FMS-like tyrosine kinase 3- internal tandem duplication (FLT3-ITD) remains as 
one of the most frequently mutated genes in acute myeloid leukemia (AML), 
especially in those with normal cytogenetics. The FLT3-ITD and FLT3-TKD 
(tyrosine kinase domain) mutations are biomarkers for high risk AML and are 
associated with drug resistance and high risk of relapse. Multiple FLT3 
inhibitors are in clinical development, including lestaurtinib, tandutinib, 
quizartinib, midostaurin, gilteritinib, and crenolanib. Midostaurin and 
gilteritinib have been approved by FDA for Flt3 mutated AML. Gilteritinib 
(ASP2215, Xospata) is a small molecule dual inhibitor of FLT3/AXL. The ADMIRAL 
study showed that longer overall survival and higher response rate are 
associated with gilteritinib in comparison with salvage chemotherapy for relapse 
/refractory (R/R) AML. These data from the ADMIRAL study may lead to the therapy 
paradigm shift and establish gilteritinib as the new standard therapy for R/R 
FLT3-mutated AML. Currently, multiple clinical trials are ongoing to evaluate 
the combination of gilteritinib with other agents and regimens. This study 
summarized clinical trials of gilteritinib for AML.