Replies to post #146951 on Biotech Values

[north40000]

Peter, thank you for the one informed, but conservative, response so far. It is a shame you have not followed the company. I hope the exchange has piqued further curiosity and study on your and everyone's part.

As you know, I have considerable time with MEDX and Yervoy. I look on Bavi somewhat similarly, but less toxic. In a way, both mabs release the brakes on the immune system, albeit through different targets and MOA. iMO, both also then call into play our immune systems that were heretofore blocked or stymied--- otoh, by CTLA-4 and otoh, by PS. It may take some time for the parts of the immune system to be activated--- we are all different with different immune systems and health.

The next few weeks or months should be interesting.

Now at Dulles, and our flight has been called for Paris and onto Barcelona.

Thank you for the reading and listen. WE will pick up later.

North

[dia76ca]

Thanks for the intelligent post biomaven0.

It is of course the second line NSCLC study which is of most interest. They(under Dr. Garnick's influence)designed it as they would a registrational trial as they have all(including Garnick) expressed the possibility of an application for Accelerated Approval if the results are outstanding. Some time ago it was announced that the Doce alone arm has achieved a MOS of less than 6 months. We are awaiting the MOS from the low dose Bavi/Doce arm and the high dose Bavi/Doce arm. Those who follow this trial closely think these arms MOS may already exceed 12 months.

The MOA is very interesting but it is the MOS data that is most important. We should get that information in the next few weeks or months...the longer wait the better both for patients and investors!

[jq1234]

But what makes it unusual and complex is that he is proposing a dual MOA - both an anti-angiogenic initial action and a subsequent immune action.

There is no way of knowing if dual action actually occurred in human trials. One way to look at is via adverse event to see if they show up. I haven't seen much indication from adverse events indicating either anti-angiogenic activity or immune response.

[Robert C Jonson]

Peter, here are some comments by our "resident guru" on the PPHM board in reponse to your reaction to Dr. Thorpe's presentation. Perhaps you'll find them of interest.

Bob


freethemice Member Profile freethemice

Monday, August 13, 2012 9:41:30 AM
Re: Robert C Jonson post# 86484
Post # of 86492
Yes, he doesn't really know much about bavi and how it works. He makes the mistake, that many do,
to lump bavi in with anti-angiogenics, like Avastin. While the result of treatment with Bavi is to destroy the
tumor vasculature, the MOA is not anti-angiogenic. Anti-angiogenic are usually mAbs that target the
receptors (VEGFR-1, VEGFR-2, VEGFR-3, FGFR) or their ligands (VEGF, FGF), that is the pathway involved
in the growth factor for vascular growth. Of course, these are upregulated in tumor growth, but they
are also part of normal growth, wound healing, etc. Bavi is a mAb that targets the PS upregulated
specifically, and uniquely, on the endothelial cells of the TUMOR vasculature. PS is not upregulated
on the vasculature of normal tissue. So Bavi is not involved in the angiogenic pathway at all.
The MOA for Bavi has at least three aspects to it and they are all connected, so you can't say
maybe some parts will work and others won't. I suggest looking at the post CJ put up yesterday
which is a concise overview of how Bavi works as previously presented by Thorpe.
See post # 86429, also see this http://en.wikipedia.org/wiki/Angiogenesis
After this I am not going to respond to what people say about Bavi on other websites.
That is a hole I am not going down.