We are a clinical-stage precision oncology company focused on developing novel targeted therapies to inhibit frontier targets in RAS-addicted cancers.

At Revolution Medicines, we combine our understanding of genetic drivers and adaptive resistance mechanisms in cancer, coupled with robust drug discovery and medicinal chemistry capabilities, to create a deep pipeline targeting critical signaling nodes within the RAS and related pathways. This cohesive approach underpins our clinical strategy of exploring mechanism-based dosing paradigms and in-pathway combinations to optimize treatment for cancer patients.

Our research and development pipeline comprises RAS(ON) inhibitors that bind directly to RAS variants, which we refer to as RAS(ON) Inhibitors, and RAS Companion inhibitors that target key nodes in the RAS pathway or associated pathways (e.g., mTOR), which we refer to as RAS Companion Inhibitors. Our RAS Companion Inhibitors (e.g., SHP2, mTORC1 and SOS1 inhibitors) are designed primarily to enable combination treatment strategies involving both combinations with our own RAS(ON) Inhibitors and other pathway inhibitors.

Our most advanced RAS Companion Inhibitor product candidate, RMC-4630, is a potent and selective inhibitor of SHP2, a central node in the RAS signaling pathway. In collaboration with our partner, Sanofi, we are evaluating RMC-4630 in a multi-cohort Phase 1/2 clinical program for a range of tumor types harboring specific oncogenic mutations.

We are also developing a portfolio of potent, cell-active inhibitors of the active, GTP-bound form of RAS, or RAS(ON). Oncogenic RAS variants are responsible for the vast majority of RAS-addicted cancers and represent a large unmet medical need. Our proprietary technology platform has produced inhibitors for variants driving a vast majority of RAS-addicted cancers including development candidates RMC-6291 (KRAS^G12C and NRAS^G12C), and RMC-6236 (KRAS^MULTI).

A frontier oncology target is a protein that plays an important role in cancer and for which there is either: (1) no approved drug that directly inhibits it, or (2) one or more approved drugs that directly inhibit it but through a mechanism of action that doesn’t maintain suppression of the full range of its biologic contributions to cancer.