4.4 Review

Which FLT3 Inhibitor for Treatment of AML?

Journal

CURRENT TREATMENT OPTIONS IN ONCOLOGY
Volume 23, Issue 3, Pages 359-380

Publisher

SPRINGER
DOI: 10.1007/s11864-022-00952-6

Keywords

AML; FLT3 inhibitor; Sorafenib; Midostaurin; Gilteritinib; Quizartinib

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Treatment options in acute myeloid leukemia (AML) have significantly improved over the last decade, with better understanding of disease biology and availability of targeted therapies. The use of FLT3 inhibitors (FLT3i) in FLT3-mutated (FLT3(mut)) AML is an important development, but the clinical decisions and choice of FLT3i are still evolving.
Opinion statement Treatment options in acute myeloid leukemia (AML) have improved significantly over the last decade with better understanding of disease biology and availability of a multitude of targeted therapies. The use of FLT3 inhibitors (FLT3i) in FLT3-mutated (FLT3(mut)) AML is one such development; however, the clinical decisions that govern their use and dictate the choice of the FLT3i are evolving. Midostaurin and gilteritinib are FDA-approved in specific situations; however, available data from clinical trials also shed light on the utility of sorafenib maintenance post-allogeneic stem cell transplantation (allo-SCT) and quizartinib as part of combination therapy in FLT3(mut) AML. The knowledge of the patient's concurrent myeloid mutations, type of FLT3 mutation, prior FLT3i use, and eligibility for allo-SCT helps to refine the choice of FLT3i. Data from ongoing studies will further precisely define their use and help in making more informed choices. Despite improvements in FLT3i therapy, the definitive aim is to enable the eligible patient with FLT3(mut) AML (esp. ITD) to proceed to allo-SCT with regimens containing FLT3i incorporated prior to SCT and as maintenance after SCT.

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