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]

NCT05620914

/ Withdrawn临床2期IIT

A Window of Opportunity Study of Patritumab Deruxtecan in Patients With Brain Metastases

The purpose of this study is to determine if the study drug, patritumab deruxtecan (HER3-DXd), can be measured in brain tumor tissue after recieving one dose of patritumab deruxtecan before surgery.

开始日期2025-07-01

申办/合作机构

Duke University

[+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）

2026-05-01·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.

2026-05-01·SUPPORTIVE CARE IN CANCER

Prevalence of antibody drug conjugated–induced nausea and vomiting (ADCINV) in patients with cancer

Review

作者: Kannout, Samy ; Eng, Lawson ; Affronti, Mary Louise ; Scotté, Florian ; Zheng, Cindy ; Blayne, Ayden ; Fazelzad, Rouhi ; Ruhlmann, Christina H ; Rugo, Hope S ; Talwar, Sumeet ; Dou, Aaron ; Chow, Ronald ; Ma, Andreas ; Zhang, Daniel ; Iihara, Hirotoshi ; Leigh, Jennifer

Abstract:

Introduction:

Antibody–drug conjugates (ADC) have emerged as an important part of systemic treatment across disease sites. To date, there is no robust pooled prevalence estimate of nausea and vomiting induced by ADCs. Establishing such estimates is essential to determine if ADC-induced nausea and vomiting (ADCINV) represents a clinically significant problem warranting further research into antiemetic prophylaxis. Our aim is to report the prevalence of reported ADCINV across literature.

Methods:

A systematic search of Medline, Embase, Cochrane CENTRAL and Web of Science was conducted from database inception until September 24, 2025. Articles were included if they reported nausea and/or vomiting due to ADCs used in cancer treatment, in the abstract. Pooled prevalence was reported. Subgroup analysis was conducted by ADC. Meta-regression was conducted by age and sex. Quality assessment was conducted. Type I error was set at 0.05.

Results:

A total of 209 studies with 15,493 patients were included. Thirty-nine percent (95%CI, 36–42%) of patients experience any nausea, and 26% (95%CI, 23–29%) experience any vomiting. Younger patients are more likely to experience nausea; each 10-year increase in age is associated with a 12% decrease in nausea rates. Higher emetogenic ADCs include trastuzumab deruxtecan, sacituzumab govitecan, brentuximabvedotin and patritumab deruxtecan. Lower emetogenic agents include disitimab vedotin, telisotuzumab vedotin and rovalpituzumab tesirine.

Discussion:

This is the first study to report prevalence of ADCINV across ADCs. It is a prevalent adverse effect akin to chemotherapy-induced nausea and vomiting that should be viewed as clinically relevant and further investigated to help develop optimal strategies related to antiemetics.

2026-02-01·CANCER TREATMENT REVIEWS

Intracranial activity of antibody-drug conjugates in advanced non-small cell lung cancer: What have we accomplished so far?

Review

作者: Remon, Jordi ; Hendriks, Lizza E L ; Huang, Derek De-Rui ; Cheo, Seng Wee ; Voon, Pei Jye ; Saw, Stephanie P L ; Addeo, Alfredo ; Li, Molly S C ; Menis, Jessica

Antibody-drug conjugates (ADCs) represent a rapidly evolving class of therapeutics in non-small cell lung cancer (NSCLC), offering targeted delivery of cytotoxic payloads to tumor cells while minimizing off-target toxicity. Although ADCs have demonstrated promising results in NSCLC, their efficacy in treating central nervous system (CNS) metastases has been uncertain due to concerns over blood-brain barrier (BBB) penetration and the lack of dedicated CNS-specific evaluations in clinical trials. However, emerging evidence challenges this paradigm. While earlier-generation ADCs such as T-DM1 exhibited limited CNS efficacy, newer ADCs employing optimized linkers and cytotoxins demonstrate more favorable efficacy and toxicity profiles. Selected agents, including trastuzumab deruxtecan, datopotamab deruxtecan and patritumab deruxtecan, have all shown intracranial responses in patients with advanced NSCLC with brain metastases (BM). Proposed mechanisms facilitating CNS activity include BBB disruption by BM, membrane-permeable and highly potent cytotoxic payloads, and bystander effects that enable tumor cell killing beyond the target antigen. Nevertheless, several limitations remain, including variability in trial designs, limited number of patients with untreated CNS disease, and a lack of CNS-specific endpoints. Given the high incidence of BM in NSCLC and their significant impact on patient outcomes, there is an urgent need to better understand the intracranial activity of ADCs and whether they can prevent the development of CNS metastases, especially as some of these ADCS are being tested in the curative-intent setting. This review synthesizes current evidence and highlights ongoing trials, with a focused examination of the evolving role of ADCs in the management of BM.

673

项与德帕瑞妥单抗相关的新闻（医药）

2026-06-12

·上海丰能数字健康技术研究院

【文献解读171】抗体偶联药物在晚期非小细胞肺癌中的研究进展

——基于《肿瘤防治研究》2022年第49卷第8期综述的深度解读导语：晚期非小细胞肺癌（NSCLC）的治疗在靶向与免疫治疗时代取得了长足进步，但获得性耐药仍是横亘在临床疗效前的核心障碍。当标准治疗线用尽，后线治疗选择有限且疗效有限时，临床亟需新的作用机制药物。抗体偶联药物（ADC）以其“精准投递”细胞毒药物的独特模式，正成为破局的新锐力量。本文将基于陈雅蕊、王江涛等作者在《肿瘤防治研究》（2022, 49(8): 855-860）上发表的综述，系统梳理ADC在晚期NSCLC各靶点的研究进展，并分析其临床潜力与挑战。一、 ADC：重塑肿瘤治疗范式的“生物导弹” 抗体偶联药物（ADC）由三个核心部件构成：特异性单克隆抗体、连接子和高活性细胞毒性载荷。其设计原理类似于精确制导的“生物导弹”：抗体负责识别并结合肿瘤细胞表面的特定抗原，通过内吞作用进入细胞内部；随后，在溶酶体环境下，连接子断裂释放细胞毒药物，从而在肿瘤细胞内“引爆”，实现高效杀伤。与传统化疗相比，ADC旨在降低全身毒性，提高治疗窗口。1.1 ADC的“三驾马车” 抗体：通常选用人源化IgG，需具备高特异性、高亲和力及低免疫原性。连接子：其稳定性至关重要，分为可切割型（允许药物在靶细胞外发挥“旁观者效应”）和不可切割型（降低脱靶毒性）。细胞毒载荷：多为微管抑制剂（如美坦辛衍生物）或DNA损伤剂（如拓扑异构酶I抑制剂），需在皮摩尔级别即有强效毒性。1.2 理想靶点的甄选一个合格的ADC靶点需满足：在肿瘤组织高表达/特异性表达，而在正常组织低表达；能被抗体有效结合并介导内化；具备高效的细胞内转运途径。在NSCLC领域，HER2、Trop-2、MET、HER3等已成为明星靶点，相关药物研发进展迅速。二、 HER2靶向ADC：从乳腺癌到肺癌的跨越式突破 HER2靶点在肺癌中的应用最初受启发于其在乳腺癌的成功。研究发现，HER2突变而非单纯扩增，能促进受体内化，为ADC治疗提供了更佳的生物学基础。2.1 T-DM1：开创先河的探路者作为首个在HER2阳性晚期NSCLC中测试的ADC，T-DM1（曲妥珠单抗-美坦辛）在一项II期研究中，针对HER2突变/扩增患者，取得了客观缓解率（ORR）51%，中位无进展生存期（PFS）5个月的疗效，且安全性可控。基于此，NCCN指南推荐其用于治疗HER2突变NSCLC（2A类证据）。2.2 DS-8201：树立新标杆的明星药物 DS-8201（德曲妥珠单抗）是新一代抗HER2 ADC，其采用拓扑异构酶I抑制剂作为载荷，并具有更高的药物/抗体比（DAR），从而增强了抗肿瘤活性。关键的DESTINY-Lung01II期临床研究结果令人瞩目：在42例经治HER2突变NSCLC患者中，ORR高达61.9%，中位PFS长达14个月。基于此，FDA于2020年批准其用于经治的转移性HER2突变NSCLC，并已纳入NCCN指南。对比研究显示，DS-8201在HER2突变队列的疗效显著优于HER2过表达队列（PFS 14月 vs. 5.4月）。药物研究阶段患者人群关键疗效数据 T-DM1 II期 HER2突变/扩增 ORR: 51%; PFS: 5个月 DS-8201 II期 (DESTINY-Lung01) HER2突变 (经治) ORR: 61.9%; PFS: 14个月 DS-8201 II期 (DESTINY-Lung01) HER2过表达 (经治) PFS: 5.4个月三、多靶点并进：Trop-2、MET与HER3的探索除了HER2，针对其他在NSCLC中高表达的靶点，ADC药物也在积极布局。3.1 Trop-2靶向：SG与DS-1062 Sacituzumab govitecan (SG)针对难治性NSCLC的I/II期研究显示，中位PFS为4.4个月，中位OS为7.3个月，且疗效与Trop-2表达水平无关。DS-1062（Datopotamab deruxtecan）的I期研究证实了其安全性，并已启动III期临床，对比多西他赛，并探索与PD-1抑制剂的联合一线治疗。3.2 MET靶向：克服信号通路耐药 Teliso-V是抗MET的ADC。I期研究显示其单药或联合EGFR-TKI在MET阳性NSCLC中具有抗肿瘤活性，其机制可能绕过EGFR TKI耐药中常见的MET扩增。然而，后续在鳞状NSCLC的II期研究因疗效不佳和毒性问题而提前终止，提示MET靶向ADC的临床开发需更精准的患者筛选。3.3 HER3靶向：克服EGFR TKI耐药的新策略 HER3是EGFR TKI耐药的重要旁路激活机制。Patritumab Deruxtecan (HER3-DXd)在EGFR突变NSCLC的I期研究中显示良好安全性。临床前研究表明，EGFR TKI可上调HER3表达，从而增强HER3-DXd的疗效。此外，HER3-DXd与PD-1抑制剂的联合也展现出协同抗肿瘤活性。靶点代表药物当前最高阶段核心发现/优势 Trop-2 SG II期 (篮式试验) 疗效与Trop-2表达水平无关，为泛癌种应用提供可能 Trop-2 DS-1062 III期单药与联合PD-1抑制剂的临床研究同步推进 MET Teliso-V II期 (已终止) 单药/联合EGFR-TKI在MET阳性患者中显示活性；鳞癌研究失败 HER3 HER3-DXd I期高内化率；与EGFR TKI和免疫治疗均有协同潜力四、探索中的新兴靶点与未来策略除上述靶点外，针对EGFR（MRG003）、B7-H3（MGC018）、PTK7（Cofetuzumab Pelidotin）、NaPi2b（XMT-1536）等靶点的ADC药物也处于I/II期临床研究阶段，初步数据展示了安全性与一定的抗肿瘤活性。值得注意的是，部分药物（如MGC018）的高级别治疗相关不良事件发生率较高，凸显了ADC毒性管理的重要性。未来ADC的发展将聚焦于：1.载荷优化：开发具有更强效、不同作用机制或可穿透血脑屏障的新型载荷。2.联合治疗：与免疫检查点抑制剂、靶向药物或其他ADC联用，以克服耐药、增强疗效。3.伴随诊断：寻找能精准预测ADC疗效的生物标志物，实现个体化治疗。核心要点总结与展望 ADC为耐药晚期NSCLC提供了全新治疗范式：以DS-8201为代表的HER2靶向ADC已在HER2突变患者中确立了卓越疗效和标准治疗地位。靶点探索呈现多元化格局：Trop-2、MET、HER3等靶点ADC药物研究活跃，各有优势与挑战，尤其HER3-DXd在克服EGFR TKI耐药方面潜力突出。临床应用需平衡疗效与毒性：ADC的安全性特征（如血液学毒性、间质性肺炎）需密切关注，精准的患者筛选和不良反应管理是成功应用的关键。联合治疗是未来重要方向：ADC与靶向、免疫等药物的联合方案正在积极探索，有望进一步提升疗效并扩大获益人群。伴随诊断与个体化治疗不可或缺：明确ADC的疗效预测标志物，实现“对号入座”，是未来研究的核心课题。临床实践启示笔者认为，ADC的临床应用策略应基于循证医学证据分层展开：对于HER2突变的经治晚期NSCLC患者，DS-8201是优先考虑的治疗选择之一。对于其他靶点（如Trop-2、HER3），目前多数药物仍处于临床研究阶段，鼓励符合条件的患者积极参与相关临床试验。在临床实践中，需对患者进行全面的基因检测（包括HER2、MET等），并充分评估患者的体能状态和既往治疗史。治疗过程中，应密切监测并及时处理ADC相关不良反应，尤其是与载荷相关的特异性毒性。参考文献： [1] Herbst RS, Morgensztern D, Boshoff C. 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Trop-2 is a novel target for solid cancer therapy with sacituzumab govitecan (IMMU-132), an antibody-drug-conjugate (ADC). Oncotarget, 2015, 6(26): 22496-22512. [29] Jiang A, Gao X, Zhang D, et al. Expression and clinical significance of the Trop-2 gene in advanced non-small cell lung carcinoma. Oncol Lett, 2013, 6(2): 375-380. [30] Bardia A, Messersmith WA, Kio EA, et al. Sacituzumab Govitecan, a Trop-2-Directed Antibody-Drug Conjugate, for Patients with Epithelial Cancer:Final Safety and Efficacy Results from the Phase 1/2 IMMU-132-01 Basket Trial. Ann Oncol, 2021, 32(16): 746-756. [31] Heist RS, Guarino MJ, Masters G, et al. Therapy of advanced non-small-cell lung cancer with an SN-38-anti-T rop-2 drug conjugate, sacituzumab govitecan. J Clin Oncol, 2017, 35(24): 2790-2797. [32] Meric-Bernstam F, Spira AI. TROPION-Pan Tumor 01: Dose analysis of The TROP2-directed antibody-drug conjugate (ADC) datopotamab deruxtecan (Dato-DXd, DS-1062) for the treatment (Tx) of advanced or metastatic non-small cell lung cancer (NSCLC). J Clin Oncol, 2021, 39(15): 9058. [33] Ko B, He T, Gadgeel S, et al. MET/HGF pathway activation as a paradigm of resistance to targeted therapies. Ann Transl Med, 2017, 5(1): 4. [34] Salgia R. MET in Lung Cancer: Biomarker Selection Based on Scientific Rationale. Mol Cancer Ther, 2017, 16(4): 555-565. [35] Wang J, Anderson MG, Oleksijew A, et al. ABBV-399, a c-Met Antibody Drug Conjugate that Targets Both MET Amplified and c-Met OverexpressingTumors, Irrespective of MET Pathway Dependence. Clin Cancer Res, 2016, 23(4): 992-1000. [36] Goldman J, Angevin E, Strickler J, et al. MA 02.10 Phase I Study of ABBV-399 (Telisotuzumab Vedotin) as Monotherapy and in Combination with Erlotinib in NSCLC. J Thoracic Oncol, 2017, 12(11): 1805-1806. [37] Strickler JH, Weekes CD, Nemunaitis J, et al. First-in-human phaseⅠ, dose-escalation and expansion study of telisotuzumab vedotin, an antibody-drug conjugate targeting c-Met, in patients with advanced solid tumors. J Clin Oncol, 2018, 36(33): 3298-3306. [38] Waqar SN, Redman MW, Arnold SM, et al. A phase Ⅱ study of telisotuzumab vedotin in patients with c-MET-positive stage Ⅳ or recurrent squamous cell lung cancer (LUNG-MAP Sub-study S1400K, NCT03574753). Clin Lung Cancer, 2020, 22(3): 170-177. [39] Kawakami H, Yonesaka K. HER3 and its ligand, heregulin, as targets forcancer therapy. Recent Pat Anticancer Drug Discov, 2016, 11(3): 267-274. [40] Yonesaka K, Hirotani K, Kawakami H, et al. Anti-HER3 monoclonal antibody patritumab sensitizes refractory non-small cell lung cancer to the epidermal growth factor receptor inhibitor erlotinib. Oncogene, 2016, 35(7): 878-886. [41] Watanabe S, Yonesaka K, Tanizaki J, et al. Targeting of the HER2/HER3signaling axis overcomes ligand-mediated resistance to trastuzumab in HER2-positive breast cancer. Cancer Med, 2019, 8(3): 1258-1268. [42] Hashimoto Y, Koyama K, Kamai Y, et al. A novel HER3-targeting antibody-drug conjugate U3-1402 exhibits potent therapeutic efficacy through the delivery of cytotoxic payload by efficient internalization. Clin Cancer Res, 2019, 25(23): 7151-7161. [43] Yu HA, Baik CS, Gold K, et al. LBA62 Efficacy and safety of patritumab deruxtecan (U3-1402), a novel HER3 directed antibody drug conjugate, in patients (pts) with EGFR-mutated (EGFRm) NSCLC-Science Direct. Ann Oncol, 2020, 31: 1189-1190. [44] Yonesaka K, Takegawa N, Watanabe S, et al. An HER3-targeting antibody-drug conjugate incorporating a DNA topoisomeraseI inhibitor U3-1402 conquers EGFR tyrosine-kinase-inhibitor-resistant NSCLC. Oncogene, 2019, 9(38): 1398-1409. [45] Haratani K, Yonesaka K, Takamura S, et al. U3-1402 sensitizes HER3-expressing tumors to PD-1 blockade by immune activation. J Clin Invest, 2020, 130(1): 374-388. [46] Jiang Z, Hao Y, Ding X, et al. The effects and mechanisms of SLC34A2on tumorigenicity in human non-small cell lung cancer stem cells. Tumor Biol, 2016, 37(8): 10383-10392. [47] Heynemann S, Yu H, Churilov L, et al. NaPi2b expression in a large surgical Non-Small Cell Lung Cancer (NSCLC) cohort. Clin Lung Cancer, 2022, 23(2): e90-e98. [48] Bodyak ND, Mosher R, Yurkovetskiy AV, et al. The dolaflexin-based antibody-drug conjugate XMT-1536 targets the solid tumor lineage antigen SLC34A2/NaPi2b. Mol Cancer Ther, 2021, 20(5): 896-905. [49] Richardson DL, Barve MA, Strauss JF, et al. PhaseⅠ expansion study of XMT-1536, a novel NaPi2b-targeting antibody-drug conjugate (ADC): preliminary efficacy, safety, and biomarker results in patients with previously treatedmetastatic ovarian cancer (OC) or non-small cell lung cancer (NSCLC). Clin Oncol, 2020, 38(15_suppl): 3549. [50] Kato S, Okamura R, Mareboina M, et al. Revisiting Epidermal Growth Factor Receptor ( EGFR) Amplification as a Target for Anti-EGFR Therapy: Analysis of Cell-Free Circulating TumorDNA in Patients With Advanced Malignancies. JCO Precis Oncol, 2019, 3: PO.18.00180. [51] Ramalingam SS, Vansteenkiste J, Planchard D, et al. Overall survival with osimertinib in untreated, EGFR-mutated advanced NSCLC. N Engl J Med, 2020, 382(1): 41-50. [52] Xu RH, Qiu MZ, Zhang Y, et al. First-in-human dose-escalation study of anti-EGFR ADC MRG003 in patients with relapsed/refractory solid tumors. Clin Oncol, 2020, 38(15_suppl): 3550. [53] Jang S, Powderly JD, Spira AI, et al. Phase 1 dose escalation study of MGC018, an anti-B7-H3 antibody-drug conjugate (ADC) in patients with advanced solid tumors. Clin Oncol, 2021, 39(15_suppl): 2631-2632. [54] Radovich M, Solzak JP, Hancock BA, et al. Abstract PS10-26: An initialsafety study of gedatolisib plus cofetuzumab pelidotin for metastatic triple-negative breast cancer. Cancer Res, 2021, 81(4): 10-26. [55] Gébleux R, Stringhini M, Casanova R, et al. Non-internalizing antibody-drug conjugates display potent anti-cancer activity upon proteolytic release of monomethyl auristatin E in the subendothelial extracellular matrix. Int J Cancer, 2017, 140(7): 1670-1679. [56] Whalen KA, White BH, Quinn JM, et al. Targeting the Somatostatin Receptor 2 with the Miniaturized Drug Conjugate, PEN-221: A Potent and Novel Therapeutic for the Treatment of Small Cell Lung Cancer. Mol Cancer Ther, 2019, 18(11): 1926-1936. （解读基于陈雅蕊, 王江涛, 关泉林, 姬薇, 焦福智. 抗体偶联药物在晚期非小细胞肺癌中的研究进展. 肿瘤防治研究, 2022, 49(8): 855-860.）

2026-06-11

·亿药前谈

ADC赛道再变天：当"魔法子弹"遇上肺癌，谁才能真正突围？

点击蓝字,立即关注 FOLLOW US 近日，一项备受关注的肺癌联合用药III期临床研究被按下暂停键。与此同时，中国创新药企的一款同类产品却刚刚交出亮眼成绩单。在ADC药物狂飙突进的年代，这两件事放在一起，值得我们好好聊聊。 01 一项重磅联合疗法研究的提前终止 6月初，国际医药巨头默沙东与吉利德联合宣布，提前终止Trodelvy（一款靶向Trop2的ADC药物）与默沙东明星PD-1抑制剂Keytruda（K药）联合用于一线治疗晚期非小细胞肺癌（NSCLC）的III期临床研究——KEYNOTE-D46/EVOKE-03。这项研究针对的是PD-L1高表达（TPS≥50%）的初治转移性非小细胞肺癌患者，原计划要到2027年才能完成主要数据收集。是什么让两大药企决定提前"止损"？独立数据监测委员会在审查了当前的无进展生存期（PFS）最终分析和总生存期（OS）中期数据后给出了建议：联合用药组虽然在延缓疾病进展方面观察到了一定趋势，但未达到统计学意义上的显著差异；而想要在接下来的随访中观察到总生存期的显著获益，可能性也不大。好消息是，联合用药没有发现新的安全性问题——这明确指向了一个结论：不是安全性问题，而是疗效确实不够看。 02 科普小课堂：ADC是个啥？在聊清楚这件事为什么重要之前，不妨先简单科普一下什么是ADC。 ADC全称抗体偶联药物（Antibody-Drug Conjugate），江湖人称"魔法子弹"。它的设计思路非常精妙：通过一个"导航系统"（单克隆抗体）精准识别肿瘤细胞表面的特定蛋白，再 tether 上一颗"炸弹"（细胞毒性药物，也叫载荷/payload），中间用一根"保险绳"（连接子/linker）拴住。理论上，ADC进入体内后，抗体部分负责带路，找到癌细胞并与之结合，然后整体被癌细胞"吃掉"。进入癌细胞内部后，连接子断裂，释放出毒性载荷，从内部炸死癌细胞。这种"精准制导"的设计，本意是让药物主要杀伤癌细胞，减少对正常组织的伤害。但现实世界往往比设计图纸复杂得多——连接子太不稳定，药物可能在到达肿瘤之前就提前"松绑"，导致炸弹在血液循环中提前释放，不仅增加了全身毒性，还削弱了到达肿瘤的药物剂量。 03 Trodelvy的困境：两次折戟，问题出在哪？其实，这不是Trodelvy在肺癌领域的第一次失利。早在这次一线治疗研究之前，Trodelvy在二线非小细胞肺癌的EVOKE-01研究中就已经碰壁——对比传统化疗药物多西他赛，未能显示出显著优势。如果我们仔细复盘EVOKE-01的数据，就能发现一些端倪，也能理解为什么这次的联合用药研究同样走不通：首先，疗效衰减明显。研究预设Trodelvy能将患者的死亡风险降低约25%（HR=0.75），但实际观察到的数值为0.84，随着随访时间延长甚至进一步恶化到0.89。这说明Trodelvy可能能带来短暂的肿瘤控制效果，但难以转化为真正的生存获益。其次，免疫治疗应答者反而"拖后腿"。在亚组分析中，那些此前对免疫治疗有应答的患者，使用Trodelvy后的表现反而更差（HR=1.09）；而对免疫治疗无应答的患者，数据相对好一些（HR=0.75）。这个反直觉的现象说明，Trodelvy的加入某种程度上"稀释"了免疫治疗的优势效果。第三，肿瘤缓解数据并不漂亮。 Trodelvy组的客观缓解率（ORR）只有13.7%，甚至低于化疗组的18.1%；中位无进展生存期（mPFS）方面，4.1个月对比3.9个月，几乎可以说是没有差异。第四，安全性问题突出。约50%的患者出现严重中性粒细胞减少（≥3级），约10%出现严重腹泻。如此高的血液学毒性和胃肠道毒性，提示药物的连接子可能不够稳定，导致载荷提前释放，一方面让患者承受了更多副作用，另一方面到达肿瘤组织的有效药物浓度反而不足。此外，Trodelvy使用的载荷是SN-38，这种拓扑异构酶I抑制剂虽然在三阴性乳腺癌和尿路上皮癌中表现尚可，但对非小细胞肺癌的杀伤力似乎并不理想。把这些因素综合起来，再看这次的一线联合用药研究：研究对象是PD-L1高表达（TPS≥50%）的人群，而这恰恰是K药单药疗效最强的领域。在EVOKE-01中，免疫应答亚组就已经出现了"反向稀释"效应，到了K药"主场"的一线高表达人群中，Trodelvy能带来的额外获益空间自然就更小了。再加上其本身偏窄的治疗窗口和安全性负担，这次提前终止，其实在意料之中。 04 中国创新药的高光时刻：Sac-TMT做对了什么？就在Trodelvy遭遇滑铁卢的同时，科伦博泰旗下靶向同样靶点（Trop2）的ADC药物Sac-TMT（也称SKB264/MK-2870）却传来了好消息。其在中国开展的OptiTROP-Lung05研究中，Sac-TMT联合K药用于一线PD-L1阳性（TPS≥1%）的非小细胞肺癌患者，结果显示：联合用药组相较于K药单药组，疾病进展或死亡风险降低了65%（HR=0.35）。虽然中位PFS数据尚未成熟，但这一降幅已经显著超越了既往经典联合治疗研究所达到的水平。更"聪明"的是研究设计——不同于EVOKE-03只纳入PD-L1高表达（TPS≥50%）患者，OptiTROP-Lung05研究覆盖了所有PD-L1阳性人群（TPS≥1%），其中PD-L1低/中表达（TPS 1-49%）和高表达（TPS≥50%）的患者比例约为四六开。亚组分析显示，PD-L1低/中表达亚组的获益更为突出。这恰恰打在了K药的"软肋"上——K药单药在PD-L1低/中表达人群中的疗效相对有限，联合一个强力搭档才有更大的改善空间。 05 从分子设计看差异：为什么Sac-TMT更强？两款药物靶向同一个靶点，联合的是同一个免疫治疗药物，为何结果天差地别？答案藏在分子设计里。更稳定的连接子： Sac-TMT的连接子在体内更不容易提前断裂，这意味着载荷能在血液循环中保持"栓牢"状态，直到抵达肿瘤组织才释放。带来的直接好处有两个：一是血液中游离的载荷浓度更低，全身毒性（尤其是骨髓抑制和腹泻）显著减少；二是更多药物被递送到肿瘤内部，杀伤效率更高。更强的载荷： Trodelvy使用的是SN-38，Sac-TMT则采用了代号为KL610023的载荷——这是一种贝洛替康衍生物，同样靶向拓扑异构酶I，但细胞杀伤效力更强，半衰期也更长。这种设计理念的差异，直接反映在安全性数据上：Sac-TMT的血液学毒性和腹泻发生率远低于Trodelvy，其主要毒性表现为与靶点相关的"在靶毒性"，临床管理难度更小，患者的用药体验和治疗依从性自然也更好。简单来说，Trodelvy像是"导航系统还行但炸弹容易半路掉链子"，而Sac-TMT则是"导航精准、炸弹给力且保险绳更牢靠"。 06 默沙东的ADC版图：Sac-TMT的地位为何愈发重要？默沙东围绕K药打造的联合用药矩阵中，ADC是重要的战略方向。除了科伦博泰的Sac-TMT，2023年默沙东还与日本第一三共达成了一笔高达220亿美元的重磅合作，涉及HER3-DXd、I-DXd和R-DXd三款药物。但从目前的开发进展来看，Sac-TMT的重要性正在不断攀升： HER3-DXd虽然在治疗奥希替尼耐药后的EGFR突变非小细胞肺癌的III期研究中PFS达到了主要终点，但出现了2例致命的间质性肺炎（5级ILD），今年5月已主动撤回上市申请。这一安全性挫折显然影响了其后续开发节奏。 I-DXd目前主要集中在小细胞肺癌和前列腺癌领域的探索，在非小细胞肺癌方面仅有早期临床数据。 R-DXd的开发重心则在卵巢癌领域。此外，虽然默沙东也在参与第一三共/阿斯利康的T-DXd（靶向HER2的ADC）联合K药在肺癌领域的DESTINY-Lung06和TROPION-Lung08研究，但这些试验的主导权在第一三共/阿斯利康手中，T-DXd也并不在默沙东自己的产品矩阵内。此消彼长之下，Sac-TMT几乎成了默沙东在一线非小细胞肺癌领域最倚重的ADC伙伴。目前，默沙东已经布局了两项以"K药+Sac-TMT"为核心的III期大临床： TroFuse-007：针对PD-L1高表达（TPS≥50%）的转移性非鳞状非小细胞肺癌患者，预计2028年完成； TroFuse-023：针对转移性鳞状非小细胞肺癌患者的维持治疗，覆盖所有PD-L1表达水平。这两项研究瞄准的都是一线非小细胞肺癌的大适应症人群，足见默沙东对这一组合的信心。值得注意的是，全球III期设计并未采用中国研究中PD-L1 TPS≥1%的入组标准，而是分别针对特定人群精准出击——这或许既是对两款药物协同效应的信心，也是在K药核心适应症专利到期日渐临近的背景下，未雨绸缪、巩固优势的策略考量。 07 这对行业意味着什么？ Trodelvy在肺癌领域的连续失利，并不意味着ADC这条路走不通，而是提醒我们：ADC不是简单的"抗体+毒素"拼盘，连接子的稳定性、载荷的选择、适应症的差异化定位，每一个细节都决定成败。对中国创新药企而言，Sac-TMT的成功是一个极具意义的信号。它证明中国本土研发的创新药物，在分子设计和临床开发策略上，完全有能力做到全球领先水平，甚至在同靶点竞争中后来居上。与此同时，这一事件也在重塑一线非小细胞肺癌的未来竞争格局。随着K药专利悬崖的逼近，默沙东迫切需要找到能够延长其产品生命周期的黄金搭档。在这个叙事中，Sac-TMT正从"重要选项"逐步走向"C位主角"。在ADC药物竞争日趋白热化的今天，科学设计的力量正在重新定义谁是真正的赢家。免责声明本公众号专注收集发布全球生物医药行业资讯。本文仅作信息交流之目的，本文中所涉及的信息旨在科普，部分内容为AI生成，文中观点仅具有参考价值，不对所包含内容的准确性、可靠性或者完整性提供任何明示或暗示的保证。亿药前谈扫描二维码，关注更多生物医药资讯

抗体药物偶联物临床3期

2026-06-11

·熊猫的研究笔记

把研发做好，把公司买回来

即便在正确的方向上，人生也会走过许多难走的路。这段时间，国内市场对于创新药行业非常沮丧。海外XBI指数持续上行，与国内创新药指数的剪刀差持续扩大。在同样的AI叙事与降息走弱预期下，海外big pharma通过M&A的方式为biotech持续提供流动性，我们面临着“Coins法案以及政策交困”的预期，随着市场持续失血，部分优质药企的估值跌回了过去几年的新低。对我而言，这是一个如何看待“公司内在价值持续增长，股价不断下跌”的问题，考验的是自己能力圈的真实边界。对于公司而言，考验的是能否保持战略定力，去做更多长远的布局，当然也包括在有能力的情况下启动股份回购计划。恒瑞、药明、映恩、中生、先声、加科思等等都在回购股份，这既是股东导向，也是很好的股权激励与人才长期利益绑定的时机。我始终相信，股东的长期收益基于公司最终创造的价值。价值来自解决的问题，以及解决问题的能力在较长一段时间中是否具备差异性。上篇文章探讨了ASCO后，ArriVent得到海外投资者认可的原因竞品数据披露后，为什么ArriVent反而得到市场认可？，核心还是伏美替尼成药概率的提升以及海外竞争格局的向好。同样的逻辑并没有映射到国内，不过给不给估值也不重要，“海外商业化”以及“大分子临床”两张期权最后能刮出什么结果，核心还是看艾力斯是否努力地做好当下。 1.当前重点：解决NSCLC后线耐药，延长一线治疗时间在我看来，目前的重点不是去做一个“什么前沿靶点都布局”的ADC药企，而是围绕NSCLC耐药人群构建一个“联合用药”的闭环生态。做好药是第一步，卖好药是第二步，药物之间能不能形成闭环是第三步——也是真正拉开差距的一步。从EGFR耐药机制看，除了C797S突变外，MET扩增是EGFR-TKI获得性耐药的主要机制之一（MET扩增、过表达通常占约10–15%），HER3与TROP2也在EGFR NSCLC中常见高表达，对上述机理的研究以及同相关药物的联用也是布局肺癌药企的重点。此前，伏美替尼与荣昌的RC108 c-Met ADC，以及康宁杰瑞的JSKN016 Her3/Trop2 ADC也做了临床联用。 MET方面，赛沃替尼+奥希替尼在二/三线治疗中有着不错的数据，Ⅱ期SAVANNAH研究显示研究者评估ORR为56%，mPFS约7.4个月，Ⅲ期SACHI研究中患者mPFS为8.2个月，验证了EGFR与MET通路双重阻断的临床价值。一线FLOWERS研究样本量较小（N=44），随访时间尚短，其信号强度有待更大规模确证性研究验证，目前Ⅲ期SANOVO试验正在进行中。Ami+Laz已于2024年获FDA批准用于EGFR ex19del/L858R一线，但需管理皮疹/甲沟炎/ILD样事件与静脉血栓栓塞风险，作为奥希替尼单药或奥希替尼+化疗之外的可选方案。 TROP2方面，科伦博泰的sac-TMT，在OPTITROP-Lung04 Ⅲ期试验中，sac-TMT组mPFS达到8.3个月，显著优于化疗的4.3个月（HR 0.49），预设OS期中分析也显示获益趋势（HR 0.60），3级以上TRAE约58%，需重点管理中性粒细胞减少、口腔炎、眼部毒等，并建立标准化监护流程。 HER3方面，默沙东/第一三共去年自愿撤回HER3-DXd的BLA，核心压力来自确证性Ⅲ期HERTHENA-Lung02 OS未显现优势。百利天恒的EGFR×HER3双抗ADC iza-bren，单药治疗EGFR-TKI耐药NSCLC患者，整体mPFS达12.5个月，19del亚组达14.1个月；联合奥希替尼一线治疗EGFR突变NSCLC，2.5mg/kg组12个月PFS率92.1%。安全性方面，3级以上TEAE以血液学毒性为主，因TRAE导致的停药率为1.9%，ILD发生率1.4%，无3级以上ILD事件。基于上述，我对艾力斯的理解是，在Met、Trop2、Her3三条大分子药物的开发路径上，无论是做单抗还是双抗ADC，核心要做好三点：第一，在靶点组合和连接子设计上做出差异化，验证平台的价值。第二，在安全性上守住底线，现有ADC药物的痛点在于治疗窗、剂量、长期耐受性能否做稳定联合，伏美替尼最大的差异化优势就是安全性优异，如果自研ADC安全性差了，联用的逻辑就站不住。第三，关注与伏美替尼的联用数据，从后线推到一线。伏美还没有像奥希替尼那样有大规模的联用ADC数据，这个空白本身就是机会。 2.不追热点：找适合自己的双载荷ADC 众所周知，双载荷ADC的核心理念是通过双重杀伤机制突破单载荷的耐药天花板，但问题同样在于毒性控制。两个高效载荷叠加往往放大骨髓/黏膜/脱靶毒性，且均一偶联、连接子时序释放与稳定性显著抬升了CMC的门槛。根据公开进度，HER2相关双载荷关注度较高，但也有企业走差异化路线，例如康弘的KH815靶向TROP2，载荷为TOP1i+TPL，已获CDE临床许可并推进I期，预计2026年年内有数据读出；信达的IBI3020靶向CEACAM5，基于DuetTx平台开发的双载荷ADC，已在I期临床完成首例患者给药。对艾力斯而言，如果要往“免疫重塑”的方向努力，可以考虑两个维度，一是通过ADC把冷肿瘤变成热肿瘤，用伏美替尼维持肿瘤负荷与TKI可能的免疫微环境调节，二是把TLR/STING激动剂作为第二载荷，前提是能证明治疗窗（脱靶炎症、irAE-like综合征、给药途径与释放控制比较苛刻），并能给出与伏美联用时的监测与中止规则，这个问题解决不了，后面的路会比较难。 3.强化特点：深化小分子研发的基本盘这几年小分子药物研发做得不够好，这是需要反思的。对于艾力斯而言，大分子和小分子药物的布局不是二选一的关系，而是一条路的不同阶段，小分子继续深耕EGFR通路的耐药突变覆盖（如C797S）以及RAS/MAPK等下游旁路通路，大分子则针对旁路激活（MET扩增、HER3上调、TROP2高表达）和肿瘤免疫微环境，两者是互补的，共同构成EGFR耐药后的闭环生态。从3-5年的科学储备看，DDR调控剂（如ATR/CHK1/PRAP类）、表观遗传调控（EZH2/BRD4等）目前还是作为平台能力的储备，目前是否具备与ADC、TCE联合协同重塑免疫微环境的潜力还要验证。共价抑制剂、环肽抑制剂、降解剂，这些新药形式针对的是传统小分子难以作用的PPI等大界面靶点，Protac从机理上确实可能避开C797S造成的活性位点“锁孔变形”的问题，但也需要更多的时间来验证。把以上思考放在一起，在高博和尤博带领下沉下心来做研发，，艾力斯还是有机会的。第一，Q3首个自研ADC的中美同步IND申报，验证自主linker-payload的安全性以及平台价值。第二，从机制紧迫性与伏美替尼联合生态出发，MET过表达/扩增人群是当前最可能第一个承接自研ADC+伏美替尼联用的入口，若平台安全窗口能力验证，可以考虑开发HER3/C-MetADC或者EGFR/c-Met双抗ADC（虽然也逐步拥挤，AZ等10家药企也进行了布局），以精准对标MET扩增驱动的耐药人群。此外，围绕Trop2、Her3相关靶点，利用其在NSCLC中的广泛表达与高效内吞特性，克服异质性耐药，与伏美替尼形成产品矩阵闭环。第三，探索后续双载荷/双机制payload、免疫激活型ADC（TLR/STING agonist conjugate等）技术，在载荷组合和连接子技术上做出真正差异化的创新。 My friend Dean once said，don't give a shit about the stock price.乐观和悲观都对，但都不重要。重要的是围绕患者的需求，把药做好，把药卖好，走出一条自己的路，好的公司最后会把自己买回来。

100 项与德帕瑞妥单抗相关的药物交易

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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
EGFR突变的非小细胞肺癌	申请上市	美国	Merck & Co., Inc.	2023-12-22
EGFR突变的非小细胞肺癌	申请上市	美国	Daiichi Sankyo Co., Ltd.	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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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


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	壓築壓鬱願鏇鹽鏇鏇壓(醖網網顧網鹽願齋遞齋) = 願鬱構製簾願鬱繭壓製積糧衊範遞願獵築鬱鏇 (製鬱鑰鏇製襯築遞鹹製 ) 更多	积极	2026-05-29
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	Treatment of physician’s choice (TPC)	壓築壓鬱願鏇鹽鏇鏇壓(醖網網顧網鹽願齋遞齋) = 衊齋夢壓淵獵壓衊製鏇積糧衊範遞願獵築鬱鏇 (製鬱鑰鏇製襯築遞鹹製 ) 更多	积极	2026-05-29
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)	餘繭襯積觸窪構醖獵襯 = 遞鬱夢簾鑰餘糧構衊齋範鑰願齋範鏇淵窪鏇鏇 (鹹膚獵憲築鬱構夢構憲, 壓淵壓選範遞築鑰鏇膚 ~ 築餘製淵淵夢繭鬱願製) 更多	-	2026-05-07
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 B)	餘繭襯積觸窪構醖獵襯 = 範鬱範鑰簾網製夢製遞範鑰願齋範鏇淵窪鏇鏇 (鹹膚獵憲築鬱構夢構憲, 製鑰膚餘選壓獵獵衊壓 ~ 艱簾餘範憲襯積齋鏇簾) 更多	-	2026-05-07
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	簾繭製壓構糧簾積遞糧(遞糧簾糧艱網壓廠簾糧) = 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. 獵鏇淵夢餘鬱網觸觸襯 (觸鏇遞餘醖廠淵製積衊 )	积极	2025-12-05
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 + pertuzumab		积极	2025-12-05
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	襯製憲壓壓遞蓋觸繭鹹(顧襯糧範鏇鹽糧繭鏇遞) = neutropenia in three (15%) patients and febrile neutropenia in two (10%). 築鏇鑰膚構廠鹽願鬱憲 (齋簾壓窪淵遞壓鑰觸窪 ) 更多	积极	2025-11-01
NCT05865990 (TUXEDO-3, Pubmed \| Lancet Oncol)	临床2期	脑转移瘤	21	Patritumab deruxtecan (HER3-DXd) 5·6 mg/kg	鑰顧網淵網蓋壓餘繭範(餘選願構積齋構壓鑰膚) = 繭顧築齋糧餘淵醖觸醖範糧觸鹽襯遞獵壓網選 (鬱顧糧簾夢遞鑰顧鹽鏇 ) 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)	鏇醖觸廠鹽顧築衊齋衊(遞餘衊簾糧繭憲觸簾鏇) = 選淵艱鏇觸窪齋觸獵鏇觸製簾選鑰築製獵鬱願 (範淵夢窪壓顧蓋願醖壓 ) 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	鏇製窪鏇艱膚蓋願構衊(餘顧鬱鹽遞夢積繭選淵) = 壓艱淵鑰積網製憲簾鏇繭願選蓋窪選簾積蓋顧 (鏇餘鹹壓壓醖壓構範憲, 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	範衊範淵鹹鏇糧鹽夢鏇(憲蓋鏇衊淵積積艱膚憲) = 積壓廠鏇繭窪醖範顧蓋網網鏇鬱積衊繭膚簾構 (鹽廠範鹹蓋憲夢鹽廠憲, 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)	鬱窪獵遞衊窪鑰遞選憲(願鏇鬱夢糧網繭淵衊夢) = 簾鬱餘夢積觸鑰願網衊築齋衊齋襯鹹膚糧衊構 (築網淵簾築鏇築鹽築艱, 5.5 ~ 6.8) 更多	积极	2025-05-30
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	Platinum-based chemotherapy (PBC)	鬱窪獵遞衊窪鑰遞選憲(願鏇鬱夢糧網繭淵衊夢) = 壓構齋鏇廠壓觸壓糧襯築齋衊齋襯鹹膚糧衊構 (築網淵簾築鏇築鹽築艱, 5.0 ~ 5.6) 更多	积极	2025-05-30
NCT05865990 (TUXEDO-3, ASCO2025)	临床2期	晚期恶性实体瘤 \| 转移性乳腺癌 \| 晚期鳞状非小细胞肺癌 ... HER3 更多	61	HER3-DXd 5.6 mg/kg	遞餘窪鏇壓襯衊衊夢鏇(窪鹹淵艱壓壓廠鬱鹹範) = 構簾願網鹽鹹製艱壓齋鏇築憲網鹽鹹獵淵構顧 (鏇構窪積鹽壓糧蓋鹹獵 )	积极	2025-05-30