Ridaforolimus (formerly known as deforolimus) is a novel small-molecule inhibitor of the protein mTOR, a “master switch” in cancer cells. Blocking mTOR creates a starvation-like effect in cancer cells by interfering with cell growth, division, metabolism and angiogenesis.
ARIAD is collaborating with Merck & Co., Inc. (“Merck”) to globally develop and commercialize ridaforolimus (see Merck collaboration). This collaboration supports our strategic objective to build a fully integrated oncology company that discovers, develops and markets breakthrough medicines for cancer patients.
In collaboration with Merck, we are conducting a broad-based global oncology development program in multiple cancer indications. Together, we will pursue at least five cancer indications for ridaforolimus: sarcomas, endometrial, prostate, breast and non-small cell lung cancers. We are studying ridaforolimus both as a single agent and in combination with various targeted agents driven by mechanisms of action and biology. During 2008, ARIAD and Merck initiated Phase 2 clinical studies evaluating ridaforolimus in patients with breast, endometrial and prostate cancer. In March 2009, ARIAD and Merck announced a fourth Phase 2 clinical trial of ridaforolimus in patients with non-small cell lung cancer. Read Recent Press Release on Ridaforolimus.
For specific information on sites and enrollment status on clinical trials with ridaforolimus in various cancers, please visit www.clinicaltrials.gov or please email us at TrialDesk@ariad.com.
Ridaforolimus: beyond cancer
Beyond our focus area of oncology, ridaforolimus has potential to provide important clinical benefits in other therapeutic areas, including cardiovascular disease. We are leveraging the market potential of ridaforolimus by licensing the compound to other companies for non-cancer development and commercialization. For example, we have collaborations with Medinol, Ltd. (“Medinol”) and ICON Medical Corp. (“ICON”) to develop stents and other medical devices that deliver ridaforolimus to prevent re-blockage at sites of vascular injury following stent-assisted angioplasty.
