Compugen disclosed new data demonstrating the potential of CGEN-15032 as a target for the development of first-in-class cancer therapy. CGEN-15032 is a novel myeloid and epithelial immuno-oncology target, which may serve as an immuno-suppressive target within the tumor microenvironment. Addressing the immuno-suppressive environment of the tumor through myeloid drug targets has the potential for developing treatments that may expand the patient population responsive to current treatments.
The data, demonstrating the target's immunomodulatory effect and its effect on tumor growth, were generated as part of the research collaboration with the Johns Hopkins University School of Medicine (JHU), under the direction of Prof. Drew Pardoll, MD, PhD, Director of the Bloomberg-Kimmel Institute for Cancer Immunotherapy at Johns Hopkins and Chairman of Compugen's Scientific Advisory Board.
Compugen also announced today the extension of its multi-year immuno-oncology research collaboration with JHU. The research collaboration, originally announced in December 2014 is now expanded to include new additional targets discovered by Compugen which have the potential to serve as a basis for the development of cancer immunotherapy treatments. This highly valuable collaborative research provides ongoing assessment of the biology and mechanisms of action of Compugen's novel immune checkpoint proteins and expedites their expected translation towards the clinic.
Anat Cohen-Dayag, PhD, President and CEO of Compugen said, "The data we achieved with CGEN-15032, together with JHU exemplifies the tremendous value of our collaboration, providing us with access to world-class immuno-oncology knowledge and expertise to successfully develop our immuno-oncology programs, and accelerate their path towards future human testing."
CGEN-15032 was discovered by the company's immune checkpoint discovery platform, which also served as the cornerstone for the identification of TIGIT and PVRIG – two novel immune checkpoints which are currently in preclinical development by Compugen. Tumor growth in CGEN-15032-deficient mice (knock-out mice) is reduced relative to wild-type mice, and treatment of CGEN-15032-deficient mice with an anti-PD-L1 antibody further reduced tumor growth as compared with anti-PD-L1 treated wild-type mice. Together, these data suggest that CGEN-15032 may serve as an immuno-suppressive component of the tumor microenvironment, and that drugs inhibiting CGEN-15032 either alone or in combination with checkpoint inhibitors may activate anti-cancer immune responses.