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Teva, Checkpoint Therapeutics sign license agreement for Oral PARP inhibitor

Teva Pharmaceutical Industries and Checkpoint Therapeutics have signed a license agreement in which Checkpoint will obtain the exclusive worldwide rights to develop and commercialize CEP-8983 and its small molecule prodrug, CEP-9722, an oral poly (ADP-ribose) polymerase (PARP) inhibitor in early clinical development for solid tumors.

CEP-9722 is a novel, orally active, small molecule selective inhibitor of PARP-1 and PARP-2 enzymes that will be developed by Checkpoint as both a monotherapy and in combination with other anti-cancer agents, including Checkpoint’s novel immuno-oncology and checkpoint inhibitor antibodies currently in development.

Teva president of global R&D and chief scientific officer Michael Hayden said: "Teva is committed to facilitating the development of its early clinical stage oncology programs, which hold promise for the oncology community, by identifying targeted opportunities with companies who have unique R&D capabilities in this therapeutic area.

"We believe Checkpoint’s development capabilities, in combination with its immuno-oncology antibodies already under development, will enable these molecules to move forward with future potential for patients."

Checkpoint Therapeutics president and CEO James Oliviero said: "The acquisition of worldwide rights to CEP-9722 immediately transforms Checkpoint Therapeutics into a clinical-stage biopharmaceutical company, expanding our proprietary portfolio with an exciting targeted therapy that, when combined with our immuno-oncology antibodies under development, can potentially create wholly-owned proprietary combinations that leverage the immune system and other complimentary mechanisms with the goal of providing significant benefit to patients.

"PARP inhibitors have been associated with promising activity across multiple tumor types, including breast, ovarian and prostate cancer." Mr. Oliviero, continued, "We appreciate Teva’s belief in our organization and our development strategy for this drug candidate in multiple strategic indications."

About PARP

Poly (ADP-ribose) polymerase (PARP) enzymes are involved in normal cellular homeostasis, such as DNA transcription, cell cycle regulation, and DNA repair. DNA repair enzymes such as PARP, whose activity and expression are up-regulated in tumor cells, are believed to contribute to resistance and dampen the effects of chemotherapy and radiation.

By inhibiting PARP, certain cancer cells may be rendered unable to repair single strand DNA breaks, which in turn causes double strand DNA breaks and can lead to cancer cell death.

Across multiple tumor types, including breast, ovarian and prostate cancer, PARP inhibitors have shown promising activity as a monotherapy against tumors with existing DNA repair defects, such as BRCA1 and BRCA2, and as a combination therapy when administered together with anti-cancer agents that induce DNA damage.