START-lung is an international, multicentre, single-arm phase II trial. Protocol treatment consists of tarlatamab administered as an intravenous infusion until disease progression according to RECIST v1.1 criteria, unacceptable toxicity, or patient decision, whichever comes first. The primary objective of the trial is to assess the clinical efficacy of tarlatamab, in terms of 12-month OS rate, in patients with ES-SCLC and ECOG PS 2 who have previously received only one line of platinum-etoposide doublet chemotherapy with immune-checkpoint inhibition and whose disease has progressed.

开始日期2026-05-01

申办/合作机构

European Thoracic Oncology Platform

[+1]

NCT07423585

/ Recruiting临床2期IIT

A Front-Line Window-of-Opportunity Phase 2 Study of Tarlatamab (Bispecific T Cell Engager: DLL3-CD3) in Patients With Extensive-Stage Small-Cell Lung Cancer

This phase II trial tests the effect of tarlatamab in treating patients with small cell lung cancer (SCLC) that has spread from where it first started to other parts of the body (extensive-stage). SCLC is an aggressive cancer which has a low 5-year survival rate. Tarlatamab is a bispecific antibody that can bind to two different antigens at the same time. Tarlatamab binds to DLL3 which is a protein found on the surface of some types of tumor cells, including small-cell lung cancer, and to CD3 which is present on immune system T-cells (a type of white blood cell) and may interfere with the ability of tumor cells to grow and spread. This may increase the length of time to progression (growing, spreading, or getting worse) and help patients with extensive-stage SCLC live longer.

开始日期2026-04-01

申办/合作机构

Ohio State University Comprehensive Cancer Center

[+1]

NCT07328490

/ Not yet recruiting临床1/2期IIT

A Phase I/II Study to Assess the Safety and Antitumor Activity of Bispecific T-cell Engager Tarlatamab and TROP2 Targeted Antibody Drug Conjugate Sacituzumab Govitecan in Previously Treated Extensive-Stage Small Cell Lung Cancer and Extrapulmonary Neuroendocrine Cancer

Background:
Small-cell lung cancer (SCLC) is the most deadly form of lung cancer. It kills at least 250,000 worldwide each year. Extra-pulmonary neuroendocrine cancer (EP-NEC) is a similar type of cancer that develops anywhere other than the lungs. EP-NEC is also very aggressive. Better treatments are needed for these cancers.
Objective:
To test 2 drugs (tarlatamab combined with sacituzumab govitecan [SG]) in people with SCLC or EP-NEC.
Eligibility:
People aged 18 years and older with SCLC or EP-NEC that either did not respond to or returned after treatment.
Design:
Participants will be screened with a physical exam, blood tests, heart function testing, and imaging scans.
Both study drugs are given intravenously (through a needle in the arm). Participants will receive a small starter dose of tarlatamab (1 mg) 2 weeks before beginning regular treatment, followed by the full dose (10 mg) one week later. Treatment then follows a repeating 4-week cycle: tarlatamab (10 mg) on days 1 and 15, and sacituzumab govitecan (7.5 or 10 mg/kg) on days 1 and 8. Treatment continues for up to 2 years, unless the cancer worsens, the participant passes away, or side effects become too severe.
Participants will have regular check-ups including physical exams, blood tests, and imaging scans to monitor safety and treatment response. Blood and tumor samples will be collected for research purposes.
After stopping treatment, participants will return for a safety check at 30 days, then be contacted every 3 months to check on their health and survival. Those who stop treatment for reasons other than cancer progression will continue CT scans every 8 weeks until their disease progresses.

开始日期2026-03-30

申办/合作机构

National Cancer Institute

100 项与塔拉妥单抗相关的临床结果

登录后查看更多信息

100 项与塔拉妥单抗相关的转化医学

登录后查看更多信息

100 项与塔拉妥单抗相关的专利（医药）

登录后查看更多信息

项与塔拉妥单抗相关的文献（医药）

2026-04-01·LUNG CANCER

Safety evaluation of tarlatamab: A pharmacovigilance study based on the FAERS database

Article

作者: Huang, Chunxia ; Li, Yaxin ; Wang, Xue ; Xu, Xiaopeng ; Wang, Jiesong ; Zhang, Mei

OBJECTIVES:

Tarlatamab (Imdelltra, AMG757) has been approved for extensive-stage small cell lung cancer (ES-SCLC) treatment, yet post-marketing data remain limited. Existing studies lack conclusive evidence on its real-world safety profile.

MATERIALS AND METHODS:

Leveraging the FDA Adverse Event Reporting System (FAERS), this study evaluated adverse events (AEs) attributed to Tarlatamab between Q2 2024 and Q1 2025. Disproportionality analysis using reporting odds ratio (ROR) and Bayesian confidence propagation neural network (BCPNN) quantified associations between Tarlatamab and AEs.

RESULTS:

Among 448 analyzed AE reports, the median time to AE onset was 5.0 days. Tarlatamab-associated AEs reports showed elevated hospitalization (21.7 %) and fatality rates (16.7 %). Significant signals emerged across 5 System Organ Classes (SOCs) and 31 Preferred Terms (PTs), including unlabeled events: atrial fibrillation (IC025: 0.77), ageusia (IC025: 3.79), mental status changes (IC025: 2.45), and unresponsiveness to stimuli (IC025: 2.22). Notable discrepancies with labeled information included dual hypertension (IC025: 0.18) and hypotension (IC025: 1.61) signals, suggesting complex blood pressure effects, and a higher mortality risk in male patients. Mild AEs correlated with reduced severe outcome risks.

CONCLUSION:

These findings offer critical insights for clinicians to identify and manage Tarlatamab-related AEs, highlighting underestimated risks and informing tailored practice.

2026-03-01·Clinical Lung Cancer

Optimizing Tarlatamab Delivery in Small Cell and Neuroendocrine Lung Cancer: Real-World Insights into Step-Up Dosing and Prophylactic Tocilizumab Use

Article

作者: Puglianini, Omar Castaneda ; Puri, Sonam ; Joshi, Utsav ; Creelan, Benjamin ; Gaballa, Sameh ; Saltos, Andreas ; Haura, Eric ; Ma, Joanna C ; Kareem, Syeda Saba ; Pellini, Bruna ; Tanvetyanon, Tawee ; Shafique, Michael ; Chiappori, Alberto ; Lu, Charles ; Ong, Faustine ; Naqvi, Syeda Mahrukh Hussnain ; Budhathoki, Pravash ; Gray, Jhanelle E ; Melzer, Daniel ; Solarte, Daniela C Bravo

PURPOSE:

Tarlatamab, a DLL3-targeted bispecific T-cell engager, has emerged as a second-line therapy for extensive-stage small cell lung cancer (ES-SCLC) following progression on platinum-based chemoimmunotherapy. While clinical trials have demonstrated promising efficacy, real-world data on safety remain limited.

METHODS:

This retrospective study included 40 patients with SCLC or high-grade neuroendocrine carcinoma treated with tarlatamab at Moffitt Cancer Center between May 2024 and February 2025. Clinical, laboratory, and treatment-related variables including cytokine release syndrome (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS) were reviewed. Predictive models for these toxicities were developed using Firth logistic regression based on data from 30 patients who did not receive prophylactic tocilizumab.

RESULTS:

The median age was 66.5 years; 55% were male, and 87.5% had an ECOG performance status of 0 to 1. Among patients who did not receive prophylactic tocilizumab (N = 30), 53.3% developed CRS and 23.3% developed ICANS after Cycle 1 Day 1, with 10% experiencing grade ≥ 3 severity for each. Three patients discontinued treatment due to severe CRS/ICANS, with 2 deaths and 1 transition to hospice. Among those who received prophylactic tocilizumab (N = 10), 1 patient developed grade 2 CRS and none developed ICANS. Elevated LDH and liver metastasis were independent predictors of CRS; LDH was also predictive of grade ≥ 2 CRS. Diabetes and cardiovascular disease were independently associated with ICANS.

CONCLUSION:

Tarlatamab is associated with higher CRS and ICANS rates in real-world settings than observed in trials. Prophylactic tocilizumab may mitigate these toxicities in high-risk patients and should be considered for incorporation into treatment protocols.

2026-03-01·Clinical Lung Cancer

Management of Pulmonary Large-Cell Neuroendocrine Carcinoma (LCNEC): An Updated Review

Review

作者: Chow, James Chung Hang ; Yeung, Anson Man Lok

Pulmonary large-cell neuroendocrine carcinoma (LCNEC) is an uncommon and aggressive malignancy, accounting for approximately 3% of all primary lung malignancies. Due to its rarity, the treatment paradigm for LCNEC is primarily derived from retrospective data from non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC). This review synthesizes current evidence and discusses emerging treatment strategies. For medically fit patients with resectable disease, surgical resection, in particular lobectomy, should be offered, while stereotactic body radiation therapy can be reserved for medically inoperable patients. Adjuvant chemotherapy is suggested for most resected tumors, with SCLC regimens (eg, etoposide-cisplatin) associated with better outcomes; however, very early-stage tumors (stage IA) warrant individualized decision-making. There is currently no evidence supporting the use of adjuvant immunotherapy in LCNEC. The role of adjuvant radiotherapy, neoadjuvant therapy and prophylactic cranial irradiation in LCNEC remains undefined. For unresectable, locally advanced disease, concurrent chemoradiation with etoposide-cisplatin followed by consolidation durvalumab is recommended, although the optimal dose-fractionation and the duration of consolidation immunotherapy remain to be investigated. In metastatic disease, etoposide-platinum chemotherapy remains the first-line treatment, while targeted therapy can be considered if tumors harbor actionable genomic alterations. The potential benefit of immunotherapy is currently under investigation. While several second-line treatment options have been reported with modest efficacy, local ablative treatment has shown promise in oligometastatic LCNEC. Among the most promising emerging treatment strategies are DLL3-targeting therapies, buoyed by the recent success of tarlatamab in SCLC. The evolving role of molecular profiling in prognostication and treatment decision-making is also examined.

877

项与塔拉妥单抗相关的新闻（医药）

2026-03-25

·抗体密码

究竟是什么影响了TCE的疗效？

Amgen的DLL3/CD3的双特异抗体tarlatamab已经获得FDA加速批准上市，用于治疗广泛期小细胞肺癌（ES-SCLC）成人患者。这是首个正在意义上靶向实体瘤的TCE，也成功打破了TCE实体成药难的魔咒，同时也为广泛期小细胞肺癌患者带来了新的希望。后续BI（勃林格殷格翰）的TCE双抗obrixtamig，Harpoon（被默克收购）的HPN328,和泽镜的ZG006也陆续进入临床并披露疗效。虽然都是靶向DLL3 的TCE抗体，但是这些抗体在临床中确各有不同，最近，荣昌生物的对tarlatamab，obrixtamig和HPN328进行解析，揭示了这些药物临床药效差异的可能原因。表位各不相同：AMG757特异性靶向DLL3的EGF3结构域，其与相应截短抗原的结合信号显著证实了此点。相比之下，HPN328与BI764532更倾向于结合DLL3结构上靠近细胞膜区域的表位，它们的结合模式集中位于更邻近细胞膜的区域，而非较远的EGF3结构域。这些截然不同的表位结合模式，为后续双特异性抗体在免疫突触形成和T细胞活化过程中呈现差异化的功能行为，奠定了关键的结构基础。通过分子建模解析了DLL3与各双抗间的相互作用，HPN328采用三特异性结构（抗DLL3/抗CD3/抗白蛋白），形成结构紧密的免疫突触，总间距约15纳米（如CD3与DLL3-EGF6间的距离约80Å），利于T细胞与肿瘤细胞紧密接合（图3b）。BI764532基于IgG样结构，形成中等紧密度的免疫突触，间距约15-18纳米（如CD3与DLL3-EGF6间距约115Å），实现灵活的T细胞-肿瘤细胞桥接（图3c）。AMG757因结合DLL3远端的EGF3结构域（DLL3跨膜区至EGF3间距约93Å），形成相对延展的免疫突触，间距约18.8纳米（如CD3结合臂与DLL3-EGF3间距约75Å）为系统评估三种双特异性抗体活性差异并模拟肿瘤微环境，研究者选用SCLC来源SHP77及神经内分泌瘤SKMEL-30细胞，在体外比较其T细胞激活与杀伤能力。在SHP77模型中，BI764532对CD4⁺/CD8⁺T细胞的激活效能（EC₅₀ 7.6–18.5 pM）均最优，HPN328次之，而结合远端表位的AMG757活性最弱，与其形成的较长免疫突触距离（18.8 nm）相符。在SKMEL-30模型中，BI764532与HPN328活性相当，均显著优于AMG757。整体表明，HPN328与BI764532凭借紧凑的免疫突触结构更有效激活T细胞，而AMG757因较长的空间距离需更高浓度才能引发应答，印证了结构差异决定功能效能的规律。平行比较三个抗体对肿瘤细胞的杀伤：在SHP77细胞中，HPN328的杀伤效力最强（EC₅₀ 1.94 pM），显著优于BI764532（12.06 pM）和AMG757（7.61 pM）。而在SKMEL-30细胞中，BI764532展现出最强细胞毒性（EC₅₀ 15.21 pM），优于HPN328（0.84 nM）和AMG757（4.02 nM）。AMG757在两种细胞系中活性均最弱，与其较长的免疫突触距离和较高的激活阈值相符。同型对照无显著杀伤作用，证实了双抗介导细胞毒性的特异性。为评估双特异性抗体的免疫刺激潜力，分析了其与不同肿瘤细胞共培养时的细胞因子释放谱。在SHP77细胞中，HPN328诱导IL-2和TNF-α的能力最强（EC₅₀分别为86.83 pM和3.94 pM），而BI764532诱导IFN-γ更强（EC₅₀ 19.69 pM）。在SKMEL-30细胞中，仅BI764532可微弱诱导IL-2，但其IFN-γ诱导能力最强（EC₅₀ 0.03452 nM），三者对TNF-α诱导均弱。结果表明，细胞因子释放与肿瘤杀伤无线性关联：HPN328以杀伤优先，BI764532呈现更平衡的炎症谱，而AMG757免疫刺激潜力整体最弱。临床前研究揭示了三种双特异性抗体（BsAb）的特性：HPN328在T细胞激活和肿瘤杀伤上最强（CD8⁺ T细胞激活EC₅₀ 82.43 pM，杀伤EC₅₀ 1.94 pM）；BI764532具有平衡的细胞因子释放谱和中等的免疫突触紧密性；AMG757则需更高激活浓度且免疫突触较长（18.8 nm）。临床数据显示，这些特性转化为了不同的疗效与安全性结果：HPN328 的临床效力最强，在小细胞肺癌（SCLC）II期试验中客观缓解率达50%，尤其在非神经内分泌亚型中达45%，与临床前高效杀伤的预期相符。 BI764532 的临床疗效因癌症类型和治疗方案差异显著（ORR范围18%-70%），体现了其“平衡效力”的特点，但尚缺乏全面的毒性数据来验证临床前推测的“可控毒性”。 AMG757 通过阶梯递增给药和患者选择策略，克服了其较长免疫突触带来的潜在空间障碍，在SCLC的III期试验中显著延长了中位总生存期（13.6个月 vs 化疗8.3个月），且毒性可控，与临床前的平衡免疫激活预测一致。总结 TEC的活性是一个非常复杂的问题，与抗体的结构，靶向CD3的亲和力，CD3抗体的表位，靶点等相关。其本质上与免疫突触相关，在之前的文章中我们也介绍过免疫突触的稳定性，及形成的免疫突触的距离会影响TCE的活性。这篇文章首次利用模拟的结构，对临床中的三款DLL3 TCE双抗进行了解读，从结构上解析了TCE疗法不同的原因。们已经建立抗体密码读者交流群，有兴趣的可以扫描下方二维码添加微信进群，请主动备注姓名-公司-职位（高校-专业），非诚勿扰！因为你的分享、点赞、在看我足足的精气神儿！声明本公众号所发表文章以宣传知识为目的，因此不构成投资，病人用药等建议。如果文章侵您的权益及时联系小编进行删除！参考文献 https://doi.org/10.1007/s12032-025-03232-z

2026-03-25

·allsci.com

Moonlight Bio prepares potency-enhanced DLL3 CAR-T for first-in-human in SCLC

Moonlight Bio, Inc., a Seattle-based cell therapy company founded in 2023, has registered a Phase I first-in-human clinical trial (NCT07488923) of ML261, an autologous anti-DLL3 CAR T-cell therapy engineered with a CARD11-PIK3R3 fusion transgene, in patients with relapsed or refractory small cell lung cancer and select neuroendocrine carcinomas. The trial, named SPECTRAL-1, is listed as not yet recruiting, with an estimated start date of May 2026 and planned enrollment of 110 participants. ML261 is the first CAR T-cell product to incorporate the CARD11-PIK3R3 potency-enhancement platform in a clinical setting, a technology derived from academic research at Northwestern University and the University of California, published in Nature in February 2024. The Moonlight Bio SCLC program enters a competitive DLL3-targeting landscape but does so with a distinct biological approach that has not previously been tested in humans. SPECTRAL-1 is an open-label, sequential dose-escalation study. The primary endpoint is the incidence of dose-limiting toxicities within a 28-day observation period, while treatment-emergent adverse events, preliminary efficacy, and pharmacokinetics will also be assessed. ML261 is administered as an intravenous infusion of autologous T cells collected via leukapheresis and engineered ex vivo. Eligible participants must have confirmed relapsed or refractory SCLC, gastroenteropancreatic neuroendocrine carcinoma, high-grade neuroendocrine prostate cancer, or extrapulmonary neuroendocrine carcinoma, with documented DLL3 expression, and have received at least one prior line of systemic therapy (excluding prior DLL3 CAR-T). Primary completion is estimated for Q1 2028. The biological rationale for ML261 rests on two elements. First, DLL3 is an inhibitory Notch pathway ligand aberrantly expressed on the surface of neuroendocrine tumor cells — present in approximately 80–90% of SCLC tumors — while largely absent from normal adult tissues. This expression pattern makes it a tumor-selective target. Second, the CARD11-PIK3R3 fusion gene, originally identified as a gain-of-function driver mutation in CD4+ cutaneous T-cell lymphoma by Jaehyuk Choi’s laboratory at Northwestern University, was repurposed by researchers including Kole Roybal at UCSF to enhance CAR T-cell function. The fusion amplifies signaling through the CARD11-BCL10-MALT1 complex, increasing cytokine production, T-cell persistence, and proliferation in preclinical solid tumor models. The modification reduced the CAR T-cell dose required for tumor control and diminished dependence on lymphodepletion preconditioning. Moonlight Bio licensed this technology from its academic originators; both Choi and Roybal serve on the company’s strategic advisory team, alongside Sean Parker of the Parker Institute for Cancer Immunotherapy. ML261 enters a DLL3-targeting field that already includes an approved product. Tarlatamab (Imdelltra, Amgen), a DLL3×CD3 bispecific T-cell engager, received FDA approval for relapsed SCLC and is being studied in Phase 3 trials and in extrapulmonary neuroendocrine carcinomas. HPN328 (Harpoon Therapeutics), a DLL3-targeting tri-specific T-cell engager, is in Phase 1/2 development. Among CAR T approaches, academic-sponsored programs in China — including GC511B and an anti-PD-L1/4-1BB DLL3 CAR T from Sichuan University — are in early-phase testing. ML261 is differentiated by its CARD11-PIK3R3 potency-enhancement platform, which is designed to address the persistent failure of conventional CAR T cells in solid tumors due to T-cell exhaustion and immunosuppressive microenvironments. Whether this translates into clinical benefit over bispecific engagers or unmodified CAR T constructs remains to be determined by SPECTRAL-1 data. Moonlight Bio initiates first-in-human trial of ML261, a potency-enhanced anti-DLL3 CAR T therapy, in relapsed SCLC and neuroendocrine carcinomas. Your email address will not be published. Required fields are marked * Comment * Name * Email * Website

免疫疗法临床1期细胞疗法临床3期上市批准

2026-03-24

·今日头条

水到渠成，复宏汉霖要做中国MNC

从复宏汉霖2025年报看到了王者之相。复宏汉霖2025年营收66.666亿元，同比增长16.5%，净利润8.27亿元，持续三年营收、利润双增长，其中，2025H2营收38.47亿元，环比增长高达36.4%。复宏汉霖加速了，而且还有更震撼的数据。 2025年研发投入25亿元，在新生代创新药企（不包括传统Big pharma）中仅次于百济神州。全球化大药云集，不仅有PD-1单抗H药、PD-L1 ADC HLX43、HER2单抗HLX22、EGFR单抗HLX07，还有喷薄而出的超20款早研新分子，以FIC/BIC为主。全球化网络建设也对标百济神州，销售网络覆盖60个国家/地区，供应网络2025年圆满完成超30次海外交付，临床研究网络覆盖近30个国家，全球同步注册（2025年递交海外BLA 29项，获批28项）覆盖60个国家/地区。复宏汉霖今年首次提出要成为C-MNC（以中国为总部的跨国生物制药企业），一切都水到渠成。 01 苦心经营6年，全球化网络进入收获期以2020年汉曲优在欧盟获批为起点，复宏汉霖在全球化版图上落下第一子。当中国创新药产业开始思考如何跳出BD“卖青苗”困局时，复宏汉霖的全球化网络已然成熟，为2030年实现20+款产品全球上市，其中15+款登陆欧美市场，做好了所有准备。复宏汉霖出海自主参与程度较高，具备主导自有产品海外临床开发、药政注册、生产供应的能力。全球朋友圈日益扩大，深度绑定国际一流药企雅培、卫材，2025年海外产品收入同比增长翻倍。截至目前，公司共有10款产品（40项适应症）在全球60个国家/地区获批上市，其中7款已在中国获批，4款获得美国FDA批准、4款获得欧盟EC批准，惠及全球超100万患者。与百济神州一样摆脱对CRO的依赖，自建国际化临床团队。目前临床团队规模增至670人，临床研究网络覆盖近30个国家、1000+家研究中心，入组10000+患者（中国以外1700+患者），具备独立开展国际多中心临床试验的能力。合作的sites包括美国的安德森癌症医学中心、斯隆—凯特林癌症研究所，日本的日本国立癌症研究中心(NCCH)、日本国立癌症研究中心东院(NCCHE)、近畿大学医学部(Kindai University Hospital)、癌研有明医院(JFCR)。具备与全球主要监管机构直接沟通的能力。2025年递交海外BLA 29项，获批28项，覆盖60个国家和地区，彰显强劲国际化注册能力。最新总产能达8.4万升，常态化供应全球市场。全球上市核查100%通过率，拥有中美欧三地GMP通行证。高频次稳定交付保障，全球产品供应超2000万支，2025年圆满完成超30次海外交付。出海效率创行业标杆，地舒单抗类似药美国首发仅用10天即完成出厂，创造公司出海交付新纪录。复宏汉霖已站稳主要海外市场。美国市场：复宏汉霖是迄今为止获得美国FDA批准上市产品最多的中国生物医药企业，肿瘤和自免产品16款中占到4款。公司产品在全球各地的上市申报和再注册中，现场核查通过率达到100%，而2020-2024年FDA受理BLA约170件，仅有50%大分子药物一次申请通过。欧洲市场：深度布局，多款产品实现上市销售。2025年，H药广泛期小细胞肺癌在英国、欧盟获批上市，已在12个欧洲国家实现上市销售，进入7国医保目录，2026年，H药鳞状非小细胞肺癌、非鳞状非小细胞肺癌、食管鳞癌也有望在欧盟获批。HLX14两款产品2025年获欧盟、英国批准上市，并在德国、西班牙、英国开始销售。HLX11有望于2026年在欧盟获批上市。日本市场：2025年与卫材达成H药日本市场合作，创下中国药品在日本单地区授权最大规模纪录。本土布局落地、MAH资质获批创纪录，设立日本子公司，涵盖临床运营、质量、药政注册等本土化核心团队，12天取得日本上市许可持有人（MAH）资质（仅为标准流程1/3），构建管线上市基础。新兴市场：构建起多产品、广泛且深入的商业化网络，2025年，与雅培进一步深化合作，授权其在亚太、非洲、中亚、东欧及其他新兴市场的部分国家和地区，就H药开展包括广泛期小细胞肺癌（ES-SCLC）在内的多项适应症的商业化合作。复宏汉霖以生物类似药、H药为开路先锋，打通全球化基建，为承接下一波FIC/BIC大单品海外放量，提供了成熟条件。 02 密集冲击全球大药，一波接一波 H药是大药首秀，让复宏汉霖体系化能力、系统性优势得到一次全面验证。 H药目标是，挟三大重磅适应症，2030年前冲击全球终端销售百亿人民币大关。一线小细胞肺癌：美国已完成201例桥接试验入组，有望于ESMO期间读出数据，并于2026年提交BLA；围手术期胃癌：有望成为全球首个以免疫单药替代辅助化疗的围手术期胃癌方案，中国胃癌适应症获突破性疗法认定，数据有望于ASCO期间公布，并有望于2026年中获批上市，日本桥接试验准备中；一线转移性结直肠癌：有望成为首个用于一线转移性结直肠癌的PD-(L) 1 联合VEGF疗法，中国、日本及东南亚III期试验已完成入组，预计2027年公布MRCT临床结果。第二波大药是HLX43（PD-L1 ADC）、HLX22（新型HER2单抗)、HLX07（创新EGFR单抗），国际化全面爆发。三大重磅炸弹今年推进至临床后期。HLX43是最强广谱ADC、潜在BIC PD-L1 ADC，“单药即管线”的巨大能量接近于兑现，2026年将启动二线治疗EGFR野生型非鳞状非小细胞肺癌（nsqNSCLC）、三线及后线治疗鳞状非小细胞肺（sqNSCLC）以及二线治疗sqNSCLC的三项全球关键临床研究；HLX22具有改变目前一线胃癌标准疗法的潜力，2026年一线HER2+胃癌III期国际多中心临床试验预计完成入组；HLX07有望开辟EGFR高表达肺鳞癌一线治疗新路径，2026年启动用于皮肤鳞状细胞癌的II期临床研究、用于一线sqNSCLC的国际多中心II/III期临床研究。复宏汉霖早期研发管线据复宏汉霖2025年度业绩推介资料第三波大药群星璀璨，高壁垒、多元化新分子井喷而出。 2025年，复宏汉霖强化平台化创新体系建设，形成涵盖下一代IO平台、Hanjugator™ ADC平台、三特性T细胞衔接器及AI驱动的一站式抗体药物早期研发HAI Club平台在内的多维技术平台，为打造具备全球竞争力的中长期创新管线提供可持续的系统能力支撑。早期新分子超过20款，从数月亮到数星星，根本看不过来。 3款FIC/BIC创新管线最近IND获批。HLX3901（DLL3 x DLL3 x CD3 x CD28 四抗TCE）通过精巧的分子设计，兼具持久的特异性T细胞激活、攻克低T细胞浸润肿瘤及显著降低细胞因子释放综合征（CRS）的多重优势，旨在克服第一代TCE（安进Tarlatamab）在实体瘤治疗中的主要障碍；HLX97（KAT6A/B小分子抑制剂）相比同类产品辉瑞PF-07248144，展现出更强的KAT6A/B抑制活性和对KAT5/7/8更高的选择性，在更低剂量下即展现出相当或更优的抗肿瘤活性，在相近抑瘤水平时引发的血液学毒性显著更低，预示其在临床上可能拥有更宽的治疗窗口；HLX316（B7H3×唾液酸酶融合蛋白）有潜力靶向PD-1/PD-L1以外的免疫抑制生物学机制，拓宽免疫治疗在实体瘤中的应用范围，突破现有治疗方案局限。肿瘤：HLX3902（STEAP1 x CD3 x CD28三抗TCE）在前列腺癌中展现强效、持久的抗肿瘤应答；HLX48（EGFR x cMET双抗ADC）高效低毒设计，中等potency payload 可最大限度发挥抗体功能，并具备更强的旁观者效应，疗效、耐受性优于竞品，用于治疗NSCLC和结直肠癌；HLX49（新型HER2双表位ADC）采用跟HLX48同款自研Linker-payload，且抗体部分同时靶向HLX22特色的HER2表位和曲妥珠HER2表位，强效提高对HER2二聚体尤其是HER2/EGFR 的内吞，在多种模型中疗效均优于德曲妥珠单抗，同时拥有比同类药物更好的耐受性，有望成为同类最佳的HER2 ADC治疗乳腺癌和胃癌；HLX403（CDH17 ADC）在多个CDX模型（如SNU16胃癌和GP2D结直肠癌）中，疗效优于第一三共/阿斯利康DS-8201，并且在耐药性/低表达肿瘤中具有治疗潜力，有望为消化道肿瘤治疗提供一款更优的ADC分子；HLX402（ADAM9 ADC）为潜在BIC的新兴肿瘤靶点ADC；HLX85（ALPP/ALPPL2 ADC）为潜在FIC的新兴肿瘤靶点ADC。自免：HLX109（IL-1R3 单抗）同时抑制多组发炎信号，比现有自免疗法有更强治疗效力与更多适应症，靶向IL-1/IL-33/IL-36三大炎症通路的生物制剂市场预计2030年超720亿美元，潜在BIC上游靶点，体内外实验药效优于临床竞争对手，具备延长的半衰期，并可开发为皮下制剂。减脂增肌：HLX203为BIC单抗药物，ActRIIA亲和力比礼来Bima高10-20倍，相比Bima大幅增加减脂效果，显著保护肌肉，而且半衰期延长，可皮下给药；HLX204是用于体重控制的FIC GPCR激动剂，可与GLP-1RA联用，既减脂，又维持肌肉，既减少脂质吸收，又增强能量代谢。罗马不是一天建成的，复宏汉霖自2019年港股上市以来，穿越疑云和迷雾，大器终成，建立起全链条、广覆盖的全球化能力，建立起高产量、FIC/BIC品质的创新能力。大单品爆发力+管线纵深度，复宏汉霖有了底气，为转型跨国Biopharma而战斗。

100 项与塔拉妥单抗相关的药物交易

登录后查看更多信息

研发状态

批准上市

10 条最早获批的记录,

后查看更多信息

适应症	国家/地区	公司	日期
小细胞肺癌	加拿大	Amgen, Inc.	2024-09-01
广泛期小细胞肺癌	美国	Amgen, Inc.	2024-05-16

未上市

10 条进展最快的记录,

后查看更多信息

适应症	最高研发状态	国家/地区	公司	日期
局限期小细胞肺癌	临床3期	美国	百济神州（北京）生物科技有限公司	2024-01-23
局限期小细胞肺癌	临床3期	美国	Amgen, Inc.	2024-01-23
局限期小细胞肺癌	临床3期	日本	Amgen, Inc.	2024-01-23
局限期小细胞肺癌	临床3期	日本	百济神州（北京）生物科技有限公司	2024-01-23
局限期小细胞肺癌	临床3期	阿根廷	Amgen, Inc.	2024-01-23
局限期小细胞肺癌	临床3期	阿根廷	百济神州（北京）生物科技有限公司	2024-01-23
局限期小细胞肺癌	临床3期	澳大利亚	Amgen, Inc.	2024-01-23
局限期小细胞肺癌	临床3期	澳大利亚	百济神州（北京）生物科技有限公司	2024-01-23
局限期小细胞肺癌	临床3期	奥地利	Amgen, Inc.	2024-01-23
局限期小细胞肺癌	临床3期	奥地利	百济神州（北京）生物科技有限公司	2024-01-23

登录后查看更多信息

临床结果

适应症

分期

评价

查看全部结果

研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


Tandem Meetings ASTCT and CIBMTR2026	N/A	实体瘤 \| 血液肿瘤	61	Bispecific Therapies	構淵憲網衊積製廠積蓋(鑰醖選製網範艱衊鹽艱) = 餘糧齋夢壓襯構網範壓襯衊獵鹽製鹽鏇淵繭獵 (醖壓襯網鑰鹽夢選淵衊 ) 更多	积极	2026-02-04
NCT05740566 (DeLLphi-304 \| DeLLphi-301, CTgov)	临床3期	小细胞肺癌	509	lurbinectedin+amrubicin+topotecan (Standard of Care (SOC))	顧範繭廠鹹顧鏇廠獵築(鑰艱糧築衊顧鑰鬱夢醖) = 繭築糧繭築艱遞網壓鹽膚鬱築廠蓋壓夢壓衊鑰 (範鬱簾夢壓糧網夢網衊, 蓋製壓糧壓觸築襯餘廠 ~ 願廠壓艱觸觸願廠齋膚) 更多	-	2026-01-05
				Tarlatamab (Tarlatamab 1 mg to 10 mg Q2W)	顧範繭廠鹹顧鏇廠獵築(鑰艱糧築衊顧鑰鬱夢醖) = 選簾鏇淵膚顧齋夢簾膚膚鬱築廠蓋壓夢壓衊鑰 (範鬱簾夢壓糧網夢網衊, 膚蓋積築選製膚艱網蓋 ~ 鹽選顧鹹簾觸醖壓夢構) 更多
ESMO_ASIA2025	N/A	小细胞肺癌	17	Tarlatamab	製衊醖膚淵衊鏇願餘齋(膚膚願鏇顧顧選製簾糧) = 齋獵糧繭選鑰壓積獵壓網構顧壓遞艱遞鹽顧膚 (鑰醖構淵製衊膚遞製選 ) 更多	积极	2025-12-05
ESMO_ASIA2025	N/A	小细胞肺癌	10	Tarlatamab	鹹鬱膚選願壓構製膚醖(鑰夢鏇範積構糧窪顧淵) = 積糧繭鑰構製構顧糧餘簾積襯鏇鏇蓋淵壓鹽蓋 (衊艱糧簾窪醖糧鹹壓鏇 ) 更多	积极	2025-12-05
NCT05740566 (DeLLphi-304, Company_Website) 人工标引	临床3期	广泛期小细胞肺癌	-	IMDELLTRA	衊糧鹽窪積廠選醖衊襯(簾製顧遞廠鬱鬱積製醖) = 廠齋衊願壓廠觸顧觸選觸衊繭蓋壓壓鏇網淵繭 (鹹鑰蓋襯襯選簾醖鹽衊 ) 更多	积极	2025-11-19
				SOC	衊糧鹽窪積廠選醖衊襯(簾製顧遞廠鬱鬱積製醖) = 簾築簾膚獵廠醖顧壓憲觸衊繭蓋壓壓鏇網淵繭 (鹹鑰蓋襯襯選簾醖鹽衊 ) 更多
SITC2025	N/A	广泛期小细胞肺癌	13	Tarlatamab	簾網構鹹夢廠餘製獵壓(襯壓醖願網膚淵製膚鏇) = 蓋糧醖簾積積襯顧製遞網積獵壓襯構觸構膚糧 (製鏇繭壓築選齋構鏇鹹 ) 更多	积极	2025-11-05
				Tarlatamab (No PD)	簾網構鹹夢廠餘製獵壓(襯壓醖願網膚淵製膚鏇) = 齋網選願遞餘鹹獵壓膚網積獵壓襯構觸構膚糧 (製鏇繭壓築選齋構鏇鹹 ) 更多
NCT05740566 (DeLLphi-304, ESMO2025) 人工标引	临床3期	小细胞肺癌	509	Tarlatamab	選夢遞鏇獵壓鑰鏇鹽衊(顧鏇窪憲淵鏇範願廠憲) = 廠選憲遞範窪艱遞遞鏇壓願廠顧簾壓餘築醖憲 (餘廠顧醖積範齋醖壓積 ) 更多	积极	2025-10-17
				Chemotherapy (topotecan/lurbinectedin/amrubicin)	選夢遞鏇獵壓鑰鏇鹽衊(顧鏇窪憲淵鏇範願廠憲) = 鏇廠鑰糧繭繭鹹鬱壓廠壓願廠顧簾壓餘築醖憲 (餘廠顧醖積範齋醖壓積 ) 更多
NCT05740566 (DeLLphi-304, ESMO2025)	临床3期	小细胞肺癌二线	496	Tarlatamab	構獵製齋夢鬱鏇範齋築(廠夢鏇積壓遞繭膚夢網) = 鏇鹹鹹鏇簾憲顧膚窪觸願鹽構鹽觸壓淵遞選選 (鑰艱願餘膚鏇窪齋遞齋 ) 更多	积极	2025-10-17
				Chemotherapy (CTx): topotecan, lurbinectedin, or amrubicin	構獵製齋夢鬱鏇範齋築(廠夢鏇積壓遞繭膚夢網) = 鏇鹹範簾艱醖襯餘醖鏇願鹽構鹽觸壓淵遞選選 (鑰艱願餘膚鏇窪齋遞齋 ) 更多
ESMO2025	N/A	广泛期小细胞肺癌三线	3,009	3L systemic therapy	衊窪餘醖膚淵艱衊願選(遞齋壓淵願餘觸蓋遞鹹) = 鬱範積築淵壓醖鏇窪鬱獵積窪淵淵糧壓蓋窪製 (範齋鬱鑰製糧憲壓艱獵, 4.6 ~ 6.5) 更多	积极	2025-10-17
				3L systemic therapy	衊窪餘醖膚淵艱衊願選(鏇鬱齋範憲衊夢膚淵鏇) = 鹹顧顧範簾鹹築遞齋觸顧網鏇衊廠簾艱鑰鹹製 (窪夢鏇遞構簾鏇網遞製, 7.2 ~ 9.2)
NCT07016230 (UNLOCK TARLATAMAB, ESMO_IO2025)	临床2期	小细胞肺癌 \| 神经内分泌癌 DLL3 expression	40	Tarlatamab (relapsed SCLC)	窪鏇觸窪衊襯窪齋糧繭(鹽齋顧膚夢糧憲積壓範) = 鑰繭廠餘夢憲鏇繭築鏇膚築繭鹹網顧選範餘構 (餘範繭艱簾壓簾艱齋願 ) 更多	积极	2025-10-12
				Tarlatamab (DLL3-positive NECs)	窪鏇觸窪衊襯窪齋糧繭(積網積範遞艱製顧鑰壓) = 鏇齋積蓋鑰鏇齋簾廠淵鹽選襯壓鬱繭膚憲積遞 (鹹淵顧廠獵鑰廠製齋獵 )