[Breakthroughs in FLT3-mutated acute myeloid leukemia treatments]

Rinsho Ketsueki. 2023;64(9):932-941. doi: 10.11406/rinketsu.64.932.
[Article in Japanese]

Abstract

FMS-like tyrosine kinase 3 (FLT3) mutation is present in 25% of acute myeloid leukemia (AML) cases. It is associated with poor prognosis due to a high relapse rate and short remission duration. Consequently, various FLT3 inhibitors were developed. Two second-generation FLT3 inhibitors, including gilteritinib and quizartinib, are used for treating relapsed/refractory FLT3-mutated AML. Additionally, in May 2023, quizartinib was approved for newly-diagnosed FLT3-mutated AML, in combination with standard remission induction, consolidation, and maintenance therapies based on a phase 3 trial. Furthermore, high relapse rates were observed even in patients who underwent allogeneic hematopoietic cell transplantation while in their first complete remission, and post-transplant maintenance therapy using oral FLT3 inhibitors has been tried. This review summarizes breakthroughs in treatments of FLT3-mutated AML aiming for a better prognosis.

Keywords: Acute myeloid leukemia; FMS-like tyrosine kinase 3; Gilteritinib; Quizartinib.

Publication types

  • Review
  • English Abstract

MeSH terms

  • Humans
  • Leukemia, Myeloid, Acute* / drug therapy
  • Leukemia, Myeloid, Acute* / genetics
  • Mutation
  • Phenylurea Compounds
  • Protein Kinase Inhibitors / therapeutic use
  • Recurrence
  • fms-Like Tyrosine Kinase 3* / genetics

Substances

  • quizartinib
  • fms-Like Tyrosine Kinase 3
  • Phenylurea Compounds
  • Protein Kinase Inhibitors
  • FLT3 protein, human