Highlights
FLT3 inhibitor resistance in FLT3-ITD acute myeloid leukemia frequently emerges through acquired RAS-pathway mutations, particularly NRAS, creating a major barrier to durable disease control.
In this preclinical study, the clinically available sphingosine-1-phosphate receptor modulators fingolimod (FTY720) and mocravimod (KRP-203) restored sensitivity to FLT3 inhibition in multiple NRAS-mutated FLT3-ITD AML models, including primary patient blasts.
