R1-ICR-5 is a highly selective RIPK1 PROTAC degrader. Mediated by VHL, R1-ICR-5 induces the degradation of RIPK1, which in turn dysregulates the TNFR1 and TLR3/4 signaling hubs, enhances the signaling outputs of NF-kappaB, MAPK and IFN, and simultaneously promotes RIPK3 activation and necroptosis (necroptosis). R1-ICR-5 can be used in the research of triple-negative breast cancer and skin inflammation[1].
