Evotec 566480, wohin geht die Reise??? (Seite 6609)

[Kalinstorte]

Antwort auf Beitrag Nr.: 41.966.872 von mawasch am 18.08.11 07:38:06

Guten Morgen,

das sind doch wieder einmal echt gute Nachrichten. Der Freitag verspricht einen ganz angenehmen Verlauf, was Evo angeht. Hier ist man auf einem "gesunden und vielversprechenden Weg".....

LG

k-torte

[mawasch]

TR ONE-News: Evotec erhält im Rahmen ihrer Allianz mit Boehringer Ingelheim präklinische Meilenste
Evotec erhält im Rahmen ihrer Allianz mit Boehringer Ingelheim präklinische Meilensteinzahlung

Evotec AG / Evotec erhält im Rahmen ihrer Allianz mit Boehringer Ingelheim präklinische Meilensteinzahlung . Verarbeitet und übermittelt durch Thomson Reuters ONE. Für den Inhalt der Mitteilung ist der Emittent verantwortlich.

Hamburg, Deutschland - 18. August, 2011: Evotec AG (Frankfurt Stock Exchange: EVT, TecDAX) gab heute bekannt, dass ihre Forschungsallianz mit Boehringer Ingelheim einen Meilenstein erreicht hat, der eine Zahlung in Höhe von 4 Mio. Euro auslöst. Der Meilenstein wurde für die Identifizierung und Auswahl eines Wirkstoffkandidaten erzielt, der im Rahmen des Onkologie-Programmes in die präklinische Entwicklung gehen wird. Es handelt sich um den vierzehnten Meilenstein in dieser mehrjährigen und umfassenden Kooperation.

Dr. Mario Polywka, Chief Operating Officer von Evotec kommentierte: "Dieser wichtige Meilenstein, der als Teil der Allianz mit Boehringer Ingelheim erreicht wurde, ist der vierte aus dem Onkologie-Projekt. Damit wurde in diesem Onkologie-Programm die erste Substanz in die Phase der präklinischen Entwicklung überführt. Wir genießen diese hochkarätige wissenschaftliche Zusammenarbeit mit den Kollegen von Boehringer Ingelheim und sind bestrebt im Rahmen unserer gemeinsamen Projekte weitere Kandidaten für die klinische Entwicklung zu identifizieren". Über die Zusammenarbeit Im Jahr 2004 startete Evotec eine mehrjährige Wirkstoffforschungskooperation mit Boehringer Ingelheim, um gemeinsam präklinische Entwicklungskandidaten für die Behandlung diverser Erkrankungen zu entwickeln. Gemäß den vertraglich getroffenen Vereinbarungen hat Boehringer Ingelheim das ausschließliche Eigentumsrecht und die Verantwortung für die klinische Entwicklung, die Produktion und die Vermarktung der identifizierten Substanzen. Im Gegenzug erhält Evotec laufende Forschungszahlungen sowie präklinische Meilensteinzahlungen. Darüber hinaus birgt der Vertrag für Evotec beträchtliches langfristiges Potenzial über Erfolgszahlungen bei Erreichen von Meilensteinen während der klinischen Entwicklung sowie über Umsatzbeteiligungen an der Vermarktung neuer Wirkstoffe.

Kontakt Evotec AG: Dr. Werner Lanthaler, Vorstandsvorsitzender, Tel.: [phone], [e-mail]

Forward-Looking Statements: Information set forth in this press release contains forward-looking statements, which involve a number of risks and uncertainties. The forward-looking statements contained herein represent the judgement of Evotec as of the date of this report. Such forward-looking statements are neither promises nor guarantees, but are subject to a variety of risks and uncertainties, many of which are beyond our control, and which could cause actual results to differ materially from those contemplated in these forward- looking statements. We expressly disclaim any obligation or undertaking to release publicly any updates or revisions to any such statements to reflect any change in our expectations or any change in events, conditions or circumstances on which any such statement is based.



--- Ende der Mitteilung ---

[Finee]

http://www.4-traders.com/EVOTEC-436047/news/EVOTEC-Receives-…
EVOTEC : Receives Pre-clinical Milestone Payment as Part of its Discovery Alliance with Boehringer Ingelheim
Evotec AG / Evotec Receives Pre-clinical Milestone Payment as Part of its Discovery Alliance with Boehringer Ingelheim . Processed and transmitted by Thomson Reuters ONE. The issuer is solely responsible for the content of this announcement.

Hamburg, Germany - 18 August 2011: Evotec AG (Frankfurt Stock Exchange: EVT, TecDAX) today announced that its research alliance with Boehringer Ingelheim has achieved a milestone triggering a payment of EUR 4 million to Evotec. The milestone was achieved for the identification and selection of a compound to be advanced into pre-clinical development within an oncology programme and represents the fourteenth milestone achieved in this multi-year, multi-target collaboration.
Dr Mario Polywka, Chief Operating Officer of Evotec commented: "This important milestone achieved as part of our alliance with Boehringer Ingelheim is the fourth against an oncology target and importantly the first oncology programme to enter pre-clinical development for this collaboration. We continue to enjoy a fruitful scientific relationship with our colleagues at Boehringer in our efforts to drive new drug candidates to the clinic".

About the Evotec & Boehringer Ingelheim alliance
In 2004, Evotec entered into a multi-year, multi-target drug discovery alliance with Boehringer Ingelheim to jointly identify and develop preclinical development candidates for the treatment of various disease areas including central nervous system, inflammation, cardiometabolic and respiratory diseases. In 2009, the collaboration was extended for an additional four years and the scope expanded to include oncology targets. Under the terms of the agreement, Boehringer Ingelheim has full ownership and global responsibility for clinical development, manufacturing and commercialisation of the compounds identified. In return, Evotec receives ongoing research payments and preclinical milestones. Furthermore, the contract provides long-term upside for Evotec through potential payments for successful milestone achievements during clinical development and undisclosed royalties when new drugs reach the market.
Contact Evotec AG: Dr Werner Lanthaler, Chief Executive Officer, Phone: [phone], [e-mail]:
mailto:[e-mail]

[Ackergaul]

Zwei Artikel von der Seite http://www.outsourcing-pharma.com
1. CRL steigt in das Evotec Geschäft ein (durch geplante, kleine Zuküfe). Ein weiterer Hinweis dafür das hier mit starkem, anhaltendem Wachstum zu rechnen ist
2. Die CRO "Übernahmewelle" rollt nach wie vor...

Breaking News on Contract Research,
Manufacturing & Clinical Trials
Big pharma thirst for pre-IND services driving
CRL deals
By Nick Taylor, 08-Aug-2011
Related topics: Preclinical, Preclinical Research, Globalisation
Charles River is hunting for acquisitions with capabilities to meet big pharma’s newfound
interest in discovery services.
Big pharma has historically kept discovery and pharmacology work in-house but this is beginning to
change. In response, Charles River wants to bolster its pre-IND (investigational new drug) capabilities by
making acquisitions, at least one of which could be completed this year.
“We are evaluating a number of small, strategic acquisitions and in-licensing opportunities which would
enhance the [discovery and pharmacology] services we can offer our clients”, James Foster, CEO of
Charles River, said in a conference call with investors.
Big pharma clients have identified niche vendors with these capabilities but would prefer to work with a
bigger, more established company. Charles River plans to buy one or more of these niche players, some of
which big pharma clients have recommended.
“Clients are finding very high quality, but very small companies to do this work for them but they’re very
uncomfortable. [They’re unsure if the vendor’s] going to stay in business, or if they’ll have the sort of
regulatory rigor and financial staying power that are essential to them”, Foster said.
Making niche players part of Charles River could ease these concerns. “[Outsourcing] discovery is new for
[our clients] and they’re not going to be comfortable until companies like us to have the scientific capability
to do the work”, Foster said.
Charles River could work to develop the capabilities in-house but is set on an acquisition strategy.
“Probably it’s best to [expand services] through small high quality acquisitions where you are acquiring
some very good science and some marquee scientists”, Foster said.
Some of the targets would expand Charles River therapeutically and geographically, but Foster stressed
any deals will be small. Last year Charles River agreed to buy China-based WuXi PharmaTech for $1.6bn
(€1.1bn) but abandoned the deal after opposition from shareholders.
Diversification
Expanding discovery services would give Charles River an extra revenue source at a time when one of its
core offerings, preclinical services, is struggling. Toxicology overcapacity remains a problem and the way
clients approach these studies has also shifted in response to cost-cutting actions.
“For those compounds that do enter animals studies the more expensive toxicology studies are being
delayed until shorter-term data can validate the investment. This has resulted in a smaller overall market
for the toxicology providers”, David Windley, equity analyst at Jefferies & Company, said.
Copyright - Unless otherwise stated all contents of this web site are © 2011 - William Reed Business
Media SAS - All Rights Reserved - For permission to reproduce any contents of this web site, please email
our Syndication department [e-mail] - Full details for the use of materials on this site can be
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© 2011 - William Reed Business Media SAS - All rights reserved


Breaking News on Contract Research,
Manufacturing & Clinical Trials
Private equity firm in talks to buy PPD in $4bn
deal; reports
By Nick Taylor, 16-Aug-2011
Related topics: Phase I-II, Phase III-IV, Clinical Development
Carlyle Group is in exclusive talks to buy PPD in a deal valuing the CRO at around $4bn
(€2.8bn), according to reports.
Bids from private equity firms valuing PPD at up to $4.3bn have been made as part of the strategic review
the company confirmed in July , reports Bloomberg . PPD was only interested in private equity bids and
Carlyle is now said to lead the pack as it seeks to re-enter the clinical services sector.
“Carlyle knows the space. It may have been many years ago, but Carlyle owned PRA International for
many of its early growth years prior to selling to Genstar and then the IPO [initial public offering]”, David
Windley, equity analyst at Jefferies & Company, said in a note to investors.
A sale price of $35 to $36 a share, close to $4bn in total, “seems achievable”, Windley said. Before news
of the Carlyle bid broke PPD shares were trading at $27 and analyst target prices seen by Outsourcing-
Pharma range from $36 to $38.
Valuing PPD in light of private equity takeovers of smaller CROs (contract research organisations), such as
INC Research, would make $38 reasonable. However, Windley said PPD lacks the top-line growth forecast,
cost savings synergies or asset sale opportunities that would justify this price.
“It is not hard to imagine the management of a better positioned company believing they should be worth
a higher valuation”, Windley said.
Private benefits
As well as unlocking value for shareholders, the stated goal of the strategic review, going private would
free PPD from the reporting requirements of publicly traded companies.
“Quintiles has been "the next IPO" in the CRO industry for about four years. Meanwhile, [the CEO] seems
to enjoy the communication luxuries of being a private company. In other words, he doesn't have to tell
the world what he is up to”, Windley said.
As a private company Quintiles has entered into “some fairly exotic contract structures and strategic
relationships” that would be disliked by some shareholders, Windley said. PPD could have more scope to
enter into these types of deals if it enters private ownership.
Copyright - Unless otherwise stated all contents of this web site are © 2011 - William Reed Business
Media SAS - All Rights Reserved - For permission to reproduce any contents of this web site, please email
our Syndication department [e-mail] - Full details for the use of materials on this site can be
found in the Terms & Conditions
© 2011 - William Reed Business Media SAS - All rights reserved.


Grüße

[submersus]

....sieht ja irgendwie scheisse aus insges.

[Ackergaul]

GEN News Highlights : Aug 15, 2011
Scientists Find High-Fat Diet Causes Beta
Cell Dysfunction Leading to Type 2 Diabetes
Studies suggest elevated levels of fatty acids impact key enzyme that promotes
glucose sensing in pancreatic beta cells.
Scientists report new insights into the mechanisms by which a high fat diet can lead to type 2 diabetes.
Mouse and human studies by researchers in the U.S. and Japan suggest that elevated levels of free fatty
acids leads to both reduced expression of the transcription factors FOXA2 and HNF1A in pancreatic
beta cells, and their exclusion from the cell nuclei. This in turn results in a deficit of GnT-4a
glycosyltransferase expression in beta cells, leading to the characteristic signs of metabolic disease,
including hyperglycemia, impaired glucose tolerance, hyperinsulinemia, hepatic steatosis and diminished
insulin action in muscle and adipose tissues.
The scientists, from the Sanford-Burnham Medical Research Institute at the University of California
Santa Barbara, the RIKEN Advanced Science Institute in Japan, and the University of California San
Diego, further showed that protection from disease could be provided by enforced beta cell–specific
GnT-4a protein glycosylation, which supported the maintenance of glucose transporter expression and
the preservation of glucose transport.
Co-authors Kazuaki Ohtsubo, Ph.D., Mark Z. Chen, Ph.D., Jerrold M. Olefsky, Ph.D., and Jamey D.
Marth, Ph.D., report their findings in Nature Medicine, in a paper titled, “Pathway to diabetes through
attenuation of pancreatic beta cell glycosylation and glucose transport.”
Insulin resistance is a metabolic hallmark of type 2 diabetes, and pancreatic beta cell dysfunction
represents a diagnostic determinant of the disease, causing the loss of glucose-stimulated insulin
secretion (GSIS), the authors explain. Clues as to the molecular pathways involved in type 2 diabetes
development are embodied in a mouse model of the disease that lacks GnT-4a glycosyltransferase, an
enzyme encoded by the Mgat4a gene. GnT-4a is involved in positioning of the Slc2a2-encoded glucose
transporter-2 (Glut-2) glycoprotein on the cell surface.
The Sanford-Burnham-led team set out to search for factors that control GnT-4a function and glucose
transporter expression, and to see whether a deficiency in GnT-4a protein glycosylation and glucose
transport are truly causal in disease pathogenesis in the mouse model, and potentially in humans.
The researchers first showed that wild-type mice fed a high-fat diet (HFD) became deficient in Mgat4a
and Slc2a2 RNA in pancreatic islet cells, when compared with animals fed a regular diet. Through
promoter region DNA sequence analyses of the mouse Mgat4a and Slc2a2 genes, the orthologous
human genes MGAT4A and SLC2A1 (also known as GLUT1), and the human SLC2A2 gene, they
identified potential binding sites on multiple transcription factors including mouse and human FOXA2
and HNF1A.
In mice Foxa2 and Hnf1a binding to the Mgat4a and Slc2a2 genes was significantly reduced in
pancreatic islets from mice eating a HFD. This reduced binding coincided with decreased abundance of
the Foxa2 and Hnf1a proteins, a marked reduction in their nuclear localization of both, and increased
cytoplasmic localization. Decreased protein abundance and changes in localization combined to varying
degrees, resulting in an 80% drop in the levels of both Foxa2 and Hnf1a in the cell nuclei.
Studies in mouse islet cells confirmed that Foxa2 and Hnf1a normally contribute to Mgat4a and Slc2a2
transactivation in normal mice fed the standard diet, but that this transactivation was impaired in islets of
mice fed HFD. Significantly, when cultured islet cells from mice fed a normal diet were treated with
palmitic acid (a lipid used to model the diabetogenic effect of increased free fatty acids) nuclear
exclusion of Foxa2 and Hnf1a again resulted, and was associated with the downregulation of Mgat4a
and Slc2a2 gene expression.
Importantly, similar studies in human islets from healthy nondiabetic donors showed that in the absence
of exogenouse palmitic acid, FOXA2 and HNF1A proteins localized primarily in the nucleus, whereas the
addition of palmitic acid caused nuclear exclusion and increased cytoplasmic localization of both factors.
The addition of palmitic acid also diminished FOXA2 and HNF1A binding to the promotor regions of
MGAT4A, SLC2A1 and SLC2A2 genes, and attenuated mRNA expression of the three genes, which
coincided with the loss of GSIS.
“The similarities we observed in the responses of normal mouse and human islet cells to palmitic acid
suggested that islets from human type 2 diabetes donors may show defects comparable to those of mice
rendered diabetic by high-fat diet administration,” the authors note.
Further analyses showed that FOXA2 and HNF1A were excluded by more than 70% from the nuclei of
islet cells in tissue from type 2 diabetic patients. In the diabetic islet tissue expression of SLC2A1 and
SLC2A2 mRNAs encoding the human GLUT1 and GLUT2 glucose transporters was also decreased by
70–90%, and MGAT4A mRNA expression was reduced by 60%. The reduction in MGAT4A expression
translated to a 10-50-fold reduction of the GnT-4a glycan product. Importantly, islet cells from donors
with type 2 diabetes were 80-90% deficient in cell surface expression of both GLUT1 and GLUT2
glycoproteins, had very low glucose transport activity, and lacked the GSIS response.
The team moved on to evaluate the impact of diminished GnT-4a glycosylation on glucose transporter
expression and the onset of disease signs in a HFD–induced mouse model of type 2 diabetes. They
generated transgenic mice that constitutively expressed the human MGAT4A gene specifically in beta
cells, but in no other cell type or tissue. Both wild-type and transgenic mice fed a HFD became obese,
but while the HFD wild-type mice displayed hyperglycemia and hyperinsulinemia, MGAT4A transgenic
littermates maintained much lower concentrations of blood glucose and insulin.
Fasted MGAT4A transgenic animals also displayed markedly greater glucose tolerance, reduced
insulinemia and preserved GSIS. Circulating free fatty acid and triglyceride concentrations in these
animals were in addition markedly reduced in comparison with wild-type littermates, “indicating that
enforced beta cell GnT-4a protein glycosylation diminished multiple and systemic disease signs,” the
authors write.
Moreover, insulin tolerance tests in mice fed a HFD indicated greater glucose clearance in MGAT4A
transgenic mice than in wild-type animals, and glucose infusion rate studies suggested whole-body
insulin sensitivity was significantly greater in MGAT4A transgenic mice. Hepatic steatosis was evident in
wild-type mice that received the high-fat diet, whereas the livers of HFD MGAT4A transgenic mice
notably lacked signs of steatosis.
To test whether the disease protection afforded by GnT-4a involves maintenance of beta cell glucose
sensing, the researchers then generated transgenic mice bearing constitutive beta cell–specific
expression of the human SLC2A2 gene. In these animals there was greater beta cell GLUT-2
glycoprotein expression and glucose transport in comparison with beta cells from wild-type and MGAT4A
transgenic mice that received the standard diet.
In fact, the SLC2A2 transgene conferred an intermediate degree of improvement at the biochemical level
between wild-type and MGAT4A transgenic mice. For example, the SLC2A2 transgene provided an
intermediate reduction in hyperglycemia and hyperinsulinemia, whereas the development of obesity was
unaffected. Glucose transporter glycosylation by GnT-4a remained optimal in islet cells of MGAT4A
transgenic mice receiving the high-fat diet, whereas corresponding SLC2A2 transgenic beta cells
showed a decrease in GLUT-2 glycosylation among mice fed the high-fat diet, consistent with the
downmodulation of endogenous Mgat4a expression, diminished GnT-4a activity and decreased GLUT-2
abundance.
The overall results suggest a molecular and pathogenic pathway that includes a key role of pancreatic
beta cell GnT-4a glycosylation and glucose transport in the origin and severity of disease signs including
insulin resistance that are together diagnostic of type 2 diabetes, the authors conclude.
“A pathogenic tipping point in this pathway may occur when elevated free fatty acid (FFA) concentrations
impair the expression and function of FOXA2 and HNF1A transcription factors sufficiently in beta cells to
deplete GnT-4a glycosylation and glucose transporter expression. The resulting dysfunction of beta cells
leads to impaired glucose tolerance and failure of GSIS and further contributes to hyperglycemia, hepatic
steatosis and systemic insulin resistance. Preservation of beta cell GnT-4a glycosylation and glucose
transporter expression breaks this pathogenic cycle and its link to diet and obesity.”
The impact of enforced beta cell-specific expression of MGAT4A and SLC2A2 on metabolic
abnormalities including GSIS and insulin resistance was particularly notable, they add. “Constitutive beta
cell expression of GnT-4a or Glut-2 preserved considerable systemic insulin sensitivity, indicating that
beta cell function influences insulin action on these peripheral target tissues.”
The results were something of a surprise, however, Dr. Marth notes. “The observation that beta cell
malfunction significantly contributes to multiple disease signs, including insulin resistance, was
unexpected.” However, the findings do provide pointers to new potential therapeutic approaches, he
adds. “Now that we know more fully how states of over-nutrition can lead to type 2 diabetes, we can see
more clearly how to intervene. The identification of the molecular players in this pathway to diabetes
suggests new therapeutic targets and approaches towards developing an effective preventative or
perhaps curative treatment. This may be accomplished by beta cell gene therapy or by drugs that
interfere with this pathway in order to maintain normal beta cell function.”
© 2010 Genetic Engineering & Biotechnology News, All Rights Reserved

[Kalinstorte]

Antwort auf Beitrag Nr.: 41.942.485 von brooker69 am 12.08.11 10:57:57

und nun????Ruckzuck über €2,50????

Ich denke schon. Jetzt gehts los....jetzt gehts los.....

LG

k-torte

[baracuda1982]

Evotec unterzeichnet Partnerschaft zur Entwicklung ihres P2X7 Antagonisten EVT 401 im Bereich Tiergesundheit
Lizenz an ein führendes Unternehmen zur Entwicklung der proprietären Substanz im Bereich Tiergesundheit exklusiv gewährt

Teilen

15.08.2011: Evotec AG gab bekannt, dass sie eine weltweite Lizenz- und Kooperationsvereinbarung mit einem führenden Unternehmen im Bereich der Tiergesundheit eingegangen ist. Ziel ist es, Evotecs proprietäre Substanz EVT 401, ein selektiver niedermolekularer P2X7 Antagonist, als Wirkstoff zur Behandlung von Entzündungskrankheiten in Haustieren, zu entwickeln.

Wie vertraglich vereinbart wird Evotec eine „Technology-Transfer-Zahlung“, Entwicklungs- und kommerzielle Meilensteinzahlungen sowie Nettoumsatzbeteiligungen bei erfolgreicher Markteinführung von Produkten erhalten. Evotec behält sämtliche Rechte auf dieses Programm zur Entwicklung von Wirkstoffkandidaten für die human- therapeutische Verwendung.

Dr. Werner Lanthaler, Chief Executive Officer von Evotec, kommentierte: “Wir sind stolz darauf, mit einem weltweit führenden Unternehmen zusammen zu arbeiten, dass die Fähigkeit besitzt, Medikamente für Tierkrankheiten zu entwickeln. Damit erreichen wir nicht nur zusätzlichen Produktmehrwert, sondern unterstreichen unsere Stärke in der Anwendung der Medizinalchemie. Wir freuen uns über eine enge Zusammenarbeit mit einem der weltweit führenden Unternehmen im Bereich Tiergesundheit, um dieses Produkt erfolgreich zu entwickeln.”

Einzelheiten zu finanziellen Details wurden nicht bekanntgegeben.
http://www.bionity.com/de/news/133942/evotec-unterzeichnet-p…

[brooker69]

der Kurs wird unten gehalten da steigen erst noch ein paar ein! Ihr wißt schon wie das läuft und dann Rackzack übe 2,10€

[Ackergaul]

Moin auch,

denke dass Du mit Deiner Pipeline Betrachtung richtig liegst, allerdings glaube ich nach wie vor an gute Aussichten bei H3: In der Präsentation „Evotec_H1-2011“ stehen bei den R&D Ausgaben:
CureBeta initiative, EVT 501, response prediction, etc.
Für mich ist die Aussage wenn, Evotec hier noch investiert glaubt man noch an das Programm. P2X3 sollte ebenfalls gute Chancen haben einen Partner zu finden: potentiell first & best in class…
Dass 401 noch verpartnert werden konnte, ist auf jeden Fall positiv zu sehen (war für mich auf dem gleichen Nullpunkt wie EVT-302 – aber auch EVT-201), allerdings hätte ich mir trotzdem für dieses Jahr eine bessere Partnerschaftsmeldung erhofft. Ähnlich zumindest dem BI Deal mit Alt-Develogen oder Medimmune.

Aber zurück zu den Umsätzen. Ich glaube das hier noch einige am Jahresende sich umschauen werden. Ich halte meine angestrebten 72 bis 74 Mil für durchaus realistisch, sogar konservativ:
Der Umsatz im 1.H lag bei etwa 33,4 Mil, bedenkt man das kaum dicke Meilensteine im 1.H geflossen sind und das Evotec von Anfang an gesagt und damit rechnet dass die Meilensteine im Jahre 2011 ähnlich hoch wie 2010 ausfallen, ist noch mit einigen zu rechnen!
Also: würde der Umsatz im 2.H genauso hoch sein wie im ersten hätten wir 33,4 Mil. schon mal im Sack (SEHR konservativ gerechnet). Zuzüglich zwei weiteren dicken Meilensteinen nochmals 4 Mil. kommen wir dann schon auf 37,4 Mil.
Zudem wird der Umsatz von Compound Management von etwa nochmals 4 Mil. hinzukommen (Übernahme war im Juni, also noch keine wesentlichen Umsätze im 1.H). Damit komme ich auf etwa 41 Mil. Euro Umsätze für dass 2.H ohne dass ich die Umsätze vom 1.H „raufgeschraubt“ habe.
Da Compound Management äußerst profitabel arbeitet denke ich dass Evotec in diesem Jahr einen Nettoumsatz von 5-6 Mil. erzielen wird (und das obwohl R&D Ausgaben 60% erhöht werden). Und der Umsatz wird aus meiner Sicht ein bischen größer als 74 Mil.!

Grüße