CytomX - ein bahnbrechender Ansatz in der Tumortherapie (Seite 90)

[Joschka Schröder]

Antwort auf Beitrag Nr.: 56.351.594 von Ville7 am 03.12.17 18:17:21

Ich habe mir Eure Diskussion jetzt einmal in toto durchgelesen. Der einzige Optimist bist Du , was markttechnisch sehr positiv ist. Ansonsten überrascht es mich, auf welch niedrigem Niveau Deine US-Diskussionspartner argumentieren. Die scheinen ähnlich ahnungslos zu sein wie der von ihnen gewählte Präsident.

[Ville7]

Antwort auf Beitrag Nr.: 56.350.865 von Joschka Schröder am 03.12.17 15:32:05

Sehe ich weitgehend auch so und habe ich ihm das auch versucht zu erklären... die ganze Diskussion von mir mit ihm dazu gibt's auf www.investorvillage.com im Board "Biotech" nachzulesen.

[Joschka Schröder]

Antwort auf Beitrag Nr.: 56.350.028 von Ville7 am 03.12.17 11:45:33

Aussage 5: falsch
Aussage 4: falsch
Aussage 3: falsch
Aussage 1 und 2: Aus diesem Grund gibt es klinische Studien. Andernfalls könnte man Medikamente bereits nach der Präklinik zulassen. Im Tiermodell ist die Wirksamkeit ebenso überzeugend wie es die Reduktion der Nebenwirkungen ist.

Mehr gibt es dazu eigentlich nicht zu sagen.

[Joschka Schröder]

Antwort auf Beitrag Nr.: 56.350.028 von Ville7 am 03.12.17 11:45:33

Natürlich muss sich die Probody-Technologie erst noch im Menschen bewähren. Wäre dem nicht so, stände der Kurs nicht bei 21 USD. Der entscheidende Punkt wird die proteolytische Spaltung des Linkers bzw. die Stabilität der Maske außerhalb des Tumors sein ... das ist trivial.

Die Einwände bzw. Beiträge des zitierten Users biotech2k halte ich jedoch inhaltlich für wenig geistreich, er scheint von der Materie wenig Ahnung zu haben., seine Aussagen sind inhaltlich zum Teil völliger Nonsens.

[Ville7]

Und weiter ....

I said it at the beginning. We love CTMX here. I owned it for a while when it got cheap at $14. I don't like when people blindly look at only the positives and try to ignore all the negatives. There is little to no data to prove this even works in humans. There are tons that can go wrong. When science isn't proven, the only limit is of ones own imagination. We don't invest in hopes and dreams. We invest to make money. Money gets made off of proven data not what could be. Maybe, everything does go right for CTMX and it is worth billions. I would love that and would buy it once the data proves it.

I actually think that 80% of the uses you think it can be used for are completely trivial and not worth the cost. The big issue will be the cost vs the benefit of the mask. I would bet that 90% of T-cell or Antibody therapies have little to no need for this technology. Does Soliris need a mask? What about OMS-721?

Our bodies target antigens every single day using T cells and Antibodies in a safe, effective and side effect free manor. Not every antigen will need a mask. Most of them are safe enough to not warrant the cost.

[Ville7]

Nicht verschweigen möchte ich kritische Meinungen anderer (erfolgreicher) Biotech Investoren zum Ansatz und zu den Erfolgschancen, auch wenn ich sie nicht unbedingt teile.

Hier die Ansicht des Users "biotech2k" aus einem amerikanischen Forum:

Since only about 10% of theoretical science actually proves out in clinical trials, I have several questions that need to answered by CTMX in human trials.

1. The data showed lower toxicity in animal models. Will that translate to real clinical benefit in humans? The amount of lower toxicity my be negligible.

2. The data showed that not 100% of the masks got removed in the tumor micro environment and converted into active antibodies. Will that translate into lower efficacy?

3. CAR-T already has safety switches. Why reinvent the wheel?

4. Most ADC's aren't very toxic. Do they even need the help?

5. It only applies to cytotoxic T-cell and B-cell therapies with highly toxic antigen targets. Most of the toxicity in PD-1 and CTLA-4 doesn't even come from the antigen (off target). It comes from removing all the safeties from the immune system. The indiscriminate ability of cytotoxic cells to suddenly target healthy tissue.

[BReal]

Antwort auf Beitrag Nr.: 56.298.755 von Ville7 am 28.11.17 15:10:51

Mal sehen, ob und wann es eine Kombinationsstudie dieses Probodys mit dem unternehmenseigenen PD-L1-Probody gibt. Sofern die Technologie wie gewünscht funktioniert, könnte das ein Dreamteam werden.

[Ville7]

Antwort auf Beitrag Nr.: 56.298.662 von Joschka Schröder am 28.11.17 15:05:27

Erneut ein netter Meilenstein in Höhe von 10 Mio USD und das für einen IND. Wenn es so weiter geht kann das Geld gar nie ausgehen.... Sehr schön!

[Joschka Schröder]

CytomX Therapeutics Announces FDA Acceptance of Investigational New Drug Application for CTLA-4 Probody Therapeutic

Goal is a safer, more effective version of Yervoy®

Triggers $10 Million Milestone Payment to CytomX from Bristol Myers Squibb

NEW YORK and SOUTH SAN FRANCISCO, Calif., Nov. 28, 2017 (GLOBE NEWSWIRE) -- CytomX Therapeutics, Inc. (Nasdaq:CTMX) today announced that Bristol-Myers Squibb has received acceptance of the Investigational New Drug application (IND) from the U.S. Food and Drug Administration (FDA) for a CTLA-4-directed Probody™ therapeutic. CTLA-4, the clinically validated target of the Bristol-Myers Squibb checkpoint inhibitor Yervoy® (ipilimumab), is the first target to advance into the clinic under the companies’ strategic collaboration formed in May 2014. The IND acceptance results in a $10 million milestone payment to CytomX.

“Immune checkpoint inhibitors are making a profound impact in the treatment of people with cancer,” said Sean McCarthy, D.Phil., president and chief executive officer of CytomX Therapeutics. “By localizing antibody binding and therapeutic activity to the tumor microenvironment, our goal with Probody therapeutics is to deliver the same or potentially greater potency as first-generation checkpoint inhibitors, while reducing unwanted side effects. We are excited to see the CTLA-4 Probody advancing into the clinic and look forward to additional progress in our foundational alliance with Bristol-Myers Squibb.”

About the Collaboration
In March 2017, Bristol-Myers Squibb and CytomX Therapeutics expanded their 2014 worldwide collaboration to discover, develop and commercialize novel therapies using CytomX‘s proprietary Probody platform taking total upfront payments to CytomX to $275 million. The collaboration provides Bristol-Myers Squibb with the opportunity to select up to ten oncology targets and two non-oncology targets. To date, Bristol-Myers Squibb has selected five oncology targets under the collaboration, including CTLA-4. CytomX is eligible to receive additional preclinical payments and development, regulatory and sales milestone payments totaling up to $4.7 billion across all 12 collaboration targets, as well as tiered royalties from mid-single digit to low-double digits on net sales of each product commercialized by Bristol-Myers Squibb.

[Ville7]

Antwort auf Beitrag Nr.: 56.232.539 von Gustl24 am 21.11.17 09:46:21

Nach Verständnis diesen Artikels sollten Probodys bei mit Chemotherapie vorbehandelten Patienten noch besser demaskiert werden als bei unbehandelten Patienten, da die Menge an Proteasen (metalloproteinases) danach im (tumor) microenviroment stark erhöht ist. Das Video ist m.E. indirekt unterstützend für den Ansatz von Cytomx.

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https://thetruthaboutcancer.com/plant-compounds-video/?utm_c…

Video Transcript: Cancer-killing Plant Compounds Every Oncologist Should Know About

Dr. Blaylock: What most people don’t know, particularly oncologists don’t seem to understand, is that chemotherapy, radiation, conventional treatments all are inflammatory.

The source of cancer is chronic inflammation. So once you change that microenvironment to even more inflammatory by pumping in these chemotherapeutic agents, or radiating it, you make it more inflammatory and that changes it to more malignance.

Ty Bollinger: So it’s adding fuel to the fire.

Dr. Blaylock: So if the chemotherapy and radiation doesn’t kill everything, all the cancer cells, and wipe out the stem cells, you’ve really made things worse and not better. And that’s what we’re finding. In fact, I just wrote an article on that — it’s going to be published real soon — about the effect of microenvironment and inflammation; microenvironment and cancer growth.

And invasion, particularly invasion, it makes the cancer more invasive. And that’s because once you stimulate that cell with this inflammation it starts secreting what they call “metalloproteinases,” which are enzymes that dissolve the blood vessel wall. So all these cancers start pouring into blood vessels and that makes the cancer spread. And that’s what it’s doing.

The inflammation turns on these enzymes that make the cancer penetrate tissue, break through these barriers that the body tried to put around the cancer to keep it from spreading, and that makes it worse.

Ty Bollinger: And that’s what the tumor really is; that wall of the tumor is the body walling off those cells.

Dr. Blaylock: Right. Usually, it tries to form a capsule around it, a fibrous capsule. This is why vitamin C and things that increase that fibrous capsule’s strength help out in cancer because it’s helping contain it. And certain flavonoids, for instance, will suppress those proteinase enzymes. For instance, like curcumin, quercetin, ellagic acid, they suppress those enzymes so that the cancer can’t penetrate. And then it’s a localized cancer and then it’s easy to get rid of.

Ty Bollinger: Do we have medical literature that backs up the use of flavonoids? Are there studies where the literature shows—?

Dr. Blaylock: Numerous, numerous studies. This is one of the hottest fields of research in cancer. It’s flavonoids, plant extracts, and their effect on cancer. The problem is is that clinician is not reading the journal articles in his own journal. All these—they’re in there, the clinical journals, they’re in the research for oncology journals. They’re just not reading them because they don’t understand it. It’s a lot of biochemistry. It’s a lot of mechanism they’re not familiar with.

They’re not familiar with the plants. They don’t know how to give it. They don’t know that these extracts are purified and available. For instance, you see in leukemia research, they have absolutely shown that leukemia is much more curable if you use quercetin. Most of the leukemias are very sensitive to quercetin.

Lymphomas, all of these things, are curcumin, quercetin, ellagic acid, and resveratrol. All of these things inhibit the cancer stem cell. And that’s what’s interesting about this. For instance, curcumin actually kills the stem cell, this cancer stem cell. It doesn’t bother normal stem cells but only cancer stem cells.

Ty Bollinger: Curcumin?

Dr. Blaylock: Curcumin. And that’s the other thing about flavonoids and these plant extracts is that they’re very selective. They only damage, inhibit, and kill cancer cells. They have no effect on the normal cells except to make the normal cells stronger.

Ty Bollinger: So that selective toxicity. That’s a big thing because you don’t want to kill the good cells. You want to kill only the cancerous.

Dr. Blaylock: That’s what they always look for, what they call the “magic bullet.” Something that will kill the cancer cell and not hurt the normal cell. Well, this does even more. It kills the cancer cell, but it makes the normal cell stronger.

And so what they found out, for instance, in radiation treatment of breast cancers, colon cancers, and lung cancers, is that it actually makes the radiation much more effective. And it protects the tissue that’s being radiated that’s normal around the cancer.

Ty Bollinger: Really? And all of these do, the ellagic acid, the resveratrol, curcumin.

Dr. Blaylock: It’s a long list of them. Naringenin and ellagic acid, and resveratrol.

Ty Bollinger: And they affect the stem cells?

Dr. Blaylock: They kill the stem cells and suppress the stem cell growth. They kill the daughter cancer cells. They help encase the cancer. They suppress these invasion enzymes and reduce the metastasis. And they protect the tissue, the normal tissue, to help keep it from converting to the same process.

Because when they did this study to see if inflammation is the cause of cancer, most people who have cancer should have chronic inflammation. So they did this large study and that’s exactly what they found. For instance, in certain people, 70% of them had definable inflammation—you know, arthritis, chronic atherosclerosis, some chronic infections. And that’s what caused the cancer. If you stop inflammation you stop the cancer from ever forming.

Ty Bollinger: So do these substances you’re talking about, these flavonoids, do they have any effect on the inflammation?

Dr. Blaylock: They’re powerful anti-inflammatories. They’re very powerful anti-inflammatories. That’s how they are preventing the cancer from occurring. And then they have other mechanisms that affect the cell signaling that kills the cancer, turns on the cancer suicide gene like p21, p53. And that’ll make this cancer cell commit suicide – what we call apoptosis.

Ty Bollinger: Dr. Blaylock, in light of the fact that these flavonoids are so beneficial why is not every oncologist using them to treat cancer?

Dr. Blaylock: Well, because they don’t read their articles, and they don’t know what these flavonoids are because they don’t know the chemistry. They’ve never heard of it. They go to a meeting and the meeting is about the latest protocol and the latest chemotherapeutic drug.

And who sponsors the meeting? Makers of the chemotherapeutic drug. So you have a room full of oncologists listening to the latest drug and they’ll say, “Oh, this one. We’re getting incredible responses with this drug.” Well, as I explained, what happens to that incredible response, it causes dramatic shrinkage of the tumor initially because it’s just killing the daughter cells.

And some are not even malignant cells. But it’s not affecting the stem cell so then the cancer grows tremendously. But they can say, “Oh, we get a good response from this chemotherapeutic drug.”

Ty Bollinger: And when they say “good response” they mean the tumor shrunk. Dr. Blaylock: They mean initially it shrinks the tumor but they don’t say, “well, six months later or less it’s actually going to grow a lot faster. And it’s more likely to metastasize.”

So they’re using the wrong measurement stick for success.