MERTK and acute myeloid leukemia: Though UNC1666 was able to reduce prosurvival signaling downstream of MERTK and FLT3 and induced apoptosis in AML cell lines, it showed poor bioavailability in preclinical studies.162 This led to the development of MRX-2843, a small-molecule inhibitor of both MERTK and FLT3 with improved bioavailability compared to UNC1666.163 MRX-2843 has demonstrated significant induction of AML cell death that is proportionate to inhibition of MERTK phosphorylation and downstream signaling pathways and is dose dependent in AML cells (Fig. 3).