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.

[+1]

NCT06922591

/ Recruiting临床1/2期

A Phase 1/2, Multicenter, Open-Label Study to Evaluate Safety, Tolerability & Antitumor Activity of TNG462 in Combination With Other Agents in Patients With Pancreatic Cancer With MTAP Loss and Pancreatic or Non-Small Cell Lung Cancer With MTAP Loss & RAS Mutation

TNG462-C102 is a Phase 1/2, open-label, multicenter study designed to determine the safety, tolerability, PK, PD, and preliminary antineoplastic activity of oral TNG462 in combination with RMC-6236, RMC-9805, mFOLFIRINOX or gemcitabine/nab-paclitaxel. The study comprises a dose escalation phase and a dose expansion phase.

开始日期2025-05-31

申办/合作机构

Tango Therapeutics, Inc.

[+1]

NCT06445062

/ Recruiting临床1/2期

A Platform Study of RAS(ON) Inhibitors in Patients With Gastrointestinal Solid Tumors

The purpose of this platform study is to evaluate the safety, tolerability, pharmacokinetics (PK), and preliminary antitumor activity of novel RAS(ON) inhibitors combined with Standard(s) of Care (SOC) or with novel agents.
The current subprotocols include the following:
Subprotocol A: RMC-6236 + 5-fluorouracil-based regimens
Subprotocol B: RMC-6236 + cetuximab with or without mFOLFOX6
Subprotocol C: RMC-6236 + gemcitabine + nab-paclitaxel
Subprotocol D: RMC-9805 with or without RMC-6236 + 5-fluorouracil-based regimens
Subprotocol E: RMC-9805 with or without RMC-6236 + cetuximab with or without mFOLFOX6
Subprotocol F: RMC-9805 with or without RMC-6236 + gemcitabine + nab-paclitaxel

开始日期2024-05-24

申办/合作机构

Revolution Medicines, Inc.

100 项与 Zoldonrasib 相关的临床结果

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100 项与 Zoldonrasib 相关的转化医学

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100 项与 Zoldonrasib 相关的专利（医药）

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项与 Zoldonrasib 相关的文献（医药）

2025-07-07·Cancer Biology & Medicine

Drugging the 'undruggable' KRAS: breakthroughs, challenges, and opportunities in pancreatic cancer.

Review

作者: Ali Zaidi, Syed Aqib ; Khan, Nawaz ; Abudurousuli, Kayisaier ; Zhou, Wenting ; Aikebaier, Alifeiye ; Nuer, Muhadaisi ; Paerhati, Yipaerguli ; Raza, Umar

Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy with a poor prognosis that is driven primarily by oncogenic KRAS mutations present in > 90% of cases. KRAS mutations, particularly the G12D mutation which dominates in PDAC, fuel tumor initiation, progression, and immune evasion, thereby contributing to therapy resistance. Nevertheless, KRAS has long been considered "undruggable" due to its structure. Recent advances have spurred transformative progress in direct KRAS inhibition. While FDA-approved mutation-specific and pan-KRAS inhibitors show limited efficacy in PDAC, emerging agents (MRTX1133 and RMC-9805) have demonstrated preclinical promise. However, resistance remains a critical hurdle and is driven by pathway reactivation, secondary mutations, and metabolic adaptations. Alternative strategies targeting upstream regulators (SHP2 and SOS1) aim to block KRAS activation and associated resistance mechanisms. Preclinical studies have also highlighted synergistic benefits of combining KRAS inhibitors with MEK, PI3K, or CDK4/6 inhibitors, which are now undergoing clinical evaluation. Immunotherapies, including KRAS-targeted vaccines and adoptive T-cell therapies, have further expanded the therapeutic landscape of enhancing KRAS-targeted therapies in PDAC. The molecular basis of KRAS-driven PDAC, current inhibitors, resistance mechanisms, and innovative strategies are discussed herein to address treatment barriers. Opportunities to improve clinical outcomes are underscored in this challenging malignancy by integrating insights from preclinical and clinical research.

Cancers

Treatment of KRAS-Mutated Pancreatic Cancer: New Hope for the Patients?

Review

作者: Włoszek, Emilia ; Budzik, Michał P. ; Mękal, Dominika ; Fudalej, Marta ; Deptała, Andrzej ; Badowska-Kozakiewicz, Anna M. ; Czerw, Aleksandra ; Miski, Hanna ; Krupa, Kamila

Pancreatic cancer, specifically pancreatic ductal adenocarcinoma (PDAC), ranks among the most lethal malignancies, with a 5-year survival rate of under 10%. The most prevalent KRAS mutations occur in three hotspot residues: glycine-12 (G12), glycine-13 (G13), and glutamine-61 (Q61), leading to the constant activation of the Ras pathway, making them the primary focus in oncologic drug development. Selective KRAS G12C inhibitors (e.g., sotorasib, adagrasib) have demonstrated moderate efficacy in clinical trials; however, this mutation is infrequent in PDAC. Emerging therapies targeting KRAS G12D and G12V mutations, such as MRTX1133, PROTACs, and active-state inhibitors, show promise in preclinical studies. Pan-RAS inhibitors like ADT-007, RMC-9805, and RMC-6236 compounds provide broader coverage of mutations. Their efficacy and safety are currently being investigated in several clinical trials. A major challenge is the development of resistance mechanisms, including secondary mutations and pathway reactivation. Combination therapies targeting the RAS/MAPK axis, SHP2, mTOR, or SOS1 are under clinical investigation. Immunotherapy alone has demonstrated limited effectiveness, attributed to an immunosuppressive tumor microenvironment, although synergistic effects are noted when paired with KRAS-targeted agents. Furthermore, KRAS mutations reprogram cancer metabolism, enhancing glycolysis, macropinocytosis, and autophagy, which are being explored therapeutically. RNA interference technologies have also shown potential in silencing mutant KRAS and reducing tumorigenicity. Future strategies should emphasize the combination of targeted therapies with metabolic or immunomodulatory agents to overcome resistance and enhance survival in KRAS-mutated PDAC.

321

项与 Zoldonrasib 相关的新闻（医药）

2026-04-17

·药明康德

从“不可成药”到多点突破，KRAS靶向治疗迈向新阶段 | AACR

2026年美国癌症研究协会（AACR）年会已经在美国圣地亚哥开幕。AACR是规模最大的癌症研究会议之一，多家医药公司将在大会上汇报创新疗法的研究结果。其中，针对RAS的靶向药物开发是产业关注的抗癌药物研发重点之一。本周Revolution Medicines公司宣布，其泛RAS抑制剂daraxonrasib在治疗经治转移性胰腺导管腺癌（PDAC）患者的3期临床试验中获得积极结果。与化疗相比，daraxonrasib显著延长患者的中位总生存期（OS），显示了业界在开发RAS靶向疗法方面的长足进步。本文将与读者分享在AACR大会上部分RAS靶向疗法的最新进展。多款KRAS G12D抑制剂亮相AACR KRAS突变是在胰腺癌、结直肠癌和非小细胞肺癌（NSCLC）等肿瘤中常见的肿瘤驱动基因突变。KRAS蛋白在细胞内承担信号“开关”功能，一旦发生特定突变，这一开关便会被持续锁定在激活状态（ON），不断驱动肿瘤生长。过去数十年，由于缺乏明确的药物结合位点，加之担心靶向KRAS可能影响正常细胞的生理功能，KRAS一度被贴上“不可成药”的标签。直到KRAS G12C抑制剂sotorasib和adagrasib相继获批，为整个RAS靶向领域打开了新的突破口。在针对KRAS G12C突变体的药物研发获得突破后，科学家们把目光也转向其它KRAS突变体，其中KRAS G12D抑制剂的研发备受关注，这一突变在多种癌症类型中与KRAS G12C相比更为常见。在AACR大会上，多家生物技术公司展示了它们开发的KRAS G12D抑制剂。例如，Revolution Medicines公司将展示其KRAS G12D抑制剂zoldonrasib治疗携带KRAS G12D突变的经治NSCLC患者的临床试验结果。Zoldonrasib是一款RAS（ON）三元复合体抑制剂，此前公布的早期临床试验结果显示，在推荐2期剂量下，既往治疗后的NSCLC患者中客观缓解率达到61%，疾病控制率为89%，且未观察到剂量限制性毒性。 Verastem Oncology公司将公布其核心在研疗法VS-7375的多项研究结果，VS-7375是一款能够与激活状态和失活状态的KRAS G12D突变体结合（ON/OFF）的抑制剂。它已经获得FDA授予的快速通道资格，用于治疗携带KRAS G12D突变的局部晚期或转移性胰腺癌。此外，Eilean Therapeutics等公司也将公布其KRAS G12D抑制剂的最新研究结果。泛KRAS靶向疗法成为重要研究方向除了针对特定KRAS突变体，产业界亦在开发可同时靶向多种RAS突变体及野生型蛋白的泛RAS抑制剂。由于临床耐药往往通过野生型RAS同工型的代偿性激活实现，泛RAS抑制策略在机制层面或更有助于阻断适应性逃逸通路。本周已经公布3期试验结果的daraxonrasib就是一款泛RAS抑制剂。此外，Cogent Biosciences公司将在大会上发布泛KRAS（ON）抑制剂CGT1263的研究结果。临床前研究显示这款抑制剂对KRAS的选择性是HRAS和NRAS的500倍以上。新闻稿还指出，CGT1263在表现出抗癌活性的同时，对皮肤的pERK信号抑制有限，支持CGT1263可能具有更大的治疗窗口。 BlossomHill Therapeutics公司也将在大会上发布泛KRAS抑制剂BH-501284的研究结果。摘要显示，BH-501284是一种高效、选择性强、可口服的非共价泛KRAS抑制剂，靶向KRAS的别构switch-II口袋。BH-501284可在KRAS失活（OFF）状态下结合KRAS突变体，其结合亲和力达到皮摩尔级别。细胞洗脱实验进一步证实BH-501284能够紧密结合KRAS，其效果类似于共价抑制剂。值得注意的是，BH-501284的抗增殖活性仅受到生长因子（例如EGF）轻微影响，而这些生长因子通常会驱动KRAS进入活化状态并导致耐药。此外，在携带KRAS G12D、G12V和G12C突变的细胞来源异种移植（CDX）肿瘤模型中，BH-501284表现出持久且强效的活性。药代动力学（PK）研究显示，BH-501284在多种物种中具有良好的口服生物利用度。这些研究结果表明BH-501284是一个具有进一步开发潜力的有力候选药物。安进（Amgen）、英矽智能（Insilico Medicine）、中外制药株式会社（Chugai Pharmaceutical）、Ensem Therapeutics等公司也将公布各自泛KRAS抑制剂的研究结果。在泛KRAS抑制剂之外，泛KRAS降解剂也是靶向RAS突变体的另一种研发策略。Arvinas公司将在AACR大会上公布其泛KRAS蛋白降解靶向嵌合体的研究结果。研究人员在KRAS G12D小鼠结直肠癌模型CT-26中比较了蛋白降解靶向嵌合体介导的KRAS降解与RAS抑制的抗肿瘤活性。摘要显示，在CT-26模型中，口服泛KRAS降解剂单药治疗可导致显著的KRAS降解（>85%）以及显著的肿瘤生长抑制，包括完全缓解（CR）。一体化平台赋能RAS靶向药物开发长期以来，药明康德都在支持全球合作伙伴从药物研究（R）、开发（D）到商业化生产（M）各个阶段的需求，通过独特的一体化、端到端CRDMO模式，助力包括RAS靶向药物在内的突破性疗法加速研发进程、早日惠及患者。例如，药明康德生物学业务平台（WuXi Biology）聚焦KRAS G12D这一高度关注且具有挑战性的肿瘤靶点，构建了覆盖耐药机制研究与转化验证的一体化模型体系，为创新药物研发提供系统化支持。基于对KRAS信号通路生物学及肿瘤适应性进化机制的深入理解，平台成功开发多种KRAS G12D抑制剂诱导的耐药肿瘤模型，涵盖结直肠癌、胰腺癌及肺癌等典型KRAS驱动肿瘤类型，并通过体外诱导与体内筛选相结合的策略，实现耐药细胞系与动物模型的系统构建与验证。相关模型能够有效复现临床中常见的耐药机制，包括KRAS获得性突变、RTK反馈激活、MAPK与PI3K–AKT–mTOR信号重编程、细胞表型可塑性及肿瘤微环境影响等关键生物学过程，为下一代KRAS抑制剂及联合治疗策略评估提供可靠工具。同时，依托一体化体内外药效评价体系和生物标志物评价平台，实现从机制研究到药效评价的闭环验证，支持候选药物在耐药背景下的差异化活性评估与作用机制解析。依托标准化、可扩展的模型开发能力，WuXi Biology能够帮助合作伙伴更早识别潜在耐药风险，加速KRAS G12D靶向疗法的优化与临床转化进程。合作伙伴对药明康德的工作也给予了高度评价，曾领导一款KRAS抑制剂开发的原Mirati Therapeutics高级副总裁，药物发现负责人Matt Marx博士表示，“药明康德是我们合作时间最长的合作伙伴之一，我们与药明康德的化学、DMPK、毒理学、癌症生物学和结构生物学团队紧密合作。”他补充道：“药明康德团队一直是一个稳定、高效且富有成效的合作伙伴，在我们努力为癌症患者创造有意义新疗法的过程中，我们深深感谢他们在其中的支持。” 从长期被认为“不可成药”，到KRAS G12C抑制剂获批上市，再到多种新一代（K）RAS抑制剂和降解剂崭露头角，RAS靶向治疗已实现从概念验证到体系化拓展的重要跨越。治疗策略也从针对单一突变体走向覆盖多种突变体。对于患者而言，这意味着未来有望获得更广泛、更持久的治疗选择。依托端到端的一体化CRDMO赋能平台，药明康德将继续帮助客户将创新成果高效转化为造福全球患者的解决方案，共同践行“让天下没有难做的药，难治的病”的愿景。参考资料： [1] Verastem Oncology Announces Late Breaking and Regular Abstracts Accepted for Presentation at the AACR Annual Meeting 2026. Retrieved April 15, 2026, from https://investor.verastem.com/news-releases/news-release-details/verastem-oncology-announces-late-breaking-and-regular-abstracts [2] Abstract 4604: Preclinical efficacy of a PROTAC pan-KRAS degrader in a KRAS G12D syngeneic mouse model and concurrent immune tumor microenvironment changes. Retrieved April 15, 2026, from https://aacrjournals.org/cancerres/article/86/7_Supplement/4604/782435/Abstract-4604-Preclinical-efficacy-of-a-PROTAC-pan?searchresult=1 [3] Abstract 5120: Design and discovery of BH-501242, a novel pan-KRAS on/off inhibitor targeting KRAS switch II pocket. Retrieved April 15, 2026, from https://aacrjournals.org/cancerres/article/86/7_Supplement/5120/780846/Abstract-5120-Design-and-discovery-of-BH-501242-a?searchresult=1 [4] Abstract 425: ISM7713, a novel oral pan-KRAS (ON/OFF) inhibitor, shows robust anti-tumor activity in solid tumors with KRAS alterations. Retrieved April 15, 2026, from https://aacrjournals.org/cancerres/article/86/7_Supplement/425/775825/Abstract-425-ISM7713-a-novel-oral-pan-KRAS-ON-OFF?searchresult=1 [5] Abstract 6736: Discovery and characterization of BH-501284: A non-covalent, pan-KRAS inhibitor for treatment of diverse KRAS-mutant tumors. Retrieved April 16, 2026, from https://aacrjournals.org/cancerres/article/86/7_Supplement/6736/778502/Abstract-6736-Discovery-and-characterization-of-BH?searchresult=1 [6] Abstract 5866: Preclinical combination approaches with the pan-KRAS inhibitor AMG 410 in KRAS-mutant cancers. Retrieved April 16, 2026, from https://aacrjournals.org/cancerres/article/86/7_Supplement/5866/781779/Abstract-5866-Preclinical-combination-approaches?searchresult=1 [7] Abstract 1008: Effect of the KRAS G12C inhibitor MK-1084 on circulating tumor DNA levels in participants with KRAS G12-mutated tumors. Retrieved April 16, 2026, from https://aacrjournals.org/cancerres/article/86/7_Supplement/1008/776576/Abstract-1008-Effect-of-the-KRAS-G12C-inhibitor-MK?searchresult=1 [8] Abstract 418: ETX-929, a potential best-In-class, oral, highly potent and selective dual ON/OFF state Pan-KRAS small molecule inhibitor for the treatment of KRAS mutant and wild-type amplified cancers. Retrieved April 16, 2026, from https://aacrjournals.org/cancerres/article/86/7_Supplement/418/776245/Abstract-418-ETX-929-a-potential-best-In-class?searchresult=1 [9] Ensem Therapeutics Highlights Novel, Potent, and Selective Oral pan-KRAS and WRN Inhibitors with Best-in-Class Potential. Retrieved April 17, 2026, from https://www.businesswire.com/news/home/20260417371738/en/Ensem-Therapeutics-Highlights-Novel-Potent-and-Selective-Oral-pan-KRAS-and-WRN-Inhibitors-with-Best-in-Class-Potential [10] Daraxonrasib Demonstrates Unprecedented Overall Survival Benefit in Pivotal Phase 3 RASolute 302 Clinical Trial in Patients with Metastatic Pancreatic Cancer. Retrieved April 17, 2026, from https://ir.revmed.com/news-releases/news-release-details/daraxonrasib-demonstrates-unprecedented-overall-survival-benefit [11] Cogent Biosciences Announces Poster Presentations at the American Association for Cancer Research (AACR) Annual Meeting 2026. Retrieved April 17, 2026, from https://investors.cogentbio.com/news-releases/news-release-details/cogent-biosciences-announces-poster-presentations-american 免责声明：本文仅作信息交流之目的，文中观点不代表药明康德立场，亦不代表药明康德支持或反对文中观点。本文也不是治疗方案推荐。如需获得治疗方案指导，请前往正规医院就诊。版权说明：欢迎个人转发至朋友圈，谢绝媒体或机构未经授权以任何形式转载至其他平台。转载授权请在「药明康德」微信公众号回复“转载”，获取转载须知。分享，点赞，在看，聚焦全球生物医药健康创新

2026-04-17

·EndPoints

Pancreatic cancer data, the RAS bonanza and China ADC standouts are ready for AACR

The oncology field is buzzing after a landmark readout from Revolution Medicines, known colloquially as RevMed, showed that a targeted “pan-RAS” drug doubled the survival time for patients whose pancreatic cancer has returned or stopped responding to previous treatment. As cancer researchers and drugmakers head to San Diego this weekend for the annual AACR meeting, here’s what we’re watching: → RevMed will be reporting more data at AACR , both on its drug daraxonrasib as well as another KRAS-targeted therapy zoldonrasib. The Phase 1/2 daraxonrasib readout will give an updated look at how the drug fares as a first-line treatment in metastatic pancreatic cancer, both alone and alongside chemotherapy. Revolution Medicines reported an initial cut of data in the first-line setting last year, showing overall response rates of 47% and 55% alone and with chemotherapy respectively. The company will also be showcasing new data around its KRAS G21D-targeted drug zoldonrasib in previously treated lung cancer patients who bear that mutation. A key feature of zoldonrasib to keep an eye on is its safety profile, which has thus far been impressive, MD Anderson oncologist David Hong said. Hong is an investigator on the early-stage study. And questions will certainly be floating around the future of RevMed. The company was embroiled in rumors of a $30 billion buyout earlier this year that never materialized. → And China biotech continues to stand out, especially in ADCs. At a Sunday clinical trial plenary session on antibody-drug conjugates, three of four presentations are of trials conducted in China. That includes studies on a EGFR-targeted ADC from CSPC Pharmaceutical Group, a Claudin 6 asset from Qilu, and a B7-H3 drug called risvutatug rezetecan from Hansoh Pharma, with which GSK is partnered. Another key presentation is of a next-generation KRAS G12C inhibitor called elisrasib in advanced lung cancer. The drug is being developed by Shanghai-based D3 Bio, which in December raised $108 million to fund Phase 3 studies of the drug. → Cancer vaccines and CAR-Ts: On Monday, Moderna will share more data on its “off-the-shelf” cancer vaccine mRNA-4359 plus Keytruda in advanced melanoma. The data come after the Danish cancer vaccine developer IO Biotech filed for bankruptcy when a Phase 3 trial on another similar off-the-shelf cancer vaccine narrowly failed. At the same session, researchers from Dana-Farber Cancer Institute will be presenting an interesting use case of the CAR-T cell therapy Carvykti in high-risk smoldering multiple myeloma, which is a precursor condition to multiple myeloma.

临床3期疫苗临床结果AACR会议

2026-04-17

·科途医学K2Oncology

今日焦点 |2026年AACR年会全瞻

2026年4月17日至22日，AACR年会将在美国加州圣迭亚戈会议中心举行。为期六天的会议，将系统性揭示癌症生物学的底层机制与临床转化的最新成果。今年的议程特别强调了几个关键维度的突破：微小残留病灶（MRD）在实体瘤中的监测、早发性癌症的生物学异质性、人工智能在药物发现中的代理化，以及癌症预防的终极愿景——“0期”拦截。生物学前沿：MRD监测与早发性癌症的生物学本质MRD：从血液系统向实体瘤的全面进军微小残留病灶（MRD）监测已在血液恶性肿瘤中重写了治疗算法，但在实体瘤领域，这一技术正处于爆发前夜。当前，研究的焦点已从简单的ctDNA检测转向理解“从持久性到复发”的演化过程。UCLA的研究团队发现，利用分泌型高斯荧光素酶（Gaussia luciferase）或流式细胞术监测脑脊液中的循环肿瘤细胞，其灵敏度甚至超过了传统活检，这一进展暗示，未来的MRD监测将是多模态、高频次且深度集成的。早发性癌症：不只是“变年轻”的疾病 4月21日的全体会议（PL04）聚焦于一个令人担忧的现象：为何越来越多的年轻人患上癌症？现有的数据显示，50岁以下成年人的大肠癌发病率自20世纪90年代以来几乎翻了一番。早发性癌症并非老年患者疾病的简单提前，而是具有独特的生物学特征。空间分析显示，早发性大肠癌肿瘤携带更强的免疫抑制微环境，具有更高的Treg浸润和M2巨噬细胞存在。这意味着，针对老年患者验证有效的免疫治疗策略，在年轻患者中可能因微环境差异而失效。Andrew Chan教授等学者将从出生队列的角度探讨环境暴露、生命早期突变以及饮食因素如何共同驱动这一趋势。AI革命：从计算工具到生物学发现的代理人工智能在2026年AACR年会上首次获得了独立的全体会议待遇，这标志着AI已从辅助性的技术展示转变为决策关键点上的核心驱动力。最受瞩目的“数字孪生”技术已在ALK重排的NSCLC中得到验证，展示了其作为真实世界证据与临床试验设计之间桥梁的巨大潜力。这意味着，未来的药物临床试验可能在现实患者招募前，就已经在硅基模型中完成了初步的剂量优化和响应预测。地平线新药：分子胶与双/多靶向ADC的群雄逐鹿 AACR年会的“地平线新药”环节是药企披露其核心研发管线机密的首选之地。2026年的发布名单显示，靶向蛋白降解（TPD）和多功能抗体偶联药物（ADC）已成为创新的核心支。分子胶降解剂：挑战“不可成药”靶点分子胶（Molecular Glues）技术在今年的会议上大放异彩。Neomorph公司披露了其针对ARNT（HIF-1β）的分子胶降解剂NEO-811。ARNT是透明细胞肾细胞癌中关键的信号节点，长期以来因缺乏传统结合口袋而被认为“不可成药”。NEO-811通过将ARNT与E3泛素连接酶结合，诱导其高效降解，目前已进入I/II期临床研究。 Triana Biomedicines则带来了首创的ALK分子胶降解剂TRI-611。与现有的ALK激酶抑制剂不同，TRI-611结合在远离激酶结构域的远端位点，通过招募Cereblon（CRBN）降解ALK融合蛋白。其临床优势在于，无论患者是否存在TKI结合域的突变，TRI-611均能诱导肿瘤退缩，且具有极佳的脑渗透性，可应对肺癌患者常见的脑转移。进化中的ADC：双靶点、双载荷与差异化策略 ADC领域的竞争已从单靶点竞速转向多功能设计的博弈。基石药业在本次年会上将展示三款具有潜力的ADC资产： CS5007 (EGFR/HER3双抗ADC)：采用拓扑异构酶I抑制剂载荷，旨在解决肿瘤异质性导致的耐药问题，特别是在NSCLC和三阴性乳腺癌（TNBC）中。 CS5008 (SSTR2/DLL3双抗ADC)：针对神经内分泌肿瘤和小细胞肺癌，这两类肿瘤中SSTR2和DLL3常共同表达。 CS5006 (ITGB4-靶向ADC)：针对新型抗原Integrin β4，具有首创（FIC）潜力。此外，Araris Biotech（大冢制药子公司）披露了其三载荷ADC技术ARC-401，这种极端的设计理念旨在通过三种不同机制的毒素同时杀伤肿瘤，从而彻底杜绝耐药发生的途径。临床试验全会：KRAS与免疫治疗的巅峰决战临床试验全会是AACR最具“火药味”的环节，这里公布的数据往往直接决定了生物技术公司的市值走向。KRAS赛道：从“能否成药”到“谁能胜出” 在2026年，KRAS抑制剂的研发重点已转向G12D靶点以及克服G12C的耐药性。 Elisrasib (D3S-001)：迪哲医药将在临床全会1披露这款新一代GDP结合态KRAS G12C抑制剂的Phase 1/2数据。Elisrasib在既往接受过G12C抑制剂治疗的患者中仍显示出强效的靶点拦截能力和CNS渗透性。 Zoldonrasib (RMC-9805)：Revolution Medicines将展示这款RAS(ON) G12D选择性三复合物抑制剂的临床首秀。作为首个具有临床数据的口服G12D靶向药物，其对胰腺癌和结直肠癌的意义不言而喻。 Daraxonrasib (RMC-6236)：这款多选择性RAS(ON)抑制剂被Drug Hunter评为“2025年度分子”，在预处理的胰腺癌中展现了“前所未有”的生存获益。实体瘤免疫治疗：CAR-T的破局与疫苗的加持宾夕法尼亚大学的Carl June教授将在开幕全会分享CAR-T疗法在实体瘤中的演进。其中，一种名为KIR-CAR的新型多链CAR-T细胞疗法备受关注，它模拟NK细胞受体，旨在克服T细胞在实体瘤（如卵巢癌、间皮瘤）中的耗竭难题。同时，mRNA疫苗在肿瘤免疫中的增效作用也得到了实证。MD Anderson的研究指出，接种mRNA新冠疫苗后的患者，在接受免疫检查点抑制剂治疗时，三年的存活概率翻了一番。这提示，全身性的免疫启动可能为冷肿瘤的“加热”提供全新思路。0期癌症（Stage 0）：精准预防的终极愿景 Raymond DuBois教授将主持“靶向0期：基于精准的预防”环节。这一命题的提出，标志着癌症研究重心正在从“治愈中晚期”向“拦截超早期”转移。这一领域的关键进展包括：新生儿筛查：Sharon Plon教授将讨论如何将癌症风险评估纳入新生儿基因筛查，实现终身风险管理。药物拦截：宾大医学院的Minh Than展示了如何消除胰腺中的癌前细胞，在肿瘤形成前将其“斩草除根”。 HPV自我采样：SHIP试验的结果表明，通过HPV自采样技术，可以极大地提升欠发达地区的子宫颈癌预防效率，体现了癌症研究的“全球使命”。结语：在精准中寻求合作，以使命驱动科学 2026年AACR年会向我们展示了一个充满复杂性但也极具希望的未来。在这个未来里，癌症不再被视为一种不可避免的绝症，而是一系列可以在分子水平上被预测、监测和拦截的生物学事件。从圣迭戈会议中心的讨论中，我们可以清晰地看到，“精准”已经不再局限于基因检测，而是向多模态数据集成进化；“合作”不再只是跨院系的交流，而是人类与AI代理的并肩作战；而“使命”则要求每一项实验室的突破，最终都要惠及包括早发性癌症患者和欠发达地区人群在内的全球每一个角落。欢迎各位咨询——科途官方客服：关于科途医学科途医学是一家专注于类器官培养全流程产品、类器官建模服务、类器官疾病模型库建设、临床前药物发现、转化医学CRO服务的高科技公司，可提供类器官一站式解决方案。基于分泌蛋白质组学筛选技术，公司已经建立了40多种组织的类器官培养方法。产品包括EHSgel 基质胶、多种类器官培养基、类器官相关细胞因子、组织消化酶解液、类器官分离回收液、类器官冻存液等。我们致力于提供高质量、更可靠的类器官产品，助力客户科学研究的进展，欢迎您来电咨询。使用科途医学类器官产品或模型发表的科研文献列表(部分) 订购及业务咨询：info@K2Oncology.com 技术服务咨询：TechSupport@k2oncology.com 联系电话：010-67889128，13371633638（微信同步），17778038351 网址：www.K2Oncology.com 地址： ●北京市北京经济技术开发区经海六路5号院东尚·E园10号楼1层109 ●浙江省湖州市红丰路1366号6幢10楼1001室 ●河北省廊坊市固安县新兴园肽谷生物医药加速器产业园1号楼A1-1-4室

100 项与 Zoldonrasib 相关的药物交易

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适应症	最高研发状态	国家/地区	公司	日期
RAS突变非小细胞肺癌	临床2期	美国	Revolution Medicines, Inc.	2024-01-18
RAS突变非小细胞肺癌	临床2期	澳大利亚	Revolution Medicines, Inc.	2024-01-18
RAS突变非小细胞肺癌	临床2期	丹麦	Revolution Medicines, Inc.	2024-01-18
RAS突变非小细胞肺癌	临床2期	法国	Revolution Medicines, Inc.	2024-01-18
RAS突变非小细胞肺癌	临床2期	德国	Revolution Medicines, Inc.	2024-01-18
RAS突变非小细胞肺癌	临床2期	希腊	Revolution Medicines, Inc.	2024-01-18
RAS突变非小细胞肺癌	临床2期	意大利	Revolution Medicines, Inc.	2024-01-18
RAS突变非小细胞肺癌	临床2期	荷兰	Revolution Medicines, Inc.	2024-01-18
RAS突变非小细胞肺癌	临床2期	韩国	Revolution Medicines, Inc.	2024-01-18
RAS突变非小细胞肺癌	临床2期	西班牙	Revolution Medicines, Inc.	2024-01-18

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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


NCT06040541 (RMC-9805-001, AACR2025) 人工标引	临床1期	KRAS G12D突变实体瘤 \| KRAS G12D突变非小细胞肺癌 KRAS G12D	211	Zoldonrasib 150-1200 mg daily (KRAS G12D solid tumors)	製齋夢鑰齋築構簾廠廠(廠憲獵齋築襯範鑰糧鑰) = 鹹繭齋觸願窪餘淵糧積鹹壓觸構糧淵膚蓋壓憲 (衊鹹顧獵積窪築糧構鬱 ) 更多	积极	2025-04-27
NCT06040541 (RMC-9805-001, AACR2025) 人工标引	临床1期	KRAS G12D突变实体瘤 \| KRAS G12D突变非小细胞肺癌 KRAS G12D	211	Zoldonrasib 1200 mg QD (KRAS G12D NSCLC)	製齋夢鑰齋築構簾廠廠(廠憲獵齋築襯範鑰糧鑰) = 繭衊獵蓋鑰齋鹹齋夢衊鹹壓觸構糧淵膚蓋壓憲 (衊鹹顧獵積窪築糧構鬱, 36 ~ 83) 更多	积极	2025-04-27
NCT06040541 (Company_Website) 人工标引	临床1期	晚期胰腺导管腺癌 KRAS G12D	99	RMC-9805 1200 mg	廠鏇繭齋繭選衊蓋齋廠(襯簾蓋積窪築構鏇範觸) = in greater than 10% of patients were GI-related toxicities (nausea, diarrhea and vomiting) and rash that were primarily Grade 1 in severity and typically of limited duration. 築餘艱淵蓋襯衊範觸窪 (願醖願壓壓構觸淵範膚 ) 更多	积极	2024-10-25