Design and SAR of pyrimidine-based inhibitors targeting the ABL-T315I mutation

MEDI 357

Elena Dneprovskaia1, Jianguo Cao, jcao@targegen.com1, Chun P. Chow, chow@targegen.com1, Richard Fine2, Ehab Hanna, hanna@targegen.com1, John Hood, jhood@targegen.com1, Xinshan Kang, jasonkang2005@yahoo.com2, Boris Klebansky, bk@biopredict.com2, Dan Lohse, dlohse@targegen.com1, Chi-Ching Mak, cmak@targegen.com1, Andrew McPherson1, Glenn Noronha, gnoronha@targegen.com1, Moorthy S. S. Palanki, palanki@targegen.com1, Ved P. Pathak, pathak@targegen.com1, Joel Renick, jrenick@targegen.com1, Richard Soll, rsoll@targegen.com1, Binqi Zeng1, and Hong Zhu, hzhu@targegen.com1. (1) TargeGen, Inc, 9380 Judicial Drive, San Diego, CA 92121-3830, (2) BioPredict, Inc, 660 Kinderkamack Road, Suite 201, Oradell, NJ 07649-1525
Imatinib, a BCR-ABL kinase inhibitor, is the standard of care for patients with chronic myelogenous leukemia. Mutations in the ABL kinase domain of the BCR-ABL protein result in interference with imatinib binding. Resistance to imatinib treatment leads to 50-90% of relapses of the disease. The T315I mutation accounts for 10-20 % of all observed mutations and is resistant to all approved and clinically advanced kinase inhibitors. TargeGen has designed and synthesized a new series of compounds based on a pyrimidine template by exploiting a unique binding interaction with Glu286 of the αC helix deep within the hydrophobic pocket. Optimization efforts guided by molecular modeling resulted in compounds with low nM ABL and ABL-T315I activity. Here we present the design and SAR of inhibitors with low nM activity against the ABL-T315I.
 

Poster Session
7:00 PM-9:00 PM, Wednesday, August 22, 2007 BCEC -- Exhibit Hall - B2, Poster

Division of Medicinal Chemistry

The 234th ACS National Meeting, Boston, MA, August 19-23, 2007