Quick Search  in all journalsin this journalin this issue Journals Home Drugs of the Future Issues Drugs of the Future Policies & Guidelines Permissions My Profile Contact Us Shopping Cart Purchase History

	Drugs of the Future		Register or sign in
	Drugs Fut 2009, 34(4): 261 ISSN 0377-8282 e-ISSN 2013-0368 Copyright 2009 Clarivate CCC: 0377-8282 DOI: 10.1358/dof.2009.034.04.1338544
	Bafetinib Takeuchi, M., Kimura, S., Ashihara, E., Maekawa, T., Castaner, R., Bolos, J.
	The treatment of chronic myeloid leukemia (CML) has changed dramatically with the emergence of the ABL tyrosine kinase inhibitor (TKI) imatinib mesilate. However, primary and secondary imatinib resistance has been frequently reported, particularly in patients with advanced-stage disease. To override imatinib resistance, three second-generation ABL TKIs, i.e., dasatinib, nilotinib and bosutinib, were developed. Bafetinib (INNO-406, NS-187) is a dual ABL/Lyn inhibitor developed by our team at Kyoto University Hospital in collaboration with Nippon Shinyaku. Bafetinib was 25-55 times more potent than imatinib in blocking BCR/ABL autophosphorylation, while otherwise retaining specificity for ABL and Lyn. Bafetinib had antiproliferative effects against cells bearing wild-type or most mutated BCR/ABL proteins, except T315I, and also inhibited BCR/ABL-positive leukemic cell growth in the central nervous system. A phase I study on bafetinib was completed and the agent was well tolerated and demonstrated clinical activity across a range of doses. Responses occurred even in the setting of a heavily pretreated population, thus making bafetinib a viable option for CML therapy. Full Text: HTML, PDF

	© Clarivate. All rights reserved.
	Copyright Notice	Terms of Use	Privacy Statement	Cookie Policy	Manage cookie preferences