Erasca Announces Multiple Presentations at the Upcoming 38th EORTC-NCI-AACR Symposium
Oral presentation to share updated monotherapy clinical data for ERAS-0015 including additional patients and longer follow-up, expanding on the previously reported preliminary results from the ongoing AURORAS-1 Phase 1 trial
Poster presentation to share nonclinical combination data of ERAS-0015 and ERAS-4001 demonstrating synergy in KRAS G12X-driven models
SAN DIEGO, Sept. 10, 2026 (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 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 (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.
“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.
About Erasca
At Erasca, our name is our mission: To erase cancer. We are a clinical-stage precision oncology company singularly focused on discovering, developing, and commercializing therapies for patients with RAS/MAPK pathway-driven cancers. Our company was co-founded by leading pioneers in precision oncology and RAS targeting to create novel therapies and combination regimens designed to comprehensively shut down the RAS/MAPK pathway for the treatment of patients with cancer. We believe our team’s capabilities and experience, further guided by our scientific advisory board which includes the world’s leading experts in the RAS/MAPK pathway, uniquely position us to achieve our bold mission of erasing cancer.
Cautionary Note Regarding Forward-Looking Statements
Erasca cautions you that statements contained in this press release regarding matters that are not historical facts are forward-looking statements. The forward-looking statements are based on our current beliefs and expectations and include, but are not limited to: the potential of ERAS-0015 to meaningfully improve outcomes for patients with RAS-mutant cancers; our ability to rapidly advance toward three potentially registration-enabling trials in pancreatic and lung cancers; the potential for ERAS-0015 to be best-in-class; the potential for ERAS-4001 to be first-in-class and best-in-class; and our expectations regarding the potential therapeutic benefits of our product candidates, including ERAS-0015 and ERAS-4001. Actual results may differ from those set forth in this press release due to the risks and uncertainties inherent in our business, including, without limitation: the timing of our clinical data readouts, including for the AURORAS-1 and BOREALIS-1 trials, may be delayed; our product candidates, including ERAS-0015 and ERAS-4001, may not demonstrate therapeutic benefits that we expect; interim, topline and preliminary results of a clinical trial (including observations regarding the first dosage level at which a clinical response is detected) are not necessarily indicative of final results and one or more of the clinical outcomes may materially change as patient enrollment continues, following more comprehensive reviews of the data and as more patient data becomes available, including the risk that an unconfirmed partial response to treatment may not ultimately result in a confirmed partial response to treatment after follow-up evaluations; our approach to the discovery and development of product candidates is based on our singular focus on shutting down the RAS/MAPK pathway, a novel and unproven approach; results from preclinical studies not necessarily being predictive of future results; our assumptions around which programs may have a higher probability of success may not be accurate, and we may expend our limited resources to pursue a particular product candidate and/or indication and fail to capitalize on product candidates or indications with greater development or commercial potential; potential delays in the commencement, enrollment, data readout, and completion of clinical trials and preclinical studies; our dependence on third parties in connection with manufacturing, research, and preclinical and clinical testing; unexpected adverse side effects or inadequate efficacy of our product candidates that may limit their development, regulatory approval, and/or commercialization, or may result in recalls or product liability claims; our planned potentially registration-enabling trials may be delayed based on Food and Drug Administration (FDA) feedback or requirements, as the FDA retains broad discretion to require additional clinical data prior to the conduct of a registrational trial or submission for regulatory approval; even if our planned trials are successful, they may not support regulatory approval; the inability to realize any benefits from our current licenses, acquisitions, and collaborations, and any future licenses, acquisitions, or collaborations, and our ability to fulfill our obligations under such arrangements; regulatory developments in the United States and foreign countries; our ability to obtain and maintain intellectual property protection for our product candidates and maintain our rights under intellectual property licenses, including our ability to successfully defend against allegations raised by, or any future litigation initiated by, Revolution Medicines (RevMed) that ERAS-0015 infringes patents held by RevMed or was derived from RevMed trade secrets; the sufficiency of our cash, cash equivalents, and marketable securities; we may use our capital resources sooner than we expect; and other risks described in our prior filings with the Securities and Exchange Commission (SEC), including under the heading “Risk Factors” in our annual report on Form 10-K for the year ended December 31, 2025, and any subsequent filings with the SEC. You are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date hereof, and we undertake no obligation to update such statements to reflect events that occur or circumstances that exist after the date hereof. All forward-looking statements are qualified in their entirety by this cautionary statement, which is made under the safe harbor provisions of the Private Securities Litigation Reform Act of 1995.
Contact:
Joyce Allaire
LifeSci Advisors, LLC
jallaire@lifesciadvisors.com
Media Contact:
Michael Fitzhugh
LifeSci Communications
mfitzhugh@lifescicomms.com
Source: Erasca, Inc.
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