Erasca Announces Strategic In-Licensing of RAS-Targeting Franchise

Pan-RAS molecular glue ERAS-0015 and pan-KRAS inhibitor ERAS-4001 are potent, oral inhibitors with potential best-in-class profiles in RASm solid tumors

Pipeline prioritization and workforce restructuring sharpens focus on programs targeting the highest unmet needs and with highest probability of success

Priced concurrent $160 million equity offering

Erasca to host conference call and webcast Friday, May 17, 2024 at 8:30 am ET

SAN DIEGO, May 16, 2024 (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 it has entered into exclusive license agreements for two preclinical RAS programs—a potential best-in-class pan-RAS molecular glue (ERAS-0015) and a potential first-in-class pan-KRAS inhibitor (ERAS-4001)—and provided a pipeline update. ERAS-0015 and ERAS-4001 are highly potent, orally bioavailable molecules with complementary RAS inhibitory mechanisms that have the potential to address unmet needs in nearly 2.7 million patients who are diagnosed annually globally with RAS-mutant (RASm) tumors, of which over 2.2 million patients are diagnosed with KRAS-mutant (KRASm) tumors.

As separately announced, Erasca has priced an equity offering of $160 million with a high quality group of new and existing healthcare-focused investors.

“We’re thrilled to add ERAS-0015 and ERAS-4001 to our pipeline. Successful in-licensing of this RAS-targeting franchise with such broad potential to address unmet needs in patients helps advance our mission to erase cancer and is consistent with our focus on eradicating RAS/MAPK pathway-driven tumors,” said Jonathan E. Lim, M.D., Erasca’s chairman, CEO, and co-founder. “Based on the compelling preclinical data generated to date, we believe both molecules have the potential to demonstrate best-in-class (BIC) profiles within their respective categories of RAS inhibition. Over the long term, we have a unique opportunity to combine these two BIC molecules with distinct and complementary RAS inhibitory mechanisms to ‘clamp’ RAS and shut down MAPK signaling for the benefit of patients with these common RAS mutations.”