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.