CAMBRIDGE, Mass.--(BUSINESS WIRE)--Cyteir Therapeutics, Inc., a leader in the development of novel therapeutics based on the biology of DNA repair, today announced that it will present preclinical data elucidating a mechanism of cell death response that can be utilized to preferentially target lymphoid malignancies at the American Society of Hematology Annual Meeting in San Diego, California.
“These data demonstrate that the DNA mutase activation induced cytidine deaminase (AID) can be leveraged to effectively target AID-expressing cancers, and has shown promise in a xenograft cancer model,” said Kevin D. Mills, Ph.D., Chief Scientific Officer of Cyteir. “We know that the B-cell specific enzyme AID initiates DNA double-strand breaks and that these breaks, if not quickly repaired, can trigger cancer cell death by mitotic catastrophe. These exciting findings support the notion that modulation of the DNA repair protein RAD51 in AID-expressing malignancies could be an effective new therapeutic approach in oncology.”
“The results of these studies validate the promise of our approach and provide momentum for the continued development of our novel RAD51 modulators for use in lymphoid cancers, a program that we plan to expand into solid tumor indications,” said Donald F. Corcoran, President and Chief Executive Officer of Cyteir. “We are on an excellent path as we optimize our lead compounds into a clinical candidate, which is expected to be identified in 2017.”
Cyteir’s approach leverages the identification of activation induced cytidine deaminase (AID) as both a biomarker and driver of DNA damage. By modulating the DNA repair protein RAD51 in AID-positive cells, Cyteir seeks to induce selective self-destruction of cancer cells. Preclinical studies to date have demonstrated Cyteir’s early RAD51 modulators to be potent, selective for AID-positive cells, effective against cancer cells in vitro and in vivo, and well tolerated in preclinical animal models.
Details of the presentation are as follows:
Title: RAD51 Modulators Induce Mitotic Catastrophe in AID
Session: 802. Chemical Biology and Experimental Therapeutics: Poster III
Date: Monday, December 5, 2016
Time: 6:00pm – 8:00pm PST
Location: Hall GH, San Diego Convention Center
Preclinical data demonstrate that AID-initiated DNA double-strand breaks can trigger mitotic catastrophe, a non-apoptotic cell death mechanism, involving multiple pathways including mTOR. In a xenograft cancer model, AID-induced cytotoxicity, activated by RAD51 modulation, was used to effectively and preferentially target AID-expressing lymphoid malignancies.
Cyteir Therapeutics is a leader in the discovery and development of novel therapeutics based on the biology of DNA repair for the treatment of cancer and autoimmune diseases. Our initial approach takes advantage of DNA damage overload to induce selective self-destruction of cells by targeting disease-induced RAD51 transport. www.cyteir.com