Among them, compound 50 potently inhibited FLT3, CDK2, CDK4 and CDK6, resulting in the suppression of phosphorylation of RB, FLT3, ERK, AKT and STAT5, cell cycle arrest at the G0/G1 phase, induction of apoptosis and in vivo activity in AML. This evidence concerns the gene RB1 and acute myeloid leukemia.