The FMS-like tyrosine kinase 3 (FLT3) protein is a receptor tyrosine kinase that is expressed at high levels in 70-100% of cases of AML(Acute myeloid leukemia) and has been identified as potential target for molecular therapy. Internal tandem duplications (ITD) of the juxtamembrane domain in FLT3 occur regularly in de novo AML, resulting in constitutive activation of FLT3 tyrosine kinase activity. [1]In cell-based assays tandutinib inhibited FLT3 ,PDGFR, and KIT with IC50 values of 95-122 ng/mL, but had no significant effect against a broad range of other kinases. In Ba/F3 cells expressing various FLT3-ITD mutants, tandutinib inhibited IL-3-independent growth and FLT3-ITD auto-phosphorylation with IC50 values of 6-17 ng/ml. Tandutinib also inhibited in vitro proliferation of human leukemia cell lines containing FLT3-ITD mutations with IC50 values of approximately 6 ng/mL. [2]Tandutinib has a very limited spectrum of activity outside the type III receptor kinase family. Evaluation of tandutinib in rats, dogs, and monkeys showed it to be orally bioavailable, metabolically stable.Phase I clinical results with tandutinib (MLN518) in patients with acute myelogenous leukemia or high-risk myelodysplastic syndrome: safety, pharmacokinetics, and pharmacodynamics.

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