利妥昔单抗(Rituximab) - 药物靶点：CD20_在研适应症：自身免疫性溶血性贫血，心脏移植排斥反应，肝移植排斥反应_专利_临床

概要

基本信息

药物类型

单克隆抗体

别名

IDEC-C2B8-anti-CD20、Ristova、Rituximab (Genetical Recombination)

+ [15]

靶点

CD20

作用方式

抑制剂

作用机制

CD20抑制剂(B淋巴细胞抗原CD20抑制剂)、ADCC(抗体依赖的细胞毒作用)、CD20定向的溶细胞作用

治疗领域

肿瘤免疫系统疾病感染+ [11]

在研适应症

自身免疫性溶血性贫血心脏移植排斥反应肝移植排斥反应+ [145]

非在研适应症

急性双系白血病急性移植物抗宿主病成人急性髓性白血病+ [144]

原研机构

Genentech, Inc.

在研机构

Roche Registration GmbH

Celgene Corp.Janssen Research & Development LLC

+ [43]

非在研机构

Memorial Sloan Kettering Cancer Center

Biogen, Inc.

Fred Hutchinson Cancer Research Center

+ [57]

权益机构

上海罗氏制药有限公司

青岛百洋医药股份有限公司

Biogen, Inc.

+ [1]

最高研发阶段批准上市

首次获批日期

美国 (1997-11-26),

非霍奇金淋巴瘤

最高研发阶段(中国)批准上市

特殊审评孤儿药 (美国)、孤儿药 (欧盟)、孤儿药 (日本)

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结构/序列

Sequence Code 27145L

来源: *****

Sequence Code 83181H

来源: *****

关联

2,584

项与利妥昔单抗相关的临床试验

NCT07365306

/ Not yet recruiting临床2期IIT

A Phase 2 Study of Epcoritamab-R-GemOx With Consolidative ASCT and Additional Epcoritamab in Relapsed/Refractory Transplant-Eligible DLBCL

This phase II trial tests how well epcoritamab in combination with rituximab, gemcitabine and oxaliplatin (R-GemOx) works as treatment given after the cancer has not responded to other treatments (salvage therapy) before autologous stem cell transplant in treating patients with diffuse large B-cell lymphoma (DLBCL) that has come back after a period of improvement (relapsed) or that does not respond to treatment (refractory). Epcoritamab is a so-called bispecific antibody, a molecule that can bind simultaneously to two different receptors (proteins present on the cell surface). Epcoritamab binds to a receptor called CD3 with one part of the antibody and to a receptor called CD20 with another part of the antibody. CD3 is expressed on T cells, which are important cells of the immune system that help the body fight cancers and infections. CD20 is expressed on the surface of DLBCL cells. By simultaneous binding to CD3 and CD20, epcoritamab brings T cells and DLBCL cells close together and activates the T cells to kill the lymphoma cells. Rituximab is a so-called monoclonal antibody, a molecule that binds to a single receptor. Like epcoritamab, rituximab binds to CD20. After binding to CD20, rituximab activates the immune system to kill the lymphoma cell through several different mechanisms. Gemcitabine is a chemotherapy drug that blocks the cells from making DNA and may kill cancer cells. Oxaliplatin is in a class of medications called platinum-containing antineoplastic agents. It damages the cell's DNA and may kill cancer cells. Giving epcoritamab-R-GemOx as therapy before an autologous stem cell transplant may help kill cancer cells in the body and help make room in the patient's bone marrow for new blood-forming cells (stem cells) to grow.

开始日期2026-12-30

申办/合作机构

City of Hope National Medical Center

[+1]

NCT06015750

/ Withdrawn临床4期

An Interventional, Prospective Open-Label Study of Immunosuppressive Therapies to Mitigate Immune-Mediated Loss of Therapeutic Response to Asfotase Alfa (STRENSIQ®) for Hypophosphatasia (RESTORE)

The primary objective of this study is to evaluate the effect of immunosuppressive therapy (IST) in participants treated with asfotase alfa who demonstrate immune-mediated loss of effectiveness (LoE).

开始日期2026-07-29

申办/合作机构

Alexion Pharmaceuticals, Inc.

NCT06965114

/ Recruiting临床1/2期IIT

A Phase 1 Study of Combination Tovorafenib (DAY101) and Rituximab Treatment in Relapsed or Refractory Classical Hairy Cell Leukemia and Phase 2 Randomized Study Comparing Tovorafenib (DAY101) and Rituximab With Cladribine and Rituximab for Front-Line Treatment of Classical Hairy Cell Leukemia

This phase I/II trial tests the safety, side effects, and effectiveness of tovorafenib in combination with rituximab in patients with classical hairy cell leukemia (cHCL) that has come back after a period of improvement (recurrent) or that has not responded to previous treatment (refractory) and compares the effect of tovorafenib and rituximab to current standard treatment of cladribine and rituximab in cHCL patients that have not yet received treatment. Tovorafenib blocks certain proteins made by the mutated BRAF gene, which may help keep cancer cells from growing. It is a type of kinase inhibitor. Rituximab is a monoclonal antibody. It binds to a protein called CD20, which is found on B cells (a type of white blood cell) and some types of cancer cells. This may help the immune system kill cancer cells. Cladribine damages the cell's deoxyribonucleic acid and may kill cancer cells. It is a type of antimetabolite. Giving tovorafenib in combination with rituximab may be safe and tolerable and more effective than cladribine with rituximab in treating patients with untreated, recurrent or refractory cHCL.

开始日期2026-06-27

申办/合作机构

National Cancer Institute

100 项与利妥昔单抗相关的临床结果

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100 项与利妥昔单抗相关的转化医学

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100 项与利妥昔单抗相关的专利（医药）

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9,522

项与利妥昔单抗相关的文献（医药）

2026-12-31·RENAL FAILURE

Early posttransplant rituximab use in kidney transplant recipients with preexisting donor-specific antibodies

Article

作者: Molnar, Miklos Z. ; Fornadi, Katalin ; Yamauchi, Junji ; Jweehan, Duha ; Marineci, Silviana ; Pole, Ann ; Lazar-Molnar, Eszter ; Raghavan, Divya ; Jain, Dharmendra ; Oygen, Suayp

The presence of pretransplant anti-human leukocyte antigen (HLA) donor-specific antibodies (DSAs) is still a significant barrier to successful kidney transplantation, as it increases the risk of rejection and graft failure. Rituximab (anti-CD20 antibody) has been administered in hopes of suppressing DSA production and rejection in those with preformed DSAs. However, existing studies report conflicting outcomes, underscoring the need for more data to guide clinical practice. Thus, we evaluated the efficacy of early posttransplant rituximab administration in a cohort of kidney transplant recipients with pretransplant anti-HLA DSAs. In this retrospective study of 77 patients, we compared 1-year transplant outcomes between patients treated with and without rituximab for pretransplant anti-HLA DSAs. Infectious complications tended to occur more often in the rituximab group (BK polyomavirus DNAemia >10,000 copies/mL, 3 [19%] vs. 8 [13%]; quantifiable cytomegalovirus DNAemia, 8 [50%] vs. 19 [31%]; infection requiring hospitalization, 5 [31%] vs. 11 [18%]), but none of these differences reached statistical significance. The incidence of biopsy-proven rejection (2 [13%] vs. 12 [20%]) and high plasma donor-derived cell-free DNA (2 [18%] vs. 12 [27%]) tended to be more frequent in the no-rituximab group, but none of these reached statistical significance. Preexisting DSA persisted or recurred in 44% of the patients that received rituximab, and in 46% of patients who did not receive rituximab. Similarly, de novo DSA occurred in 31% of those who received rituximab versus in 25% of those who did not. Rituximab administration did not result difference in graft and patient survival or rejection rates or recurrence of preexisting DSA.

2026-12-31·RENAL FAILURE

Long-term real-world outcomes of rituximab in primary membranous nephropathy: a 154-patient cohort study from China

Article

作者: Fang, Ying-xin ; Shang, Wen-ya ; Zheng, Zhen-feng ; Wei, Li ; Cao, Xin ; Jia, Jun-ya ; Zhang, Xin-xin ; Yan, Tie-kun ; Xu, Peng-cheng ; Qi, Yan ; Gao, Xi-qian ; Gu, Qiu-hua ; Cheng, Xi

To investigate the long-term efficacy and safety of rituximab (RTX) in treating patients with primary membranous nephropathy (pMN), a total of 154 patients with pMN receiving RTX treatment were retrospectively enrolled in this study. The study included 92 patients who received RTX as an initial therapy, and 62 patients who received it as an alternative therapy. Over a median follow-up of 30.0 (24.0, 47.0) months after RTX treatment, 102/121 (84.3%) patients achieved immunological remission. And 128/154 (83.1%) patients achieved clinical remission (including 37.7% of CR and 45.5% of PR), accompanied by significant reduction in proteinuria and increase in serum albumin levels. Clinical response rates were comparable between the initial and alternative therapy groups (87.0 vs. 77.4%, p = 0.131), though patients in the alternative therapy group required a longer time to achieve remission. Among the 21 patients with eGFR < 60 mL·min^-1·(1.73 m²)^-1, 12 (57.1%) responded to RTX. Though two patients progressed to end-stage renal disease (ESRD) during follow-up, the remaining 19 patients showed an improvement in eGFR from 48.0 (38.0, 55.0) to 62.0 (36.0, 73.0) mL·min^-1·(1.73 m²)^-1. The clinical response in the RTX monotherapy group did not differ significantly from that in patients who received RTX in combination with glucocorticoids or other immunosuppressive agents. Twenty-eight patients experienced adverse events, most of which were mild and manageable. RTX, utilized as either an initial or alternative therapy, induced a significant clinical response in patients with pMN, including those with compromised renal function. These findings support RTX as an effective and well-tolerated option across various pMN patient profiles.

2026-04-01·SEMINARS IN ARTHRITIS AND RHEUMATISM

IgG4 related coronary artery involvement: A scoping review of the literature

Review

作者: Litterio, Marianna ; Di Vincenzo, Fabiana ; Alunno, Alessia ; Carubbi, Francesco ; Carugno, Maria Ester ; Ferri, Claudio ; Di Bartolomeo, Salvatore

OBJECTIVES:

Immunoglobulin (Ig)G4-related disease (IgG4-RD) can affect any organ, but coronary artery involvement (CAI) is a potentially life-threatening manifestation of this disease. In this scoping review, we critically appraised the literature on IgG4-related CAI, aiming to explore clinical, radiological and histopathological characteristics as well as treatment strategies and prognosis.

METHODS:

A comprehensive search was performed on January 02, 2025 in PubMed® to identify studies describing individuals with IgG4-related CAI, including both coronaritis (true arteritis of the coronary vessel wall) and periarteritis (peri-coronary involvement), and considering case reports, case series, retrospective cohort studies and observational studies. Two reviewers independently conducted the revision of literature under the guidance of the methodologist to identify eligible studies. Data extraction included clinical presentation, imaging findings, histopathology, treatment, and outcomes. Given the heterogeneity of the studies, descriptive statistical analysis was used whenever possible to summarise the data.

RESULTS:

Out of 964 screened references, 143 articles met the above-mentioned inclusion criteria. Most CAI cases were included in case reports (90.2 %), 7 % in case series and 2.8 % in retrospective cohort studies or observational studies. CAI predominantly affected males in the sixth decade of life and frequently coexisted with aortic and large vessel involvement. All segments of the coronary arterial tree could be involved, even the smallest branches. Images detected by various methods revealed several types of lesions: stenosis, wall-thickening, aneurysm, ectasia, pseudotumor, pseudoaneurysm, dissection, and soft tissue masses. Increase serum IgG4 levels and increased inflammatory markers were reported. Histopathology was consistent with IgG4-RD in all coronary samples obtained. Glucocorticoid therapy, alone or combined with immunosuppressants and/or surgical interventions, was the most commonly reported treatment. Rituximab seemed to be an effective therapy for IgG4-related CAI even without associated glucocorticoids. Despite treatment, relapse and progression of coronary lesions were noted in some cases.

CONCLUSIONS:

Early identification and multidisciplinary management og IgG4-related CAI are crucial to reduce morbidity and mortality. Available data on the response to various treatments are limited, as dedicated coronary artery imaging was not consistently obtained soon enough after treatment to assess response. In addition, long-term follow-up was not available for all patients. Further studies are required to understand the real prevalence, natural history, optimal diagnostic strategies, and therapeutic approaches for this serious condition.

2,970

项与利妥昔单抗相关的新闻（医药）

2026-02-27

·医伴旅

治疗B细胞淋巴瘤！伊布替尼(亿珂、Imbruvica)的适应症、不良反应及注意事项

伊布替尼（Ibrutinib，Imbruvica）是一款革命性的小分子靶向药物，由美国杨森制药研发。该药通过抑制BTK活性，阻断B细胞受体信号通路，显著抑制恶性B细胞增殖，适用于套细胞淋巴瘤、慢性淋巴细胞白血病/小淋巴细胞淋巴瘤、华氏巨球蛋白血症等血液肿瘤的治疗。（图片来源：clinicaltrialsarena.com）适应症慢性淋巴细胞白血病/小淋巴细胞淋巴瘤（CLL/SLL）适用于成人患者，包括初治和复发难治病例，尤其是伴17p缺失的高危人群。临床研究显示，单药或联合利妥昔单抗等方案可显著延长无进展生存期（PFS）。华氏巨球蛋白血症（WM）作为一线或后续治疗选择，单药或联合利妥昔单抗可快速降低IgM水平，缓解症状。慢性移植物抗宿主病（cGVHD）针对1岁及以上儿童及成人患者，用于激素治疗失败后的二线治疗，有效改善皮肤、口腔等器官的纤维化病变。不良反应 B 细胞恶性肿瘤患者中最常见（≥30%）的不良反应：血小板减少、腹泻、疲劳、肌肉骨骼疼痛、中性粒细胞减少、皮疹、贫血、瘀青、恶心。成人或儿科慢性移植物抗宿主病（cGVHD）患者中最常见（≥20%）的不良反应：疲劳、贫血、瘀青、腹泻、血小板减少、肌肉骨骼疼痛、发热、肌肉痉挛、口腔炎、出血、恶心、腹痛、肺炎、头痛。（图片来源：老挝卢修斯制药）注意事项出血：监测出血情况并进行处理。感染：监测患者发热及感染症状，及时评估并治疗。心律失常、心力衰竭与猝死：监测心律失常及心力衰竭症状并进行处理。高血压：监测血压并进行治疗。血细胞减少：每月检查全血细胞计数。第二原发恶性肿瘤：患者可能发生其他恶性肿瘤，包括皮肤癌及其他癌种。肝毒性（包括药物性肝损伤）：治疗期间全程监测肝功能。肿瘤溶解综合征（TLS）：评估基线风险并采取预防措施，监测并治疗肿瘤溶解综合征。胚胎‑胎儿毒性：可造成胎儿伤害。告知育龄女性对胎儿的潜在风险，并使用有效避孕措施。常见问题解答 Q：服用期间有哪些饮食禁忌？ A:避免葡萄柚及塞维利亚橙类产品，因其抑制CYP3A酶，可能增加血药 Q：能否与抗生素联用？ A:强效CYP3A抑制剂（如克拉霉素）需调整剂量；短期使用抗感染药（≤7天）建议暂停伊布替尼。 Q：长期用药的监测重点？ A:每月检测血常规、肝功能；每3-6个月评估心脏功能及血压。 Q：药物相互作用如何处理？ A：避免与强效CYP3A抑制剂（如伊曲康唑）合用，若必须联用时应减量至140mg/d；与CYP3A诱导剂（如利福平）合用可能降低疗效，应避免联用。如有相关需求可添加二维码联系我们将尽心为您服务免责声明：以上内容整理于drugs及网络，仅作信息交流之目的，而非提供医疗建议。文中观点不代表医伴旅立场，亦不代表医伴旅支持或反对文中观点。本文不构成任何治疗方案的推荐。本公众号内容仅供医学药学专业人士阅读参考，具体用药请咨询主治医师。本公众号仅提供信息展示服务，不销售药品，如需专业治疗方案，请前往正规医院接受诊疗。参考资料： https://www.drugs.com/pro/imbruvica.html 传递药讯信息、分享前沿资源↓↓↓ 往期推荐伊布替尼(Ibrutinib)的用法用量：常用剂量、剂量调整伊布替尼（亿珂、Imbruvica）作用机制、副作用管理及常见问答白血病、淋巴瘤等用药！伊布替尼（亿珂、Ibrutinib、Imbruvica）说明书：作用功效、如何用药、副作用及对策

临床结果免疫疗法

2026-02-26

·癌度

《癌度快报》2026年2月26日：美国妙佑国际配置首台“纳米热疗”系统，让癌细胞自热而凋亡！

临床试验病友交流群（点击）一、新药快讯 1、微卫星高度不稳定型结直肠癌免疫治疗联合化疗，早期进展风险降低10倍！ 2026年ASCO GI研讨会上报道了一项研究进展，靶向PD-L1的免疫治疗药物联合FOLFOX 化疗、加上抗血管生成靶向药贝伐单抗。用于错配修复缺陷（dMMR）/微卫星不稳定高（MSI-H）转移性结直肠癌的一线治疗。中位无进展生存期达到了24.5个月，而单药阿替利珠单抗的中位无进展生存期为5.3个月，早期患者的进展风险降低了10倍。这项研究表明对于特定类型的结直肠癌患者，相比单独用免疫治疗，免疫联合化疗和抗血管生成药物能让患者受益更多。 2、肝癌新药PLT012获得快速通道资格，开辟了肝癌免疫治疗的新策略！近日，美国食品药品监督管理局FDA授予靶向CD36的单抗PLT012快速通道资格，用于治疗肝细胞癌。该药通过阻断CD36介导的脂质摄取，重塑肿瘤微环境、逆转免疫抑制状态，临床前研究显示其对“冷肿瘤”及肝转移灶具有单药及联合PD-1抑制剂协同活性。目前I期临床试验正在美国招募36例晚期实体瘤患者，每3周静脉给药一次，旨在评估其安全性、药代动力学及初步疗效，为代谢免疫联合治疗提供新方向。 3、抗CD19和CD20的双抗三联药方案治疗滤泡性淋巴瘤，疗效显著！近日发布于《Nature Reviews Clinical Oncology》的研究表明，抗CD19的抗体药物塔法西妥单抗（Tafasitamab）或埃普奈妥单抗（Epcoritamab，CD20×CD3 双特异性抗体）+来那度胺联合利妥昔单抗（R²方案）。治疗复发/难治性滤泡性淋巴瘤（FL）患者。在两项三期临床试验都显示出阳性结果，对于处于复发/难治性滤泡性淋巴瘤二线及后线治疗中的患者来说值得关注。二、抗癌前沿 1、美国妙佑国际配置首台“纳米热疗”系统，让癌细胞自热而凋亡！近日，妙佑医疗国际（原梅奥诊所）安装全美首台磁性纳米颗粒介导肿瘤热疗系统（NHT），首位美国患者已于2025年12月完成临床试验治疗。该技术通过静脉注射氧化铁纳米颗粒（靶向富集于肿瘤组织），结合交变磁场诱导肿瘤局部发热（≤50℃），实现“电磁炉式”精准热疗，可同步攻击深部及多发病灶，目前正用于对多线治疗耐药的转移性实体瘤（除脑瘤）患者研究，未来拟探索与放疗联用方案，为热疗技术提供新突破路径。 “吉爱3000”惠民检项目，最低2000+可及的基因检测专属福利，全球新药临床试验免费用药、基因检测报告解读，详情微信“长按”下图扫码联系癌度王博进行咨询。另外，由于微信公众平台的机制调整，恳请各位粉丝朋友花一两秒钟帮我们点亮文章下方的【小手】和【爱心】，这对我们至关重要。谢谢大家！点亮小手爱心，送来温暖鼓励

2026-02-26

·抗体圈

单克隆抗体 50 年：从实验室到临床的进化之旅

摘要：1975年杂交瘤技术的诞生，开启了单克隆抗体的新时代。50年间，这项技术从基础研究工具，逐步发展为全球获批212款的主流治疗手段，惠及数千万患者。从鼠源抗体的局限性突破，到人源化、双特异性抗体、抗体药物偶联物的迭代，再到生物制造与给药技术的升级，单克隆抗体的进化从未停止。如今AI赋能抗体设计，口服、中枢递送等新方向探索，让这款疗法的未来充满更多可能。一、一次实验室突破，开启50年的疗愈征程 1975年，Köhler和Milstein在实验室做出了一个改变医学的发现——杂交瘤技术。简单说，就是把小鼠免疫后的B细胞和骨髓瘤细胞融合，造出能无限分泌特异性抗体的杂交瘤细胞（图1a，来源：Nature Reviews Immunology, 2025）。这一发现直接拿下1984年诺贝尔奖，也让单克隆抗体从概念变成了可量产的科研工具。最初的鼠源单抗虽能精准结合抗原，但作为药物的短板很快显现，免疫原性强、半衰期短、效应功能弱，直到1986年首款鼠源单抗muromonab-CD3获批，才迈出临床第一步，而真正的爆发，还要等上十余年。图1 从杂交瘤技术到抗体疗法的发展路径 a为杂交瘤技术制备鼠源单克隆抗体的核心步骤；b为从杂交瘤技术诞生到抗体疗法获批的关键环节，涵盖抗体工程、生物制造、临床研究等多个阶段二、抗体的“改头换面”，突破鼠源的先天局限鼠源单抗的临床短板，逼着科研人员开始给抗体“做改造”。嵌合化是第一步，把鼠源抗体的抗原结合区嫁接到人源抗体的恒定区，降低了部分免疫原性。随后的人源化技术更精细，只保留鼠源抗体的抗原结合环，其余全部替换成人源序列，这一改造让抗体的临床兼容性大幅提升（Box1，来源：Nature Reviews Immunology, 2025）。后来全人源抗体技术出现，通过转基因小鼠、噬菌体展示等方法，直接获得全人源序列的抗体，彻底解决了免疫原性问题，2002年获批的阿达木单抗，就是首款全人源IgG抗体，也成了首款年销售额超200亿美元的抗体药。三、212款获批药的背后，是疗法格局的全面进化截至2025年5月，全球获批的抗体治疗药物已达212款，这个数字还在以每年至少18款的速度增长（图2a，来源：Nature Reviews Immunology, 2025）。这些药物不再只是单一的IgG抗体，双特异性抗体、抗体药物偶联物（ADCs）、CAR-T细胞疗法等新形式百花齐放。从疾病领域看，肿瘤占比48%，自身免疫性疾病25%，感染、神经、代谢疾病等领域也在不断拓展（图2b，来源：Nature Reviews Immunology, 2025）。给药方式也从最初的静脉输注，发展出皮下注射、玻璃体内注射等多种形式，让患者的治疗体验大幅提升（图2d，来源：Nature Reviews Immunology, 2025）。图2 全球获批抗体治疗药物的发展格局 a为不同抗体形式的累计获批数量；b为抗体疗法获批的疾病领域分布；c为不同制备技术的抗体累计获批数量；d为抗体疗法的给药途径分布；e为获批抗体药物偶联物的作用机制与数量；f为获批双特异性抗体的结构形式与数量四、精准靶向的进阶，从单一抗体到多元治疗体系抗体疗法的魅力，在于对疾病的精准靶向，而这一点在B细胞疾病和HER2+癌症的治疗中体现得淋漓尽致。针对B细胞的CD20靶点，从首款嵌合抗体利妥昔单抗，到糖基化改造的奥滨尤妥珠单抗，再到双特异性T细胞衔接器、CAR-T细胞、ADCs，形成了多代产品的治疗矩阵（图3，来源：Nature Reviews Immunology, 2025）。HER2+乳腺癌的治疗更是如此，曲妥珠单抗开启靶向时代后，帕妥珠单抗的联合、ADCs的升级、双特异性抗体的出现，让这款癌症的治疗效果不断突破，甚至能覆盖HER2低表达的患者（图4，来源：Nature Reviews Immunology, 2025）。图3 靶向B细胞的各类抗体治疗药物涵盖单克隆抗体、双特异性抗体、CAR-T细胞、抗体药物偶联物等多种形式，标注了各药物的靶点、结构改造及给药方式特点图4 靶向HER2的抗体治疗药物格局展示了单克隆抗体、双特异性抗体、抗体药物偶联物及联合制剂的靶点结合特点、结构改造和获批适应症五、给药的革新，让治疗从“医院专属”变“居家可及” 静脉输注是抗体疗法最初的给药方式，虽能保证100%的生物利用度，但每次治疗需要数小时，对患者来说既耗时又费力。皮下注射的出现改变了这一现状，给药时间缩短到10分钟内，还能实现居家给药。为了突破皮下注射的剂量和体积限制，科研人员想出了多种办法：和透明质酸酶共制剂，把给药体积从2ml提升到15ml；通过工程改造让抗体更稳定、低黏度，能制备高浓度制剂；甚至改造抗体的Fc区，延长半衰期，减少给药频率（表1，来源：Nature Reviews Immunology, 2025）。如今多款抗体药已实现皮下给药，让治疗的便捷性提升了一个台阶。表1 提升抗体皮下递送效率的核心策略涵盖增加给药体积、提高给药浓度、降低用药剂量、提升生物利用度四大方向，及各方向对应的具体技术手段六、生物制造的升级，撑起抗体药的量产底气抗体药能从实验室走向临床，生物制造的进步功不可没。最初的CHO细胞培养，抗体滴度只有1-2g/L，如今通过细胞系改造、培养基优化、灌流培养等技术，滴度能稳定在5-8g/L，部分抗体甚至能突破10g/L（Box2，来源：Nature Reviews Immunology, 2025）。生产设备也从传统的不锈钢生物反应器，发展出一次性设备，降低了污染风险，提升了生产灵活性。连续加工技术的探索，还让抗体的生产周期缩短、成本降低，让更多患者能用上这款疗法。七、未来的方向，从AI设计到全新递送的无限探索其实单克隆抗体的进化，从来没有停下脚步。现在的科研人员，已经开始用AI设计抗体了，从结构预测到多参数优化，AI能让抗体的研发效率大幅提升，甚至能设计出自然界不存在的抗体序列。除了AI，条件性抗原结合抗体、IgM/IgA等新型抗体亚型、激动性抗体的探索，都在让抗体的功能更丰富。而口服抗体、中枢神经系统递送的研究，更是试图突破抗体给药的最后壁垒，让这款疗法能覆盖更多疾病、更多患者。当然，降低高工程化抗体的免疫原性，仍是未来需要持续攻克的难题（图5，来源：Nature Reviews Immunology, 2025）。八、50年回望，抗体疗法的初心与远方从1975年杂交瘤技术的实验室发现，到如今212款药物获批、数千万患者获益，单克隆抗体的50年，是基础研究向临床转化的典范。这50年里，我们解决了鼠源抗体的局限，打造了多元的抗体形式，优化了给药和制造技术，让这款疗法从“小众工具”变成了“主流疗法”。某种程度上，抗体疗法的进化，也是人类对抗疾病的缩影——从发现到突破，从优化到创新，永远向着更精准、更便捷、更有效的方向前行。而下一个50年，随着AI、合成生物学等技术的融合，抗体疗法还会带来更多惊喜。识别微信二维码，添加抗体圈小编，符合条件者即可加入抗体微信群！请注明：姓名+研究方向！版权声明本公众号所有转载文章系出于传递更多信息之目的，且明确注明来源和作者，不希望被转载的媒体或个人可与我们联系(cbplib@163.com)，我们将立即进行删除处理。所有文章仅代表作者观不本站。

100 项与利妥昔单抗相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D02994	利妥昔单抗	L01XC02	DB00073

研发状态

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10 条最早获批的记录,

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适应症	国家/地区	公司	日期
自身免疫性溶血性贫血	日本	Zenyaku Kogyo Co., Ltd.	2026-02-19
心脏移植排斥反应	日本	Zenyaku Kogyo Co., Ltd.	2023-12-22
肝移植排斥反应	日本	Zenyaku Kogyo Co., Ltd.	2023-12-22
肺移植排斥反应	日本	Zenyaku Kogyo Co., Ltd.	2023-12-22
胰腺移植排斥反应	日本	Zenyaku Kogyo Co., Ltd.	2023-12-22
肾移植排斥反应	日本	Zenyaku Kogyo Co., Ltd.	2023-12-22
小肠移植排斥	日本	Zenyaku Kogyo Co., Ltd.	2023-12-22
狼疮性肾炎	日本	Zenyaku Kogyo Co., Ltd.	2023-08-23
视神经脊髓炎	日本	Zenyaku Kogyo Co., Ltd.	2022-06-20
巴西天疱疮	日本	Zenyaku Kogyo Co., Ltd.	2021-12-24
家族性寻常型天疱疮	日本	Zenyaku Kogyo Co., Ltd.	2021-12-24
获得性血栓性血小板减少性紫癜	日本	Zenyaku Kogyo Co., Ltd.	2020-02-21
CD20阳性B细胞慢性淋巴细胞白血病	日本	Zenyaku Kogyo Co., Ltd.	2019-03-26
淋巴细胞白血病	日本	Genentech, Inc.	2019-03-26
淋巴细胞白血病	日本	IDEC Pharmaceuticals Corp.	2019-03-26
慢性特发性血小板减少性紫癜	日本	Zenyaku Kogyo Co., Ltd.	2017-06-26
血小板减少性紫癜	日本	Genentech, Inc.	2017-06-26
血小板减少性紫癜	日本	IDEC Pharmaceuticals Corp.	2017-06-26
肾病综合征	日本	Zenyaku Kogyo Co., Ltd.	2014-08-29
肾病综合征	日本	IDEC Pharmaceuticals Corp.	2014-08-29

未上市

10 条进展最快的记录,

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适应症	最高研发状态	国家/地区	公司	日期
纵隔大b细胞淋巴瘤	临床3期	美国	Genmab, Inc.	2023-02-08
纵隔大b细胞淋巴瘤	临床3期	中国	Genmab, Inc.	2023-02-08
纵隔大b细胞淋巴瘤	临床3期	日本	Genmab, Inc.	2023-02-08
纵隔大b细胞淋巴瘤	临床3期	澳大利亚	Genmab, Inc.	2023-02-08
纵隔大b细胞淋巴瘤	临床3期	奥地利	Genmab, Inc.	2023-02-08
纵隔大b细胞淋巴瘤	临床3期	比利时	Genmab, Inc.	2023-02-08
纵隔大b细胞淋巴瘤	临床3期	巴西	Genmab, Inc.	2023-02-08
纵隔大b细胞淋巴瘤	临床3期	保加利亚	Genmab, Inc.	2023-02-08
纵隔大b细胞淋巴瘤	临床3期	加拿大	Genmab, Inc.	2023-02-08
纵隔大b细胞淋巴瘤	临床3期	克罗地亚	Genmab, Inc.	2023-02-08

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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


NCT04268277 (CTgov)	临床2期	边缘区B细胞淋巴瘤	22	Pembrolizumab+Rituximab	範範餘淵艱鹽顧鹽遞鏇 = 觸選繭構願選繭淵積鬱獵襯積壓選範觸膚醖蓋 (範觸窪鹹蓋憲製壓觸築, 構窪獵膚積齋範鑰窪願 ~ 繭齋積範簾製壓遞簾醖) 更多	-	2026-02-27
NCT03919175 (CTgov)	临床2期	滤泡性淋巴瘤 \| 边缘区B细胞淋巴瘤	18	Umbralisib+Rituximab	餘範膚壓顧夢廠鑰蓋範 = 選製遞鏇淵艱鑰繭壓蓋淵構構願襯憲顧網獵築 (鏇膚鏇繭蓋蓋範觸廠廠, 獵醖遞鹽積窪製襯鹹範 ~ 積網選廠糧廠網選餘鹽) 更多	-	2026-02-27
NCT03286556 (STRIVE-IPF, CTgov)	临床2期	特发性肺纤维化	82	Autoantibody Reductive Therapy (Autoantibody Reductive Therapy)	膚夢簾齋簾築蓋鹹夢蓋(鏇壓簾鑰襯醖壓衊網製) = 壓窪醖襯積餘構鑰構餘襯顧壓憲獵蓋壓製憲積 (鑰願鏇淵觸衊願選範餘, 9) 更多	-	2026-02-24
				Treatment as Usual (TAU) (Treatment as Usual (TAU))	膚夢簾齋簾築蓋鹹夢蓋(鏇壓簾鑰襯醖壓衊網製) = 構廠範顧壓製簾積鏇遞襯顧壓憲獵蓋壓製憲積 (鑰願鏇淵觸衊願選範餘, 6) 更多
NCT04002401 (ZUMA-14, Pubmed \| Nat Cancer)	临床2期	难治性弥漫性大 B 细胞淋巴瘤 CD19-negative	26	Axicabtagene ciloleucel +Rituximab	觸廠夢艱積衊鏇遞構鏇(觸願築鬱築鹹願繭廠艱) = 夢蓋鹽鏇製艱積壓鹹壓繭選製醖衊鹽網築遞壓 (醖蓋醖淵製膚顧蓋齋鹹 ) 更多	积极	2026-01-05
NCT05409066 (EPCORE FL-1, Pubmed \| Lancet)	临床3期	难治性滤泡性淋巴瘤二线	488	Epcoritamab + Lenalidomide + Rituximab	鏇醖壓簾製鑰鹽夢鹹簾(膚鬱積醖製夢蓋鏇齋艱) = 餘鬱淵獵繭積積鬱簾糧觸膚遞衊憲遞廠網遞遞 (簾壓鹹遞獵鏇網憲鬱網, 92 ~ 97) 更多	优效	2026-01-01
				Lenalidomide + Rituximab	鏇醖壓簾製鑰鹽夢鹹簾(膚鬱積醖製夢蓋鏇齋艱) = 獵遞窪蓋願顧築衊膚糧觸膚遞衊憲遞廠網遞遞 (簾壓鹹遞獵鏇網憲鬱網, 74 ~ 84) 更多
AGMT‑NHL‑16 \| GLA2022‑10 \| IKF062 (ASH2025) 人工标引	临床2期	侵袭性 B 细胞非霍奇金淋巴瘤一线 \| 诱导	80	R-Pola-Glo(rituximabrituximab+polatuzumab vedotin+glofitamabglofitamab)	糧簾鹹壓壓淵鹹衊鑰糧(艱艱鹽遞淵淵獵網製齋) = 醖鹹鬱壓顧艱願顧築遞糧憲鹽獵鹹網糧壓簾鹹 (獵憲醖廠鏇憲鑰鹽窪製, 77 ~ 93) 更多	积极	2025-12-06
NCT04624906 (BRAWm, ASH2025)	临床2期	巨球蛋白血症一线	63	Bendamustine+Rituximab+Acalabrutinib	齋範餘憲網積顧廠壓糧(構鏇艱觸製膚鹹構壓繭) = 製窪餘遞夢淵積鹹鑰醖醖築網齋積窪糧蓋壓廠 (鏇鏇廠選廠鏇鹽遞範醖 )	积极	2025-12-06
				Bendamustine+Rituximab+Acalabrutinib (≥70 years old)	齋範餘憲網積顧廠壓糧(構鏇艱觸製膚鹹構壓繭) = 廠鹹繭鏇醖鏇簾鑰廠鹹醖築網齋積窪糧蓋壓廠 (鏇鏇廠選廠鏇鹽遞範醖 ) 更多
NCT04978584 (Smart Stop, ASH2025)	临床2期	弥漫性大B细胞淋巴瘤一线	61	Lenalidomide+Tafasitamab+Rituximab+Acalabrutinib (2 cycles of CHOP)	憲蓋鹹膚憲壓獵觸壓憲(選壓繭簾憲獵餘觸艱淵) = 範淵衊顧衊積夢繭網醖夢夢淵選積淵願鏇鬱鹹 (壓鬱築壓蓋網觸蓋願製 ) 更多	积极	2025-12-06
				Lenalidomide+Tafasitamab+Rituximab+Acalabrutinib (no cycles of CHOP)	憲蓋鹹膚憲壓獵觸壓憲(選壓繭簾憲獵餘觸艱淵) = 壓廠鏇獵衊膚餘顧範窪夢夢淵選積淵願鏇鬱鹹 (壓鬱築壓蓋網觸蓋願製 ) 更多
ASH2025	N/A	副蛋白血症	46	Plasma cell-directed therapy	獵積構蓋顧繭遞鹽觸壓(窪願願憲壓艱衊齋鏇積) = 齋壓鹽夢繭鹹壓鏇範獵網淵鬱獵夢壓願築鏇襯 (衊觸艱顧鹽構鹹簾範遞 ) 更多	积极	2025-12-06
				Non-plasma cell-directed therapy	獵積構蓋顧繭遞鹽觸壓(窪願願憲壓艱衊齋鏇積) = 遞鑰壓顧窪構餘顧構範網淵鬱獵夢壓願築鏇襯 (衊觸艱顧鹽構鹹簾範遞 ) 更多
NCT03010202 (PROLONG, ASH2025)	临床2期	免疫性血小板减少症	127	Rituximab	鹽膚壓鏇鏇鏇糧築鏇築(襯醖繭築鹽築憲糧艱衊) = 齋築蓋範憲顧憲願淵餘窪襯顧鏇獵鏇鹹夢簾選 (觸簾憲獵鏇衊觸鬱遞觸 ) 更多	积极	2025-12-06
				Rituximab+Dexamethasone	鹽膚壓鏇鏇鏇糧築鏇築(襯醖繭築鹽築憲糧艱衊) = 餘範醖醖鹽顧簾構簾鏇窪襯顧鏇獵鏇鹹夢簾選 (觸簾憲獵鏇衊觸鬱遞觸 ) 更多