Ambit Biosciences today announced the publication in the January 15, 2006 issue of the journal Cancer Research of a crystal structure that explains why the Aurora kinase inhibitor VX-680 is active against Gleevec(R) (imatinib)-resistant forms of the kinase BCR-ABL, including the T315I mutant variant. The T315I mutation is the most common drug-resistant mutation in chronic myelogenous leukemia (CML) and confers resistance not only to Gleevec, but to all second generation BCR-ABL inhibitors currently in clinical development. The interaction between VX-680 and BCR-ABL variants was initially identified using Ambit’s proprietary KinomeScan kinase profiling platform.