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FLT3 Inhibitors in Development for AML

Harry Erba, MD, PhD
Published Online:6:57 PM, Thu May 29, 2014
Harry Erba, MD, PhD, professor of medicine, director, Hematologic Malignancy Program, University of Alabama at Birmingham, discusses the excitement around FLT3 inhibitors for the treatment of acute myeloid leukemia (AML).

Clinical Pearls

  • 25-30% of patients with AML with normal karyotype will have activating mutations in FLT3.
  • Sorafenib has shown activity in FLT3/ITD-positive AML.
  • Quizartinib has shown high response rates as monotherapy, though data have shown responses tend to be mostly complete remissions with incomplete blood count recovery.
  • Quizartinib may be an important agent to bridge patients to an allogeneic stem cell transplant, which would be the only curative option for patients with relapsed FLT3/ITD-positive AML.
  • Patients who respond to quizartinib can develop a D835 mutation, but an agent is being developed that is active against both FLT/ITD and D835 mutations.
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