Avid Bioservices Inc (CDMO)

[sulaco]

Abe, Bavi is NOT Avastin


Saying that Bavi arrives "late on the scene" with anti-angiogenesis activity (due to late eversion of PS) is patently incorrect.

May I refer you to Dr. Thorpe's outstanding New York Academy of Sciences May 1, 2012 presentation?

insert-text-here

Bavituximab repolarizes macrophages to their M1 state, which allows them to kill cells that express PS, including the tumor vascular endothelium. It also leads to differentiation of the MDSCs and prompts DCs to mature and to present tumor antigens to T cells.

What does this mean? Well, macrophages float around the bloodstream in a depolarized state in the presence of cancer. Bavi repolarizes them, and thereby "re-magnetizes" them. This has NOTHING to do with whatever stage the cancer is in, and the efficacy of the Mab would not be present if "late eversion" of PS occurred as you say.

It's clear that everted PS occurs early on in the cancer timeline.
This is why Bavi is showing MOS numbers your friend can only dream of. (60% percent change in second-line NSCLC MOS that was really 100%!!)

Additionally:

Bavituximab can also prompt the development of tumor-specific immunity. In experiments with rats with treatment-resistant glioma tumors, 15% of the animals treated both with radiation and with antibody therapies did not die from those tumors. When the researchers reintroduced glioma tumor cells into these surviving rats, the rats were immune to the cancer. The team determined that spleen cells from these animals could kill gliomas, which indicated the antibody treatment had induced T cell immunity.

OK, so now Bavi fires up CD4 null cells to differentiate into the Th1 arm. This means, your Natural Killers, interferon-gammas, and other T-cell "Cluster of Designation" (CD) players are fired up to attack the cancer. Again, NOTHING to do with cancer staging and is counterintuitive to your "late PS eversion" hypothesis.

I could go on and on, but you get the point. So few people read, really.

Best,

Joe