Ariad Pharmaceuticals, Inc. announced, for the first time, results of studies conducted by the Cleveland Clinic Brain Tumor Institute on its lead oncology product candidate, currently in clinical trials. Low doses of AP23573 reduced by 40 per cent the growth of brain tumor cells, known as glioblastoma. Rarely cured by currently available treatments, this form of brain cancer is one of the most deadly cancers. Following diagnosis, median survival is approximately one year.

The potency and anti-tumor activity of AP23573 were even more striking, because the reduction of tumor cell growth was achieved both in brain cancer cells over-expressing the epidermal growth factor (EGF) receptor - a known marker of tumor aggressiveness - and in brain cancer cells without EGF receptor over-expression, suggesting broad applicability for treating these tumors.

"The latest studies on AP23573 underscore the therapeutic potential of our lead oncology product candidate and support accelerated phase 2 clinical trials in patients with solid tumors, such as gliomas," said Harvey J. Berger, MD, chairman and chief executive officer of Ariad.

The small molecule, AP23573, was designed to treat solid tumors and other cancers by inhibiting the critical cell-signaling protein mTOR, which causes tumor shrinkage by novel mechanisms of action - blockage of growth factor stimulation and cancer-cell starvation through inhibition of nutrient utilization.

Michael A Vogelbaum, MD, Ph.D, who will be presenting these findings tomorrow at the eighth annual meeting of the Society for Neuro-Oncology, led the Cleveland Clinic team.

Ariad is engaged in the discovery and development of breakthrough medicines that regulate cell signaling with small molecules. The company is developing a comprehensive approach to the treatment of cancer and is primarily focused on a series of product candidates for targeted oncology indications. Ariad also has an exclusive license to pioneering technology and patents related to the discovery, development and use of drugs that regulate NF- (kappa) B cell-signaling activity, which has been implicated in many major diseases.