These results suggest that further exploration of SU11248 activity in AML patients is warranted...SU11248 inhibited phosphorylation of FLT3-ITD with an IC50 of less than 10 nM. Similarly, phosphorylation of activation loop mutants Asp835Tyr, Asp835Val, and Asp835His was inhibited by SU11248, with IC50 values of 30 to 300 nM (Figure 2)...SU11248 also inhibited phosphorylation of Asp835 point mutations, Asp835Val, Asp835His, and Asp835Tyr.

...we tested the effect of combining the FLT3 inhibitor SU11248 with cytarabine or daunorubicin on the proliferation and survival of cell lines expressing either mutant (FLT3 ITD or FLT3 D835V) or wild-type (WT) FLT3. SU11248 had additive-to-synergistic inhibitory effects on FLT3-dependent leukemic cell proliferation when combined with cytarabine or daunorubicin...Combining SU11248 and cytarabine synergistically inhibited the proliferation of primary AML myeloblasts expressing FLT3 ITD but not WT FLT3 protein.