A Phase 1b/2, Multicenter, Open-label, Dose Regimen Determination and Dose Expansion Trial to Evaluate the Safety, Tolerability, Anti-tumor Activity, and an Optimal Dose Regimen of Patritumab Deruxtecan (HER3-DXd) With Trastuzumab Deruxtecan (T-DXd) in Participants With Hormone Receptor Positive, HER2-low or HER2-ultralow, Unresectable or Metastatic Breast Cancer (HERTHENA-Breast02)

The primary purpose of the study is to assess the safety, tolerability, and anti-tumor activity of HER3-DXd and T-DXd in the combination dosing regimens in participants with hormone receptor positive, HER2-low or HER2-ultralow, unresectable, or metastatic breast cancer.

开始日期2026-08-03

申办/合作机构

Daiichi Sankyo Co., Ltd.

[+1]

NCT07286149

/ Recruiting临床1/2期

KEYMAKER-U01 Substudy 01F: A Phase 1b/2 Umbrella Study With Rolling Arms of Investigational Agents for Previously Treated Participants With Advanced or Metastatic Nonsquamous Non-small Cell Lung Cancer (NSCLC) With KRAS G12C Mutations

Researchers want to learn if MK-1084, the study medicine, can treat advanced or metastatic non-squamous NSCLC. MK-1084 is a targeted therapy, which is a treatment that works to control how specific types of cancer cells grow and spread. The goals of this study are to learn:
* About the safety of MK-1084 and if people tolerate it when taken with other treatments
* How many people have the cancer respond (get smaller or go away) to the treatments

开始日期2026-04-30

申办/合作机构

Merck Sharp & Dohme LLC

[+1]

NCT07060807

/ Recruiting临床3期

An Open-label, Randomized, Phase 3 Study to Evaluate Patritumab Deruxtecan Monotherapy Versus Treatment of Physician's Choice in Hormone Receptor-positive, HER2-negative Unresectable Locally Advanced or Metastatic Breast Cancer (HERTHENA-Breast04).

Researchers are looking for other ways to treat breast cancer (BC) that is hormone receptor-positive and human epidermal growth factor receptor 2-negative (HR+/HER2-) and either unresectable locally advanced or metastatic.
* HR positive (HR+) means the cancer cells have proteins that attach to estrogen or progesterone (hormones) which help the cancer to grow and spread
* HER2 negative (HER2-) means the cancer cells have a low amount of a protein called HER2
* Unresectable locally advanced means the cancer cannot be completely removed by surgery and has spread into nearby tissue or muscles
* Metastatic means the cancer has spread to other parts of the body
Treatment for this type of breast cancer usually includes endocrine therapy (ET) and sometimes a second treatment. The main goal of this study is to learn if people who receive patritumab deruxtecan (also known as HER3-DXd and MK-1022) live longer overall or without the cancer growing/spreading, compared to people who receive chemotherapy or a different drug called trastuzumab deruxtecan.

开始日期2025-07-21

申办/合作机构

Merck Sharp & Dohme LLC

[+1]

100 项与德帕瑞妥单抗相关的临床结果

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100 项与德帕瑞妥单抗相关的转化医学

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100 项与德帕瑞妥单抗相关的专利（医药）

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项与德帕瑞妥单抗相关的文献（医药）

2026-07-05·BRITISH JOURNAL OF CANCER

ATR inhibition potentiates the antitumor efficacy of HER3-DXd in HER3-positive/HR-positive breast cancer by increasing DNA damage

Article

作者: Fuson, Jon A ; Gi, Young Jin ; Fukui, Jami A ; Lee, Jangsoon ; Ueno, Naoto T ; Tripathy, Debu ; Fan, Pang-Dian ; Poullikkas, Thanasis ; Xie, Xuemei

BACKGROUND:

Endocrine resistance remains a major challenge in hormone receptor-positive (HR+) breast cancer (BC), where up to 70% of tumours overexpress HER3, a receptor associated with poor prognosis and therapeutic resistance. HER3-DXd (patritumab deruxtecan) is currently under clinical investigation for HER3-expressing metastatic BC. However, strategies to further enhance its efficacy, particularly in endocrine therapy-resistant settings, are urgently needed. We hypothesised that targeting ATR, a key regulator of DNA damage repair (DDR), potentiates HER3-DXd in HER3+/HR+ BC, including tamoxifen-resistant (TMR) disease.

METHODS:

Synergistic partners for HER3-DXd were identified by whole-genome RNAi screening. Treatments' effects on cell cycle, DNA damage, and protein expression were analysed using flow cytometry, comet assay, and Western blotting, respectively. Treatments' antitumor efficacy was assessed using xenograft mouse models. TCGA and CPTAC databases were analysed for clinical relevance.

RESULTS:

HER3-DXd inhibited growth in both parental and TMR MCF7 and T47D cells. Compared to monotherapies, combining HER3-DXd with an ATR inhibitor enhanced DNA damage, sub-G1 arrest, apoptosis, downregulation of DDR and cell cycle regulatory proteins, and tumour growth inhibition. TCGA and CPTAC analyses confirmed high HER3 expression and correlation of ATR, CHEK1, and TOP1 gene expression with poor prognosis in HR+ BC.

CONCLUSION:

Combining HER3-DXd with an ATR inhibitor could benefit HER3+/HR+ BC patients with both endocrine-sensitive and -resistant diseases.

2026-06-01·CANCER

Mapping the antibody–drug‐conjugates landscape in non–small cell lung cancer: Where are we and where are we going?

Review

作者: Parisi, Claudia ; Planchard, David ; Barlesi, Fabrice

Abstract:

Antibody–drug conjugates (ADCs) represent a rapidly advancing therapeutic class in the treatment of non‐small cell lung cancer (NSCLC), offering targeted delivery of cytotoxic agents to tumor cells while minimizing off‐target toxicity. In recent years, several ADCs have emerged in both early (phase 1–2) and late (phase 3) clinical development, reflecting a growing recognition of their potential to improve outcomes in defined subsets of patients with advanced NSCLC. Late‐phase ADCs include trastuzumab deruxtecan (targeting HER2 [human epidermal growth factor receptor 2]), datopotamab deruxtecan and sacituzumab govitecan (targeting TROP2 [trophoblast cell‐surface antigen 2]), patritumab deruxtecan (targeting HER3), telisotuzumab vedotin (targeting c‐MET [cellular‐mesenchymal epithelial transition factor]), and sigvotatug vedotin (targeting IB6 [integrin beta‐6]). Research efforts are ongoing to explore novel payloads, linker technologies, and targets to expand the applicability of ADCs across broader NSCLC populations, including those with limited treatment options (e.g., EGFR ‐mutant disease in the context of treatment resistance). Despite their promise, challenges remain in optimizing patient selection, overcoming resistance mechanisms, and managing unique toxicity profiles. Ongoing, biomarker‐driven trials and combination strategies with immunotherapy or tyrosine kinase inhibitors hold the potential to further enhance the efficacy of ADCs. In this review, the authors highlight the current landscape and future directions of ADCs in NSCLC, emphasizing available results for compounds in late‐stage clinical development and different disease settings.

2026-05-01·CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY

Resistance mechanisms and post-trastuzumab deruxtecan (T-DXd) strategies in HER2+ and HER2-low breast cancer: From biology to clinical practice

Review

作者: Xue, Wenwu ; Chen, Minna ; Wen, Xiaofen ; Li, Xiaozhi ; Zeng, De ; Lin, Danxia ; Song, Junwei ; Wang, Wende ; Zhang, Weichun ; Shen, Jiaxin

Trastuzumab deruxtecan (T-DXd), a HER2-directed antibody-drug conjugate (ADC), has revolutionized the treatment landscape for HER2-positive and HER2-low breast cancer, offering unprecedented improvements in progression-free survival (PFS) and overall survival (OS). However, the emergence of resistance limits its long-term efficacy and highlights the need for rational post-progression strategies. This review summarizes current understanding of resistance mechanisms to T-DXd, including dynamic HER2 expression loss, dysregulation of DNA damage repair, tumor microenvironment remodeling, and immune evasion. Building upon these mechanistic insights, we explore therapeutic strategies following T-DXd resistance, including sequential ADCs with alternative targets or payloads, combinations with HER2-targeted tyrosine kinase inhibitors (TKIs), CDK4/6 or PARP inhibitors, endocrine therapy, and immunotherapy. Novel agents such as ARX788, patritumab deruxtecan, and Dato-DXd demonstrate promise in overcoming resistance through diversified mechanisms. Real-world data further support a "three-step strategy" involving ADC rechallenge after interim non-ADC therapies, offering a practical, mechanism-informed treatment model. This review provides a framework for precision-guided care in patients with advanced breast cancer and supports ongoing efforts to extend the therapeutic window beyond initial T-DXd benefit.

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项与德帕瑞妥单抗相关的新闻（医药）

2026-08-28

·癌度

从"没有靶点就没有药"到"降瘤+延寿",肺癌治疗正在被超级ADC与双抗药物改写！

点击蓝字关注我们没有基因突变可以"打靶",不代表没有药可以用——这两年,答案正在被两类新药一点点改写。一、"无靶点突变"的肺癌患者,到底难在哪非小细胞肺癌里,大约一半左右的患者能查到EGFR、ALK、ROS1这类明确的驱动基因突变,针对这些靶点的口服靶向药已经用了十几年,效果也比较确切。但剩下的这一半患者,基因检测报告上往往是"未见明确驱动基因突变",尤其是鳞状细胞癌这个亚型,驱动基因阳性率本来就低,可选的治疗方案基本就是化疗联合免疫治疗这一条路。一旦这条路走到头,后线治疗的选择会变得非常有限,这也是这几年ADC药物和双特异性抗体扎堆往这个方向发力的原因。顺带说一句,今年的世界肺癌大会9月12日到15日才在韩国首尔召开,现在会议还没开,以下这些数据大多来自今年上半年到年中陆续公布的III期和II期研究结果,不是大会现场公布的内容,大会届时预计会展示这些项目的进一步更新,值得持续关注。二、ADC药物:把化疗"绑"在抗体上,专打耐药后的硬骨头抗体偶联药物(ADC)的思路,是把一个能精准识别肿瘤表面标志物的抗体,和一个杀伤力很强的化疗小分子连在一起,让药物像"精确制导"一样直接送到癌细胞跟前再释放毒素,理论上能兼顾疗效和安全性。 TROP2是目前进展最快的靶点之一,这个蛋白在大多数非小细胞肺癌肿瘤表面都有不同程度的表达。靶向TROP2的ADC药物Dato-DXd(通用名达托泊塔单抗-德鲁替康)在此前完成的TROPION-Lung01这项III期研究里,对比传统化疗药多西他赛,治疗过既往接受过化疗和免疫治疗、没有明确驱动基因突变的非鳞非小细胞肺癌患者,总生存期达到14.6个月,比化疗组延长了2.3个月。基于这个结果和后续对TROP2表达水平的深入分析,研发方今年启动了一项新的III期研究TROPION-Lung17,专门针对经过特定检测方法确认TROP2高表达、没有可用驱动基因突变的非鳞癌患者,进一步验证疗效——这类患者正是你选题里说的"无靶点突变"这群人里最典型的代表。需要说清楚的是,ADC药物不是只给"无靶点"患者准备的。针对HER3靶点的ADC药物HER3-DXd(通用名帕妥珠单抗-德鲁替康),它的核心适应人群其实是EGFR突变、已经用过三代靶向药和化疗都失败了的患者,在II期HERTHENA-Lung01研究里,这部分患者的客观缓解率将近三成,中位无进展生存期5.5个月,中位总生存期11.9个月。这说明ADC这条技术路线覆盖的人群其实很广,既能给"没有靶点"的患者提供化疗之外的新选择,也能给"有靶点、但耐药了"的患者续上一条命。三、双特异性抗体:一支抗体打两个靶,想突破单药免疫治疗的天花板另一条路是双特异性抗体,简单说就是把两种不同的抗体功能合并进同一个分子里,同时打击两个不同的信号通路,理论上比单纯联用两种药物毒性更可控。 PD-1/VEGF双抗ivonescimab(通用名依沃西单抗)是这个方向里进展最快的一个,它把免疫检查点抑制剂PD-1抗体和抗血管生成的VEGF抗体做进了同一个分子里。在今年上半年公布、并同步发表在《柳叶刀》上的III期研究HARMONi-6里,针对既往未经治疗的晚期鳞状非小细胞肺癌患者(这类患者驱动基因突变本来就很少见),依沃西单抗联合化疗对比现有PD-1单抗联合化疗,中位总生存期达到27.9个月,对照组是23.7个月,死亡风险降低了34%,而且不论患者PD-L1表达高低,这个获益都能看到。这是目前少数几个在晚期肺癌一线治疗里,新方案对比现有标准治疗、在总生存期这个硬指标上拿出统计学显著获益的双抗研究。另一类是PD-1/CTLA-4双抗,代表药物是cadonilimab(通用名卡度尼利单抗)。它主要瞄准的是一群更难治的人:PD-L1表达阴性的晚期非小细胞肺癌患者。这部分患者单用PD-1抗体或者PD-1联合化疗,效果一直不太理想。今年发表的一项II期研究显示,卡度尼利单抗联合化疗用于这部分PD-L1阴性患者的一线治疗,客观缓解率达到66%,疾病控制率100%,中位无进展生存期9.7个月,中位总生存期在数据截止时还没有达到——对于这个历史上一直"不太吃"免疫治疗的人群来说,这组数据是比较少见的积极信号,不过样本量还不算大,需要更大规模的研究去验证。四、这些新药离普通患者有多远从时间线看,依沃西单抗这类双抗药物在国内已经有产品获批上市,针对不同肺癌人群和治疗线数的多项III期研究还在同步推进,包括面向更广泛全球人群、不区分PD-L1表达的HARMONi-3研究。ADC药物这边,Dato-DXd已经在申请美国上市,国内同类的TROP2 ADC产品也已经有获批品种。也就是说,这两类药物有一部分已经不是纯粹的"实验室概念",而是正在从临床研究走向实际可用的阶段,但具体到某一款药、某一个适应症能不能用、要花多少钱,还是要结合病理类型、基因检测结果、PD-L1表达水平这些具体指标,和主治医生一起判断。对于确实符合入组条件、又想尝试这类前沿方案的患者,参加正规的临床试验是目前接触这些新药相对现实、也更有保障的一条路——正规临床试验通常用药免费,还有全程的检查和随访,比自己想办法海外购药要靠谱得多。写在最后没有基因突变可以"打靶",过去常常意味着能选的路更窄。但这两年ADC和双特异性抗体这两条技术路线的进展,正在慢慢把这条路拓宽——一个是把化疗药精准送到肿瘤跟前,一个是让免疫治疗打得更准、打得更狠。这些数据大多还在向着更大规模的III期确证性研究推进,不是每一个都已经尘埃落定,但方向是实打实的。标准治疗失败不是终点,持续关注前沿进展、认准正规临床试验,总比病急乱投医要稳妥。关注癌度,带你同步全球抗癌前沿。如果你或家人是无驱动基因突变、或者多线治疗失败的晚期肺癌患者,想了解相关全球临床试验的申请渠道,欢迎直接私信咨询我们。您可通过【下面3个方式】联系癌度！ 👉 点击文末【阅读原文】；或关注公众号后点菜单栏“联系我们”；或微信直接扫描下图二维码；免责声明:本文仅为科普参考,不构成任何医疗建议。文中涉及的部分疗法或适应症尚在临床研究阶段或审批过程中,具体是否获批、能否使用以当地药监部门批准信息及主治医生评估为准。所有治疗决策请在专业医生指导下进行。往期推荐一位肺癌患者用了亚硒酸钠后活了10年——同一批32人里只有她成功了——这到底说明了什么？沿用近30年的肝癌"教科书"要更新了，"北美新标准":新框架发布,专家决策一致率达96.6%！《抗癌孙子兵法》第五篇：军形篇——读懂战场形势，才能顺势而为！ Moderna股价一天暴涨177%,全球首个III期"成功"的个体化mRNA癌症疫苗,到底成功在哪？点赞收藏分享点亮小手爱心，送来温暖鼓励

抗体药物偶联物临床3期免疫疗法临床结果临床成功

2026-08-27

·BioDialectics

丹娜法伯癌症研究所发表PARP抑制剂与HER3-DXd协同机制

HER3在80%以上非小细胞肺癌（NSCLC）中存在表达上调，与耐药及不良预后密切相关。HER3-DXd（Patritumab-deruxtecan，U3-1402）是靶向HER3的抗体药物偶联物，载荷DXd为拓扑异构酶Ⅰ抑制剂，Ⅰ期临床证实其对经治EGFR突变NSCLC具备可观疗效。既往研究证实奥希替尼可提升肿瘤细胞HER3膜表达，增强HER3-DXd内化与杀伤，但该协同效应严格依赖EGFR突变背景，临床亟需不局限于驱动基因突变的通用联合策略。DNA损伤应答（DDR）通路是ADC药物发挥药效的关键下游环节，PARP抑制剂阻断DNA单链断裂修复，理论上可放大拓扑异构酶抑制剂造成的DNA损伤，但二者在HER3靶向ADC体系下的协同模式、是否同时调控抗肿瘤免疫尚缺少系统解析。近期，丹娜法伯癌症研究所（Dana-Farber Cancer Institute）依托高通量DDR/细胞周期抑制剂筛选、NSG异种移植模型等系列验证：发现奥拉帕利等PARP抑制剂可与HER3-DXd产生广谱协同抗肿瘤作用，一方面加剧不可修复DNA损伤诱导肿瘤凋亡，另一方面释放胞质DNA激活cGAS-STING通路，强化NK细胞介导的抗肿瘤效应，该协同效应在EGFR突变、KRAS突变NSCLC模型中均可观察到。一：高通量DDR抑制剂筛选确定PARP抑制剂与HER3-DXd存在广谱协同效应选取14种DNA损伤应答与细胞周期调控抑制剂，在多株EGFR突变NSCLC细胞系开展7天活细胞成像增殖筛选，计算协同比值。结果显示奥拉帕利（PARPi）协同效应在全部受试细胞中稳定突出，ATRi、WEE1i仅表现出细胞株特异性协同。进一步拓展多种PARP抑制剂，均能和HER3-DXd产生协同，基于临床应用成熟度选择奥拉帕利开展后续机制研究。承接体外细胞功能验证，无论EGFR突变还是KRAS突变细胞，HER3-DXd联合奥拉帕利均可显著提升caspase-3/7介导的凋亡水平。HER3低/阴性细胞株对单药及联合方案均无应答，提示肿瘤细胞HER3表达是联合药效的必要基础，但并非唯一决定因素。为更好模拟体内药物经血管递送生理场景，采用搭载血管内皮管道的肿瘤器官芯片（tumor-on-chip），利用患者来源EGFR、KRAS突变类器官开展测试，发现类器官芯片结果复现体外细胞表型，联合处理组肿瘤细胞死亡比例显著高于单药组。由此推断，HER3-DXd通过HER3介导胞内递送TOP1抑制剂，PARP抑制剂阻断单链断裂修复，二者形成合成致死效应，该协同作用不局限于特定驱动基因突变，适用HER3阳性的EGFR、KRAS突变肿瘤。二：联合方案放大DNA双链断裂，触发细胞周期阻滞。体内模型证实生存获益 HER3-DXd载荷DXd抑制TOP1，造成DNA单链断裂。PARP被奥拉帕利抑制后，既丧失单链断裂修复能力，还会发生DNA捕获，将单链损伤进一步转化为双链断裂。为解析联合处理的DNA损伤应答变化，对EGFR突变HCC4006、KRAS突变H358细胞开展检测，Western blot与流式结果证实，相较于单药处理，联合组p-ATM、γ-H2AX（pH2AX）DNA损伤标志物显著升高，p21上调，细胞发生明显G2/M期周期阻滞，最终驱动肿瘤细胞走向凋亡。继而在NSG免疫缺陷小鼠构建EGFR-mutHCC4006、KRAS-mutH1573皮下异种移植瘤模型，设置溶剂对照、奥拉帕利单药、HER3-DXd单药、联合治疗四组。体内结果显示，联合组肿瘤体积得到最显著抑制，小鼠生存时间获得明显延长。在给药周期内小鼠体重无明显下降，血常规大体稳定，仅观察到长期给药后血清ALT轻度升高，提示存在潜在肝脏毒性风险。综合体内外证据，证实联合策略可在体内有效发挥抗肿瘤活性，主要通过加剧DNA损伤、诱导周期阻滞实现肿瘤细胞杀伤。同时NSG小鼠缺乏功能性适应性免疫，提示该DNA损伤介导的细胞毒性效应不依赖适应性淋巴细胞。三：联合治疗释放胞质DNA，激活cGAS-STING通路，增强NK介导的抗肿瘤免疫 DNA双链断裂损伤会造成基因组DNA泄露至胞质，激活胞质DNA感受器cGAS-STING先天免疫轴。尽管NSG小鼠无完整适应性免疫，但仍保留NK细胞，因此进一步探究联合方案的免疫调节作用。体外肿瘤细胞与NK细胞共培养杀伤实验表明，HER3-DXd+奥拉帕利预处理肿瘤细胞后，NK介导的肿瘤杀伤能力明显提升。siRNA敲低cGAS或者STING后，该NK杀伤增强效应被部分削弱，证明cGAS-STING通路参与该免疫调控过程。机制层面，联合处理上调肿瘤细胞cGAS、STING、p-TBK1通路分子，诱导IFN刺激基因以及IP-10、MIP-1α等促炎趋化因子分泌。但同时观察到不同细胞株之间存在明显异质性，部分细胞系STING通路本底表达低下，联合后免疫激活幅度有限。异种移植瘤组织免疫组化证实联合组肿瘤cGAS蛋白表达上调。据此推断，HER3-DXd联合PARP抑制剂具备双重作用模式：一方面直接造成肿瘤细胞DNA损伤杀伤。另一方面胞质DNA积累激活cGAS-STING，招募并增强NK细胞抗肿瘤功能。而肿瘤细胞cGAS-STING通路本底状态，会影响免疫激活的强弱，是潜在疗效分层标志物。总结思考研究提出一套不依赖肿瘤驱动基因突变的联合治疗策略，证实PARP抑制剂奥拉帕利与HER3-DXd具备协同抗肿瘤活性，建立HER3-DXd造成TOP1抑制-PARP抑制阻断损伤修复-累积DNA双链断裂的合成致死轴。同时还可以通过胞质DNA激活cGAS-STING，增强NK细胞介导的先天抗肿瘤免疫，实现细胞毒效应与免疫调节双重获益，拓展HER3-DXd联合用药思路，不限于既往EGFR-TKI联合模式。理论上拓展了TOP1抑制剂-PARP抑制剂合成致死的应用场景，将该组合概念迁移到抗体药物偶联物领域。同时证实ADC不仅是靶向杀伤工具，还可与DDR抑制剂协同重塑肿瘤先天免疫，也提示肿瘤细胞cGAS-STING通路完整性是影响联合方案免疫获益的重要内在因素，为患者分层提供分子依据。 Lin L, Moradi N, Lähdeniemi IA,et al. PARP inhibition enhances the antitumor activity of HER3-DXd in non-small cell lung cancer. Cell Rep Med. 2026 Aug 21:103002. doi: 10.1016/j.xcrm.2026.103002.

2026-08-27

·BioSpace

DS1025 Enters Clinical Development in Patients with Advanced Solid Tumors as Novel CD25 Directed ADC in Industry-Leading ADC Portfolio of Daiichi Sankyo

TOKYO--(BUSINESS WIRE)--The first patient has been dosed in a first-in-human phase 1 trial evaluating DS1025 in adult patients with advanced or metastatic solid tumors with disease progression on or after at least one prior line of standard therapy. DS1025 is a specifically engineered, investigational, potential first-in-class CD25 directed antibody drug conjugate (ADC) containing an immuno-oncology optimized cytotoxic payload discovered by Daiichi Sankyo (TSE:4568). CD25 is a cell surface protein that is highly expressed on regulatory T cells (Treg cells) which suppresses the response of the immune system against cancer, 1 making it a promising therapeutic target. Currently, there are no CD25 directed ADCs approved for any type of cancer. “While immunotherapies have transformed cancer treatment, continued innovation in leveraging pathways that can activate the immune system is needed,” said John Tsai, MD, Global Head, R&D, Daiichi Sankyo. “The initiation of this trial evaluating DS1025 reflects continued progress in advancing our pipeline through the development of novel antibody drug conjugates in order to deliver medicines that improve outcomes for patients with cancer.” About the Phase 1 Trial The multicenter, open-label, first-in-human, dose escalation phase 1 trial will assess the safety, tolerability, pharmacokinetics and preliminary efficacy of DS1025 in patients with advanced or metastatic solid tumors with disease progression on or after at least one prior line of standard therapy. The trial will evaluate primary endpoints of safety and tolerability, including dose-limiting toxicities and adverse events. Secondary endpoints include pharmacokinetics and immunogenicity. Exploratory endpoints include overall response rate, duration of response and time to response. The trial is expected to enroll up to 45 patients across multiple sites in Asia and Europe. For more information, please visit ClinicalTrials.gov . About CD25 CD25 is a cell surface protein that is highly expressed on regulatory T cells (Treg cells). Treg cells work to suppress the immune system, helping tumors evade the body’s natural ability to destroy abnormal cells and are thought to be a key contributor to resistance that develops with currently available immunotherapies. 2 About DS1025 DS1025 is an investigational, potential first-in-class CD25 directed ADC that builds on the DXd ADC Technology of Daiichi Sankyo by delivering an immuno-oncology optimized cytotoxic payload that works to deplete immunosuppressive T cells (Treg cells) in the tumor microenvironment and activate the immune system to detect and destroy cancer cells. About the ADC Portfolio of Daiichi Sankyo The Daiichi Sankyo ADC portfolio consists of nine ADCs in clinical development crafted from ADC technology discovered in-house by Daiichi Sankyo. The DXd ADC Technology platform of Daiichi Sankyo consists of seven ADCs in clinical development where each ADC is comprised of a monoclonal antibody attached to a number of topoisomerase I inhibitor payloads (an exatecan derivative, DXd) via tetrapeptide-based cleavable linkers. The DXd ADCs include Enhertu ® and Datroway ® , which are being jointly developed and commercialized globally with AstraZeneca, and ifinatamab deruxtecan (I-DXd), raludotatug deruxtecan (R-DXd) and patritumab deruxtecan (HER3-DXd), which are being jointly developed and commercialized globally with Merck & Co., Inc, Rahway, NJ, USA. DS3939 and DS3790 are being developed by Daiichi Sankyo. Additional ADCs being developed by Daiichi Sankyo include DS3610, which consists of an antibody attached to a novel payload that acts as an agonist of STING, and DS1025, which consists of a CD25 directed antibody attached to an immuno-oncology optimized cytotoxic payload. Ifinatamab deruxtecan, raludotatug deruxtecan, patritumab deruxtecan, DS3939, DS3610, DS3790 and DS1025 are investigational medicines that have not been approved for any indication in any country. Safety and efficacy have not been established. About Daiichi Sankyo Daiichi Sankyo (TSE: 4568) is a global healthcare company committed to becoming a trusted healthcare innovator, transforming the lives of people through its strength in science and technology. The company discovers and develops new standards of care to address diverse medical needs to fulfill its purpose of contributing to the enrichment of quality of life around the world. With a strategic focus on oncology, Daiichi Sankyo is advancing an industry-leading antibody drug conjugate portfolio along with identifying new breakthrough generating technologies to deliver practice-changing medicines to patients, healthcare professionals and society. For more information, please visit . REFERENCES: 1 Sureka N, et al. Cell Biol Int . 2025;49(8):897-928. 2 Fares C, et al. Am Soc Clin Oncol Educ Book . 2019 Jan;39:147-164. Contacts MEDIA CONTACTS: Global: Jennifer Brennan jennifer.brennan@daiichisankyo.com +1 908 900 3183 (mobile) Japan: DS-PR_jp@daiichisankyo.com INVESTOR RELATIONS CONTACT: DaiichiSankyoIR_jp@daiichisankyo.com

抗体药物偶联物免疫疗法临床1期

100 项与德帕瑞妥单抗相关的药物交易

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适应症	最高研发状态	国家/地区	公司	日期
EGFR突变的非小细胞肺癌	申请上市	美国	Daiichi Sankyo Co., Ltd.	2023-12-22
EGFR突变的非小细胞肺癌	申请上市	美国	Merck & Co., Inc.	2023-12-22
HR阳性/HER2阴性乳腺癌	临床3期	美国	Merck Sharp & Dohme LLC	2025-07-21
HR阳性/HER2阴性乳腺癌	临床3期	中国	Merck Sharp & Dohme LLC	2025-07-21
HR阳性/HER2阴性乳腺癌	临床3期	日本	Merck Sharp & Dohme LLC	2025-07-21
HR阳性/HER2阴性乳腺癌	临床3期	阿根廷	Merck Sharp & Dohme LLC	2025-07-21
HR阳性/HER2阴性乳腺癌	临床3期	澳大利亚	Merck Sharp & Dohme LLC	2025-07-21
HR阳性/HER2阴性乳腺癌	临床3期	巴西	Merck Sharp & Dohme LLC	2025-07-21
HR阳性/HER2阴性乳腺癌	临床3期	加拿大	Merck Sharp & Dohme LLC	2025-07-21
HR阳性/HER2阴性乳腺癌	临床3期	智利	Merck Sharp & Dohme LLC	2025-07-21

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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


NCT07060807 (HERTHENA-Breast04, ASCO2026)	临床3期	局部晚期不能切除的乳腺癌 HR positive \| HER2 negative	500	HER3-DXd 5.6 mg/kg IV on day 1 Q3W	齋鹽襯願鑰顧衊衊壓願(膚齋壓願鬱齋淵夢選選) = 蓋鏇醖願鹹範選壓糧糧餘襯觸壓積積淵膚網糧 (網構範範餘積願壓繭糧 ) 更多	积极	2026-05-29
				Treatment of physician’s choice (TPC)	齋鹽襯願鑰顧衊衊壓願(膚齋壓願鬱齋淵夢選選) = 遞蓋鹹夢積艱淵餘築齋餘襯觸壓積積淵膚網糧 (網構範範餘積願壓繭糧 ) 更多
NCT04699630 (ESMO_BC2026)	临床2期	转移性乳腺癌 HER3 Expression	121	Patritumab deruxtecan (Part A: HR+/HER2- or TNBC, ADC naïve)	鹹鏇顧繭積繭鹹顧憲鹽(鑰衊夢選壓憲壓範襯糧) = 鏇遞遞衊蓋顧糧網鬱艱糧製蓋製膚積鹹繭糧齋 (淵憲製鬱醖積窪繭鬱艱 ) 更多	积极	2026-05-07
				Patritumab deruxtecan (Part B: HR+/HER2- or TNBC, prior ADC)	鹹鏇顧繭積繭鹹顧憲鹽(鑰衊夢選壓憲壓範襯糧) = 願構範構網構窪繭齋獵糧製蓋製膚積鹹繭糧齋 (淵憲製鬱醖積窪繭鬱艱 ) 更多
NCT04699630 (CTgov)	临床2期	局部晚期乳腺癌 \| HER2阳性转移性乳腺癌 \| 转移性乳腺癌	121	U3-1402 (Part A)	鹹觸淵膚遞繭觸顧壓網 = 夢艱艱製淵艱淵鏇觸鏇構衊齋獵遞簾膚廠鹹構 (膚積鑰顧餘廠廠鏇範網, 製襯願憲餘簾壓繭觸壓 ~ 網獵網壓鑰齋糧膚糧廠) 更多	-	2026-05-07
				U3-1402 (Part B)	鹹觸淵膚遞繭觸顧壓網 = 簾獵製膚鏇醖衊構憲餘構衊齋獵遞簾膚廠鹹構 (膚積鑰顧餘廠廠鏇範網, 遞製鏇繭觸願襯鬱衊製 ~ 願鬱簾遞鑰觸構遞觸鑰) 更多
NCT06686394 (HERTHENA-Breast01, ESMO_ASIA2025)	临床1/2期	晚期 HER2 阳性乳腺癌 HER2+ \| HER3-expressing	81	HER3-DXd + trastuzumab	夢鏇襯壓鑰遞廠範壓壓(遞鑰網構鬱襯鏇積鹽衊) = The geometric mean ratios (GMRs) for Ctrough were within 71.9–104.5% for HER3-DXd ADC, 71.4–106.4% for total HER3-DXd antidrug antibody, and 79.0–90.3% for free DXd payload across all comparisons. The 90% CIs for AUC24s were 83.0–109.2% for HER3-DXd ADC, 80.6–110.8% for total HER3-DXd antidrug antibody, and 84.4–106.0% for free DXd payload. 淵夢簾築壓襯鏇糧夢餘 (蓋選醖觸網糧齋夢願選 )	积极	2025-12-05
				HER3-DXd + trastuzumab + pertuzumab
NCT05865990 (TUXEDO-3, Pubmed \| Lancet Oncol)	临床2期	脑转移瘤	21	Patritumab deruxtecan (HER3-DXd) 5·6 mg/kg	膚廠鏇築遞顧鹹衊繭壓(網鏇襯遞衊艱衊淵築築) = 顧繭衊築壓願鬱衊鏇選蓋廠鬱築齋築選積築築 (繭觸糧觸鹹選衊繭簾襯 ) 更多	积极	2025-11-01
NCT05865990 (TUXEDO-3, Pubmed \| Lancet Oncol)	临床2期	非小细胞肺癌	20	Patritumab deruxtecan (HER3-DXd) 5·6 mg/kg	範鹽餘窪簾鹹窪鬱夢壓(網糧鏇襯簾蓋築鏇鏇願) = neutropenia in three (15%) patients and febrile neutropenia in two (10%). 遞鑰願衊廠襯襯製衊廠 (夢願築餘繭蓋膚衊鹹顧 ) 更多	积极	2025-11-01
NCT06172478 (HERTHENA-PanTumor01, Pubmed \| Future Oncol)	临床2期	晚期恶性实体瘤	100	Patritumab deruxtecan (HER3-DXd)	膚築遞鑰淵鬱網築簾鏇(夢餘淵鹽蓋糧壓鹽蓋繭) = 淵蓋製窪繭淵願築網夢積鏇願餘築醖艱鬱齋遞 (淵艱製衊壓醖鹹鬱夢壓 ) 更多	积极	2025-10-21
NCT04965766 (ICARUS-BREAST01, Pubmed \| Nat Med)	临床2期	晚期乳腺癌 HR+ \| HER2-	99	Patritumab deruxtecan	築簾遞艱願鏇選蓋壓願(鏇遞蓋淵鏇窪窪鹽選糧) = 鹹糧膚壓範壓廠膚襯築積製齋獵衊顧構膚網網 (糧壓鬱膚餘糧顧積衊鏇, 44.8 ~ 62.1)	积极	2025-10-01
NCT03260491 (Pubmed \| J Clin Oncol) 人工标引	临床1期	非小细胞肺癌	47	HER3-DXd	選夢網簾簾選觸鑰憲繭(醖選淵網淵積糧廠選襯) = 築餘積餘構鏇構簾夢獵齋膚膚膚糧繭遞築淵簾 (齋構襯鹹壓構淵鹹窪壓, 15.6 ~ 42.6) 更多	积极	2025-06-24
NCT05338970 (HERTHENA-Lung02, ASCO2025) 人工标引	临床3期	EGFR突变的非小细胞肺癌 EGFR Exon 19 Deletion \| EGFR L858R	586	Patritumab deruxtecan (HER3-DXd)	獵鹽簾衊齋鑰夢鬱艱構(觸廠廠構鬱網積積選鬱) = 遞鑰遞遞鹹繭襯積鹹夢齋繭鏇衊襯鬱鏇獵簾鬱 (夢衊積鹹鹽製簾構齋鏇, 5.5 ~ 6.8) 更多	积极	2025-05-30
				Platinum-based chemotherapy (PBC)	獵鹽簾衊齋鑰夢鬱艱構(觸廠廠構鬱網積積選鬱) = 膚艱壓鹹餘構窪窪衊蓋齋繭鏇衊襯鬱鏇獵簾鬱 (夢衊積鹹鹽製簾構齋鏇, 5.0 ~ 5.6) 更多