Revolution Medicines Announces Dosing of First Patient in Clinical Study of RMC-4630 (SAR442720) Combined with PD-1 Inhibitor
Combination of Investigational SHP2 Inhibitor and Anti-PD-1 Antibody to be Evaluated in Patients with Solid Tumors
REDWOOD CITY, Calif., June 22, 2020 (GLOBE NEWSWIRE) -- Revolution Medicines, Inc. (Nasdaq: RVMD), a clinical-stage oncology company focused on developing targeted therapies to inhibit frontier
cancer targets, today announced dosing of the first patient in a multicenter Phase 1 clinical trial evaluating the combination of RMC-4630 (SAR442720), the company’s investigational SHP2 inhibitor,
and pembrolizumab (Keytruda), an anti-PD-1 antibody. The trial, which is being sponsored and conducted by the company’s collaboration partner Sanofi, is an open-label, safety, preliminary efficacy
and pharmacokinetics study in participants with advanced malignancies. This will include patients with non-small cell lung cancer (NSCLC) who have progressed on or after platinum-based
chemotherapy, and patients with colorectal cancer who have progressed on or after standard of care therapy.
RMC-4630 (SAR442720) is a potent and orally bioavailable small molecule that is designed to selectively inhibit the activity of SHP2, an upstream cellular protein that plays a central role in modulating cell survival and growth by transmitting signals from receptor tyrosine kinases to RAS. Pembrolizumab, a humanized antibody used in cancer immunotherapy, is designed to selectively inhibit the activity of PD-1, a key immune checkpoint that can prevent the immune system from targeting and killing cancer cells. Pembrolizumab is an approved standard of care for the treatment of NSCLC, including lung cancers harboring RAS pathway mutations.
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The company’s recently published research in the journal Cancer Research described the anti-tumor effects of a SHP2 inhibitor such as RMC-4630 (SAR442720) through modulation of key elements of the immune system in preclinical cancer models. These findings demonstrated that inhibition of SHP2 may exert therapeutic anti-tumor effects by modulating multiple arms of the immune response to the tumor in addition to reducing oncogenic signaling within tumor cells themselves. Importantly, these data indicate that these two mechanisms may be additive in their anti-tumor impact. Additionally, company findings from the same preclinical study showed that when the SHP2 inhibitor was combined with an immune checkpoint inhibitor (anti-PD-1), deep and durable tumor growth inhibition was observed, with complete tumor regressions and sustained immunological memory in some mice.