c-Myc is a basic helix-loop-helix leucine zipper (bHLH-LZ) transcription factor that is important for cell proliferation, differentiation and survival. Heterodimerization of c-Myc with Max is an obligatory requirement for c-Myc to become transcriptionally functional. Importantly, overexpression and/or dysregulation of c-Myc has been associated with tumorigenesis, contributing to the development and progression of a wide variety of human cancers, including lung, breast, pancreatic and colorectal cancers. Inactivation of c-Myc results in cell cycle arrest, apoptosis and tumor regression. Hence, inhibition of c-Myc with small-molecules is an attractive goal towards the development of novel, and urgently-needed, anti-cancer agents. We have recently disclosed the novel small-molecule c-Myc inhibitor JY-3-094, which selectively inhibits c-Myc�Max dimerization with an IC50 of 33 �M (Max�Max: IC50 > 100 �M). However, JY-3-094 exhibits poor cytotoxicity in c-Myc-overexpressing cell lines. Our efforts to optimize the in vitro and cellular c-Myc inhibitory activities of JY-3-094 will be presented.

Towards the optimization of c-Myc inhibitor JY-3-094

245th National Meeting (2013)

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