Nilotinib, a novel, selective BCR-ABL inhibitor, fits into the ATP-binding site of the BCR-ABL protein with higher affinity than imatinib. Nilotinib is not only more potent than imatinib against wild-type BCR-ABL (IC50 < 30 nM), but also significantly active against 32/33 imatinib-resistant BCR-ABL mutants. Nilotinib was as potent as imatinib in inducing apoptosis (IC50 = 0.54 nM) and inhibiting proliferation (IC50 = 0.20 nM) of EOL-1 cells.