Article

A noncanonical FLT3 gatekeeper mutation disrupts gilteritinib binding and confers resistance

2021-01-28

Abstract excerpt

<h4>ABSTRACT</h4> The recent FDA approval of the FLT3 inhibitor, gilteritinib, for AML represents a major breakthrough for treatment of FLT3 mutated AML. However, patients only respond to gilteritinib for 6-7 months due to the emergence of drug resistance. Clinical resistance to gilteritinib is often associated with expansion of NRAS mutations, and less commonly via gatekeeper mutations in FLT3, with F691L being...

Topics

Open a Topic to create a Post that cites this publication.

Identifiers and source

Literature Corpus work: 3544efd5-7a72-5fe9-9bbf-08dd5a8a478f
DOI: 10.1101/2021.01.27.428336

Open publication

Related research

Semantic proximity does not establish scientific evidence.

Click a neighbor to travelStep 1 · 12 closest

A noncanonical FLT3 gatekeeper mutation disrupts gilteritinib binding and confers resistanceDOI 10.1101/2021.01.27.428336Read

The FLT3N701K mutation causes clinical AML resistance to gilteritinib and triggers TKI sensitivity switch to quizartinibSemantic proximity Read

Gilteritinib is a clinically active FLT3 inhibitor with broad activity against FLT3 kinase domain mutations.Semantic proximity Read

Clinical and molecular response of AML harboring non-canonical <i>FLT3</i> N676K driver mutations to contemporary FLT3 inhibitorsSemantic proximity Read

Mechanisms Underlying Resistance to FLT3 Inhibitors in Acute Myeloid LeukemiaSemantic proximity Read

Gilteritinib: potent targeting of FLT3 mutations in AML.Semantic proximity Read

Understanding gilteritinib resistance to FLT3-F691L mutation through an integrated computational strategy.Semantic proximity Read

FLT3 Mutations in Acute Myeloid Leukemia: Key Concepts and Emerging ControversiesSemantic proximity Read

Gilteritinib: An FMS-like tyrosine kinase 3/AXL tyrosine kinase inhibitor for the treatment of relapsed or refractory acute myeloid leukemia patients.Semantic proximity Read

BMX kinase mediates gilteritinib resistance in FLT3-mutated AML through microenvironmental factors.Semantic proximity Read

Deciphering the mechanism of HM43239 inhibiting the mutant F691L resistant to gilteritinib in FMS-like tyrosine kinase 3.Semantic proximity Read

The AML microenvironment catalyzes a stepwise evolution to gilteritinib resistanceSemantic proximity Read

Gilteritinib use in the treatment of relapsed or refractory acute myeloid leukemia with a FLT3 mutation.Semantic proximity Read