RegulationBreakthrough Therapy (United States), Orphan Drug (United States), Orphan Drug (European Union), Commissioner's National Priority Voucher (United States)

Structure/Sequence

Molecular FormulaC44H58N8O5S

InChIKeyFVICRBSEYSHKFY-UHFFFAOYSA-N

CAS Registry2765081-21-6

Clinical Trials associated with Daraxonrasib

NCT07492680

/ Not yet recruitingPhase 2

A Phase 2 Open-Label, Multi-Center Study of BMS-986504 as Monotherapy and in Combination With Other Agents in Participants With Advanced and/or Metastatic Solid Tumors With Homozygous MTAP Deletion

This is an open-label, multicenter Phase 2 study evaluating BMS-986504 in participants with advanced and/or metastatic solid tumors that have MTAP deletion. The study includes a monotherapy component and a combination component in which BMS-986504 is given with other anti-cancer agents. The trial will assess the safety, tolerability, pharmacokinetics, pharmacodynamics, and preliminary anti-tumor activity of BMS-986504 alone and in combination regimens.

Start Date17 Jul 2026

Sponsor / Collaborator

Bristol Myers Squibb Co.

NCT07491445

/ RecruitingPhase 3

RASolute 303: A Phase 3 Global, Multicenter, Open-label, Randomized, 3-Arm Study of Daraxonrasib Monotherapy or Daraxonrasib Plus Gemcitabine and Nab-paclitaxel Versus Gemcitabine and Nab-paclitaxel as a First-Line Treatment for Patients With Metastatic Pancreatic Adenocarcinoma

The purpose of this study is to evaluate the safety and efficacy of an investigational RAS(ON) inhibitor administered as monotherapy or in combination with chemotherapy, compared with standard of care (SOC) chemotherapy alone.

Start Date09 Mar 2026

Sponsor / Collaborator

Revolution Medicines, Inc.

NCT07397338

/ RecruitingPhase 1/2

A Phase 1/2 Open-Label, Multicenter Study of RAS(ON) Inhibitors in Combination With Ivonescimab With or Without Other Anti-Cancer Agents in Patients With Solid Tumors

The purpose of this study is to evaluate the safety, tolerability, pharmacokinetics (PK), and preliminary antitumor activity of RAS(ON) inhibitors in combination with ivonescimab in adults with advanced or metastatic solid tumors with a RAS mutation.

Start Date30 Jan 2026

Sponsor / Collaborator

Revolution Medicines, Inc.

[+1]

100 Clinical Results associated with Daraxonrasib

100 Translational Medicine associated with Daraxonrasib

100 Patents (Medical) associated with Daraxonrasib

Literatures (Medical) associated with Daraxonrasib

01 Jul 2026·PHARMACOLOGICAL RESEARCH

Daraxonrasib (RMC-6236) pharmacokinetics: impact of transporters and drug-metabolizing enzymes on a first-in-class pan-RAS molecular glue

Article

Author: Beijnen, Jos H ; Bui, Viët ; Lebre, M Cristina ; van Tellingen, Olaf ; Tissier, Renaud ; Schinkel, Alfred H ; Arguedas, Davinia ; Law, Tjon ; Rijmers, Jamie

Daraxonrasib (RMC-6236) is an innovative, first-in-class oral pan-RAS inhibitor leveraging a unique molecular glue mechanism to target all RAS protein isoforms. Ongoing phase III clinical trials aim to treat solid tumors harboring RAS mutations, including non-small cell lung cancer (NSCLC), pancreatic ductal adenocarcinoma (PDAC), and colorectal cancer (CRC). KRAS-mutant NSCLC develops brain metastases in 30% of patients. Effective therapies are urgently needed and the blood-brain barrier (BBB) may pose an additional therapeutic hurdle. We assessed how drug efflux transporters expressed at the BBB (ABCB1, ABCG2), drug-metabolizing enzymes (CYP3A, CES1, CES2), and drug uptake transporters (OATP1A/1B) affect the plasma exposure and organ disposition of oral daraxonrasib. In vitro, human ABCB1 transported daraxonrasib. Oral daraxonrasib pharmacokinetics were studied in transporter- and enzyme-deficient mice, and in CYP3A4-humanized mice. Compared to wild-type controls, Abcb1a/1b- and Oatp1a/1b-deficient mice had significantly increased plasma exposure of daraxonrasib (P < 0.01), suggesting that these proteins transport daraxonrasib in vivo. Abcb1a/1b-mediated transport of daraxonrasib across the BBB was validated by oral co-administration of the ABCB1/ABCG2 inhibitor elacridar, resulting in 20-fold increased brain penetration in wild-type mice (P < 0.01). In CYP3A4-humanized Cyp3a^-/- mice, the plasma exposure of daraxonrasib was significantly reduced (>3-fold, P < 0.05). Ces1 and Ces2 deficiency left daraxonrasib pharmacokinetics mostly unchanged. Thus, ABCB1 efflux and OATP1A/1B uptake transporters and human CYP3A4 are important determinants of daraxonrasib pharmacokinetics. ABCB1 function could limit brain penetration and possibly efficacy of daraxonrasib against brain metastases. Collectively, these preclinical findings may help in optimizing the application of daraxonrasib in clinical settings.

01 Jul 2026·CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY

From G12C To pan-RAS: The expanding therapeutic landscape of KRAS-mutant NSCLC

Review

Author: Başbınar, Yasemin ; Canaslan, Kübra ; Öztop, İlhan

KRAS mutations represent the most prevalent oncogenic drivers in non-small cell lung cancer (NSCLC), defining a clinically heterogeneous subset that was historically considered "undruggable." The identification of a mutant-specific allosteric pocket in KRAS G12C led to the development of sotorasib and adagrasib, fundamentally altering the treatment paradigm for pretreated patients. However, modest response durability and the rapid emergence of resistance underscore the limitations of current monotherapies. This review provides a comprehensive synthesis of the expanding therapeutic landscape, moving beyond G12C-selective inhibition toward next-generation allele-specific agents, such as G12D inhibitors, and groundbreaking pan-RAS/RAS(ON) tri-complex inhibitors like RMC-6236. The molecular biology of the KRAS conformational cycle is examined alongside the critical role of co-mutations, specifically STK11, KEAP1, and TP53, which act as gatekeepers of metabolic reprogramming and modulate the tumor immune microenvironment. Furthermore, primary and acquired resistance mechanisms are delineated into on-target pocket alterations and off-target bypass signaling, involving the reactivation of the MAPK and PI3K pathways via RTKs like EGFR and MET. The review also explores the integration of KRAS inhibitors with immune checkpoint blockade, chemotherapy, and SHP2/MEK inhibitors, highlighting a shift toward biology-driven combination strategies. As the field transitions from single-allele blockade to multi-selective RAS(ON) inhibition and rational vertical pathway targeting, personalized, biomarker-guided treatment algorithms will be essential. By outlining the trajectory from G12C to pan-RAS strategies, this review captures the evolving precision oncology framework necessary to achieve durable clinical benefit in KRAS-mutant NSCLC.

09 Jun 2026·PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA

A targeted combination therapy achieves effective pancreatic cancer regression and prevents tumor resistance

Article

Author: Liaki, Vasiliki ; Lechuga, Carmen G ; Barbacid, Mariano ; Acosta-Gallego, Domingo ; Drosten, Matthias ; Guerra, Carmen ; Poli, Valeria ; Sánchez-Bueno, Francisco ; Álvarez, Ruth ; Dusetti, Nelson ; Sun, Pian ; Barrero, Rebeca ; Sainz, Bruno ; Morales-Cacho, Lucía ; Caleiras, Eduardo ; López-Gil, Juan Carlos ; Jiménez-Parrado, Silvia ; Kostopoulou, Myrto ; Barrambana, Sara ; López-García, Alejandra ; Zamorano-Dominguez, Elena ; San Roman, Marta ; Musteanu, Monica ; Rosas-Perez, Blanca

Pancreatic ductal adenocarcinoma (PDAC) has one of the lowest cancer survival rates. Recent studies using RAS inhibitors have opened the door to more efficacious therapies although their beneficial effect is still limited mainly due to the rapid appearance of tumor resistance. Here, we demonstrate that genetic ablation of three independent nodes involved in downstream (RAF1), upstream (EGFR), and orthogonal (STAT3) KRAS signaling pathways leads to complete and permanent regression of orthotopic PDACs induced by Kras / Tp53 mutations. Likewise, a combination of selective inhibitors of KRAS (RMC-6236/daraxonrasib), EGFR family (afatinib), and STAT3 (SD36) induced the complete regression of orthotopic PDAC tumors with no evidence of tumor resistance for over 200 d posttreatment. This combination therapy also led to significant regression of genetically engineered mouse tumors as well as patient-derived tumor xenografts (PDX) in the absence of tumor relapses. Of importance, this combination therapy was well tolerated. In sum, these results should guide the development of new clinical trials that may benefit PDAC patients.

260

News (Medical) associated with Daraxonrasib

06 Jul 2026

·www.biospace.com

Revolution Medicines Presents Phase 1/2 Clinical Data for Zoldonrasib Combination Regimens in Patients with RAS G12D Metastatic Pancreatic Cancer at ESMO Gastrointestinal Cancers Congress 2026

July 02, 2026 -- Revolution Medicines, Inc. (Nasdaq: RVMD), a late-stage clinical oncology company developing targeted therapies for patients with RAS-addicted cancers, today announced results from two Phase 1/2 clinical trials evaluating zoldonrasib, its oral RAS(ON) G12D-selective covalent inhibitor, in combination regimens for patients with RAS G12D metastatic pancreatic ductal adenocarcinoma (PDAC). The results, which will be presented today in a proffered paper session at the 2026 European Society for Medical Oncology (ESMO) Gastrointestinal Cancers Congress, include zoldonrasib in combination with standard of care chemotherapy in previously untreated patients and zoldonrasib in combination with daraxonrasib, the company’s oral RAS(ON) multi-selective inhibitor, in previously treated patients. “The Phase 3 RASolute 302 results provided clinical validation of RAS(ON) inhibition with daraxonrasib in second line metastatic pancreatic cancer and established a strong foundation for evaluating this therapeutic approach across additional RAS genotypes, treatment settings and combination strategies. The results presented at ESMO GI demonstrate compelling proof-of-concept for two zoldonrasib-based regimens in RAS G12D disease: combination with standard of care chemotherapy in previously untreated patients and a RAS(ON) inhibitor doublet with daraxonrasib in previously treated patients. Together, these findings are the foundation of two distinct Phase 3 strategies we are pursuing in previously untreated metastatic RAS G12D pancreatic cancer: the ongoing RASolute 305 trial evaluating zoldonrasib plus standard of care chemotherapy, and the planned RASolute 309 trial evaluating the combination of zoldonrasib plus daraxonrasib,” said Alan Sandler, M.D., chief development officer of Revolution Medicines. RMC-GI-102 (NCT06445062) is an ongoing Phase 1/2 trial evaluating zoldonrasib 1200 mg once daily in combination with investigator's choice of standard of care chemotherapy in patients with previously untreated metastatic RAS G12D PDAC. Investigator's choice of chemotherapy includes modified FOLFIRINOX (mFFX) or gemcitabine plus nab-paclitaxel (GnP). As of the February 8, 2026 data cutoff, the trial enrolled 41 patients in the zoldonrasib plus mFFX arm and 40 patients in the zoldonrasib plus GnP arm. Zoldonrasib demonstrated a manageable safety and tolerability pro combination with standard chemotherapy. The safety pro zoldonrasib in combination with chemotherapy was broadly consistent with the established profiles of each respective chemotherapy regimen. Grade 3 or greater treatment-related adverse events (TRAEs) occurred in 61% of patients who received the zoldonrasib plus mFFX and 80% of patients who received zoldonrasib plus GnP. The most common Grade 3 or greater TRAEs with zoldonrasib plus mFFX were decreased neutrophil count (37%), anemia (12%), and platelet count decreased (7%). The most common Grade 3 or greater TRAEs with zoldonrasib plus GnP were decreased neutrophil count (35%), anemia (28%), and fatigue (25%). No Grade 5 TRAEs were reported in either arm. The mean dose intensity was 86% with zoldonrasib plus mFFX and 90% with the zoldonrasib plus GnP. In the trial, zoldonrasib with chemotherapy showed compelling antitumor activity, with an objective response rate (ORR) of 82% (95% confidence interval [CI]: 60, 95) and disease control rate (DCR) of 96% (95% CI: 77, 100) in the mFFX population, and an ORR of 61% (95% CI: 42, 78) and DCR of 90% (95% CI: 74, 98) in the GnP population. These preliminary safety and clinical activity data support the ongoing RASolute 305 pivotal trial (NCT07621718), a global, randomized, double-blind placebo-controlled Phase 3 clinical trial evaluating zoldonrasib plus investigator’s choice of standard of care chemotherapy compared with placebo plus investigator’s choice of chemotherapy in patients with previously untreated metastatic RAS G12D PDAC. RMC-9805-001 (NCT06040541) is a Phase 1 trial evaluating zoldonrasib 1200 mg once daily plus daraxonrasib 300 mg once daily in advanced solid tumors with RAS G12D mutations. As of the February 9, 2026 data cutoff, 60 patients with RAS G12D metastatic PDAC who had previously received one or more prior lines of therapy were treated with the combination. Zoldonrasib plus daraxonrasib demonstrated a manageable safety and tolerability pro was broadly consistent with the established pro daraxonrasib monotherapy. Grade 3 or greater TRAEs occurred in 35% of patients who received the combination. Among TRAEs occurring in 10% or more of all patients, the most common Grade 3 or greater events were rash (12%), anemia (10%), and stomatitis/mucositis (7%). Few patients discontinued due to TRAES; 2% discontinued zoldonrasib and 5% discontinued daraxonrasib. The mean dose intensity was 88% for zoldonrasib and 76% for daraxonrasib. The zoldonrasib plus daraxonrasib combination demonstrated compelling antitumor activity in patients with previously treated metastatic PDAC. In the second line cohort (2L) (N=30), the ORR was 50% (95% CI: 31–69) and DCR was 97% (95% CI: 83–100). Median progression-free survival (PFS) in the 2L cohort was 9.6 months (95% CI: 7.1–NE), with a 6-month PFS rate of 71%. Median overall survival (OS) in the 2L cohort was not yet estimable, with a 6-month OS rate of 89%. In the third line and beyond (3L+) cohort (N=30), the ORR was 47% (95% CI: 28–66) and DCR was 90% (95% CI: 74–98). Median PFS in the 3L+ cohort was 7.6 months (95% CI: 4.6–10.5), with a 6-month PFS rate of 59%. Median OS in the 3L+ cohort was 10.5 months (95% CI: 6.7–NE), with a 6-month OS rate of 82%. These safety and clinical activity data support the planned pivotal global, Phase 3 RASolute 309 clinical trial of zoldonrasib plus daraxonrasib versus GnP in patients with previously untreated RAS G12D metastatic PDAC. Pancreatic cancer is one of the most lethal malignancies, characterized by its typically late-stage diagnosis, resistance to standard chemotherapy, and high mortality rate. Pancreatic ductal adenocarcinoma, or PDAC, is the most common form of pancreatic cancer. Due to the lack of early symptoms and effective detection methods, approximately 80% of patients are diagnosed with advanced or metastatic disease. PDAC is the most commonly RAS-driven malignancy of all major cancers, with more than 90% of patients having tumors that harbor RAS mutations.1 RAS G12D is the most prevalent RAS mutation subtype in PDAC, occurring in 40% of patients, and has been associated with poorer outcomes than RAS wild-type disease and certain other RAS-mutant subgroups.1-4 Zoldonrasib is an investigational, oral RAS(ON) G12D-selective covalent tri-complex inhibitor. RAS G12D is the most prevalent RAS mutation, accounting for 29% of all RAS cancers.1 Across tumor types, approximately 61,000 new patients with RAS G12D cancers are estimated each year in the U.S., and no targeted therapy is currently approved for these patients.5 Zoldonrasib is currently being evaluated as a monotherapy and in combination with other therapies, including with Revolution Medicines’ RAS(ON) multi-selective inhibitor daraxonrasib (RMC-6236), as well as standard of care regimens in lung and gastrointestinal cancers. Daraxonrasib is an investigational, oral RAS(ON) multi-selective, non-covalent tri-complex inhibitor. The U.S. Food and Drug Administration (FDA) granted daraxonrasib Breakthrough Therapy Designation and Orphan Drug Designation for the treatment of patients with previously treated metastatic pancreatic ductal adenocarcinoma (PDAC) harboring G12 mutations. In addition, daraxonrasib was selected for the FDA Commissioner’s National Priority Voucher pilot program, which is intended to accelerate the development and review of therapies aligned with U.S. national health priorities. Daraxonrasib is designed to target cancers driven by a broad range of common RAS genotypes, including PDAC, non-small cell lung cancer (NSCLC), and colorectal cancer. Daraxonrasib is being advanced through a global Phase 3 registrational program comprising four trials, including the completed RASolute 302 trial and three additional trials in patients with PDAC and metastatic RAS mutant NSCLC. 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). References 1 Lee JK, Sivakumar S, Schrock AB, et al. Comprehensive pan-cancer genomic landscape of KRAS altered cancers and real-world outcomes in solid tumors. NPJ Precis Oncol. 2022;6(1);91. doi:10.1038/s41698-022-00334-z 2 Yousef, A., Yousef, M., Chowdhury, S. et al. Impact of KRAS mutations and co-mutations on clinical outcomes in pancreatic ductal adenocarcinoma. NPJ Precis Oncol. 2024;8:27. 3 Qian ZR, Rubinson DA, Nowak JA, et al. Association of Alterations in Main Driver Genes With Outcomes of Patients With Resected Pancreatic Ductal Adenocarcinoma. JAMA Oncol. 2018;4(3):e173420. doi:10.1001/jamaoncol.2017.3420 4 Norton C, Shaw MS, Rubnitz Z, et al. KRAS Mutation Status and Treatment Outcomes in Patients With Metastatic Pancreatic Adenocarcinoma. JAMA Netw Open. 2025;8(1):e2453588. doi:10.1001/jamanetworkopen.2024.53588 5 Estimated using tumor mutation frequencies from Foundation Medicine Insights March 2022 and scaled to estimated patient numbers using cancer incidence from ACS Cancer Facts and Figures 2023. The content above comes from the network. if any infringement, please contact us to modify.

29 Jun 2026

·www.prnewswire.com

At a Turning Point for RAS-directed Therapies, Break Through Cancer and the Lustgarten Foundation Launch New Pancreatic Cancer Initiative

Backed by a $16M investment, this collaborative effort will help define the next generation of combination therapy strategies for pancreatic cancer CAMBRIDGE, Mass., June 29, 2026 /PRNewswire/ -- At a pivotal moment for pancreatic cancer, Break Through Cancer and the Lustgarten Foundation today, with support from the Cinelli Family Foundation, announced a $16 million investment in the Conquering KRAS for Patients with Pancreatic Cancer TeamLab. Spanning six world-class cancer research institutions, this initiative aims to improve outcomes for one of the deadliest cancers by focusing on KRAS, a gene that is mutated in more than 90% of pancreatic cancer cases. Continue Reading New initiative builds on one of the most deeply profiled pancreatic cancer studies to accelerate future therapies. Post this Break Through Cancer and the Lustgarten Foundation, with support from the Cinelli Family Foundation, are partnering to accelerate the next generation of pancreatic cancer therapies. The initiative comes amid a sea of change in the field. After decades in which oncogenic RAS proteins were considered 'undruggable' a new generation of RAS-directed therapies is showing promise and delivering encouraging results for patients with pancreatic cancer. Yet, while these advances offer invaluable hope for patients and their families, important questions remain about how pancreatic tumors respond to RAS-directed therapy and how future treatment strategies may achieve more durable benefit. Through a first-of-its-kind correlative research study launched in 2024, researchers in the original Conquering KRAS in Pancreatic Cancer TeamLab have already assembled an unprecedented collection of patient tumor and blood samples that may help answer those questions. Building on years of progress, the new initiative will support this multi-disciplinary team of scientists and clinicians from six world-class cancer research institutions including Dana-Farber Cancer Institute, Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Memorial Sloan Kettering Cancer Center, MIT's Koch Institute for Integrative Cancer Research, The University of Texas MD Anderson Cancer Center, and NYU Langone Health Perlmutter Cancer Center, to tackle these challenges through an integrated program of translational science and clinical research. "Recent advances in RAS-targeted therapies have opened a new chapter in pancreatic cancer research" said Tyler Jacks, PhD, president of Break Through Cancer and renowned pancreatic cancer researcher. "This initiative is focused on what comes next – understanding how these therapies work in patients, the nature of primary and acquired resistance, and how we can develop treatment strategies that build upon the improvements of RAS-directed therapy alone." The new funding will support two complementary efforts. First, researchers will continue and build on the research emerging from the first-of-its-kind clinical correlative study launched in 2024 through the Conquering KRAS in Pancreatic Cancer TeamLab which collected tumor and blood samples before, during, and after treatment with Revolution Medicine's daraxonrasib – an investigational novel multi-selective RAS(ON) inhibitor that recently made headlines following phase 3 trial results in patients with previously treated metastatic pancreatic cancer. Researchers now have the unprecedented opportunity to analyze these samples and create one of the most comprehensive pictures to date of how pancreatic cancers respond and adapt to RAS-directed therapy. Insights from this work will help identify biomarkers of response, uncover mechanisms of resistance and adaptation, and inform combination therapy strategies. Second, researchers will establish a clinical study to evaluate next-generation treatment strategies informed by those discoveries. The TeamLab will explore combination therapies designed to enhance the benefit of KRAS-directed treatments, bringing together expertise in cancer biology, immunology, computational science, and patient care. The effort builds upon the unique model of radical collaboration that defines Break Through Cancer, connecting researchers across leading cancer centers to share data, expertise, technologies, and patient insights in real-time. This approach is synergistic with Lustgarten's impact-driven research strategy, fueling bold science that deepens our understanding of pancreatic cancer and improves treatment outcomes. "Pancreatic cancer research is entering a new era of possibility, and we must invest in the kind of collaborative science that transforms promising advances into meaningful progress for patients," said Linda Tantawi, CEO of the Lustgarten Foundation. "We are incredibly excited to support the next phase of the Conquering KRAS for Patients with Pancreatic Cancer TeamLab, uniting leading experts across institutions and disciplines to build on the momentum of recent discoveries. By accelerating collaboration and innovation, this initiative will answer critical questions, unlock new opportunities, and drive breakthroughs that shape the future of pancreatic cancer treatment." The initiative reflects a shared commitment by Break Through Cancer, the Lustgarten Foundation, and the Cinelli Family Foundation to accelerate progress against pancreatic cancer by investing in collaborative science capable of moving discoveries from the laboratory to patients more quickly. As RAS-directed therapies continue to advance, researchers believe the greatest opportunity may lie not in any single treatment, but in understanding how to deploy these therapies in combinations with other approaches to achieve lasting benefit. About Break Through Cancer Founded in 2021, Break Through Cancer empowers outstanding researchers and physicians to both intercept and find cures for several of the deadliest cancers by stimulating radical collaboration among outstanding cancer research institutions, including its founding partners: Dana-Farber Cancer Institute, Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Memorial Sloan Kettering Cancer Center, MIT's Koch Institute for Integrative Cancer Research, and The University of Texas MD Anderson Cancer Center. The Foundation is supported by a Board of Directors from the five partner institutions and a Scientific Advisory Board of U.S. cancer experts. The Foundation was launched with an extraordinary challenge pledge of $250 million from Mr. and Mrs. William H. Goodwin, Jr. and their family, and the estate of William Hunter Goodwin III. For further information, please visit the Foundation's website at . About The Lustgarten Foundation The Lustgarten Foundation is the largest private funder of pancreatic cancer research in the world, funding preeminent pancreatic cancer research, driving the pursuit of bold and innovative science toward earlier detection and better treatments, and transforming pancreatic cancer into a curable disease. The Foundation funds research where creative risks yield high rewards to accelerate and expand life-saving treatment options. We believe time is everything to patients and their families, and that community is power. Lustgarten programs and events provide people affected by pancreatic cancer a voice and a place to create hope, together. For more information about the Lustgarten Foundation, visit lustgarten.org and follow us on Facebook , Instagram, Bluesky, LinkedIn, and YouTube . About The Cinelli Family Foundation The Cinelli Family Foundation (CFF) was established in 2021 to honor the dreams of Al and Sharon Cinelli. Inspired by the transformative power of education and shaped by cancers that impacted the Cinelli family, the Foundation invests in two areas where progress is both urgent and possible: accelerating breakthroughs in blood, breast, and pancreatic cancer prevention and treatment, and supporting education research, innovative programs, and technologies to help reimagine educational ecosystems and radically improve learning outcomes. Based in Lawrence, Kansas, CFF is a national funder driven by the belief that science and learning are among the most powerful forces for human progress. For more information, visit . Media Contact: Soracha Ward [email protected] SOURCE Break Through Cancer 21% more press release views with Request a Demo

Phase 3

26 Jun 2026

·www.biopharmadive.com

FDA accepts Replimune filing; Merck KGaA drops $11B on life sciences services

Today, a brief rundown of news involving Replimune, Revolution Medicines and Merck KGaA, as well as updates from Eli Lilly, Otsuka Pharmaceutical and Definium Therapeutics that you may have missed.On Friday, Replimune said that the Food and Drug Administration has accepted the resubmission for its cancer drug RP1, with a decision expected by Aug. 2 and an advisory committee set to convene in July to discuss the twice-rejected application. The latest move is another signal of the changing attitude of the FDA, which was accused of moving the goal post or providing conflicting feedback to companies, leading to delayed or rejected applications under the now-exited leaders Marty Makary and Vinay Prasad. Multiple other companies that faced hurdles under the prior leadership are now gaining new chances for their applications. Delilah AlvaradoRevolution Medicine outlined data from Phase 2 trials of its second RAS-blocking cancer drug, zoldonrasib, showing it can shrink or eliminate tumors in pancreatic cancer patients when combined with chemotherapy or Revolutions lead drug, daraxonrasib. In the chemo-combo trial, 82% of enrollees with RAS-mutated disease who got zoldonrasib and one type of chemotherapy regimen as a first-line treatment responded, as did 61% who got the experimental drug plus another type of chemo. In the trial that combined the two Revolution drugs in a second- or third-line setting in RAS-mutated enrollees, 50% of patients in the second-line setting and 47% in the third-line setting saw their tumors shrink or disappear. The data are scheduled for presentation at the European Society of Medical Oncology Gastrointestinal Cancers meeting next week. Revolution just began dosing patients in a Phase 3 trial with the chemo combination, and is planning to begin a daraxonrasib-zoldonrasib Phase 3 trial later this year. Jonathan GardnerGermany-based Merck KGaA is spending more than $11 billion to acquire Bio-Techne, a U.S. life-sciences analytics and diagnostics provider, the companies said Thursday. Per deal terms, German Merck will pay $73 per share in cash, a 36% premium to Bio-Technes average price over the past month. Merck KGaA executives stated the transaction will help build the companys life science business that serves drugmakers with materials and manufacturing by adding protein analysis, biomarker discovery and diagnostics capabilities. The deal is expected to close later this year, pending regulatory and shareholder approval, and Merck KGaA will finance it with a combination of cash on hand and new debt. Jonathan GardnerPsychedelic drug developer Definium Therapeutics is issuing $805 million worth of stock, proceeds from which will go toward research and development of its pipeline, and potential commercialization of its candidate DT120 against major depression. The public offering closing announced Thursday comes just a few days after the company unveiled positive late-stage results of DT120, an LSD-based oral drug. The company is still awaiting data from a second pivotal trial. Delilah AlvaradoEli Lilly is widening a research collaboration with China-based Abbisko, paying an undisclosed upfront fee and pledging up to $1.9 billion in potential payouts based on achievement of development and commercial milestones for drugs developed under the agreement, Abbisko said Tuesday. The two companies will work on multiple targets, advancing novel drug candidates with global potential, growing from work from a deal signed in 2022 on discovery, development, and potential commercialization of a novel small-molecule therapeutic. Abbisko has established deals with multiple drugmakers, including Merck KGaA and AstraZeneca, with the former company seeking FDA approval for a medicine called pimicotinib thats part of their deal. Jonathan GardnerOtsuka Pharmaceuticals experimental drug met its primary endpoint in a late-stage trial of adults with ADHD and comorbid anxiety, showcasing statistically significant and clinically relevant improvements when compared to placebo, the company said Thursday. Compared to placebo, centanafadine a norepinephrine, dopamine, and serotonin reuptake inhibitor had improved ADHD after eight weeks, as measured by a rating scale. The Phase 3b trial enrolled 315 adults. The experimental therapy is currently under regulatory review in the U.S. as a treatment for ADHD in children and adults, with a decision target of July 24. Delilah Alvarado '

Phase 3Phase 2AcquisitionClinical Trial FailureLicense out/in

100 Deals associated with Daraxonrasib

R&D Status

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Pancreatic adenocarcinoma metastatic	Phase 3	United States	Revolution Medicines, Inc.	09 Mar 2026
Pancreatic adenocarcinoma metastatic	Phase 3	Japan	Revolution Medicines, Inc.	09 Mar 2026
Pancreatic Ductal Adenocarcinoma	Phase 3	Japan	Revolution Medicines, Inc.	15 Dec 2025
Pancreatic Ductal Adenocarcinoma	Phase 3	France	Revolution Medicines, Inc.	15 Dec 2025
Pancreatic Ductal Adenocarcinoma	Phase 3	Italy	Revolution Medicines, Inc.	15 Dec 2025
Pancreatic Ductal Adenocarcinoma	Phase 3	Spain	Revolution Medicines, Inc.	15 Dec 2025
Pancreatic Ductal Adenocarcinoma	Phase 3	United Kingdom	Revolution Medicines, Inc.	15 Dec 2025
RAS Mutation Non-Small Cell Lung Cancer	Phase 3	United States	Revolution Medicines, Inc.	06 May 2025
RAS Mutation Non-Small Cell Lung Cancer	Phase 3	Japan	Revolution Medicines, Inc.	06 May 2025
RAS Mutation Non-Small Cell Lung Cancer	Phase 3	Australia	Revolution Medicines, Inc.	06 May 2025

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT06625320 (RASolute 302, Pubmed \| N Engl J Med)	Phase 3	Metastatic Pancreatic Ductal Adenocarcinoma RAS G12 mutations	500	Daraxonrasib	lyxmowhvxq(wvdvdsryty) = unrllxkjke iqvdoygupa (kzdpodinrp ) View more	Positive	31 May 2026
				Chemotherapy	lyxmowhvxq(wvdvdsryty) = vpzlzysgmf iqvdoygupa (kzdpodinrp ) View more
NCT06625320 (RASolute 302, ASCO2026)	Phase 3	Pancreatic adenocarcinoma metastatic Second line RAS G12 \| RAS G13 \| Q61	500	Daraxonrasib 300 mg PO QD	vkxonsneez(pwidktnzcr) = djwfcyfngd hlpxyuuofa (nvwtlmxyak, 10.0–NE) View more	Positive	29 May 2026
				Investigator’s choice of SOC cytotoxic chemo	vkxonsneez(pwidktnzcr) = bzxtaydjtg hlpxyuuofa (nvwtlmxyak, 5.4–8.2) View more
NCT05379985 (RMC-6236-001, NEWS 1 \| NEWS 2 \| NEWS 3 \| Literature) Manual	Phase 1/2	KRAS mutant pancreatic ductal adenocarcinoma RAS mutations	168	Daraxonrasib (RAS-mutated Pancreatic Ductal Adenocarcinoma)	eluijyduoi(mhwuljduxd) = ktwbvhsnlg miiqrloorn (jedwzmosio ) View more	Positive	14 May 2026
				Daraxonrasib (RAS G12 mutations)	inkmszkekw(kieonsiuqr) = swpwpiichr axbgvttfpu (etrcblwtcp, 17 - 56) View more
NCT05379985 (AACR2026)	Phase 1/2	Pancreatic adenocarcinoma metastatic First line RAS mutations	40	Daraxonrasib 300 mg QD	wqbyurkomc(xfvcgobtud) = bdodytiqmh diuvapjrul (gogvwvbgbz, 79 - 98) View more	Positive	21 Apr 2026
NCT06881784 (RASolve 301, AACR2026)	Phase 3	RAS mutation	420	Daraxonrasib	ceeqxscgxw(wjflunqdpr) = iaitnvwqqo hozankgmaj (spwlpjranl, 6 - 12.3) View more	Positive	21 Apr 2026
				Docetaxel	qkwcsysnvu(jgqtlyjjat) = tsljkszozr zhresajnsg (lvribwhiha, 8.1 - 10.8) View more
NCT06445062 (AACR2026)	Phase 1/2	Pancreatic adenocarcinoma metastatic First line RAS mutations	40	Daraxonrasib + gemcitabine/nab-paclitaxel (GnP)	ocygzzjumw(rhvfppvlzq) = zenghwezbe ncumewpmqo (kqygfjaxxj, 76 - 97) View more	Positive	21 Apr 2026
				Daraxonrasib + gemcitabine/nab-paclitaxel (GnP) (Pts with measurable disease at baseline and either had ≥ 1 post-baseline tumor assessment or had clinical progression or death prior to such assessment.)	ocygzzjumw(rhvfppvlzq) = azgrhgrzuh ncumewpmqo (kqygfjaxxj, 79 - 98) View more
NCT06625320 (RASolute 302, Company_Website)	Phase 3	Metastatic Pancreatic Ductal Adenocarcinoma Second line	500	Daraxonrasib 300 mg	ucvtrvwzit(covylwopuu) = yoknqmzcyw onbcxgiuvc (luqnwythdr ) View more	Positive	13 Apr 2026
				Chemotherapy	ucvtrvwzit(covylwopuu) = yjuijzancp onbcxgiuvc (luqnwythdr ) View more
Company_Website Manual	Phase 1	Pancreatic Ductal Adenocarcinoma First line RAS-mutant	40	Daraxonrasib	jwsxmvranz(meaopkvahi) = xchurwdwtx cjijdmjcdx (smzpdheect ) View more	Positive	10 Sep 2025
Company_Website Manual	Phase 1	Pancreatic Ductal Adenocarcinoma Second line RAS G12X mutation \| RAS mutation	83	Daraxonrasib 300 mg	pcsinwtybi(gmpjeemppu) = acrmpjspzb ejvdigmwlo (vunlxzfiiw )	Positive	10 Sep 2025
				Daraxonrasib 300 mg (RAS G12X mutation)	pcsinwtybi(gmpjeemppu) = htnwgpbbwk ejvdigmwlo (vunlxzfiiw ) View more
Company_Website Manual	Phase 1	Pancreatic Ductal Adenocarcinoma First line RAS mutations	40	Daraxonrasib + Gemcitabine + nab-Paclitaxel	wqbfivupnt(rloyhagydg) = lubzhyipgr gxeuuvuhas (lcicxntcgf ) View more	Positive	10 Sep 2025

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