Patients with acute myeloid leukemia and an activating mutation in FLT3 respond to a small-molecule FLT3 tyrosine kinase inhibitor, PKC412.

@article{Stone2005PatientsWA,
  title={Patients with acute myeloid leukemia and an activating mutation in FLT3 respond to a small-molecule FLT3 tyrosine kinase inhibitor, PKC412.},
  author={Richard M Stone and Daniel J. Deangelo and Virginia M. Klimek and Ilene Galinsky and Eli Estey and Stephen D. Nimer and Wilson Grandin and David Edward Lebwohl and Yanfeng Wang and Pamela B. Cohen and Edward A. Fox and Donna S Neuberg and Jennifer J. Clark and Dwight Gary Gilliland and James D Griffin},
  journal={Blood},
  year={2005},
  volume={105 1},
  pages={
          54-60
        }
}
Leukemic cells from 30% of patients with acute myeloid leukemia (AML) have an activating mutation in the FLT3 (fms-like tyrosine kinase) gene, which represents a target for drug therapy. We treated 20 patients, each with mutant FLT3 relapsed/refractory AML or high-grade myelodysplastic syndrome and not believed to be candidates for chemotherapy, with an FLT3 tyrosine kinase inhibitor, PKC412 (N-benzoylstaurosporine), at a dose of 75 mg 3 times daily by mouth. The drug was generally well… CONTINUE READING

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