Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
MYC, one of the most commonly dysregulated proteins in cancer, has long seemed ‘undruggable’. Can a clinical-stage cell-penetrating peptide — or preclinical small-molecule inhibitors and degraders — prove otherwise?
When Laura Soucek first used Omomyc to block MYC signalling in mice, she spent most of the night in the lab. “People thought that these mice would liquefy,” recalls Soucek, then a postdoc at the University of California San Francisco. “I really didn’t want to harm the animals.” MYC is dysregulated in up to 70% of cancers, but the transcription factor’s role is central to so much biology that researchers thought MYC inhibition would be catastrophically unsafe — and certainly too toxic for a drug. When Soucek’s mice were alive in the morning, her first thought was that Omomyc hadn’t worked at all.