stem cells grafted in the brain, in another part of the study, were identified to induce cell division and neuro differentiation of endogenous neuro progenitor cells around the hippocampus and its surrounding cells and increase in great deal the stability of dendrites and synapses. Stem cell also contributed various anti-inflammatory and neuro growth factors, especially increased the expression of IL-10. This again suppressed apoptosis of brain neurons, the prevention effect against Alzheimer's disease.

Dr. Ra of RNL Bio noted that, "RNL Bio has already completed government-approved clinical trials confirming the efficacy of RNL Bio stem cells in the management and treatment of other diseases, including osteoarthritis, limb ischemia, and progressive hemifacial atrophy (Romberg's disease)."

This study was published in a recent volume of the renowned, peer-reviewed U.S. medical journal PLOS ONE. Images, plans for future efforts, and impact on this crushing disease will be discussed when the scientists discuss the details of this revolutionary study in a press conference in Seoul on September 27th.

SOURCE: RNL BIO CO., LTD.

[Fruehrentner]

Prana Scientist to Participate in Webcast to Discuss Alzheimer's Disease Therapeutics

28.09.2012


Melbourne - September 28, 2012; Prana Biotechnology (NASDAQ: PRAN; ASX: PBT) today announced that Chief Scientific Advisor, Rudy Tanzi, Joseph P. and Rose F. Kennedy Professor of Neurology, Harvard Medical School will take part in a webcast hosted by George Zavoico, Ph.D., Managing Director and Senior Analyst, of MLV & Co. The topic of the webcast will be: "Alzheimer's Disease Therapeutics: Recent Setbacks and Emerging Alternatives." The webcast will take place on Monday, October 1, at 2:00 pm Eastern Daylight Time (New York City).

The session will consider what are the most promising new technologies for fighting Alzheimer's Disease which currently affects more than 36 million people worldwide. Participants will hear about innovative technologies and the best way forward for combating Alzheimer's and other age related diseases. Professor Tanzi will address the potential impact of the recent failures of Pfizer's bapineuzumab and Eli Lilly's solanezumab Phase 3 trials and discuss the possible scientific reasons why they did not succeed.

Investors are invited to participate. To obtain dial-in information please contact: Leslie Goedken at 646-556-9206, [e-mail]; or Scott Ammaturo at 646-556-9218, [e-mail]. A toll free number from Australia will be provided for callers when they RSVP by phone or by email to the MLV names provided.

[Fruehrentner]

Prana Announces A$6 Million Capital Raising

02.10.2012

Melbourne - October 1, 2012 : Prana Biotechnology Limited (NASDAQ: PRAN; ASX: PBT) today announced that it has raised A$6.0 million (approx.) through a placement of 32,500,000 ordinary fully paid shares (equivalent to 3.25 million Nasdaq listed ADRs) at a price of A$0.185 per share. The placement attracted strong demand even though the amount raised was restricted by the number of shares which could be issued by the Company under ASX listing rule 7.1, thereby not requiring a separate meeting of shareholders.

The placement was subscribed by a range of leading Australian institutional investors within the healthcare sector in Australia, as well as several High Net Worth Investors. The placement was managed by JM Financial Group Limited, based in Melbourne.

The capital was raised in order to support Prana's two ongoing Phase 2 clinical trials, the IMAGINE trial and Reach2HD trial, testing the effects of its lead drug candidate, PBT2, in Alzheimer's and Huntington disease patients, respectively. Results are anticipated to be reported in 2H13.

"The funds raised by Prana via this placement, reflect strong commitment to Prana's clinical development programmes and the commercial opportunity this provides. The endorsement of and participation by some of Australia's leading healthcare investors is very welcome" said Geoffrey Kempler, Prana's Executive Chairman.

Prana management and scientific advisors are on a roadshow this week in Melbourne New York, Boston and London, updating the investment community on Prana's progress.

[Finee]

Das kann sehr interessant werden!

Targeting Metals in Alzheimer's and Other Neurodegenerative Diseases

Thursday, November 29, 2012 | 12:00 PM - 4:00 PM
The New York Academy of Sciences

Presented by the Brain Dysfunction Discussion Group at the New York Academy of Sciences

Alzheimer's disease (AD) is characterized by elevated brain iron levels and accumulation of copper and zinc in cerebral β-amyloid deposits. Both ionic zinc and copper accelerate the aggregation of Aβ, the principle component of β-amyloid deposits. Copper and iron can also promote the neurotoxic redox activity of Aβ and induce oxidative cross-linking into stable oligomers. Recent reports documented the release of Aβ together with ionic zinc and copper in cortical glutaminergic synapses following excitation, leading to the formation of Aβ oligomers. Excessive accumulation of Aβ oligomers in the synaptic cleft is thought to adversely affect synaptic neurotransmission, and transition metals have been implicated in the misfolding and accumulation of a-synuclein and Huntington protein in Parkinson's and Huntington's diseases (PD and HD), respectively, as well as tau hyperphosphorylation in AD, contributing to disease pathogenesis and progression. The "Metal Hypothesis of Neurodegenerative Diseases" is proposed to describe the underlying, possibly causative, events, leading to the neuropathology that drives AD, PD, and HD. This symposium examines how these findings led to the discovery of small molecules designed to restore the physiologic balance of transition metals in the brain, prevent further accumulation of misfolded proteins, and possibly even have a disease-modifying effect. A review of the early clinical experience of one such compound, PBT2, will be presented.

Organizers
Rudolph Tanzi, PhD (PRANA)
Massachusetts General Hospital and Harvard Medical School

George Zavoico, PhD
MLV & Co.

Jennifer Henry, PhD
The New York Academy of Sciences

Speakers
Robert A. Cherny, PhD (PRANA)
The Florey Institute of Neuroscience and Mental Health, Australia

Steven M. Hersch, MD, PhD
Massachusetts General Hospital and Harvard Medical School

Rudolph Tanzi, PhD
Massachusetts General Hospital and Harvard Medical School

Dan Tardiff, PhD
Whitehead Institute for Biomedical Research

http://www.nyas.org/Events/Detail.aspx?cid=1c84a5bc-6abb-4a6…

[Finee]

Notice of Annual General Meeting and
Explanatory Memorandum
http://hotcopper.com.au/announcements.asp?id=497325

[Finee]

Folgendes gefunden:

(Forum: ASX - By Stock (Back)
Code: PBT - PRANA BIOTECHNOLOGY LIMITED
Post: 8770233
Reply to: #8769274 from skint Views: 100
Posted: 13/11/12 09:46)

There is a replay about to start if anyone is interested.
http://www.blogtalkradio.com/help4hd/2012/11/12/help-4-hd-ne…
Fantastic show. 63 patients enrolled and on track for december finish on enrollment.
The doctors seemed very positive on the outcome, although careful to say they will not know till the reults are tallied.
They described PBT2 as a potential new treatment which will address the need for a treatment for cognition.
I heard it called a unique trial a few times.
With two dosages, there is a two in 3 chance of getting the drug, better than the 50/50 chance in many trials.
They said the Alzheimers trial efficacy was real and it gives them a real hope results here will be positive.
Behavior is another thing they are checking. Patients can get really cranky as their body control is being lost.
One doc called it a unique opportunity to contribute to a leap forward in finding a treatment for Huntingtons.
Called it the first time to be addressed at the ill nerve cell level.
Should make it easy for the cell to protect itself and clear excess Huntingtin protein.
We think we have something very interesting here.
Study is being run as a very tight ship and December deadline will be met.
The trial is designed by statisticians and powered for a meaningful result.
Most productive site is SanDiego with 12 already enrolled.
They say with positive results a phase 3 is sure to follow.
Could that be a post approval trial The docs seemed excited.

[Finee]

Prana Provides Huntington Disease Trial Update
in conjunction with the Huntington Study Group Annual Conference
Melbourne – 14 November, 2012; Prana Biotechnology (NASDAQ:PRAN; ASX:PBT)
today reported on its progress in the Reach2HD trial, following a resentation by the Ms Dianne Angus, Prana’s Chief Operating Officer, at the Huntington Study Group Annual Conference held in Seattle this past weekend.
The Reach2HD trial is a Phase IIa, 6 month trial in 100 patients with early to mid-stage Huntington disease that are treated with one of two doses of PBT2 or placebo.
Enrollment commenced in April 2012 following approval from the FDA to conduct the trial across sites in the USA and Australia. All twenty Reach2HD sites are open and recruiting. Based on current recruitment activity, it is expected that over 80% of patients will be in dosing by the end of this month in line with Prana’s recruitment completion target at the end of the year and reporting of results in 2H13.
During the presentation, Ms Angus noted that PBT2 has a unique therapeutic action because of its specialized ability to prevent the toxic relationship between disease proteins and biological metals in the brain. Of special relevance to Huntington disease,PBT2 has been shown in animal modeling that it can reduce the aggregation of a mutant form of the Huntingtin protein that is associated with the disease, improve motor function, preserve euronal tissue and significantly improve life expectancy*. Moreover
PBT2 has demonstrated a significant ability to improve cognitive Executive Function (“thinking ability”) in a Phase IIa study in Alzheimer’s disease**. Based on the breadth of pre-clinical and clinical data to date, Prana’s Reach2HD trial has been designed to investigate safety and tolerability of PBT2 in Huntington disease patients and to measure potential cognitive, functional and motor benefits in patients and also explore mechanistic biomarker readouts.
"There is mounting evidence that compounds that can restore metal homeostasis in the neuron can stop and even reverse cognitive decline associated with neurodegenerative diseases. We think Prana's PBT2 could be such a compound," said New York based MLV & Co. Equity Research, Senior Biotech Analyst George Zavoico, Ph.D.
“The first patient has already completed the 6 month treatment period and no patients have withdrawn from the trial for any safety or other reasons, so we are very pleased with our progress to date. The Data Safety Monitoring Board will report again next February” said Mr Kempler, Prana’s Chairman and CEO.
Huntington disease is a complex and severely debilitating genetic, neurodegenerative disease, for which there is no cure. The disease often affects young adults and, whilst associated with severe physical movement symptoms, it progressively impacts the mind and emotions as well. The disease causes incapacitation and death about 15-25 years after onset. The disease affects over 30,000 people in the US and about 70,000 worldwide. There is only one marketed drug for Huntington disease, with limited utility and notably there are no drugs either available or in development that have established clinical evidence for treating the cognitive decline associated with Huntington disease.

* Manuscript in preparation
**PBT2 has completed a Phase IIa trial in Alzheimer’s patients and significantly improved the Executive Function of patients treated with the drug. Executive Function is an integrated set of cognitive abilities,
including thinking flexibility, concept formation, and self-monitoring. Executive Function has overarching control of cognitive processes needed for organizing, strategizing, problem solving, verbal reasoning and
multi-tasking. Loss of Executive Function is the main cognitive loss experienced by those with Huntington
disease.

[Fruehrentner]

Prana Completes Recruitment In Alzheimer's Trial

Melbourne - 27 November, 2012

Prana Biotechnology (NASDAQ: PRAN; ASX: PBT) today announced that it has completed recruitment in the IMAGINE trial, a 12 month Phase II trial testing PBT2, the Company's drug in development for Alzheimer's Disease.

The double-blind placebo controlled trial has enrolled 41 patients with prodromal or mild Alzheimer's Disease in Melbourne, Australia. One additional patient may be included in the trial, subject to final screening procedures this week. All trial participants are undergoing brain scans to measure PBT2's effect on amyloid deposits in the brain (using PiB-PET scanning) and effects on increasing brain activity (F-FDG PET). Cognition effects are being measured by the Neuropsychological Test Battery (NTB), a test that measures the type of cognitive problems experienced by prodromal and early Alzheimer's patients.

In an earlier 12 week Alzheimer's Disease trial, PBT2 significantly reduced the level of Abeta protein in the spinal fluid of treated patients as well as significantly improving their cognitive Executive Function1,2,3.

"We expect that the current 12 month IMAGINE trial will provide further evidence of PBT2's ability to have a positive effect in the brain and help Alzheimer's patients," said Prana's Executive Chairman, Mr Geoffrey Kempler.

The scientific data supporting the belief that PBT2 will bring meaningful clinical benefit to patients is extensive. PBT2 restores neuronal health by selectively binding and redistributing brain metals (copper, zinc) that have become imbalanced due to disease or the ageing process. Furthermore PBT2 is able to prevent Abeta protein induced toxicity and promote its disaggregation in the brain.

The trial has received funding from the Alzheimer's Drug Discovery Foundation (ADDF). Howard Fillit, MD, the ADDF's Executive Director commented that "PBT2 stands out as one of the few remaining orally available agents with clinical trial evidence of cognitive benefit for Alzheimer's patients. Success in this trial will demonstrate target engagement by PBT2 in the brains of people with Alzheimer's Disease, and accelerate the clinical development of PBT2 to patients".

Alzheimer's Disease and dementia affects over 26 million people worldwide. The cost to society has been reported as $600 billion per annum. Currently all available treatments are approved to provide some degree of symptomatic relief. None change the course of the disease and the eventual decline in patient's cognition and health. PBT2 has the potential to be an effective treatment for Alzheimer's Disease that is supported by an extensive body of scientific and clinical work.



References

1. Lannfelt et al. "Safety, Efficacy, and biomarker findings of PBT2 in targeting Abeta modifying therapy for Alzheimer's disease: a controlled phase IIa, double-blind, randomized, placebo-controlled trial", Lancet Neurology (2008) vol. 7, pp. 779-86.
2. Lannfelt et al. Errata: Lancet Neurology (2009) vol. 8, pp. 981.
3. Faux et al "PBT2 Rapidly Improves Cognition in Alzheimer's Disease: Additional Phase II Analyses", Journal of Alzheimer's Disease (2010) vol. 20 pp. 509-516


For further information please visit the Company's web site at www.pranabio.com.

[Finee]

PRANA Biotechnology (PRAN) Release: Metal Hypothesis for Alzheimer's, Huntington and Other Neurodegenerative Diseases Declared Promising Therapeutic Strategy by Scientists at New York Academy of Sciences Symposium

12/5/2012 9:17:53 AM
MELBOURNE, AUSTRALIA--(Marketwire - December 05, 2012) - Prana Biotechnology (NASDAQ: PRAN) (ASX: PBT) today announced that leading scientists discussing the Metal Hypothesis at the New York Academy of Science on November 29th at a symposium titled "Targeting Metals in Alzheimer's and Other Neurodegenerative Diseases," highlighted the promise that therapies like Prana's PBT2 could offer for sufferers of neurodegenerative diseases.
This symposium examined findings that have led to the discovery of small molecules designed to restore the balance of transition metals in the brain that are critical for normal neuronal function, that reduce the accumulation of aggregated target proteins associated with disease, and that could have a disease-modifying effect.
Dr. Rudy Tanzi, the Joseph P. and Rose F. Kennedy Professor of Neurology at Harvard University and Prana's Chief Scientific Advisor, said, "Researchers are increasingly focusing on the role of metals in neurodegenerative disease, providing data that promotes optimism for the outcome of Prana's trials. As we learn more about the genetics of Alzheimer's disease it increasingly appears that the disease is triggered by the excessive accumulation of the amyloid beta protein in the brain. Prana's therapeutic strategy for treating neurodegenerative disease involves a highly differentiated mechanism of action as an anti-beta-amyloid drug therapy." Rather than simply trying to stop production of all native amyloid beta protein, PBT2 (i) prevents the metal dependent conversion of amyloid beta protein into oligomers that are toxic to synapses and (ii) restores normal brain metal distribution that is essential for neuronal health and synaptic function.
Dr. Steven M. Hersch, of Massachusetts General Hospital and Harvard Medical School said, "Transition metals, especially iron and copper, have been implicated in the pathogenesis of Huntington disease. Copper may directly modulate the toxicity of the huntingtin protein (Htt) while iron accumulation in response to neurodegeneration likely potentiates the damage to the central nervous system, making both metals potential therapeutic targets. PBT2 is the first clinical candidate that modulates Htt directly."
Dr. Dan Tardiff, of the Whitehead Institute for Biomedical Research, said, "We have screened multiple validated yeast cells of proteotoxicity and identified numerous compounds that restore protein homeostasis and rescue cells from death. We have several compounds that rescue cell death through altering metal homeostasis. Though it is not clear the precise mechanism in some cases, it is becoming more apparent that, along with molecules like PBT2, targeting metals may ultimately be a productive therapeutic strategy in several neurodegenerative diseases."
The presentations explored the causative events leading to the neuropathology that drives Alzheimer's disease, Parkinson's disease and Huntington disease. Dr. Robert Cherny of The Florey Institute of Neuroscience and Mental Health, Melbourne, and Prana's Head of Research, said, "We have been investigating the therapeutic potential of drugs which act to inhibit pathological metal-protein interactions and promote neuronal function by restoring metal homeostasis. We believe that cognition can be improved significantly with drugs like PBT2."
http://www.biospace.com/News/prana-biotechnology-release-met…

[Finee]

Journal of Huntington’s Disease Publishes Benefits of PBT2
Melbourne – December 13, 2012;
Prana Biotechnology (NASDAQ:PRAN; ASX:PBT) today announced that the Journal of Huntington’s Disease has in its December, 2012 edition, published data showing the benefits of PBT2 in Huntington Disease*. The paper describes PBT2’s ability to inhibit the development of the symptoms and pathological features of Huntington Disease in pre-clinical transgenic animal models.
“PBT2 markedly reduced neurodegeneration, significantly increased lifespan and improved motor function and coordination in an aggressive animal model of the disease”, said lead author and Head of Research at Prana, Associate Professor Robert Cherny.
“It is already well established that PBT2 prevents the aggregation of the Abeta protein outside neurons, in Alzheimer’s Disease. It is also established that the mutant Huntingtin (Htt) protein aggregates inside the neuron in Huntington Disease. There is published evidence that the protein aggregation in both diseases is driven by the interaction with metals. Our work has shown that PBT2 can prevent this protein aggregation caused by interaction with metals”, he added.
At a recent New York Academy of Sciences symposium on targeting metals to treat neurodegenerative diseases, Professor Steven M. Hersch, of Massachusetts General Hospital and Harvard Medical School commented that “transition metals, especially iron and copper, have been implicated in the pathogenesis of Huntington Disease. Copper may directly modulate the toxicity of the Htt protein while iron accumulation in response to neurodegeneration likely potentiates the damage to the central nervous system, making both metals potential therapeutic targets. PBT2 is the first clinical candidate that modulates Htt directly.”
PBT2 is being trialed in Huntington Disease patients in 20 sites across the USA and Australia. Results are expected in the second half of 2013.

[Finee]

Speculative Biotech Stocks To Consider In The Wake Of Early-Stage Developments
December 13, 2012

When it comes to the biotech sector, many stocks that trade under $5/share are considered to be very speculative, and as a result I wanted to focus on two that could benefit from developments within their specific markets. In this article I've chosen two companies that have met the follow criteria:
Prana Biotechnology Ltd. (PRAN) which is based in Parkville, Australia engages "in the research and development of therapeutic drugs for the treatment of neurological disorders in Australia. The company primarily focuses on the Alzheimer's, Parkinson's, and Huntington's diseases, as well as various cancer, age-related macular degeneration and cataract, Motor Neuron, and Creutzfeldt-Jakob diseases". (Yahoo! Finance)
From a fundamental perspective shares of Prana currently carry a market cap of $72 million, have traded up 50.13% since July 1st and are currently trading at a 3.69% discount to their 50 DMA and at a 16.17% premium to their 200 DMA.
On December 13th it was announced that the Journal of Huntington's Disease has published data showing the benefits of its experimental drug PBT2, for the treatment of Huntington's Disease. The results highlight PBT2's ability to inhibit the development of the symptoms and pathological features of the disease in animal models. The drug is currently being tested on patients in 20 sites across the USA and Australia, with results expected in Q2 of 2013.
IInvestors should also note that "PBT2 has markedly reduced neuro-based degeneration, significantly increased lifespan and improved motor function and coordination in an aggressive animal model of the disease," said lead author and Head of Research at Prana, Associate Professor Robert Cherny. If Prana can continue to demonstrate significant strides, especially in terms of the reduction of neuro-based degeneration with regard to PBT2, in both the US and Australia, I see no reason why a small to moderate sized position should not be established at current levels.
http://seekingalpha.com/article/1063461-2-speculative-biotec…

[Fruehrentner]

Gilead übernimmt eine kleine australische Firma.

Könnte mit PRANA auch passieren ...


Gilead Sciences to Acquire YM BioSciences

13 Dec 2012

Adds Selective JAK Inhibitor to Growing Oncology and Inflammation Pipeline

FOSTER CITY, CA, USA & MISSISSAUGA, Canada I December 12, 2012 I Gilead Sciences, Inc. (Nasdaq: GILD) and YM BioSciences Inc. (NYSE MKT: YMI, TSX: YM) announced today that the companies have signed a definitive agreement under which Gilead will acquire YM for U.S.$2.95 per share in cash. The transaction has received the unanimous approval of YM’s Board of Directors, and values YM at approximately U.S.$510 million, with YM reporting C$125.5 million in cash and cash equivalents as of September 30, 2012. Gilead plans to fund the acquisition with cash on hand. The transaction is expected to close in the first quarter of 2013.

YM’s lead drug candidate, CYT387, is an orally-administered, once-daily, selective inhibitor of the Janus kinase (JAK) family, specifically JAK1 and JAK2. The JAK enzymes have been implicated in a number of disorders including myeloproliferative diseases, inflammatory disorders and certain cancers. YM has reported positive results from a Phase 1/2 clinical trial of CYT387 in 166 patients with myelofibrosis, a life-threatening myeloproliferative disease. Pending completion of the acquisition, Gilead intends to initiate a pivotal Phase 3 clinical trial of CYT387 in myelofibrosis in the second half of 2013.

“This acquisition represents an opportunity to add a complementary clinical program in the area of hematologic cancers to our growing oncology portfolio,” said Norbert W. Bischofberger, PhD, Gilead’s Executive Vice President, Research and Development and Chief Scientific Officer. “Based on promising Phase 2 data, we believe CYT387 could provide important clinical benefit for patients with myelofibrosis, including potential improvements with regard to anemia and decreased dependence on blood transfusions. We look forward to advancing CYT387 into a Phase 3 study as quickly as possible and to exploring its potential in other myeloproliferative diseases with significant unmet medical need.”

Myelofibrosis is a progressive, chronic bone marrow disorder in which the marrow is replaced by fibrous scar tissue, making it difficult for the bone marrow to sufficiently produce blood cells, leading to anemia (low red blood cell count) and thrombocytopenia (low blood platelet count), severe constitutional symptoms and spleen enlargement. JAK inhibitors modulate cytokine-stimulated intracellular signalling and decrease the circulating levels of proinflammatory cytokines associated with the pathogenesis of myelofibrosis.

“This agreement represents a positive outcome both for myelofibrosis patients and for our shareholders. Gilead has the research and development capabilities and the resources needed to more fully realize the potential of CYT387 as a therapeutic advance for myelofibrosis patients and potentially for other indications,” said Dr. Nick Glover, President and CEO of YM.

“Since our acquisition of CYT387 nearly three years ago, YM has made great progress in advancing CYT387 through the clinical, regulatory, manufacturing and business development processes. While Gilead's acquisition will end a long, varied and interesting journey for YM, we are pleased to have this transaction crystallize the present value of this important therapeutic candidate,” said Mr. David Allan, Chairman of YM.

In recent years, Gilead has sought to expand its R&D expertise in the area of oncology through the appointment of leading cancer researchers and clinicians, the establishment of external scientific partnerships and through strategic acquisitions. Gilead’s lead compound in oncology, idelalisib (formerly referred to as GS-1101), is an investigational, first-in-class specific inhibitor of the phosphoinositide-3 kinase (PI3K) delta isoform. Five Phase 3 studies of idelalisib in chronic lymphocytic leukemia (CLL) and indolent non-Hodgkin’s lymphoma (iNHL) are progressing.

Gilead is also conducting Phase 2 clinical trials of simtuzumab (formerly referred to as GS-6624), an investigational monoclonal antibody (mAb) candidate targeting the human lysyl oxidase-like 2 (LOXL2) protein, in myelofibrosis, colorectal cancer, pancreatic cancer and certain fibrotic diseases.

CYT387, idelalisib and simtuzumab are investigational products and their safety and efficacy have not yet been established.

Terms of the Transaction

Under the terms of the agreement, upon closing of the proposed transaction, shareholders of YM will receive U.S.$2.95 per common share in cash, and holders of warrants and stock options will receive a cash payment equal to the difference between U.S.$2.95 and the exercise price of such warrant or stock option. The proposed transaction will be completed through a plan of arrangement under the provisions of the Companies Act (Nova Scotia).

The transaction will require the approval of YM shareholders at a special meeting of YM shareholders, to be held as soon as reasonably practicable and in any event on or before February 11, 2013. In addition to YM’s shareholder approval, closing of the transaction is subject to the satisfaction of certain other customary conditions, including court approval of the transaction, and applicable government and regulatory approvals, including expiration or termination of the waiting period under the United States Hart Scott Rodino Antitrust Improvements Act, and the review period under the Competition Act (Canada). The approval of Gilead shareholders is not required in connection with the proposed transaction.

The arrangement agreement contains customary non-solicitation provisions, but permits YM, in certain circumstances, to terminate the arrangement and accept an unsolicited superior proposal, subject to fulfilling certain conditions.

BofA Merrill Lynch and Bloom Burton & Co. serve as financial advisors, and Gowling Lafleur Henderson LLP, Heenan Blaikie LLP and Dorsey & Whitney LLP serve as legal advisors to YM in connection with the transaction. Gilead is advised by Wilson Sonsini Goodrich & Rosati, Professional Corporation and Blake Cassels and Graydon LLP.

About YM

YM BioSciences Inc. is a drug development company primarily focused on advancing CYT387, an orally administered inhibitor of both the JAK1 and JAK2 kinases, which have been implicated in a number of hematological and immune cell disorders including myeloproliferative neoplasms and inflammatory diseases as well as certain cancers. Positive interim results have been reported from a Phase 1/2 trial of CYT387 in 166 patients with myelofibrosis. In addition, YM has several preclinical programs underway with candidates from its library of novel compounds identified through internal research conducted at YM BioSciences Australia.

About Gilead Sciences

Gilead Sciences is a biopharmaceutical company that discovers, develops and commercializes innovative therapeutics in areas of unmet medical need. The company’s mission is to advance the care of patients suffering from life-threatening diseases worldwide. Headquartered in Foster City, California, Gilead has operations in North America, Europe and Asia Pacific.

SOURCE: Gilead Sciences

[Finee]

Prana Completes Recruitment in Huntington Trial 6 month Phase II study with PBT2 in Huntington patients
Melbourne – 19 December, 2012: Prana Biotechnology (NASDAQ:PRAN; ASX:PBT) today announced that it has completed recruitment in the Reach2HD Phase IIa clinical trial using PBT2 in patients with Huntington Disease (HD).
The 6 month double-blind, placebo-controlled Phase II trial in patients with early to midstage Huntington Disease met its enrolment target of 100 patients ahead of schedule. Additional patients may be included in the trial, subject to final procedures this week.
The Principal Investigator on the study, Dr Ray Dorsey of Johns Hopkins University Medical Center, commented that “interest in PBT2 is high in part because PBT2 offers a novel mechanistic approach to the treatment of HD. We thank the clinical sites and the Huntington community for their wonderful support”. The Reach2HD trial was coordinated in conjunction with the Huntington Study Group (HSG) across 20 clinical sites in the USA and Australia.
Huntington Disease is a complex and severely debilitating genetic, neurodegenerative disease, for which there is no cure. The disease often affects young adults and, whilst associated with severe physical movement symptoms, progressively impacts the mind and emotions as well. The disease causes incapacitation and death about 15-25 years after onset. At this time there is only one marketed drug for the alleviation of some of the involuntary motor symptoms associated with the disease.
Professor Ira Shoulson, Professor of Neurology, Pharmacology and Human Science at Georgetown University (Washington DC) and the Chair of the Executive Committee of the Huntington Study Group said “PBT2 attracted our attention as an experimental drug with the potential to bring real benefit to Huntington Disease patients who suffer from a range of motor, ehavioural and cognitive symptoms. The favourable signals from the PBT2 trial in Alzheimer’s Disease are particularly promising”.
http://hotcopper.com.au/announcements.asp?id=514024

[Finee]

Analyst Actions:
Last updated: 12/20/2012
Coverage of Prana Biotechnology Limited (PRAN) ADRs have been initiated at Burrill Institutional Research with an Outperform rating and a price target of $5 a share.

[Finee]

Antwort auf Beitrag Nr.: 43.948.738 von Finee am 20.12.12 15:50:32

http://www.aktiencheck.de/analysen/Artikel-Prana_Biotechnolo…

[Finee]

Antwort auf Beitrag Nr.: 43.948.738 von Finee am 20.12.12 15:50:32

http://www.pranabio.com/downloads/analyst_reviews/PRAN%20-%2…

[Fruehrentner]

Antwort auf Beitrag Nr.: 43.959.276 von Finee am 24.12.12 22:19:26

Danke für diesen link.

Frohe Weihnachten

[Finee]

Antwort auf Beitrag Nr.: 43.959.738 von Fruehrentner am 25.12.12 15:42:30

Frohe Weihnachten, und ein gesundes, glückliches und zufriedenes neues Jahr 2013.

[dottore]

Zitat von Finee: Das kann sehr interessant werden!

Targeting Metals in Alzheimer's and Other Neurodegenerative Diseases

Thursday, November 29, 2012 | 12:00 PM - 4:00 PM
The New York Academy of Sciences

Presented by the Brain Dysfunction Discussion Group at the New York Academy of Sciences

Alzheimer's disease (AD) is characterized by elevated brain iron levels and accumulation of copper and zinc in cerebral β-amyloid deposits. Both ionic zinc and copper accelerate the aggregation of Aβ, the principle component of β-amyloid deposits. Copper and iron can also promote the neurotoxic redox activity of Aβ and induce oxidative cross-linking into stable oligomers. Recent reports documented the release of Aβ together with ionic zinc and copper in cortical glutaminergic synapses following excitation, leading to the formation of Aβ oligomers. Excessive accumulation of Aβ oligomers in the synaptic cleft is thought to adversely affect synaptic neurotransmission, and transition metals have been implicated in the misfolding and accumulation of a-synuclein and Huntington protein in Parkinson's and Huntington's diseases (PD and HD), respectively, as well as tau hyperphosphorylation in AD, contributing to disease pathogenesis and progression. The "Metal Hypothesis of Neurodegenerative Diseases" is proposed to describe the underlying, possibly causative, events, leading to the neuropathology that drives AD, PD, and HD. This symposium examines how these findings led to the discovery of small molecules designed to restore the physiologic balance of transition metals in the brain, prevent further accumulation of misfolded proteins, and possibly even have a disease-modifying effect. A review of the early clinical experience of one such compound, PBT2, will be presented.

Organizers
Rudolph Tanzi, PhD (PRANA)
Massachusetts General Hospital and Harvard Medical School

George Zavoico, PhD
MLV & Co.

Jennifer Henry, PhD
The New York Academy of Sciences

Speakers
Robert A. Cherny, PhD (PRANA)
The Florey Institute of Neuroscience and Mental Health, Australia

Steven M. Hersch, MD, PhD
Massachusetts General Hospital and Harvard Medical School

Rudolph Tanzi, PhD
Massachusetts General Hospital and Harvard Medical School

Dan Tardiff, PhD
Whitehead Institute for Biomedical Research

http://www.nyas.org/Events/Detail.aspx?cid=1c84a5bc-6abb-4a6…

also das mit dem Zink hat schon dazu geführt, dass die Firma Adeona eine größere Studie zunächst vielversprechend durchführte, dem Aktienwert eine geile Performance gab und dann das Präparat doch floppte, damit auch die Aktie.

[dottore]

noch einen kleinen Nachtrag. Charttechnisch siehrt es hier bescheiden aus, insbesondere wenn mann sieht, dass seit 2004 ein intakter Abwärtstrend besteht.
Schaut man nur 1 Jahr zurück, dann ist der "Kursausbruch derzeit am konsolidieren und an einem spannenden Punkt. Wenn keine positive Überraschung, oder wenigstens die Hoffnungen unterstützende News kommt, dann geht e schon bald wieder runter, bis wo sie vor dem Ausbruch war.

[Fruehrentner]

Antwort auf Beitrag Nr.: 44.016.319 von dottore am 13.01.13 19:24:18

qdottore,

danke für deinen Hinweis auf ADEOAN. Wie weit war diese Firma denn gekommen, also in welcher klin. Phase floppte deren Wirkstoffkandidat?

[Fruehrentner]

Antwort auf Beitrag Nr.: 44.016.319 von dottore am 13.01.13 19:24:18

Ohne Zweifel ist PRANA high risk im derzeitigen Stadium.

Aber selbst wenn es nur auf der watch list ist, spannend zu verfolgen und Hoffnung für die Alzheimerpatienten.

[Finee]

Antwort auf Beitrag Nr.: 44.016.319 von dottore am 13.01.13 19:24:18

Synthetic Biologics (SYN), formerly Adeona Pharmaceuticals, and its reaZin®

Although the secondary data were somewhat disappointing, the company still indicated that it would stick with the indication and follow through with marketing the reaZin medical food for the dietary management of Alzheimer's disease and mild cognitive impairment.

http://seekingalpha.com/article/543211-synthetic-biologics-z…

[Fruehrentner]

Antwort auf Beitrag Nr.: 44.017.966 von Finee am 14.01.13 11:43:56

Also reaZin hat für mich wenig mit dem Wirkmenachanismus von Pranas Wirkstoffkandidaten zu tun; kaum miteinander vergleichbar.

[Finee]

Antwort auf Beitrag Nr.: 44.021.254 von Fruehrentner am 14.01.13 22:24:22

Das stimmt natürlich auch wieder!

[Fruehrentner]

Antwort auf Beitrag Nr.: 44.021.685 von Finee am 15.01.13 06:52:12

Schön, dass Du es eingesehen hast

[Finee]

Prana Biotechnology has released data demonstrating their drug, PBT2, is effective in animal models of HD

By Dr Jeff Carroll on January 14, 2013
Edited by Dr Ed Wild

The Huntington Study Group and Prana Biotechnology are currently running a clinical trial, Reach2HD, to determine whether the drug PBT2 is effective in HD patients. Now, they've released the preclinical data behind the rial, showing the drug is effective in two animal models of HD.

History of PBT2

Many Huntington’s disease families have been excited by word of a new layer developing a novel treatment for HD. Prana Biotechnology, a drug development company in Australia, has developed a new drug they call PBT2.
HDBuzz has previously written about Prana and their drug, which works in a surprising and novel way. While all the details are not understood, the drug is designed to interfere with interactions between the huntingtin protein and the metal copper.
Interfering with copper in the body may sound like a strange and surprising way to attack Huntington’s disease, but there is a history of investigating changes in copper in the brain of HD patients.
Another genetic disease called Wilson’s disease is caused by mutations in a gene that helps cells get rid of excess copper. The cells of patients with Wilson’s disease accumulate too much copper because they don’t know how to get rid of it, thanks to their defective gene.
It turns out that Wilson’s disease patients have brain damage in the same areas of the brain as Huntington’s disease patients, and that in HD, these parts of the brain accumulate copper too. This supports the idea that copper might be important for the particular parts of the brain that die in HD.
Based on in-house work that suggested PBT2 was effective in Huntington’s disease, Prana Biotechnology began working with the Huntington Study Group to initiate a trial of their drug in human HD patients. The trial, currently running in the US and Australia, is called Reach2HD. This trial happened so fast that few people outside the company had seen the data that suggested their drug was effective. They’ve now published this data for everyone to see in the new Journal of Huntington’s Disease.

The animal models
Before testing a drug in humans, scientists like to have an idea of whether it is safe and effective. The only way to study this is to give the drug to animals who have been genetically modified to carry the same mutant HD gene as human patients.
These animals have problems that mimic, in some ways, those experienced by HD patients. While the animals don’t have Huntington’s disease, they do provide an objective way of testing whether a drug has an impact on the problems caused by expression of the mutant HD gene.
To test PBT2, the team of scientists, lead by Stephen Massa of the University of California at San Francisco, turned to two different animal models of HD. First, they used a tiny worm with a big name — ´Caenorhabditis elegans’. Unlike humans, with their billions and billions of brain cells, C. Elegans has precisely 302 brain cells.
Forcing C. elegans’ worms to express a gene similar to the one that causes Huntington’s disease in people causes these worms to become paralyzed and unable to move. Because the mice are so small and have a very short lifespan, they can be used to quickly test whether a drug reduces the harm associated with the mutant gene.
The second animal used to investigate the effectiveness of PBT2B was a mouse that has been genetically engineered to express a mutant HD gene. This gene makes them very sick, very fast — they have problems with coordinating their movements, show shrinkage in the brain similar to that seen in HD patients and ultimately die very young. These mice provide a simple tool for testing a Huntington’s disease drug — scientists can simply give the mice a drug and see if it can improve any of their symptoms.

The results
In the worm model, PBT2 was very effective — worms treated with PBT2 were able to live for much longer without becoming paralyzed. Rescuing worms is nice, but it’s a long way from people! The mice, despite being small and having fairly simple behaviors, are much closer to people. How did PBT2 do in HD mice?
While alive, HD mice treated with PBT2 showed some improvements in the coordination of their movements — that is, they were slightly less clumsy. More interestingly, treatment with PBT2 prolonged the survival of HD mice by a significant amount: mice treated with the drug lived about 26% longer than untreated mice. That’s a pretty decent extension, though we should remember that the mice were still quite sick during the extended period of their life.
Other measures were improved by PBT2 treatment as well. Like many HD patients, these HD mice lose weight. Weight loss can be a major problem for HD patients, and is difficult to combat. Treatment with PBT2 helped HD mice maintain body weight in a fairly dramatic fashion.
In the brain, HD mice showed shrinkage similar to that experienced by HD patients. This loss was significantly, but not completely, rescued by treating the mice with PBT2. This suggests the drug isn’t just masking symptoms, but might actually be stopping the brain cell death that causes symptoms to occur.

Caveats and questions
All in all, it’s easy to see why these scientists were excited about the results of PBT2. The beneficial effects in the mice, in particular, are pretty impressive.
As with any trial conducted in animals, it’s worth thinking about the limitations. The mice, for example, were treated with PBT2 from 3 weeks of age — essentially from when they first start eating and drinking on their own, rather than nursing from their mothers. This is not what will happen in people, who are only being given the drug after their symptoms start. Can PBT2 work, even if it’s only given when someone is already sick? We just don’t know yet.
PBT2 has advantages over some other experimental drugs in HD. For one, it is known to get into the brain, where it needs to be to work. Furthermore, it has already been shown to be well tolerated in human Alzheimer’s Disease patients, making it less likely that the drug will fail because of side-effects.
The clinical trial currently investigating PBT2 in HD patients is formally only designed to study whether the drug is safe in HD patients when administered for 26 weeks. But the investigators are also measuring a host of changes in these patients caused by HD, including behavior changes, thinking problems and biological changes in the blood, urine and brain. Looking at these things now may give us a hint of whether PBT2 is effective.
Especially in light of these positive results in animal models, HDBuzz is encouraged to hear that the trial is now fully recruited, and we look forward to hearing the results."

http://www.hdsa.org/research/hdbuzz/hdbuzz-prana-biotech-pub…

[Finee]

Prana Announces NYAS Symposium eBriefing Available Online

http://www.asx.com.au/asxpdf/20130130/pdf/42cnvk8j5grpwv.pdf

[Fruehrentner]

Antwort auf Beitrag Nr.: 44.080.469 von Finee am 30.01.13 09:02:28

Prana Announces NYAS Symposium eBriefing Available Online

Datum: 29.01.2013

Melbourne - January 30, 2013; Prana Biotechnology (NASDAQ:PRAN; ASX:PBT) today announced that the New York Academy of Sciences eBriefing which provides information and video footage of the symposium which took place on November 29th titled "Targeting Metals in Alzheimer's and Other Neurodegenerative Diseases" is now available for viewing by the public by going to: www.nyas.org/MetalsandAD-eB

The eBriefing features multimedia presentations of speakers' slides and audio, written meeting summary, and links to related resources.

Dr. Rudy Tanzi, the Joseph P. and Rose F. Kennedy Professor of Neurology at Harvard University and Prana's Chief Scientific Advisor, and Dr. Robert Cherny, Prana's Head of Research, are featured in the eBriefing. The presentations explore in depth the causative events leading to the neuropathology that drives Alzheimer's disease, Parkinson's disease and Huntington disease. This symposium examined how these findings led to the discovery of small molecules designed to restore the balance of transition metals in the brain that are critical for neuronal function, reduce the accumulation of aggregated target proteins, and could have a disease-modifying effect. A review of Prana's PBT2 clinical history is also presented.

According to Geoffrey Kempler, Chairman of Prana, "We are pleased to make available to the public the eBriefing of the Symposium which recently took place at the New York Academy of Sciences. We believe it provides a clear synopsis and overview of the potential of Prana's PBT in treating Alzheimer's and Huntington diseases." Recently, Prana announced that it has completed enrollment in its ongoing 6 month Phase 2 trial in Huntington patients and 12-month Phase 2 trial in Alzheimer's disease patients.

Dr. Tanzi said, 'As more and more scientists in the Alzheimer's field generate data on the role of metals in neurodegenerative disease, we are becoming increasingly optimistic about the prospects for Prana's trials. Elucidation of new Alzheimer's genes continues to support the excessive accumulation of the amyloid beta protein in the brain as the triggering event for this devastating disease. Prana's therapeutic strategy for treating neurodegenerative disease involves a very different mechanism of action than that of other anti-beta-amyloid drugs, which have largely failed. In light of these failures, many in the field have deemphasized efforts to treat existing Alzheimer's patients and are focusing on prevention. I believe that PBT2 has a very good chance of success for not only helping to prevent Alzheimer's, but also for providing real benefit to the millions of existing patients in need of effective treatments".

[Finee]

Copper/zinc chelation by clioquinol reduces spinal cord white matter damage and behavioral deficits in a murine MOG-induced multiple sclerosis model.

Abstract
The present study aimed to evaluate the therapeutic potential of clioquinol (CQ), a metal chelator, on multiple sclerosis pathogenesis. Experimental autoimmune encephalomyelitis was induced by immunization with myelin oligodendrocyte glycoprotein (MOG(35-55)) in female mice. Three weeks after the initial immunization, demyelination and immune cell infiltration in the spinal cord were analyzed. CQ (30mg/kg) was given by gavage once per day for the entire experimental course. CQ profoundly reduced the daily clinical score and incidence rate of EAE mice. The CQ-mediated inhibition of the clinical course of EAE was accompanied by suppression of demyelination and reduced infiltration by encephalitogenic immune cells including CD4, CD8, CD20 and F4/80 positive cells. CQ also remarkably inhibited EAE-associated BBB disruption and MMP-9 activation. Autophagy contributes to clearance of aggregated proteins in astrocytes and neurons. The present study found that EAE increased the induction of autophagy and CQ further increased this expression. Furthermore, the present study found that post-treatment with CQ also reduced the clinical course of EAE and spinal cord demyelination. These results demonstrate that CQ inhibits the clinical features and neuropathological changes associated with EAE. The present study suggests that transition metals may be involved in several steps of multiple sclerosis pathogenesis. HIGHLIGHT: EAE mice spinal cord shows aberrant vesicular zinc staining in the white matter. Clioquinol inhibited the daily clinical score and incidence rate of EAE mice. Clioquinol suppressed demyelination and reduced infiltration of encephalitogenic immune cells. Clioquinol inhibited the EAE-associated BBB disruption and MMP-9 activation. Clioquinol increased the induction of autophagy in EAE mice.

http://www.sciencedirect.com/science/article/pii/S0969996113…

In August 2004, Prana Biotechnology, an Australian company and P.N Gerolymatos S.A (PNG) agreed to recognize each others rights to market clioquinol in their respective territories, with PNG holding right for European territories, and Prana holding rights for US and Japan. Prana has performed research into the use of hydroxyquinolines drugs in the treatment of Alzheimers disease. (From Wikipedia, the free encyclopedia)

[Finee]

The Life Sciences Report Watchlist 2013
February 1st, 2013 by The Life Sciences Report

... Prana Biotechnology Ltd. (PBT:ASX) is taking on serious neurodegenerative diseases that disrupt the lives of patients and their families. The company has a miniscule $70M market cap, and shares should move dramatically on positive data. Results of phase 2b studies of the company’s orally bio-available PBT2 small molecule for the treatment of Huntington’s disease should be forthcoming in H2/13, and from an Alzheimer’s disease trial by the end of Q4/13. “This represents one of the biggest risk/reward opportunities of 2013,” says Senior Biotechnology Analyst George Zavoico of MLV & Co. “We are awaiting proof of concept and if it pans out, it should position Prana for a major partnership deal.” ...

http://www.trefis.com/stock/celg/articles/166582/the-life-sc…

[Finee]

07.02.2013, 09:19 Uhr
USA erwartet dreimal mehr Alzheimer-Kranke bis 2050

Alt und vergesslich: Forscher gehen davon aus, dass sich die Zahl der Alzheimer-Erkrankten in den USA bis 2050 verdreifachen wird. Ähnliches sagen Experten für Deutschland voraus.
Von Anja Mia Neumann

Im Jahr 2050 werden einer Studie zufolge etwa dreimal so viele Menschen in den USA an Alzheimer erkrankt sein wie heute. Zu diesem Ergebnis kommen Forscher im Fachjournal "Neurology". Die Zahl der Erkrankten werde von 4,7 Millionen im Jahr 2010 auf 13,8 Millionen Menschen steigen, prophezeit das Team um Liesi Hebert vom Rush University Medical Center in Chicago. Alzheimer ist die häufigste Form von Demenz.
Auch in Deutschland sagen Experten einen starken Anstieg der Patienten voraus. Nach jüngsten Angaben der Deutschen Alzheimer Gesellschaft (DAlzG) wird sich die Zahl der Demenzkranken bis 2050 mehr als verdoppeln – von derzeit 1,4 Millionen auf rund 3 Millionen Betroffene. Etwa zwei Drittel von ihnen haben demnach Alzheimer.
Die Zahl der älteren Menschen nehme zu. Und mit dieser Entwicklung wächst der DAlzG zufolge auch die Zahl der Demenzkranken – sofern kein Durchbruch in der Therapie gelingt. Bislang ist Alzheimer unheilbar.

Weiter lesen:
http://web.de/magazine/gesundheit/krankheiten/17104404-usa-e…

[Finee]

Antwort auf Beitrag Nr.: 44.114.548 von Finee am 07.02.13 14:35:30

Eigentlich nichts Neues - nur zur Erinnerung...

[Finee]

Obama Seeking to Boost Study of Human Brain

The Obama administration is planning a decade-long scientific effort to examine the workings of the human brain and build a comprehensive map of its activity, seeking to do for the brain what the Human Genome Project did for genetics.

Francis S. Collins, the director of the National Institutes of Health, one of the federal agencies involved in the project.

George M. Church, a molecular biologist at Harvard, said he was helping to plan the project, the Brain Activity Map.
The project, which the administration has been looking to unveil as early as March, will include federal agencies, private foundations and teams of neuroscientists and nanoscientists in a concerted effort to advance the knowledge of the brain’s billions of neurons and gain greater insights into perception, actions and, ultimately, consciousness.

Scientists with the highest hopes for the project also see it as a way to develop the technology essential to understanding diseases like Alzheimer’s and Parkinson’s, as well as to find new therapies for a variety of mental illnesses...

http://www.nytimes.com/2013/02/18/science/project-seeks-to-b…

[Finee]

Prana Announces that PBT2 Reduces Cognitive Impairment
Caused by Tau Protein Accumulation
New data to be presented at the 11th International Conference on Alzheimer’s and Parkinson’s Disease
Melbourne – 4 March, 2013 Prana Biotechnology (NASDAQ:PRAN; ASX:PBT) today
announced the upcoming presentation of new data demonstrating the ability of PBT2 to reduce the damage to brain cells, caused by the accumulation of the tau protein and preventing subsequent cognitive impairment. The tau protein, along with the Abeta protein, are the two major proteins associated with Alzheimer’s Disease.
The findings are consistent with the improvement in cognition previously reported in transgenic Alzheimer's mice studies* and in patients in a Phase IIa clinical trial with PBT2** and further validate the metal targeting mechanism of action of PBT2. New data will be presented by Prana scientist Associate Professor Paul Adlard at the 11th International Conference on Alzheimer’s and Parkinson’s Disease, to be held in Florence, Italy, March 6th to 10th, 2013.
To date, Abeta has been the primary therapeutic target for disease modifying drugs developed for Alzheimer’s disease. However, the clinical failure of several anti-Abeta drugs supports the view that targeting Abeta alone may be insufficient to improve outcomes for patients. The other hallmark pathological feature of Alzheimer’s disease is the presence of neurofibrillary tangles, composed of abnormal tau protein. In his presentation, entitled “Metal Chaperones are novel therapeutic agents for tauopathy’, Associate Professor Adlard will present new data showing that treatment with PBT2 significantly improves cognition and reduces the abundance of tau aggregates through metal mediated mechanisms in a transgenic mouse model of tau overexpression.
Commenting on the significance of the new data, Rudy Tanzi, the Rose and Joseph Kennedy Professor of Neuroscience at Harvard Medical School and Prana’s Chief Scientific Advisor said, "These findings provide further evidence for PBT2 as a highly attractive therapeutic for Alzheimer's disease that targets both beta amyloid deposition and tangle formation. Translating these dual effects into the clinic could potentially provide tremendous benefit for patients."
PBT2 is currently in a Phase II clinical trial, the IMAGINE trial, which is now fully enrolled and will be completed at the end of the year.

* Adlard et al. Neuron (2008) vol. 59, pp. 43-55.
** Lannfelt et al. Lancet Neurology (2008) vol. 7, pp. 779-86. Lannfelt et al. Errata: Lancet Neurology (2009)
vol. 8, pp. 981.

[Finee]

ASX Compliance Pty Limited
Senior Adviser, Listings (Melbourne)
Level 4, Rialto North Tower
525 Collins Street
Melbourne VIC 3000
Dear Kobe,
Announcement: “Prana’s PBT2 Reduces Tau Related Cognitive Impairment”
I refer to your letter of 5th March 2013 and note the letter was issued by ASX in response to the volume of shares traded on Monday 4th March, before the release of the above named announcement. It should be noted that the Chairman and CEO, Mr Geoffrey Kempler, is currently undertaking a road show in the USA and presenting at a conference as announced to the market earlier. This has coincided with an increase in market activity, particularly in the USA preceding the 4th March increased volumes on the ASX.
Your specific questions relate to continuous disclosure around PBT 2 impact on Tau. We provide the following responses as listed below:
1. Whether the Company considers the information included in the Announcement as material to the Company?
Yes
2. If the answer to question 1 is “no”, please advise the basis on which the Company does not consider the information to be material.
Not applicable.
3. If the answer to question 1 if “yes”, when did the Company first become aware of the information in the Announcement concerning the new data demonstrating the ability of PBT2 to reduce the damage to brain cells, caused by accumulation to the tau protein and preventing subsequent cognitive impairment?
The announcement referred to above is reflective of the ongoing scientific development that dates back to the commencement of the Company. An announcement dated 10 July 2008 which outlined the potential of PBT2 to reduce brain cell damage caused by accumulation of the Tau protein, and the announcement of 4 March 2013 continues the progression, interpretation and validation of this concept.
4. If this was before the release of the Announcement, please identify an earlier announcement from the Company which disclosed this information.
The following announcements relate to the same underlying material on Tau.
10/07/2008
Neuron to Publish Prana’s PBT2 Preclinical Research
19/09/2011
Prana`s PBT2 Directly Restores Neurons Critical to Cognition
26/03/2012
PLoS ONE Journal Publishes Model of Alzheimers Disease
20/09/2012
Further information - Clinical Trials Cited as Most Advanced
5. If there was no earlier announcement, and the Company became aware of the information prior to the release of the Announcement, why was the information not released to the market at an earlier time? Please comment specifically on the application of listing rule 3.1 and the exceptions to the rule in listing rule 3.1A.
Not applicable
6. The Announcement mentioned that new data will be presented by the Company’s scientist Associate Professor Paul Adlard at the 11th International Conference on Alzheimer’s and Parkinson’s disease, to be held in Florence, Italy, March 6th to 10th 2013. Please advise when the new data will be released to ASX. Please comment specifically on the application of listing rule 3.1 and the exceptions to the rule in listing rule 3.1A.
Friday March 8th 2013, before the Conference presentation on Saturday, the Company will release a summary of the new data on PBT2.
7. Please confirm that the Company is in compliance with listing rule 3.1.
The company is in compliance with listing rule 3.1
The Company continues to comply with all ASX Listing Rules.
Yours sincerely,
Richard Revelins, Company Secretary
Thursday 7th March 2013
5 March 2013
Mr Richard Revelins
Company Secretary
Prana Biotechnology Limited
By e-mail only
Dear Richard,
Prana Biotechnology Limited (the "Company")
ASX Limited (“ASX”) refers to the following.
1. The Company’s announcement titled “Prana’s PBT2 Reduces Tau Related Cognitive Impairment” lodged with ASX at 3.06pm on Monday 4 March 2013, and released at 3:12pm on the same day, announcing the upcoming presentation of new data demonstrating the ability of PBT2 to reduce the damage to brain cells, caused by accumulation of the tau protein and preventing subsequent cognitive impairment (the “Announcement”).
2. Listing rule 3.1, which requires an entity, once it becomes aware of any information concerning it that a reasonable person would expect to have a material effect on the price or value of the entity’s securities, to immediately tell ASX that information.
3. The definition of “aware” in Chapter 19 of the listing rules. This definition states that:
“an entity becomes aware of information if a director or executive director (in the case of a trust, director or executive officer of the responsible entity or management company) has, or ought reasonably to have, come into possession of the information in the course of the performance of their duties as a director or executive officer of that entity.”
4. Paragraph 17 of Guidance Note 8 which states:
“Once a director or executive officer becomes aware of information, he or she must immediately consider whether that information should be given to ASX. An entity cannot delay giving information to ASX pending formal sign-off or adoption by the board, for example.”
5. Listing rule 3.1A, which sets out an exception from the requirement to make immediate disclosure, provided that each of the following are satisfied.
“3.1A.1 A reasonable person would not expect the information to be disclosed.
3.1A.2 The information is confidential and ASX has not formed the view that the information has ceased to be confidential.
3.1A.3 One or more of the following applies.
ASX Compliance Pty Limited
ABN 26 087 780 489
Level 4
Rialto North Tower
525 Collins Street
Melbourne VIC 3000
GPO Box 1784
Melbourne VIC 3001
Telephone [phone]
Facsimile 61 3 9614 0303
www.asx.com.au
 It would be a breach of a law to disclose the information.
 The information concerns an incomplete proposal or negotiation.
 The information comprises matters of supposition or is insufficiently definite to warrant disclosure.
 The information is generated for the internal management purposes of the entity.
 The information is a trade secret.”
6. ASX’s policy position on the concept of “confidentiality” which is detailed in paragraphs 33 to 39 of Guidance Note 8. In particular, paragraphs 34 and 35 of the Guidance Note state that:
“‘Confidential’ in this context has the sense of ‘secret’…” and “Loss of confidentiality may be indicated by otherwise unexplained changes to the price of the entity’s securities, or by reference to the information in the media or analysts reports”.
Having regard to the above, we ask that you answer the following questions in a format suitable for release to the market in accordance with listing rule 18.7A.
1. Whether the Company considers the information included in the Announcement as material to the Company?
2. If the answer to question 1 is “no”, please advise the basis on which the Company does not consider the information included in the Announcement to be material.
3. If the answer to question 1 is “yes”, when did the Company first become aware of the information in the Announcement concerning the new data demonstrating the ability of PBT2 to reduce the damage to brain cells, caused by accumulation of the tau protein and preventing subsequent cognitive impairment?
4. If this was before the release of the Announcement, please identify any earlier announcement from the Company which disclosed this information.
5. If there was no earlier announcement, and the Company became aware of the information prior to the release of the Announcement, why was the information not released to the market at an earlier time? Please comment specifically on the application of listing rule 3.1 and the exceptions to the rule in listing rule 3.1A.
6. The Announcement mentioned that new data will be presented by the Company’s scientist Associate Professor Paul Adlard at the 11th International Conference on Alzheimer’s and Parkinson’s Disease, to be held in Florence, Italy, March 6th to 10th 2013. Please advise when the new data will be released to ASX. Please comment specifically on the application of listing rule 3.1 and the exceptions to the rule in listing rule 3.1A.
7. Please confirm that the Company is in compliance with listing rule 3.1.
Your response should be sent to me by return e-mail or by facsimile on facsimile number [phone]. It should not be sent to the Company Announcements Office.
Unless the information is required immediately under listing rule 3.1, a response is requested as soon as possible and, in any event, not later than before the start of trading (ie before 9.30 a.m. AEDT) on Thursday, 7 March 2013.
If you are unable to respond by the time requested, you should consider a request for a trading halt in the Company’s securities. As set out in listing rule 17.1 and Guidance Note 16 - Trading Halts, we may grant a trading halt at your request. We may require the request to be in writing. We are not required to act on your request. You must tell each of the following.
 The reasons for the trading halt.
 How long you want the trading halt to last.
 The event you expect to happen that will end the trading halt.
 That you are not aware of any reason why the trading halt should not be granted.
 Any other information necessary to inform the market about the trading halt, or that we may ask for.
The trading halt cannot extend past the commencement of normal trading on the second day after the day on which it is granted. If a trading halt is requested and granted and you are still unable to reply to this letter before the commencement of trading, suspension from quotation would normally be imposed by us from the commencement of trading if not previously requested by you. The same applies if you have requested a trading halt because you are unable to release information to the market, and are still unable to do so before the commencement of trading.
If you have any queries regarding any of the above, please let me know.
Yours sincerely,
[sent electronically without signature])
Kobe Li
Senior Adviser, Listings (Melbourne)

[Finee]

4 Healthcare Stock Stories Not To Be Overlooked

http://wallstcheatsheet.com/category/business-recaps/

[Finee]

FDA proposes to dramatically lower the bar on Alzheimer's drugs

March 14, 2013 | By John Carroll

Just weeks after pointing R&D groups engaged in Alzheimer's drug research to early-stage patients, the FDA is proposing to lower the bar biotechs will have to clear in order to gain an approval. And faced with a string of blockbuster collapses in Phase III, regulators are signaling a greater willingness to offer early, accelerated approvals for the most promising therapies that come out of the pipeline.
Up to now, the FDA has required drug developers to demonstrate improvements in both cognition and function in order for a drug developer to gain an approval. Simply put, patients in the study would not only have to demonstrate improved memory and acuity compared to a placebo group, they would also have to do better at simple daily chores like dressing themselves.
That's proven a devilishly hard target, eluding Big Pharma groups which have poured billions of dollars into new drugs only to come up short on late-stage development. But there's been a growing belief that patients diagnosed with the disease are often too damaged to benefit from therapies. As a result, the FDA has been urging drug developers to move their target to early-stage or high-risk patients, and the agency is now looking to adopt new guidances to assist the biopharma companies on trial designs that can use a new standard focused on cognitive improvements alone or preventive measures proven with biomarkers.
These new standards--initially addressed in a new draft guidance last month--could radically alter the R&D landscape for Alzheimer's drugs, widely perceived as a golden ticket to instant blockbuster status. They could also open a pathway to new therapies that could help millions of patients grapple with a mysterious and terrible disease.

[Fruehrentner]

Melbourne - March 27, 2013

Prana Biotechnology (NASDAQ: PRAN; ASX: PBT), today announced that it has secured funding of A$7 million through a placement of approximately 35.9 million fully paid ordinary shares at a price of A$0.195 per share (equivalent to approximately US$2.03 per Nasdaq listed ADR).

The funding amount includes A$2 million as part of a underwritten Share Purchase Plan (SPP).

The placement attracted strong demand from a range of Australian Institutions and High Net Worth Investors. The placement was managed by JM Financial Group Limited, based in Melbourne, Australia.

Capital is being raised by Prana in order to accelerate the regulatory pathway of its key clinical asset PBT2, now in two concurrent Phase II clinical trials in Huntington Disease and Alzheimer's Disease. Recruitment was completed for both clinical trials on time and within budget. Results are expected to be reported in October 2013 for Huntington's Disease and 1Q 2014 for Alzheimer's Disease.

Chairman and CEO Geoffrey Kempler said, "these funds allow us to accelerate our drug development schedule and move towards commercialization of PBT2 a year sooner than would otherwise be possible. We are grateful for the support of both our existing and new investors."

Share Purchase Agreement (SPP)

Prana will offer eligible shareholders the right to participate in the SPP which will enable shareholders to apply for up to A$15,000 of shares (subject to any scale back) at the same price as the Placement. The first A$2 million under the SPP will be underwritten by JM Financial Group Ltd.

The maximum amount to be raised under the SPP is A$4 million. The SPP will be available to all eligible shareholders who were on the Company's share register as at 7.00 pm AEDT on Tuesday 26th March 2013 (record date).


The SPP will allow each eligible shareholder to apply for up to approximately 76,900 new fully paid ordinary shares at an issue price of A$0.195 per share (a total of A$15,000). The full terms of the SPP offer, and how to accept and apply for new shares will be set out in an SPP Offer document which will be sent to all eligible shareholders.

The subscription price of the shares to be offered under the Plan represents a 13.3% discount to the market closing price on the ASX as at the Record Date.

The funds raised under the Offer will be used to accelerate the regulatory pathway of the Company's key clinical asset, PBT2, as referred to above.

The proposed timetable for the SPP is as follows:

Indicative Timetable
Record Date 26 March 2013
Announcement of Share Purchase Plan 27 March 2013
Dispatch of Offer and Application Forms to Eligible Shareholders 11 April 2013
Share Purchase Plan Opens 11 April 2013
Share Purchase Plan Offer Closes 26 April 2013
Allotment and Issue of SPP Shares 3 May 2013
Dispatch of Holding Statements 8 May 2013
Quotation of SPP Shares on ASX 9 May 2013

Subject to the ASX Listing Rules and Corporations Act, the Company reserves the right to vary the above dates in consultation with the Underwriter. If the Offer is oversubscribed, the Company in consultation with the Underwriter reserves the right to close the Offer early.

The above timetable is subject to change - shareholders should consult the SPP offer document which will be mailed to them.

The Company will apply for quotation of the new shares issued under the SPP. The new shares will rank equally in all respects with the Company's existing fully paid ordinary shares.

[Fruehrentner]

27.03.2013

Alzheimer-Forschung

Goldener Schuss

Pharmakonzerne und Biotech Start-ups liefern sich ein spektakuläres Rennen um das erste Alzheimer-Medikament. Dem Gewinner winken Milliardenprofite. Eine Reportage über die Jäger des größten Schatzes der Medizin.

http://www.manager-magazin.de/magazin/artikel/0,2828,885507,…

[Finee]

MELBOURNE, AUSTRALIA--(Marketwired - Apr 3, 2013) -
Prana Biotechnology (NASDAQ: PRAN) (ASX: PBT) today reported on the progress of its lead development asset PBT2 in Phase II trials for Huntington disease and Alzheimer's disease.
Across the two trials approximately 37% have been dosed to 6 months or longer, twice the duration of the previous Phase II Alzheimer's trial.1,2 PBT2 has been well tolerated and both trials are on schedule with very pleasing retention rates and compliance. Each Independent Data Safety Monitoring Board for the two trials met at the end of March and recommended that each trial continue as planned without any protocol changes.
Prana's PBT2 represents a novel and differentiated therapeutic action in the treatment of neurodegenerative diseases based on its specialized ability to prevent the toxic relationship between disease proteins and biological metals in the brain which otherwise can lead to protein amyloid formation. Moreover, the redistribution of such metals by PBT2 promotes neurotransmission and neuronal function.
Alzheimer's disease Trial Update - the "IMAGINE" trial
In an earlier 12 week trial PBT2 both significantly changed amyloid levels in spinal fluid and improved the cognition of patients with Alzheimer's disease.1,2 The IMAGINE trial, with 12 months of treatment, aims to establish PBT2 as a safe and effective treatment for Alzheimer's disease. The following provides an update on the trial:
Last Patient recruited November 2012;
Last Patient to be Dosed November 2013;
Trial will be completed in December 2013;
7% of patients have completed 12 months of dosing, over 4 times longer than the previous longest exposure to PBT2;
50% of patients have reached 26 weeks of dosing;
Data Safety Monitoring Board met on 27 March, 2013, with the recommendation to continue the trial without any changes to the original protocol.
The randomized, double-blind, placebo controlled trial has enrolled 41 patients with prodromal or mild Alzheimer's disease in five sites in Melbourne, Australia. Brain Imaging is being used to measure PBT2's effect on amyloid deposits in the brain (using PiB-PET scanning) and effects on increasing brain activity (FDG PET). Cognition effects are being measured by the Neuropsychological Test Battery (NTB).
The trial has received funding from the Alzheimer's Drug Discovery Foundation (ADDF).
Howard Fillit, MD, the ADDF's Executive Director commented, "PBT2 stands out as one of the few orally available agents with clinical trial evidence of cognitive benefit for Alzheimer's patients. Success in this trial will demonstrate target engagement by PBT2 in the brain of people with Alzheimer's disease, and accelerate the clinical development of PBT2 to patients."
The protocol for the IMAGINE trial is available by clicking here.
Huntington Disease Trial Update - the "Reach2HD" trial
The Reach2HD trial is a 6 month trial in 109 patients with early to mid-stage Huntington disease. The trial is being conducted across sites in the USA and Australia. The following provides an update on the trial:
Last Patient recruited December 2012;
Last Patient to be Dosed June 2013;
Results anticipated October 2013;
97% of patients have completed 12 weeks of dosing (equal to previous longest exposure of PBT2);
32% of patients have completed 6 months of dosing;
Data Safety Monitoring Board met on 28 March, 2013, with the recommendation to continue the trial without any changes to the original protocol.
Only one drug is marketed for Huntington disease and that is only for the relief of the severe motor or chorea symptoms. There are no approved treatments for the significant cognitive and behavioural components of the disease, which typically manifest before motor problems.

[Fruehrentner]

Und wieder ist einer weg vom Fenster:



Lilly halts Alzheimer's drug trial due to liver problems

Thu Jun 13, 2013 6:51pm EDT

(Reuters) - Eli Lilly and Co. said on Thursday it halted a mid-stage study of an experimental Alzheimer's disease treatment due to potential liver toxicity, the latest setback in the quest to find a treatment that can slow or cure the memory-robbing condition.

Lilly said the Phase II study of the drug, LY2886721, from a class known as beta secretase, or BACE, inhibitors, was stopped after safety monitors identified cases of abnormal liver tests.

The Indianapolis-based drugmaker said the liver issues do not appear related to the drug's mechanism, and that it remains interested in developing BACE inhibitors to treat the progressive brain disease.

Oral drugs to block beta secretase, although still unproven, have been one of the biggest hopes for slowing progression of the disease after another class of medicines being developed by Lilly and Pfizer Inc. last summer fell short in big trials.

Those injectable drugs, Lilly's solanezumab and Pfizer's bapineuzumab, directly block beta-amyloid, a protein that forms brain plaques considered a prime cause of Alzheimer's disease.

Solanezumab failed to slow progression of Alzheimer's among patients with mild to moderate disease. It is now being tested in patients with mild disease because it was shown to slow loss of memory in that narrower population. Bapineuzumab has been largely written off by investors after failing to slow progression of Alzheimer's in its late-stage trials.

BACE inhibitors, including rival products being developed by Merck & Co., Roche Holding AG and Eisai Co. Ltd, are meant to prevent buildup of beta-amyloid by blocking an enzyme called BACE1.

Industry analysts have said any of the BACE inhibitors could become huge sellers, with annual sales of $3 billion or more, if they prove effective and are approved. That is because no drugs currently slow progression of Alzheimer's, the biggest cause of dementia, which is believed to affect an estimated 5 million Americans.

Even so, Wall Street is not assuming the drugs will succeed, because they are in relatively early development and there have been few clues on their safety and effectiveness.

An estimated 35 million people worldwide are believed to have dementia, including Alzheimer's disease, and those numbers are expected to rise as more people live longer.

Lilly shares closed up 0.1 percent on Thursday, amid a 1 percent gain for the drug sector.

http://www.reuters.com/article/2013/06/13/us-lilly-alzheimer…

[Finee]

Prana presents new benchmark test to assess Huntington’s Disease
patients in clinical trials
New testing method created by clinical investigators in Prana’s REACH2HD trial highlighted at the 17th Annual Congress of Parkinson’s Disease and Movement Disorders
Wednesday, 19 June, 2013: Melbourne-based Prana Biotechnology (ASX:PBT / NASDAQ:PRAN) has unveiled a world first, patient-reported outcomes study for Huntington’s Disease (HD) in a poster presentation at the 17th Annual Congress of Parkinson’s Disease and Movement Disorders being held in Sydney this week.
The Poster entitled: “The Huntington‘s Disease patient-reported outcome of problems: feasibility and applicability in clinical research (HD-PROP)” details a new benchmarking system to assess the problems experienced by people with HD. The HD-PROP test aims to overcome some of the challenges associated with assessing clinically relevant outcomes in HD where progressive motor, cognitive and psychiatric symptoms can interfere with comprehension of lengthy patient self-report questionnaires and communication of responses. The HD-PROP test may be a useful tool to evaluate Prana’s clinical trial results.
The HD-PROP test asks trial participants three questions in relation to their HD at the commencement of the trial. What problem is most bothersome? In what way is this problem bothersome? How severe is this problem?
The HD-PROP test was created by clinical investigators involved in Prana’s Phase 2 clinical trial of PBT2 known as the REACH2HD Study. This 109 patient trial is fully recruited and nearing completion.
Professor Ira Shoulson, one of four authors of the Poster and an internationally renowned clinical investigator, said: “This is the first time this type of patient response testing has been applied to HD, and we expect it will form an important part of future trials in HD."
“Patient-reported outcomes are an important area of focus for the US Food and Drug Administration (FDA) and along with clinical measures provide a more complete understanding of the relevance as well as safety and effectiveness of potential treatments.”
At the commencement of Prana’s Phase 2 trial, 97% of participants reported at least one bothersome problem, 87% reported at least two problems, and 67% reported at least three problems. Motor symptoms, cognitive symptoms, functional decline, and behavioral symptoms were the most commonly reported first, second and third problems.
Geoffrey Kempler, Chief Executive Officer of Prana Biotechnology added: “This new assessment gives us great insight into the issues and concerns of people with HD and has established an important benchmark that we can consider when assessing the final clinical results of our
REACH2HD trial.”

[Finee]

Antwort auf Beitrag Nr.: 44.874.281 von Finee am 19.06.13 07:03:33

http://www.aspecthuntley.com.au/asxdata/20130619/pdf/0141814…

[Finee]

PBT434 drug candidate shows potential as “next-generation” diseasemodifying treatment in Parkinson’s Disease
Data featured in Plenary Lecture and ‘Blue Ribbon Highlights’ conference presentations at the 17th Movement Disorders Congress of Parkinson’s Disease and Movement Disorders.

Thursday, 20 June, 2013: Melbourne-based Prana Biotechnology (ASX:PBT / NASDAQ:PRAN) today welcomed the release of data which indicates its drug candidate PBT434 shows significant disease-modifying capability in multiple animal models of Parkinson’s Disease (PD) with potential utility in a range of movement disorders.
PD is caused by the death of specialized neurons in the region of the brain called the substantia nigra.
This is the only part of the brain where iron, dopamine (a neurotransmitter) and the alpha synuclein protein are all present at high concentrations. In PD, iron binds to dopamine, preventing it from functioning normally, and creating toxic free radicals. Iron also binds to alpha synuclein, causing it to aggregate. The aggregation of this protein is a well-established pathological feature of PD, and a target for new disease-modifying therapies.
PBT434 prevents alpha synuclein from aggregating and also prevents the toxic consequences of iron combining with dopamine,
In a further sign of the potential of PBT434 as an effective treatment, its therapeutic benefits were seen to be dose-dependent. Increasing increments of the drug resulted in increased preservation of neurons and increased improvement in motor function.
“These data are highly positive and support the advancement of PBT434 as a first-in-class drug that could change the course of Parkinson’s Disease and related movement disorders,” said Geoffrey Kempler, Prana’s Chairman and CEO. “This would be a major step forward in therapy as existing treatments are focused on symptomatic relief and offer little in the way of halting neurodegenerative decline once it has begun. The drug is progressing through the development process, with the aim of first clinical trials in 2015”.
These findings are being presented today at the 17th Annual Congress of Parkinson’s Disease and Movement Disorders in Sydney by Professor Colin Masters, Director of The Mental Health Research Institute at the Florey Institute of Neuroscience, in a plenary presentation, and Associate Professor David Finkelstein, Head of the Parkinson’s Disease Laboratory also at the Florey Institute.
“What we have known for some time is that dopamine and iron, together in the brain, form a combustible mix and this drives alpha synuclein aggregation and toxicity,” said Associate Professor Finkelstein.

[Fruehrentner]

hier der komplette heutige Pressetext, da fehlte etwas:


Prana's PBT434 shows potential as "next-generation" treatment in Parkinson Disease

Thursday, 20 June, 2013

Melbourne-based Prana Biotechnology (ASX: PBT / NASDAQ: PRAN) today welcomed the release of data which indicates its drug candidate PBT434 shows significant disease-modifying capability in multiple animal models of Parkinson's Disease (PD) with potential utility in a range of movement disorders.

PD is caused by the death of specialized neurons in the region of the brain called the substantia nigra. This is the only part of the brain where iron, dopamine (a neurotransmitter) and the alpha synuclein protein are all present at high concentrations. In PD, iron binds to dopamine, preventing it from functioning normally, and creating toxic free radicals. Iron also binds to alpha synuclein, causing it to aggregate. The aggregation of this protein is a well-established pathological feature of PD, and a target for new disease modifying therapies.

PBT434 prevents alpha synuclein from aggregating and also prevents the toxic consequences of iron combining with dopamine,

In a further sign of the potential of PBT434 as an effective treatment, its therapeutic benefits were seen to be dose-dependent. Increasing increments of the drug resulted in increased preservation of neurons and increased improvement in motor function.

"These data are highly positive and support the advancement of PBT434 as a first-in-class drug that could change the course of Parkinson's Disease and related movement disorders," said Geoffrey Kempler, Prana's Chairman and CEO. "This would be a major step forward in therapy as existing treatments are focused on symptomatic relief and offer little in the way of halting neurodegenerative decline once it has begun. The drug is progressing through the development process, with the aim of first clinical trials in 2015".

These findings are being presented today at the 17th Annual Congress of Parkinson's Disease and Movement Disorders in Sydney by Professor Colin Masters, Director of The Mental Health Research Institute at the Florey Institute of Neuroscience, in a plenary presentation, and Associate Professor David Finkelstein, Head of the Parkinson's Disease Laboratory also at the Florey Institute.

"What we have known for some time is that dopamine and iron, together in the brain, form a combustible mix and this drives alpha synuclein aggregation and toxicity," said Associate Professor Finkelstein.

"What we've seen with PBT434 is two beneficial modes of action - it prevents cell death by inhibiting the interaction between dopamine and iron and it also stops this accumulation of alpha synuclein."

This is the first molecule designed to inhibit the neurotoxic build-up of alpha synuclein in the brain and PBT434 could support the "next generation for PD therapies," Associate Professor Finkelstein also said.

The full Poster can be viewed at:

http://www.pranabio.com/downloads/Media%20Releases/Media%20R…



Contacts:
Prana Biotechnology Limited
[phone]

Investor Relations
ebecca Wilson
T: 0417 382 391
E: [e-mail]

[Fruehrentner]

hatten wir das eigentlich auch?

Wieder kürzlich einer weg vom Fenster:



May 7, 2013

Another Alzheimer's Drug Fails Phase III Trial

Baxter International acknowledged today that its Phase III drug candidate Gammagard (immunoglobulin) failed to meet its co-primary endpoints of reducing cognitive decline and preserving functional abilities in patients with mild to moderate Alzheimer’s disease.

According to topline results released by Baxter, patients with mild to moderate Alzheimer's who took Gammagard at either the 400 mg/kg or 200 mg/kg dose did not demonstrate a statistically significant difference in the rate of cognitive decline as compared to placebo. Those means stood at 7.4 for the 400 mg/kg patients, 8.9 for 200 mg/kg patients, and 8.4 for placebo patients. Results also showed a lack of statistically significant change in functional ability compared with placebo—means were -11.4 among both 400 mg/kg and placebo patients, rising slightly to -12.4 for 200 mg/kg patients.

But as Abbott acknowledged in a statement, the study was not powered to show statistical significance among subgroups. And instead of ending its clinical study of the experimental drug, however, Baxter cited a proverbial silver lining in the cloud of data released on Gammagard.

Patients with moderate Alzheimer’s, and carriers of the ApoE4 genetic marker—which increases risk of developing the disease—who were dosed at 400 mg/kg, showed cognition improvement of between 16% and 29% after taking the experimental drug vs. placebo, as measured by the Alzheimer’s Disease Assessment Scale—Cognitive Subscale (ADAS-Cog) and Modified Mini-Mental State (3MS) examination.

“The study missed its primary endpoints. However, we remain interested by the prespecified subgroup analyses, particularly among patients with moderate disease and those who carry a genetic risk factor for Alzheimer’s disease, two patient groups that are in great need of advances in care,” Ludwig Hantson, Ph.D., president of Baxter’s BioScience business, said in the statement. “A detailed analysis of the results from the GAP study continues, and we look forward to a greater understanding of the full dataset.”

The Phase III results came from the Gammaglobulin Alzheimer’s Partnership study conducted by Baxter with the Alzheimer’s Disease Cooperative Study, a clinical trial consortium supported by NIH’s National Institute on Aging.

The results contrast with promising Phase II findings for Gammagard released in July 2012. They showed improvements in thinking, behavior, and routine day-to-day functions in 11 of 16 patients receiving the drug for three years. Four patients who received the most effective dose of 0.4 g/kg experienced no decline in cognition, daily functioning, memory, and mood.

Gammagard joins a growing number of Alzheimer’s drug candidates in failing pivotal-stage clinical trials despite much optimism last year. Last year, Eli Lilly endured two Phase III flops for solanezumab, an amyloid beta monoclonal antibody that failed in effectiveness against beta-amyloid plaques. Solanezumab did not meet both cognitive and functional primary endpoints in two Phase III EXPEDITION trials.

Both EXPEDITION trials showed no statistically significant slowing of cognitive decline in patients with moderate Alzheimer's. Lilly cited a prespecified secondary subgroup analysis in patients with mild Alzheimer's disease, which showed a statistically significant reduction in cognitive decline. Even when Lilly modified EXPEDITION2 to specify a single primary endpoint of cognition, the revised endpoint did not achieve statistical significance.

However, Lilly said in December it plans to launch by Q3 a new Phase III study of the drug in patients with mild Alzheimer’s.

Also last year, Johnson & Johnson’s Janssen Alzheimer Immunotherapy unit and Pfizer ended development of Alzheimer’s drug candidate bapineuzumab after it failed to meet co-primary clinical endpoints in one Phase III study of patients who are ApoE4 carriers (Study 302), and another Phase III study of noncarriers (Study 301). J&J took a $700 million in-process R&D charge in Q3 2012.

And early in 2012, Pfizer wrote down $225 million in up-front cash and $500 million in potential milestone payments after Dimebon (latrepirdine), an Alzheimer’s drug developed with Medivation, flunked a Phase III study in patients with mild to moderate Alzheimer’s who were also being treated with donepezil HCL tablets. Dimebon failed to meet endpoints for cognitive improvement as well as for self-care and daily function.

http://www.genengnews.com/gen-news-highlights/another-alzhei…

[Fruehrentner]

LMTX von TauRX Therapeutics ist noch im Rennen. Es werden bereits Patienten für die Phase III rekrutiert:

http://taurx.com/lmtx-for-ad/

http://taurx.com/dementiaweek-2013.pdf


Das wird spannend.

[Finee]

Prana Biotech receives approval for 12-month open-label extension study in Alzheimer's Disease

(PRAN) announced that it has received approval from the Austin Health Human Research Ethics Committee (HREC) to commence a 12-month open-label extension study with Alzheimer's Disease patients participating in Prana's IMAGINE trial. The approval follows a full review by Austin Health HREC of the potential benefit to patients and safety data collected during the ongoing IMAGINE trial, a 12-month double-blind Phase II clinical trial of PBT2 in Alzheimer's patients. Fifteen percent of participants in IMAGINE have now finished the full 12 months of treatment and one hundred percent have completed at least 6 months of treatment. Patients who have completed the full 12-month term of the IMAGINE trial are eligible for participation in the open-label extension study. All participants in the extension study will receive a 250mg once daily oral dose of PBT2 for an additional 12 months, with the first patient expected to start next month.

http://finance.yahoo.com/news/prana-receives-approval-12-mon…

[Finee]

Prana Completes Phase 2 Huntington Disease Trial With PBT2

MELBOURNE, AUSTRALIA--(Marketwired - Jul 23, 2013) - Prana Biotechnology (NASDAQ: PRAN) (ASX: PBT) today announced the successful completion of Reach2HD, a phase 2 clinical trial in patients with early to mid-stage Huntington disease. The Company expects to announce the results arising from the trial in October.
Reach2HD is a randomised, double-blind, placebo-controlled Phase 2 trial testing the safety and efficacy of PBT2, the Company's lead compound under development for both Huntington disease and Alzheimer's disease.
"We have been extremely pleased with the conduct of the trial, at all levels including recruitment and patient retention," said Dr. Ray Dorsey, Principal Investigator of the Reach2HD study and Director of the Huntington Study Group Coordination Center.
Reach2HD had planned to recruit 100 patients with Huntington disease in 9 months. In fact, 109 participants were enrolled in the trial within that period. "The strong rate of recruitment reflects support for the Reach2HD trial within the Huntington disease clinical research community," said Dr Dorsey. Of the 109 enrolled, 104 patients completed the trial, reflecting a retention rate of over 95%.
A Data Safety Monitoring Board met on five occasions throughout the trial and on each occasion recommended that no changes or modifications to the study protocol be made based on their review of the safety data.
The primary outcome of the trial is safety and tolerability. The trial also includes a number of secondary outcome measures from the cognitive, motor and behavioural domains affected in Huntington disease. A positive result of Reach2HD will identify signals of therapeutic benefit in one or more of the domains measured, which will inform the design of the next clinical trial.
Mr. Geoffrey Kempler, Prana's Chairman and CEO, said: "Assuming we achieve the positive results we are hoping for in Reach2HD, we plan to meet with the US regulator, the Food and Drug Administration, and other regulatory agencies to discuss the next steps in the clinical development of PBT2 for the treatment of Huntington disease."
"We plan to discuss the design of the next trial and agree on a set of clinical outcomes that, when achieved, will allow us to submit a New Drug Application for approval to start to market PBT2 for Huntington disease."
Huntington disease is a complex and severely debilitating genetic, neurodegenerative disease, for which there is no cure. The disease often affects young adults and, whilst associated with severe physical movement symptoms, progressively impacts the mind and emotions as well. The disease causes incapacitation and death about 15-25 years after onset. The disease affects over 30,000 people in the US and 70,000 worldwide.
The Huntington Study Group (HSG) collaborated with Prana to coordinate the Reach2HD trial across 20 sites in the USA and Australia.

http://finance.yahoo.com/news/prana-completes-phase-2-huntin…

[Fruehrentner]

Was geht denn hier jetzt ab??!!

Kursfeuerwerk! Und ich bin nicht drin!

[Finee]

Prana Doses First Patient in PBT2 Alzheimer’s Extension Study
Melbourne – Monday 29th July, 2013

Prana Biotechnology (NASDAQ:PRAN; ASX:PBT)today announced that the first patient has been dosed in the 12-month open-label extension study with Alzheimer’s Disease patients participating in Prana’s Phase 2 IMAGINE trial.
Patients who have completed the full 12-month term of the IMAGINE trial are eligible for participation in the open-label Extension study. All participants in the Extension study will receive a 250mg once daily oral dose of PBT2 for an additional 12 months.
The IMAGINE trial is a 12-month double-blind Phase 2 clinical trial of PBT2 in mild or prodromal Alzheimer’s patients. The Extension study does not alter the completion and reporting on the IMAGINE trial with results expected in March 2014.
Prana’s Chairman and CEO, Geoffrey Kempler, said: “We anticipate a high level of patient interest in participating in this Extension study given the support expressed from the physicians involved."

http://www.asx.com.au/asxpdf/20130729/pdf/42h98ksfldkwsc.pdf

[Finee]

Antwort auf Beitrag Nr.: 45.130.887 von Finee am 29.07.13 08:33:59

Besonders den folgenden Satz hat mir sehr gut gefallen: "support expressed from the physicians involved"

[Finee]

Antwort auf Beitrag Nr.: 45.130.887 von Finee am 29.07.13 08:33:59

Prana announces dosing of first patient in PBT2 Phase II trial for Alzheimer’s disease

Fortsetzung folgt!

Professor Rudy Tanzi, the Joseph P. and Rose F. Kennedy Professor of Neurology at Harvard University and Prana’s Chief Scientific Advisor, added: “PBT2 is the most promising therapy currently in clinical trials for the treatment of Alzheimer’s disease”.

http://healthmedicinet.com/i/prana-announces-dosing-of-first…

[Finee]

4 Healthcare Stock Stories Causing Commotion On Monday
By Mark Lawson

http://wallstcheatsheet.com/stocks/4-healthcare-stock-storie…

[Finee]

Prana Prepares for Next Steps in the PBT2 Development Path to Market and Commercialization With Key Appointments Strategy

MELBOURNE, AUSTRALIA--(Marketwired - Aug 1, 2013) -
Prana Biotechnology (NASDAQ: PRAN) (ASX: PBT) has today announced the first of several key appointments in the near term to advance PBT2 into late stage and pre-market clinical development of PBT2 as a treatment for Alzheimer's and Huntington's diseases.
Dr. Peter Smith has been engaged to drive business development for Prana's lead drug PBT2 globally at an important time for Prana with results from Phase II clinical trials for Huntington's and Alzheimer's diseases expected in October 2013 and March 2014 respectively.
Prana will shortly also be making senior appointments in Toxicology, Manufacturing and Clinical Operations to support the company's plans to accelerate PBT2 into prospective Phase III studies.
Dr. Peter Smith is a seasoned senior executive in the biotechnology industry with substantial experience in negotiating global licensing deals, finance and operational roles, including CEO of Alchemia from 2006 until earlier this year where he secured a global partnership with Dr. Reddy's. Prior to Alchemia, Dr Smith was CEO and Managing Director of Amrad, Chairman and CEO of Cerylid Biosciences and founded the UK-based cancer vaccine company Onyvax. He has also held senior roles in the banking industry.
Prana Biotechnology Executive Chairman Geoffrey Kempler said: "Prana is entering an exciting period of its history as we near reporting on our two Phase II trials of PBT2.
"These appointments are essential as we plan for the future in delivering innovative therapies in these diseases for which today, there is no cure. We are very pleased to have someone of Peter's calibre working alongside us to capitalize on the growing interest in PBT2 as we progress its path to market and look forward to announcing future appointments shortly."
About Prana Biotechnology Limited Prana Biotechnology was established to commercialise research into age-related neurodegenerative disorders. The Company was incorporated in 1997 and listed on the Australian Securities Exchange in March 2000 and listed on NASDAQ in September 2002. Researchers at prominent international institutions including The University of Melbourne, The Mental Health Research Institute (Melbourne) and Massachusetts General Hospital, a teaching hospital of Harvard Medical School, contributed to the discovery of Prana's technology.
For further information please visit the Company's web site at www.pranabio.com.

[Fruehrentner]

Prana Prepares for Next Steps in the PBT2 Development Path to Market and Commercialization With Key Appointments Strategy

MELBOURNE, AUSTRALIA - Aug 1, 2013

Prana Biotechnology (NASDAQ: PRAN) (ASX: PBT) has today announced the first of several key appointments in the near term to advance PBT2 into late stage and pre-market clinical development of PBT2 as a treatment for Alzheimer's and Huntington's diseases.

Dr. Peter Smith has been engaged to drive business development for Prana's lead drug PBT2 globally at an important time for Prana with results from Phase II clinical trials for Huntington's and Alzheimer's diseases expected in October 2013 and March 2014 respectively.

Prana will shortly also be making senior appointments in Toxicology, Manufacturing and Clinical Operations to support the company's plans to accelerate PBT2 into prospective Phase III studies.

Dr. Peter Smith is a seasoned senior executive in the biotechnology industry with substantial experience in negotiating global licensing deals, finance and operational roles, including CEO of Alchemia from 2006 until earlier this year where he secured a global partnership with Dr. Reddy's. Prior to Alchemia, Dr Smith was CEO and Managing Director of Amrad, Chairman and CEO of Cerylid Biosciences and founded the UK-based cancer vaccine company Onyvax. He has also held senior roles in the banking industry.

Prana Biotechnology Executive Chairman Geoffrey Kempler said: "Prana is entering an exciting period of its history as we near reporting on our two Phase II trials of PBT2.

"These appointments are essential as we plan for the future in delivering innovative therapies in these diseases for which today, there is no cure. We are very pleased to have someone of Peter's calibre working alongside us to capitalize on the growing interest in PBT2 as we progress its path to market and look forward to announcing future appointments shortly."

http://www.pranabio.com/default.asp?contentID=629

[Finee]

The Role Of Transition Metals & Reactive Oxygen Species (ROS) In Alzheimer's Disease
von Pırıl Erel am 08. August 2013

http://de.slideshare.net/pirilerel8/ssa-presentation-final

[Finee]

The Past, Present and Future of Alzheimer’s Treatments
By Leo Sun - August 19, 2013

Alzheimer’s disease, the most common form of dementia, is one of the greatest medical mysteries of our day. 5.2 million Americans are diagnosed with this debilitating disease, which is the sixth leading cause of death in the country. Alzheimer’s disease usually occurs in patients over 65 years old, and is expected to affect one in every 85 people in the world by 2050 -- a startling figure considering that scientists still don’t fully understand what causes the disease.
Those factors make the race to bring a real treatment for Alzheimer’s disease a top priority for the biotech industry. Let’s take a look at the past, present and future of these treatments to better understand the challenges that patients, scientists and biotech investors face.

Current treatments

The current market for Alzheimer’s treatments generates roughly $20 billion in revenue annually, according to Deutsche Bank. However, these treatments only treat the main symptoms of Alzheimer’s -- memory loss, confusion, and cognitive problems -- rather than the actual cause.
Aricept, developed by Eisai and Pfizer (NYSE: PFE), is the most popular of these treatments. Aricept is a cholinesterase inhibitor which prevents the breakdown of acetylcholine, a chemical messenger needed for learning and memory. By keeping acetylcholine levels elevated, Alzheimer’s symptoms can be held at bay for an average of six to twelve months in roughly half of the patients.
Aricept had peak sales of $2.4 billion in 2010, but have fallen dramatically over the past three years after its patent expiration. Today, generic Aricept is widely available from generics companies such as Actavis and Teva Pharmaceutical.
Namenda, which was first synthesized by Eli Lilly & Co. (NYSE: LLY) in 1968, is another common treatment for Alzheimer’s disease. Namenda attempts to protect the brain’s nerve cells against glutamate, a chemical messenger which is released in excess amounts by cells damaged by Alzheimer’s disease and other neurological disorders. If glutamate binds to a patient’s brain cells, it allows calcium to freely enter the cells, causing cell degeneration.
Namenda is currently manufactured by Forest Pharmaceuticals, a subsidiary of Forest Laboratories (NYSE: FRX). Last quarter, sales of Namenda rose 7.9% year-on-year to $397.5 million, accounting for 48% of Forest Laboratories’ top line. However, the patent for Namenda expires in 2015, which could send Forest over the edge of the cliff as generics enter the market.

The brain plaque problem

To treat the root cause of Alzheimer’s, scientists are currently working on the theory of brain plaques -- extracellular deposits of beta amyloid in the gray matter of the brain. These brain plaques are believed to be neurotoxic and a major cause of the primary symptoms of dementia. The quest to clear away the plaque, however, has not been an easy one.
Pfizer, along with Johnson & Johnson (NYSE: JNJ) and Elan Corporation (recently acquired by Perrigo Company), initially approached this problem with a plaque-clearing humanized monoclonal antibody known as bapineuzumab. Bapineuzumab attempts to use monoclonal antibodies to bind to beta amyloids directly to clear them individually. However, bapineuzumab was shown to be ineffective in patients with mild to moderate Alzheimer’s disease. Development of an intravenous formulation of the drug was halted last August, and a Phase II subcutaneous formulation of the drug was discontinued in July.
Eli Lilly, on the other hand, has been working a different angle with its experimental drug, solanezumab -- a BACE inhibitor which seeks to block the creation of beta amyloid deposits altogether, rather than simply clearing them out. However, Lilly hit a major roadblock last year when its experimental drug, solanezumab, showed poor efficacy on advanced Alzheimer’s patients in Phase III trials. Rather than give up as its peers have done, Lilly went back to the drawing board by focusing the treatment on mild Alzheimer’s cases instead, on a larger group of 2,100 patients, compared to the 1,300 in its original trial.
Lilly faces some tough competition going forward. Merck and AstraZeneca are also developing BACE inhibitors like solanezumab, and Merck has already presented positive results for its Phase Ib study of its drug, MK-8931.

Smaller competitors at the gates

Big Pharma is not alone in its quest to uncover the elusive treatment for Alzheimer’s. Last year, over 1,000 clinical trials were conducted to test various methods of treating the disease. Many of these trials were conducted by smaller, developmental stage companies, like Prana Biotechnology (NASDAQ: PRAN).
Prana’s lead drug, PBT2, is a copper/zinc ionophore which was shown to restore cognition in animal models of Alzheimer’s disease. The drug targets the zinc and copper ions that are necessary for the assembly of the beta amyloid deposits, diffusing them and effectively detoxifying them. PBT2 is currently in Phase IIb clinical studies for Alzheimer’s and Phase IIa clinical trials for Huntington’s disease, a neurodegenerative genetic disorder. The full results from the Alzheimer’s trial will be released in October, and the results of the Huntington’s trial will be available next March.
Although Prana is a small fish in a sea of much larger competitors, its progress with PBT2 makes it one of the more important names to watch in the race to treat Alzheimer’s.

http://beta.fool.com/leokornsun/2013/08/19/the-past-present-…

[Fruehrentner]

DAS war wohl der Grund für den fulminanten Kursanstieg der letzten Tage:


Alzheimer: Kupferhaltige Lebensmittel könnten Krankheitsrisiko erhöhen

Im Tierversuch verursacht die Zufuhr geringer Mengen des Metalls, wie sie bei normaler Ernährung aufgenommen werden, mit der Zeit krankhafte Veränderungen im Gehirn


Rochester (USA) - Mit der Nahrung aufgenommenes Kupfer kann sich in Blutgefäßen des Gehirns ansammeln. Das verhindert den Abtransport des Eiweißstoffs Beta-Amyloid, was dessen Ablagerung im Hirngewebe begünstigt – ein charakteristisches Merkmal der Alzheimer-Demenz. Das berichten amerikanische Forscher nach Experimenten mit Mäusen und menschlichen Hirnzellen. Bei Alzheimer-Mäusen erhöhte schwach kupferhaltiges Trinkwasser zusätzlich die Produktion von Beta-Amyloid im Gehirn und verstärkte Entzündungsreaktionen. Diese Ergebnisse eröffnen neue Möglichkeiten zur Vorbeugung und Therapie der Alzheimer-Krankheit, schreiben die Wissenschaftler im Fachjournal „Proceedings of the National Academy of Sciences (PNAS)“.

„Die langfristige Wirkung des Kupfers besteht darin, einen Prozess zu schädigen, durch den Beta-Amyloide aus dem Gehirn entfernt werden“, sagt Rashid Deane von der University of Rochester. Sein Forscherteam hatte zunächst jungen, gesunden Mäusen drei Monate lang täglich über das Trinkwasser sehr geringe Mengen an Kupfer verabreicht. Die Dosierung sei vergleichbar gewesen mit dem, was Menschen bei normaler Ernährung konsumieren würden, so Deane. Die Forscher entdeckten, dass sich das Kupfer mit der Zeit in den Zellen von Blutgefäßwänden im Gehirn der Tiere ansammelte. Diese Zellen bilden die sogenannte Blut-Hirn-Schranke, die den Stofftransport zwischen Blut und Hirngewebe reguliert. Die Zellen verhinderten zwar den Übertritt von Kupfer in das Gehirn. Aber die erhöhten Mengen des Metalls hemmten auch ein wichtiges Transportprotein (LRP1). Dieses sorgt normalerweise dafür, dass Beta-Amyloide ständig aus dem Gehirn in das Blut gelangen und so abtransportiert werden. Ist der Abtransport blockiert, sammelt sich der Eiweißstoff an und bildet unlösliche Ablagerungen, die Hirnzellen abtöten. Dieser Effekt des Kupfers ließ sich auch in Zellkulturen menschlicher Hirnzellen nachweisen. Genauere, biochemische Untersuchungen zeigten: Das Transportprotein wird durch den erhöhten Kupferspiegel oxidiert und dann von der Zelle abgebaut.

In weiteren Experimenten untersuchten die Forscher die Wirkung von Kupfer bei Mäusen, die bereits an Alzheimer erkrankt waren. Bei diesen Tieren war die Blut-Hirn-Schranke schon geschädigt und durchlässiger geworden. Das bewirkte, dass das Kupfer nicht nur in die Blutgefäßzellen, sondern auch in das Hirngewebe eindrang. Dadurch verstärkten sich die normale Produktion von Beta-Amyloid und damit auch das Ausmaß an Ablagerungen. Zusätzlich löste dies Entzündungsreaktionen aus, die die Funktion der Blut-Hirn-Schranke noch weiter schädigten. Die unterschiedlichen Wirkungen des Kupfers könnten dazu beitragen, die Entwicklung einer Alzheimer-Demenz zu beschleunigen. Kupferbindende Wirkstoffe, die eine Ansammlung in den Blutgefäßen des Gehirns und das Durchbrechen der Blut-Hirn-Schranke verhindern, wären möglicherweise geeignet, das Fortschreiten der Demenz aufzuhalten, schreiben die Autoren.

Dabei sei aber zu bedenken, dass Kupfer auch ein lebensnotwendiges Spurenelement ist und unter anderem die Nervenfunktion unterstützt. Es wird in Form von Kupferionen mit dem Trinkwasser und mit verschiedenen Nahrungsmitteln zugeführt – darunter Getreide, Nüsse, Innereien und Schalentiere. Im Körper liegt es überwiegend an Proteine gebunden vor. Für Erwachsene beträgt der geschätzte Tagesbedarf an Kupfer 1 bis 1,5 Milligramm. Es wäre nun wichtig, genauer zu wissen, welche Mengen gesundheitlich unbedenklich sind. Jedenfalls dürfte die Ernährung eine bisher unterschätzte Rolle für das Demenzrisiko spielen und eine überhöhte Kupferzufuhr könnte den Krankheitsverlauf verschlimmern. Die Ursache der Alzheimer-Demenz ist unbekannt und es gibt bisher keine Therapie, die sich in klinischen Studien als wirksam erwiesen hat.

http://www.wissenschaft-aktuell.de/artikel/Alzheimer__Kupfer…

[Fruehrentner]

interessant! Die Firma D-PHARM entwickelt auf derselben Arbeitshypothese wie Prana einen Wirkstoffkandidaten gegen Alzheimer. Jedoch ist D-Pharm in einem viel früheren, präklinischem Entwicklungsstadium als Pranas Molekül.

Ich glaube, PRANA hat hier was ganz großes in Händen ...


DP-460:

DP-460 is in preclinical development for Alzheimer's disease. It is a MAC derivative of BAPTA. Its membrane-dependent modulation of transition metals like copper, zinc and iron, enables DP-460 to interfere in oxygen radical generation and plaque formation associated with neurodegeneration.


DP-460 is a small molecule, NCE, and is the second most advanced product utilizing MAC technology. DP-460 is a selective modulator of copper and zinc homeostasis in the vicinity of cell membranes. Accumulation of aggregated β-amyloid and phospho-tau protein is the hallmark of Alzheimer's disease and is believed to be metal ion dependent. Moreover, contemporary scientific publications suggest that aggregation of β-amyloid and accumulation of phospho-tau precipitates may trigger the processes that lead to damage and degeneration of brain cells. D-Pharm is developing DP-460 to prevent and modify the course of Alzheimer's disease; DP-460 is currently in preclinical development.

DP-460 exhibited significant efficacy in a transgenic mouse model of Alzheimer's disease. Treatment with DP-460 dramatically reduced amyloid plaque load in the mice brains. In addition, in vitro and ex vivo studies demonstrate suppression of degeneration of brain cells induced by β-amyloid, free radicals and oxygen-glucose deprivation. Preliminary safety data indicates that DP-460 is safe and non-toxic even at doses far in excess of the efficacious dose.

http://www.dpharm.com/DP109.asp

[Fruehrentner]

Seit Jahren beobachte ich diese Firma und jetzt verpass ich den Einstieg!

[Fruehrentner]

Antwort auf Beitrag Nr.: 45.305.633 von Fruehrentner am 22.08.13 18:58:45

...

[Finee]

Antwort auf Beitrag Nr.: 45.305.649 von Fruehrentner am 22.08.13 18:59:54

Eine vorgefasste Meinung ist schwieriger zu zertrümmern als ein Atom.
Albert Einstein

[orion1983]

Fruehrentner....ich habe genau dasselbe problem. erstmals gekauft im januar 2011 für 3 wochen, dann mal kurz rein und wieder raus. hab 20-seitigen analystenstudien dazu gelesen und fand deren medikament sehr vielversprechend. wollte nach dem ausbrechen der eeewig anhaltenden 2,3$-pendelei warten, bis die aktie zurück kommt. darauf habe ich jetzt ewig umsonst gewartet und bin vor kurzem mit nem deutlich kleineren betrag bei 4,55$ rein....trotz großen risikos hat das tägliche kursplus zum glück noch angehalten. bin gespannt, wie´s weitergeht...

[orion1983]

achja...da ja anscheinend neben den fundamental überzeugten investoren (wie mir) auch chart-player auf den prana-zug aufgesprungen zu sein scheinen, ist´s evtl von wichtigkeit, dass bei 5$ ein gap gerissen wurde. da der gestrige handelsverlauf auch zudem größtenteils parabolisch nach oben zeigte, denke ich schon, dass es nochmal bis 5$ runter geht, und evtl auch darunter....sofern die nächsten tage noch keine news bzw pusher-artikel kommen. deshalb ist es meiner meinung nach gestern zuuu heiß gelaufen und ich habe diesmal meine gier ausgeschaltet und bin bei 6$ wieder raus gesprungen...und warte mal ab, um definitiv wieder einzusteigen. 225 mio $ wert sind zwar immer noch unglaublich billig, WENN die ergebnisse passen, aber wenn fast-money-players eingestiegen sind, stehe ich lieber an der seitenlinie, auch wenn das bei steigenden kursen oft genauso weh tut wie bei fallenden kursen investiert zu sein

mitte/ende september bis oktober sollen ja wieder news kommen soweit ich mich erinnern kann, also hat die aktie noch zeit zum durchatmen bis dahin würde ich meinen....aber ich dachte andererseits ja auch, dass 4$ das absolute ende der fahnenstange gewesen wären. also man darf gespannt sein auf die nächsten tage hoffe, die leser dieses forums finden auch noch den richtigen einstiegspunkt....bis 2,25 $ geht´s wohl nur mit schlechten daten zurück...und DANN wäre ja eh vorsicht geboten...

[orion1983]

so..gap ist geschlossen bei 5$ jetzt wird´s interessant!!

[Finee]

Prana drug treatment PBT2 named one of TopNeuroscience Projects to Watch
Highlights
• PBT2 selected as one of the most attractive neuroscience opportunities in the industry
• Independent panel says PBT2 potentially meets a large, unmet market
• Prana to present at Therapeutic Area Partnerships on Nov 18-20, 2013 in Boston, USA
MELBOURNE, September 3, 2013 :
Prana Biotechnology (ASX:PBT / NASDAQ:PRAN), a leading global developer of first-in-class treatments for neurodegenerative disease, is pleased to announce Elsevier Business Intelligence has named clinical drug PBT2 as one of the Top 10 Neuroscience Projects to Watch.
Prana is developing PBT2 as a treatment for Huntington’s and Alzheimer’s disease.
The top 10 list isselected by an independent panel each year to highlight compounds which address a large, unmet market, strong science and a diversity of indications. Other criteria include the potential for new opportunities beyond initial indications, multi-level partnering opportunities and a strong company behind the compound.
Companies selected in the Top 10 Neuroscience Projects to Watch were screened against strict criteria and are considered the most attractive neuroscience opportunities in the industry. Past Top 10 candidates have signed $US17 billion in potential acquisitions and alliances including Vectura, AVEO, Trophos, BiPar, Myogen, Sirtris and Kosan.
Prana will present the latest research on PBT2 to more than 250 guests at Windhover’s Therapeutic Area Partnerships meeting on November 18-20, 2013 at the Hyatt Regency in Boston, USA.
“We are very pleased to have PBT2 recognised as one of the most promising treatments under development,” said Prana’s Chairman and CEO Mr Geoffrey Kempler.
“There currently exists very limited treatment options for Huntington’s disease, which affects about 30,000 in the US and 1200 people in Australia. Current treatment options for Alzheimer’s disease are also limited and focus on the symptoms of the disease rather than the cause.”
In July, Prana completed Reach2HD, a Phase II clinical trial investigating PBT2 as a treatment for Huntington’s disease, and is expected to release results in October 2013.
Results from the Phase II IMAGINE trial of PBT2 in patients suffering Alzheimer’s disease are expected to be announced in March 2013.
Data from an earlier trial on PBT2 has been published in Lancet Neurology and Journal of Alzheimer’s Disease, showing PBT2 significantly changed Abeta levels in spinal fluid and significantly improved the cognition of Alzheimer’s disease patients.

[Finee]

Parkinson’s UK Awards £150,000 to Study Prana’s PBT434
Dr James Duce of University of Leeds – Principal Investigator
Melbourne – Wednesday 4 September, 2013:
Prana Biotechnology (NASDAQ:PRAN; ASX:PBT) today announced that Parkinson’s UK has awarded £150,000 (AU$260,000) to The University of Leeds to study the mechanism of action of PBT434.
Principal Investigator Dr James Duce, from The University of Leeds UK, will collaborate with Professor David Finkelstein of The Florey Institute of Neuroscience and Mental Health (FINMH) in Australia and Associate Professor Robert Cherny of FINMH and Prana’s Head of Research on the Study.
Dr Duce has published extensively on the role of iron in both the healthy and diseased brain.
The funds will be used over 18 months to study the mechanism of action of PBT434 in animal models of Parkinson’s disease and Parkinsonian syndromes. In particular, the work will focus on the ability of PBT434 to reduce the elevated iron levels in the Parkinsonian brain, attenuate oxidative stress and alter the function or abundance of iron regulated proteins.
Dr Kieran Breen, Director of Research and Innovation at Parkinson’s UK commented: “This is a really exciting time for Parkinson’s research. We are now starting to identify drugs that will treat Parkinson’s – possibly slowing down or halting its progression – rather than just treating the symptoms”.
“This research has been funded by our innovative translational research programme. This takes basic research findings and helps to bring them closer to the clinic. Research such as this could ultimately bring us closer to our ultimate goal – a cure for Parkinson’s.”
PBT434 is Prana’s lead drug under development for Parkinson’s disease, Parkinsonian
syndromes, and other movement disorders. The drug has completed the first stage of preclinical toxicology studies, with the support of The Michael J Fox Foundation, and is now completing further toxicology studies to be ready to start Phase 1 clinical trials at the end of 2014.
“PBT434 has proven effective in preventing neuronal loss and preserving motor function in three different animal models of Parkinson’s disease. PBT434 also inhibits the accumulation of alpha synuclein, a hallmark of the disease, which is promoted by increasing iron levels in the brain. Elevation of iron in the brain is a well-established pathological feature of
Parkinson’s disease,” said Associate Professor Cherny, Prana’s Head of Research on the Study, “The evidence so far suggests that PBT434 targets the biochemical pathways that influence the trafficking and distribution of iron in the brain. This generous award will allow us to gain more refined insights into PBT434’s therapeutic activity and better understand the
pathological events underlying the disease.”

[Fruehrentner]

MELBOURNE, AUSTRALIA--(Marketwired - Sep 13, 2013)

Prana Biotechnology (ASX: PBT) (NASDAQ: PRAN), a leading global developer of first-in-class treatments for neurodegenerative disease, has today provided an update on three clinical trials testing its proprietary drug, PBT2, in Alzheimer's and Huntington's diseases.

Huntington REACH 2HD Trial
The Reach 2HD trial is a six month double-blind placebo controlled Phase 2 trial on 109 early-to-mid stage Huntington's disease patients. The trial was successfully completed at the end of July 2013 with 95% of participants completing the entire six months of treatment. There has been a delay in finalising the database to achieve 'database lock', required before statistical analysis of the data may begin. The results, originally anticipated in the last quarter of 2013, are now expected to be reported early in 2014.

"Apart from the timing delay, which is disappointing, nothing has changed. The trial was conducted and completed to protocol, and will provide the robust data needed to meet with the FDA in 2014 as we prepare for the next PBT2 trial," said Geoffrey Kempler, Chairman and Chief Executive Officer.

Alzheimer's IMAGINE Trial
The IMAGINE trial is a 12 month double-blind placebo controlled Phase 2 trial in 42 prodromal and mild Alzheimer's disease patients. The last patient was enrolled on 28 November 2012 and now 17 (40%) of patients have completed the entire 12 months of treatment. The Data Safety Monitoring Board has met on four occasions and recommended that the trial continue without changes to the protocol. The last patient will finish dosing at the end of November. Results are anticipated to be available in the first quarter of 2014.

IMAGINE Extension Trial
In July, the IMAGINE Extension open label trial was approved allowing all patients who have completed the IMAGINE trial to participate for a further 12 months.

Enrolment into the Extension trial opened (at the first site) on 23 July 2013, at which time 12 patients had already completed dosing in the initial IMAGINE trial, some up to five months prior. Of these 12 patients, eight (67%) have elected to join the Extension trial. Since the opening of the Extension trial, a further five patients have completed treatment in the initial IMAGINE trial and all five (100%) have elected to continue onto the Extension trial and receive PBT2 for an additional 12 months.

"We are very excited as we approach the release of clinical trial data in the coming months. Building on a body of scientific research developed over many years, our clinical trials are designed to demonstrate the safety and efficacy of PBT2 in two devastating diseases," said Mr Kempler.

[orion1983]

da nun für 2013 keine ordentlichen news mehr zu erwarten sind und alle in Q1 2014 verschoben wurden, denke ich der kurs bröckelt noch weiter ab.... und aufgrund des enormen anstiegs auf über 6$ sind sicher einiger shorter mit aufgesprungen und haben den schönen wert etwas verhunzt. mittel- und langfristig bin ich jedoch sehr positiv eingestellt! ob ich nochmal zu 3$ nachkaufen kann wird sich noch zeigen....

[Fruehrentner]

Welt-Alzheimer-Bericht 2013: Zahl Demenzkranker soll sich verdreifachen

http://www.spiegel.de/gesundheit/diagnose/welt-alzheimer-ber…

[Finee]

MELBOURNE, AUSTRALIA--(Marketwired - Oct 30, 2013) -
Prana Biotechnology (ASX: PBT) (NASDAQ: PRAN),
PBT2 Increases numbers of Neurons in the brain
PBT2 increases numbers of Synapses in the brain
PBT2 increases NMDA and AMPA levels
PBT2 increases Protein Phosphatase 2a (PP2a)
Prana Biotechnology (ASX: PBT) (NASDAQ: PRAN), a leading global developer of first-in-class treatments for neurodegenerative disease, has today announced the publication of an article in the peer reviewed Aging Cell showing the effects of PBT2 on neurogenesis and in reversing the memory and learning losses associated with the aging process, in normal (ie non transgenic) old mice.
The paper, entitled "A Novel Approach To Rapidly Prevent Age-Related Cognitive Decline", appears in the journal Aging Cell available now online here*. The authors were led by Associate Professor Paul Adlard, Head, Synaptic Neurobiology Laboratory, The Florey Institute of Neuroscience and Mental Health.
"It is very exciting to discover that PBT2 not only helps clear amyloid from the brain, but is promoting the birth of new nerve cells in a part of the brain that is particularly affected by Alzheimer's disease, the hippocampus. This now adds to the predicted beneficial properties of PBT2 for the treatment and prevention of Alzheimer's disease," commented Dr Rudy Tanzi, Professor of Neurology at Harvard Medical School, Vice Chair of Neurology at Massachusetts General Hospital, and Prana's Chief Scientific Advisor.
Age-related cognitive decline occurs in humans along with all other mammals. Data in this publication, describes how PBT2 reversed both memory and cognitive loss in aged mice.
Previously Prana reported the positive effects of PBT2 on increasing neuronal number, synaptic density and up regulation of critical markers of synaptic function and plasticity in an transgenic animal model of Alzheimer's disease, as well as significantly improved cognition (see Prana press release 21 March 2011 here). These new findings are in normal old mice that have not been genetically modified and do not form amyloid.
"In my view, these data help explain why other Alzheimer's therapies that solely target Abeta or tau pathology may, at best, be only partially effective. PBT2, by addressing metal induced oligomer formation, restoring metal balance in affected brain regions, and by promoting new neuronal cell growth, elicits a distinct set of disease modifying effects. Thus PBT2 may not only ameliorate Alzheimers pathology, but perhaps other detrimental aspects of aging on the brain," concluded Dr Tanzi.
Synopsis of the Aging Cell publication
Typically mice live for 24 to 30 months, developing progressive cognitive impairment from 16 to 18 months. Age related cognitive decline is associated with measurable structural and biochemical changes in the brain, which were significantly improved by PBT2. In the study 22 month old mice were treated with PBT2 for a total of 12 days.
PBT2 restored learning and memory. The old mice treated with PBT2 performed learning and memory tasks to the same level exhibited by young mice and significantly better than untreated old mice (p
PBT2 Increases markers of neurogenesis and neuron number:
a) Increased number of mature neurons by up to 27% in the hippocampus
b) Increased markers of cell proliferation by 67% and markers of numbers of immature neurons by 130% in the hippocampus.
c) Neuronal proliferation markers were elevated around the lateral ventricles by 214% (atrophy of peri-ventricular tissue is a feature of Huntington's disease)
PBT2 increases numbers of synapses in the hippocampus:
a) Synaptophysin levels increased by 38%
b) Dendritic spine density increased by 15%
PBT2 increases glutamate receptor levels in the hippocampus:
a) NMDA R2b levels increased by 88%
b) AMPA levels increased by 97%
PBT2 increases Protein Phosphotase 2a (PP2a) in the hippocampus:
a) PP2a increased by 22%
b) Phosphorylated Tau levels decreased by 81%
* Adlard et al, A Novel Approach To Rapidly Prevent Age-Related Cognitive Decline
http://onlinelibrary.wiley.com/doi/10.1111/acel.12178/pdf

[Finee]

The biotech winning the age fight
Published 06 November 2013 12:32

Investors looking to play the anti-ageing theme might want to consider a look at ASX and Nasdaq-listed Prana Biotechnology.

The share price of the clinical-stage company jumped more than 50 per cent in a day at the end of October on the back of a peer-reviewed article in the medical journal Aging Cell that showed the positive effect its compound has on neurogenesis and in reversing the memory and learning losses associated with the ageing in mice.

During a visit to Australia for the AusBiotech conference in Melbourne recently, biotech analyst for boutique investment and brokerage firm MLV & Co George Zavoico, who covers Prana in the United States, points to the Prana’s phase II trial results early in the new year as the next potential catalyst to unlock value in the company.

Prana’s test drug PBT2 is the subject of the phase II trial for Alzheimer’s and Huntington’s diseases. Both trials are expected to report results in Q1 2014.

“The positive review now puts the trial results in the spotlight,” says Zavoico, who is employed by the research arm of a company which is also retained by Prana in an advisory capacity.

News brings big swings

Like most small biotech companies listed on the ASX, Prana’s share price can swing significantly on news even remotely related to its drug trials...

http://www.afrsmartinvestor.com.au/p/shares/the_biotech_winn…

[Finee]

http://au.news.yahoo.com/today-tonight/health/article/-/1982…

[Finee]

http://www.asx.com.au/asxpdf/20131128/pdf/42l733lvn04gxb.pdf
Finde ich sehr interessant, wenn auch nicht bahnbrechend neu...

[Finee]

2 small biotech firms with big potential
By Tom Richardson - December 2, 2013

Innovative pharmaceutical business Acrux (ASX: ACR) recently signed a distribution deal in Brazil for its flagship testosterone deficiency drug Axiron. The drug can improve sex drive and energy levels in men, and is particularly popular in the billion-dollar U.S market.
Approval for sale in Brazil follows on from recent approval in Germany and Acrux has identified 142 countries with potential for the drug’s distribution. 2010 was Acrux’s breakthrough year, after it received approval to market Axiron from the U.S Food and Drug Administration (FDA). It recently had that patent extended until 2027.
The innovative aspect of the Acrux business is that it develops drugs that can be administered topically through the skin in simple spray or liquid form. This is an increasingly patient-preferred method, rather than less convenient methods like injection.
Acrux is also in the process of commercialising Estradiol, a spray therapy for female menopause symptoms. The company has a market cap around $420 million and shows how the biotech sector can deliver big profits for shareholders who get in early enough.

Another small-cap biotechnology company gaining publicity recently is Prana Biotechnology (ASX PBT). It’s attempting to develop treatments for some of the world’s most common diseases, in particular Alzheimer’s and Parkinson’s. Success has blockbuster potential for shareholders, with the company expected to release the results of its latest Alzheimer’s drug trials in March 2014.
In the last year, shares in the business have tripled in value then almost halved again as investors speculate on the company’s success in developing and commercialising the Alzheimer’s drugs. Eventual U.S FDA approval for any Alzheimer’s treatment is the Holy Grail, but that’s a long way off yet, with the company giving no further clues as to the status of the trials after its AGM last week. Even reported trial success is absolutely no guarantee of FDA approval to market the drugs.
Current market cap is $216 million, although investors can expect this to gyrate sharply as the results of its drug trials become clearer.

http://www.fool.com.au/2013/12/02/2-small-biotech-firms-with…" target="_blank" rel="nofollow ugc noopener">http://www.fool.com.au/2013/12/02/2-small-biotech-firms-with…

[Finee]

Prana completes PBT2 dosing in IMAGINE Alzheimer’s Disease clinical trial
95% patient retention level achieved in IMAGINE trial

MELBOURNE, December 9, 2013:
Prana Biotechnology (ASX:PBT; NASDAQ:PRAN), a developer of best-in-class treatments for neurodegenerative disease, today announced the completion of the treatment phase of its IMAGINE Alzheimer’s Disease (AD) clinical trial.
There were 42 patients with prodromal or mild AD enrolled in the Phase II double-blind placebo-controlled clinical trial of Prana’s novel drug, PBT2. A total of 40 patients completed the planned 12 months of treatment with PBT2, or placebo, bringing the treatment phase of the trial to a close.
The IMAGINE trial received funding from the New York based Alzheimer’s Drug Discovery Foundation (ADDF). ADDF’s Executive Director Howard Fillit, MD, said the results were now keenly anticipated.
“At the time of initiating the trial, we noted that PBT2 stood out as one of the few remaining orally available agents with clinical trial evidence of cognitive benefit for Alzheimer’s patients,” Dr Fillit said.
“Since then the relevance of this trial and its design has only increased, in light of the changing competitive and regulatory landscape for Alzheimer’s drugs in development.”
“The ADDF is proud to have supported this PBT2 trial design that reflects the US Food and Drug Administration’s new guidelines encouraging companies to look at treating patients earlier in the disease process.”
The primary outcome of IMAGINE is the effect of 12 months of treatment with a daily oral dose of 250mg of PBT2 on beta amyloid deposits in the brain.
Other outcomes include the effects of PBT2 on increasing brain activity (F-FDG PET), brain volume (MRI) and cognition, measured by a Neuropsychological Test Battery (NTB).
To qualify for participation in the trial, patients completed a PiB-PET brain scan to confirm a level of beta amyloid deposit consistent with prodromal or early disease.
Only two patients withdrew during the trial representing a trial retention rate of 95%. An independent Data Safety Advisory Board met five times during the course of the trial and on no occasion made any recommendations to vary the original trial protocol.
The data compilation and statistical analysis will commence shortly after the last few patients complete their follow up visit, with results expected in March 2014.
Currently all available treatments for AD are approved to provide some degree of symptomatic relief. None change the course of the disease and the eventual decline in patient’s cognition and health. The IMAGINE study design aims to demonstrate PBT2’s potential as an effective disease modifying treatment available to patients.
IMAGINE protocol: https://www.anzctr.org.au/Trial/Registration/TrialReview.asp…

http://www.asx.com.au/asxpdf/20131209/pdf/42lh3g56c23zbj.pdf

[Finee]

Alzheimer’s Theory That’s Been Drug Graveyard Facing Test
http://www.bloomberg.com/news/2013-12-12/merck-s-bid-to-trea…

...und der Kommentar dazu (intéressant, complet et très instructif )

Dr. Rudy Tanzi
This is not the only anti-abeta therapy still standing. Prana Biotechnology, founded in my lab in 1997 and now based in Melbourne, Australia, has already conducted a positive phase 2A trial for their anti-amyloid beta drug PBT2. The drug is based on findings from my lab at MGH dating back to 1993 showing that the interactions of the amyloid beta protein with copper causes aggregation and neurotoxicity of beta-amyloid. The same is true for the neural aggregates in Huntington's disease. We will get read outs of trials of PBT2 for Alzheimer's disease and Huntington's disease next year.

I am very concerned about the safety of BACE inhibitors used over extended periods of time given that the BACE enzyme has many critical substrates, including sodium channel components, myelin regulating enzymes, and seizure related proteins. We already saw that inhibiting gamma secretase, e.g. Lilly's gamma secretase inhibitor, led to major safety issues that led to termination of the clinical trial. This was because it turned out to be detrimental to block gamma secretase from cleaving its other substrates, beyond the amyloid beta-protein precursor (APP). Once again, pharma has made a huge leap of faith to block cleavage of APP by beta-secretase (BACE) with inhibitors. Why do they think that this will be safe over extended periods of time? BACE inhibitors will need to be used either before pre-symptomatically or the earliest stages of the disease. So, long term use will be required. There is a real concern that like gamma secretase inhibitors, BACE inhibitors will not be safe in then long run due to the many other natural substrates of BACE.

For the sake of the patients I hope this is not the case. But, luckily, there are other options like PBT2 that can be used early or late in the disease since it not only blocks accumulation of beta-amyloid in the brain but also neutralizes toxicity of beta-amyloid. While the newspapers will only update you on big pharma trials like Merck's, if you care about this disease, keep track of the little guys, like Prana and PBT2, as well. We don't know what will work in the end and big pharma has historically shown that they do not always think these things through by reading all of the literature regarding potential safety issues down the line. We already saw this with gamma secretase inhibitors. There is similar reason to worry about BACE inhibitors. For the sake of the patients, let's hope for the best...and be thankful for the alternative therapies you may not frequently read about...

Dr. Rudolph E. Tanzi
Joseph P. and Rose F. Kennedy Professor of Neurology,
Harvard Medical School
Vice-Chair, Neurology Research,
Director, Genetics and Aging Research Unit,
Massachusetts General Hospital

[Finee]

Viel diskutiertes Video (seit ein paar Tagen auf YouTube):

Hope for Alzheimer's
http://www.youtube.com/watch?v=pVNcjb3UEnY

[Fruehrentner]

Was empfiehlt sich eigentlich beim Kauf einer australischen Aktie:

Besser direkt an der Heimatbörse in Sydney (ASX) oder lieber ADRs an der Nasdaq?

Beides wäre ja hier möglich.

[Finee]

Antwort auf Beitrag Nr.: 46.093.494 von Fruehrentner am 20.12.13 19:53:20

WKN: 937103: Über meine Bank (ComDirect), ist der handel an ASX relativ kompliziert, so werde ich immer Tradegate vorziehen.
WKN: 753907: Nasdaq - gut möglich.

[Finee]

What is the global impact of dementia?
JANUARY 4, 2014, 4:36 AM
http://www.cbsnews.com/videos/what-is-the-global-impact-of-d…

[Finee]

Antwort auf Beitrag Nr.: 46.158.029 von Finee am 05.01.14 09:27:02

Professor Rudy Tanzi - Prana's co-founder and Chief Scientific Advisor.

[Fruehrentner]

Antwort auf Beitrag Nr.: 46.158.059 von Finee am 05.01.14 09:42:55

Prof. Tanzi hält Aktien von Prana, das sollte man der Vollständigkeit halber erwähnen.
Welchen Schluss man daraus zieht, bleibt jedem selbst überlassen.

[Finee]

Antwort auf Beitrag Nr.: 46.159.919 von Fruehrentner am 05.01.14 17:03:05

Ist das nicht immer so, daß Insider-Kauf für das Unternehmen und die Geschäftsentwicklung förderlich ist?

[Fruehrentner]

Antwort auf Beitrag Nr.: 46.163.083 von Finee am 06.01.14 11:41:20

Normalerweise ja.

Und dass er durch die Medien tingelt und trommelt, ist daher verständlich

[Fruehrentner]

Vor wenigen Sekunden rausgekommen:

http://hotcopper.com.au/announcements.asp?id=651283

[Fruehrentner]

http://www.asx.com.au/asxpdf/20140122/pdf/42m7lpxxz8jk62.pdf

[me_2]

Antwort auf Beitrag Nr.: 46.273.805 von Fruehrentner am 22.01.14 00:35:27

was steht denn da bei hotcopper ??

[Fruehrentner]

Antwort auf Beitrag Nr.: 46.277.215 von me_2 am 22.01.14 13:17:54

Der hotcopper link führt(e) zum selben pdf-Dokument wie der ASX-link darunter.

[Fruehrentner]

Enorm hohes PRAN Handelsvolumen in den ersten 15 Min. an der ASX (> 500.000) bei einem momentanen Kursplus von über 4 %.

Das ist doch was im Busch!!

[Fruehrentner]

Antwort auf Beitrag Nr.: 46.283.135 von Fruehrentner am 23.01.14 00:41:04

5,4 % Kursplus in Australien bei hohem Handelsvolumen (> 1,8 Mill. gehandelte shares).

http://www.asx.com.au/asx/research/companyInfo.do?by=asxCode…

[me_2]

Antwort auf Beitrag Nr.: 46.284.125 von Fruehrentner am 23.01.14 09:17:27

Frührentner, wenn es News gibt, wann würden die üblicherweise veröffentlicht, nach unserer bzw. Nasdaq-Zeit?

[Fruehrentner]

Antwort auf Beitrag Nr.: 46.286.855 von me_2 am 23.01.14 13:22:59

Die Handelszeiten in Australien/Sydney sind hier wohl maßgeblich, meine ich. Zumindest war es so bei der letzen news, die ich quasi live mitbekommen habe.

Also news kommen wohl kurz vor oder kurz nach Handelsbeginn in Sydney. Auszuschliessen ist aber nicht, dass news während der gesamten Handelszeiten in Australien herauskommen oder (kurz) nach Börsenschluss in Sydney.

Du musst also länger aufbleiben

Aber alles ohne Gewähr! Frag bei Prana direkt nach.

[me_2]

Antwort auf Beitrag Nr.: 46.287.971 von Fruehrentner am 23.01.14 14:54:17

Danke. nach meiner Rechnung wird in AUS von 19h bis 1 h unserer Zeit gehandelt, stimmt das so?

[Fruehrentner]

Antwort auf Beitrag Nr.: 46.288.247 von me_2 am 23.01.14 15:15:25

Nein, stimmt nicht.

[Fruehrentner]

Die Ergbnisse der Huntington disease clinical trails werden in Kürze erwartet.

Die Ergebnisse des Alzheimer clinical trials sind für den März angekündigt.

Fallen die Huntington disease Daten gut aus, wird dies quasi auf die Alzheimer Studie "extrapoliert" werden vom Markt. Kommen dann noch positive Ergebnisse im März, geht's vollends durch die Decke!

Die Kursrakete zündet also idealerweise in 2 gewaltigen Stufen.

Hoffen wir, dass es keine Fehlzündung wird.

Hier geht es nochmal zur letzten news und der neuesten Unternehmenspräsentation mit allen Details (pdf):

http://www.pranabio.com/downloads/Media%20Releases/Media%20R…

[Fruehrentner]

PRANAs Ansatz zur Behandlung von Alzheimer mittels des Wirkstoffkandidaten PBT2 beruht auf einem völlig anderen Ansatz als alle anderen prominenteren Wirkstoffkandidaten. Letztere sind in Phase II oder Phase III bei den Big Pharmas reihenweise gescheitert. Deren Scheitern untermauert indirekt Pranas Arbeitshypothese.

Prana hat deren Scheitern übrigens vorhergesagt, aber lest selbst:

http://www.pranabio.com/downloads/Prana%20Positioning%20stat…

[Fruehrentner]

PRAN schließt heute nahezu auf Tageshoch an der heute eher schwachen Nasdaq.

Und gleich geht's in Sydney weiter ...

[Fruehrentner]

Sydney öffnet um Mitternacht (10:00 Ortszeit)

[Fruehrentner]

Die 1 AU$ Marke wurde in Sydney geknackt.

[me_2]

Feuerstein äußert sich zu PRAN zurückhaltend bis negativ.

http://www.thestreet.com/story/12265416/1/biotech-stock-mail…

[Fruehrentner]

Die Unternehmenswebseite wurde jetzt neu gestaltet:

www.pranabio.com

[Fruehrentner]

Antwort auf Beitrag Nr.: 46.298.419 von me_2 am 24.01.14 15:31:34

Komischerweise äussert sich Feuerstein nur zum HD trial mit PBT2. Zum Alzheimer trial mit PBT2 sagt er nichts.

Folgendes Szenario ist denkbar:

1.) Die anstehenden HD Ergebnisse erfüllen nicht die Erwartung => Kurs sackt deutlich ab

2a) Bekanntgabe positiver Alzheimer-Ergebnisse im März: Kurs steigt wieder deutlich, da Alzh. das weitaus größere Marktpotential hat und PBT2 ein Alleinstellungsmerkmal hätte. Die negativen HD-Ergebnisse wären schnell vergessen.

oder 2.b) Alzheimer-Ergebnisse nur neutral oder sogar negativ => Kursabsturz ins Bodenlose.

[Fruehrentner]

Nasdaq deutlich rot - und PRAN im Plus!

Keinerlei Abgabedruck, im Gegenteil, schwer an Stücke zu kommen.

[Fruehrentner]

Forthcoming Clinical Trial Results Could Push Prana Shares Even Higher

http://seekingalpha.com/article/1965671-forthcoming-clinical…

[Fruehrentner]

Impfstoffe enttäuschen
Pleiten im Kampf gegen Alzheimer

26.01.2014

Gegen Alzheimer impfen und damit die fürchterliche Zerstörung des Gehirns verhindern - bleibt es ein Traum? Gleich vier große Patientenstudien mit zwei Antikörpern endeten enttäuschend.

http://www.faz.net/aktuell/wissen/impfstoffe-enttaeuschen-pl…

[Fruehrentner]

Jetzt zieh durch!

[Fruehrentner]

[Fruehrentner]

Eins ist klar:

Sollten sich die bisherigen Erkenntnisse über PBT2 und die zugrundeliegende Arbeitshypothese bestätigen, wird es den Nobelpreis dafür geben.

[Fruehrentner]

Heute hat's BUMM gemacht!

Und dass ohne News.

Tag 12 in Folge im plus geschlossen. Habe ich noch nie gesehen!

[Finee]

These are the best and worst-performing medical and biotech stocks from Jan. 24 to Jan. 31, a period during which the American Stock Exchange’s Biotechnology Index r0se 0.4%. This screen includes biotechnology and medical companies traded on the New York Stock Exchange, the Nasdaq or the American Stock Exchange that had market capitalizations of more than $300 million at the beginning of the week. The data come from Interactive Data and Thomson Reuters Fundamentals via FactSet Research Systems.

http://www.forbes.com/sites/matthewherper/2014/02/01/the-bes…

[Fruehrentner]

Zitat von Fruehrentner: Eins ist klar:

Sollten sich die bisherigen Erkenntnisse über PBT2 und die zugrundeliegende Arbeitshypothese bestätigen, wird es den Nobelpreis dafür geben.

Vor nicht allzu langer Zeit glaubte man einem australischen Mediziner nicht - und dann bekam er 2005 den Nobelpreis:

http://de.wikipedia.org/wiki/Barry_Marshall


Wenn bei PRAN weiterhin positive Daten kommen, wird Rudolph Tanzi nach meiner Meinung den Nobelpreis erhalten - ihm glaubt die Mehrheit der Alzheimer Forschergemeinde bisher nicht ...

[Fruehrentner]

Fixing the Metal Brain: Why PBT2 Could Be the First Effective Treatment For Alzheimer's Disease [Kindle Edition]

Joe Dever (Author)

Book Description
Publication Date: February 1, 2014
Could a breakthrough in the treatment of Alzheimer’s disease be at hand? If the Metal Hypothesis of Alzheimer’s Disease is correct, then the first effective treatment may not be far off.

Over 5 million Americans currently have the disease, and that number will climb dramatically as the baby boom generation ages. Millions more worldwide are afflicted with Alzheimer’s, threatening to overwhelm governments. A disease that slowly robs you of your mind can be especially cruel to its victims, but it also takes a heavy toll on families and caregivers as well.

So a treatment that can alter the course of the disease is desperately needed, yet so far there has only been failure and frustration. However, a drug called PBT2 is currently in clinical trials, and the anticipation is running high. PBT2 operates by a novel mechanism based on what has been called the Metal Hypothesis of Alzheimer’s. It’s believed that PBT2 can restore the natural balance of metals at the synapse of neurons damaged by Alzheimer’s disease.

http://www.amazon.com/Fixing-Metal-Brain-Effective-Alzheimer…

[Finee]

HotCopper 05.02.2014

The role of zinc and copper in autism spectrum (tomsilver39)

PBT2 can be HUGE!!!

http://www.ncbi.nlm.nih.gov/pubmed/23823984

[Finee]

Antwort auf Beitrag Nr.: 46.381.670 von Finee am 05.02.14 11:29:26

http://www.academia.edu/4079689/The_Role_of_Zinc_and_Copper_…

[Fruehrentner]

PBT2 (Alzheimer trial) ist bekanntlich auf Bitten der teilnehmenden Studienärzte derzeit in der Open-Label Extension.

Hier ein kurzes Buchkapitel zu Open-Label extensions allgemein:

http://books.google.de/books?id=9X-YPkWvwokC&pg=PA193&lpg=PA…

Demnach werden OLE beantragt und genehmigt, wenn die Probanden zuvor in der verblindeten Studie deutlich positiv angesprochen haben und es unethisch wäre, ihnen das Testmedikament vorzuenthalten.

Im Falle von PBT2 doch wohl ein vielversprechendes Zeichen, oder?

[Fruehrentner]

Die französ. Firma PALUMED scheint jedenfalls vom wissenschaftlichen Konzept Pranas/PBT2 überzeugt zu sein und startete jüngst ein Entwicklungsprogramm mit einem anderem Molekül:

http://www.palumed.fr

[me_2]

Ganz schön erschreckend dieser Kursverfall, ohne News !?? oder ist mir was entgangen?

[Geldgeier0815]

Hmm , ich denke mal das die die große Anteile in australien haben einfach mal kasse machen.....ist doch n gutes zeichen das täglich mehr als 1 mio papiere dort gehandelt werden,
sofern die testphase 3 beginnt und n top abschlußbericht erscheint gibt es dann neuer aktionäre den kurs durch käufe wieder nach oben schieben....

ich sehe die pennystocks durchaus bei erfolg ihrer pipeline
bei 5€ in rund 3 jahren.

habe bemerkt das durch die re-gesplitteten papiere hier das "eigentliche" forum ist , und hoffe das die aktie nachdem sie luft geholt hat wieder steigt.

das hiv virus wurde gestoppt also wenn man nicht gerade in afrika lebt stirbt man daran nicht mehr (sorry das ist us-aussenpolitik mit generika...etc),
und das zugpferd alzheimer denke ich ist auch im medizinischem interesse
und hat ne menge potenzial bei erfolgreicher patentierung. $$$

man wird alzheimer dann wohl nur stoppen oder deutlich veringern können, das reicht aber für die fantasie des aktienkuses hin.

freundliche grüße

[Fruehrentner]

A New Target in Fighting Brain Disease: Metals

http://online.wsj.com/news/articles/SB1000142405297020474090…

[Fruehrentner]

Trading Halt in Australien heute morgen

http://www.asx.com.au/asx/research/companyInfo.do?by=asxCode…


Hopp oder Top!

[me_2]

Antwort auf Beitrag Nr.: 46.465.471 von Fruehrentner am 17.02.14 00:31:14

oder weder noch ... der Kursverlauf der letzten 10 Tage hat wohl das Hopp schon eingepreist.

[Finee]

Nicht schlecht!
http://www.asx.com.au/asxpdf/20140218/pdf/42msyn3fyhd0sv.pdf

[Finee]

Antwort auf Beitrag Nr.: 46.473.291 von Finee am 18.02.14 07:34:47

Ehrlich gesagt:

S U C C E S S ! ! !

[Fruehrentner]

Antwort auf Beitrag Nr.: 46.473.303 von Finee am 18.02.14 07:39:18

[Finee]

Dr. Rudy Tanzi - Tweets

vor 2 Std.
Our drug PBT2 was safe and successfully improved cognition in Huntington's disease patients!

vor 9 Min.
Some who *bet* our PBT2 trial would fail are now trying to find negatives in results. Let's put patient benefit over profits and losses..

vor 6 Min.
This is the second time PBT2 has improved the cognitive domain of executive function -first in 2008 in Alzheimer's and now in Huntington's.

[Finee]

US Pre-Market : 9.54 Up 2.29 (31.59%) 6:26AM EST -
Nasdaq Real Time Price

[Finee]

Antwort auf Beitrag Nr.: 46.475.615 von Finee am 18.02.14 12:28:15

+ 31.59%

[Geldgeier0815]

ich erinnere mich noch an den positiven kursverlauf von vertex.... und erdenke mir mal positive paralelen bei prana



jetzt muß nur noch die alzheimer-geschichte funzen...

[me_2]

Antwort auf Beitrag Nr.: 46.475.619 von Finee am 18.02.14 12:29:13

wo sind die +31% ? ich kann noch nirgends irgendwelche kursreaktionen sehen.

[Finee]

Antwort auf Beitrag Nr.: 46.475.943 von me_2 am 18.02.14 13:10:10

US Pre-Market
02/14/2014
6:26AM EST

[me_2]

Antwort auf Beitrag Nr.: 46.476.001 von Finee am 18.02.14 13:18:17

danke. ich sehe dort derzeit +12,69 % . und was Feuerstein schreibt, ist (leider) genau das, was ich mir beim lesen der Meldung auch gedacht habe. eine kursexplosion würde mich wundern.

[Finee]

Antwort auf Beitrag Nr.: 46.475.943 von me_2 am 18.02.14 13:10:10

Pre-Market Change
7:23:30 AM EST

Leider nur:

8.30 USD +1.05 (+14.48%)

249,874 Volume

[me_2]

Antwort auf Beitrag Nr.: 46.476.051 von Finee am 18.02.14 13:26:35

na jetzt schauts ja schon wieder ganz anders aus, +33%. Trotzdem seltsamer kursverkauf da bei Nasdaq .

[Finee]

Antwort auf Beitrag Nr.: 46.478.401 von me_2 am 18.02.14 17:20:45

Also doch nicht so schlecht!

[me_2]

Antwort auf Beitrag Nr.: 46.478.451 von Finee am 18.02.14 17:24:54

jetzt nicht mehr. ich fands irritierend dass wir bei fast 0% starten und dann langsam bis auf jetzt 38% hochgehen. die Ergebnisse sind ambivalent. ich denke die phantasie kommt von der leichten kognitiven verbesserung und deren Bedeutung für die Indikation alzheimer. für m. huntington ist das eher bedeutungslos, da stehen andere symptome im vordergrund, und für die gabs keine positiven Ergebnisse. ich bleibe jedenfalls vorsichtig und jeder zeit verkaufsbereit.

[Fruehrentner]

Antwort auf Beitrag Nr.: 46.478.817 von me_2 am 18.02.14 18:01:20

Wie bitte?! "Die Ergebnisse sind ambivalent?"

Weisst Du, was HD für eine harte "Nuss" ist? Es gibt nur ein einziges sehr bescheiden wirksames zugelasenes Medikament bei HD. PBT2 wäre dagegen ein bedeutender Fortschritt und Segen für HD-Patienten, wenn hoffentlich die Zulassung für PBT2 kommt.

Selbst alle bisher für AD zugelassenen Wirkstoffe wie Donepezil. Memantin und wie sie alle heissen, verzögern nur einige Zeit die Symptome bei Alzheimer. Hält PBT2 in Phase 2 und Phase 3 das, was es bisher verspricht bzw. schon gezeigt hat bei AD, ist es gegenüber den jetzigen AD-Mittelchen ein riesiger Fortschritt.

Ich rechne mit Orphan Drug Status und Fast-Track Status bei PBT2 in der Indikation HD.

[Fruehrentner]

Prana: Expect Success In Massive Binary Event

Feb. 17, 2014 1:19 PM ET |

Executive summary:

Prana is an Australian biotech with a potential treatment for Alzheimer's disease.
Potential future revenues of at least $5 billion, but market cap is only $295 million.
Lead compound backed by spectacularly good science.
Imminent catalyst: results from Phase 2b IMAGINE trial due in March.

http://seekingalpha.com/article/2026281-prana-expect-success…

[Fruehrentner]

Posting #10187101 von user Ralphptf heute auf dem hotcopper.com.au Forum:


Congratulations to Prana.
Congratulations to longs.
This is a tremendous result!

A lot of the discussion on expectations to the lead up I believe did not consider the limitations of a iia study. Again, which is primarily about safety.

So here is my take on those who are dubious about these results. AD and HD are slow progressive diseases. They are marked primarily by a slow and functional decline over time.

Let us take hypertension as a juxtaposition. You have high blood pressure, you take a pill that takes your blood pressure down almost instantly. You cannot have the same proof of concept for a slow progressive disease it just is not possible.

So what have prana achieved here. In six months that have proof of concept that they can slow functional decline and loss of executive function. The most fundamentally debilitating aspects of these disease. IN SIX MONTHS!!! The actual functional decline can often take years, so sensitivity to measuring decline and proving statistical significance is extremely tricky. But prana have done this, IN SIX MONTHS.

If you really want a magic pill that makes it all go away instantly, go and talk to santa or the easter bunny. If you want a viable treatment that slows the functional decline in progressive illnesses that have no current treatments, then go and knock on prana's door.

Furthermore, in the other tests, there was minimal difference noticed. However, are these some of the functional aspects of the diseases that decline after executive function and functional capacity is lost? I leave that for others to answer and I look forward to seeing the full results with comparative graphs.

Make no mistake people. This is a successful trial and the outcomes are more than I dreamed of.

Well done again to the team at Prana.

[Finee]

Antwort auf Beitrag Nr.: 46.480.233 von Fruehrentner am 18.02.14 20:32:54

Ich bin der gleichen Meinung!!

[me_2]

das war ja ne kurze Euphorie, da haben einige doch genauer hingeschaut ...

[Fruehrentner]

Positive Phase 2 Results For Prana Biotechnology In Huntington's Disease: Behind The Smoke And Mirrors

Feb. 21, 2014

http://seekingalpha.com/article/2039103-positive-phase-2-res…

[Finee]

Tech & Innovation Daily
Published Sat, Feb 22, 2014
Marty Biancuzzo, Chief Technology Analyst

http://www.techandinnovationdaily.com/2014/02/22/prana-biote…

[Finee]

Drug Appears Safe in Huntington’s; Experts Split on Claims of Functional Benefit
19 Feb 2014

http://www.alzforum.org/news/research-news/drug-appears-safe…

[Finee]

Nicht mehr ganz neu, aber interessant...

http://pranabio.com/wp-content/uploads/2014/02/14-0218_PRAN-…

[Finee]

Do NOT buy or sell PRAN until you have read everything.

What’s the Best Small Cap Huntington's Disease Stock? RPTP, PRAN & OMER

http://www.smallcapnetwork.com/What-s-the-Best-Small-Cap-Hun…

[Finee]

Antwort auf Beitrag Nr.: 46.489.191 von me_2 am 19.02.14 18:51:06

Prana Biotechnology Limited Message Board

djnato2007 • 10 minutes ago

Adam F has bacically cost me $15000 in 1 month
He and the Stinking Alpha guys basically made me fail, along with my lack of understanding of the Short bash trickery and being a fearful idiot. Good luck to all you rich guys that can handle the swings. Just another failure for me. Thanks Adam F and the stinking alpha scam.

[Finee]

Shining a Light on Overlooked and Underfollowed Biotechs: George Zavoico

Source: George S. Mack of The Life Sciences Report (3/6/14)

George Zavoico Prospecting for hidden biotech gems makes sense, says H.C. Wainwright & Co. Managing Director George Zavoico, who recently joined the firm's healthcare equity research team. The digging can be hard, but the rewards of successful diligence are huge. In this interview with The Life Sciences Report, Zavoico takes readers on a discovery tour that follows clinical trial data to new ideas that could bring windfalls to portfolios down the road.


The Life Sciences Report: What theme do you see working for investors in 2014?

TLSR: Could you talk about Prana Biotechnology Ltd. (PBT:ASX), which you've just initiated on?

GZ: Certainly. Prana has a compound called PBT2 in clinical trials. On Feb. 18, the company announced results of its phase 2a trial in Huntington's disease (HD). The primary endpoint in this randomized, double-blind study was the safety and tolerability of PBT2 in patients with HD. The exact primary endpoint was the frequency of adverse events over 26 weeks, and it turned out that the compound met that endpoint. This was not surprising, because the drug had been safely administered to Alzheimer's disease (AD) patients in a previous phase 2a trial.
Here's where things get interesting. I cautioned investors not to overinterpret and expect statistically significant data on efficacy from phase 2 trials at the start of this interview. This trial, called Reach2HD, was first and foremost a phase 2a safety trial, since PBT2 had never before been given to HD patients. A panel of secondary endpoints—a long list actually—were examined with no expectation of finding statistically significant efficacy results. Recall what I said earlier about looking for trends, not statistical significance. Prana was looking for trends in cognitive function that could then be fashioned into a confirmatory phase 2b trial that would increase the likelihood of showing a clinically significant benefit—a meaningful improvement in cognitive function.
A surprising thing was discovered in this phase 2a trial. One of the cognitive measures, specifically the Trail Making Test Part B, demonstrated a statistically significant improvement in performance versus placebo at both 12 and 26 weeks. This test is an assessment of executive function—a patient's capacity to plan and organize things and to multitask, which is weakened early on in both HD and AD. The same cognitive function showed a statistically significant improvement with PBT2 in an earlier, phase 2a AD trial, and it is also a secondary endpoint in an ongoing AD trial that's going to read out before the end of March, according to the company's guidance. If this same secondary endpoint is met in the phase 2b trial, that would be confidence building, to say the least.

TLSR: The results of the high dose of 250 mg versus the low dose of 100 mg are delineated in the phase 2a PBT2 trail. Is the efficacy of the high-dose arm strong compared to the low-dose arm?

GZ: That's right. Also, in that regard, a very small substudy was performed, in which the brains of four patients in both PBT2 trial arms were imaged. Just as in Alzheimer's disease, the brain shrinks in Huntington's disease. There was some evidence that brain atrophy was reduced in the HD patients taking PBT2. Understand that this was a trend toward conservation of brain volume with PBT2, and was not statistically significant because of the small patient population. But it was an exciting result, nevertheless.

TLSR: What is it about PBT2 that makes it potentially efficacious in Alzheimer's and Huntington's diseases?

GZ: The common pathogenesis of these diseases is protein misfolding. The misfolding is facilitated and enhanced by metals—zinc and copper, in particular. The physiologic mechanisms that remove zinc and copper, which are released and exist very transiently in the synapse during neurotransmission, just don't work as well as we age. In younger people, the metals are immediately bound and transported back to their intracellular storage sites. If they stay longer in the synapse—that space between nerve cells—they can interact with those proteins and aggregate. As disease progresses, these metal-binding proteins, or metalloproteins, form plaques, which cause dysfunction in neurotransmission and ultimately an inflammatory response that kills the affected and surrounding neurons. That's when patients begin to get overt symptoms.
In Alzheimer's and Huntington's diseases, the misfolded proteins are beta-amyloid and mutant huntingtin protein, respectively. PBT2 has a chaperone-type activity that appears to strip zinc and copper from these metalloproteins, then transports them across the neuronal cell membrane and delivers them to intracellular proteins, where the metals are normally stored. In animal models, PBT2 has been shown to reduce the amyloid burden in the brain, meaning that the amount of amyloid plaques is reduced. This is the primary endpoint in the ongoing Alzheimer's disease trial, called IMAGINE, that is expected to read out before the end of March.
Here's where it may get very exciting. If PBT2 reduces the amyloid burden in Alzheimer's disease patients after a year of treatment, and improves cognitive function, then it will be the only drug candidate to have shown this. In our view, the risk-reward ratio for PBT2 is tremendous.

Let me just caution readers that PBT2 may also fail to show a reduction in amyloid burden, in which case we expect Prana's stock to take a big hit. But having reviewed the preclinical and early clinical results to date, we think this trial has a better chance of succeeding than failing.

http://www.thelifesciencesreport.com/pub/na/shining-a-light-…

[Fruehrentner]

U.a. mit Beitrag über Prana:


March 07, 2014

Alzheimer's Research Stocks - Technical And Other Considerations

http://seekingalpha.com/article/2074203-alzheimers-research-…

[Fruehrentner]

Eins steht fest:

im März kommen die P-II Alzheimer Ergebnisse - ein binärer Event für Prana!