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This enzyme leads to the malignant transformation of primitive hematopoietic cells and to the consequent disease. The central role of Bcr\u2010Abl in the pathogenesis of CML culminated in the discovery of imatinib (an ATP\u2010competitive inhibitor), which is currently the frontline therapy for CML. Unfortunately, the initial enthusiasm generated by its high response rate has been dampened by the development of resistance, especially in the advanced phases of CML. To overcome imatinib resistance, several second\u2010generation ATP\u2010competitive inhibitors endowed with increased potency against imatinib\u2010resistant mutants have been developed: the dual Src\/Abl inhibitor dasatinib and the Abl inhibitor nilotinib have been recently approved by US\u2010FDA for the treatment of imatinib\u2010resistant CML, and many other compounds are currently in clinical trial. Although second\u2010generation TK inhibitors have shown to be clinically effective against most of the imatinib\u2010resistant mutants, to date poor results have been obtained in the treatment of the Bcr\u2010Abl T315I mutant. In this review we will report the most interesting second\u2010generation Abl and dual Src\/Abl inhibitors recently entered in clinical trial, but also the new ATP\u2010competitive and uncompetitive inhibitors published in the last few years, focusing on their chemical structure, mechanism of action, and structure\u2013activity relationship.\u2003\u2003\u00a9 2009 Wiley Periodicals, Inc. Med Res Rev, 31, No. 1, 1\u201341, 2010<\/jats:p>","DOI":"10.1002\/med.20175","type":"journal-article","created":{"date-parts":[[2009,8,27]],"date-time":"2009-08-27T17:21:31Z","timestamp":1251393691000},"page":"1-41","source":"Crossref","is-referenced-by-count":41,"title":["New insights into small\u2010molecule inhibitors of 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