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FMS-like receptor tyrosine kinase-3(Flt3), a member of class III tyrosine kinase receptor family, is predominantly expressed in hematopoietic progenitor cells and plays an important role in the pathogenesis of acute myeloid leukemia (AML). Flt3 is expressed in blast cells of most patients with AML including wild-type and two forms of Flt3 mutations. These two mutations identified in the AML patients are internal tandem duplication (ITD) mutations in the juxtamembrane domain and point mutations (TKD) in the activation loop of the TKD. The relapse rates in the Flt3/ITD mutation AML patients are significantly increased and the overall survival rates decreased compared with the AML patients without the Flt3 mutation. So development of a drug inhibited both wide type and mutant Flt3 kinase could provide an effective way to treat AML.
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