预约演示
更新于：2026-07-07
Etentamig
更新于：2026-07-07
概要
基本信息
药物类型 双特异性T细胞结合器 |
别名 ABBV-383、TNB 383B、TNB-383B + [1] |
作用方式 抑制剂、刺激剂 |
作用机制 BCMA抑制剂(B细胞成熟蛋白抑制剂)、CD3刺激剂(T细胞表面糖蛋白CD3复合体刺激剂) |
在研适应症 |
非在研适应症- |
原研机构 |
在研机构 |
非在研机构- |
最高研发阶段临床3期 |
首次获批日期- |
最高研发阶段(中国)临床3期 |
特殊审评孤儿药 (美国) |
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结构/序列
Sequence Code 524306457L
来源: *****
Sequence Code 631408146H
来源: *****
Sequence Code 931729375H
来源: *****
关联
13
项与 Etentamig 相关的临床试验NCT07600151
A Clinical Phase I/II, Multicenter, Open-label, National Study Evaluating Quintuplet Treat-ment With ISaTuximab, Bortezomib, Lenalidomide and Dexamethasone Plus Etentamig (Etenta-Isa-VRd) in Primary DiagnOsed High-Risk Multiple Myeloma Patients
This study is researching an experimental five-drug combination called etentamig, isatuximab, bortezomib, lenalidomide, and dexamethasone. The study is focused on participants with newly diagnosed multiple myeloma (NDMM) and high-risk disease who are eligible for autologous stem cell transplantation.
开始日期2026-12-01 |
申办/合作机构 |
NCT07420959
Phase 1/2 Trial of ABBV-383 for Patients With Relapsed Refractory Waldenström Macroglobulinemia
This phase I/II trial studies the side effects and best dose of ABBV-383 and to see how well it works in treating patients with Waldenström macroglobulinemia that has come back after a period of improvement (relapsed) or that does not respond to treatment (refractory). ABBV-383 is a monoclonal antibody that may interfere with the ability of cancer cells to grow and spread. A monoclonal antibody is a type of protein that can bind to certain targets in the body, such as molecules that cause the body to make an immune response (antigens).
开始日期2026-03-25 |
申办/合作机构 |
NCT07095452
Phase 2/3, Multicenter, Randomized, Open-Label Study Evaluating the Efficacy and Safety of Etentamig and Daratumumab (Etentamig+D) Compared to Daratumumab, Lenalidomide, and Dexamethasone (DRd) in Subjects With Newly Diagnosed Multiple Myeloma Not Eligible for Transplant
Multiple myeloma (MM) is a cancer of the blood's plasma cells. The cancer is typically found in the bones and bone marrow (the spongy tissue inside of the bones) and can cause bone pain, fractures, infections, weaker bones, and kidney failure. This is a study to determine the adverse events, change in disease activity, and pharmacokinetics of Etentamig in adult participants with MM.
Etentamig is an investigational drug being developed for the treatment of MM. This study is broken into 2 phases; phase 2 with 3 study arms and phase 3 with 2 study arms. Participants in phase 2 will receive 1 of 3 doses of etentamig in combination with daratumumab. Participants in phase 3 will receive etentamig at RP3D in combination with daratumumab, or daratumumab, lenalidomide, and dexamethasone (DRd). Around 660 adult participants with MM will be enrolled at approximately 155 sites worldwide
Participants in phase 2 will receive 1 of 3 doses of etentamig as intravenous (IV) infusions, combination with subcutaneous (SC) injections of daratumumab. Participants in phase 3 will receive RP3D doses of etentamig as IV infusions, combination with SC injections of daratumumab, or SC injections of daratumumab, capsules of lenalidomide, and tablet/ IV injections of dexamethasone (DRd). The study duration is approximately 16 years.
There may be higher treatment burden for participants in this trial compared to their standard of care. Participants will attend regular visits during the study at a hospital or clinic. The effect of the treatment will be checked by medical assessments, blood tests, checking for side effects and questionnaires.
Etentamig is an investigational drug being developed for the treatment of MM. This study is broken into 2 phases; phase 2 with 3 study arms and phase 3 with 2 study arms. Participants in phase 2 will receive 1 of 3 doses of etentamig in combination with daratumumab. Participants in phase 3 will receive etentamig at RP3D in combination with daratumumab, or daratumumab, lenalidomide, and dexamethasone (DRd). Around 660 adult participants with MM will be enrolled at approximately 155 sites worldwide
Participants in phase 2 will receive 1 of 3 doses of etentamig as intravenous (IV) infusions, combination with subcutaneous (SC) injections of daratumumab. Participants in phase 3 will receive RP3D doses of etentamig as IV infusions, combination with SC injections of daratumumab, or SC injections of daratumumab, capsules of lenalidomide, and tablet/ IV injections of dexamethasone (DRd). The study duration is approximately 16 years.
There may be higher treatment burden for participants in this trial compared to their standard of care. Participants will attend regular visits during the study at a hospital or clinic. The effect of the treatment will be checked by medical assessments, blood tests, checking for side effects and questionnaires.
开始日期2026-01-08 |
申办/合作机构 |
100 项与 Etentamig 相关的临床结果
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100 项与 Etentamig 相关的转化医学
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100 项与 Etentamig 相关的专利（医药）
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5
项与 Etentamig 相关的文献（医药）2025-12-03·Cureus Journal of Medical Science
Safety and Efficacy of Anti-B-cell Maturation Antigen (Anti-BCMA) Bispecific Antibodies for Relapsed/Refractory Multiple Myeloma: A Systematic Review of Clinical Trials
Review
作者: Jawed, Inshal ; Khan, Asad Ali ; Sajjad, Muhammad ; Rahman, Mansoor ; Khan, Muhammad Musa
Relapsed/refractory multiple myeloma (RRMM) remains a challenging condition with a need for more effective treatment options. There are ongoing clinical trials analyzing the effects of anti-B-cell maturation antigen (BCMA) bispecific antibodies (Abs) against RRMM with early, promising results. This study aims to systematically evaluate the safety and efficacy of anti-BCMA bispecific antibodies in patients with RRMM. PubMed, Embase, Web of Science, and the American Society of Hematology (ASH) website were searched for published evidence on the safety and efficacy of anti-BCMA bispecific Abs. Screening was performed using original clinical trials published in English, RRMM, and anti-BCMA-CD3 bispecific Abs as our inclusion criteria. Our search yielded a total of 2211 articles. After screening, we found 11 relevant clinical trials (five phase I, one phase I/II, two phase Ib, two phase II, one phase III). Across the trials, 910 patients with ages ranging from 32 to 82 years were analyzed. A majority of patients were exposed to and/or refractory to triple-class and penta-drugs (prior therapies ranged from 1 to 25). AMG-420, AMG-701, elranatamab, REGN5458, teclistamab (Tec), alnuctamab (ALNUC), and ABBV-383 are the seven anti-BCMA-CD3 bispecific Abs currently being assessed in clinical trials as monotherapy and in combination with immunomodulators/proteasome inhibitors against RRMM. Across the included trials, elranatamab demonstrated overall response rates (ORRs) of 61-64%, while teclistamab ranged from 40% to 78% depending on the regimen. ALNUC and ABBV-383 achieved ORRs of 51% and 57%, respectively. Among patients previously exposed to and/or refractory to anti-BCMA therapies (including antibody-drug conjugates and CAR-T cell therapy), ORRs were 54% for elranatamab and 40% for teclistamab. Incidence of cytokine release syndrome (CRS) or immune effector cell-associated neurotoxicity syndrome (ICANS) was low with subcutaneous (SC) administration of tec, elranatamab, and ALNUC. Across the studies, no death was reported due to CRS, although it led to treatment discontinuation in one patient in AMG-420, two patients in AMG-701, and dose reduction in three patients in ABBV-383 trials. Our analysis of the trials revealed that bispecific Abs showed efficacy in RRMM, with CRS and hematologic toxicities being the most common adverse events, mostly low-grade and manageable. Based on the promising efficacy and safety of BCMA targeting bispecific Abs, these drugs are emerging as a new therapeutic option for patients with advanced and RRMM.
2025-05-01·Clinical Lymphoma Myeloma & Leukemia
Comprehensive Review of Bispecific Antibody Constructs In Multiple Myeloma: Affinities, Dosing Strategies and Future Perspectives
Review
作者: Rasche, Leo ; Einsele, Hermann ; Waldschmidt, Johannes M ; Kortüm, K Martin
Despite significant advancements, multiple myeloma (MM) remains incurable, and there is still a pressing need for new therapeutic strategies with highly selective mechanisms of action and balanced off-target toxicity. In recent years, the development of "off-the-shelf" bispecific antibodies (bsAbs) has significantly enhanced our ability to treat relapsed or refractory MM. Teclistamab, elranatamab (both BCMA × CD3), and talquetamab (GPRC5D × CD3) are approved for treating MM patients who have received at least 3 prior lines of therapy, including a proteasome inhibitor, an immunomodulatory drug, and an anti-CD38 monoclonal antibody. Meanwhile, the range of available bsAbs is rapidly expanding, offering patients and healthcare providers a broad selection of options that vary in target antigens, binding domains, construct designs, dosing regimens, and side effects. As linvoseltamab, alnuctamab, and ABBV-383 (all BCMA × CD3), as well as forimtamig (GPRC5D × CD3) and cevostamab (FcRH5 × CD3) progress through late-stage clinical development, emerging trispecific antibodies are now available that target either 2 different MM-associated antigens or provide additional co-stimulatory signals to prevent T-cell exhaustion. Despite this plethora of therapeutic options, resistance to bsAbs is an inevitability, and the optimal positioning of these drugs within the current MM treatment landscape remains to be determined. In this review, we examine the available data on all clinically accessible bsAbs, evaluating their potential, current limitations, and implications for efficacy and safety, with the aim of achieving deeper responses and longer overall survival for MM patients.
2022-11-02·Cancer discovery
ABBV-383 Demonstrates Tolerability and Efficacy in Relapsed/Refractory MM
Article
Abstract:
The T cell–engaging bispecific antibody ABBV-383 was well tolerated in relapsed/refractory multiple myeloma (RRMM).
89
项与 Etentamig 相关的新闻（医药）2026-06-21
·焕药深研
应合规要求，仅呈现部分报告信息，完整全文内容欢迎阅读外发报告
#小程序://国金证券研究服务/DdGrzPur6mLtGfJ
+
目录
摘要
■ 投资逻辑
T细胞衔接器(TCE)正从早期机制验证进入产业兑现阶段。TCE通过同时结合疾病相关靶点与T细胞CD3等分子，将T细胞定向募集至靶细胞附近并诱导杀伤。相较CAR-T，TCE具备现货型供应、生产放大相对容易、剂量和给药方案更灵活等优势；相较传统单抗，TCE能够实现更深度的B细胞/浆细胞清除或肿瘤细胞杀伤。2021年以来，全球TCE获批数量明显增加，2025-2026年BD交易和投融资热度再度升温，TCE赛道已从技术平台故事进入临床数据、商业化放量和适应症拓展共同驱动的新阶段。
血液瘤是TCE最成熟的应用场景，已形成从机制验证到商业化兑现的闭环。CD19/CD3、CD20/CD3、BCMA/CD3等靶点在B-ALL、B细胞淋巴瘤和多发性骨髓瘤中相继取得临床突破。Blinatumomab率先验证CD3重定向T细胞杀伤的可行性，随后CD20/CD3和BCMA/CD3产品进一步推动TCE从单一品种走向多靶点、多适应症商业化。我们认为，血液瘤TCE后续增长主要来自三方面：一是已上市产品持续放量；二是从末线治疗向更早线、维持治疗和MRD清除场景前移；三是双靶点、多特异性和联合治疗提升缓解深度与持续时间。
自免有望成为TCE第二增长曲线，投资逻辑从“杀伤肿瘤”转向“免疫重置”。多类自身免疫病由B细胞、浆细胞及自身抗体驱动，BCMA/CD3、CD20/CD3、CD19/CD3及多靶点TCE具备实现深度B细胞/浆细胞清除的潜力，理论上可带来比传统B细胞清除疗法更深、更持久的疾病控制。2025年以来，UCB、Gilead、Cullinan、Candid、康诺亚、德琪医药等公司围绕MG、SLE、IgA肾病、RA、系统性硬化症、AIHA、ITP等适应症加速布局。随着早期临床数据逐步披露，自免TCE有望成为继血液瘤之后最值得关注的方向。
实体瘤是TCE远期空间最大的方向，但也是研发风险最高的方向。实体瘤TCE面临靶点正常组织表达、肿瘤微环境免疫抑制、T细胞浸润不足、抗原异质性和CRS/ICANS等多重挑战。DLL3×CD3在小细胞肺癌中率先实现突破，PSMA、STEAP1、CLDN18.2、GPC3、EGFR、CDH6等靶点持续推进。我们认为，实体瘤TCE的关键并非简单复制血液瘤经验，而在于通过遮蔽型TCE、2+1结构、低亲和CD3、条件激活、半衰期优化、CD28共刺激和联合治疗等方式改善治疗窗。具备明确靶点生物学、差异化工程平台和早期人体疗效信号的公司，具备较高弹性。
建议关注三条主线：第一，血液瘤TCE商业化兑现主线，重点关注已上市或接近上市、具备适应症前移和联合治疗潜力的品种；第二，自免TCE从0到1主线，重点关注BCMA/CD20/CD19等B细胞或浆细胞清除路径，以及已获得早期临床验证或大型药企BD背书的平台公司；第三，实体瘤TCE技术破局主线，重点关注DLL3、PSMA、STEAP1、CLDN18.2等靶点，以及遮蔽、2+1设计和多抗及共刺激平台。海外建议关注Roche、Johnson & Johnson、Genmab/AbbVie、Regeneron、Merck/Harpoon、Janux、Xencor、CytomX、UCB、Gilead、Cullinan等公司在TCE领域的临床数据、适应症拓展。国内建议关注康诺亚、泽璟制药、智翔金泰、德琪医药等具备TCE管线或出海交易验证的创新药公司，同时关注国内双抗/多抗平台公司在自免和实体瘤方向的后续布局。
风险提示：临床研发失败风险；商业化放量不及预期风险；临床进度不及预期风险
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正文
一、TCE：从双抗到多抗，从血液瘤向自免领域跃进，实体瘤逐步突破
（一）TCE疗法：新一代免疫疗法，靶向性强且起效快，成为近几年研究热点
过去二十年，免疫疗法革新癌症治疗模式，核心是通过多种手段调动宿主免疫系统清除肿瘤，目前研究重点集中在T淋巴细胞（适应性免疫系统，可直接杀伤肿瘤细胞）。有效T细胞抗肿瘤应答的关键是肿瘤相关抗原（TAA），主要包括DNA突变产生的新抗原、癌胚抗原、癌睾丸抗原（CTA）及肿瘤细胞过度表达的蛋白，如 CD19、PSMA、DLL3等。临床应用最成功的免疫疗法为免疫检查点抑制剂和CAR-T细胞，此外TAA疫苗、肿瘤浸润淋巴细胞（TILs）疗法研究广泛但疗效不一。目前免疫疗法的获益仅局限于部分患者和特定癌种，生存获益因适应症而异。
相较于传统免疫治疗手段，T细胞衔接器（TCE）抗肿瘤靶向性强、疗效确切且起效更快，能够绕开T细胞活化、识别并杀伤肿瘤的多个复杂环节，为提升机体抗肿瘤免疫能力提供了全新路径。TCE的作用机制十分特殊：它可以同时结合一种或多种肿瘤相关抗原，以及T细胞表面T细胞受体（TCR）复合物的CD3ε亚基。通过这种双重结合使得TCE能将T细胞定向招募至肿瘤细胞周围，跨接形成稳定有效的免疫突触，且整个过程不受T细胞原有表位特异性的限制。后续T细胞被激活后，会发生增殖、分泌细胞因子，并释放穿孔素与颗粒酶，特异性杀伤肿瘤细胞。其中穿孔素可在肿瘤细胞膜上形成孔洞，颗粒酶作为丝氨酸蛋白酶家族成员，能够切割胞内多种功能蛋白，最终诱导肿瘤细胞发生凋亡。不同于机体自发产生的抗肿瘤免疫，也区别于免疫检查点抑制剂、肿瘤疫苗、肿瘤浸润淋巴细胞疗法所诱导的免疫反应，TCE起效完全不依赖主要组织相容性复合体（MHC）的抗原呈递识别。凭借这一特性，T细胞可以有效攻击两类癌细胞：一是不表达MHC分子的肿瘤细胞，二是肿瘤相关抗原无法有效搭载于MHC分子表面的肿瘤细胞。而这两种情况，正是肿瘤实现免疫逃逸、进而产生免疫治疗耐药的重要机制。此外，与免疫检查点抑制剂、肿瘤疫苗不同，T细胞衔接器无需抗原呈递细胞介导激活，也不需要共刺激分子参与协同作用，就能直接触发T细胞裂解杀伤肿瘤细胞；同时其药效发挥也不依赖T细胞受体的表位特异性。
以TCE双抗为例，根据是否含Fc区结构主要分为三大类：IgG-like和非IgG-like（片段化）以及两者的混合体。
非IgG样TCE双抗： 不含Fc段，如串联scFv的BiTE®分子及DART平台（具有稳定的异源二聚体scFv组装体）。其设计初衷是利用其较小的分子量实现快速的组织渗透。这类分子一端结合肿瘤相关抗原（TAA），另一端结合T细胞受体复合物中的恒定组分CD3。由于缺乏Fc区，它们不会激活巨噬细胞、中性粒细胞和NK细胞等携带Fc受体的免疫细胞，从而限制了非特异性的免疫激活。
IgG样TCE双抗：保留了Fc区，具备更长的半衰期、更高的稳定性，以及与补体蛋白和固有免疫细胞上的Fc受体相互作用的潜力。这些相互作用可能通过抗体依赖性细胞介导的细胞毒性（ADCC）、补体依赖性细胞毒性（CDC）和抗体依赖性细胞介导的吞噬作用（ADCP）增强药物的抗肿瘤作用。然而，这种设计也存在一些缺点，例如其较大的分子尺寸，这可能会限制其组织渗透和分布，以及由于TAA非依赖性T细胞活化以及针对T细胞的ADCC和CDC作用而可能出现的不良事件具备更长的半衰期和更高的稳定性，且通过Fc介导的ADCC和CDC可能在体内引起不必要的非特异性免疫反应。且在工程化上面临严峻挑战，尤其是重链与轻链的正确组装。多种多肽链的共表达极易产生错配，因此需要专门的技术手段。代表技术平台：罗氏的KiH和CrossMab，Genmab的DuoBody等。
组合型TCE：包括结合了IgG样抗体和Fv型BsAbs特征的药物，例如同时存在可结晶片段（Fc）结构域和scFv分子。这类药物既具有IgG样TCE特有的Fc区，又具有Fv样TCE典型的Fcv区。
（二）逐步步入红利期：2021年以来获批数量激增，2025-2026年相关交易热情高涨
TCE疗法相比于CAR-T疗法，发展较晚但发展迅速。与细胞疗法相比，TCE 的主要优势在于其易于生产、可现货供应、可像 mAb 一样进行静脉或皮下给药、剂量和给药方案灵活、药代动力学可控，以及可以重复给药和延长治疗及暴露时间。在2014年blinatumomab获批后的八年沉寂期之后，过去四年间，FDA又批准了九种TCE疗法，EMA也批准了两种，TCE的研发进入蓬勃发展阶段。如今，无论在血液肿瘤还是实体瘤适应症方面，TCE的获批数量，以及靶抗原的数量，均已超过CAR-T细胞疗法。
目前全球已经获批超10款TCE疗法，大多集中于血液瘤领域，但技术边界持续拓展，实体瘤领域亦有产品获批上市。从适应症分布来看，血液瘤仍是TCE疗法的主战场。目前获批品种高度集聚于CD20、BCMA等成熟靶点，覆盖了弥漫大B细胞淋巴瘤（DLBCL）、滤泡性淋巴瘤（FL）及多发性骨髓瘤（MM）等主流细分市场。其中，Amgen的Blinatumomab（CD3xCD19）作为先行者，2025年全球销售额已达16.63亿美元（+36.78%）；而针对BCMA靶点的Teclistamab（强生）与Elranatamab（辉瑞）在末线MM领域的快速渗透，进一步验证了TCE疗法在血液系统恶性肿瘤中的临床刚需。在实体瘤领域，TCE疗法正实现从“0到1”的突破。尽管实体瘤因微环境复杂等因素开发难度较高，但以Tarlatamab（CD3xDLL3，针对小细胞肺癌）和Tebentafusp（CD3xgp100，针对葡萄膜黑色素瘤）为代表的产品已相继获批，并展现出优异的放量潜力（如Tarlatamab2025年销售额超6亿美元，同比增长超400%）。这预示着TCE的技术边界正在拓宽，未来随着靶点筛选的差异化以及分子结构的持续优化，实体瘤有望成为驱动TCE赛道二次增长的核心引擎。
全球TCE的BD交易及投融资情况于2025-2026年热情再度高涨。
从BD交易的数量和金额来看，2024年交易数量创新高，2025年交易金额创新高，尽管2026年仅过去4个多月事件，但CD3相关的TCE双/多抗交易金额已经达近85亿美金（仅统计披露金额），TCE相关交易热情再现。
从投融资频次来看，2020-2021年间，在全球生物医药投融资热潮下，TCE领域事件数达到峰值，进入2022年后的行业调整期，虽然绝对数量有所回落，但2025年起全球及中国内地的活跃度出现明显拐点，事件数再度回升（2025年全球达80起），显示出市场对TCE作为下一代免疫疗法核心资产的估值修复。从地域分布看，中国内地的投融资事件数在2025-2026年的表现尤为突出，反映了国内创新药企在TCE技术路径上的快速跟进与资本认可。
在融资体量方面，融资金额在2020年创下峰值（419亿美元），2026/1/1-2026/5/7近4个月事件，全球TCE市场投融资金额已达178亿美元，已近2021年全年水平，已超2020年全年投融资金额的42%。TCE进一步获得更多投融资青睐。
在过去十年中，期刊文献和专利文献的数量显著增加，其中专利占文献总量的44%，表明TCE持续受到商业关注。进一步探索TCE的主要治疗领域，分析显示，Bi-TCE的开发主要集中在实体瘤领域，相关文献最多的癌症类型包括肺癌、乳腺癌、胰腺癌、前列腺癌和卵巢癌；血液系统恶性肿瘤构成第二大研究重点，主要由针对多发性骨髓瘤和急性白血病的研发项目推动。
二、深入血液瘤：TCE 最成熟场景，验证 B 细胞/浆细胞谱系清除能力
（一）B细胞淋巴瘤和白血病中的早期验证，以CD19/CD20等靶点为主
TCE疗法在血液瘤中的早期成功，首先来自B细胞谱系恶性肿瘤。B细胞白血病和B细胞非霍奇金淋巴瘤具有相对清晰的谱系抗原表达，例如CD19和CD20。这类抗原在B细胞发育过程中表达稳定，且恶性B细胞对其保留程度较高，因此成为早期TCE药物开发的理想靶点。CD19/CD3和CD20/CD3构成了TCE在B细胞恶性肿瘤中的两条关键验证路径。前者以Blinatumomab为代表，率先在B细胞急性淋巴细胞白血病（B-ALL）中验证了CD3重定向T细胞杀伤的临床可行性；后者以Mosunetuzumab、Glofitamab和Epcoritamab为代表，将TCE机制进一步拓展至复发/难治B细胞非霍奇金淋巴瘤（B-NHL）。这一过程不仅证明了TCE对B细胞谱系恶性肿瘤的治疗价值，也为后续BCMA/CD3和GPRC5D/CD3在多发性骨髓瘤中的成熟奠定了基础。
（二）多发性骨髓瘤推动TCE成熟化，BCMA/GPRC5D/FcRH5/CD38成为热门靶点
多发性骨髓瘤：全球每年新发约20万人，中国新发约3万人
全球每年新发患者18.8万人，我国新发约3万人。MM在很多国家是血液系统第2位常见恶性肿瘤，目前仍无法治愈。根据WHO数据，2022年全球新发MM患者18.79万人，粗发病率约2.4/10万人；死亡人数12.14万人，粗死亡率1.5/10万人。可见MM的患者群体庞大，且死亡率相对较高。根据《Cancers (Basel)》发表的相关文献，1997年之前MM的中位生存期为2.5年，此后十年内逐步提升至4年，现已超过7年，主要得益于ASCT及传统化疗药物的使用。根据WHO数据，2022年我国MM新发患者约3.03万人，死亡约1.87万人，按总人口测算粗发病率约2.2/10万人、粗死亡率约1.3/10万人。
MM为TCE疗法最成熟的应用场景之一，BCMA/GPRC5D/FcRH5等持续探索并推进前线
复发MM目前多以CAR-T疗法和TCE疗法为主，TCE疗法目前偏后线。针对不同类型的MM，治疗方式和预后都不尽相同，需要对MM进行分类与分层诊断。根据NCCN最新2026年版指南和我国2024年修订的MM诊疗指南，若出现CRAB或SLiM表现则通常需要进行治疗，初次诊断一般在评估允许的条件下首选诱导治疗+自体造血干细胞移植（ASCT）疗法。国内指南诱导治疗首选蛋白酶体抑制剂（PI）+免疫调节剂（IMID）+地塞米松的三药联合方案，也可加入CD38单抗；NCCN指南则首推达雷妥尤单抗（CD38单抗）+硼替佐米PI+来那度胺IMID+地塞米松四药联合疗法。复发治疗时，国内指南针对二线及以上复发患者，优先推荐CAR‑T细胞治疗（伊基奥仑赛、泽沃基奥仑赛、西达基奥仑赛）及TCE双抗特立妥单抗；而NCCN2026版指南分层更为精细，1‑3线且来那度胺耐药患者首选西达基奥仑赛，2线后、存在多药暴露史的患者首选伊基奥仑赛，≥4线多线治疗失败人群则将多种TCE双抗列为首选方案。
多发性骨髓瘤是当前TCE疗法最成熟的应用场景之一。BCMA是最核心靶点，teclistamab、elranatamab和linvoseltamab等BCMA×CD3双抗已在复发/难治MM中获批，验证了TCE在浆细胞肿瘤中的临床价值。GPRC5D是非BCMA靶点中进展最快的方向，talquetamab的获批为BCMA治疗后患者提供了序贯选择。FcRH5/FcRL5则是另一类重要替代靶点，cevostamab等项目显示出较强开发潜力。未来MM TCE的研发重点将从单一BCMA靶向，逐步转向GPRC5D、FcRH5以及BCMA/GPRC5D双靶或三特异性TCE，以应对抗原逃逸、耐药和复发问题。
三、自免：从“杀伤肿瘤”到“免疫重置”，有望接棒第二增长曲线
截至2026年6月，TCE尚未获批用于自身免疫病，但临床证据正在从个案和小样本研究进入专门药物的早期临床阶段。自免TCE并非简单复制肿瘤治疗，而是利用更温和、可控的B细胞或浆细胞清除，实现较长期缓解。
（一）为何血液瘤靶点能迁移到自免？
许多自身免疫病与异常B细胞、浆细胞和自身抗体持续存在有关。B细胞不仅可产生自身抗体，还可参与抗原递呈和炎症维持；长寿命浆细胞则可持续分泌自身抗体。因此，血液瘤中已验证的CD19、CD20和BCMA靶点，可自然延展至B细胞驱动或自身抗体驱动的自免疾病。二者区别在于治疗目标：血液瘤——清除恶性B细胞或浆细胞克隆；自免疾病——清除自身反应性B细胞和致病浆细胞，实现免疫重置。
传统B细胞清除疗法仍存在残留致病细胞。自身免疫病的发生与自身反应性B细胞和浆细胞密切相关。除分泌自身抗体外，B细胞还可参与抗原递呈和T细胞激活，推动慢性炎症持续存在。以rituximab为代表的抗CD20单抗已经证明，清除B细胞能够改善部分自身免疫病患者的临床症状。然而，CD20主要表达于成熟B细胞和记忆B细胞，不表达于浆母细胞和浆细胞。因此，抗CD20单抗难以清除长期存活于骨髓或组织生态位中的长寿命浆细胞，也无法完全阻断自身抗体持续产生。此外，部分记忆B细胞可残留于淋巴结、三级淋巴结构和炎症组织中。随着B细胞逐渐恢复，这些残留细胞可能再次扩增，最终导致疾病复发。传统抗CD20疗法的局限性推动了更深度、更精准的免疫细胞清除策略。
血液瘤靶点复用，为自免延展奠定基础。TCE在自身免疫病中的应用建立在血液瘤领域已经验证的靶点基础上。CD19×CD3 TCE Blinatumomab最初用于B细胞急性淋巴细胞白血病，BCMA×CD3 TCE Teclistamab最初用于多发性骨髓瘤，CD20×CD3 TCE则已在B细胞淋巴瘤中获得验证。由于CD19、CD20和BCMA分别覆盖B细胞分化过程中的不同阶段，这些靶点也可用于清除自身免疫病中的致病性B细胞或浆细胞。不同靶点对应不同的免疫清除深度。CD20主要覆盖成熟B细胞和记忆B细胞；CD19覆盖范围更广，可延伸至部分浆母细胞；BCMA则主要表达于浆母细胞和浆细胞，包括持续分泌自身抗体的长寿命浆细胞。未来，临床可根据疾病机制选择不同靶点：以B细胞异常为主的疾病可优先考虑CD19或CD20，以自身抗体和长寿命浆细胞驱动的疾病则更适合探索BCMA。
早期临床信号初步验证TCE的免疫重置潜力。目前，TCE尚未获批用于自身免疫病，但已出现多项早期人体证据。CD19×CD3 TCE Blinatumomab已在难治性类风湿关节炎中显示出快速B细胞清除和疾病活动度下降。BCMA×CD3 TCE Teclistamab则在难治性系统性红斑狼疮以及其他自身抗体介导的自身免疫病中显示出浆细胞清除、自身抗体下降和临床症状改善。此外，专门面向自身免疫病开发的TCE正在进入早期临床阶段。A-319、Mosunetuzumab、Imvotamab和YK012分别围绕CD19×CD3或CD20×CD3展开探索。现阶段的证据仍以病例报告、小样本研究和早期临床试验为主，尚需更大规模研究验证缓解持续时间、适用人群和长期安全性。
（二）自免中已有部分产品初现疗效，期待后续产品管线
Mosunetuzumab在SLE患者中可诱导快速且深度的外周B细胞清除，并呈现一定剂量相关性。低剂量1.6mg队列未观察到CD19+B细胞低于定量下限（0/1BLOQ），5mg队列中2/5例达到BLOQ；而在更高剂量队列中，5+15mg、5+45mg和5+60mg均有3/3例达到BLOQ，提示随剂量提升，B细胞清除的深度和一致性明显增强。时间维度上，多数患者在皮下注射后早期CD19+B细胞迅速下降至极低水平，但部分患者在后续随访中出现B细胞回升，说明该疗法具备强药效学活性，但清除持续性及是否需要维持/重复给药仍需进一步观察。
Candid Therapeutics早期临床数据显示，TCE 在MG、SLE等自免疾病中已展现出初步药效学活性和临床疗效信号。药效学层面，clutamig可实现深度组织 B 细胞/浆细胞清除，并在后续观察到以naive B 细胞为主的外周 B 细胞重建，提示其可能通过清除既有自身反应性 B 细胞库、促进免疫系统重置发挥作用。临床层面，在重症肌无力和系统性红斑狼疮患者中，治疗后均观察到疾病活动度指标改善，显示TCE机制在不同自身免疫病中具备初步可转化性。整体来看，尽管当前数据仍处早期、样本量有限，TCE 已从机制验证推进至患者层面的疗效信号验证，后续建议关注更大样本、更长随访下疗效持续性和安全性表现。
CM336用于CD19CAR-T后复发的多重难治性自身免疫性溶血性贫血患者的治疗，两例患者既往均接受多线免疫抑制治疗，并在CD19 CAR-T后获得短暂无药缓解，但随后复发；其中患者1再次接受CD19 CAR-T未获应答。CM336采用短期阶梯递增给药方案，治疗后两例患者均快速进入缓解，血红蛋白水平在约3周内恢复至正常范围，同时间接胆红素、网织红细胞比例和LDH等溶血指标显著下降，并在6个月随访中维持改善。药效学方面，CM336治疗后外周CD19+B细胞和IgG水平下降，骨髓流式显示第12周浆细胞比例由0.86%降至0.00881%，B细胞比例由8.96%降至0.20%，提示其可通过深度清除B细胞和浆细胞，实现对CD19 CAR-T后复发AIHA的快速控制。
三、实体瘤：DLL3率先突破SCLC，PSMA、GPC3等靶点持续进展
实体瘤是TCE疗法远期空间最大的方向，但也是研发难度最高的方向。与血液瘤相比，实体瘤细胞并不天然暴露于循环免疫系统中，肿瘤微环境更复杂，抗原表达异质性更强，且许多实体瘤靶点在正常组织中亦有低水平表达，容易带来on-target/off-tumor毒性。因此，实体瘤TCE的核心矛盾并不是“能否激活T细胞”，而是能否在足够安全的前提下，把T细胞激活限制在肿瘤局部，并形成持续有效的杀伤。
我们认为，实体瘤TCE正处于从早期概念验证走向差异化平台验证的阶段。DLL3×CD3在小细胞肺癌中的突破证明，实体瘤并非TCE不可及场景；PSMA、STEAP1、CLDN18.2、GPC3、EGFR、CDH6等靶点持续推进，则显示不同瘤种仍存在较多可探索空间。但与血液瘤不同，实体瘤TCE的成败更依赖靶点筛选、分子工程、安全窗口和联合治疗策略。
（一）实体瘤TCE的核心难点：安全性、疗效持续性与抗原异质性
1. 靶外毒性限制治疗窗口
实体瘤靶点往往不是肿瘤细胞独有，而是在正常组织中存在一定表达。TCE一旦通过CD3端激活T细胞，可能对低表达靶点的正常组织产生杀伤，导致on-target/off-tumor毒性。相比传统单抗或ADC，TCE引发的是T细胞介导的级联免疫杀伤，安全窗口要求更高。
因此，实体瘤TCE需要优先选择肿瘤高表达、正常组织低表达或空间上相对隐蔽的靶点。例如DLL3在小细胞肺癌中高表达，而正常组织表达相对有限；PSMA在前列腺癌中具有较明确的肿瘤相关表达；CLDN18.2、GPC3、STEAP1等靶点也因其肿瘤表达特征而受到持续关注。
2. CRS/ICANS等免疫相关不良反应仍需管理
TCE通过CD3重定向T细胞，天然存在细胞因子释放综合征（CRS）和免疫效应细胞相关神经毒性综合征（ICANS）风险。血液瘤TCE已经形成递增给药、预处理、皮下注射和给药节奏优化等管理经验，但实体瘤患者肿瘤负荷、基础状态和联合治疗背景更复杂，安全性管理仍是决定商业化可及性的关键因素。
3. 肿瘤微环境抑制导致疗效不足
实体瘤常呈现T细胞浸润不足、免疫抑制细胞富集、T细胞耗竭、基质屏障明显等特点。即使TCE能够把T细胞募集到肿瘤细胞附近，也可能因为T细胞功能不足、局部免疫抑制强或免疫突触形成效率低，导致疗效不及血液瘤。
4. 抗原异质性导致复发和耐药
实体瘤内部抗原表达常呈高度异质性，单一靶点TCE可能只能清除部分抗原阳性细胞，残留的抗原低表达或阴性克隆可能继续进展。因此，多靶点覆盖、联合治疗和动态伴随诊断将成为实体瘤TCE长期发展的重要方向。
（二）破局方向：从“强激活”转向“精准激活”
实体瘤TCE的开发思路正在从单纯提高CD3激活强度，转向提高肿瘤选择性和治疗窗口。我们认为，未来具备竞争力的平台主要有以下几类：
1. 低亲和力CD3设计：降低系统性T细胞激活
CD3端亲和力是TCE安全性和疗效平衡的关键参数。若CD3结合过强，药物可能在外周循环中更容易诱导T细胞激活，带来CRS和非特异性炎症反应；若CD3结合过弱，则可能无法形成足够稳定的免疫突触，影响杀伤效率。低亲和力CD3设计的核心，是让TCE更依赖肿瘤端抗原高密度结合所带来的多价效应，在高抗原密度肿瘤细胞表面形成稳定桥接，而在低抗原密度正常组织中不易触发充分T细胞活化。该策略尤其适合肿瘤/正常组织表达差异明确但并非绝对肿瘤特异的靶点。
2. 双抗2+1结构：增强肿瘤端结合，提高抗原密度选择性
2+1结构通常通过两个肿瘤抗原结合臂和一个CD3结合臂构建分子。两个肿瘤端结合臂可以增强对高抗原密度肿瘤细胞的结合稳定性，而低抗原密度正常组织较难同时满足二价结合条件，从而提高肿瘤选择性。且2+1结构一般可与IgG样抗体工程、半衰期延长和可规模化生产兼容，在实操层面可实现。代表性公司包括Xencor，且已实现对多个MNC的平台授权，外部验证获得认可。
3. 条件激活/遮蔽型TCE：把活性限制在肿瘤微环境
遮蔽型TCE通过遮蔽肽、可切割linker或前药化设计，使分子在外周循环中保持低活性，进入肿瘤微环境后被肿瘤相关蛋白酶激活。Janux、CytomX、Harpoon等公司的平台均围绕这一方向展开。
以CytomX的Probody为例，这些分子通过肽基掩蔽CD3或TAA结合域，使其在体内保持非活性状态，仅在被肿瘤相关蛋白酶（例如基质金属蛋白酶MMPs或组织蛋白酶）切割后才会释放。这种肿瘤限制性激活通过将CD3结合限制在肿瘤微环境中，降低了全身毒性，减少了CRS发生率，并扩大了治疗窗口。当然，条件激活型TCE并不局限于传统遮蔽肽，而是包括多种前药化设计，TRACTr、ProTriTAC、PROTECT等平台均通过在CD3或TAA结合结构域上引入可移除的遮蔽模块，使TCE在外周血和正常组织中保持低活性，并在肿瘤微环境中经蛋白酶切割后恢复CD3结合和T细胞重定向功能。其中，遮蔽模块可以是短肽、蛋白结构域，或PD-1/PD-L1等蛋白-蛋白相互作用对。部分平台还引入白蛋白结合域以延长未激活前药的循环半衰期，而蛋白酶切割后释放的活性TCE因失去半衰期延长模块而快速清除，从而降低全身毒性。此外，酸性pH、高胞外ATP等肿瘤特异性理化特征也可作为TCE激活信号，用于进一步提高肿瘤选择性。
4.多抗/共刺激：应对抗原异质性、实现T细胞定向激活
多特异性/共刺激型TCE不再局限于TAA×CD3，而是进一步加入第二肿瘤抗原、CD28共刺激臂、4-1BB共刺激臂、checkpoint调控模块，或局部释放型细胞因子/免疫调节模块。CD3信号主要提供T细胞激活信号，但在实体瘤免疫抑制微环境中，单纯CD3激活可能不足以维持持续杀伤。CD28共刺激双抗、4-1BB共刺激、PD-1/PD-L1联合、ADC联合、放化疗联合等方式，有望增强T细胞扩增、浸润和持续杀伤能力。目标是从单纯提供TCR/CD3信号，升级为提供更完整的T细胞激活、扩增、持续杀伤与抗耗竭支持。主要设计类型包括：
·TAA×CD3×第二TAA：通过双靶点识别提高选择性，降低单一抗原低表达正常组织风险，并减少抗原丢失导致的逃逸。适合两个肿瘤抗原在肿瘤中共表达，而在关键正常组织中不共表达的场景。
·TAA×CD3×CD28：CD3提供TCR-like signal1，CD28提供共刺激signal2，从而增强T细胞扩增和效应功能。代表方向包括EGFR×CD28与PSMA×CD28共刺激双抗，常与PD-1抑制剂等免疫治疗联合开发。REGN7075是EGFR×CD28共刺激双抗，REGN5678是PSMA×CD28共刺激双抗开发项目。
·TAA×CD3×4-1BB：4-1BB共刺激更偏向增强已被抗原启动的T细胞效应、存活和记忆样功能；肿瘤定位的4-1BB激动可尝试降低传统系统性4-1BB激动剂的肝毒性和全身免疫毒性风险。
·TAA×CD3×checkpoint/cytokine：在肿瘤局部同步提供杀伤信号与微环境重塑信号，但结构更复杂，药代、暴露、安全性和CMC难度显著上升。
（三）肺部肿瘤：DLL3攻克小细胞肺癌难题，早线进一步探索中
肺部肿瘤是实体瘤TCE双抗临床验证最重要的方向之一，其中突破主要集中在小细胞肺癌（SCLC）。SCLC具有增殖快、早期转移、复发率高和后线治疗选择有限等特点，长期以来二线及以后治疗疗效有限。传统一线治疗以铂类/依托泊苷联合PD-L1抑制剂为标准，但患者多数会在短期内复发，复发后化疗带来的生存获益有限。因此，SCLC成为TCE双抗最具临床价值的肺部肿瘤切入点。
（四）前列腺癌：PSMA仍为前列腺癌TCE核心靶点，且向掩蔽型、长半衰期和多靶方向演进，KLK2、STEAP1、DLL3早期展现出较强疗效和安全性，国内管线尚处早期布局阶段
从现有临床数据看，前列腺癌TCE双抗的开发已从早期以PSMA为主，逐步扩展至KLK2、STEAP1、DLL3等差异化靶点。其中，KLK2和STEAP1目前显示出较好的综合潜力。KLK2靶向药物pasritamig在2L及以上mCRPC中表现出较高的PSA应答，单药研究中亚洲患者PSA50可达50.0%，联合多西他赛后整体PSA50达64.7%，taxane-naive人群PSA50进一步提高至75.0%，且CRS发生率较低或可控，提示KLK2作为前列腺特异性较强的靶点，可能具备较优治疗窗。STEAP1靶向药物Xaluritamig也展现出较明确的剂量相关疗效，在较高剂量队列中PSA50可达62.1%，PSA90可达31.0%，ORR最高约26.4%，但CRS和≥3级TRAE仍需关注。
PSMA仍是前列腺癌中验证最充分的靶点，但传统PSMA×CD3项目整体表现分化明显。早期药物如JNJ-63898081、JNJ-80038114、Acapatamab、TNB-585等虽证明了PSMATCE的机制可行性，但普遍存在疗效有限、CRS发生率较高、ADA或停药率较高等问题，限制了进一步开发价值。相比之下，新一代工程化PSMATCE更值得关注，例如JANX007采用掩蔽型设计，在2L及以上mCRPC中显示出较强PSA下降和影像学缓解信号，目标剂量≥2mg人群PSA50达73%、PSA90达26%，可测量病灶患者ORR达30%，但CRS发生率仍高达96%，其中≥3级CRS为8%，后续仍需观察其安全性优化和疗效持续性。AMX-500同样显示出PSA50/PSA90信号，但目前样本量和随访仍有限。
对于神经内分泌前列腺癌，DLL3是更具针对性的靶点。Tarlatamab和Gocatamig均在2L及以上NEPC中显示一定抗肿瘤活性，其中Gocatamig在NEPC全人群ORR为17.4%，高剂量队列ORR可达30%，提示DLL3 TCE在NEPC这一高未满足需求亚型中具有探索价值。但该方向患者基数较小，且CRS、ICANS等免疫相关毒性仍需重点管理。
五、老牌玩家多以拓展适应症切入，新进入者引领新兴技术平台
（一）老牌玩家：头部企业策略多为拓展产品适应症，罗氏、强生积极求新
（1）Amgen：已从血液瘤验证推进至实体瘤商业化，并正在通过剂型优化、适应症前移和联合治疗拓展平台价值
技术平台由早期的BiTE更新升级为HLE-BiTE，半衰期显著延长。Amgen的TCE平台主要称为BiTE（Bispecific T-cell Engager）技术，通过分子工程方法，将两种不同的scFv连接为一条链式分子，实现双特异性。一个scFv特异性识别T细胞表面CD3分子，另一个scFv特异性识别肿瘤细胞相关抗原（如CD19、BCMA等）。早期经典BiTE结构小、效力强，但半衰期短，代表是Blinatumomab。传统BiTE通常由两个单链抗体片段连接而成，不含完整Fc结构，因此分子量较小、组织渗透性较好，但也容易经肾脏清除，血清半衰期通常只有数小时。这也是Blinatumomab需要连续静脉输注的重要原因。经典BiTE的优势是机制清晰、T细胞重定向杀伤效率高，并已在B-ALL中完成充分临床验证；不足则是给药便利性差，长期输注对患者依从性和医疗资源占用较高。为解决经典BiTE半衰期短的问题，Amgen开发了HLE BiTE（half-life extended BiTE）平台。HLE BiTE在BiTE分子中加入Fc结构，目的在于延长体内暴露时间，减少给药频率，提高患者便利性。Tarlatamab就是Amgen HLE-BiTE平台最重要的成功案例，其靶向DLL3/CD3，已经在小细胞肺癌中获批，证明HLE-BiTE不仅可用于血液瘤，也能在实体瘤中实现临床突破。
Amgen当前TCE布局已形成三条核心主线：Blinatumomab作为CD19/CD3经典BiTE，继续围绕B-ALL推进皮下注射剂型和前线治疗拓展，同时外推至SLE和难治RA等自免疾病；Tarlatamab作为DLL3/CD3实体瘤TCE代表，已在ES-SCLC获批，并通过多项DeLLphi研究向一线维持、局限期SCLC、皮下注射给药及联合ADC/免疫治疗等方向扩展；Xaluritamig则是下一代STEAP1/CD3实体瘤TCE，已在mCRPC进入两项Phase3，并进一步探索前列腺癌早期疾病阶段和尤文肉瘤。整体来看，Amgen TCE平台已从血液瘤验证推进至实体瘤商业化，并正在通过剂型优化、适应症前移和联合治疗拓展平台价值。
（2）Genmab：DuoBody平台驱动TCE商业化，Epcoritamab持续向前线治疗拓展
Genmab是全球抗体工程领域的重要平台型公司，其TCE布局主要建立在DuoBody双抗平台之上。DuoBody技术通过可控Fab-armexchange生成双特异性IgG抗体，保留天然IgG样结构和较长血浆半衰期，同时实现两个不同靶点的精准结合。对于TCE而言，DuoBody可将CD3端与肿瘤抗原端组合，从而招募T细胞杀伤肿瘤细胞。Genmab最具代表性的TCE资产为Epcoritamab（EPKINLY/TEPKINLY），靶向CD3×CD20，由Genmab和AbbVie共同开发，是目前全球核心CD20/CD3双抗之一。此外，Genmab通过技术授权在骨髓瘤TCE中也具备影响力。J&J的Tecvayli（BCMA×CD3）和Talvey（GPRC5D×CD3）均来自Genmab与J&J的DuoBody合作协议，虽然由J&J负责开发和商业化，但Genmab获得里程碑和销售特许权使用费，进一步验证平台能力。
2026年已上市管线Epcoritamab即将迎来3项数据读出催化（1项已读出）：①EPCORE DLBCL-1完整数据已披露：该Phase3已显示PFS、CR、DOR和至下一治疗时间改善，但OS未达到统计学显著；②3期联合来那度胺对比化疗用于2L+ DLBCL的DLBCL-4数据预计于26H1读出；③3期单药治疗1L DLBCL的数据预计于2026年内读出。
（3）Roche/Genentech：探索4-1BB双抗联合及三抗疗法，自免SLE早期探索中
Roche在TCE领域可实现血液瘤产品生态协同。公司长期深耕B细胞淋巴瘤，拥有Rituxan/MabThera和Gazyva等CD20单抗、Polivy（CD79b ADC）、Venclexta（BCL-2抑制剂），以及Lunsumio和Columvi两款CD20/CD3 TCE。上述资产覆盖B细胞肿瘤的不同治疗机制：CD20单抗负责基础免疫清除和预处理，ADC提供细胞毒载荷杀伤，TCE招募T细胞重定向杀伤，BCL-2抑制剂诱导凋亡。依托这一组合，Roche设计了包括Columvi+Polivy+R-CHP、Lunsumio+Polivy、Lunsumio+lenalidomide等联合方案，推动TCE从后线单药向前线联合治疗迁移。除成熟CD20xCD3资产外，Roche也在临床前探索条件激活型TCE，通过蛋白酶可切割mask遮蔽CD3结合端，使TCE在肿瘤微环境中被激活，以扩大实体瘤治疗窗。
通过子公司中外制药探索4-1BB双抗联合及三抗疗法。罗氏下一代TCE选用的是4-1BB（CD137）共刺激信号。其子公司中外制药在2024年AACR上公开过Dual/LINC-Ig平台，用于解决共刺激 TCE 的细胞交联的隐患。Dual-Ig 的核心在于通过工程化的Fab区域，让同一个Fab同时具备 CD3 与 CD137 的双特异性，但两者结合是竞争性的：一旦 Fab 已经结合了 CD3，就无法再结合 CD137，反之亦然。这样可以避免在缺乏 DLL3 结合的情况下，发生非特异性的 T 细胞交联，从而降低系统性激活的风险。LINC-Ig 则通过在两个 Fab 之间引入二硫键，进一步限制其空间构象，来避免交联。当 Dual-Ig和 LINC-Ig 两种技术合体，就形成了Dual/LINC-Ig平台，该平台下的代表产品为 RG6524（DLL-3/CD3/CD137三抗TCE），目前处于临床一期。RG6524 是在这两个技术平台的基础上，设计了两个CD3/CD137靶向臂，一个肿瘤抗原靶向臂，形成完整的三特异TCE架构。此外，罗氏还探索过Englamours alfa（CD19x4-1BBL）+Glofitamab的Signal1+Signal2策略，通过CD20xCD3 TCE提供T细胞激活信号，并由4-1BBL共刺激分子增强T细胞持续活性，此前于2024ASH在R/R B-NHL中披露早期临床数据，但已于2026Q1管线中被移出。
Roche 2026-2027年TCE催化剂主要集中在两款已上市CD20/CD3 TCE的适应症扩张。2026年，Lunsumio+Polivy用于2L+DLBCL已在美国申报NDA，Lunsumio+lenalidomide用于2L+FL预计年内申报NDA；2027年，Columvi将推进Columvi+Polivy+R-CHP用于1L DLBCL以及单药用于r/rMCL的申报。
目前Roche也在积极探索TCE在自免（SLE）的运用。已上市的Lunsumio已于2025EULAR披露早期临床结果，在SLE中展现剂量依赖性的快速、深度B细胞清除潜力。另有一款RG6382（CD19xCD3）正处于SLE的I期，预计2027年11月完成I期临床。
（4）强生：BCMAxGPRC5DxCD3三抗早期疗效优异，KLK2xCD3等加速推进实体瘤研发
强生为当前多发性骨髓瘤TCE领域最核心的公司之一，截止2026.5已拥有两款上市TCE产品：TECVAYLI(teclistamab)和TALVEY(Talquetamab)，分别靶向BCMAxCD3和GPRC5DxCD3。两款产品均基于Genmab授权的DuoBody平台开发。此外，强生继续推进下一代TCE资产：一方面Ramantamig布局BCMAxGPRC5DxCD3三抗TCE，升级多发性骨髓瘤管线，JNJ-8543这一CD79xCD20xCD3三抗TCE进军B细胞血液瘤；另一方面用JNJ-8343（KLK2xCD3）布局实体瘤（前列腺癌），并已经进入临床III期，早期披露数据表现优异。
Ramantamig早期数据已展现出接近CAR-T级别的深度缓解潜力，同时具备现货型、Q4W皮下注射、单次step-up dose和低级别CRS等便利性/安全性优势，有望成为强生骨髓瘤TCE平台从双抗向三特异升级的核心资产。2025 ASH更新数据显示，强生的Ramantamig（JNJ-5322）作为BCMA×GPRC5D×CD3三特异TCE，在末线复发/难治性多发性骨髓瘤中展现出较强早期疗效。RP2D确定为100mg Q4W皮下注射，并仅需1次5mg step-up dose；在BCMA/GPRC5D-naive患者中，ORR达100.0%，≥VGPR为96.3%，≥CR为88.9%，且缓解随随访延长继续加深。疗效持续性方面，12个月和18个月PFS分别为92.6%和79.6%，中位PFS尚未达到。安全性方面，CRS发生率为53%，主要为1/2级，未报告ICANS，提示其在维持高疗效的同时具备较便利的给药和可管理安全性。
（5）Regeneron：内部推进CD3xTAA与CD28xTAA共刺激联用，外部合作补齐条件激活TCE
Regeneron积极探索CD3双抗与CD28共刺激双抗联用。CD3双抗提供T细胞激活/杀伤信号（Signal1），CD28双抗通过肿瘤抗原定位补充共刺激信号（Signal2），从而增强T细胞杀伤强度和持续性。2024年再生元在《Nature Reviews Immunology》发表相关文章，指出：当与 CD3 双特异性抗体联合使用时，TAA × CD28 双特异性抗体不仅在 T 细胞和靶细胞之间形成人工免疫突触，而且与单独使用CD3双特异性抗体相比，在异种和同种肿瘤模型中均增强了抗肿瘤反应；CD22×CD28通过增强T细胞活化和细胞毒性功能，提高了CD20×CD3双抗Odronextamab在弥漫性大B细胞淋巴瘤小鼠模型中的疗效。公司已形成CD20xCD3、BCMAxCD3、MUC16xCD3、PSMAxCD3等CD3 TCE管线，并配套开发PSMAxCD28、EGFRxCD28、MUC16xCD28、CD22xCD28等共刺激双抗。相比单纯CD3 TCE，Regeneron更强调“激活+增强”的组合式免疫治疗平台，可能提高实体瘤和复发难治血液瘤中的T细胞功能维持。
CD28共刺激也是高风险路线，需要格外关注安全性问题。CD28是较强的早期T细胞共刺激信号，理论上能更直接增强T细胞活化，但历史上全身性CD28激动曾出现严重安全性事件。因此Regeneron平台成败的关键，在于能否通过肿瘤抗原定位把CD28激活限制在肿瘤局部，既提升疗效，又避免系统性免疫激活。后续需要重点跟踪REGN5837、REGN5678和REGN7075等项目的临床安全窗口及疗效兑现情况。
与CytomX合作探索条件激活双抗。6月3日，CytomX Therapeutics宣布扩大其与Regeneron的合作和许可协议，利用CytomX的Probody治疗平台和Regeneron的Veloci-Bi双特异性抗体开发平台创建条件激活的双抗。Regeneron和CytomX的合作最初于2022年开始，其战略重点是将CytomX生物掩蔽策略与Regeneron双特异性抗体相结合，开发出在肿瘤微环境中被蛋白酶激活之前保持非活性的双特异性抗体。2022年AACR发表文章显示：与激活的TCB相比，掩蔽EGFR和CD3结合域可显著降低其与表达EGFR或CD3的细胞的结合，并在蛋白酶活性极低的条件下，减弱CI107介导的细胞毒性和T细胞活化作用。此外，CI107 对移植了人类 PBMC 的小鼠的异种移植肿瘤显示出强大的疗效，并且与食蟹猴体内活化的TCB相比，具有更好的耐受性和暴露量。
（6）Abbvie：从CD20×CD3商业化延伸至下一代TCE平台，外部合作补强共刺激与肿瘤激活技术
AbbVie与Genmab共同开发的Epcoritamab为CD20×CD3双抗，已在R/RDLBCL、R/RFL等B细胞淋巴瘤中实现商业化，并持续向更早线和联合治疗拓展；多发性骨髓瘤方向，公司通过Etentamig（ABBV-383，BCMA×CD3）和ISB2001（BCMA/CD38/CD3三抗）补强浆细胞肿瘤布局，试图覆盖BCMA单靶及双靶三抗两代TCE资产。平台端，AbbVie近年通过外部合作补充下一代TCE设计能力：其与Evolve Immune合作，引入基于CD2共刺激机制的新一代TCE平台，目标是在CD3介导T细胞激活之外进一步增强T细胞功能，用于实体瘤和血液系统恶性肿瘤；同时，公司又与Xilio Therapeutics达成合作，基于后者肿瘤激活技术开发新型免疫疗法，其中包括掩蔽型TCE分子。
（二）新兴平台公司：遮蔽肽等技术平台逐步兴起
（1）Janux: 遮蔽型TCE新锐代表，PSMA×CD3率先验证实体瘤治疗窗优化
Janux核心技术为TRACTr（Tumor Activated T Cell Engager）平台，基于结合位点竞争性封闭实现遮蔽效果。根据公司招股书披露，TRACTr/TRACIr分子由肿瘤抗原结合域、T细胞结合域、结构域优化遮蔽肽、白蛋白结合域和蛋白酶可切割linker组成。未进入肿瘤微环境前，遮蔽肽限制CD3/CD28或肿瘤抗原结合，从而降低系统性T细胞激活、CRS和正常组织毒性；进入肿瘤组织后，肿瘤相关蛋白酶切割linker，解除遮蔽，使分子恢复T细胞重定向杀伤或共刺激活性。与此同时，白蛋白结合域用于延长激活前循环半衰期，而激活后遮蔽结构和白蛋白结合域脱落，活性分子半衰期缩短，有助于降低其逃逸出肿瘤后的系统性毒性。其PSMA×CD3（JANX007）已获得早期临床验证。此外，TRACIr平台在TRACTr基础上进一步探索CD28共刺激，JANX013为PSMA×CD28共刺激双抗，拟与PSMA×CD3JANX007联用，以增强T细胞杀伤深度和持续性。目前Merck和BMS均与JANUX达成平台合作协议。
JANX007是Janux目前最重要的临床资产，I期数据显示其在mCRPC中观察到PSA下降、影像学缓解和可管理安全性，初步验证PSMA×CD3肿瘤激活型TCE在实体瘤中的可行性。与非遮蔽型PSMA/CD3TCE相比，JANX007的关键差异在于通过遮蔽降低外周CD3激活，试图在保留抗肿瘤活性的同时减少CRS和正常组织毒性。2025年12月公布的I期临床数据显示，PSA50达73%，ORR=30%，m-PFS=7.3mon。公司后续重点将转向taxane-naïve mCRPC人群，并探索与AR通路抑制剂或CD28共刺激平台联用。JANX014同样靶向PSMA×CD3，但采用双遮蔽设计，同时遮蔽PSMA端和CD3端，旨在进一步扩大安全窗口。需要注意的是，2026年4月，公司宣布终止开发JANX008（EGFR×CD3），考虑到当下该平台尚无已上市管线验证，遮蔽型TCE高度依赖靶点选择和肿瘤生物学，JANUX平台仍需更多临床验证。
（2）CytomX：再生元合作背书技术平台，核心管线CX-908仍在临床前期
CytomX核心技术为Probody平台，主要通过affinity masking实现遮蔽效果。公司通过细菌表面展示的合成肽库，针对待遮蔽抗体筛选能够特异性结合其CDR区域的遮蔽肽，并将其通过蛋白酶可切割linker连接至抗体N端。未切割状态下，遮蔽肽与抗原竞争CDR结合，从而降低外周组织中的抗原结合和药物活性；进入肿瘤微环境后，linker被肿瘤相关蛋白酶切割，遮蔽肽脱落，抗体恢复靶点结合和效应功能。
早前CX-904管线停止开发，当前核心TCE管线CX-908仍处于临床前期。CX-904靶向EGFRxCD3，此前为CytomX代表性条件激活TCE资产。CX-904曾显示出一定安全性和初步抗肿瘤活性，但出于管线优先级和资金原因，CX-904于2025年暂停开发。当下核心管线CX-908靶向CDH3×CD3，CDH3在肺癌、乳腺癌等多种实体瘤中高表达，但正常组织亦有表达，传统未遮蔽CDH3/CD3TCE容易面临on-target/off-tumor毒性。临床前研究显示，CX-908在未激活状态下对CDH3阳性肿瘤细胞和CD3阳性Jurkat细胞结合明显减弱，蛋白酶激活后结合与体外杀伤活性恢复；在H1975和HCC1806肿瘤模型中可诱导肿瘤退缩。安全性方面，食蟹猴研究显示CX-908较未遮蔽TCE显著降低IFNγ、IL-2、IL-6、MCP-1等细胞因子释放，最大耐受剂量约为3mg/kg，而未遮蔽TCE约为0.03mg/kg，耐受性提升约100倍。CX-908则进一步证明遮蔽型TCE在高正常组织表达实体瘤靶点上的潜在安全窗优势。
进一步加深与Regeneron的合作，外部验证Probody平台的潜力。CytomX和Regeneron最早于2022年达成战略合作，围绕条件激活双特异性抗体开展多靶点研发，Regeneron负责靶点选择和双抗工程能力，CytomX则提供Probody遮蔽与肿瘤微环境激活技术，将Regeneron在CD3/CD28双抗和抗体工程上的积累，与CytomX的遮蔽肽平台结合，用于开发条件激活TCE。2026年6月，双方进一步扩大合作，Regeneron新增两个研究项目，并保留最多六个未来靶点的选择权；CytomX将获得预付款，并有资格获得研发、监管和商业化里程碑，潜在总额约40亿美元。
（3）Xencor：Xmab平台构建2+1结构及长半衰期双抗，已与多MNC合作技术平台
Xencor核心技术为XmAb平台，优势主要在于Fc结构工程和IgG样多特异性抗体设计。公司通过XmAb Bispecific Fc Domain构建稳定、长半衰期、易生产的双抗骨架，并进一步发展出XmAb 2+1结构，即两个肿瘤抗原结合域加一个CD3或CD28结合域。两个肿瘤抗原结合臂可以增强对高抗原密度肿瘤细胞的结合，而低抗原密度正常组织较难形成稳定结合，从而提高肿瘤选择性；单个CD3结合臂则用于降低过度T细胞激活风险。
Xencor自有TCE资产以XmAb819和XmAb541为代表。XmAb819为ENPP3×CD3的2+1TCE，面向晚期透明细胞肾癌，ENPP3在肾癌中表达较高、正常组织表达较低，公司计划在2026年确定推荐III期剂量，并支持2027年启动关键性研究。XmAb541为CLDN6×CD3TCE，主要探索卵巢癌及其他CLDN6阳性实体瘤。除CD3TCE外，Xencor也在推进CD28共刺激双抗，代表资产XmAb808为B7-H3×CD28，定位是与已有CD3TCE联用，通过CD3提供T细胞激活Signal1、CD28提供共刺激Signal2，以增强T细胞扩增和抗肿瘤效应。Plamotamab则是CD20×CD3TCE，最初用于B细胞淋巴瘤，Xencor在2024年从J&J收回全球权益后，正在将其转向类风湿关节炎等自免疾病探索，体现TCE从肿瘤向B细胞清除型自免适应症延展的趋势。
已实现对多个MNC的平台授权，外部验证获得认可。Amgen的Xaluritamig（STEAP1×CD3）即采用XmAb 2+1 Bispecific结构，已进入前列腺癌III期；Astellas的ASP2138（CLDN18.2×CD3）也采用XmAb 2+1结构，目前处于胃癌/胃食管结合部癌I期；J&J合作管线中还包括PSMA×CD28和CD20×CD28共刺激双抗。
Xencor 2026H2预计将迎来多个实体瘤TCE数据读出及自免TCE进展。重点推进的两款实体瘤CD3TCE：XmAb819为ENPP3×CD3，适应症为透明细胞肾癌（ccRCC），2026年上半年已启动CRC、NSCLC和乳头状肾癌（pRCC）肿瘤扩展队列，预计2026年下半年在医学会议披露RP3D单药数据；XmAb541为CLDN6×CD3，面向CLDN6阳性肿瘤，包括卵巢癌和生殖细胞肿瘤，预计2026年下半年披露RP3D单药数据。此外，公司探索TCE在自免中的运用，、Plamotamab（CD20×CD3）预计26H2更新RA Ib期进展，XmAb657（CD19×CD3）预计更新首次人体剂量爬坡研究进展。
（4）MSD/Harpoon：以DLL3×CD3为核心切入实体瘤TCE
Merck通过2024年收购Harpoon Therapeutics切入下一代TCE疗法。Harpoon的TriTAC平台分子由三部分组成：用于T细胞结合的CD3结合域、专有的半衰期延长域和抗原结合域。TriTAC由一条单链多肽组成，该多肽旨在结合肿瘤表面抗原、人血清白蛋白以及T细胞受体（TCR）的CD3ε亚基。肿瘤靶向和白蛋白结合由单域抗体（sdAb）实现，而CD3则由单链可变区片段（scFv）结合。当TriTAC同时结合细胞表面抗原和T细胞时，它们会诱导形成细胞溶解性突触，模拟TCR和MHC之间的天然相互作用，激活T细胞杀伤靶细胞。此外，Harpoon还开发了ProTriTAC™平台，将前药概念应用于其TriTAC®平台，在CD3和白蛋白之间加入可以被肿瘤微环境特异性酶切割的linker和掩蔽肽，因此，该抗体仅在肿瘤组织中被酶切后激活，减少脱靶毒性；同时被酶切后激活的CD3xTAA不含白蛋白抗体，半衰期缩短，安全性提升。
核心资产MK-6070目前已经进入临床I/II期。MK-6070（原HPN328，gocatamig），为DLL3×CD3 TriTAC，用于DLL3阳性小细胞肺癌、神经内分泌肿瘤及其他DLL3表达肿瘤。目前正在探索单药，也探索与atezolizumab及ifinatamab deruxtecan（I-DXd）联用，且在往1L SCLC探索。对Merck而言，MK-6070的战略意义在于补齐其在实体瘤TCE，尤其DLL3赛道中的布局。除MK-6070外，Harpoon还带来了BCMA×CD3资产HPN217和条件激活EpCAM靶向项目HPN601等早期管线。
（6）UCB/Candid：收购Candid切入TCE，围绕BCMA/CD20/CD19拓展血液瘤及自免
UCB通过收购Candid切入TCE赛道，预计于2026年Q2末至Q3初完成交割。2026年5月UCB签署收购Candid的协议，交易对价为20亿美元现金首付款，另有最高2亿美元开发里程碑。Candid成立于2024年，是目前自免TCE领域推进速度最快的公司之一。其核心是利用CD3 TCE实现对致病B细胞/浆细胞的深度清除，从而达到免疫重置。从UCB角度看，Candid补强了其免疫疾病管线，使UCB从传统抗炎/免疫调节进一步进入“靶向免疫重置”赛道。从技术路径看，Candid并非押注单一靶点，而是在探索不同深度B细胞清除的适应症匹配：BCMA×CD3更偏向清除浆细胞，适合自身抗体驱动更强的疾病；CD20×CD3更偏向广谱B细胞清除，可借鉴利妥昔单抗等CD20疗法在RA、SLE、硬皮病等疾病中的经验；CD19×CD20×CD3及BCMA×CD19×CD3则进一步扩大靶细胞覆盖范围，在难治自免疾病中实现比传统单抗更深、更持久的免疫重置。2025年以来，Candid已披露Cizutamig和CND261进入IgA肾病、MG、RA、SLE、系统性硬化症等多项临床研究。Cizutamig采用2+2结合构型并进行Fc沉默和CD3结合优化，通过高亲和力BCMA结合清除BCMA阳性B细胞/浆细胞，同时通过优化CD3端降低过度T细胞激活和细胞因子释放。体外数据显示，cizutamig在保持B细胞杀伤活性的同时，相较其他BCMATCE可减少细胞因子释放。
Candid目前布局较为完整，围绕BCMA、CD20、CD19三类B细胞/浆细胞靶点构建多款TCE。目前在研的几款管线：（1）Cizutamig（BCMA×CD3）：已在多发性骨髓瘤中完成I期研究，并已在中国和欧洲多个自免适应症中积累超过100例受试者、其中68例为自免患者的早期数据，具备潜在BIC BCMA TCE特征，安全性表现为CRS多为低级别且可管理、未观察到ICANS，并计划推进MG和SARD-ILD全球II期研究。（2）CND261（CD20×CD3）：已给药超过110例患者，其中自免患者超过20例，在自免患者中观察到组织深度B细胞清除，CRS均为1级且发生率低于20%，未见ICANS。（3）CND319（CD19×CD20×CD3）：处于IND-enabling阶段，计划进入首次人体研究。（4）CND460（BCMA×CD19×CD3）处于IND-enabling阶段。
（7）Gilead/Ouro/康诺亚：CM336安全性优异，积极拓展自免适应症
Gilead 2026年3月拟收购Ouro，核心资产为BCMAxCD3双抗CM336，预计2027年开展多个自免适应症注册性III期。2024年11月，康诺亚将CM336在大中华区以外的全球研发、生产、注册及商业化权益授权给OuroMedicines子公司PlatinaMedicines，康诺亚保留大中华区权益，并获得首付款/近期付款、Ouro股权及潜在里程碑和销售分成。2026年3月，Gilead宣布以16.75亿美元首付款及最高5亿美元里程碑收购Ouro Medicines，从而获得CM336海外权益。CM336/OM336旨在通过有限疗程皮下注射实现快速、深度B细胞清除，并已在AIHA、ITP等严重抗体介导罕见疾病中显示出早期疗效和差异化安全性，同时已获得FDA针对AIHA和ITP的快速通道及孤儿药资格，预计2027年进入注册性研究。
（8）Cullinan：深度布局自免领域，引进智翔金泰GR1803加速推进SLE等自免适应症
Cullinan目前自免TCE布局包括两条主线：（1）自研CLN-978（CD19×CD3双抗）：采用皮下注射给药，主要覆盖SLE、RA和干燥综合征等B细胞驱动疾病。2026年EULAR披露的初步I期数据显示，CLN-978在难治SLE和难治RA患者中，单次目标剂量后即观察到临床获益，包括部分患者达到缓解；同时外周血及组织中出现深度、剂量依赖性B细胞清除，且单次目标剂量最高至30μg及初始多剂量方案整体安全性较好；具备深度B细胞清除能力，同时具备皮下注射、剂量可控、无需淋巴清除预处理等潜在便利性。（2）从智翔金泰引进的velinotamig/GR1803（BCMA×CD3双抗）：预计2026Q4披露SLE初始多剂量数据。GR1803在肿瘤端也已有较显著进展：已完成/推进GR1803在复发/难治多发性骨髓瘤中的I期及关键II期研究，并于2026年1月获得NMPA附条件上市申请受理，随后被纳入优先审评，拟用于既往至少接受过三线治疗的复发/难治多发性骨髓瘤成人患者。Cullinan2026年5月材料显示，velinotamig在RP2D目标剂量下的RRMM患者中ORR为87.5%、≥VGPR率为70.8%、CR率为37.5%，且在髓外病变患者中ORR为83.3%；安全性方面，RP2D目标剂量组CRS发生率较高但≥3级CRS为6.3%，未观察到ICANS。
（三）国内创新药企：近年来陆续布局多抗及新兴技术平台
（1）德琪医药：空间位阻及2+1靶点组合平台，积极探索实体瘤及血液瘤领域
德琪医药的TCE布局主要依托其自主AnTenGager平台，核心设计包括“2+1”二价靶点结合、空间位阻遮蔽，以及具备快速结合/解离动力学的自有CD3序列。其逻辑与Xencor 2+1结构、Janux/CytomX遮蔽设计有一定相似之处：一方面，通过两个肿瘤或疾病靶点结合臂增强对低表达靶细胞的识别；另一方面，通过空间位阻遮蔽降低未结合靶细胞时的CD3端暴露和T细胞激活，从而减少CRS风险。
目前德琪TCE平台最重要的资产是ATG-201（CD19×CD3），采用“2+1”CD19靶向结构，并结合空间位阻遮蔽和自有CD3序列。2026年3月，德琪与UCB达成全球授权协议，UCB获得ATG-201全球独家开发、生产和商业化权益；德琪获得6000万美元首付款及2000万美元近期里程碑，并有资格获得超过11亿美元开发、注册和商业化里程碑及销售分成。该交易是德琪首个TCE出海交易，也验证了AnTenGager平台在自免TCE方向的全球化价值。根据公告，德琪计划在中国和澳大利亚提交ATG-201临床试验申请，并完成首次人体I期研究后将后续开发移交UCB。除ATG-201外，德琪正在推进多款实体瘤和血液瘤TCE。（1）实体瘤方向，ATG-106为CDH6×CD3双抗用于卵巢癌和肾癌；ATG-112为ALPPL2/ALPP/G×CD3探索妇科肿瘤、消化道肿瘤、膀胱癌和NSCLC；ATG-110为LY6G6D×CD3，用于微卫星稳定型结直肠癌。（2）血液瘤方向，公司还布局GPRC5D×CD3（ATG-021）、LILRB4×CD3（ATG-102）和FLT3×CD3（ATG-107）。其中，ATG-106和ATG-112已在AACR2026披露临床前数据：ATG-106在CDH6阳性卵巢癌和肾癌模型中显示强T细胞依赖性杀伤和体内抑瘤效果，且在非人灵长类替代分子研究中耐受性较好；ATG-112则利用ALPP/G在正常成人组织中低表达、在多类实体瘤中异常表达的特点，通过“2+1”结构和CD3空间遮蔽实现低细胞因子释放和肿瘤选择性杀伤。
2026-2027年催化剂：（1）ATG-110预计2027H1提交IND；（2）ATG-106预计2027Q2提交IND;(3)ATG-112预计2027年前后推进IND。
（2）泽璟制药：DLL3三抗目前处于III期临床阶段，MUC17三抗消化道肿瘤I期探索中
（3）复宏汉霖：引入共刺激信号CD28重塑实体瘤免疫，实现优效、更宽治疗窗口
复宏汉霖对该TCE平台的机制设计进行了系统性优化：CD3激活采用靶点依赖性机制，在无肿瘤靶抗原存在时，不触发CD3激活信号，从而降低脱靶激活风险；CD28共刺激信号采用条件性激活设计，仅在CD3信号被触发后发生，并与CD3协同激活调控T细胞。此外，通过将CD3和CD28的结合区域置于TCE分子的同侧，促进其与同一T细胞上的CD3和CD28进行顺式结合（cis-结合），以减少非特意性的T细胞激活和互相攻击，进而有效控制了系统性毒性风险，实现了更宽的治疗窗口。2026 AACR披露早期临床数据，展现出较优的临床前潜力。
六、风险提示
研发失败风险。TCE药物研发涉及靶点选择、CD3亲和力设计、分子构型优化、半衰期调控、给药方案及安全窗管理等多个环节，技术复杂度较高。若候选药物在临床前或临床阶段出现疗效不足、CRS/ICANS、感染、低免疫球蛋白血症、肝毒性、血液学毒性或其他不可接受的不良反应，可能导致剂量受限、适应症收缩、临床暂停或项目终止。实体瘤TCE还面临靶点正常组织表达、肿瘤微环境抑制、T细胞浸润不足和抗原异质性等挑战；自免TCE则需验证深度B细胞/浆细胞清除的长期安全性和免疫重置可持续性，相关研发结果存在不确定性。
临床进度不及预期风险。TCE管线多处于早期或中期临床阶段，后续推进可能受到患者入组速度、剂量爬坡、CRS监测要求、联合用药设计、监管沟通、临床终点选择及生产供应等因素影响。若关键临床研究启动、入组、数据读出、注册申报或审批进度慢于预期，可能影响相关公司产品上市节奏和市场预期。对于自免TCE而言，目前多数数据仍来自小样本、开放标签或早期研究，后续能否进入随机对照研究并取得明确临床获益仍存在不确定性。
商业化不及预期风险。TCE产品商业化放量受适应症规模、治疗线数、竞品格局、疗效安全性差异、给药便利性、CRS管理成本、住院/门诊给药条件、医生接受度、患者支付能力及医保/商业保险覆盖等因素影响。血液瘤领域已有CAR-T、ADC、单抗、小分子及多款同靶点TCE竞争，价格和市场份额可能承压；实体瘤TCE若疗效持续性或安全性未能明显优于现有疗法，放量可能低于预期；自免TCE作为新兴治疗模式，仍需医生和患者接受深度免疫清除及潜在感染风险，商业化路径存在不确定性。
应合规要求，仅呈现部分报告信息，完整全文内容欢迎阅读外发报告
国金证券研究服务
团队介绍
＋
报告信息
证券研究报告：《TCE行业专题报告：血液瘤商业化兑现、自免接棒，实体瘤静待技术进一步突破》
对外发布时间：2026年6月17日
报告发布机构：国金证券股份有限公司
证券分析师：甘坛焕
SAC职业编号：S1130525060003
邮箱：gantanhuan@gjzq.com.cn
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2026-06-10
·雪球
一、开场介绍会议时间：2026财年主持人说明：由高盛分析师AsadHaider主持，目的为探讨艾伯维公司未来5-10年的定位、治疗领域、业务线及潜在增长支柱。管理层发言摘要：RobertA.Michael（董事会主席兼首席执行官）：强调公司战略延续性，重点为快速恢复增长；去年在修美乐（Humira）美国专利保护到期仅两年后即超过峰值销售额，未来将聚焦免疫学、肿瘤学、神经科学、美学及肥胖症四大增长驱动力。RoopalThakkar（执行副总裁、研发部主管、首席科学官）：重点介绍肿瘤学管线进展，提及ASCO会议上Temab-A（c-Met靶向ADC）、etentamig（多发性骨髓瘤TCE）等资产的积极数据。ScottT.Reents（执行副总裁、首席财务官）：概述第一季度业绩强劲，Skyrizi和Rinvoq保持23%增长，上调全年财务指引。二、财务业绩分析核心财务数据第一季度业绩：超出预期3亿美元，实现两位数增长；Skyrizi和Rinvoq：两者均增长23%，全年指引分别上调1亿美元；神经科学领域：整体增长17%，呈现广泛增长态势；营收与利润：报告营收增长10%，运营增长略高于9%，全年收益增长超过14%。关键驱动因素收入增长主要由Skyrizi和Rinvoq的持续增长驱动，两者上市第八年仍保持超20%增速；神经科学领域多产品贡献增长，成为公司第三大支柱；投资效率提升，在推动增长的同时实现利润增长。三、业务运营情况分业务线表现免疫学：Skyrizi和Rinvoq在炎症性肠病（IBD）、银屑病等领域市场份额高，Skyrizi一线治疗数据强劲，Rinvoq标签扩展后可在生物制剂治疗后使用；推进联合疗法（如α4β7+Skyrizi），克罗恩病内镜缓解效果翻倍。肿瘤学：ASCO会议上公布Temab-A（c-MetADC）在头颈癌、卵巢癌的积极数据，计划推进剂量优化和关键试验；etentamig（BCMATCE）在多发性骨髓瘤中CRS发生率0%，预计今年晚些时候公布III期数据；PD-1/VEGF联合疗法（与荣昌生物合作）在非小细胞肺癌中数据积极，计划加速III期。神经科学：三大垂直领域（精神病学、偏头痛、帕金森病）均具备超50亿美元峰值潜力，目前市场模型低估约10亿美元；Vraylar、偏头痛药物等产品增长强劲。美学及肥胖症：与Gubra合作的amylin类药物聚焦持久性和差异化，1期试验显示10%体重减轻，计划在BMI≥35患者中推进1b/2期；肥胖症与美学业务协同，覆盖患者完整美学旅程。研发投入与成果免疫学管线：布局TL1A、TREM-1、IRAK4等新机制，与Capstan合作体内CAR-T平台（B细胞耗竭），推进α4β7（ABBV-382）联合疗法；IL-23长效药物进入临床，探索延长给药周期。肿瘤学管线：三特异性TCE、KRAS抑制剂（与Kestrel合作）、PSMAADC（969）等资产推进，969在前列腺癌五线患者中ORR达45%，PFS15个月，计划进入III期。神经科学管线：cycloplastogenbretisilocin（抑郁症）、emraclidine（Cerevel合作）、下一代Aβ抗体（阿尔茨海默病）等资产处于临床阶段。市场拓展：暂无信息运营效率：暂无信息四、未来展望及规划短期目标（2026年及近期）财务目标：维持Skyrizi和Rinvoq的23%增长，实现两位数营收和利润增长；研发推进：启动α4β7联合疗法的2b期试验，探索加速III期；推进肿瘤学资产（Temab-A、etentamig）的关键试验，公布PD-1/VEGF联合疗法在非小细胞肺癌的更多数据。中长期战略（未来5-10年）核心领域：以免疫学、肿瘤学、神经科学、美学为四大支柱，拓展肥胖症领域，每个领域均目标贡献超50亿美元峰值销售额；管线策略：通过联合疗法（如Skyrizi+TL1A）和外部创新（业务发展交易）补充管线，应对专利到期风险（Rinvoq专利至2037年）；政策应对：关注340B计划滥用、最惠国待遇立法等政策风险，推动解决欧洲不公平定价做法。五、问答环节要点公司定位与增长支柱问：未来5-10年公司定位及增长支柱？答：延续“快速恢复增长”战略，四大支柱为免疫学（Skyrizi/Rinvoq）、肿瘤学（新兴管线）、神经科学（三大垂直领域）、美学及肥胖症；肿瘤学将成为重要增长部分，目前市场对其管线潜力低估。业务发展与资本部署问：如何看待后期或上市后资产的交易机会？答：不排除此类交易，重点关注免疫学、肿瘤学、神经科学、美学及肥胖症领域的差异化资产；过去两年已投入80亿美元收购管线，未来将继续补充长期增长驱动力。肥胖症市场机会问：肥胖症领域的差异化机会及商业策略？答：聚焦持久性（70%患者因不良事件1年后停药），amylin类药物1期数据显示10%体重减轻，计划在高BMI患者中推进；结合美学渠道（与医美中心合作），覆盖患者体重管理及美学需求。外部运营环境与政策风险问：关注哪些监管及政策挑战？答：重点关注最惠国待遇立法（反对，认为破坏创新生态）、340B计划滥用（支持试点解决）、欧洲不公平定价（需政府介入解决）。财务指引与管线潜力问：是否提供中期财务指引？答：暂无计划，但指出Skyrizi/Rinvoq峰值潜力被市场低估（模型预期低于公司内部预测），神经科学三大领域各被低估约10亿美元，肿瘤学资产（Temab-A、etentamig）峰值潜力达数十亿美元（当前模型仅10亿美元）。六、总结发言管理层强调公司战略聚焦“四大增长驱动力+肥胖症”，通过内部研发与外部创新（业务发展交易）构建管线深度；财务表现强劲，第一季度超预期，Skyrizi和Rinvoq持续增长，神经科学成为第三大支柱；肿瘤学管线潜力显著，ASCO会议数据验证Temab-A、etentamig等资产价值，未来将成为重要增长引擎；长期目标为在免疫学、肿瘤学、神经科学等领域保持领先，通过联合疗法和差异化资产应对竞争与专利到期风险，同时关注政策环境变化，保护创新生态。查看业绩会议全文
2026-06-08
Data being presented, including six oral presentations, reinforce AbbVie's leadership and commitment to ongoing research to improve outcomes for people living with blood cancers
NORTH CHICAGO, Ill.
,
June 8, 2026
/PRNewswire/ -- AbbVie (NYSE: ABBV) today announced it will share new data at the European Hematology Association (EHA) 2026 Congress and will showcase clinical advancements from research programs across multiple blood cancers, including multiple myeloma (MM), follicular lymphoma (FL), chronic lymphocytic leukemia (CLL), diffuse large B-cell lymphoma (DLBCL), acute myeloid leukemia (AML) and amyloidosis (AL). Featured data from AbbVie's blood cancer portfolio and pipeline include 21 oral and poster presentations, highlighting the investigational compound etentamig (ABBV-383), and approved therapies, EPKINLY
®
(epcoritamab-bysp) (TEPKINLY
®
in the EU), VENCLEXTA
®
(venetoclax) (VENCLYXTO
®
in the EU) and DECNUPAZ™ (pivekimab sunirine-pvzy).
"The compelling data we are presenting at EHA reflect AbbVie's robust portfolio and pipeline and our ongoing work to advance the treatment and understanding of hematologic cancers," said Daejin Abidoye, M.D., vice president, therapeutic area head, oncology, solid tumor and hematology, AbbVie. "With this research, we continue our commitment to pioneering innovative solutions that have the potential to elevate standards of care for patients and help address the most pressing challenges in treating blood cancers."
Key oral presentations of epcoritamab data include:
Treatment impact of epcoritamab with lenalidomide and rituximab in relapsed or refractory (R/R) FL
A subgroup analysis of the Phase 3 EPCORE FL-1 trial (
NCT05409066
) of fixed-duration epcoritamab, in combination with rituximab plus lenalidomide (E+R
2
) for patients with R/R FL (n=243), was performed to determine if the efficacy benefit and tolerability of E+R
2
extended across clinically relevant subgroups, including patients with higher- and lower-risk disease features, compared to R
2
.
1
Between Follicular Lymphoma International Prognostic Index (FLIPI) subgroups, overall response rate (ORR) was numerically higher with E+R
2
compared to R
2
(FLIPI 0–2, 96.5% vs 84.8%; FLIPI 3–5, 93.0% vs 72.6%).
1
A similar trend was seen in those with progression of disease less than or equal to two years from the date of initial frontline therapy (POD24).
1
Across the age subgroups, ORR and complete response rates (CRR) for E+R
2
and R
2
for ≥65 were (94.3% vs 80.2% and 80.7% vs 44.3%, respectively) and <65 (95.5% vs 78.4% and 83.9% vs 54.0%, respectively). Progression-free survival (PFS) hazard ratios (HRs) (95% CIs) for E+R
2
and R
2
for the NHL-5 low co-morbidity index score were (0.27 [0.17–0.42]) and NHL-5 high + intermediate were (0.14 [0.06–0.29]).
1
The E+R
2
safety pro all subgroups was consistent with the overall trial population, with no new safety signals.
1
Efficacy data of epcoritamab following systemic therapy in R/R large B-cell lymphoma
(
LBCL)
EPCORE DLBCL-1 (
EudraCT No. 2020-003016-27
) is a randomized Phase 3 trial in R/R LBCL evaluating epcoritamab, a CD3×CD20 bispecific antibody, monotherapy. The study showed a statistically significant improvement in PFS versus investigator's choice of chemoimmunotherapy (CIT) — either rituximab plus gemcitabine plus oxaliplatin or bendamustine plus rituximab (HR 0.74 [95% CI, 0.60–0.92]; P=0.0059; 24-month PFS: 30% vs 13%). The study did not demonstrate a statistically significant improvement in overall survival (OS) (HR: 0.96 [95% CI, 0.77–1.20]). There was no OS detriment per pre-specified criteria.*
2
Epcoritamab reported a CRR of 38% and CIT 26%; (nominal P value 0.0032), duration of response (DOR) (median DOR 37 vs 6 months; duration of complete response (DOCR) NR vs 11 months, respectively) and time to next treatment (TTNT) (7 vs 4 months, respectively; nominal P value <0.0001).
2
Higher rates of grade 3–4 infections (30% vs 12%) and any-grade COVID-19 (36% vs 11%) were reported in the epcoritamab arm. Grade 5 treatment-emergent adverse events (TEAEs) occurred in 17% vs 6% (exposure-adjusted, 1.5 vs 1.8 per 100 pt-mo) and were largely attributable to grade 5 COVID-19 (9% vs 2%).
2
*OUS the protocol and SAP were amended to include dual primary endpoints of OS and PFS
The following studies featuring venetoclax, etentamig and pivekimab sunirine-pvzy data will also be shared as oral and poster presentations:
Predicted efficacy of venetoclax-based therapies in CLL based on genetic biomarkers
Results from the Phase 3 GAIA/CLL13 (
NCT02950051
) trial evaluating fixed-duration venetoclax-based combinations (with rituximab, obinutuzumab and obinutuzumab plus ibrutinib) as a chemotherapy-free alternative to chemoimmunotherapy (fludarabine, cyclophosphamide and rituximab or bendamustine and rituximab) in fit, previously untreated CLL patients lacking del(17p) or TP53 mutations.
3
Venetoclax in combination with rituximab and obinutuzumab plus ibrutinib in previously untreated CLL patients lacking del(17p) or TP53 mutations are investigational combinations not approved in the EU.
Efficacy and safety data of venetoclax-obinutuzumab combination in previously untreated CLL
Results from the open-label Phase 3 CLL14 trial (
NCT02242942
) comparing the efficacy and safety of venetoclax in combination with obinutuzumab to obinutuzumab plus chlorambucil in previously untreated patients with CLL and coexisting medical conditions.
4
Real-world management practices with venetoclax-based therapy for AML
Results from the prospective observational study, REVIVE (
NCT03987958
), examining the effect of antimicrobial prophylaxis, post-remission administration of G-CSF and treatment initiation setting on safety and effectiveness outcomes with venetoclax plus hypomethylating agents (HMA) in newly diagnosed AML patients unfit for intensive chemotherapy.
5
Etentamig in patients with relapsed/refractory multiple myeloma (RRMM) with prior exposure to B-cell maturation antigen (BCMA)-targeted therapy
Results from Arm B of the MONVISO study (
NCT05650632
), evaluating a flat dose of etentamig in patients with RRMM with at least two prior lines of therapy, including triple-class and prior BCMA exposure. The Phase 1b study is assessing dose optimization and safety.
6
Etentamig is an investigational therapy not approved in the EU.
Longer term safety and efficacy data of etentamig monotherapy in R/R light chain amyloidosis
Updated results from M24-209 (
NCT06158854
), evaluating etentamig monotherapy in BCMA-targeted therapy-naïve patients with relapsed/refractory immunoglobulin light chain amyloidosis. The open-label Phase 1/2 study is assessing dose escalation safety and efficacy.
7
Etentamig is an investigational therapy not approved in the EU.
Efficacy data of pivekimab sunirine-pvzy in patients with blastic plasmacytoid dendritic cell neoplasm (BPDCN) with baseline skin involvement in the CADENZA study
Post-hoc analysis from CADENZA (
NCT03386513
), evaluating the first-line use of pivekimab sunirine-pvzy in patients with BPDCN and varying degrees of skin involvement. The open-label Phase 1/2 study is assessing overall response rate, overall survival and percentage of eligible patients approved to proceed with a stem cell transplant.
8
Pivekimab sunirine-pvzy is an investigational therapy not approved in the EU.
Details on key oral and poster presentations at the EHA 2026 Congress are available below and the full abstracts are available
here
.
Oral Presentations:
Title
Date/Time
Session
Abstract/ Presentation Number
Clinically Relevant Subgroup Analysis from the Randomized Phase 3 EPCORE FL-1 Trial: Treatment (Tx) Effect of Epcoritamab with Lenalidomide and Rituximab (R
2
) in R/R Follicular Lymphoma (FL)
Thursday, June 11,
17:45 - 18:00 CEST
Oral Session,
K1 Hall
EHA-3041
Short: S229
Results from EPCORE DLBCL-1: Randomized Phase 3 Study of Epcoritamab (Epcor) Vs Investigator's Choice Chemoimmunotherapy (CIT) in Patients with Relapsed/Refractory Large B-Cell Lymphoma (R/R LBCL)
Friday, June 12,
17:15 - 17:30 CEST
Oral Session,
Nobel Hall
EHA-2409
Short: S235
Venetoclax-obinutuzumab for Previously Untreated Chronic Lymphocytic Leukemia: Final Results of the Randomized CLL14 Study
Friday, June 12,
17:30 - 17:45 CEST
Oral Session,
AE1 Hall
EHA-2488
Short: S146
Genetic Biomarkers Predicting Sustained Efficacy of Venetoclax-based Therapies or CIT in Chronic Lymphocytic Leukemia: Final 5-year Analysis of the GAIA/CLL13 Trial
Friday, June 12,
18:15 - 18:30 CEST
Oral Session,
AE1 Hall
EHA-4841
Short: S149
Phase 1 Dose Escalation Safety and Efficacy of Etentamig in Patients with Relapsed or Refractory Light Chain Amyloidosis
Friday, June 12,
18:15 - 18:30 CEST
Oral Session,
Victoria Hall
EHA-1134
Short: S209
Fixed Duration Venetoclax Plus Epcoritamab Shows Favorable Tolerability and High Response Rates with Early Molecular Responses in R/R CLL/SLL: Interim Analysis of the Randomized HOVON 165/AETHER Trial
Sunday, June 14,
11:45 - 12:00 CEST
Oral Session,
A10-11 Hall
EHA-3784
Short: S153
Poster Presentations:
Sustained Remissions Beyond 4 Years with Epcoritamab Monotherapy: Long-term Follow-up Results from the Pivotal EPCORE NHL-1 Trial in Patients with Relapsed or Refractory Large B-cell Lymphoma
Friday, June 12,
18:45 CEST
Poster Session, Hall A
EHA-2191
Short: PF977
Epcoritamab + R-mini-chop Results In 2-year Remissions and High MRD-negativity Rates in Elderly Patients with Newly Diagnosed DLBCL: Results from the EPCORE NHL-2 Trial
Friday, June 12,
18:45 CEST
Poster Session,
Hall A
EHA-2359
Short: PF1007
Reduced CD20 Expression and Intratumoral CD3+ T Cells Following Epcoritamab Treatment Are Associated with Progressive Disease in a Subset of Diffuse Large B-cell Lymphoma and Follicular Lymphoma
Friday, June 12,
18:45 CEST
Poster Session, Hall A
EHA-2343
Short: PF1069
Pharmacodynamic Biomarkers Support the Clinical Benefit of Epcoritamab Plus Rituximab and Lenalidomide (R
2
) In Patients with Relapsed/Refractory Follicular Lymphoma (R/R FL): Analyses from EPCORE FL-1
Friday, June 12,
18:45 CEST
Poster Session, Hall A
EHA-3123
Short: PF1081
Real-world Management Practices with Venetoclax-based Therapy For AML - Results from the Prospective REVIVE Study
Friday, June 12,
18:45 CEST
Poster Session,
Hall A
EHA-3291
Short: PF536
The Efficacy of Pivekimab Sunirine (PVEK) in Patients (PTS) with Blastic Plasmacytoid Dendritic Cell Neoplasm (BPDCN) with Baseline Skin Involvement in the CADENZA Study
Friday, June 12,
18:45 CEST
Poster Session,
Hall A
EHA-1950
Short: PF500
Anchored Matching-adjusted Indirect Comparison of Epcoritamab, Lenalidomide, and Rituximab Vs Tafasitamab, Lenalidomide, and Rituximab in Relapsed/Refractory Follicular Lymphoma: EPCORE FL-1 Vs Inmind
Saturday, June 13,
18:45 CEST
Poster Session, Hall A
EHA-1124
Short: PS2035
Comparative Effectiveness of Epcoritamab, Lenalidomide, and Rituximab in EPCORE FL-1 Vs Real-world Chemoimmunotherapy in Relapsed/Refractory Follicular Lymphoma
Saturday, June 13,
18:45 CEST
Poster Session, Hall A
EHA-3065
Short: PS2042
Comparative Analyses of Epcoritamab in Combination with Lenalidomide and Rituximab Vs Obinutuzumab and Bendamustine in Relapsed/Refractory Follicular Lymphoma
Saturday, June 13,
18:45 CEST
Poster Session, Hall A
EHA-3140
Short: PS2052
Epcoritamab + Chemoimmunotherapy in Patients with Relapsed/Refractory Large B-cell Lymphoma Eligible for Autologous Stem Cell Transplant: Pooled Results from Arms 4 and 10 of EPCORE NHL-2
Saturday, June 13,
18:45 CEST
Poster Session,
Hall A
EHA-2303
Short: PS2070
Fixed-duration Epcoritamab Monotherapy Induces High Response and MRD-negativity Rates in Elderly Patients with Newly Diagnosed Large B-cell Lymphoma and Comorbidities: Results from EPCORE DLBCL-3
Saturday, June 13,
18:45 CEST
Poster Session, Hall A
EHA-2346
Short: PS2082
Epcoritamab In Relapsed/Refractory Diffuse Large B-cell Lymphoma (R/R DLBCL): Insights from the Real-world Epcoritamab Patient Characteristics and Outcomes Research (Real-epcor) Study
Saturday, June 13,
18:45 CEST
Poster Session, Hall A
EHA-2202
Short: PS2086
Epcoritamab Plus Lenalidomide and Rituximab Improves or Preserves Health-related Quality of Life in Patients with Relapsed/Refractory Follicular Lymphoma Who Had High Symptom Burden or Adverse Events
Saturday, June 13,
18:45 CEST
Poster Session, Hall A
EHA-2776
Short: PS2497
Quality of Life and Symptoms with Fixed-duration Acalabrutinib + Venetoclax ± Obinutuzumab Vs Chemoimmunotherapy in Treatment-naive Chronic Lymphocytic Leukemia: Patient-Reported Outcomes from AMPLIFY
Saturday, June 13,
18:45 CEST
Poster Session,
Hall A
EHA-4662
Short: PS1706
Etentamig In Patients (PTS) with Relapsed/Refractory Multiple Myeloma (RRMM) with Prior Exposure to B-cell Maturation Antigen (BCMA)-targeted Therapy
Saturday, June 13,
18:45 CEST
Poster Session,
Hall A
EHA-2799
Short: PS1913
Etentamig (ABBV-383) is an investigational medicine and is not approved by any health authorities worldwide. The safety and efficacy of this medicine is under evaluation as part of ongoing clinical studies. Pivekimab sunirine is not approved in the EU.
EPKINLY
®
/TEPKINLY
®
(epcoritamab) and VENCLEXTA
®
/VENCLYXTO
®
(venetoclax) are approved medicines being investigated for additional uses. Safety and efficacy have not been established for these unapproved additional uses.
EPKINLY
®
/TEPKINLY
®
(epcoritamab) is being co-developed by Genmab and AbbVie as part of the companies' oncology collaboration. The companies share commercial responsibilities in the U.S. and
Japan, with AbbVie responsible for further global commercialization.
VENCLEXTA
®
/VENCLYXTO
®
(venetoclax) is being developed by AbbVie and Roche. It is jointly commercialized by AbbVie and Genentech, a member of the Roche Group, in the U.S. and by AbbVie outside of the U.S.
Additional information on AbbVie clinical trials is available at
.
USE & IMPORTANT SAFETY INFORMATION for EPKINLY
®
(epcoritamab-bysp) in U.S.
What is EPKINLY?
EPKINLY is a prescription medicine used to treat adults with:
certain types of diffuse large B-cell lymphoma (DLBCL) or high-grade B-cell lymphoma that has come back (relapsed) or that did not respond (refractory) after 2 or more treatments.
follicular lymphoma (FL) that has come back or that did not respond to previous treatment, together with lenalidomide and rituximab
follicular lymphoma (FL) that has come back or that did not respond after 2 or more treatments.
EPKINLY for the treatment of DLBCL is approved based on patient response data. Studies are ongoing to confirm the clinical benefit of EPKINLY.
It is not known if EPKINLY is safe and effective in children.
IMPORTANT SAFETY INFORMATION
Important Warnings—EPKINLY can cause serious side effects, including:
Cytokine release syndrome (CRS)
, which is common during treatment with EPKINLY and can be serious or lead to death. To help reduce your risk of CRS, you will receive EPKINLY on a step-up dosing schedule (when you receive 2 or 3 smaller step-up doses of EPKINLY before your first full dose during your first cycle of treatment), and you may also receive other medicines before and for 3 days after receiving EPKINLY. If your dose of EPKINLY is delayed for any reason, you may need to repeat the step-up dosing schedule.
Neurologic problems
that can be serious, and can be life-threatening, and lead to death. Neurologic problems may happen days or weeks after you receive EPKINLY.
People with DLBCL or high-grade B-cell lymphoma
may be hospitalized after receiving their first full dose of EPKINLY on Day 15 of Cycle 1 due to the risk of CRS and neurologic problems.
People with FL
may be hospitalized after receiving their first full dose of EPKINLY on Day 22 of Cycle 1 due to the risk of CRS and neurologic problems.
Tell your healthcare provider or get medical help right away
if you develop a fever of 100.4°F (38°C) or higher; dizziness or lightheadedness; trouble breathing; chills; fast heartbeat; feeling anxious; headache; confusion; shaking (tremors); problems with balance and movement, such as trouble walking; trouble speaking or writing; confusion and disorientation; drowsiness, tiredness or lack of energy; muscle weakness; seizures; or memory loss.
These may be symptoms of CRS or neurologic problems.
If you have any symptoms that impair consciousness,
do not
drive or use heavy machinery or do other dangerous activities until your symptoms go away.
EPKINLY can cause other serious side effects, including:
Infections
that may lead to death. Your healthcare provider will check you for signs and symptoms of infection before and during treatment and treat you as needed if you develop an infection. You should receive medicines from your healthcare provider before you start treatment to help prevent infection. Tell your healthcare provider right away if you develop any symptoms of infection during treatment, including fever of 100.4°F (38°C) or higher, cough, chest pain, tiredness, shortness of breath, painful rash, sore throat, pain during urination, feeling weak or generally unwell, or confusion.
Low blood cell counts,
which can be serious or severe. Your healthcare provider will check your blood cell counts during treatment. EPKINLY may cause low blood cell counts, including low white blood cells (neutropenia and lymphopenia), which can increase your risk for infection; low red blood cells (anemia), which can cause tiredness and shortness of breath; and low platelets (thrombocytopenia), which can cause bruising or bleeding problems.
Your healthcare provider will monitor you for symptoms of CRS, neurologic problems, infections, and low blood cell counts during treatment with EPKINLY. Your healthcare provider may temporarily stop or completely stop treatment with EPKINLY if you develop certain side effects.
Before you receive EPKINLY, tell your healthcare provider about all your medical conditions, including if you
have an infection, are pregnant or plan to become pregnant, or are breastfeeding or plan to breastfeed. If you receive EPKINLY while pregnant, it may harm your unborn baby.
If you are a female who can become pregnant
, your healthcare provider should do a pregnancy test before you start treatment with EPKINLY and you should use effective birth control (contraception) during treatment and for 4 months after your last dose of EPKINLY. Tell your healthcare provider if you become pregnant or think that you may be pregnant during treatment with EPKINLY. Do not breastfeed during treatment with EPKINLY and for 4 months after your last dose of EPKINLY.
The most common side effects of EPKINLY when used alone in DLBCL or high-grade B-cell lymphoma or FL include
CRS, injection site reactions, tiredness, muscle and bone pain, fever, diarrhea, COVID-19, rash, and stomach-area (abdominal) pain.
The most common severe abnormal laboratory test results with EPKINLY when used alone
include decreased white blood cells, decreased red blood cells, and decreased platelets.
The most common side effects of EPKINLY when used together with lenalidomide and rituximab in FL include
rash
,
upper respiratory tract infections, tiredness, injection site reactions, constipation, diarrhea, CRS, pneumonia, COVID-19, and fever.
The most common severe abnormal laboratory test results with EPKINLY when used together with lenalidomide and rituximab
include decreased white blood cells and decreased platelets.
These are not all of the possible side effects of EPKINLY. Call your doctor for medical advice about side effects.
You are encouraged to report side effects to the FDA at (800) FDA-1088 or
or to Genmab US, Inc. at 1-855-4GENMAB (1-855-443-6622).
Please see
Full Prescribing Information
and
Medication Guide
,
including Important Warnings.
Globally, prescribing information varies. Refer to the individual country product label for complete information.
USE & IMPORTANT SAFETY INFORMATION for VENCLEXTA
®
(venetoclax tablets) in U.S.
Uses
VENCLEXTA is a prescription medicine used:
to treat adults with chronic lymphocytic leukemia (CLL) or small lymphocytic lymphoma (SLL).
in combination with azacitidine, or decitabine, or low-dose cytarabine to treat adults with newly diagnosed acute myeloid leukemia (AML) who:
‒ are 75 years of age or older, or
‒ have other medical conditions that prevent the use of standard chemotherapy.
It is not known if VENCLEXTA is safe and effective in children.
Important Safety Information
What is the most important information I should know about VENCLEXTA?
VENCLEXTA can cause serious side effects, including:
Tumor lysis syndrome (TLS).
TLS is caused by the fast breakdown of cancer cells. TLS can cause kidney failure, the need for dialysis treatment, and may lead to death. Your healthcare provider will do tests to check your risk of getting TLS before you start taking VENCLEXTA. You will receive other medicines before starting and during treatment with VENCLEXTA to help reduce your risk of TLS. You may also need to receive intravenous (IV) fluids into your vein. Your healthcare provider will do blood tests to check for TLS when you first start and during treatment with VENCLEXTA. It is important to keep your appointments for blood tests. Tell your healthcare provider right away if you get any symptoms of TLS during treatment with VENCLEXTA, including fever, chills, nausea, vomiting, confusion, shortness of breath, seizures, irregular heartbeat, dark or cloudy urine, unusual tiredness, or muscle or joint pain.
Drink plenty of water during treatment with VENCLEXTA to help reduce your risk of getting TLS.
Drink 6 to 8 glasses (about 56 ounces total) of water each day, starting 2 days before your first dose, on the day of your first dose of VENCLEXTA, and each time your dose is increased.
Your healthcare provider may delay, decrease your dose, or stop treatment with VENCLEXTA if you get symptoms of TLS. When restarting VENCLEXTA after stopping for 1 week or longer, your healthcare provider may check again for your risk of TLS and change your dose.
Who should not take VENCLEXTA?
Patients taking certain medicines during the beginning of VENCLEXTA (when the dose is being slowly increased) are at increased risk of TLS.
Tell your healthcare provider about all the medicines you take,
including prescription and over-the- counter medicines, vitamins, and herbal supplements. VENCLEXTA and other medicines may affect each other causing serious side effects.
Do not start new medicines during treatment with VENCLEXTA without first talking with your healthcare provider.
Before taking VENCLEXTA, tell your healthcare provider about all of your medical conditions, including if you:
have kidney or liver problems.
have problems with your body salts or electrolytes, such as potassium, phosphorus, or calcium.
have a history of high uric acid levels in your blood or gout.
are scheduled to receive a vaccine. You should not receive a "live vaccine" before, during, or after treatment with VENCLEXTA, until your healthcare provider tells you it is okay. If you are not sure about the type of immunization or vaccine, ask your healthcare provider. These vaccines may not be safe or may not work as well during treatment with VENCLEXTA.
are pregnant or plan to become pregnant. VENCLEXTA may harm your unborn baby.
Females who are able to become pregnant:
‒ Your healthcare provider should do a pregnancy test before you start treatment with VENCLEXTA.
‒ Use effective birth control during treatment and for 30 days after the last dose of VENCLEXTA.
‒ If you become pregnant or think you are pregnant, tell your healthcare provider right away.
are breastfeeding or plan to breastfeed. It is not known if VENCLEXTA passes into your breast milk. Do not breastfeed during treatment with VENCLEXTA and for 1 week after the last dose.
What should I avoid while taking VENCLEXTA?
You should not drink grapefruit juice or eat grapefruit, Seville oranges (often used in marmalades), or starfruit during treatment with VENCLEXTA. These products may increase the amount of VENCLEXTA in your blood.
What are the possible side effects of VENCLEXTA?
VENCLEXTA can cause serious side effects, including:
Low white blood cell counts (neutropenia).
Your healthcare provider will do blood tests to check your blood count during treatment with VENCLEXTA and may pause dosing of VENCLEXTA or give you medicines to help treat your neutropenia if it is severe.
Infections.
Death and serious infections such as pneumonia and blood infection (sepsis) have happened during treatment with VENCLEXTA. Your healthcare provider will closely monitor and treat you right away if you get a fever or any signs of infection during treatment with VENCLEXTA.
Tell your healthcare provider right away if you get a fever or any signs of an infection during treatment with VENCLEXTA.
The most common side effects of VENCLEXTA when used in combination with acalabrutinib in people with CLL or SLL include
low white blood cell count, headache, diarrhea, muscle and bone pain, and COVID-19.
The most common side effects of VENCLEXTA when used in combination with obinutuzumab or rituximab or alone in people with CLL or SLL include
low white blood cell count; low platelet count; low red blood cell count; diarrhea; nausea; upper respiratory tract infection; cough; muscle and joint pain; tiredness; and swelling of your arms, legs, hands, and feet.
The most common side effects of VENCLEXTA in combination with azacitidine or decitabine or low-dose cytarabine in people with AML include
nausea; diarrhea; low platelet count; constipation; low white blood cell count; fever with low white blood cell count; tiredness; vomiting; swelling of arms, legs, hands, or feet; fever; infection in lungs; shortness of breath; bleeding; low red blood cell count; rash; stomach (abdominal) pain; infection in your blood; muscle and joint pain; dizziness; cough; sore throat; and low blood pressure.
Your healthcare provider may temporarily stop VENCLEXTA treatment, decrease your dose, or completely stop treatment if you get severe side effects.
VENCLEXTA may cause fertility problems in males. This may affect your ability to father a child. Talk to your healthcare provider if you have concerns about fertility.
These are not all the possible side effects of VENCLEXTA. Call your doctor for medical advice about side effects.
You are encouraged to report side effects of prescription drugs to the FDA. Visit
or call 1-800-FDA-1088.
If you cannot afford your medication, contact genentech-access.com/patient/brands/venclexta for assistance.
Please see full
Prescribing Information
. Globally, prescribing information varies. Refer to the individual country product label for complete information.
U.S. Prescribing Information for AbbVie Medicines
Please see full
Prescribing Information
including BOXED WARNING for DECNUPAZ (pivekimab sunirine-pvzy)
About AbbVie
AbbVie's mission is to discover and deliver innovative medicines and solutions that solve serious health issues today and address the medical challenges of tomorrow. We strive to have a remarkable impact on people's lives across several key therapeutic areas including immunology, neuroscience and oncology – and products and services in our Allergan Aesthetics portfolio. For more information about AbbVie, please visit us at
. Follow @abbvie on
LinkedIn,
Facebook
,
Instagram
,
X
and
YouTube.
About
AbbVie in Oncology
AbbVie is committed to elevating standards of care and bringing transformative therapies to patients worldwide living with difficult-to-treat cancers. We are advancing a dynamic pipeline of investigational therapies across a range of cancer types in both blood cancers and solid tumors. We are focusing on creating targeted medicines that either impede the reproduction of cancer cells or enable their elimination. We achieve this through various, targeted treatment modalities and biology interventions, including small molecule therapeutics, antibody-drug conjugates (ADCs), immuno-oncology-based therapeutics, multispecific antibody and novel CAR-T platforms. Our dedicated and experienced team joins forces with innovative partners to accelerate the delivery of potential breakthrough medicines.
Today, our expansive oncology portfolio comprises approved and investigational treatments for a wide range of blood cancers and solid tumors. We are evaluating more than 35 investigational medicines in multiple clinical trials across some of the world's most widespread and debilitating cancers. As we work to have a remarkable impact on people's lives, we are committed to exploring solutions to help patients obtain access to our cancer medicines. For more information, please visit
.
Forward-Looking Statements
Some statements in this news release are, or may be considered, forward-looking statements for purposes of the Private Securities Litigation Reform Act of 1995. The words "believe," "expect," "anticipate," "project" and similar expressions and uses of future or conditional verbs, generally identify forward-looking statements. AbbVie cautions that these forward-looking statements are subject to risks and uncertainties that may cause actual results to differ materially from those expressed or implied in the forward-looking statements. Such risks and uncertainties include, but are not limited to, challenges to intellectual property, competition from other products, difficulties inherent in the research and development process, adverse litigation or government action, changes to laws and regulations applicable to our industry, the impact of global macroeconomic factors, such as economic downturns or uncertainty, international conflict, trade disputes and tariffs, and other uncertainties and risks associated with global business operations. Additional information about the economic, competitive, governmental, technological and other factors that may affect AbbVie's operations is set forth in Item 1A, "Risk Factors," of AbbVie's 2025 Annual Report on Form 10-K, which has been filed with the Securities and Exchange Commission, as updated by its Quarterly Reports on Form 10-Q and in other documents that AbbVie subsequently files with the Securities and Exchange Commission that update, supplement or supersede such information. AbbVie undertakes no obligation, and specifically declines, to release publicly any revisions to forward-looking statements as a result of subsequent events or developments, except as required by law.
Contacts:
Media:
Anisha Bagchi Manix
Email:
anisha.manix@abbvie.com
Investors:
Liz Shea
Email:
liz.shea@abbvie.com
_________________________________
1
Tessoulin B, Nijland M, et al. Clinically Relevant Subgroup Analysis From The Randomized Phase 3 EPCORE FL-1 Trial: Treatment (Tx) Effect Of Epcoritamab With Lenalidomide And Rituximab (R²) In R/R Follicular Lymphoma (Fl). Abstract EHA-3041 presented at the European Hematology Association Congress 2026. Stockholm, Sweden.
2
Fox C, Inchiappa L, et al. Results From EPCORE DLBCL-1: Randomized Phase 3 Study Of Epcoritamab (Epcor) Vs Investigator's Choice Chemoimmunotherapy (Cit) In Patients With Relapsed/Refractory Large B-Cell Lymphoma (R/R Lbcl). Abstract EHA-2409 presented at the European Hematology Association Congress 2026. Stockholm, Sweden.
3
Tausch E, Schneider C, et al. Genetic Biomarkers Predicting Sustained Efficacy of Venetoclax-based Therapies or CIT in Chronic Lymphocytic Leukemia: Final 5-yr Analysis of the GAIA/CLL13 Trial. Abstract EHA-4841 presented at the European Hematology Association Congress 2026. Stockholm, Sweden.
4
Fischer K, Al-Sawaf O ,et al. Venetoclax-obinutuzumab for Previously Untreated Chronic Lymphocytic Leukemia: Final Results of the Randomized CLL14 Study. Abstract EHA-2488 presented at the European Hematology Association Congress 2026. Stockholm, Sweden.
5
Moshe Y, Wolach O, et al. Real-world Management Practices with Venetoclax-based Therapy For AML- Results from the Prospective REVIVE Study. Abstract EHA- 3291 presented at the European Hematology Association Congress 2026. Stockholm, Sweden.
6
Chhabra S, Searle E, et al. Etentamig In Patients with Relapsed/Refractory Multiple Myeloma (RRMM) with Prior Exposure to B-cell Maturation Antigen (BCMA)-targeted Therapy. Abstract EHA-2799 presented at the European Hematology Association Congress 2026. Stockholm, Sweden.
7
Kastritis E, Huart A, et al. Phase 1 Dose Escalation Safety and Efficacy of Etentamig in Patients with Relapsed or Refractory Light Chain Amyloidosis. Abstract EHA-1134 presented at the European Hematology Association Congress 2026. Stockholm, Sweden.
8
Pemmaraju N, Marconi G, et al. Efficacy of pivekimab sunirine-pvzy in patients with blastic plasmacytoid dendritic cell neoplasm (BPDCN) with baseline skin involvement in the CADENZA study Abstract EHA-1950 presented at the European Hematology Association Congress 2026. Stockholm, Sweden.
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SOURCE AbbVie
临床结果临床3期临床1期上市批准临床2期
100 项与 Etentamig 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 |
|---|---|---|---|---|
| 浆细胞白血病 | 临床3期 | 美国 | 2024-05-19 | |
| 浆细胞白血病 | 临床3期 | 中国 | 2024-05-19 | |
| 浆细胞白血病 | 临床3期 | 日本 | 2024-05-19 | |
| 浆细胞白血病 | 临床3期 | 澳大利亚 | 2024-05-19 | |
| 浆细胞白血病 | 临床3期 | 奥地利 | 2024-05-19 | |
| 浆细胞白血病 | 临床3期 | 比利时 | 2024-05-19 | |
| 浆细胞白血病 | 临床3期 | 加拿大 | 2024-05-19 | |
| 浆细胞白血病 | 临床3期 | 捷克 | 2024-05-19 | |
| 浆细胞白血病 | 临床3期 | 丹麦 | 2024-05-19 | |
| 浆细胞白血病 | 临床3期 | 法国 | 2024-05-19 |
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临床结果
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适应症
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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 |
|---|
临床1期 | 34 | 顧鬱夢齋顧鏇醖蓋膚獵(鹽製夢鏇憲鬱鬱顧憲鑰) = 構製製簾獵築鹹製鹽積 夢顧顧鹹糧窪廠遞廠窪 (齋鹽鹽膚餘範獵壓醖廠 ) 更多 | 积极 | 2026-05-12 | |||
临床1期 | 多发性骨髓瘤 三线 | 85 | 窪顧膚夢醖糧蓋艱範窪(觸膚鏇廠觸選鑰鬱網構) = were neutropenia (78%), anemia (28%), and thrombocytopenia (22%). 鑰繭網膚遞衊製壓觸窪 (願壓壓艱衊繭鬱願鏇醖 ) 更多 | 积极 | 2025-12-06 | ||
临床1期 | 33 | (Relapsed/Refractory Multiple Myeloma) | 襯膚願醖廠窪網鹽鏇鹽(餘壓願範鑰窪遞築壓壓) = no recurrent CRS events were observed beyond Cycle 1 夢糧簾廠鏇製鏇壓簾餘 (醖繭築廠衊糧簾網窪觸 ) 更多 | 积极 | 2025-12-06 | ||
临床1/2期 | 12 | 鏇醖築鑰繭製築鹽壓鹽(鹽淵築鬱醖繭積醖鏇壓) = 鹹廠壓憲簾淵獵簾簾憲 選積選顧簾簾廠窪衊衊 (衊膚蓋鑰衊膚鬱夢鏇襯 ) 更多 | 积极 | 2025-12-06 | |||
临床1期 | 20 | 鬱鏇壓糧醖憲壓壓膚願(願淵淵鏇淵憲淵鹽繭襯) = 製觸淵遞齋顧鹽鏇膚淵 淵鬱壓窪繭製艱選遞鑰 (衊繭齋選醖顧襯齋淵製, 0.2) | 积极 | 2025-12-06 | |||
(MRD-negative (<10-5)) | 鬱鏇壓糧醖憲壓壓膚願(願淵淵鏇淵憲淵鹽繭襯) = 齋繭鏇糧製夢鏇蓋憲築 淵鬱壓窪繭製艱選遞鑰 (衊繭齋選醖顧襯齋淵製, 0.2) | ||||||
临床1期 | 复发性多发性骨髓瘤 BCMA | CD3 | 146 | 鑰網壓鏇蓋醖壓廠齋鑰(鏇餘構簾範壓鑰膚艱憲) = CRS incidence was 30% (4% G2; No ≥G3 events) with median time to CRS onset of 22.3 (5.5-29.6) hours; and median time to CRS resolution of 20.7 (1.8-131.7) hours 糧製構製積餘積遞淵鏇 (糧壓積蓋範製製膚夢夢 ) 更多 | 积极 | 2025-05-30 | ||
临床1期 | 复发性多发性骨髓瘤 BCMA | CD3 | 146 | 鹹淵糧襯膚蓋簾願鹹簾(鹽鑰醖鑰繭鹹餘範築鹽) = 壓範築淵鹽願窪衊製積 選夢構壓繭簾積夢獵鹹 (廠簾齋獵壓構繭獵網廠 ) 更多 | 积极 | 2025-05-14 | ||
临床1期 | 146 | Etentamig (Non-Black patients) | 鬱鬱廠膚衊襯構醖遞壓(範鹹壓齋遞膚廠淵窪憲) = 壓鏇鬱選鏇網齋憲網觸 鑰獵鑰夢製獵鹽遞鏇餘 (網鹽網夢齋鹽窪願齋遞, 21% grade 1 and 5% grade 2) 更多 | 积极 | 2025-05-14 | ||
Etentamig (Black patients) | 鬱鬱廠膚衊襯構醖遞壓(範鹹壓齋遞膚廠淵窪憲) = 簾鬱積鏇艱獵鏇築顧願 鑰獵鑰夢製獵鹽遞鏇餘 (網鹽網夢齋鹽窪願齋遞, all grade 1) 更多 | ||||||
临床1期 | 220 | ABBV-383 60mg Q4W | 壓製衊選獵衊構積艱顧(壓鏇淵築壓齋衊製鹽襯) = 築鹹齋衊願獵醖簾廠選 觸簾糧鹹壓繭顧窪鏇網 (衊願鹽鹽艱積獵製構襯 ) 更多 | 积极 | 2024-05-24 | ||
ABBV-383 40mg Q3W | 壓製衊選獵衊構積艱顧(壓鏇淵築壓齋衊製鹽襯) = 遞繭醖鑰鬱艱願獵範網 觸簾糧鹹壓繭顧窪鏇網 (衊願鹽鹽艱積獵製構襯 ) 更多 | ||||||
临床1期 | 复发性多发性骨髓瘤 BCMA- | CD3 | 220 | ABBV-383 20 mg Q3W | 積鹽糧糧餘鹹鬱餘構願(顧膚齋餘觸選廠鬱壓膚) = 鹽鬱鹹壓顧餘鏇淵築鏇 遞獵積膚齋網夢選餘鏇 (積壓鬱蓋餘積鏇醖餘憲 ) 更多 | 积极 | 2024-05-24 | |
ABBV-383 40 mg Q3W | 積鹽糧糧餘鹹鬱餘構願(顧膚齋餘觸選廠鬱壓膚) = 鬱網鬱選鏇鬱夢積齋選 遞獵積膚齋網夢選餘鏇 (積壓鬱蓋餘積鏇醖餘憲 ) 更多 |
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