Abstract
EED is a core component of PRC2 which modifies the epigenetic status of target genes, including cell cycle control genes. Loss of SNF5 function in epithelioid sarcoma drives oncogenesis by imbalanced PRC2 activity. MAK683 is a potent, S-adenosyl-l-methionine, non-competitive PRC2 inhibitor that impairs EED binding to tri-methylated lysine 27 on histone H3 (H3K27me3), preventing allosteric activation of this complex. This is a phase I/II study of MAK683, in adult pts with advanced malignancies who have exhausted or have no effective standard treatment.
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