This phase I trial tests the safety, side effects, and best dose of camonsertib in combination with stereotactic body radiation therapy in controlling disease in patients with head and neck squamous cell cancer that has come back after a period of improvement (recurrent) or that cannot be removed by surgery (unresectable). Camonsertib may stop the growth of tumor cells and may kill them by blocking some of the enzymes needed for cell growth. Stereotactic body radiation therapy is a type of external radiation therapy that uses special equipment to position a patient and precisely deliver radiation to tumors in the body (except the brain). The total dose of radiation is divided into smaller doses given over several days. This type of radiation therapy helps spare normal tissue. Giving camonsertib in combination with stereotactic body radiation therapy may help control disease in patients with recurrent or unresectable head and neck squamous cell cancers.

开始日期2025-12-26

申办/合作机构

National Cancer Institute

NCT05601440

/ Recruiting临床2期IIT

A Liquid-biopsy Informed Platform Trial to Evaluate Treatment in CDK4/6-inhibitor Resistant ER+/HER2- Metastatic Breast Cancer

This study is being done to answer the following question: Can testing breast cancer for DNA abnormalities or "biomarkers" help predict which patients are most likely to be helped by certain treatments? The pre-study screening is being done to test a sample of blood (or tumour tissue) for biomarkers to see if patients can participate in the study

开始日期2023-06-13

申办/合作机构

Canadian Cancer Trials Group

NCT05605509

/ Active, not recruiting临床2期IIT

A Phase II Study of RP-6306 in Patients With Advanced Cancer

This study is being done to answer the following questions:
* Is the new drug, RP-6306, safe to use, and what effects does it have on cancer when given with standard treatment?
* If there are specific biomarkers, do patients have an improved response to treatment compared to those without the biomarker?
This study is being done to find out if this approach is better or worse than the usual approach for this type of cancer. The usual approach is defined as care most people get for this type of cancer.

开始日期2023-05-24

申办/合作机构

Canadian Cancer Trials Group

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100 项与 Camonsertib 相关的临床结果

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100 项与 Camonsertib 相关的转化医学

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100 项与 Camonsertib 相关的专利（医药）

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项与 Camonsertib 相关的文献（医药）

2025-07-01·Science Bulletin

Molecular architecture and inhibition mechanism of human ATR-ATRIP

Article

作者: Jian, Lingfei ; Xu, Chenchen ; Cai, Gang ; Wang, Guangxian ; Zhao, Zhanpeng ; Zheng, Zexuan ; Wang, Xuejuan ; Zhang, Qingjun ; Xu, Xinyi ; Wang, Po

The ataxia telangiectasia-mutated and Rad3-related (ATR) kinase is a master regulator of DNA damage response and replication stress in humans. Targeting ATR is the focus of oncology drug pipelines with a number of potent, selective ATR inhibitors currently in clinical development. Here, we determined the cryo-EM structures of the human ATR-ATRIP complex in the presence of VE-822 and RP-3500, two ATR inhibitors currently in Phase II clinical trials, achieving an overall resolution of approximately 3 Å. These structures yield a near-complete atomic model of the ATR-ATRIP complex, revealing subunit stoichiometry, intramolecular and intermolecular interactions, and critical regulatory sites including an insertion in the PIKK regulatory domain (PRD). Structural comparison provides insights into the modes of action and selectivity of ATR inhibitors. The divergent binding modes near the solvent side and in the rear pocket area of VE-822 and RP-3500, particularly their disparate binding orientations, lead to varying conformational changes in the active site. Surprisingly, one ATR-ATRIP complex binds four VE-822 molecules, with two in the ATR active site and two at the ATR-ATR dimer interface. The binding and selectivity of RP-3500 depend on two bound water molecules, which may be further enhanced by the substitution of these bound waters. Our study provides a structural framework for understanding ATR regulation and holds promise for assisting future efforts in rational drug design targeting ATR.

2024-12-26·JOURNAL OF MEDICINAL CHEMISTRY

Discovery of ART0380, a Potent and Selective ATR Kinase Inhibitor Undergoing Phase 2 Clinical Studies for the Treatment of Advanced or Metastatic Solid Cancers

Article

作者: Ding, Yanbing ; Vijayan, R. S. K. ; Smith, Graeme C. M. ; Cross, Jason B. ; Lapointe, David ; Shepard, Hannah E. ; Jiang, Yongying ; Carroll, Christopher L. ; Do, Mary K. Geck ; Lively, Sarah ; Heald, Robert A. ; Johnson, Michael G. ; Liu, Chiu-Yi ; Kang, Zhijun ; Giuliani, Virginia ; Pang, Jihai ; Di Francesco, M. Emilia ; Heffernan, Timothy ; Wu, Qi ; Fang, Cheng ; Jones, Philip ; Williams, Christopher C. ; Suarez, Catalina ; Li, Meng ; Ma, XiaoYan ; Bardenhagen, Jennifer P. ; Yau, Anne Ju ; Yap, Timothy A. ; Lv, Xiaobing ; Robinson, Helen M. R.

One of the hallmarks of cancer is high levels of DNA replication stress and defects in the DNA damage response (DDR) pathways, which are critical for maintaining genomic integrity. Ataxia telangiectasia and Rad3-related protein (ATR) is a key regulator of the DDR machinery and an attractive therapeutic target, with multiple ATR inhibitors holding significant promise in ongoing clinical studies. Herein, we describe the discovery and characterization of ART0380 (6), a potent and selective ATR inhibitor with a compelling in vitro and in vivo pharmacological profile currently undergoing Phase 2 clinical studies in patients with advanced or metastatic solid tumors as monotherapy and in combination with DNA-damaging agents (NCT04657068 and NCT05798611). ART0380 (6) has a favorable human PK profile suitable for both intermittent and continuous once-daily (QD) dosing, characterized by a dose-proportional increase in exposure and low variability.

2024-12-16·CLINICAL CANCER RESEARCH

Genotype-Directed Synthetic Cytotoxicity of ATR Inhibition with Radiotherapy

Article

作者: Riaz, Nadeem ; Gardner, Rui ; Reis-Filho, Jorge ; Roulston, Anne ; Morris, Stephen ; McDermott, Niamh ; Novaj, Ardijana ; Pei, Xin ; Mandelker, Diana ; Ma, Jennifer ; Setton, Jeremy ; Sinha, Sonali ; Pareja, Fresia ; Ng, Victor ; Longhini, Ana Leda F. ; Powell, Simon N. ; Grimsley, Helen ; Rosen, Ezra ; Koehler, Maria ; Khan, Atif ; Lee, Nancy

Abstract:

Purpose::

The importance of the DNA damage response in mediating effects of radiotherapy (RT) has galvanized efforts to target this pathway with radiosensitizers. Yet early clinical trials of this approach have failed to yield a benefit in unselected populations. We hypothesized that ataxia–telangiectasia mutated (Atm)–null tumors would demonstrate genotype-specific synergy between RT and an inhibitor of the DNA damage response protein ataxia–telangiectasia and Rad3-related (ATR) kinase.

Experimental Design::

We investigated the synergistic potential of the ATR inhibitor (ATRi) RP-3500 and RT in two Atm-null and isogenic murine models, both in vitro and in vivo. Staining of γ-H2AX foci, characterization of the immune response via flow cytometry, and tumor rechallenge experiments were performed to elucidate the mechanism of interaction. To examine genotype specificity, we tested the interaction of ATRi and RT in a Brca1-null model. Finally, patients with advanced cancer with ATM alterations were enrolled in a phase I/II clinical trial to validate preclinical findings.

Results::

Synergy between RP-3500 and RT was confirmed in Atm-null lines in vitro, characterized by an accumulation of DNA double-strand breaks. In vivo, Atm-null tumor models had higher rates of durable control with RT and ATRi than controls. In contrast, there was no synergy in tumors lacking Brca1. Analysis of the immunologic response indicated that efficacy is largely mediated by cell-intrinsic mechanisms. Lastly, early results from our clinical trial showed complete responses in patients.

Conclusions::

Genotype-directed radiosensitization with ATRi and RT can unleash significant therapeutic benefit and could represent a novel approach to develop more effective combinatorial synthetic cytotoxic RT-based treatments.See related commentary by Schrank and Colbert, p. 5505

116

项与 Camonsertib 相关的新闻（医药）

2025-10-28

·N C S

License-in模式成为企业研发管线快速扩充重要手段

1. License-in 模式概述与发展历程1.1 License-in 模式的概念界定与核心特征 License-in（许可引进）是企业通过支付 “首付款 + 里程碑付款 + 销售提成”，从外部获取技术、专利等商业化权利的合作模式。相较于自主研发，可缩短周期、快速补管线；相较于并购，成本低、灵活性高，但存在合作深度不足、易削弱自主研发能力的风险。1.2 License-in 模式的发展历程与演变全球起源：20 世纪 80 年代美国生物医药行业兴起，21 世纪成为跨国药企管线扩充重要策略。中国阶段：起步（2015-2017）：再鼎医药、云顶新耀等 Biotech 借其快速建管线。爆发（2018-2021）：2021 年交易金额达 130.86 亿美元峰值，传统药企加入。调整（2022 至今）：2024 年交易仅 41 笔、金额 8 亿美元，License-out（对外授权）快速增长，产业转向 “走出去”。1.3 License-in 模式在不同行业的应用特点生物医药：交易金额高、监管严、技术评估复杂、回报周期 5-10 年，是核心应用领域。软件与信息技术：技术迭代快、标准化高，向订阅制转型。制造业：聚焦工业技术 / 工艺，需专业支持与长期服务，如日系航空企业借其降本 19%。消费品：依赖品牌授权，需快速响应市场，2024 年全球授权市场规模 3696 亿美元，娱乐 / 角色授权占比 38%。2. License-in 市场现状与发展趋势2.1 全球 License-in 市场规模与交易特征 2024 年上半年全球生物制药许可交易总价值 763 亿美元，首付款占比仅 6%（2019 年为 13%），估值更理性。 2023 年全球生命科学交易数同比降 27%，北美、欧洲为核心市场；中国跨境药品许可交易 1208 项（2019-2023），美国是中国 License-in 主要授权方（48.7%）。肿瘤是主要治疗领域（License-in 占 42.3%、License-out 占 48.9%），其次为感染性疾病。2.2 中国 License-in 市场发展状况交易数据下滑：2024 年上半年交易 23 笔，前三季度 29 笔（同比降 62%），金额 18.4 亿美元（同比降 63%）。结构变化：2024 年药品许可交易 117 笔（降 23%），金额超 230 亿美元（增 34%），单笔金额提升；44.1% 交易聚焦已获批 / NDA 阶段药物，非肿瘤药占比从 2019 年 42% 升至 2023 年 80%。2.3 License-in 市场的发展趋势分析 “引进来” 转 “走出去”：2024 年中国 License-out 达 94 笔（为 License-in 的 2 倍 +），金额 519 亿美元，东南亚成重要下游市场。模式创新：订阅制普及，“NewCo”（合资公司）模式兴起。技术多元化：ADC（占 License-out 15%+）、双抗、CGT（细胞基因疗法）、小核酸药物成热点。估值与监管：首付款占比下降，科创板加强对 License-in 企业独立性审核（如海和药物 IPO 被否）。3. License-in 模式的典型案例分析3.1 成功案例分析云顶新耀：2017 年成立，引进依嘉、耐赋康等产品，2024 年上半年收入 3.02 亿元（增 158%）并首次盈利；8 款管线覆盖 4 大领域，预期 2030 年重点产品峰值销售 100 亿。再鼎医药：2013 年成立，通过 10 余项 License-in 建管线，2024 年前三季度收入 2.9 亿美元（增 44.32%）；尼拉帕利 2020 年进医保后三年销售额破 20 亿，引进项目原研方多被跨国巨头收购（如 Tesaro 被 GSK 收购）。3.2 失败案例分析罗氏退还 camonsertib：2022 年预付 1.25 亿，2024 年因临床数据不及预期、竞争激烈退还 Repare，已支付 4000 万美元。阿斯利康退还 roxadustat：2013-2016 年累计支付 5.32 亿美元，因 FDA 担忧安全性要求补做试验，2024 年退还 FibroGen。 BMS 退还多项目：2021 年以 2 亿预付获 TIGIT 双抗等项目，2024 年因战略重组、聚焦核心领域退还，Agenus 仅获 4500 万美元里程碑款。3.3 案例总结与经验启示成功关键：精准市场判断、前瞻性选品、强执行能力（临床 / 商业化）、灵活交易结构、“自主研发 + License-in” 双轮驱动。核心风险：技术（临床数据不达标）、监管（审批受阻）、市场（竞争 / 定价压力）、合作（授权方战略调整）、财务（高额付款压力）。4. License-in 模式的成功因素分析4.1 企业内部能力要求 BD 能力：需具备项目筛选、谈判、融资能力，如再鼎医药通过 BD 快速锁定优质项目。临床推进能力：涵盖试验设计、运营、监管沟通、患者招募，云顶新耀耐赋康中国桥接试验仅 2 年获批。商业化能力：含市场准入（如尼拉帕利进医保）、销售推广，需专业团队支撑。自主研发能力：避免依赖外部，云顶新耀建 mRNA 平台、再鼎医药加强自研管线。4.2 外部环境因素监管政策：中国药审改革加速上市，但科创板对技术独立性要求提高；各国注册差异大（如 FDA 审批严）。知识产权保护：2024 年全球知识产权市场规模 1.8 万亿美元（2022 年增 20%），但侵权、泄密风险仍存。资本市场：2017-2021 年追捧 License-in，2024 年因业绩不及预期转向谨慎，更关注商业化能力。产业阶段：中国医药从仿制转创新，临床前 / I 期项目引进占比从 2019 年 30% 升至 2025 年 68%。4.3 交易结构设计要素支付结构：首付款占比 5-20%（2024 年 6%），里程碑款挂钩研发 / 注册 / 商业化，销售提成 10-30%。地域与权利：中国常见 “大中华区权益”，需明确授权类型（独家 / 非独家）、转授权权利。知识产权：需覆盖基础 / 改进专利及数据，改进专利归属影响长期权益。风险与收益：明确研发 / 市场风险分担，约定退出机制（终止条款、违约责任）。5. License-in 模式面临的挑战与风险5.1 技术与评估挑战评估复杂性：需从技术可行性（如 ADC 的抗体 / 毒素 / 连接子）、临床价值、商业潜力、知识产权多维度评估。信息不对称：授权方可能隐瞒负面信息，需通过全维度尽职调查降低风险。 l研发失败风险：创新药上市成功率不足 10%，II 期临床成功率仅 31.3%，存在临床前毒性、审批受阻等问题。5.2 商业化与市场风险竞争加剧：热门领域（如 PD-1）同质化严重，技术迭代快（化疗→靶向→免疫），医保谈判压缩定价空间。商业化执行风险：市场准入（注册 + 医保）、销售网络建设（肿瘤团队初始投入数千万）、供应链管理均需大量资源。支付风险：医保政策影响大（2024 年谈判 “以价换量”），不同市场支付体系差异显著，高价药需患者援助项目。5.3 合作与管理风险合作管理：双方目标（授权方重短期收益、引进方重长期成功）、文化差异可能引发冲突，需保障信息共享。知识产权纠纷：存在侵权、专利无效风险，技术秘密泄露可能丧失竞争优势。整合成本：技术转移（占交易金额 10-20%）、团队 / 管理体系整合需大量投入，难度高。6. License-in 模式的发展前景与展望6.1 未来发展趋势预测合作模式升级：从单一引进转向 “研发 + 生产 + 销售” 综合合作，“NewCo” 模式、长期战略联盟增多。数字化融合：AI 用于项目评估，区块链保护知识产权，云计算简化技术转移。新兴技术机遇：ADC（科伦博泰等企业领先）、双抗（2028 年市场 525 亿美元）、CGT（罕见病治愈潜力）、小核酸（舶望制药与诺华合作）、AI 制药成热点。6.2 对企业的战略建议差异化策略：聚焦细分领域（如罕见病）、新兴技术（如小核酸），探索联合开发等创新合作模式。系统化风控：组建跨领域评估团队，制定多维度评估标准，建立项目跟踪机制。能力与生态建设：强化自研能力，建专业 BD 团队，构建 “CRO+CDMO + 投资机构” 产业生态，重视复合型人才培养。7. 结论与总结市场格局：全球 License-in 进入调整期，中国从 “引进来” 转向 “走出去”，2024 年 License-out 金额为 License-in 的 60 倍 +。核心结论：成功需 “BD + 临床 + 商业化 + 自研” 四大能力，需应对技术、市场、合作多重风险，未来聚焦技术多元化与模式创新。展望：License-in 仍将发挥作用，中国企业需平衡合作与自研，实现 “合作共赢”，助力全球医药创新。

引进/卖出抗体药物偶联物并购IPO

2025-09-01

·Bioconjugate 药研备忘

专利动态|XDC专利更新：多种新型有效载荷（2025.08.28）

恒瑞医药 WO2025176180 HER2-艾日布林衍生物 SHR-4602 8月28日，恒瑞医药公开一篇ADC专利，涉及靶点HER2，抗体为 Pertuzumab，有效载荷为艾日布林衍生物，该 ADC 旨在治疗抗 HER2 ADC 耐药的肿瘤，包括乳腺癌、胃癌、结直肠癌、尿路上皮癌、胆管癌、肺癌等。 SHR-4602 是恒瑞自主研发的一种新型抗 HER2 ADC，抗体采用帕妥珠单抗，利用肽连接子偶联有效载荷 ER300（艾日布林衍生物）。恒瑞在2024年的 AACR 会议摘要中披露该药物的临床前数据。2024年12月，SHR-4602 的新药临床申请获 NMPA 批准，用于晚期实体瘤，目前该药物正在进行临床 2 期研究。 SONY WO2025177173 抗体-聚合物偶联物 8月28日，Sony 集团公开一篇抗体聚合物偶联药物专利，靶点涉及 CD33、CD30、CD7、CD123。聚合物含有侧链的脱氧尿苷基团，有效载荷为 MMAE，通过 VC 连接子裂解释放，同时聚合物含有高亲水性结构 HEG（即磷酸-PEG），通过灵调整长度可以根据需要提高或降低 ADC 药物整体水溶性。日内瓦大学 WO2025176733 ATR或CHK1抑制剂 ADC 8月28日，日内瓦大学公开一篇 ADC 专利，涉及非细胞毒载荷，专利公开采用 ATR 或 CHK1 抑制剂为 ADC 有效载荷，其中 ATR 抑制剂优选 camonsertib、Elimusertib；CHK1抑制剂优选 Prexasertib。实施例将 ATR 或 CHK1 抑制剂通过肽连接子与抗 HER2 抗体偶联，其中肽连接子包括GPVK、GGFG、GGNN、GNLK、GLVK、GPLK、GGGF、GPVR、VC-PABC 等。 Abdera WO2025179051、WO2025179031 DLL3 RDC ABD-147、5T4 RDC 8月28日，Abdera Therapeutics 公开两篇 RDC 专利，涉及靶点 DLL3 和 5T4，靶向部分为抗体片段 VHH-Fc，与螯合剂 DOTA-linker 通过四氟苯酯（OTFP）接头偶联，螯合剂-抗体比（CAR）值约为4，然后分别 111In、177Lu 或 225Ac 进行放射性标记后得到 RDC 药物。 Abdera Therapeutics 的核心研发项目之一 ABD-147 是一款靶向 DLL3 的 RDC 药物，其基于公司独特的 ROVEr™ 平台（设计和开发具有可调节药代动力学特性的放射性药物）开发，以提高治疗效果并减少副作用。ABD-147 的 IND 申请在2024年04月获得美国 FDA 批准，目前正在进行临床 1 期研究，用于治疗小细胞肺癌和肺大细胞神经内分泌癌。 ABD-147 对应的诊断性核药和治疗性核药分别为 111In-ABD147 和 225Ac-ABD147。往期分享：专利动态|XDC的新linekr或新靶点专利动态|偶联药物新专利（2025.08.14）专利动态|新一周的ADC专利（2025.08.07）专利动态|最新偶联药物（XDC）专利（2025.07.31）专利动态 | 新ADC专利公开：新机制载荷/新靶点/新项目(2025.07.24) 专利分享|糖基偶联新型二糖连接子：齐鲁 vs GlycoT 专利动态 | 最新ADC药物相关专利专利动态 | 在研ADC最新专利公开专利分享 | 先声药业FGFR2b ADC药物SIM0686 专利分享 | 亲合力生物的白蛋白偶联药物 QHL-1618，肿瘤微环境释放专利分享 | 新型ADC载荷靶向破解肿瘤耐药专利分享 | "孤勇者"的妥协？Heidelberg Pharma获华东医药投资后转向TOP1i ADC 专利分享 | 先声药业ADC偶联"接头"新技术公开专利分享 | MTG酶定点偶联+点击化学：Hummingbird 双载荷ADC技术公开上海诗健生物新一代ADC平台专利公开 **说明：本公众号内容基于公开信息的整理和分析，如涉及侵权请联系处理；作者水平有限，对专利或文献的解读可能存在疏漏之处，请以原文为准；欢迎个人转发分享，如需转载至公众号或其他平台，请注明出处并遵守版权规范。** 参考资料： Tian Y, Sun X, Yang C, Liao C. Abstract 3195: SHR-4602, next generation of HER2-targeting ADC with potent anti-tumor efficacy overcoming the resistance of HER2 ADC with Topo I inhibitor payload in xenograft models. Cancer Research. 2024;84(6_Supplement):3195-3195. doi:10.1158/1538-7445.am2024-3195 药物临床试验登记与信息公示平台官网 clinicaltrials 官网公司官网 END 欢迎关注，与您分享偶联药物领域最新突破

抗体药物偶联物临床申请临床1期AACR会议免疫疗法

2025-07-16

·FierceBiotech

Repare finds suitor for paused PKMYT1 inhibitor in current partner Debiopharm

Debiopharm will pay $10 million upfront for the rights to lunresertib.\n Seven months after pressing pause on its plans for its PKMYT1 inhibitor, Repare Therapeutics has found a partner to take the cancer drug forward.Back in January, Repare abandoned phase 3 plans to evaluate the candidate, called lunresertib, in combination with its ATR inhibitor camonsertib for platinum-resistant ovarian cancer. While the biotech continued to assess lunresertib in combination with Debiopharm’s WEE1 inhibitor as part of a collaboration, Repare said at the time that it would halt other plans to develop lunresertib unless a partner can be found.That partner has finally appeared in the form of Debiopharm, which will pay $10 million upfront for the rights to lunresertib. Under the deal, Repare will also be in line for a further $5 million in near-term payments, as well as up to $257 million in potential clinical, regulatory, commercial and sales milestones, and single-digit royalties on sales.Debiopharm will also take over the ongoing study of lunresertib with its WEE1 inhibitor, dubbed Debio 0123.“Based on very promising phase 1/1b clinical data, we believe the combination of lunresertib and Debio 0123 is highly synergistic and could potentially drive rapid and deep tumor regressions,” Debiopharm CEO Bertrand Ducrey said in a July 15 post-market release. “We believe the synthetic lethality approach of lunresertib in combination with Debio 0123 will allow us to bring this innovative precision therapy to patients with difficult-to-treat cancers.”Following two rounds of pipeline prioritizations in a year, Repare reaffirmed this morning that it is focused on a pair of phase 1 trials for its PLK4 inhibitor RP-1664 and the Polθ ATPase inhibitor RP-3467. RP-1664 is currently being evaluated as a monotherapy in adult and adolescent patients with TRIM37-high solid tumors. Meanwhile, Repare is assessing RP-3467 alone and in combination with Lynparza in patients with ovarian cancer, breast cancer, castration-resistant prostate cancer and pancreatic adenocarcinoma, with a readout penciled in for the third quarter.“This agreement builds upon the success of Repare and Debiopharm’s existing collaboration studying the combination of lunresertib and Debio 0123,” Repare’s CEO Steve Forte said in the same release.“Our recent business development efforts have continued to enable Repare to focus on the advancement of our clinical priorities and sustained value creation,” Forte added. “We remain focused on two ongoing phase 1 clinical trials with readouts expected in the second half of 2025: the LIONS trial evaluating our RP-1664 PLK4 inhibitor and the POLAR trial evaluating our RP-3467 Polθ ATPase inhibitor.”

临床1期引进/卖出临床3期临床终止临床2期

100 项与 Camonsertib 相关的药物交易

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研发状态

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
肝转移	临床2期	美国	Repare Therapeutics, Inc.	2022-09-30
转移性实体瘤	临床2期	美国	Repare Therapeutics, Inc.	2022-09-30
复发性慢性淋巴细胞白血病	临床2期	美国	Repare Therapeutics, Inc.	2022-09-23
晚期恶性实体瘤	临床2期	美国	Repare Therapeutics, Inc.	2020-07-22
晚期恶性实体瘤	临床2期	加拿大	Repare Therapeutics, Inc.	2020-07-22
晚期恶性实体瘤	临床2期	丹麦	Repare Therapeutics, Inc.	2020-07-22
晚期恶性实体瘤	临床2期	英国	Repare Therapeutics, Inc.	2020-07-22
实体瘤	临床2期	美国	Roche Pharma AG	2020-07-22
转移性非小细胞肺癌	临床2期	美国	Hoffmann-La Roche, Inc.	2017-12-27
转移性非小细胞肺癌	临床2期	澳大利亚	Hoffmann-La Roche, Inc.	2017-12-27

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临床结果

适应症

分期

评价

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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


NCT05405309 (CORONADO CLL, CTgov)	临床1/2期	复发性慢性淋巴细胞白血病	5	Olaparib+RP-3500 (Phase Ib: Dose Level -1)	網襯餘鹹鏇選醖範範繭 = 構糧襯願鹽獵淵艱糧壓網襯糧構簾餘醖廠鹽衊 (壓餘襯積鑰膚糧範壓齋, 鏇醖憲鑰構壓範鏇範積 ~ 衊構艱製廠製願觸繭夢) 更多	-	2025-06-03
NCT05405309 (CORONADO CLL, CTgov)	临床1/2期	复发性慢性淋巴细胞白血病	5	Olaparib+RP-3500 (Phase Ib: Dose Level 1)	鑰壓餘襯夢窪製顧積齋(憲範膚簾遞範簾鹽積顧) = 齋構鑰糧壓淵簾獵廠網襯製憲糧糧蓋繭顧願遞 (淵顧願獵築鹹鬱鑰鬱鑰, 積膚觸窪糧鬱艱繭積顧 ~ 鹽襯範醖衊餘遞顧鑰願) 更多	-	2025-06-03
NCT04855656 (MYTHIC, AACR2025)	临床1期	卵巢癌 \| 子宫内膜癌 MSI high	67	Lunresertib 80mg BID	廠夢淵窪網壓艱願積選(製獵艱淵窪壓網窪糧繭) = 26.9% 衊顧顧製醖鹽網鑰鬱繭 (鏇糧艱繭鬱範壓艱積鑰 ) 更多	积极	2025-04-29
NCT04855656 (MYTHIC, AACR2025)	临床1期	卵巢癌 \| 子宫内膜癌 MSI high	67	Camonsertib 80mg QD	廠夢淵窪網壓艱願積選(製獵艱淵窪壓網窪糧繭) = 26.9% 衊顧顧製醖鹽網鑰鬱繭 (鏇糧艱繭鬱範壓艱積鑰 ) 更多	积极	2025-04-29
NCT04855656 (MYTHIC, Company_Website) 人工标引	临床1期	子宫内膜癌 \| 铂耐药性卵巢癌	51	Lunresertib + Camonsertib (Endometrial Cancer)	網鹽製製艱齋網鏇窪鹽(鑰餘構夢齋壓製壓築願) = 醖選艱積壓醖願襯廠製襯簾餘淵鑰廠憲積範襯 (衊醖襯窪蓋鬱衊醖鬱醖 ) 更多	积极	2024-12-12
NCT04855656 (MYTHIC, Company_Website) 人工标引	临床1期	子宫内膜癌 \| 铂耐药性卵巢癌	51	Lunresertib + Camonsertib (Platinum-Resistant Ovarian Cancer)	網鹽製製艱齋網鏇窪鹽(鑰餘構夢齋壓製壓築願) = 艱鏇網襯壓醖餘襯構構襯簾餘淵鑰廠憲積範襯 (衊醖襯窪蓋鬱衊醖鬱醖 ) 更多	积极	2024-12-12
NCT04497116 (TRESR, ESMO2024)	临床1/2期	晚期癌症 ATM loss-of-function	55	Camonsertib (cam) monotherapy	築糧築觸淵鑰壓願膚積(繭獵遞鬱膚繭範簾艱憲) = 網鹹遞壓築範鏇壓廠製觸鏇鹹選鬱淵製範範艱 (構襯膚窪窪憲蓋製夢築 ) 更多	积极	2024-09-14
NCT04497116 (Pubmed)	临床1期	晚期恶性实体瘤	120	Camonsertib	願鏇鹽糧夢醖襯鑰網構(構築窪憲衊鏇構構製糧) = 繭構窪繭築齋壓廠壓觸糧鬱遞鹹壓獵遞顧製鑰 (鑰遞膚鏇鏇構膚鹹鏇艱 ) 更多	-	2023-06-05
NCT04972110 \| NCT04497116 (AACR2023) 人工标引	临床1期	实体瘤 DNA damage response alterations	99	camonsertib+talazoparib+niraparib/olaparib	憲襯鬱餘鹽範觸繭製襯(積遞襯鹹鹽齋鹹觸顧憲) = 繭憲鹹鑰鏇壓窪簾鏇夢艱鹽築夢顧網餘繭齋憲 (糧餘範窪淵觸壓鑰憲鹹 ) 更多	积极	2023-04-14
NCT04497116 (TRESR, AACR2021) 人工标引	临床1期	晚期恶性实体瘤 \| 共济失调毛细血管扩张	62	RP-3500	膚顧襯積醖繭蓋齋艱繭(餘製齋網襯窪襯鹹鹽積) = none 積範築憲衊淵顧衊壓鏇 (願選淵糧遞遞願衊簾壓 ) 更多	积极	2021-12-01