REDWOOD CITY, Calif., March 17, 2026 (GLOBE NEWSWIRE) -- Revolution Medicines, Inc. (Nasdaq:RVMD), a late-stage clinical oncology company developing targeted therapies for patients with RAS-addicted cancers, today announced that nine oral and poster presentations highlighting advances across its RAS(ON) inhibitor pipeline will be featured at the American Association for Cancer Research (AACR) Annual Meeting, taking place April 17–22, 2026 in San Diego.

The presentations will include new Phase 1 data for zoldonrasib, a RAS(ON) G12D-selective inhibitor, in patients with previously treated KRAS G12D mutant non-small cell lung cancer, which will be featured in a plenary session.

The company will also present two Phase 1/2 datasets evaluating daraxonrasib, a RAS(ON) multi-selective inhibitor, in patients with first line metastatic pancreatic ductal adenocarcinoma (PDAC), including monotherapy data and daraxonrasib plus chemotherapy combination data, the latter of which will be featured in a mini-symposium session.

Additional presentations will highlight preclinical research supporting a new class of mutant-targeted catalytic RAS(ON) inhibitors, designed to maintain antitumor activity in the setting of emergent resistance.

Together, these presentations reflect the breadth of Revolution Medicines’ RAS(ON)-focused development strategy, spanning clinical studies across multiple tumor types and ongoing discovery efforts to address resistance and expand therapeutic opportunities for patients with RAS-driven cancers.

Details of the presentations are listed below.

Revolution Medicines Invited Presentation:

Title: Targeting the Oncogenic State of RAS: Lessons from Tri-Complex Inhibitors
Presenter: Mallika Singh, Ph.D., Revolution Medicines
Session: How KRAS Inhibitors Got to the Clinic: From Discovery to Patient Benefit
Date/Time: April 18; 3:00 p.m. – 3:20 p.m. PST


Revolution Medicines Oral Presentation:

Title: Preliminary Safety and Clinical Activity of Zoldonrasib (RMC-9805), an Oral, RAS(ON) G12D-Selective, Tri-Complex Inhibitor in Patients with Previously Treated KRAS G12D Non-Small Cell Lung Cancer (NSCLC)
Presenter: Jonathan Reiss, M.D., UC Davis Comprehensive Cancer Center
Abstract
Number: 		CT021
Session: New Frontiers in Precision Oncology
Date/Time: April 19; 1:30 p.m. – 1:45 p.m. PST


Revolution Medicines Mini Symposiums:

Title: Daraxonrasib plus Chemotherapy as First Line Treatment for Patients with Metastatic Pancreatic Adenocarcinoma (mPDAC)
Presenter: Brian Wolpin, M.D., Dana-Farber Cancer Institute
Abstract
Number: 		LB407
Session: Late-Breaking Research
Date/Time: April 21; 4:05 p.m. – 4:20 p.m. PST


Title: Discovery of a New Class of Mutant-Targeted Catalytic RAS(ON) Inhibitors with Retained Antitumor Activity in Setting of Emergent Resistance Due to Elevated RAS Flux
Presenter: Jacqueline (Jan) Smith, Ph.D., Revolution Medicines
Abstract
Number: 		6782
Session: Targeted Protein Degradation and Non-canonical Oncogenic Signaling
Date/Time: April 21; 4:05 p.m. – 4:20 p.m. PST


Revolution Medicines Posters:

Title: RAS(ON) Inhibition in both Cancer and Immune Cells by Daraxonrasib Drives Antitumor Immunity
Presenter: Nataliya Shifrin, Ph.D., Revolution Medicines
Abstract
Number: 		2831
Session: Immune Mechanisms Invoked by Other Therapies and Exposures
Date/Time: April 20; 2:00 p.m. – 5:00 p.m. PST


Title: RASolve 301: A Phase 3 Study of Daraxonrasib (RMC-6236) vs. Docetaxel in Patients with Previously Treated RAS-mutant NSCLC
Presenter: Ferdinandos Skoulidis, M.D., Ph.D., MRCP, MD Anderson Cancer Center
Abstract
Number: 		CT215
Session: Late-Breaking Research
Date/Time: April 21; 9:00 a.m. – 12:00 p.m. PST


Title: Daraxonrasib Monotherapy as First Line Treatment for Patients with Metastatic Pancreatic Adenocarcinoma
Presenter: Eileen O’Reilly, M.D., Memorial Sloan Kettering Cancer Center
Abstract
Number: 		LB337
Session: Late-Breaking Research: Clinical Research 3
Date/Time: April 21; 2:00 p.m. – 5:00 p.m. PST


Title: RAS(ON) Multi-Selective Inhibitors Stimulate the Hydrolysis of RAS-GTP to RAS-GDP and Drive Synergistic Combination Benefit with KRAS(OFF) Inhibitors in G12 Mutant Tumors
Presenter: Kyle Seamon, Ph.D., Revolution Medicines
Abstract
Number: 		5696
Session: Mechanisms of Anticancer Drug Action
Date/Time: April 21; 2:00 p.m. – 5:00 p.m. PST


Collaborator Mini Symposium:

Title: Active RAS Inhibition Intercepts Pancreas Cancer in Mice
Presenter: Ben Stanger, M.D., Ph.D., Penn Pancreatic Cancer Research Center
Abstract
Number: 		LB406
Session: Late-Breaking Research
Date/Time: April 21; 3:50 p.m. – 4:05 p.m. PST


About Revolution Medicines, Inc.
Revolution Medicines is a late-stage clinical oncology company developing novel targeted therapies for patients with RAS-addicted cancers. The company’s R&D pipeline comprises RAS(ON) inhibitors designed to suppress diverse oncogenic variants of RAS proteins. The company’s RAS(ON) inhibitors daraxonrasib (RMC-6236), a RAS(ON) multi-selective inhibitor; elironrasib (RMC-6291), a RAS(ON) G12C-selective inhibitor; zoldonrasib (RMC-9805), a RAS(ON) G12D-selective inhibitor; and RMC-5127, a RAS(ON) G12V-selective inhibitor, are currently in clinical development. Additional development opportunities in the company’s pipeline focus on RAS(ON) mutant-selective inhibitors, including RMC-0708 (Q61H) and RMC-8839 (G13C). For more information, please visit www.revmed.com and follow us on LinkedIn .

Forward-Looking Statements
This press release contains forward-looking statements within the meaning of the U.S. Private Securities Litigation Reform Act of 1995. Any statements in this press release that are not historical facts may be considered “forward-looking statements,” including without limitation statements regarding the company’s development strategy and its ability to build or advance its portfolio and R&D pipeline; progression of clinical studies and findings from these studies, including the tolerability, safety, and potential efficacy of the company’s candidates being studied; and the ability of the company’s RAS(ON) inhibitors to maintain antitumor activity in the setting of emergent resistance.

Forward-looking statements are typically, but not always, identified by the use of words such as “aims,” “anticipate,” "believe," "estimate," "expect," "plan," “potential,” “project,” “up to,” "will" and other similar terminology indicating future results. Such forward-looking statements are subject to substantial risks and uncertainties that could cause the company’s development programs, future results, performance, or achievements to differ materially from those anticipated in the forward-looking statements. Such risks and uncertainties include without limitation risks and uncertainties inherent in the drug development process, including the company’s programs’ development stages, the process of designing and conducting preclinical and clinical trials, the regulatory approval processes, the timing of regulatory filings, the challenges associated with manufacturing drug products, the company’s ability to successfully establish, protect and defend its intellectual property, other matters that could affect the sufficiency of the company’s capital resources to fund operations, reliance on third parties for manufacturing and development efforts, changes in the competitive landscape, and the effects on the company’s business of the global events, such as international conflicts or global pandemics. For a further description of the risks and uncertainties that could cause actual results to differ from those anticipated in these forward-looking statements, as well as risks relating to the business of Revolution Medicines in general, see Revolution Medicines’ Annual Report on Form 10-K filed with the Securities and Exchange Commission (the “SEC”) on February 25, 2026, and its future periodic reports to be filed with the SEC. Except as required by law, Revolution Medicines undertakes no obligation to update any forward-looking statements to reflect new information, events, or circumstances, or to reflect the occurrence of unanticipated events.

Revolution Medicines Media & Investor Contact:
[email protected]
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