Around one-third of patients with acute myeloid leukemia (AML) harbor FLT3 gene mutations which are associated with poor prognosis and high risk of relapse. Several compounds targeting FLT3 internal tandem duplication (ITD) have been developed in the past decades, but none has overcome myelosuppressive toxicity caused by the simultaneous inhibition of FLT3 and c-Kit. Therefore, there is a need for new treatment options.