Aminoisoquinoline benzamides FLT3 and Src-family kinase inhibitors potently inhibit proliferation of acute myeloid leukemia cell lines

摘要

Aim:Mutated or overexpressed FLT3 drives about 30% of reported acute myeloid leukemia (AML). Currently, FLT3 inhibitors have shown durable clinical responses but a complete remission of AML with FLT3 inhibitors remains elusive due to mutation-driven resistance mechanisms. The development of FLT3 inhibitors that also target other downstream oncogenic kinases may combat the resistance mechanism.