Abstract
Background and aims: Murine double minute 2 (MDM2) is the key negative regulator of the tumor suppressor protein p53. Upregulation of MDM2 contributes to MCC oncogenesis by inhibiting p53, thus promoting tumor proliferation. MDM2 is, therefore, a rational target in TP53WT MCC. Navtemadlin, a potent, selective, orally available MDM2 inhibitor, restores p53 function and drives tumor cell apoptosis. Preliminary analysis of the navtemadlin monotherapy cohort of the KRT-232-103 trial documents an ORR of 33% and an acceptable safety profile in 11 patients with advanced MCC who were relapsed/refractory to anti-PD-1/PD-L1 immunotherapy (Wong 2020).
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