SAN DIEGO, July 20, 2021 (GLOBE NEWSWIRE) -- Erasca, Inc. (Nasdaq: ERAS), a clinical-stage precision oncology company singularly focused on discovering, developing, and commercializing therapies for patients with RAS/MAPK pathway-driven cancers, today announced the closing of its initial public

Erasca Enters into Collaboration with Merck to Evaluate ERAS-0015 with KEYTRUDA in RAS-Mutant Solid Tumours. Tuesday, May 12, 2026 Erasca has entered into a clinical trial collaboration and supply agreement with Merck to evaluate ERAS-0015 in combination with KEYTRUDA for patients with RAS-mutant solid tumours. The agreement will support the AURORAS-1 clinical proof-of-concept study, which is assessing the investigational pan-RAS molecular glue ERAS-0015 together with pembrolizumab, Merck's anti-PD-1 therapy. Erasca is sponsoring the study, while Merck will provide pembrolizumab at no cost. The companies are exploring the potential of the combination therapy to improve treatment outcomes in cancers driven by RAS mutations. RAS mutations are known to activate the RAS/MAPK pathway and contribute to an immunosuppressive tumour environment. Preclinical findings suggest that ERAS-0015 may help enhance the effects of PD-1 blockade by reducing immunosuppression and supporting stronger and longer-lasting tumour responses. Globally, around 2.7 million patients are diagnosed each year with RAS-mutant tumours. Limited treatment options targeting multiple RAS mutations and the development of resistance mechanisms remain major challenges in treating these cancers. ERAS-0015 is an investigational oral therapy designed to inhibit RAS signalling across a broad range of mutations. The therapy is currently being evaluated in the Phase 1 AURORAS-1 trial in patients with RAS-mutant solid tumours. Early dose-escalation results from the study showed favourable safety and tolerability, linear pharmacokinetics, and confirmed as well as unconfirmed partial responses in patients across different tumour types and RAS mutations. Responses were observed at doses as low as 8 mg once daily. The therapy is also designed to address resistance associated with mutant-selective inhibitors through inhibition of RAS wildtype variants. In addition, ERAS-0015 demonstrated favourable absorption, distribution, metabolism, excretion, and pharmacokinetic properties in preclinical animal studies.