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MYC is a cancer-driving transcription factor with no drug because it has no binding pocket. A molecular glue or degrader that jams its required partner MAX, or recruits an E3 ligase to the MYC-MAX interface, could switch it off; gluing disordered proteins now has precedent from cereblon-binding drugs.
MYC must dimerise with MAX to bind DNA. Rather than seeking an inhibitor pocket on MYC, a molecular glue or bifunctional degrader could stabilise a non-productive MYC conformation or recruit an E3 ligase to the MYC-MAX interface. Precedent for gluing intrinsically disordered proteins now exists (for example the recruitment of transcription factors to cereblon by aryl sulfonamides and CELMoD-class agents).
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