Clinical Efficacies of FLT3 Inhibitors in Patients with Acute Myeloid Leukemia

FLT3 mutations are the most common genomic alteration detected in acute myeloid leukemia (AML) with a worse clinical prognosis. The highly frequent FLT3 mutations, together with the side effects associated with clinical prognosis, make FLT3 promising treatment targets and have provoked the advancement of FLT3 inhibitors. Recently, numerous FLT3 inhibitors were actively developed, and thus the outcomes of this aggressive subtype of AML were significantly improved. Recently, midostaurin and gilteritinib were approved as frontline treatment of AML and as therapeutic agents in the recurred disease by the United States Food and Drug Administration. Recently, numerous promising clinical trials attempted to seek appropriate management in frontline settings, in relapsed/refractory disease, or after stem cell transplantation in AML. This review follows numerous clinical trials about the usefulness of FLT3 inhibitors as frontline therapy, as relapsed/refractory conditioning, and as maintenance therapy of stem cell transplantation. The cumulative data of FLT3 inhibitors would be important clinical evidence for further management with FLT3 inhibitors in AML patients with FLT3 mutations.

Automated summary

FLT3 mutations are the most common genetic alterations in AML and have a negative impact on clinical prognosis. The development of FLT3 inhibitors has shown promise in improving outcomes for AML patients with FLT3 mutations. Midostaurin and gilteritinib have recently been approved as frontline treatments for AML by the FDA. Clinical trials are ongoing to explore the use of FLT3 inhibitors in different treatment settings. The accumulation of data on FLT3 inhibitors will be important evidence for guiding the use of these inhibitors in AML patients with FLT3 mutations.