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.

开始日期2026-07-17

申办/合作机构

Bristol Myers Squibb Co.

NCT07491445

/ Recruiting临床3期

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.

开始日期2026-03-09

申办/合作机构

Revolution Medicines, Inc.

NCT07397338

/ Recruiting临床1/2期

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.

开始日期2026-01-30

申办/合作机构

Revolution Medicines, Inc.

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100 项与达拉西布相关的临床结果

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100 项与达拉西布相关的转化医学

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100 项与达拉西布相关的专利（医药）

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项与达拉西布相关的文献（医药）

2026-04-01·CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY

From G12C To Pan-RAS: The Expanding Therapeutic Landscape of KRAS-Mutant NSCLC

Review

作者: 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.

2026-04-01·CANCER CELL

Anticancer activity of RAS-GTP inhibition in cholangiocarcinoma

Article

作者: Cueto-Ureña, Cristina ; Sin-Coscujuela, Daniel ; Banales, Jesus M ; Tian, Tian V ; Senent, Yaiza ; Kim, Alyssa ; Morali, Konstantina ; Entrialgo-Cadierno, Rodrigo ; Guruceaga, Elisabeth ; Pechuan-Jorge, Ximo ; Herranz, Jose M ; Herzberg, Benjamin O ; Garcia, Alia V ; Ponz-Sarvise, Mariano ; Yañez-Bartolome, Mariana ; Feliu, Iker ; Macaya, Irati ; Jiang, Jingjing ; Singh, Mallika ; Vicent, Silve ; Lopez, Ines ; Raghulan, Rashi ; Aronchik, Ida ; Hegde, Aparna ; Vaquero, Javier ; Macarulla, Teresa ; Evans, James W ; Wang, Yingyun ; Azad, Nilofer ; Schumpp, Alyssa

About 25% of cholangiocarcinoma (CCA) tumors harbor KRAS mutations. Here, we investigated the activity of RAS(ON) multi-selective inhibitors, which target the active, GTP-bound state of mutant and wild-type variants of canonical RAS isoforms, in preclinical models and in patients with KRAS mutant CCA. RAS(ON) multi-selective inhibitors yield strong anticancer responses in cell- and patient-derived xenografts and immunocompetent allograft models. Consistent with these preclinical findings, we describe clinical activity of the RAS(ON) multi-selective inhibitor daraxonrasib in two patients with advanced KRAS G12 CCA. RAS-GTP inhibition also potentiates the activity of current standard-of-care CCA regimens to prolong survival in cell-derived human xenografts and mouse allografts. Furthermore, we demonstrate that intrinsic and acquired resistance to RAS(ON) multi-selective inhibitors mainly rely on mechanisms that drive RAS signaling overactivation. Overall, our findings indicate that KRAS mutant CCA is addicted to RAS signaling for proliferation and support the potential clinical evaluation of RAS-GTP inhibition in CCA.

2026-04-01·CLINICAL CANCER RESEARCH

RRAS and RRAS2 Mutations Are Recurrent Oncogenic Drivers in Lung Cancer and Are Sensitive to the Pan-RAS Inhibitor RMC-6236

Article

作者: Febres-Aldana, Christopher A. ; Lai, Rachel ; Gazzo, Andrea ; Gili, Leo ; Master, Rohan P. ; Gomez Marti, Juan Luis ; Mattar, Marissa S. ; Ladanyi, Marc ; Zhang, Tom ; Dix, Jenna-Marie ; Arbour, Kathryn C. ; Yang, Soo-Ryum ; Khodos, Inna ; Pfeil, Alexander J. ; Cheng, Ryan ; Somwar, Romel ; de Stanchina, Elisa

Abstract:

Purpose::

RRAS and RRAS2 encode a subfamily of RAS-like small GTPases that share considerable structural and functional similarities with KRAS, HRAS, and NRAS. Whether homologous RRAS/RRAS2 mutations are oncogenic and actionable drivers in lung cancer remains underexplored.

Experimental Design::

An institutional cohort of 8,488 non–small cell lung carcinomas (NSCLC) sequenced by comprehensive targeted DNA sequencing (MSK-IMPACT) between 2016 and 2024 was evaluated for RRAS/RRAS2 mutations. RRASQ87L or RRAS2Q72L were modeled in murine IL3-dependent Ba/F3 cells and immortalized human bronchiolar epithelial cells (HBEC). The oncogenic potential, signaling characteristics, and sensitivity to MAPK pathway inhibitors, including the novel pan-RAS inhibitor RMC-6236, were evaluated in vitro and in vivo.

Results::

RRAS Q87L or RRAS2Q72L, homologous to KRAS-codon Q61 substitutions, were found in ∼0.45% of NSCLCs (38/8,488), with all but two lacking other MAPK pathway oncogenic drivers. RRASQ87L and RRAS2Q72L mutations transformed Ba/F3 cells and HBECs and robustly activated MAPK and PI3K–mTOR pathway signaling. RMC-6236 suppressed proliferation of RRASQ87L- and RRAS2Q72L-mutant cell lines, reduced ERK phosphorylation, induced apoptosis, and impeded cell-cycle progression. In vivo, RMC-6236 significantly inhibited growth of RRASQ87L/RRAS2Q72L-mutant HBEC-derived xenografts.

Conclusions::

RRASQ87L and RRAS2Q72L are recurrent, oncogenic, and potentially actionable drivers in NSCLC. Our study supports the inclusion of RRAS/RRAS2 into routine molecular diagnostic panels for precision oncology and provides preclinical rationale for investigating the potential therapeutic utility of pan-RAS inhibitors for patients with RRASQ87L/RRAS2Q72L-mutant lung cancers.

900

项与达拉西布相关的新闻（医药）

2026-05-12

·证券之星

“癌王”生存期翻倍！RevMed“神药”是泡沫还是未来？

（原标题：“癌王”生存期翻倍！RevMed“神药”是泡沫还是未来？）作者 | 黄绎达编辑 | 张帆知名Biotech企业Revolution Medicines（股票代码：RVMD；以下简称：RevMed）近期股价连续冲高，抢眼表现引发投资者高度关注。今年1月，公司股价也出现过一轮快速拉升，1月2日~15日的区间涨幅高达55%。图：Revolution Medicines股价走势；资料来源：wind，36氪作为一家专注于针对携带RAS突变肿瘤靶向药物的创新药企业，其核心管线主要针对有着“癌症之王“之称的，公司现阶段虽暂无药品获批上市，但核心产品Daraxonrasib是全球泛RAS分子胶领域的明星潜力品种。对于尚未兑现业绩的Biotech企业而言，短期股价大幅波动虽属行业常态，但行情的异动往往是由核心事件驱动。那么，驱动RevMed股价近期暴涨的核心因素都有哪些？后续投资RevMed又有哪些关键看点？临床数据驱动股价涨跌之所以被称为“癌症之王”，核心原因在于的生存率长期极低、预后极差。公开资料显示，2022年全球的新发病例数与在所有恶心肿瘤中分别排名第12，死亡病例则排名第6；另有统计数据显示，全球患者的5年生存率中位数仅6.2%，在全部恶性肿瘤中处于最低水平。图：2022年全球主要恶性肿瘤新发病例数与死亡病例数；资料来源：GCO，36氪死亡率居高不下，主要源于以下三大因素：1.胰腺的解刨位置相对隐蔽，早期肿瘤体积微小，缺乏典型的临床表现，容易发生漏诊、误诊；而且早期症状不明显，常被当成身体不适而被忽略，因此多数患者确诊时，已经发展至中晚期；2.的恶性程度通常较高、临床治疗难度大，主要表现为侵袭性强，易发生早期转移，导致手术的窗口期非常短，而且术后的复发率偏高；3.治疗手段长期存在局限，目前的一线治疗方案依然是标准化疗，但疗效有限不说，还容易耐药；过去数十年针对的靶向药长期缺失，相关药品的研发进展缓慢，难以满足中晚期患者的治疗需求；正是由于普遍确诊偏晚期，加之可选的临床治疗有限，患者的用药周期普遍较短，这也是当前抗药物市场规模偏小的核心原因。公开资料显示，2025年全球药物市场规模约30亿美元水平。未来，随着相关靶向新药、创新疗法的临床普及，全球药物市场将迎来一轮快速扩容，到2035年有望超过120亿美元。从本轮RevMed股价暴涨的节奏来看，刺激公司股价短期内暴涨的核心驱动因素，是公司在13日当天公布了核心产品Daraxonrasib用于二线治疗转移性胰腺导管腺癌（PDAC）的RASolute 302临床试验III期顶线结果积极。正是基于的诊疗现状，该结果显著提振抗药物市场的整体预期，推动公司股价当日股价大涨41%，创近年来单日最大涨幅记录。图：Revolution Medicines当前研发管线；资料来源：公司官网，36氪从Daraxonrasib的临床数据来看，4月13日公布的RASolute 302关键临床数据显示：Daraxonrasib组中位OS为13.2个月，化疗组为6.7个月，风险比（HR）0.40（p<0.0001）；相较化疗组，Daraxonrasib组在PFS方面同样取得了统计学显著的改善；安全性方面，Daraxonrasib总体耐受性良好、安全性可控、未出现新的安全性信号。从上述数据可知，与对照组（化疗）相比，Daraxonrasib组在该试验的两个主要终点，无进展生存期（PFS）与总生存期（OS），均取得了统计学显著且具有明确临床意义的改善。简言之，Daraxonrasib既能够有效显著延长患者的生存时间，也能显著延缓疾病进展、改善患者生活质量。在颇为严峻的诊疗现状下，Daraxonrasib临床试验取得的积极结果就具备了重要的现实意义：不仅为中晚期患者提供了全新的诊疗方案，同时也为抗药物的研发提供了重要参考。正是基于以上原因，资本市场对Daraxonrasib潜在的临床价值给予了充分认可，由此在短时间内大幅推升了企业估值。而且，公司表示上述总生存期与无进展生存期终点数据将作为最终数据，提交至全球监管机构申请新药上市。综合目前的临床数据，Daraxonrasib获批上市的概率极高，这也是资本市场给予公司高估值溢价的另一核心因素。4月21日，RevMed在美国癌症研究协会AACR的年会上，公布了Daraxonrasib一线治疗转移性的1/2期临床试验的更新数据。本次更新数据涵盖单药和联合化疗两种方案，由于总生存期和无进展生存期这两个主要终点数据未熟，本次数据更新重点披露了短期疾病控制及安全性相关的研究结果。根据此次更新数据得出的结论之一：Daraxonrasib在短期疾病控制方面表现优异。其中，单药方案的客观缓解率（ORR）为47%，疾病控制率（DCR）高达92%，6个月无进展生存率为71%，6个月生存率为83%；联合化疗的方案表现更加突出，对应的客观缓解率为58%，6个月的无进展生存率、6个月生存率则分别为84%和90%。目前，针对的标准化疗方案疗效十分有限，客观缓解率大约在20~40%区间，6个月无进展生存率在40~50%区间。由此可见，Daraxonrasib无论是单药还是联用方案，在疾病控制、短期生存获益方面，都明显突破现有疗法的疗效天花板，有望重塑的一线临床治疗格局，并凭借暂时无可替代的临床价值充分发挥先发优势，为其商业化潜力的释放提供稳定的支撑。然而，根据此次更新数据得出的结论之二：Daraxonrasib在安全性方面存在一定瑕疵，主要表现为≥3级不良事件的比例偏高。其中，单药方案≥3级不良事件的占比为38%，主要是皮疹、腹泻、口腔炎等；联用方案≥3级不良事件的占比为71%，主要是贫血、中性粒细胞计数减少、疲劳等。当前数据显示，Daraxonrasib的不良事件主要集中在皮肤毒性、消化道反应和血液毒性这三大方面，而且血液毒性主要是叠加化疗所致。所以，从各不良事件的比例来看，该药物安全性虽存在一定瑕疵，但整体风险可控且处于临床可接受范围，且没有肺炎、肝衰竭、消化道穿孔、心衰等靶向药常见的黑框风险。据此预计目前的安全瑕疵不会阻碍该药品后续的审评审批进程，但仍需关注3期临床试验的长期安全性数据。基于上述事件来复盘RevMed近期的股价表现，临床数据依旧是拉动行情的核心驱动因素。在4月13日公布Daraxonrasib三期临床顶线数据后，股价连涨三天，并不断创新高；随后的三个交易日维持高位震荡，且在4月16日盘中刷新历史峰值，反映了市场对其高估值的审慎消化。4月21日的日内涨幅不足2%，反映出尽管一线治疗更新数据疗效亮眼，但安全性存在的瑕疵，在一定程度上影响商业化预期，叠加前期估值高位，多空因素交织，股价上涨的动能随之走弱；4月22日~23日，资金获利了结主导，股价累计回撤近10%；进入5月后，虽有部分临床数据披露，但总体上为补充佐证性质，公司股价暂无大的幅波动，整体进入震荡调整阶段。年初并购凸显管线价值尽管公司当前股价较4月16日的历史高点有所回落，但总市值仍高达306亿美元（5月11日），折合人民币约2083亿元。这对于一家尚未实现盈利、核心产品仍处于临床阶段的创新药企而言，如此高的估值水平，充分反映出资本市场对公司核心研发管线的临床价值与未来商业化潜力的高度认可。2026年初，默沙东就收购RevMed曾展开谈判，据外媒消息，默沙东给出的整体收购价格区间在280~320亿美元，而公司年初时的总市值仅约150亿美元。尽管收购报价已存在明显溢价，但双方最终未能就交易对价达成一致，收购谈判于1月下旬宣告终止。在收购传闻发酵期间，公司总市值从1月初的150亿美元快速攀升至220亿美元以上；收购终止的消息放出后，股价随即承压回落。市场普遍认为，此次收购止步的核心原因，在于管理层高度认可自身研发管线价值，认为默沙东的出价明显低估了Daraxonrasib、其他在研品种以及自研RAS（ON）三元复合物技术平台等公司核心资产的长期价值与商业化潜力，所以并不急于卖身变现。近年来，以默沙东为代表的跨国药企，凭借长期以来积累的专业研判能力，其收购创新药管线的动作，已成为全球生物医药行业的重要投资风向标。其收购意向与并购谈判，都能够有效的重塑市场预期，显著提振创新药企的估值。尽管此次收购未能落地，但也为后续核心品种临床数据披露后的估值重估埋下了伏笔。投资策略Daraxonrasib的III期临床顶线数据在4月13日公布后，多家海外金融机构迅速调整对RevMed的评级与目标价。美国银行（BofA）将目标价从115美元上调至170美元，并维持买入评级不变；Oppenheimer则将目标价从150美元上调至165美元，并维持优于大市的评级不变。从机构视角来看，Daraxonrasib的临床结果符合甚至超出预期，凭借远超目前其他疗法在疗效方面的临床优势，该药品上市后的先发优势将十分明显，并有望重塑的治疗格局；同时，临床需求旺盛，叠加竞争格局向好，将为该药后续商业化潜力的释放提供坚实支撑。全球市场规模在未来10年翻四倍的一大核心逻辑，正是Daraxonrasib商业化落地后，由于临床进度靠前，竞争格局良好，在好需求的加持下，销售放量带动整个市场空间扩容，这一行业逻辑也是市场给予RevMed高估值溢价的核心因素。而且凭借RAS（ON）三元复合物技术平台这一底层技术的特性，Daraxonrasib具备明确的泛癌治疗潜力，可大幅拓宽产品受众人群与市场空间，持续贡献增量业绩，为公司估值提供另一重支撑。从公司目前的在研管线来看，除了核心适应症外，Daraxonrasib作为泛RAS抑制剂，管线还布局了携带RAS突变的非小细胞肺癌、RAS依赖型实体瘤等其他适应症。公司研发团队与管理层核心成员，均为深耕创新药领域多年的顶尖人才，是RevMed实现技术突破的基石。典型如公司首席执行官Mark A. Goldsmith博士，是行业公认的抗肿瘤药物研发领军人物；公司首席研发官Alan Sandler博士拥有深厚的肿瘤药物研发背景与全球顶尖药企研发高管的任职履历。依托公司研发团队深厚的行业积淀与药物开发能力，自主研发了三元复合物技术平台，为核心管线的后续开发提供了技术支持。目前，公司核心产品Daraxonrasib商业化落地在即，投资者一方面需要密切跟踪全球监管的审评审批进度，特别关注后续临床数据的披露，尤其是安全性数据的表现；另一方面RevMed作为典型的Biotech，自身缺乏成熟的商业化体系与销售渠道，药品获批上市后，如何推动核心产品的商业化进程，是亟待解决的现实问题。在此背景下，携手大型跨国药企开展商业化合作，是公司的理想选择之一。借助大型药企完善的销售网络、学术资源、商业化运营经验等优势，加速产品销售放量与业绩释放，也能有效降低自身的经营风险。同时，重磅商业化合作项目落地，更是资本市场重要的风向标，有助于进一步提振公司估值。其背后的核心逻辑在于，大型药企就核心产品Daraxonrasib与RevMed展开商业化合作，既是对Daraxonrasib临床价值与商业化潜力的权威背书，也将有效缓解了市场对公司自身商业化能力不足的担忧，并与Daraxonrasib的长期投资逻辑形成共振，为公司估值的上行提供强支撑。*免责声明：本文内容仅代表作者看法。市场有风险，投资需谨慎。在任何情况下，本文中的信息或所表述的意见均不构成对任何人的投资建议。在决定投资前，如有需要，投资者务必向专业人士咨询并谨慎决策。我们无意为交易各方提供承销服务或任何需持有特定资质或牌照方可从事的服务。

2026-05-12

·PRNewswire

Breakthrough Targeted Therapy Shows Promise for KRAS‑Mutated Pancreatic Cancer, with Virginia Cancer Specialists and NEXT Oncology Playing Key Role

FAIRFAX, Va., May 12, 2026 /PRNewswire/ -- Virginia Cancer Specialists announced today its participation as a leading clinical trial site in a landmark study evaluating daraxonrasib, a first‑in‑class targeted oral therapy for patients with previously treated, advanced KRAS ‑ mutated pancreatic cancer. Results from the Phase 1/2 trial, published recently in The New England Journal of Medicine, demonstrated exceptional disease control in a cancer historically resistant to targeted treatment. Positive Phase 3 results reported in April 2026 further confirmed the therapy's profound clinical benefit and signal a potential new standard of care. Pancreatic cancer has long been one of the most aggressive and difficult cancers to treat, driven in large part by KRAS mutations—genetic alterations historically considered "undruggable." Daraxonrasib was designed to directly inhibit mutant KRAS, offering a novel therapeutic approach for patients whose disease has progressed after standard chemotherapy. In the NEJM‑published study, nearly 90% of patients achieved disease control following treatment with daraxonrasib, representing a significant advance in a disease with limited options. The encouraging results were reinforced by subsequent Phase 3 data, which validated the drug's strong clinical impact and support expectations for regulatory approval. "We are witnessing a true turning point in pancreatic cancer research," said Alexander I. Spira, MD, PhD, FACP, FASCO, Co‑Director of the Virginia Cancer Specialists Research Institute and Chief Scientific Officer of NEXT Oncology. "KRAS mutations have long represented one of oncology's greatest challenges. These results demonstrate that precision‑targeted therapies like daraxonrasib may finally change outcomes for patients facing a devastating diagnosis." Virginia Cancer Specialists and NEXT Oncology were selected as prominent trial sites for this research, reflecting the strength of their nationally recognized, community‑based clinical research program. Through the joint venture between Virginia Cancer Specialists Research Institute and NEXT Oncology, patients have access to innovative therapies close to home—often years before they become widely available. "We are incredibly proud that this research, under Dr. Spira's leadership, lead to such an important advancement. It reflects the exceptional caliber of our research programs and our deep commitment to bringing promising new therapies to patients within a compassionate, community-based setting," says Chao Yin, MD, Medical Oncologist, who sees patients in Virginia Cancer Specialists' Fairfax location. "Our role in this historic study underscores our commitment to advancing cancer care through research," Dr. Spira added. "Clinical trials are how tomorrow's treatments reach patients today." At any given time, the Virginia Cancer Specialists Research Institute and NEXT Oncology enroll patients in hundreds of active clinical trials across tumor types, providing access to precision oncology and next‑generation treatments within the communities where most patients seek care. For more information about clinical trials at Virginia Cancer Specialists or to explore research opportunities, visit VirginiaCancerSpecialists.com. About Virginia Cancer Specialists Virginia Cancer Specialists, the largest private cancer practice in Northern Virginia, has been recognized as the #1 physician practice in Virginia in cancer care and across all medical specialties for 3 years running (2024-2026), as recognized by Castle Connolly Top Doctors. It features a world-class treatment team offering access to the most current treatment protocols fighting cancer and blood diseases. It's also home to the Virginia Cancer Specialists Research Institute and the largest clinical trials portfolio in the Mid-Atlantic – including a dedicated research facility for Phase I clinical trials and later-stage trials through a joint venture with Fairfax's NEXT Oncology. The practice offers medical oncology, radiation oncology, musculoskeletal tumor surgery, breast surgery, thoracic surgery, genetic counseling, support cancer care, financial counseling, onsite laboratory, onsite pharmacy, language services, telehealth, nurse advice line, and much more. Virginia Cancer Specialists is part of The US Oncology Network. This collaboration unites the practice with more than 600 sites of care across 31 states, 2,700 affiliated physicians, and research and data from thousands of patients with cancer in clinical trials across the country. Its 2024 partnership with the renowned Sara Cannon Research Institute opens the door to hundreds of additional clinical studies, increases care to more patients, and has played a role in more than 100 FDA-approved cancer therapies. For more information about The US Oncology Network, which is supported by McKesson, a trusted name and global leader in healthcare for over 180 years, visit USOncology.com. For more information about Virginia Cancer Specialists, visit: VirginiaCancerSpecialists.com Media Contact Jean Dzierzak [email protected] 703-963-5770 SOURCE Virginia Cancer Specialists 21% more press release views with Request a Demo

临床3期临床结果

2026-05-12

·今日头条

等了40年，这种癌症终于有药可救了你有没有想过，如果身体里有个开关坏了，一直在喊“快长快长”，会怎样？这就是胰腺癌患者的真实处境。我有个朋友的父亲，确诊到离世，只有四个月。化疗做了两轮，医生说肿瘤没小，但人已经扛不住了。那时候我在想：怎么就没办法呢？现在，可能真的有办法了。 0

等了40年，这种癌症终于有药可救了你有没有想过，如果身体里有个开关坏了，一直在喊“快长快长”，会怎样？这就是胰腺癌患者的真实处境。我有个朋友的父亲，确诊到离世，只有四个月。化疗做了两轮，医生说肿瘤没小，但人已经扛不住了。那时候我在想：怎么就没办法呢？现在，可能真的有办法了。 01 一个坏掉的“绿灯” 先通俗讲一下这个病的“病根”。我们每个细胞里都有一个“交通灯”，叫RAS基因。它正常工作时，红灯停、绿灯行，该分裂的时候分裂，不该分裂的时候就老实待着。但有些人的这个灯，是坏的。不是坏了不亮，而是——永远卡在绿灯上。你能想象吗？一个十字路口，绿灯永远不灭，车流就会一直涌过来，最后整个路口堵死、瘫痪。癌细胞就是这么来的，不停地分裂、分裂、再分裂，直到把正常器官挤得没法工作。医学上管这叫“RAS基因突变”。在被称为“癌王”的胰腺癌里，超过90%的患者是这种情况。肺癌、肠癌里也不少。科学家从40年前就知道这个“病根”，但一直没办法。为什么？因为这个“交通灯”的表面太光滑了，像个光滑的玻璃球，药物根本抓不住。常规思路全都不通，连诺贝尔奖得主当年都直摇头。直到最近，思路终于变了。 02 一组让人眼前一亮的数据 2026年5月初，全球顶级医学期刊《新英格兰医学杂志》发了一篇文章，讲的是一款叫daraxonrasib的新药。针对什么人？那些化疗失败、病情还在进展的晚期胰腺癌患者。说实话，这个群体以前基本等于“没有希望”。但这药的数据出来了：在26名特定突变的患者中，35%的人肿瘤明显缩小。中位总生存期达到13.1个月。 13.1个月，听起来是不是也不长？我告诉你历史数据你就明白了——传统化疗在同样的情况下，中位生存期一直是6个月上下。13.1个月，是翻倍的突破。有参与研究的医生原话说：有些患者吃药几天后，症状就明显好转了。这在化疗方案里几乎不可能看到。我不禁在想：对那些已经没有选择的家庭来说，多活几个月意味着什么？可能是看到孩子毕业，可能是陪老伴过一个生日。每一个月的延长，都不是冰冷的数字。 03 中国企业没有缺席这场全球竞赛里，中国药企的身影也很活跃。我梳理了一下目前的信息：加科思自主研发的一款pan-KRAS抑制剂，跟国际药企阿斯利康达成了总金额超20亿美元的合作，光首付款就有1亿美元。这个数字说明什么？说明国际巨头也认可中国在这个领域的研发能力。劲方医药的口服KRAS G12D抑制剂，已经在中国进入III期注册临床研究，还拿到了美国FDA的快速通道资格。中美同步推进，速度不慢。正大天晴自主研发的口服Pan-KRAS抑制剂，2026年初已经获得中美两国临床试验许可。贝达药业的一款泛RAS“分子胶”抑制剂，也在2026年1月获批临床试验。在更早的KRAS G12C抑制剂赛道，中国企业已经完成了从研发到上市的全程。三款国产药物全部获批，并且都进了国家医保目录。从零到三，从实验室到患者手中，这一步走得不容易，但走得很扎实。 04 差距在哪里，机会在哪里冷静说一句，pan-RAS这个更广谱的赛道，目前全球还没有任何一款产品获得完全批准。海外的领跑者起步更早、临床验证的成熟度更高。这是一个客观事实。但中国企业的优势也很明显：临床推进速度快，商业化执行力强。G12C赛道的成功已经证明了这一点。从“快速跟进”到“定义赛道”，这是每个创新药强国都必须走的路。我不觉得这是“差距”或者“落后”。每个主体都有自己的发展阶段和节奏，都在不断优化和调整。我更愿意理解为：中国创新药企，正在从“会做题”走向“会出题”。写在最后科学家花了四十多年，才把这个驱动近三分之一实体瘤的关键开关搞清楚。有人说创新药研发太难了，动辄十年、二十年、甚至四十年。但换个角度想：如果四十年的坚持，能让未来每一个胰腺癌患者多活半年、一年，让更多家庭少一些“来不及说再见”，这四十年值不值得？我觉得，值。每一个在实验室里没放弃的人，都在为这个世界添一份光亮。你觉得攻克“最难靶点”，中国企业还要多久？欢迎评论区聊聊你的看法。（综合整理自：NEJM、FDA官网、各企业公告）

100 项与达拉西布相关的药物交易

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研发状态

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适应症	最高研发状态	国家/地区	公司	日期
转移性胰腺腺癌	临床3期	美国	Revolution Medicines, Inc.	2026-03-09
胰腺导管腺癌	临床3期	英国	Revolution Medicines, Inc.	2025-12-15
RAS突变非小细胞肺癌	临床3期	美国	Revolution Medicines, Inc.	2025-05-06
RAS突变非小细胞肺癌	临床3期	日本	Revolution Medicines, Inc.	2025-05-06
RAS突变非小细胞肺癌	临床3期	澳大利亚	Revolution Medicines, Inc.	2025-05-06
RAS突变非小细胞肺癌	临床3期	比利时	Revolution Medicines, Inc.	2025-05-06
RAS突变非小细胞肺癌	临床3期	法国	Revolution Medicines, Inc.	2025-05-06
RAS突变非小细胞肺癌	临床3期	德国	Revolution Medicines, Inc.	2025-05-06
RAS突变非小细胞肺癌	临床3期	中国香港	Revolution Medicines, Inc.	2025-05-06
RAS突变非小细胞肺癌	临床3期	爱尔兰	Revolution Medicines, Inc.	2025-05-06

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临床结果

适应症

分期

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT06881784 (RASolve 301, AACR2026)	临床3期	RAS mutation	420	Daraxonrasib	網顧壓製鬱廠選夢簾願(衊遞簾繭選築觸窪餘鹽) = 鑰遞蓋壓遞獵艱齋繭壓範醖夢獵構襯鏇築齋鹹 (構構繭糧襯簾遞鏇顧網, 6 ~ 12.3) 更多	积极	2026-04-21
				Docetaxel	糧網餘鏇窪淵鹽顧衊遞(構窪遞築餘廠顧範獵醖) = 壓襯淵憲觸壓網夢繭襯鏇醖構顧鏇構簾觸鑰鏇 (夢範鹽願築衊鹹淵壓繭, 8.1 ~ 10.8) 更多
NCT06445062 (AACR2026)	临床1/2期	转移性胰腺腺癌一线 RAS mutations	40	Daraxonrasib + gemcitabine/nab-paclitaxel (GnP)	鬱艱鑰顧築餘襯選繭壓(製餘顧繭憲顧餘願夢鬱) = 鹹膚鑰構積製鬱鏇積鹽鏇製製選廠鏇築蓋糧獵 (構糧構遞鹽壓艱範願顧, 76 ~ 97) 更多	积极	2026-04-21
				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.)	鬱艱鑰顧築餘襯選繭壓(製餘顧繭憲顧餘願夢鬱) = 簾遞願餘糧窪願衊膚構鏇製製選廠鏇築蓋糧獵 (構糧構遞鹽壓艱範願顧, 79 ~ 98) 更多
NCT05379985 (AACR2026)	临床1/2期	转移性胰腺腺癌一线 RAS mutations	40	Daraxonrasib 300 mg QD	廠衊壓齋齋壓鏇觸壓糧(鑰積積鏇顧夢簾繭範襯) = 膚鏇廠觸網網鹽顧簾鹽蓋築憲餘蓋糧願繭構襯 (網憲鹹觸夢築網鬱築膚, 79 ~ 98) 更多	积极	2026-04-21
NCT06625320 (RASolute 302, Company_Website)	临床3期	转移性胰腺导管腺癌二线	249	Daraxonrasib 300 mg	糧蓋齋醖鹽構獵壓艱鏇(積糧鬱範顧膚餘壓廠糧) = 遞簾鹹艱鬱構觸憲壓選窪遞築繭憲壓網構鏇範 (構構繭遞鏇簾襯醖憲簾 )	积极	2026-04-13
				Chemotherapy	糧蓋齋醖鹽構獵壓艱鏇(積糧鬱範顧膚餘壓廠糧) = 選選窪夢鑰醖糧壓簾獵窪遞築繭憲壓網構鏇範 (構構繭遞鏇簾襯醖憲簾 )
Company_Website 人工标引	临床1期	胰腺导管腺癌一线 RAS-mutant	40	Daraxonrasib	膚壓觸壓鏇鏇鬱網糧窪(衊遞膚鏇選顧醖繭選構) = 餘繭憲醖淵簾範構醖醖製廠積鏇簾窪憲淵鑰廠 (齋簾獵廠醖鑰淵網積膚 ) 更多	积极	2025-09-10
Company_Website 人工标引	临床1期	胰腺导管腺癌一线 RAS mutations	40	Daraxonrasib + Gemcitabine + nab-Paclitaxel	構齋鬱觸廠網淵糧醖壓(繭壓蓋糧繭齋壓鑰糧憲) = 選願淵艱繭淵廠鏇廠蓋糧繭繭鬱鬱醖淵繭構廠 (餘淵鑰膚簾夢艱蓋糧艱 ) 更多	积极	2025-09-10
Company_Website 人工标引	临床1期	胰腺导管腺癌二线 RAS G12X mutation \| RAS mutation	83	Daraxonrasib 300 mg	繭顧鬱餘顧顧衊構膚選(製鹽範醖網繭鏇鏇願蓋) = 襯簾築蓋廠襯簾顧積積鏇製廠繭獵繭鑰選蓋鏇 (築獵遞鑰製鏇廠糧積築 )	积极	2025-09-10
				Daraxonrasib 300 mg (RAS G12X mutation)	繭顧鬱餘顧顧衊構膚選(製鹽範醖網繭鏇鏇願蓋) = 蓋網醖窪積蓋鹽夢淵顧鏇製廠繭獵繭鑰選蓋鏇 (築獵遞鑰製鏇廠糧積築 ) 更多
NEWS 人工标引	N/A	KRAS突变非小细胞肺癌一线	-	Daraxonrasib+Pembrolizumab (TPS≥50%)	遞醖獵鹽壓簾顧鑰鹹鑰(積網鹽繭獵襯夢簾繭衊) = 壓遞願憲築餘衊夢憲構淵蓋繭簾觸觸膚網糧簾 (遞鏇艱網觸壓簾鏇構窪 ) 更多	积极	2025-07-10
				Daraxonrasib+Pembrolizumab+Chemotherapy (TPS<50%)	遞醖獵鹽壓簾顧鑰鹹鑰(積網鹽繭獵襯夢簾繭衊) = 鏇鑰壓膚憲觸鹽構顧淵淵蓋繭簾觸觸膚網糧簾 (遞鏇艱網觸壓簾鏇構窪 ) 更多
NEWS 1 \| NEWS 2 人工标引	N/A	非小细胞癌一线	33	Elironrasib+daraxonrasib	範築積蓋襯鏇糧鹽壓糧(顧衊鏇積衊鏇齋夢鑰廠) = 築齋構築築繭壓網願蓋願膚鹹膚積衊鏇鏇襯壓 (艱鏇繭齋糧構選構鬱鑰 ) 更多	积极	2025-05-10
NCT06128551 (Corporate Publications \| NEWS) 人工标引	临床1期	非小细胞肺癌三线	26	Elironrasib + Daraxonrasib	艱夢構範艱鹽繭築遞壓(觸鏇夢網選獵窪構膚窪) = 艱襯選壓顧築廠積艱衊膚壓廠鏇築餘顧網糧蓋 (積鬱醖淵鏇壓網築鏇觸 ) 更多	积极	2025-05-07