Avid Bioservices Inc (CDMO)

[cjgaddy]

DawgInLife, this excerpt from 2006 IJC article may also help with your question about Bavi’s interaction on normal dying cells vs. cancerous cells…

“Apoptotic cells are engulfed silently, without evoking an inflammatory response, whereas necrotic cells do evoke an inflammatory response. It is thought that PS on the surface of apoptotic cells signals a quiescence response by macrophage lineage cells in which TGF-b secretion is induced while secretion of TNF-a and IL-1 is suppressed. Necrotic cells on the other hand, do not signal quiescence, either because PS on necrotic cells is masked by normally intracellular PS-binding molecules (e.g., annexin-5) or because proteases secreted by necrotic cells degrade the PS-receptor (PSR) on macrophages. Thus monocytes/macrophages that phagocytize necrotic cells default into the production of inflammatory cytokines, IL-1 and TNF-a. Because tumor endothelial cells are intact, viable, PS-expressing cells, it was proposed by Huang et al.,11 that activated monocytes bind to PS-expressing tumor endothelial cells, but do not induce an inflammatory response against them. However, in mice treated with 3G4, PS on tumor endothelial cells is masked and is instead coated with antibody. Thus, macrophages attracted to the Fc portion of the 3G4 antibody promote a local inflammatory response, which leads to further immune cell recruitment and vascular damage, as well as destruction of tumor cells that expose PS.”
ABOVE FROM:
ICJ 6-2006: ”Combination of a Monoclonal Anti-Phosphatidylserine Antibody with Gemcitabine Strongly Inhibits the Growth & Metastasis Of Orthotopic Pancreatic Tumors In Mice”
Adam W Beck, Troy A Luster, Andrew F Miller, Shane E Holloway, Chris R Conner, Carlton C Barnett, Philip E Thorpe, Jason B Fleming, Rolf A Brekken
Simmons Comprehensive Cancer Center and Hamon Center for Therapeutic Oncology Research, UTSW-MC/Dallas
Intl. Journal of Cancer, 6/2006; 118(10):2639-43.
http://www.researchgate.net/publication/7417166_Combination_of_a_monoclonal_anti-phosphatidylserine_antibody_with_gemcitabine_strongly_inhibits_the_growth_and_metastasis_of_orthotopic_pancreatic_tumors_in_mice
http://www8.utsouthwestern.edu/utsw/facdir/cma/fileuploads/5/facdir10808/IJC_Beck_et_al_may_2006.pdf <=Unfortunately, dead link.

= = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = =
Recall, here is the link to Dr. Thorpe’s 5-1-12 PS-Targeting talk at NYAS that FTM was referring to.
The Q&A starts at 34:26, and the question that parallels your question begins at 35:40.

• DawgInLife 106295: “Are there any research showing why normal cell death exposing PS is not effected by bavi? The lack of side effects in both animal models and clinical trials seems to imply bavi is not attaching to these normal dying cells but i can't find the reason for this.”
• FTM 106298: “If anything the presence of bavi would increase the phagocytosis of apoptotic cells (efferocytosis) and so should not be a problem. In the Q&A section of the NYAS talk by Thorpe someone asked the same question and Thorpe gave the same answer.” http://en.wikipedia.org/wiki/Efferocytosis

BAVI MOA: 5-1-12 Dr. Phil Thorpe's 46min talk at NYAS PS-Targeting Symposium http://tinyurl.com/9792gl5
. . .Symposium title: "Phosphatidylserine (PS) Asymmetry - Therapeutic Apps. in Cancer & Infectious Disease Symposium"
. . .Replays of 5 speakers: Alan Schroit, Chris Reutlingsperger, David Ucker, Ari Helenius, Philip Thorpe
. . .Direct link to Philip Thorpe’s 46 min. talk & Q&A: http://www.nyas.org/MediaPlayer.aspx?mid=25e51622-c908-46ef-bba1-95ca6a814eed
- - - - - - -
More…
BAVI MOA: 10-12-12 NMB article on how Bavi "Induces Innate & Specific Anti-tumor Responses" http://tinyurl.com/cw9odb8
BAVI MOA: 5-26-11 Dr.Thorpe's keynoter at Recombinant-Mabs/Barcelona http://tinyurl.com/3klpodc & http://tinyurl.com/3m33h33
BAVI MOA: 4-2010 Thrombosis Research article (Dr.Thorpe) http://tinyurl.com/9reso7s
BAVI MOA: See http://www.peregrineinc.com/technology/bavituximab-oncology/recent-data.html