On September 10, 2026 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, reported that updated monotherapy clinical data from the ongoing Phase 1 AURORAS-1 trial of ERAS-0015 will be shared in an oral presentation and nonclinical combination data of ERAS-0015 and ERAS-4001 will be shared in a poster presentation at the 38th EORTC-NCI-AACR (Free EORTC-NCI-AACR Whitepaper) (ENA) Symposium on Molecular Targets and Cancer Therapeutics, taking place November 18-20 in Barcelona, Spain. ERAS-0015 is a potential best-in-class pan-RAS molecular glue in development for the treatment of patients with RAS-mutant solid tumors. ERAS-4001 is a potential first-in-class and best-in-class pan-KRAS inhibitor in development for the treatment of patients with KRAS-mutant solid tumors.
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"We look forward to sharing an expanded AURORAS-1 monotherapy dataset with the medical community at the ENA Symposium, including results from more patients and with longer follow-up," said Jonathan E. Lim, M.D., Erasca’s chairman, CEO, and co-founder. "The clinical activity and favorable tolerability observed in our prior data disclosures underscore the potential of ERAS-0015 to meaningfully improve outcomes for patients with RAS-mutant cancers. We’re also excited to share nonclinical data for the combination of ERAS-0015 and ERAS-4001 showing synergy in KRAS G12X-driven models. With strong momentum across the pipeline, we are rapidly advancing toward three potentially registration-enabling trials for ERAS-0015 in pancreatic and lung cancers."
Oral Presentation Details
Title: Preliminary safety, pharmacokinetics, and efficacy of ERAS-0015: Results from the AURORAS-1 first-in-human trial
Speaker: Judy Wang, M.D., Florida Cancer Specialists, Sarah Cannon Research Institute
Date and Time: Friday, November 20, 12:30 p.m. Central European Time
Session: Plenary Session 6, Proferred Papers
Location: Room 111 + 112
Poster Presentation Details
Title: Combination of ERAS-0015 and ERAS-4001 targets active and inactive KRAS and displays synergy in nonclinical KRAS G12X-driven models
Presenter: Erin Lew, Ph.D., Erasca, Inc.
Date and Time: Friday, November 20, 9:00 a.m. – 3:00 p.m. Central European Time
Session: Combination Therapies
Location: Exhibition Hall
About ERAS-0015
ERAS-0015 is an investigational, oral, highly potent pan-RAS molecular glue designed to inhibit RAS signaling with a potential best-in-class profile. Erasca is evaluating ERAS-0015 in the AURORAS-1 Phase 1 trial in patients with RAS-mutant solid tumors. Early dose escalation data in AURORAS-1 demonstrated favorable safety and tolerability results, well-behaved, linear PK, and confirmed and unconfirmed partial responses in multiple patients across multiple tumor types with different RAS mutations, including confirmed partial responses at doses as low as 8 mg once daily (QD). ERAS-0015 is also designed to prevent resistance against mutant-selective inhibitors through inhibition of RAS wildtype variants. In addition, ERAS-0015 has demonstrated favorable absorption, distribution, metabolism, and excretion (ADME) and pharmacokinetic (PK) properties in multiple animal species.
About ERAS-4001
ERAS-4001 is an investigational, oral, highly potent, and selective pan-KRAS inhibitor with a potential first-in-class and best-in-class profile. Erasca is evaluating ERAS-4001 in the BOREALIS-1 Phase 1 trial in patients with KRAS-mutant solid tumors. ERAS-4001 demonstrated favorable preclinical in vitro potency against KRAS G12X mutations as well as KRAS wildtype amplifications, which may limit treatment resistance mediated through KRAS wildtype activation. No activity was observed for ERAS-4001 against HRAS or NRAS wildtype proteins in preclinical studies, which may enable a better therapeutic window compared to pan-RAS inhibitors. ERAS-4001 showed potent activity against both GTP-bound (active state) and GDP-bound (inactive state) KRAS with single digit nanomolar IC50s. In vivo, ERAS-4001 induced tumor regression in multiple KRAS-mutant models. In preclinical studies, ERAS-4001 showed encouraging ADME and PK properties.
(Press release, Erasca, SEP 10, 2026, View Source [SID1234670742])