Farnesyl transferase inhibitors: From peptides to a clinical compound

MEDI 266

Katerina Leftheris, katerina.leftheris@bms.com, Discovery Chemistry, Pharmaceutical Research Institute, Bristol-Myers Squibb, P.O. Box 4000, Princeton, NJ 08543-4000
A family of GTP-binding proteins (p21ras) encoded by ras genes are known to play a major role in controlling cell growth and differentiation. Mutated ras genes have been found in 15% of all human carcinomas with a much higher occurrence in pancreatic adenocarcinomas (90%) and human colon tumors (50%). Ras proteins must be membrane-associated to function and post-translational modification is critical for this localization. A conserved tetrapeptide CA1A2X sequence at the C-terminus of p21ras triggers a series of post-translational processing events including the farnesylation of Cys186 by the enzyme farnesyl transferase. Inhibition of S-farnesylation of p21ras may block the growth of ras-mediated tumors. Starting from a CAAX tetrapeptide lead, SAR development led to the identification of farnesyl transferase inhibitor BMS-214662 as a clinical candidate. Unlike known farnesyl transferase inhibitors that are cytostatic, BMS-214662 induces apoptosis and leads to curative efficacy in in vivo animal models containing human tumor xenografts. Development of BMS-214662 as well as the status of farnesyl transferase inhibitors in the clinic will be discussed.
 

Murray Goodman Memorial Symposium
8:30 AM-12:05 PM, Wednesday, 31 August 2005 Washington DC Convention Center -- Ballroom A, Oral

Division of Medicinal Chemistry

The 230th ACS National Meeting, in Washington, DC, Aug 28-Sept 1, 2005