This phase I/II trial tests the safety, side effects, best dose and how well giving daraxonrasib works for the treatment of pediatric patients with solid tumors with RAS mutations that has come back after a period of improvement (relapsed) or that has not responded to previous treatment (refractory). Daraxonrasib may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth. Giving daraxonrasib may be safe, tolerable and/or effective in treating patients with relapsed or refractory solid tumors with RAS mutations.

开始日期2027-04-09

申办/合作机构

The Children's Oncology Group Foundation, Inc.

NCT07793253

/ Not yet recruiting临床2期IIT

A Multi-Institutional Phase 2 Evaluation of Daraxonrasib in Recurrent KRAS-Mutant Biliary Tract Cancer

The purpose of this study is to evaluate the anti-tumor efficacy of daraxonrasib monotherapy in patients with unresectable or advanced/metastatic, KRAS-mutant BTC who have progressed on or are intolerant of 1st line systemic therapy.

开始日期2026-11-01

申办/合作机构

The Sidney Kimmel Comprehensive Cancer Center

[+2]

NCT07756281

/ Not yet recruiting临床1期

A Phase 1, Open-Label, Dose-Escalation and Expansion Study of SNV1521 in Combination With RAS Inhibition in Participants With Locally Advanced Unresectable or Metastatic Pancreatic Cancer

This study is a Phase 1 clinical trial testing an oral investigational drug called SNV1521 together with a RAS-targeted cancer medicine in people with pancreatic cancer that cannot be removed by surgery or has spread. The main goals are to find doses of the drug combination that are safe and tolerable and to look for early signs that the treatment may help control the cancer. Participants will receive the study medicines in repeating cycles and will have regular blood tests, scans, and other exams to monitor side effects and how their cancer responds.

开始日期2026-09-01

申办/合作机构

Synnovation Therapeutics, Inc.

[+1]

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项与达拉西布相关的文献（医药）

2026-11-01·JOURNAL OF MOLECULAR BIOLOGY

The Allosteric Revolution: From Static Structures to Conformational Ensembles and Next-Generation Therapeutics

Review

作者: Jang, Hyunbum ; Nussinov, Ruth

The rapid emergence of breakthrough allosteric drugs, together with increasing emphasis on the molecular mechanisms of disease, underscores the critical importance of understanding biological processes at the molecular level. Among these, few concepts are as fundamental as the allosteric behavior of proteins. The importance of allostery was recognized decades ago; however, at the time proteins were viewed as static molecular structures rather than dynamic conformational ensembles that continuously interconvert among states with distinct free energies. The realization that proteins exist as dynamic conformational ensembles has transformed our understanding of oncogenic mutations, molecular recognition, protein regulation, and folding. These processes arise from the intrinsic allosteric nature of proteins embodied in their dynamic conformational ensembles. This conceptual advance has also accelerated the development of allosteric therapeutics. Here, we review the conceptual evolution of allostery from classical models to the conformational ensemble paradigm and discuss its implications for biology and modern drug discovery. We highlight breakthroughs in allosteric therapeutics, including a PROTAC that induces degradation of the Cyclin E-CDK2 complex; the pan-Ras molecular glue daraxonrasib for pancreatic cancer, whose allosteric mechanism is mediated through cyclophilin A rather than directly on Ras; a COP9 signalosome exosite-targeting agent; and other emerging modalities.

2026-09-01·ANTICANCER RESEARCH

Synergy of KRAS-inhibitor Daraxonrasib Combined With Recombinant Methioninase on Pancreatic-cancer Cells But Not Normal Cells

Article

作者: Han, Qinghong ; Hoffman, Robert M ; Bouvet, Michael ; Miyashi, Yuta ; Ishiguro, Tomoyuki ; Kim, Jinsoo ; Li, Shukuan

BACKGROUND/AIM:

Approximately 30% of all cancers have mutations in the KRAS proto-oncogene, GTPase (KRAS), and approximately 88% of pancreatic cancer tumors have mutations in KRAS. Recently, a novel KRAS inhibitor, daraxonrasib, with activity against both wild-type and mutant KRAS, has been developed and has shown efficacy in a phase III clinical trial of recurrent pancreatic-cancer patients, but with significant side-effects. In the present report, we determined whether daraxonrasib is synergistic with recombinant methioninase (rMETase) on pancreatic cancer cells that have the KRAS G12D mutation, compared to normal fibroblasts.

MATERIALS AND METHODS:

Cell viability was measured with the WST-8 reagent. The half-maximal inhibitory concentrations (IC₅₀) of rMETase and daraxonrasib were determined on PANC-1 human pancreatic cancer cells and Hs-27 human normal fibroblasts in vitro. The viability of PANC-1 and Hs-27 cells treated with rMETase alone, DXR alone, or a combination of rMETase and daraxonrasib was determined at their respective IC₅₀ values.

RESULTS:

The IC₅₀ values of daraxonrasib were 10.5 μM for PANC-1 and 8.4 μM for Hs-27. The IC₅₀ values of rMETase were 0.47 U/ml for PANC-1 and 0.42 U/ml for Hs-27. Daraxonrasib alone and rMETase alone showed significantly higher cytotoxicity towards PANC-1 cancer cells than Hs-27 fibroblasts. The combination of daraxonrasib and rMETase demonstrated selective synergistic cytotoxicity toward PANC-1 cells compared to normal Hs-27 fibroblasts (p<0.05).

CONCLUSION:

The present results suggest that the combination of daraxonrasib and rMETase has clinical potential for lowering the effective dose of daraxonrasib, thereby reducing daraxonrasib-associated side-effects, as well as increasing its efficacy.

2026-09-01·DRUG DISCOVERY TODAY

Daraxonrasib in pancreatic cancer: When progress disrupts practice

Article

作者: Philip, Philip A ; Azmi, Asfar S

2,307

项与达拉西布相关的新闻（医药）

19 小时之前

·BioSpace

SELLAS Life Sciences Presents Preclinical Data Demonstrating SLS009 Activity in Pancreatic Cancer Models at the 2026 AACR Conference on Pancreatic Cancer

SLS009 increased apoptosis more than six-fold versus daraxonrasib in a MYC-amplified, daraxonrasib-resistant patient-derived pancreatic cancer organoid model - Combination of SLS009 and daraxonrasib further increased apoptosis to 36.5% and necrosis to 30.6%, supporting evaluation of CDK9 inhibition as a potential strategy to enhance RAS-directed therapy - SLS009 combined with BET inhibition demonstrated synergistic activity and sustained suppression of MYC, providing additional evidence of SLS009 activity against MYC-driven pancreatic cancer biology - Sept. 25, 2026-- SELLAS Life Sciences Group, Inc. (NASDAQ: SLS) (“SELLAS’’ or the “Company”), a late-stage clinical biopharmaceutical company focused on the development of novel therapies for a broad range of cancer indications, today announced preclinical data from studies evaluating SLS009 (tambiciclib), its highly selective cyclin-dependent kinases 9 (CDK9) inhibitor, in patient-derived organoid models of pancreatic ductal adenocarcinoma (PDAC). The data are being presented at the American Association for Cancer Research (AACR) Conference on Pancreatic Cancer: New Frontiers in Biology and Therapeutic Development, being held September 25–28, 2026, in San Diego. The timing of this announcement reflects AACR’s embargo policy, under which the data presented at the conference were restricted from publication until 1:00 p.m. ET today. The studies, conducted in collaboration with researchers at the University of Wisconsin–Madison, evaluated SLS009 in MYC-amplified PDAC models, including a model resistant to the recently approved RAS inhibitor daraxonrasib (RMC-6236), as well as in combination with the BET inhibitor ZEN3694. MYC amplification is a biologically recognized mechanism of RAS targeting resistance. “These findings provide encouraging preclinical evidence that CDK9 inhibition may enhance the activity of RAS-directed therapy in pancreatic cancer, including in the setting of MYC-associated resistance,” said Dragan Cicic, MD, Senior Vice President, Clinical Development of SELLAS. “In a daraxonrasib-resistant patient-derived model, SLS009 demonstrated substantially greater activity than daraxonrasib alone and further increased apoptosis and necrosis when the two agents were combined. Together with the synergistic activity observed with BET inhibition, these data support a broader strategy of using SLS009 to disrupt transcriptional programs that may contribute to resistance to RAS-targeted therapies and provide a strong rationale for further evaluation in pancreatic cancer patients.” In a MYC-amplified, daraxonrasib-resistant patient-derived PDAC organoid model, SLS009 at 200 nM, daraxonrasib at 100 nM, and the combination of both agents were evaluated. Daraxonrasib was administered continuously, while SLS009 was removed after 24 hours to approximate its in vivo pharmacokinetic profile, with apoptosis and necrosis assessed at 72 hours. A separate MYC-amplified patient-derived PDAC organoid model evaluated SLS009 in combination with the BET inhibitor ZEN3694. The combination demonstrated synergistic activity, including increased cancer cell death and sustained suppression of MYC transcription. Notably, these effects were observed at a ZEN3694 concentration substantially below reported physiologically achievable exposure levels. Key findings: SLS009 demonstrated substantially greater single-agent activity than daraxonrasib in the daraxonrasib-resistant model, inducing 17.9% apoptosis versus 2.8% with daraxonrasib and 14.5% necrosis versus 2.7%. The combination of SLS009 and daraxonrasib further increased cancer cell death, inducing 36.5% apoptosis and 30.6% necrosis, compared with 17.9% and 14.5%, respectively, with SLS009 alone and 2.8% and 2.7%, respectively, with daraxonrasib monotherapy. SLS009 combined with ZEN3694 demonstrated synergistic activity, producing greater apoptosis and necrosis than either agent alone. The SLS009/ZEN3694 combination produced sustained suppression of MYC RNA and reduced expression of MYC and MCL-1 proteins, consistent with disruption of transcriptional pathways supporting tumor cell survival. Together, the findings support further investigation of CDK9 inhibition as a strategy to enhance RAS-directed therapy and potentially address MYC-associated resistance in pancreatic cancer. The BET combination data provide additional mechanistic support for SLS009-based approaches designed to disrupt MYC-dependent transcriptional programs and suggest the potential to enhance BET inhibition at lower drug exposures. “MYC is a particularly challenging oncogenic driver because it has historically been difficult to target directly,” said Jeremy D. Kratz, MD, Assistant Professor of Medicine and Principal Investigator at the University of Wisconsin–Madison. “Across these studies, CDK9 inhibition produced substantial activity in MYC-amplified pancreatic cancer models through two distinct therapeutic strategies. The activity of SLS009 supports its activity in a model with de novo daraxonrasib-resistance and together with the synergistic transcriptional suppression observed with BET inhibition, provides a strong rationale for further investigation of SLS009-based combinations in molecularly defined subsets of pancreatic cancer.” Poster presentation details: Title: Elucidating MYC allelic imbalance and therapeutic response in pancreatic ductal adenocarcinoma via patient-derived organoids Authors: Sawyer AG, Flannagan LE, Esguerra PN, Hossan MS, Kratz JD Poster Number: A036 – September 27, 2026: 5-7pm PST Title: Synthetic Lethality Through Combined BET and CDK9 Inhibition in MYC-Amplified Pancreatic Ductal Adenocarcinoma Authors: Esguerra PN, Cadarso M, Livingwell S, Hossan MD, Wong O, Kratz JD Poster Number: B127 – September 27, 2026: 5-7pm PST Title: Targeting dual CDK9 and KRASG12D selective inhibition as a novel combination therapy in pancreatic ductal adenocarcinoma Authors: Cadarso M, Esguerra P, Flannagan L, Hossan MS, Kratz JD Poster Number: B043 – September 27, 2026: 5-7pm PST SELLAS is a late-stage clinical biopharmaceutical company focused on the development of novel therapeutics for a broad range of cancer indications. SELLAS’ lead product candidate, GPS, is licensed from Memorial Sloan Kettering Cancer Center and targets the WT1 protein, which is present in an array of tumor types. GPS has the potential as a monotherapy and combination with other therapies to address a broad spectrum of hematologic malignancies and solid tumor indications. The Company is also developing SLS009 (tambiciclib) – potentially the first and best-in-class differentiated small molecule CDK9 inhibitor with reduced toxicity and increased potency compared to other CDK9 inhibitors. Data suggests that SLS009 demonstrated a high response rate in AML patients with unfavorable prognostic factors including ASXL1 mutation, commonly associated with poor prognosis in various myeloid diseases. The content above comes from the network. if any infringement, please contact us to modify.

临床结果AACR会议

2026-09-30

·抗体圈

首付款4亿美元！胡滔博士与默沙东达成合作

近日上海思璞锐医药与默沙东宣布，就临床前口服KRAS G12D（ON）抑制剂SPR2015达成全球独家授权。思璞锐获4亿美元首付款，含里程碑潜在总额最高21.3亿美元。行业震动点不在金额，而在对比：三年前，创始人胡滔刚以2400万美元首付款，把UA022卖给阿斯利康。三年后，同一靶点、同一人，首付款变4亿美元，翻了16倍。一笔“反常”的交易 SPR2015尚未进入临床。按全球授权惯例，临床前资产首付款通常千万美元级，过亿已罕见。 4亿美元，放到临床阶段资产也算高价。默沙东等不了。 2026年1月，它曾试图收购Revolution Medicines，目标直指RAS(ON)组合，但因估值分歧告吹。九个月后，Revolution的daraxonrasib已获FDA批准用于转移性胰腺导管腺癌，默沙东在G12D赛道仍空缺。错过一轮，代价就是四亿美元起步。这笔钱补的是管线里“必须要有”的拼图。临床前分子的硬数据默沙东掏钱，不全是焦虑。 SPR2015是口服、选择性KRAS G12D（ON）分子胶抑制剂。正常RAS在ON/OFF态切换，G12D突变后倾向持续活化。 SPR2015直接瞄准活化态KRAS G12D，与亲环素A及突变蛋白形成三元复合物，将其锁在抑制构象。 2026年AACR数据：在超15个结直肠癌CDX和PDX模型中，单药ORR 64.7%，DCR 94.1%。关键在“单药”。目前G12D临床验证主要来自Revolution的zoldonrasib，同机制，正接受FDA审评。 SPR2015未进临床，是同一路线上的第二选择。默沙东买的，是不继续落后的选项。为什么G12D值这个钱 KRAS突变覆盖20%-30%实体瘤；胰腺癌中KRAS突变达80%-90%，G12D占比近30%。胰腺癌“癌王”，二线ORR长期低于10%，中位PFS仅2-3个月。临床需求巨大，靶向药长期空白。 G12C已验证直接靶向KRAS可行，但G12C仅占KRAS突变约11%，G12D才是最大亚型。谁先拿下G12D，谁就拿到RAS通路最大市场。竞争白热化：恒瑞HRS-464推进III期，泰励TSN1611在临床，劲方GFH375推进。默沙东此时以4亿美元锁定，是晚到但必须到的入场券。胡滔的第二次出手最值得品读的不是默沙东出价，而是胡滔路径。胡滔博士，连续创业者，20余年医药经历，曾任职默克、安进、药明康德。创立思璞锐前，他是祐森健恒联合创始人兼CEO。 2023年11月，祐森健恒将临床前KRAS G12D抑制剂UA022全球权益授权阿斯利康，首付款2400万美元，里程碑总额最高3.95亿美元。 2024年底，胡滔创立思璞锐。六个月后，公司完成超2亿元天使轮，博远资本、汉康资本联合领投；2026年初Pre-A轮再融超3500万美元，弘晖基金领投，累计约6500万美元。然后就是这笔4亿美元首付款交易。从祐森健恒到思璞锐，从UA022到SPR2015，从2400万到4亿，胡滔用三年证明：正确靶点上做出差异化分子，临床前资产一样能卖出临床阶段价格。胡滔在公告中说，思璞锐专注RAS通路创新疗法，为胰腺癌、结直肠癌、肺癌等提供突破性方案。他赌的是RAS通路，不是某一个分子。一个临床前分子卖出4亿美元首付款，表面是默沙东的焦虑定价，底子里是胡滔对KRAS G12D价值的第二次兑现。靶点没变，人没变，变的是市场认知：从“值得赌”变成“必须买”。识别微信二维码，添加抗体圈小编，符合条件者即可加入抗体圈微信群！请注明：姓名+研究方向！版权声明本公众号所有转载文章系出于传递更多信息之目的，且明确注明来源和作者，不希望被转载的媒体或个人可与我们联系(cbplib@163.com)，我们将立即进行删除处理。所有文章仅代表作者观不本站。

2026-09-30

·BioSpace

AIM ImmunoTech Discusses Ampligen®’s Potential to Complement Emerging Pancreatic Cancer Therapies in New CEO Corner Video

Company highlights supportive survival observations, potential for biomarker-driven patient selection and upcoming Phase 2 DURIPANC milestones Access it here OCALA, Fla., Sept. 30, 2026 (GLOBE NEWSWIRE) -- AIM ImmunoTech Inc. (NYSE American: AIM) (“AIM” or the “Company”) today announced the release of a new installment of its CEO Corner series featuring Chief Executive Officer Thomas K. Equels discussing how Ampligen® (rintatolimod) could fit into the evolving treatment landscape for pancreatic cancer. In the CEO Corner, Equels discusses recent advances in pancreatic cancer treatment and why AIM believes Ampligen’s distinct immune-modulating approach warrants continued investigation. Rather than directly targeting a cancer-driving pathway, Ampligen has the potential to induce a broad-spectrum therapeutic effect that amplifies a patient’s innate immune response, creating the potential for a complementary role alongside or following therapies that act through different mechanisms. The segment also highlights observations from a Dutch Named Patient Program (“NPP”) in which patients with radiologically stable pancreatic cancer after FOLFIRINOX received Ampligen as a maintenance treatment. In an exploratory analysis of 39 patients with a neutrophil-to-lymphocyte ratio (“NLR”) below 4.5, median overall survival was 34.8 months, measured from the start of FOLFIRINOX. This encouraging observation supports further investigation of Ampligen following chemotherapy. Advances with FOLFIRINOX and daraxonrasib highlight the evolving treatment landscape in pancreatic cancer. The following chart summarizes the median overall survival results from the selected patients from NPP program as well as data from the separate clinical trials of FOLFIRINOX in metastatic pancreatic cancer and a daraxonrasib clinical trial of RAS G12 mutation patients with previously treated metastatic pancreatic cancer. However, differences in patient selection, disease stage, treatment setting, and the timing of survival measurement prevent direct comparisons between the NPP findings and survival results from trials of these therapies. These findings provide a rationale for randomized studies to determine whether adding Ampligen after chemotherapy improves outcomes. Further research is also needed to establish whether NLR can identify patients more likely to benefit specifically from Ampligen, rather than patients with a generally more favorable prognosis. “Pancreatic cancer continues to present an urgent need for better treatment strategies, even as important new therapies emerge,” said Equels. “Ampligen approaches the disease differently through its potential to activate the innate immune response. We believe the powerful overall survival signal seen in the Named Patient Program, together with the clinical and biomarker data being generated through DURIPANC, will provide a compelling rationale to continue evaluating Ampligen’s potential role in pancreatic cancer. Ultimately, our goal is to get drug approval, which will be based on overall survival, in all probability focused on patients with neutrophil-to-lymphocyte ratios below 4.5.” AIM is continuing to investigate Ampligen through the ongoing Phase 2 DURIPANC study evaluating Ampligen in combination with AstraZeneca’s durvalumab in metastatic pancreatic cancer. The study’s primary endpoint is Clinical Benefit Rate at 24 weeks following initiation of combination therapy, with topline results anticipated in the first quarter of 2027. The study is also evaluating progression-free survival, overall survival and immune profiling, with overall survival analysis expected to begin in 2027. AIM anticipates topline results from DURIPANC in the first quarter of 2027, followed by its analysis of overall survival – the gold standard for drug approval – commencing in Q3 2027. If supported by the clinical and biomarker data, the Company believes the study could help define the parameters of a potential follow-up pivotal Phase 3 program and provide positive clarity around where Ampligen fits within an evolving pancreatic cancer treatment landscape. The latest CEO Corner segment is now available on the Company’s website here . About AIM ImmunoTech Inc. AIM ImmunoTech Inc. is an immuno-pharma company focused on the research and development of its lead product, Ampligen® (rintatolimod), for the treatment of late-stage pancreatic cancer, a lethal and unmet global health problem. Ampligen is a dsRNA and highly selective TLR3 agonist immuno-modulator that has shown broad-spectrum activity in clinical trials. For more information, please visit aimimmuno.com and connect with the Company on X , LinkedIn , and Facebook . Cautionary Statement This press release contains forward-looking statements within the meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended, that involve a number of risks and uncertainties. Any forward-looking statements set forth in this press release speak only as of the date hereof. Such forward-looking statements may include statements relating to: Ampligen’s potential efficacy and applicability in the treatment of pancreatic cancer; the timing of commencement, enrollment, completion, and results of clinical trials; intellectual property expansion and regulatory progress; and timing for receiving government approvals, if at all. For all forward-looking statements, the Company claims the protection of the safe harbor for forward-looking statements contained in the Private Securities Litigation Reform Act of 1995. All statements in this press release other than statements of historical fact, including statements regarding the potential of Ampligen’s mechanism of action, anticipated regulatory milestones, our future results of operations and financial position, our business strategy and plans, and our objectives for future operations, are forward-looking statements. Words such as “believe,” “may,” “might,” “will,” “could,” “should,” “can,” “estimate,” “continue,” “anticipate,” “intend,” “expect,” “envision,” “potential” and similar expressions are intended to identify forward-looking statements, but the absence of these words does not mean that a statement is not forward-looking. The Company does not undertake to update any of these forward-looking statements to reflect events or circumstances that occur after the date hereof, except as required by applicable law. The Company is in various stages of seeking to determine whether Ampligen will be effective in the treatment of multiple types of viral diseases, cancers, and immune-deficiency disorders, and disclosures in the Company’s reports filed with the SEC, on its website, and in its press releases set forth its current and anticipated future activities. These activities are subject to change for a number of reasons. Significant additional testing and trials will be required to determine whether Ampligen® will be effective in the treatment of pancreatic cancer. No assurance can be given as to whether current or planned clinical trials will be successful or yield favorable data, and the trials are subject to many factors including lack of regulatory approval(s), lack of study drug, lack of adequate funding, or a change in priorities at the institutions sponsoring other trials. Even if these clinical trials are initiated, the Company cannot assure that the clinical studies will be successful or yield any useful data. No assurance can be given that the findings in preliminary studies will prove true or that such studies will yield favorable results, or that future studies will not result in findings that are different from those reported in the studies referenced in the Company’s reports filed with the SEC, on the Company’s website, and in its press releases. Operating in foreign countries carries with it a number of risks, including potential difficulties in enforcing intellectual property rights. The Company cannot assure that its potential foreign operations will not be adversely affected by these risks. For a detailed discussion of these and other risk factors, please review the “Risk Factors” section in the Company’s most recent Annual Report on Form 10-K and subsequent Quarterly Reports on Form 10-Q filed with the SEC. These filings are available at and . You should not place undue reliance on any forward-looking statements. The information found on the Company’s website or on other websites referenced or linked to in this press release is not incorporated by reference into this press release and such information is referenced or linked for reference purposes only. A photo accompanying this announcement is available at CONTACT: Investor Contact: JTC Team, LLC Jenene Thomas 908.824.0775 AIM@jtcir.com

临床2期免疫疗法

100 项与达拉西布相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D13265	-	-	-

研发状态

批准上市

10 条最早获批的记录,

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适应症	国家/地区	公司	日期
晚期胰腺腺癌	美国	Revolution Medicines, Inc.	2026-08-26
转移性胰腺腺癌	美国	Revolution Medicines, Inc.	2026-08-26

未上市

10 条进展最快的记录,

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适应症	最高研发状态	国家/地区	公司	日期
胰腺导管腺癌	申请上市	美国	Revolution Medicines, Inc.	2026-07-22
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
RAS突变非小细胞肺癌	临床3期	意大利	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, WCLC2026)	临床3期	非小细胞肺癌二线 RAS-Mutant	420	Daraxonrasib (RMC-6236)	淵淵遞繭繭蓋網鬱鹽鹹(鏇壓遞鑰廠繭範醖構觸) = 觸鹹鬱鑰襯願醖糧鏇繭選齋網夢鏇鏇膚鹽獵夢 (醖廠築網範範遞蓋遞鏇, 6 ~ 12.3)	积极	2026-09-12
				Docetaxel	築鬱餘繭觸遞積憲膚憲(壓製築膚築廠築簾遞願) = 夢餘鹹積醖構窪鹽蓋艱夢築積蓋糧壓鬱膚鹹築 (齋齋艱鏇獵網遞糧鏇遞, 5.6 ~ 15.6)
NCT06625320 (RASolute 302, Pubmed \| N Engl J Med)	临床3期	转移性胰腺导管腺癌 RAS G12 mutations	500	Daraxonrasib	積艱壓襯衊積鏇淵鏇積(齋醖範築簾願膚夢艱顧) = 築膚顧獵膚簾衊觸夢積蓋顧鏇願範獵築製築觸 (齋餘觸範夢簾窪衊鏇構 ) 更多	积极	2026-07-23
				Chemotherapy	積艱壓襯衊積鏇淵鏇積(齋醖範築簾願膚夢艱顧) = 醖糧齋繭觸醖醖範艱觸蓋顧鏇願範獵築製築觸 (齋餘觸範夢簾窪衊鏇構 ) 更多
NCT06625320 (RASolute 302, ASCO2026)	临床3期	转移性胰腺腺癌二线 RAS G12 \| RAS G13 \| Q61	500	Daraxonrasib 300 mg PO QD	鬱築壓糧廠廠窪獵築顧(獵鹹蓋顧觸淵範繭鬱獵) = 範鑰築壓築壓衊顧範觸壓壓簾鹽遞鹽鹹壓網選 (網餘繭構夢鏇製構襯構, 10.0–NE) 更多	积极	2026-05-29
				Investigator’s choice of SOC cytotoxic chemo	鬱築壓糧廠廠窪獵築顧(獵鹹蓋顧觸淵範繭鬱獵) = 鹽選淵顧衊獵膚醖鹹製壓壓簾鹽遞鹽鹹壓網選 (網餘繭構夢鏇製構襯構, 5.4–8.2) 更多
NCT05379985 (RMC-6236-001, NEWS 1 \| NEWS 2 \| NEWS 3 \| Literature) 人工标引	临床1/2期	KRAS突变胰腺导管腺癌 RAS mutations	168	Daraxonrasib (RAS-mutated Pancreatic Ductal Adenocarcinoma)	鑰積鏇鹹願艱窪鬱襯糧(構繭衊選製襯壓鹽鹽築) = 簾選膚遞醖繭醖鹽醖壓鏇鏇衊膚選積齋鏇鹹壓 (網膚鑰鬱顧鹽憲鬱遞構 ) 更多	积极	2026-05-14
				Daraxonrasib (RAS G12 mutations)	構醖壓糧顧艱選顧糧顧(醖獵窪夢繭艱艱觸鏇鑰) = 積艱選顧窪齋鏇淵夢糧鬱觸積艱觸簾製簾製範 (衊衊壓簾積築鬱齋觸鬱, 17 ~ 56) 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)	顧窪積膚顧範選網鬱獵(醖蓋憲選壓築顧觸構鏇) = 膚糧積衊糧蓋淵廠襯餘觸範鹽鏇積構淵積獵遞 (襯觸窪選獵鹹艱鬱鹹鑰, 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.)	顧窪積膚顧範選網鬱獵(醖蓋憲選壓築顧觸構鏇) = 窪鹹鏇鹹鏇鬱範簾獵鏇觸範鹽鏇積構淵積獵遞 (襯觸窪選獵鹹艱鬱鹹鑰, 79 ~ 98) 更多
NCT06881784 (RASolve 301, AACR2026)	临床3期	RAS mutation	420	Daraxonrasib	簾淵範顧鹹積鑰選獵願(顧窪簾襯積積選製齋製) = 鏇積廠鹹構壓積夢構壓齋膚憲廠鹹獵築鏇艱鹽 (膚積蓋簾齋夢積觸遞鏇, 6 ~ 12.3) 更多	积极	2026-04-21
				Docetaxel	襯窪鑰築醖糧夢襯顧築(製憲蓋糧構糧網構顧鹽) = 夢齋願築製鏇鏇餘積鹽艱醖醖簾鏇窪構廠糧膚 (襯築衊餘艱鹽獵壓鏇憲, 8.1 ~ 10.8) 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	築鬱獵壓憲夢醖鏇壓蓋(壓構製製鹹淵夢鹽鹽襯) = 選醖鹹顧範夢鹽鏇衊繭廠糧夢鑰壓糧網簾夢構 (簾觸窪範餘醖繭艱獵膚, 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	500	Daraxonrasib 300 mg	憲衊齋壓齋築糧築鑰願(遞憲選廠窪齋廠壓壓糧) = 餘憲顧繭糧艱夢鏇積繭繭範願鹹淵餘遞網蓋壓 (積遞廠鏇鏇鑰襯簾壓鬱 ) 更多	积极	2026-04-13
				Chemotherapy	憲衊齋壓齋築糧築鑰願(遞憲選廠窪齋廠壓壓糧) = 壓鑰壓製夢膚鏇選淵醖繭範願鹹淵餘遞網蓋壓 (積遞廠鏇鏇鑰襯簾壓鬱 ) 更多
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	構餘餘遞膚蓋餘夢願鹽(簾觸憲簾鏇蓋築壓蓋鑰) = 夢網衊製窪鹽淵衊繭鹹鹽網窪簾鏇鏇選壓遞夢 (網鏇餘壓鏇簾蓋願範膚 ) 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-mutant	40	Daraxonrasib	淵廠艱餘蓋淵艱選艱構(鑰觸淵憲觸積膚簾淵窪) = 網簾選選衊鏇醖積顧壓艱網簾選醖願願壓顧顧 (憲網構膚鹽餘築範製淵 ) 更多	积极	2025-09-10