Revolution Medicines Inc. is focused on developing innovative therapies aimed at outsmarting cancer through its proprietary technologies. The company emphasizes a targeted approach to drug discovery, leveraging insights into the molecular mechanisms of cancer to design therapies that specifically inhibit cancer-causing proteins. This strategy is reflected in their pipeline of products, which includes a range of investigational drugs designed to address various cancer types by disrupting the pathways that enable tumor growth and survival.

The scientific foundation of Revolution Medicines is built on a deep understanding of the biology of cancer and the development of small molecule inhibitors. Their research is centered on the identification and validation of novel drug targets, which allows them to create compounds that can effectively engage these targets. By focusing on precision medicine, Revolution Medicines aims to provide more effective treatment options for patients, ultimately improving outcomes in the fight against cancer.

United States

Revolution Medicines, Inc., a clinical-stage precision oncology company, focuses on developing therapies to inhibit targets primarily within the RAS and mTOR signaling pathways. The company's principal product candidate is RMC-4630, an inhibitor of SHP2, which is in Phase 1b/2 study for the treatment of RAS-dependent tumors. Its products in preclinical stage include mutant RAS proteins; SOS1, a protein that converts RAS (OFF) to RAS (ON) in cells; and RMC-5552, a mTORC1 inhibitor. Revolution Medicines, Inc. has a collaboration agreement with Sanofi for the research and development of SHP2 inhibitors. The company was founded in 2014 and is headquartered in Redwood City, California.

Cancer

Revolution Medicines Inc

Pancreatic ductal adenocarcinoma

Daraxonrasib (RMC-6236)

Non-small cell lung carcinoma

RMC-6236

Breast cancer

Glioblastoma

Renal cell carcinoma

Solid tumor/s

The mTOR Complex 1 (mTORC1) is a central node within the mTOR &nbsp;signaling pathway and a critical regulator of metabolism, growth and &nbsp;proliferation within cells, including cancer cells. The abnormal &nbsp;activation of mTORC1, and subsequent inactivation of the tumor &nbsp;suppressor 4EBP1, is a mechanism that is frequently harnessed by cancer &nbsp;cells to gain a growth and proliferation advantage over normal cells. As &nbsp;such, selective inhibition of mTORC1 to prevent the phosphorylation and &nbsp;inactivation of 4EBP1 is viewed as a potential therapeutic strategy for &nbsp;several tumor types including breast cancer, glioblastoma and renal &nbsp;cell carcinoma, among others.
<a href="https://www.revmed.com/pipeline/rmc-5552">Source</a>

RMC-5552 (mTORC1 inhibitor)

SHP2 is a protein encoded by the PTPN11 gene, which has long been &nbsp;regarded as a cancer-causing gene. The SHP2 protein plays a central role &nbsp;in modulating cell survival and growth by transmitting signals from &nbsp;upstream receptor tyrosine kinases, or RTKs, to RAS. As a key signaling &nbsp;node within the RAS pathway, SHP2 acts as an important regulator of &nbsp;growth signals within normal cells and, in certain circumstances, cancer &nbsp;cells.
A traditional view was that RAS pathway oncoproteins were constitutively &nbsp;active and insensitive to upstream modulation. However, our data &nbsp;support an emerging framework in which certain oncoproteins are &nbsp;semi-autonomous and rely upon upstream signaling for oncogenic activity. &nbsp;Consistent with this hypothesis, we have demonstrated that our SHP2 &nbsp;inhibitors arrest tumor growth and/or trigger tumor cell death in mouse &nbsp;xenograft models of cancers bearing specific KRAS, NF1 and BRAF &nbsp;mutations that have been shown to rely upon SHP2 signaling. As a result, &nbsp;we believe that a potent, selective and orally bioavailable inhibitor &nbsp;of SHP2 has the potential to be a valid therapeutic option for the &nbsp;treatment of certain cancers that rely on, or are "addicted" to, &nbsp;SHP2-dependent oncogenic mutations.
<a href="https://www.revmed.com/pipeline/rmc-4630">Source</a>

RMC-4630 + sotorasib

Pancreatic cancer

RMC-6236 is an oral, selective, first-in-class RAS(ON) Inhibitor designed to treat patients with cancers driven by a wide range of common RAS mutations. Initially being evaluated as monotherapy, it may also be deployed as a RAS Companion Inhibitor in combination with mutant-selective RAS(ON) Inhibitors and in other combination treatment strategies.

RMC-6236 (RASMULTI)

RMC-6291, an oral, selective, covalent inhibitor of KRASG12C(ON) designed to treat patients with cancers driven by the KRASG12C mutant, is the first of the company’s mutant-selective RAS(ON) Inhibitors to enter clinical development and the first reported clinical-stage inhibitor of KRASG12C that uses a highly differentiated mechanism of action.

RMC-6291 (KRASG12C)

Colorectal cancer

RMC-9805 is an oral, selective, covalent inhibitor of KRASG12D(ON), the most common driver of RAS-addicted human cancers, predominantly among patients with pancreatic cancer, NSCLC, or colorectal cancer (CRC). The company believes RMC-9805 is the first oral and covalent inhibitor of

RMC-9805 (KRASG12D)

RMC-6236 is an oral, selective, first-in-class RAS(ON) Inhibitor designed to treat patients with cancers driven by a wide range of common RAS mutations. Initially being evaluated as monotherapy, it may also be deployed as a RAS Companion Inhibitor in combination with mutant-selective RAS(ON) Inhibitors and in other combination treatment strategies.
 
RMC-6291, an oral, covalent inhibitor of RASG12C(ON) designed to treat patients with cancers driven by the KRASG12C mutant

RMC-6236 + RMC-6291

RMC-6236+ pembrolizumab

RMC-6291, an oral, covalent inhibitor of RASG12C(ON) designed to treat patients with cancers driven by the KRASG12C mutant

Revolution Medicines Inc

Company Details