Curis, Inc. (NASDAQ: CRIS), a drug development company seeking to develop next generation targeted small molecule drug candidates for cancer treatment, today announced the presentation of data in a poster presentation at the 2011 AACR-EORTC-NCI International Conference on Molecular Targets and Cancer Therapeutics in San Francisco, California. The poster presentation was titled “Anti-tumor activity of CUDC-907, a single small molecule inhibitor that targets both PI3K and HDAC, in hematologic cancer models” and was presented by Rudi Bao, M.D., Ph.D., Curis’ Senior Director of Oncology.

“As is the case with our other targeted agents, CUDC-907 has been designed to disrupt multiple points in cancer networks, in this case the PI3K pathway as well as several known mechanisms of resistance to single-target PI3K inhibitors, through CUDC-907’s potent inhibition of its HDAC target,” stated Dan Passeri, Curis President and Chief Executive Officer. “We are encouraged by its broad activity in preclinical cancer models, favorable performance compared to first-in-class PI3K and HDAC inhibitors and its oral bioavailability. We are continuing to advance this molecule through IND-enabling studies and currently anticipate that we will file an IND for an orally-administered form of CUDC-907 during the first half of 2012.”

About CUDC-907

In January of 2011, Curis selected CUDC-907 as a development candidate. CUDC-907 was identified by structure-based design following an extensive structure-activity-relationship campaign. Enzymatic assays indicate that CUDC-907 potently inhibits Class I PI3K subtypes and Class I and II HDAC subtypes. Both PI3K and HDAC are validated cancer targets, the combination of which Curis scientists believe have synergistic interaction against cancer cells.

While CUDC-907 is also active on portions of PI3K pathway that have been shown to play an important role in the development of many solid tumor cancer types, the current work is focused on its activity in models of hematological cancer. Recent data suggest that in addition to the mutational path to cancer development observed in solid tumors, redundant activation of the Class I PI3K isoforms can contribute to cellular transformation in hematological cells.

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