迈泽妥单抗(Mezagitamab) - 药物靶点：CD38_在研适应症：免疫球蛋白a肾病，免疫性血小板减少症，抗体介导的排斥反应_专利_临床

概要

基本信息

药物类型

单克隆抗体

别名

Anti-CD38 mAb(Takeda)、TAK-079、TAK079

靶点

CD38

作用方式

抑制剂

作用机制

CD38抑制剂(淋巴细胞分化抗原CD38抑制剂)、ADCC(抗体依赖的细胞毒作用)

治疗领域

免疫系统疾病血液及淋巴系统疾病肿瘤+ [1]

在研适应症

免疫球蛋白a肾病免疫性血小板减少症抗体介导的排斥反应+ [1]

非在研适应症

重症肌无力复发性多发性骨髓瘤系统性红斑狼疮

原研机构

Takeda Pharmaceutical Co., Ltd.

在研机构

Spera Pharma, Inc.

Takeda Pharmaceutical Co., Ltd.

武田（中国）国际贸易有限公司

+ [1]

非在研机构

Millennium Pharmaceuticals, Inc.

权益机构

Takeda Pharmaceutical Co., Ltd.

XOMA Royalty Corp.

BioInvent International AB

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

特殊审评快速通道 (美国)、孤儿药 (美国)、孤儿药 (欧盟)、孤儿药 (日本)、儿科研究计划 (欧盟)

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结构/序列

Sequence Code 210789L

来源: *****

Sequence Code 1191632864H

来源: *****

关联

12

项与迈泽妥单抗相关的临床试验

NCT07613359

/ Not yet recruiting临床2期

A Double-Blind, Placebo-Controlled, Multicenter, Randomized, Phase 2 Trial to Evaluate the Safety and Efficacy of Mezagitamab (TAK-079) in Kidney Transplant Recipients With Late Antibody-Mediated Rejection (AMR)

Antibody-mediated rejection (AMR) is a major cause of worsening kidney function after a kidney transplant (kidney allograft dysfunction) and can lead to kidney failure. AMR happens when the kidney recipient's immune system makes antibodies that attack the donor kidney. Antibodies are proteins made by the immune system to recognize foreign cells. Over time, this attack can damage kidney tissue and cause the transplant to fail. Because AMR can be serious, there is a need for treatments that are safe, work well, and are supported by good evidence.
The main aim of this study is to find out how safe mezagitamab is and how well adults with AMR tolerate it compared with placebo. A placebo looks like medicine but has no active ingredients. The study will also look at whether mezagitamab helps to control inflammation in the transplanted kidney and helps keep kidney function stable, compared with placebo.
Participants will be placed by chance in 1 of the 3 treatment groups in equal numbers. Two groups will receive mezagitamab in two different doses. One group will receive placebo. This means that out of every 3 participants, 2 will receive mezagitamab and 1 will receive placebo.
During the study, participants will visit their study clinic several times.

开始日期2026-09-01

申办/合作机构

Takeda Pharmaceutical Co., Ltd.

NCT06948318

/ Recruiting临床3期

A Phase 3, Open-label, Multicenter Continuation Trial to Evaluate the Long-term Safety and Efficacy of Mezagitamab Subcutaneous Injection in Adults With Chronic Primary Immune Thrombocytopenia

Primary immune thrombocytopenia (ITP) is a condition where the immune system mistakenly destroys platelets, which are cells that help stop bleeding. This leads to a lower number of platelets, making it easier to bruise or bleed. The main aim of this study is to check how safe mezagitamab is and how well it is tolerated by adults with chronic primary ITP, if given over a longer time. Other aims are to learn how effective treatment with mezagitamab is and how the body processes it (called pharmacokinetics or PK) over a longer time.
Participants of the following previous mezagitamab studies will be invited to join this continuation study: TAK-079-3002 and TAK-079-1004. In this continuation study, participants will receive mezagitamab when certain protocol criteria are met.
During the study, participants will visit their study clinic several times.

开始日期2025-08-14

申办/合作机构

Takeda Pharmaceutical Co., Ltd.

NCT06963827

/ Recruiting临床3期

A Phase 3 Multicenter, Randomized, Double-Blind, Placebo Controlled Trial to Evaluate Efficacy and Safety of Mezagitamab (TAK-079) in Study Participants With Primary IgA Nephropathy in Combination With Stable Background Therapy

Immunoglobulin A nephropathy (IgAN) is a kidney condition. It happens when the body's immune system creates groups of proteins (called immune complexes) that build-up in the kidneys causing swelling (inflammation). Over time, this inflammation may lead to kidney damage and cause the kidneys to no longer work properly. The main aim of this study is to check how well mezagitamab changes protein levels in the urine (proteinuria) compared to placebo in adults with primary IgAN. A placebo looks like medicine but doesn't have any active ingredients in it. Other aims are to check how safe mezagitamab is and how well participants with primary IgAN can tolerate it compared to placebo, and to find out if and how well mezagitamab continues to maintain kidney function over the long term compared to placebo.
Participants will be placed in 1 of the 2 treatment groups; the main group and the open-label group. In the main group, participants will be placed in 1 of the 2 treatment groups by chance (either mezagitamab or placebo) at a 2:1 ratio. This means that out of 3 participants, 2 will receive mezagitamab and 1 will receive placebo. The participants will receive either mezagitamab or placebo for almost half a year in two 1-year cycles. They will be observed for another half year in each 1-year cycle and will have check-ups about every month during this time.
In the open-label group, a small number of participants who have lower levels of protein in their urine or have kidneys that do not filter the blood well, will receive mezagitamab treatment. This will include participants who have previously received mezagitamab in another study, TAK-079-1006. Every participant will receive mezagitamab in the same way as those in the main group receiving mezagitamab.
During the study, participants will visit their study clinic several times.

开始日期2025-07-15

申办/合作机构

Takeda Pharmaceutical Co., Ltd.

100 项与迈泽妥单抗相关的临床结果

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100 项与迈泽妥单抗相关的转化医学

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100 项与迈泽妥单抗相关的专利（医药）

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55

项与迈泽妥单抗相关的文献（医药）

2026-04-09·NEW ENGLAND JOURNAL OF MEDICINE

A Phase 2 Randomized Trial of Mezagitamab in Primary Immune Thrombocytopenia

Article

作者: Syrigou, Antonia ; Miura, Katsuhiro ; Nguyen, Van Anh ; Radinoff, Atanas ; Skelton, Emily ; Yang, Renchi ; Patriarca, Andrea ; Sapunarova, Katya ; Wang, Scarlett ; Patwari, Parth ; Pulanić, Dražen ; Yee, Donald L. ; Kuter, David J.

BACKGROUND:

Immune thrombocytopenia (ITP) is a disorder of increased platelet destruction and reduced platelet production and is associated with an increased bleeding risk and a compromised quality of life. Available therapies are ineffective in at least 20% of cases. Mezagitamab is an anti-CD38 antibody that targets plasma cells, plasmablasts, and natural killer cells.

METHODS:

We conducted this multicenter, double-blind, randomized, placebo-controlled trial to assess the safety and efficacy of mezagitamab at a dose of 100 mg, 300 mg, or 600 mg, as compared with placebo, administered subcutaneously once weekly for 8 weeks in adults with persistent or chronic ITP (mean platelet count on ≥2 measurements, <30,000 per microliter). The primary end point was adverse events. A key secondary efficacy end point was a platelet response (defined by a platelet count of ≥50,000 per microliter and ≥20,000 per microliter above the baseline value) on at least two visits at any time through week 16.

RESULTS:

In the combined mezagitamab groups (28 participants), the mean age was 50 years (range, 24 to 88) and the mean number of previous ITP therapies was 4 (range, 1 to 9); in the combined placebo groups (13 participants), the mean age was 39 years (range, 20 to 65) and the mean number of previous ITP therapies was 4 (range, 1 to 13). The mean baseline platelet count was 19,100 and 17,300 per microliter, respectively. Adverse events were reported in 19 of 28 participants (68%) in the combined mezagitamab groups and in 9 of 13 participants (69%) in the combined placebo groups; adverse events of grade 3 or higher in 5 of 28 participants (18%) and in 3 of 13 participants (23%), respectively; and serious adverse events in 4 of 28 participants (14%) and in 1 of 13 participants (8%). Through week 16, a platelet response was observed in 10 of 11 participants (91%) in the mezagitamab 600-mg group and in 3 of 13 participants (23%) in the combined placebo groups.

CONCLUSIONS:

Treatment with mezagitamab led to increased platelet counts, with a safety profile that appeared to be similar to that of placebo among participants with persistent or chronic ITP. (Funded by Takeda Development Center Americas; ClinicalTrials.gov number, NCT04278924.).

2026-04-01·Current Opinion in Organ Transplantation

Managing the highly sensitized kidney transplant patient

Review

作者: Jackson, Kyle R. ; Parsons, Ronald F.

Purpose of review:

Highly sensitized kidney transplant candidates, particularly those with calculated panel reactive antibody (CPRA) ≥99.9%, face significant immunologic barriers to transplantation. This review highlights recent clinical strategies that have improved transplant access and outcomes in this population, with a focus on allocation policy, kidney-paired donation, and desensitization.

Recent findings:

Updates from national allocation systems and kidney-paired donation programs have demonstrated substantial gains in transplant access for many highly sensitized candidates. However, those with CPRA at least 99.9% remain difficult to match. Novel desensitization approaches, such as imlifidase, proteasome inhibitors, anti-CD38 mAbs, and early-phase CAR T-cell therapies have shown promise in selected patients. Increasingly, immunologic phenotyping or gene expression profiling may help tailor desensitization strategies to individual recipients.

Summary:

Most highly sensitized candidates now achieve transplant through allocation policy or paired donation. For those with CPRA at least 99.9%, desensitization will likely remain an important tool to facilitate transplantation. Emerging therapies and immunologic profiling may help individualize treatment and expand transplant access for this challenging group.

2026-01-06·CLINICAL AND EXPERIMENTAL IMMUNOLOGY

Evolving understandings for the roles of CD38 protein in autoimmunity and autoimmune disease

Review

作者: Ares, Irma ; Zhang, Jieying ; Maximiliano, Jorge-Enrique ; Lopez-Torres, Bernardo ; Wang, Ping ; Ye, Xiaochun ; Anadón, Arturo ; Wang, Xu ; Martínez-Larrañaga, María-Rosa ; Song, Mengping ; Martínez, Marta ; Martínez, María-Aránzazu

Abstract:

Autoimmune diseases are chronic idiopathic disorders characterized by inflammatory responses. Cluster of differentiation 38 (CD38), a surface molecule with enzymatic and signalling capabilities, contributes to the regulation of NAD+ metabolism and mediates various intracellular pathways. Recent research has revealed the influence of the CD38 protein in the pathogenesis of autoimmune diseases. During inflammation, CD38 is involved in regulating biological processes such as cell recruitment, cell activation, cytokine and chemokine release, antigen presentation, and phagocytosis. Dysfunctional CD38 induces autoimmune diseases. CD38 is expressed at low levels in various haematopoietic systems and tissues but exhibits elevated expression in multiple myeloma and plasma cells. CD38-targeted monoclonal antibodies with favourable therapeutic effects have been discovered, such as isatuximab, daratumumab, and mezagitamab. Although CD38-targeted antibodies were originally developed to eliminate malignant immune cells and inhibit their strong activation, these monoclonal antibodies can also inhibit autoantibodies production in autoimmune diseases. CD38 protein is a promising biomarker of autoimmune disease diagnosis and a potential therapeutic target for the treatment of autoimmune diseases. In this review article, we will focus on the latest findings on the involvement of CD38 in autoimmunity and autoimmune disease and assess the value of research and therapeutic application of CD38 in disease control.

78

项与迈泽妥单抗相关的新闻（医药）

2026-05-29

·聊聊血液

追寻治愈：概述免疫性血小板减少症的现代疗法

免疫性血小板减少症是一种自身免疫性疾病，历史上脾切除术和干细胞移植可使部分患者获得长期缓解甚至“治愈”。近年来，多种现代药物（如TPO-RA、利妥昔单抗、BTK抑制剂等）改善了ITP的治疗，且部分患者可在停药后仍维持缓解。近日一篇综述探讨了如何定义ITP的“治愈”，回顾了历史与当前疗法，分析了有潜力的疾病修饰策略。点击文字下载原文The hunt for a cure modern medical approaches for immune thrombocytopenia.pdf 文章核心亮点历史疗法（如脾切除术、强化免疫抑制）可在部分患者中实现治愈因副作用和长期后遗症，历史疗法在现代已较少使用早期使用TPO-RA（血小板生成素受体激动剂）或免疫调节疗法可诱导SROT 靶向性生物制剂可在难治性患者中诱导持久缓解现代药物治疗实现疾病修饰乃至治愈是有希望的如何定义ITP的“治愈” 理论定义：血小板计数恢复正常 + 自身免疫反应完全消除现实局限：目前无验证方法可确定自身免疫记忆是否被根除；ITP病理异质性大，缺乏可靠诊断/追踪/预测复发的标志物实际可行的治愈标准：长期稳定的正常血小板计数 + 异常实验室指标（如抗血小板抗体、细胞因子紊乱等）恢复正常。注意：即便“治愈”，治疗本身可能带来长期后遗症，影响生活质量。脾切除术是否可治愈ITP？疗效：初始反应率80–90%，5年以上持续缓解率约50–70%。问题：并发症率~10%，存在感染和静脉血栓的不可逆风险患者满意度低（I-WISh调查中仅38%满意）即使血小板正常的患者中，9%后悔手术，14%报告长期后遗症脾切除术后20+年仍可复发术后存在持续性免疫表型改变，本质上创造了"无脾"这一新疾病状态结论：脾切除可能治愈部分患者，但因缺乏生物标志物无法识别谁被治愈，且代价显著。哪些患者适合追求“治愈”？文章提出四个典型病例，强调治疗需个体化：自然缓解率：儿童70–80%，成人约30%。高危人群：Evans综合征、继发于自身免疫病或淋巴增殖疾病者、需多线治疗者。 ITP病理生理与治愈策略关键机制：脾：血小板破坏的主要场所，也是自身免疫记忆细胞（长寿命浆细胞、记忆B细胞）的“巢穴”。 B细胞：BAFF促进B细胞生存与复发。 T细胞：Treg功能下降，Th1/Th17极化，CD8+ TEMRA细胞克隆扩增与难治性相关。两大治疗策略：早期免疫调节：防止疾病复杂化、记忆固化。深度免疫清除：用于难治性患者，如CAR-T、双特异性抗体。接近“治愈”的现代治疗策略早期使用利妥昔单抗（抗CD20）与高剂量地塞米松联用，6个月缓解率提高（63% vs 36%），但不良反应增加。低剂量方案在某些中心使用，效果良好。早期免疫抑制剂（如霉酚酸酯） FLIGHT试验显示MMF联合激素可降低治疗失败率（22% vs 44%），但影响生活质量。 TPO-RA 免疫调节作用：改善Treg功能，降低抗血小板抗体。停药后持续缓解率：约30–40%（尤其在早期使用患者中更高）。多项研究表明越早使用，SROT率越高。 BAFF抑制剂（如ianalumab、belimumab）联合利妥昔单抗或TPO-RA可提高停药后缓解率，延长无治疗失败时间。抗CD38单抗（达雷妥尤单抗、mezagitamab）可清除长寿命浆细胞，部分难治性患者获得长期缓解（>20个月）。其他尝试全反式维甲酸：提高6个月缓解率，但可能只是延迟复发。奥司他韦：抑制血小板去唾液酸化，联合激素提高6个月缓解率。深度免疫清除策略高剂量环磷酰胺 + 自体HSCT 难治性患者中约43%获得持续完全缓解，但存在治疗相关死亡风险（~7–11%）。 CAR-T细胞治疗 CD19 CAR-T在难治性ITP和AIHA中显示出持久缓解（如11例AIHA中82%持续缓解）。复发者可能出现BCMA+长寿命浆细胞，提示可靶向BCMA。双特异性抗体（如特立妥单抗、贝林妥欧单抗）可引导T细胞攻击浆细胞或B细胞，副作用较CAR-T小。个案报道显示可诱导完全缓解，相关临床试验正在进行。专家观点总结主要结论理想的ITP治愈应实现：正常血小板计数恢复疾病潜在的免疫紊乱平衡不良反应与长期后遗症风险三大研究主题靶向新通路/免疫区室：BTK、Syk、FcRN抑制；浆细胞或补体靶向治疗早期免疫调节：一线TPO-RA、利妥昔单抗、免疫抑制深度免疫抑制：双特异性抗体、CAR-T、联合方案现存挑战与未来方向时间局限：现有SROT和治疗失败时间数据多为6个月至数年，是否等于疾病修饰或治愈仍未知，亟需>2年的长期随访数据。生物标志物匮乏：目前无可靠标志物可诊断ITP、预测治疗反应、评估复发潜力或预后。无法区分暂时缓解与疾病生物学改变，也无法在诊断时识别将进展为慢性的患者。异质性：ITP不是单一疾病，而是多种免疫病理状态共享同一表型。不存在"一刀切"方案。患者中心：追求治愈不能以牺牲生活质量为代价。脾切除术虽可"治愈"，但长期后遗症令许多患者无法接受。治疗选择需平衡患者偏好、目标、副作用与生活质量。核心观点："追寻治愈"并非寻找单一解决方案，而是定义多种有效策略。挑战在于证明现代疗法能够实现疾病修饰，并明确何时、在哪些患者中可实施以治愈为目的的治疗。参考文献 Expert Rev Hematol . 2026 May 20. doi: 10.1080/17474086.2026.2678348.

2026-05-20

·新浪看点

CD38赛道为何再次升温？从浆细胞标志物到代谢免疫核心节点

（来源：ACROBiosystems官方）在多发性骨髓瘤（MM）治疗逐步迈向深度缓解与早期干预的背景下，CD38的研究定位正在发生变化。从最初仅被视作浆细胞表面特异性标志物，到其在NAD⁺代谢调控及肿瘤免疫微环境中的作用逐渐受到关注，并推动其在多发性骨髓瘤及部分自身免疫疾病中的潜力逐渐释放。跨膜拓扑结构与“腺苷轴”免疫逃逸机制：CD38功能的重新认识CD38兼具受体与酶的双重属性，是NAD⁺代谢相关的重要外酶，可催化NAD⁺水解生成ADPR和烟酰胺。其主要以催化域朝向胞外的II型跨膜构象存在，同时也有研究报道少量III型取向（催化域朝向胞质）的存在，使其可能参与不同空间来源的NAD⁺代谢调控。在肿瘤微环境中，CD38相关代谢通路与腺苷生成过程密切相关。CD38可与CD203a及CD73共同参与NAD⁺向腺苷（Adenosine）的转化过程，使骨髓微环境中腺苷水平升高。研究显示，多发性骨髓瘤患者骨髓微环境中的腺苷水平高于SMM及MGUS阶段。这种代谢演进通过A2AR/A2BR信号通路抑制效应T细胞和NK细胞的杀伤功能，并与肿瘤免疫逃逸及免疫治疗响应降低相关，这一代谢免疫机制也为CD38靶向干预提供了核心理论依据。]article_adlist-->临床干预节点的战略前移：从SMM到自免领域基于CD38在NAD⁺代谢及腺苷生成中的作用，其在不同疾病中的表达差异，逐渐被用于解释其在多疾病谱中的分布特征。在病理状态下，CD38异常高表达与多种疾病进展相关。在多发性骨髓瘤中，恶性浆细胞普遍高表达CD38，使其成为核心治疗靶点；在IgA肾病、免疫性血小板减少症（ITP）等自身免疫疾病中，CD38⁺浆细胞持续产生自身抗体，参与疾病进展。多疾病谱的异常表达特征，赋予了CD38广谱靶点开发潜力。2025年11月，达雷妥尤单抗（CD38单抗，Darzalex Faspro）获FDA批准用于高风险冒烟型多发性骨髓瘤（SMM），标志着CD38靶向治疗开始进入疾病早期干预阶段。在此基础上，基于PERSEUS III期研究结果，达雷妥尤单抗四药联合方案（DVRd）获中国NMPA批准，用于治疗适合自体干细胞移植的新诊断多发性骨髓瘤成年患者，进一步扩展治疗场景。（来源：https://doi.org/10.1186/s12967-024-05768-6）在自身免疫疾病领域，CD38靶向治疗也在持续拓展。Felzartamab（菲泽妥单抗）通过清除长寿浆细胞降低自身抗体水平，在IgA肾病及原发性膜性肾病（PMN）中显示出临床活性，目前已在多个适应症中推进全球III期临床研究。今年4月，渤健（Biogen）以最高8.5亿美元对价，Felzartamab大中华区独家开发与商业化权益，标志着这款CD38单抗全球权益正式收归单一主体，全球化临床与商业化进入加速期。除肾脏相关自身免疫疾病外，CD38靶向策略也开始向更多B细胞及浆细胞驱动疾病拓展。美国哈佛医学院麻省总医院血液科David J. Kuter教授团队近期发表于《NEJM》的II期研究显示，CD38单抗Mezagitamab（TAK-079）可提升慢性或持续性提升免疫性血小板减少症（ITP）患者血小板水平，并表现出较好的安全性，验证了CD38作为ITP治疗新靶点的可行性。16周时不同剂量Mezagitamab与安慰剂对照组在血小板反应指标上的疗效对比药物形态演进：多技术路线并行发展随着CD38靶点机制解析不断深入，药物研发已从传统单抗主导，升级为单抗、多特异性抗体、ADC、DAC及基因编辑细胞治疗多技术路线并行的格局。单抗仍是当前临床应用的基础框架，主要通过ADCC、CDC效应清除CD38高表达细胞，达雷妥尤单抗为该赛道标杆药物。新一代差异化单抗持续推进适应症拓展，康诺亚自主研发的CM313已完成全球除大中华区外的独家授权，布局复发 / 难治性骨髓瘤、系统性红斑狼疮、ITP等自免疾病。CD38、用于治疗多发性骨髓瘤的制剂CD38/CD3双抗、BCMA/CD38/CD3三抗等多特异性抗体，通过桥接T细胞与靶细胞强化定向杀伤，早期临床已展现高客观缓解率，是提升治疗应答深度的重要方向。CD38 ADC药物研发同样稳步推进，Sorrento公司的CD38 ADC药物STI6129已获FDA批准开展复发 / 难治性骨髓瘤临床，依托定点偶联与特殊连接子设计优化稳定性有效提升分子整体结构稳定性。在新一代偶联药物研发赛道中，DAC凭借独特作用机制展现出广阔研发前景。在2026年AACR年会披露的前沿研发成果中，两款靶向CD38的DAC药物表现亮眼，ADC-2419以IKZF1/3降解剂P5为载荷，DAC-002以IKZF1/3降解剂CY001-80为载荷，均通过可切割连接子与抗CD38抗体偶联；动物实验显示，DAC-002单次给药即可抑制肿瘤生长，高剂量可实现肿瘤完全消退，且初步非人灵长类毒理研究未发现明显安全问题。此外，基于CRISPR-Cas9的CD38基因编辑技术，可有效规避CAR-T/NK细胞的同类相残效应，提升其体内持久性，相关探索仍在持续推进。高质量CD38系列产品助力创新药物发现为全方位助力CD38相关创新药物高效研发，ACROBiosystems百普赛斯可提供完善的CD38系列研发配套试剂，包含纯度超90%、覆盖人、小鼠、食蟹猴等多种属的CD38重组蛋白；特异性CD38检测抗体以及CD38蛋白预偶联磁珠等产品。这一系列产品全面适配抗体药物筛选、分子互作分析、细胞功能实验、免疫结合活性验证等各类研发场景，加速CD38靶点创新管线落地。验证数据蛋白均一结构及高纯度经SEC-MALS验证The purity of Human CD38, Fc Tag is more than 95% and the molecular weight of this protein is around 115-145 kDa verified by SEC-MALS.CD38与抗体的结合活性经ELISA验证Immobilized Human CD38, His Tag at 5 μg/mL (100 μL/well) can bind Anti-CD38 MAb, Human IgG1 with a linear range of 0.2-4 ng/mL (QC tested).CD38与Anti-CD38 CAR的结合活性经FACS验证2e5 of Anti-CD38 CAR-293 cells were stained with 100 μL of 10 μg/mL of Human CD38 Protein, His Tag (MALS verified) and negative control protein respectively, washed and then followed by His Antibody, PE and analyzed with FACS (Routinely tested).CD38蛋白预偶联磁珠与抗体的结合活性经验证Immobilized 26.6 μg CD38 protein to 1 mg Beads , can bind the Anti-CD38 Antibody with an EC50 of 0.9196 μg/mL.

2026-05-20

·新浪看点

CD38赛道为何再次升温？从浆细胞标志物到代谢免疫核心节点

（来源：ACROBiosystems官方）在多发性骨髓瘤（MM）治疗逐步迈向深度缓解与早期干预的背景下，CD38的研究定位正在发生变化。从最初仅被视作浆细胞表面特异性标志物，到其在NAD⁺代谢调控及肿瘤免疫微环境中的作用逐渐受到关注，并推动其在多发性骨髓瘤及部分自身免疫疾病中的潜力逐渐释放。跨膜拓扑结构与“腺苷轴”免疫逃逸机制：CD38功能的重新认识CD38兼具受体与酶的双重属性，是NAD⁺代谢相关的重要外酶，可催化NAD⁺水解生成ADPR和烟酰胺。其主要以催化域朝向胞外的II型跨膜构象存在，同时也有研究报道少量III型取向（催化域朝向胞质）的存在，使其可能参与不同空间来源的NAD⁺代谢调控。在肿瘤微环境中，CD38相关代谢通路与腺苷生成过程密切相关。CD38可与CD203a及CD73共同参与NAD⁺向腺苷（Adenosine）的转化过程，使骨髓微环境中腺苷水平升高。研究显示，多发性骨髓瘤患者骨髓微环境中的腺苷水平高于SMM及MGUS阶段。这种代谢演进通过A2AR/A2BR信号通路抑制效应T细胞和NK细胞的杀伤功能，并与肿瘤免疫逃逸及免疫治疗响应降低相关，这一代谢免疫机制也为CD38靶向干预提供了核心理论依据。]article_adlist-->临床干预节点的战略前移：从SMM到自免领域基于CD38在NAD⁺代谢及腺苷生成中的作用，其在不同疾病中的表达差异，逐渐被用于解释其在多疾病谱中的分布特征。在病理状态下，CD38异常高表达与多种疾病进展相关。在多发性骨髓瘤中，恶性浆细胞普遍高表达CD38，使其成为核心治疗靶点；在IgA肾病、免疫性血小板减少症（ITP）等自身免疫疾病中，CD38⁺浆细胞持续产生自身抗体，参与疾病进展。多疾病谱的异常表达特征，赋予了CD38广谱靶点开发潜力。2025年11月，达雷妥尤单抗（CD38单抗，Darzalex Faspro）获FDA批准用于高风险冒烟型多发性骨髓瘤（SMM），标志着CD38靶向治疗开始进入疾病早期干预阶段。在此基础上，基于PERSEUS III期研究结果，达雷妥尤单抗四药联合方案（DVRd）获中国NMPA批准，用于治疗适合自体干细胞移植的新诊断多发性骨髓瘤成年患者，进一步扩展治疗场景。（来源：https://doi.org/10.1186/s12967-024-05768-6）在自身免疫疾病领域，CD38靶向治疗也在持续拓展。Felzartamab（菲泽妥单抗）通过清除长寿浆细胞降低自身抗体水平，在IgA肾病及原发性膜性肾病（PMN）中显示出临床活性，目前已在多个适应症中推进全球III期临床研究。今年4月，渤健（Biogen）以最高8.5亿美元对价，Felzartamab大中华区独家开发与商业化权益，标志着这款CD38单抗全球权益正式收归单一主体，全球化临床与商业化进入加速期。除肾脏相关自身免疫疾病外，CD38靶向策略也开始向更多B细胞及浆细胞驱动疾病拓展。美国哈佛医学院麻省总医院血液科David J. Kuter教授团队近期发表于《NEJM》的II期研究显示，CD38单抗Mezagitamab（TAK-079）可提升慢性或持续性提升免疫性血小板减少症（ITP）患者血小板水平，并表现出较好的安全性，验证了CD38作为ITP治疗新靶点的可行性。16周时不同剂量Mezagitamab与安慰剂对照组在血小板反应指标上的疗效对比药物形态演进：多技术路线并行发展随着CD38靶点机制解析不断深入，药物研发已从传统单抗主导，升级为单抗、多特异性抗体、ADC、DAC及基因编辑细胞治疗多技术路线并行的格局。单抗仍是当前临床应用的基础框架，主要通过ADCC、CDC效应清除CD38高表达细胞，达雷妥尤单抗为该赛道标杆药物。新一代差异化单抗持续推进适应症拓展，康诺亚自主研发的CM313已完成全球除大中华区外的独家授权，布局复发 / 难治性骨髓瘤、系统性红斑狼疮、ITP等自免疾病。CD38、用于治疗多发性骨髓瘤的制剂CD38/CD3双抗、BCMA/CD38/CD3三抗等多特异性抗体，通过桥接T细胞与靶细胞强化定向杀伤，早期临床已展现高客观缓解率，是提升治疗应答深度的重要方向。CD38 ADC药物研发同样稳步推进，Sorrento公司的CD38 ADC药物STI6129已获FDA批准开展复发 / 难治性骨髓瘤临床，依托定点偶联与特殊连接子设计优化稳定性有效提升分子整体结构稳定性。在新一代偶联药物研发赛道中，DAC凭借独特作用机制展现出广阔研发前景。在2026年AACR年会披露的前沿研发成果中，两款靶向CD38的DAC药物表现亮眼，ADC-2419以IKZF1/3降解剂P5为载荷，DAC-002以IKZF1/3降解剂CY001-80为载荷，均通过可切割连接子与抗CD38抗体偶联；动物实验显示，DAC-002单次给药即可抑制肿瘤生长，高剂量可实现肿瘤完全消退，且初步非人灵长类毒理研究未发现明显安全问题。此外，基于CRISPR-Cas9的CD38基因编辑技术，可有效规避CAR-T/NK细胞的同类相残效应，提升其体内持久性，相关探索仍在持续推进。高质量CD38系列产品助力创新药物发现为全方位助力CD38相关创新药物高效研发，ACROBiosystems百普赛斯可提供完善的CD38系列研发配套试剂，包含纯度超90%、覆盖人、小鼠、食蟹猴等多种属的CD38重组蛋白；特异性CD38检测抗体以及CD38蛋白预偶联磁珠等产品。这一系列产品全面适配抗体药物筛选、分子互作分析、细胞功能实验、免疫结合活性验证等各类研发场景，加速CD38靶点创新管线落地。验证数据蛋白均一结构及高纯度经SEC-MALS验证The purity of Human CD38, Fc Tag is more than 95% and the molecular weight of this protein is around 115-145 kDa verified by SEC-MALS.CD38与抗体的结合活性经ELISA验证Immobilized Human CD38, His Tag at 5 μg/mL (100 μL/well) can bind Anti-CD38 MAb, Human IgG1 with a linear range of 0.2-4 ng/mL (QC tested).CD38与Anti-CD38 CAR的结合活性经FACS验证2e5 of Anti-CD38 CAR-293 cells were stained with 100 μL of 10 μg/mL of Human CD38 Protein, His Tag (MALS verified) and negative control protein respectively, washed and then followed by His Antibody, PE and analyzed with FACS (Routinely tested).CD38蛋白预偶联磁珠与抗体的结合活性经验证Immobilized 26.6 μg CD38 protein to 1 mg Beads , can bind the Anti-CD38 Antibody with an EC50 of 0.9196 μg/mL.

100 项与迈泽妥单抗相关的药物交易

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KEGG	Wiki	ATC	Drug Bank
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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
免疫球蛋白a肾病	临床3期	美国	Takeda Pharmaceutical Co., Ltd.	2025-07-15
免疫球蛋白a肾病	临床3期	中国	Takeda Pharmaceutical Co., Ltd.	2025-07-15
免疫球蛋白a肾病	临床3期	日本	Takeda Pharmaceutical Co., Ltd.	2025-07-15
免疫球蛋白a肾病	临床3期	阿根廷	Takeda Pharmaceutical Co., Ltd.	2025-07-15
免疫球蛋白a肾病	临床3期	澳大利亚	Takeda Pharmaceutical Co., Ltd.	2025-07-15
免疫球蛋白a肾病	临床3期	奥地利	Takeda Pharmaceutical Co., Ltd.	2025-07-15
免疫球蛋白a肾病	临床3期	加拿大	Takeda Pharmaceutical Co., Ltd.	2025-07-15
免疫球蛋白a肾病	临床3期	哥伦比亚	Takeda Development Center Americas, Inc.	2025-07-15
免疫球蛋白a肾病	临床3期	捷克	Takeda Pharmaceutical Co., Ltd.	2025-07-15
免疫球蛋白a肾病	临床3期	法国	Takeda Pharmaceutical Co., Ltd.	2025-07-15

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临床结果

适应症

分期

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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


NCT06722235 (ASH2025)	临床3期	免疫性血小板减少症	171	Mezagitamab 600 mg	鏇蓋糧製顧艱憲糧壓憲(壓鬱構網構艱窪遞齋壓) = similar between mezagitamab and placebo (50% vs 45%) 窪構顧製衊製蓋餘構艱 (廠網蓋獵蓋築餘簾蓋膚 ) 更多	积极	2025-12-06
NCT05174221 (ASN2025 \| Company_Website)	临床1期	免疫球蛋白a肾病	17	Mezagitamab	醖築獵憲願夢觸艱艱淵(築壓獵獵鏇醖鹽築憲鹽) = 鏇鹽獵範蓋憲繭積衊鑰鏇膚糧膚鬱夢願餘淵廠 (餘鑰觸艱窪遞繭鹹餘艱 ) 更多	积极	2025-11-07
NCT04278924 (TAK-079-1004, CTgov)	临床2期	免疫性血小板减少症	41	Placebo (Part A & B: Double Blind Period: Placebo)	夢窪齋製築糧獵衊艱蓋 = 壓壓網願衊膚顧顧製醖製糧獵鬱製構簾糧鬱艱 (顧夢簾觸製築鏇窪鹹觸, 艱窪醖構艱夢衊顧餘餘 ~ 鏇淵範簾齋憲願淵構選) 更多	-	2025-06-15
				TAK-079 (Part A: Double Blind Period: TAK-079 100 mg)	夢窪齋製築糧獵衊艱蓋 = 鹽構蓋鑰繭艱鹽鹽醖簾製糧獵鬱製構簾糧鬱艱 (顧夢簾觸製築鏇窪鹹觸, 鹹獵簾觸餘鬱壓獵選鹽 ~ 艱鏇齋鬱遞膚鏇壓築繭) 更多
NCT05174221 (ERA2025)	临床1期	免疫球蛋白a肾病	17	Mezagitamab 600 mg + Angiotensin-converting enzyme inhibitor and/or angiotensin receptor blocker (IgA nephropathy)	窪蓋鑰製網鏇顧構衊鹽(壓窪鬱蓋蓋鑰淵簾夢獵) = 觸窪遞蓋蓋獵壓遞觸網網衊積蓋艱顧廠獵獵鑰 (鑰繭窪願繭鑰蓋網願膚 ) 更多	积极	2025-06-04
NCT03439280 (Phase 1b study, Pubmed)	临床1期	复发性多发性骨髓瘤 CD38	-	Mezagitamab monotherapy	簾齋鏇壓願構選餘齋遞(鹽網窪鑰廠築窪憲醖選) = Three patients discontinued treatment due to TEAEs 築遞衊顧築網淵遞構願 (構簾鏇襯餘壓選淵遞艱 ) 更多	积极	2024-12-01
NCT05174221 (ASN2024) 人工标引	临床1期	免疫球蛋白a肾病	17	Mezagitamab	蓋壓糧選餘繭衊廠築範(淵簾淵鬱衊醖夢積鬱齋) = None 網選壓選壓網繭窪鏇膚 (廠衊觸積顧鹽築繭觸鏇 ) 更多	积极	2024-10-25
NCT04278924 (TAK-079-1004, PipelineReview) 人工标引	临床2期	免疫性血小板减少症	-	Mezagitamab	鹽鏇鑰鬱膚網鑰繭壓鹹(壓餘簾壓膚顧顧鹹窪遞) = 醖遞顧簾糧壓繭鹹蓋淵壓網簾製構願窪蓋膚蓋 (積鬱積餘製選鹹構醖糧 ) 更多	积极	2024-06-22
				Placebo	鹽鏇鑰鬱膚網鑰繭壓鹹(壓餘簾壓膚顧顧鹹窪遞) = 艱窪網鹽選憲憲鹹鏇鏇壓網簾製構願窪蓋膚蓋 (積鬱積餘製選鹹構醖糧 ) 更多
NCT03724916 (CTgov)	临床1期	系统性红斑狼疮	23	TAK-079 Placebo (Pooled Placebo)	網製糧簾簾艱觸醖膚廠 = 醖顧衊醖鑰獵夢壓積襯窪鑰選簾襯糧蓋醖網衊 (簾艱範膚鹽膚夢簾觸築, 網鏇壓糧顧簾糧憲願窪 ~ 繭鬱遞膚願糧觸遞齋艱) 更多	-	2024-03-29
				TAK-079 (TAK-079 90 mg)	網製糧簾簾艱觸醖膚廠 = 壓築糧獵醖憲範繭構艱窪鑰選簾襯糧蓋醖網衊 (簾艱範膚鹽膚夢簾觸築, 範蓋壓積壓遞淵齋艱淵 ~ 鏇築鹹憲夢夢簾糧蓋簾) 更多
NCT04278924 (TAK-079-1004, Biospace) 人工标引	临床2期	免疫性血小板减少症	-	Mezagitamab	構鏇醖繭壓廠製襯鬱鹹(願鏇觸簾糧膚窪選範鏇) = Mezagitamab has been generally safe and well tolerated across all three cohorts. 醖醖簾艱襯衊糧蓋衊鹽 (選襯簾窪艱願獵鹽鑰糧 ) 更多	积极	2024-03-13
				Placebo
NCT04159805 (CTgov)	临床2期	重症肌无力	36	TAK-079 Placebo (TAK-079 Placebo-matching)	齋選膚顧觸蓋鬱積膚廠 = 艱願繭鹹齋遞網廠憲網簾構鹹範壓夢餘齋簾窪 (壓淵簾鑰願襯餘憲壓齋, 餘廠窪鹽構齋鑰遞觸壓 ~ 艱製簾蓋築襯淵鏇衊膚) 更多	-	2023-06-02
				TAK-079 (TAK-079 300 mg)	齋選膚顧觸蓋鬱積膚廠 = 範範壓壓窪醖襯鏇壓鹹簾構鹹範壓夢餘齋簾窪 (壓淵簾鑰願襯餘憲壓齋, 憲範選繭鏇鹽齋鏇膚壓 ~ 餘醖齋糧網衊廠淵艱憲) 更多