SAN DIEGO, March 5, 2026 — Leads & Copy — Erasca, Inc. (Nasdaq: ERAS), a clinical-stage precision oncology company, has entered into a clinical trial collaboration and supply agreement with Tango Therapeutics, Inc. (Nasdaq: TNGX; “Tango”) to evaluate Erasca’s pan-RAS molecular glue, ERAS-0015, in combination with Tango’s PRMT5 inhibitor, vopimetostat (TNG462).
The agreement supports a Phase 1/2 clinical trial assessing ERAS-0015 combined with vopimetostat in patients with MTAP-deleted pancreatic or MTAP-deleted RASm non-small cell lung cancer (NSCLC). Erasca will provide ERAS-0015 at no cost, while Tango will be the trial sponsor. Both companies retain commercial rights to their respective compounds, and the agreement is non-exclusive.
Jonathan E. Lim, M.D., Erasca’s chairman, CEO, and co-founder, stated that the company has disclosed encouraging early clinical activity for ERAS-0015, including initial clinical responses in several patients with different tumor types and RAS mutations at a fraction of the dose compared to RMC-6236. Lim added that combining ERAS-0015 with Tango’s PRMT5 inhibitor offers a promising opportunity to improve the standard of care for patients with MTAP-deleted RAS-mutant cancers.
Nearly all MTAP-deleted pancreatic cancers and 30% of MTAP-deleted NSCLC tumors have co-occurring RAS mutations. This creates a dependency making these cancer cells more sensitive to simultaneous RAS and PRMT5 inhibition. Combining a pan-RAS molecular glue with a PRMT5 inhibitor is designed to shut down the RAS signaling pathway and more strongly suppress PRMT5 in MTAP-deleted tumor cells. This dual-targeted approach has the potential to produce deeper and more durable responses and reduce the likelihood of resistance in difficult-to-treat cancers.
ERAS-0015 is an oral pan-RAS molecular glue intended to inhibit RAS signaling. Erasca is currently evaluating ERAS-0015 in the AURORAS-1 Phase 1 trial involving patients with RAS-mutant solid tumors. Early data from AURORAS-1 has shown favorable safety and tolerability, linear pharmacokinetics, and confirmed and unconfirmed responses in multiple patients across multiple tumor types with different RAS mutations, including confirmed and unconfirmed partial responses at doses as low as 8 mg once daily.
Preclinical studies comparing ERAS-0015 to RMC-6236 showed that ERAS-0015 had approximately 8-21 times higher binding affinity to cyclophilin A (CypA), approximately 5 times greater potency in RAS inhibition, and greater in vivo antitumor activity, achieving comparable or greater tumor growth inhibition or regression at doses as low as approximately one-tenth to one-fifth of the dose of RMC-6236. ERAS-0015 is also designed to prevent resistance against mutant-selective inhibitors through inhibition of RAS wildtype variants.
ERAS-0015 has also demonstrated favorable absorption, distribution, metabolism, and excretion (ADME) and pharmacokinetic (PK) properties in multiple animal species.
Erasca is focused on discovering, developing, and commercializing therapies for patients with RAS/MAPK pathway-driven cancers.
Source: Erasca, Inc.
