Avid Bioservices Inc (CDMO)

[biopharm]

Ambit / Peregrine collaboration.... trying to pull a needle from a haystack this has become and darnet, this puzzle will be pieced together sooner or later....

Read the link and at the very end I seen this portion below, not sure what that "..propietary CSF1R inhibitor program" would be or if any collaborators are involved and my guess is there is more to the story. I like how they place that at the very end... Peregrine like. Peregrine Falcon like... just swarming in the high skies above just waiting for that perfect moment for an appearance that is like a knife in the back to some other Big Pharma predators.

June 12, 2014
...
..
..

....Quizartinib is also being studied in newly diagnosed patients in combination with chemotherapy as well as maintenance following a hematopoietic stem cell transplantation (HSCT). In addition to quizartinib, Ambit's clinical pipeline includes AC410, an oral JAK2 inhibitor, and CEP-32496, a BRAF inhibitor licensed to Teva Pharmaceutical Industries Ltd. Ambit's preclinical portfolio includes a proprietary CSF1R inhibitor program.

http://www.bizjournals.com/sanfrancisco/prnewswire/press_releases/California/2014/06/12/LA46577

..... now remember Peregrine with MDSC's / TAM (tumor associated macrophages) .. T-cells..etc?? which is all part of "Notch Signaling .. or that intracellular pathway of communication among cells and ultimately all part of the new understanding of the MOA of Bavituximab - PS Targeting.

--------------------------------------

Well...I find this associated with CSF1R and this abstract below and "Novartis" backed it looks like but what if CSF1R was attempted in combination with PS Targeting is the question ?? Hell... the question is PS Targeting in combination with many other treatments may prove more successful than current SOC's! So... what is inside that CSF1R inhibitor PROGRAM ... from Ambit ?? Will never let the hopium fade...

CSF1R inhibition delays cervical and mammary tumor growth in murine models by attenuating the turnover of tumor-associated macrophages and enhancing infiltration by CD8+ T cells

Dec 4, 2013

Abstract

Increased numbers of tumor-infiltrating macrophages correlate with poor disease outcome in patients affected by several types of cancer, including breast and prostate carcinomas. The colony stimulating factor 1 receptor (CSF1R) signaling pathway drives the recruitment of tumor-associated macrophages (TAMs) to the neoplastic microenvironment and promotes the differentiation of TAMs toward a pro-tumorigenic phenotype. Twelve clinical trials are currently evaluating agents that target the CSF1/CSF1R signaling pathway as a treatment against multiple malignancies, including breast carcinoma, leukemia, and glioblastoma. The blockade of CSF1R signaling has been shown to greatly decrease the number of macrophages in a tissue-specific manner. However, additional mechanistic insights are needed in order to understand how macrophages are depleted and the global effects of CSF1R inhibition on other tumor-infiltrating immune cells. Using BLZ945, a highly selective small molecule inhibitor of CSF1R, we show that CSF1R inhibition attenuates the turnover rate of TAMs while increasing the number of CD8+ T cells that infiltrate cervical and breast carcinomas. Specifically, we find that BLZ945 decreased the growth of malignant cells in the mouse mammary tumor virus-driven polyomavirus middle T antigen (MMTV-PyMT) model of mammary carcinogenesis. Furthermore, we show that BLZ945 prevents tumor progression in the keratin 14-expressing human papillomavirus type 16 (K14-HPV-16) transgenic model of cervical carcinogenesis. Our results demonstrate that TAMs undergo a constant turnover in a CSF1R-dependent manner, and suggest that continuous inhibition of the CSF1R pathway may be essential to maintain efficacious macrophage depletion as an anticancer therapy.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3902121/

...now back to mowing grass, which happens to grow a lot faster than how this Peregrine story is playing out.