Replies to post #102574 on Avid Bioservices Inc (CDMO)

[freethemice]

I can not believe you have not read the fact that bavi (2aG4, 3G4) binds to beta2-GPI. This has been known
since 2006 when this paper was published by Thorpe's lab.
http://www.ncbi.nlm.nih.gov/pubmed/16905548
Plasma protein beta-2-glycoprotein 1 mediates interaction between the anti-tumor monoclonal antibody
3G4 and anionic phospholipids on endothelial cells.
Luster TA, He J, Huang X, Maiti SN, Schroit AJ, de Groot PG, Thorpe PE.
Journal of Biological Chemistry, 2006 Oct 6;281(40):29863-71.
I even posted this picture recently

That is why I said "conveniently" because you seemed to be ignoring facts that did not fit your theory.
The whole notion that bavi is not an antibody is the same thing. The idea that there is a vaccine-like
effect is not new. My post from yesterday shows how it can be used to make a vaccine.
http://investorshub.advfn.com/boards/read_msg.aspx?message_id=81917943
http://investorshub.advfn.com/boards/read_msg.aspx?message_id=81918470
In addition, the existence of long-term survivors in the second-line NSCLC would be strong evidence that
those patients have developed immunity to metastasis of the disaease. The MOA as it is now understood has an
explanation for that and doesn't really require anything else. Thorpe says this in his talks as reactivating the
innate and adaptive immunity. By blocking the immunosuppression the adaptive arm of the immune system is
then allowed to function normally, which results in the generation of antigen-specific CD8 T cells and antigen-specific
B cells and memory T and B cells, which give rise to immunity. Yes, the MOA is a hypothesis and has been, and will be,
revised as new facts become known, but any new version of the MOA has to still explain the current facts.
Thorpe has mentioned several times this study of glioblastoma in rats and how the surviving rats were shown to have immunity.
http://www.ncbi.nlm.nih.gov/pubmed/19887482
He even specifically mentions it in his NYAS talk and shows the survival curve.

He has also talked about the study of prostate cancer in the mouse model and how those 38% survived.
The poster from this year's AACR meeting
Cure of castration-resistant prostate cancer in TRAMP mice by reactivating tumor immunity
with a phosphatidylserine-targeting antibody
Yi Yin, Xianming Huang, Gustavo Barbero, Dan Ye, Philip E. Thorpe
http://www.peregrineinc.com/images/stories/pdfs/aacr_2012_prostate_cure.pdf

I just don't feel that entirely new ideas are needed here. The MOA will be added to and revised, but the MOA as is,
is actually quite radical when you view it in the context of the past. That is all I have to say about it.

[koman]

FTM, CP, Bavi binds a complex of PS and beta2-glycoprotein based on what I've read so far. Unless FTM can show a reference that bavi does not bind to PS he is wrong in his statement. Also, all this ranting about MOA, interesting mentally, but I'm more interested in whether bavi combo will increase MOS and leave the MOA as a black box. I still stand by my statement that bavi alone or with this current combo does not elicit an adaptive immune response in humans based on results so far- but that it unlocks one of several locks that holds back the adaptive immune response. I wonder if there is a difference in the binding mechanism of the murine version vs the human bavi that may be one of the causes of the difference in the results seen in murine/rat models vs humans so far. FTM, do you know if the the murine anti-PS antibody also binds to a complex of PS and beta2-glycoprotein? Thanks