MCL1, a highly regulated member of the BCL2 family, is frequently found to be amplified or overexpressed in both solid tumors and hematologic cancers. It is induced by a wide range of survival signals and rapidly downregulated during apoptosis. Inhibition of MCL1 expression and/or function is therefore of considerable therapeutic interest in cancer, as it is thought to mediate cancer cell survival in myelodysplastic syndrome, acute myeloid leukemia, non-Hodgkin’s lymphoma, and multiple myeloma. Small molecule MCL1 inhibitors have been shown to be efficacious as monotherapy in preclinical models of multiple myeloma, acute myeloid leukemia, and lymphoma.
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