Degrade the damaged p53 protein rather than trying to repair it

Gain-of-function mutant p53 accumulates to high levels because it escapes MDM2-mediated turnover, and it drives invasion and chemoresistance in mouse models. A selective degrader exploiting the mutant's dependence on HSP90 or its distinct conformation could deplete it. Precedent: HSP90 inhibitors destabilise mutant p53 and prolong survival in mutant-p53 mouse models, but are too toxic; a targeted degrader would separate the effect from global chaperone inhibition.