依库珠单抗(Eculizumab) - 药物靶点：C5_在研适应症：水通道蛋白4抗体阳性视神经脊髓炎谱系疾病，非典型溶血性尿毒症综合征，重症肌无力_专利_临床

概要

基本信息

药物类型

单克隆抗体

别名

Anti-C5 monoclonal antibody 5G1-1、Eculizumab (Genetical Recombination)、Eculizumab (genetical recombination) (JAN)

+ [16]

靶点

C5

作用方式

抑制剂

作用机制

C5抑制剂(补体C5抑制剂)

治疗领域

肿瘤免疫系统疾病感染+ [5]

在研适应症

水通道蛋白4抗体阳性视神经脊髓炎谱系疾病非典型溶血性尿毒症综合征重症肌无力+ [2]

非在研适应症

原研机构

Alexion Pharmaceuticals, Inc.

在研机构

Alexion Europe SAS

Alexion Pharmaceuticals, Inc.Astrazeneca Korea Ltd.

+ [3]

非在研机构-

权益机构

Alexion Pharmaceuticals, Inc.

AstraZeneca PLC

最高研发阶段批准上市

首次获批日期

美国 (2007-03-16),

阵发性睡眠性血红蛋白尿症

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)、孤儿药 (韩国)、孤儿药 (澳大利亚)、优先审评 (中国)

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结构/序列

Sequence Code 66437L

来源: *****

Sequence Code 66453H

来源: *****

关联

65

项与依库珠单抗相关的临床试验

NCT05646563

/ Not yet recruiting临床2期

A Phase II, Open-Label Study of NM8074 in Soliris®-Treated Patients with Paroxysmal Nocturnal Hemoglobinuria (PNH)

This is a Phase II, open-label study designed to evaluate the safety, efficacy, and immunogenicity of NM8074 in PNH patients undergoing complement-inhibitor therapy with Soliris.

开始日期2026-01-01

申办/合作机构

NovelMed Therapeutics, Inc.

NCT07010302

/ Not yet recruiting临床4期IIT

A Comparative Clinical Effectiveness Trial of Rituximab Versus Ravulizumab, Inebilizumab, Satralizumab and Eculizumab To Prevent Relapses in Neuromyelitis Optica Spectrum Disorder

Neuromyelitis Optica Spectrum Disorder (NMOSD) is a rare autoimmune condition that mainly affects the eyes and spinal cord, causing serious symptoms such as vision loss, paralysis, and severe pain. This trial compares the effectiveness and safety of five medications commonly used to prevent NMOSD relapses: rituximab, ravulizumab, inebilizumab, satralizumab, and eculizumab.
In this study, 160 adults with NMOSD who test positive for a specific antibody (AQP4-IgG) will participate. They will be randomly assigned to receive either rituximab or one of the four other FDA-approved medications. The main goal is to find out which treatment best prevents relapses and has fewer serious side effects. The trial will also measure disability, patient satisfaction, quality of life, and biomarkers that help track disease activity.
Participants will have regular assessments, including medical exams, surveys, and tests for vision, walking ability, and brain function. They will report any side effects or health issues experienced during the study. The trial will last from one to four years for each participant.
This research aims to help patients and doctors make better-informed treatment decisions by providing clear evidence about the best available therapies for NMOSD.

开始日期2025-11-01

申办/合作机构

The Massachusetts General Hospital

[+1]

NCT06673394

/ Withdrawn临床2期IIT

Eculizumab For Acute Attack of Neuromyelitis Optica Spectrum Disorder (NMOSD): a Multi-Center, Phase 2, Open Label Trial (EASE-NMO)

Neuromyelitis optica spectrum disorder (NMOSD) is a relapsing, inflammatory autoimmune disorder of the central nervous system characterized by the pathogenic anti-aquaporin 4 antibody (AQP4-IgG). The objectives of this study are to assess the efficacy and safety of eculizumab for treatment of patients with neuromyelitis optica spectrum disorders during acute phase who are anti-aquaporin-4 (AQP4) antibody-positive. Eculizumab, a humanized monoclonal antibody, inhibits the terminal complement protein C5 and prevents its cleavage into C5a and the formation of C5b-9 (MAC), has approved for preventive treatment of NMOSD. Given the high efficacy of C5 inhibition, eculizumab is proposed to potentially provide rapid relief from astrocyte destruction by reducing MAC formation, which could contribute to the fast alleviation of neurological deficit during NMO acute attack. The potential of eculizumab warrants further investigation as a treatment for acute neuromyelitis optica spectrum disorders attacks.

开始日期2025-09-03

申办/合作机构

天津医科大学总医院

100 项与依库珠单抗相关的临床结果

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100 项与依库珠单抗相关的转化医学

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100 项与依库珠单抗相关的专利（医药）

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2,430

项与依库珠单抗相关的文献（医药）

2026-12-31·JOURNAL OF MEDICAL ECONOMICS

Cost per responder analysis of iptacopan versus eculizumab and ravulizumab in treatment of paroxysmal nocturnal hemoglobinuria: implications for decision-making

Article

作者: Shafrin, Jason ; Muthukrishnan, Sanjana ; Kuypers, Nicholas ; Bilano, Ver ; Than, Kyi-Sin ; Paulose, Jincy

OBJECTIVE:

Paroxysmal nocturnal hemoglobinuria (PNH) is a rare and debilitating hematological disease with significant economic burden. Despite the availability of multiple therapies, there is a lack of consensus on optimal treatment strategies among physicians and payers in the United States. This study aimed to evaluate the economic value of iptacopan, a novel oral treatment option, compared to terminal complement inhibitors (specifically, complement component C5 inhibitor or C5i)-including eculizumab and ravulizumab-among patients with PNH who are either (i) C5i-experienced or (ii) complement-inhibitor-naïve.

METHODS:

A cost per responder analysis was conducted based on treatment efficacy from clinical trials comparing iptacopan with C5i treatments. Treatment response was defined as the proportion of patients achieving red blood cell transfusion independence. Treatment costs were estimated as pharmaceutical wholesale acquisition cost and treatment administration costs, accounting for discontinuation. Outcomes evaluated included the number needed to treat to achieve a response and the cost per responder over the treatment duration of 24 weeks.

RESULTS:

Over 24 weeks, the number needed to treat to achieve an additional response was lower for iptacopan than all C5i comparators (C5i-experienced: 1.05 with iptacopan vs. 3.86 with C5is; complement-inhibitor-naïve: 1.02 with iptacopan vs. 1.69 with C5is). Cost per responder was lower for iptacopan than C5i comparators for both C5i-experienced ($264,337 for iptacopan vs. $975,298 for ravulizumab, $1,060,511 for eculizumab, and $744,561-$955,194 for eculizumab biosimilar with 10%-30% discount from eculizumab cost) and complement-inhibitor-naïve patients ($256,754, vs. $428,139 for ravulizumab, $465,546 for eculizumab, and $326,849-$419,314 for eculizumab biosimilar).

CONCLUSION:

Among both C5i-experienced and complement-inhibitor-naïve patients, treatment with iptacopan resulted in higher response rates and lower cost per responder compared to C5is.

2026-03-01·Neurology-Neuroimmunology & Neuroinflammation

Complement C5 Inhibitor Ameliorates a Case of Dysferlinopathy

Article

作者: Yu, Meng ; Yuan, Yun ; Lu, Xin ; Wang, Qingqing ; Zhang, Wei ; Lv, He ; Kang, Shuaikun ; Deng, Jianwen ; Wang, Zhaoxia ; Zheng, Fuze

OBJECTIVES:

Dysferlinopathy is an autosomal recessive muscular dystrophy caused by pathogenic variants of the DYSF gene. Currently, no clinical effective treatment is available. Given the myopathologic and animal model evidence on complement activation in dysferlinopathy, we explored the potential therapeutic effect of complement inhibition.

METHODS:

We reported a case of teenager-onset dysferlinopathy with progressive proximal weakness, markedly elevated serum creatine kinase levels, and assistance requirement for ambulation when admission. Muscle biopsy showed dysferlin deficiency and marked deposition of complement C5b-9 on nonnecrotic sarcolemma. Based on these findings and previous preclinical studies, the patient received eculizumab (900 mg weekly for 4 weeks) with informed consent.

RESULTS:

Clinical improvement was observed following complement inhibition therapy. By week 5, all tested muscle groups reached Medical Research Council grade 5/5, and the North Star Assessment for Dysferlinopathy score increased from 28 to 39. The 6-minute walk test (6MWT) improved from 220 m to 363 m. The muscle MRI revealed reduced muscle edema after eculizumab treatment. These benefits were sustained at 13-month follow-up.

DISCUSSION:

Complement inhibition showed promising clinical improvement in this single case of dysferlinopathy. Further studies with larger sample sizes are needed to investigate the efficacy and safety of complement inhibitors in dysferlinopathy.

2026-03-01·Neurology-Neuroimmunology & Neuroinflammation

Real-World Efficacy and Safety of Neuromyelitis Optica Spectrum Disorder Disease-Modifying Treatments

Article

作者: Narasimhan, Sathya S. ; Ganguly, Avanteeka ; Levy, Michael ; Bilodeau, Philippe A. ; Healy, Brian C. ; Bhattacharyya, Shamik ; Jiang, Mulan ; Wruble Clark, Mattia ; Harowitz, Jenna Bernice ; Pua, Danielle Kei ; Mateen, Farrah Jasmine ; Mahler, Joao Vitor

BACKGROUND AND OBJECTIVES:

Neuromyelitis optica spectrum disorder (NMOSD) is characterized by inflammatory relapses that result in severe disability, including blindness and paralysis. Relapse prevention with safe and effective treatments is key to reducing long-term disability. We aim to compare the efficacy and safety of rituximab-the most commonly used treatment-with recently approved NMOSD-specific treatments-eculizumab, inebilizumab, satralizumab-and other common off-label NMOSD treatments-mycophenolate mofetil (MMF) and azathioprine. The primary outcomes are relapse-free survival and annualized relapse rate. Secondary outcomes are serious infectious adverse event (SIAE) and treatment-limiting adverse event (TLAE)-free survival.

METHODS:

A retrospective cohort study of NMOSD was conducted on patients at the Mass General Brigham hospital network. Patients meeting 2015 NMOSD diagnostic criteria, who were seen between 2000 and 2024 were included. Poisson regression, frequentist negative binomial analysis with inverse probability of treatment weighting, and Cox proportional hazard models were used to assess relapse rates, relapse-free survival, and SIAEs.

RESULTS:

A total of 176 patients with NMOSD were followed for a median of 9 years (interquartile range: 5-14), contributing 691 relapse assessments. The median age at first attack was 42 years, and 83% were female. Compared with rituximab, relapse risk was significantly lower with C5 inhibitors (HR 0.12, 95% CI 0.07-0.24), inebilizumab (HR 0.22, 95% CI 0.12-0.65), and satralizumab (HR 0.19, 95% CI 0.11-0.42). Annualized relapse rates were the lowest for C5 inhibitors (0, 95% CI 0-0.063) and the highest for azathioprine (0.34, 95% CI 0.18-0.56). A composite outcome of relapse, SIAE, and TLAE favored C5 inhibitors (HR 0.22, 95% CI 0.05-0.67), while azathioprine (HR 2.33, 95% CI 1.08-4.86) and MMF (HR 1.75, 95% CI 1.02-2.95) showed increased risk compared with rituximab. C5 inhibitors had the lowest incidence of serious infections (incidence rate ratio 0.16, 95% CI 0.05-0.42 vs rituximab).

DISCUSSION:

Clinicians should consider using NMOSD-approved treatments given their favorable efficacy and safety profiles in the real-world setting. MMF and azathioprine should be avoided. We caution against rituximab as a default first-line given the cumulative risk of relapse, SIAEs, and TLAEs over time.

CLASSIFICATION OF EVIDENCE:

This study provides Class III evidence that, in patients with NMOSD, FDA-approved disease-modifying therapies are associated with lower relapse rates and fewer serious adverse events compared with rituximab.

647

项与依库珠单抗相关的新闻（医药）

2026-01-27

·药时代

12.55亿美元！先声药业双抗出海

出海机会来了！寻找PCSK9小分子抑制剂产品，全球权益，目前所处阶段不限。请感兴趣的公司立即联系：药时代BD团队 BD@drugtimes.cn 正文共：1000字预计阅读时间：4分钟 2026年1月27日，先声药业宣布与勃林格殷格翰达成许可合作协议，双方将共同开发先声药业的临床前阶段TL1A/IL23p19双特异性抗体SIM0709，用于炎症性肠病的治疗。截图来源：先声药业根据协议，勃林格殷格翰获得该项目在大中华区以外的全球权益。先声药业可获得首付款，以及基于开发、注册和商业里程碑的成功，最高可达10.58亿欧元（约12.55亿美元）的付款，此外还可获得大中华区以外净销售额提成的特许权使用费。 SIM0709是先声药业多抗技术平台开发的长效人源化双特异性抗体，可同时靶向肿瘤坏死因子样细胞因子1A（TL1A）和白介素23（IL-23），阻断导致IBD发生发展的两条核心通路。更关键的是，其超长半衰期设计有望降低给药频率，极大提升患者依从性，项目预计将于2026年上半年进入人体研究。临床前数据显示，SIM0709在体外原代细胞实验和体内动物实验中均表现出优异的药效协同效果，甚至优于两个单药的联用。此外，本次交易是先声药业自免领域第二个创新药海外授权。截至2026年1月，先声药业集团共实现5项自研创新药早研项目对外技术授权许可，潜在交易总金额超46亿美元。封面图/摘要图来源：药时代数亿元投资！晶泰科技与东阳光药成立新公司 2026-01-27 默沙东300亿美元收购谈判搁浅！ 2026-01-26 康诺生物叩响港股大门，加入全球“抗衰老”科学竞速 2026-01-26 中国首款！阿斯利康「依库珠单抗」新适应症在华获批 2026-01-26 版权声明/免责声明本文为汇编文章。本文仅作信息交流之目的，不提供任何商用、医用、投资用建议。文中图片、视频、字体、音乐等素材或为药时代购买的授权正版作品，或来自微信公共图片库，或取自公司官网/网络，部分素材根据CC0协议使用，版权归拥有者，药时代尽力注明来源。如有任何问题，请与我们联系。衷心感谢! 药时代官方网站:www.drugtimes.cn 联系方式: 电话:13651980212 微信:27674131 邮箱:contact@drugtimes.cn 点击查看更多精彩内容！

2026-01-27

·药物临床试验信息

填补儿童罕见病治疗空白！首个靶向药舒立瑞®在华获批，惠及6岁以上难治性重症肌无力患儿

2026年1月26日，国家药品监督管理局正式批准舒立瑞®（依库珠单抗注射液）适应症扩展至6岁及以上抗AChR抗体阳性的难治性全身型重症肌无力儿童患者。这是目前中国首个且唯一获批用于该疾病儿童患者的靶向治疗，填补了长期存在的临床空白，为患儿及其家庭带来新的治疗希望。什么是儿童难治性全身型重症肌无力？全身型重症肌无力是一种罕见的自身免疫性神经肌肉疾病，可导致患儿肌肉无力、行走困难、言语不清、吞咽障碍甚至呼吸衰竭，严重影响生长发育与生活质量。约85%患者为AChR抗体阳性，其中部分患儿对现有免疫抑制治疗反应不佳，疾病控制困难，被称为“难治性”，临床亟需有效靶向药物。二、临床数据支持：症状显著改善，安全性良好获批基于一项全球多中心III期临床试验，结果显示，依库珠单抗治疗26周后，患儿重症肌无力定量评分较基线显著改善，具有高度统计学与临床意义。其疗效与安全性特征与成人患者一致，为儿童长期治疗提供了可靠依据。该药通过抑制补体C5激活，精准阻断自身免疫攻击，从机制上干预疾病进程。三、里程碑意义：从成人到儿童，完整生命周期的治疗覆盖舒立瑞®此前已在中国获批用于成人难治性gMG，此次扩展至儿童患者，实现了该靶向疗法在成人与儿童患者中的全覆盖。作为全球首个C5补体抑制剂，其获批不仅意味着治疗选择的丰富，更体现了我国对罕见病患儿群体的高度关注与政策支持，助力“健康中国2030”在罕见病领域的落地。注：以上信息基于公开信息与学术资料整合，不构成任何投资或医疗建议。往 / 期 / 回 / 顾 4600万哮喘患者福音！首个“哮喘+慢阻肺”三联疗法在中国获批外周动脉疾病（也称下肢动脉硬化闭塞症）：一种易被忽视的血管疾病挑战从中国到澳洲，22天获批！亚虹医药创新药APL-2401开启国际多中心临床新里程

临床3期申请上市

2026-01-27

·制药网

阿斯利康重磅创新药新适应症在中国获批，重症肌无力领域再迎利好

【制药网产品资讯】重症肌无力是一种自身免疫性神经肌肉接头疾病，由神经-肌肉接头传递功能障碍引起，其特征是波动性肌肉无力，具有病程长、难治愈、易复发的特点。近日，国内市场在全身型重症肌无力(gMG)领域迎来好消息。　　1月26日，阿斯利康宣布，其罕见病创新药依库珠单抗注射液(商品名：舒立瑞)，适应证扩展至用于治疗6岁及以上抗乙酰胆碱受体(AChR)抗体阳性的难治性全身型重症肌无力(gMG)儿童患者。这标志着我国儿童罕见病治疗领域取得重要突破。　　gMG是一种罕见的慢性自身免疫性神经肌肉疾病，可导致肌肉功能丧失、严重衰弱，影响患者行走、说话、吞咽及呼吸能力。该病在任何年龄段均可发病，儿童及青少年患者正处在生长发育关键期，疾病对其肌肉功能、生活质量和身心发育造成严重影响。此前，我国对于难治性儿童gMG患者缺乏针对性的靶向治疗选择。　　此次舒立瑞的获批，是基于依库珠单抗治疗难治性gMG儿童患者的III期临床试验(ECU-MG-303)积极结果。研究显示，治疗第26周时，患者重症肌无力定量评分(QMG)总分较基线显著改善，均值变化为-5.8(95%置信区间：-8.4，-3.13)，统计学差异显著(p=0.0004)，且疗效具有明确临床意义。　　阿斯利康相关人士表示，依库珠单抗为儿童难治性gMG患者带来全新治疗选择，有望改善患者治疗结局与生活质量。据悉，作为全球头个C5补体抑制剂，依库珠单抗通过选择性抑制末端补体C5激活发挥作用，给药方式为诱导剂量期后每两周静脉注射一次。　　近年来，国际上新型靶向药物被广泛研究和应用于重症肌无力治疗中，包括靶向B细胞、C5补体抑制单抗、白介素6单抗等药物，重症肌无力的治疗已经进入了生物靶向新阶段。　　舒立瑞的获批落地，是我国重症肌无力治疗领域的重大突破。据悉，近年来多款作用于不同靶点的创新药物相继问世，为患者提供了多元化治疗选择。如再鼎医药的新生儿受体单抗(艾加莫德)是一款获批准上市的FcRn(新生儿受体)拮抗剂，通过竞争性的结合FcRn来靶向清除体内的致病性IgG抗体，用于治疗抗乙酰胆碱受体(AChR)抗体阳性的全身型重症肌无力(gMG)成人患者的辅助疗法。艾加莫德在起效时间、疗效、安全性等方面特点突出，为攻克gMG提供了全新的治疗手段。其帮助患者改善肌肉力量，改善生活质量，达到“微小带病，但不发病”的正常生活状态，改写重症肌无力患者治疗结局。　　荣昌生物自主研发的BLyS/APRIL双靶点融合蛋白创新药物泰它西普(RC18，商品名：泰爱®)与常规治疗药物联合用于治疗抗乙酰胆碱受体(AChR)抗体阳性的成人全身型重症肌无力(gMG)患者的新适应症于2025年5月获批上市。作为全球头个上市的BLyS/APRIL双靶治疗重症肌无力的原研生物药，泰它西普由人跨膜激活剂及钙调亲环素配体相互作用因子(TACI)受体的胞外域以及人免疫球蛋白G(IgG)的可结晶片段(Fc)域构成，可同时靶向B细胞激活因子(又称BLyS)和增殖诱导配体(APRIL)，直击致病性抗体产生的源头——B细胞及浆细胞，其获批上市为患者带来了新疗法。　　有数据显示，全球重症肌无力患者约120万人，其中中国患者约22万人，庞大的患者群体背后是巨大的未满足临床需求。此前，儿童患者、难治性患者的治疗困境，成人患者对更优疗效、更低副作用方案的追求，都推动着医疗界不断探索创新。随着更多创新药物的引入与本土研发的突破，重症肌无力患者的治疗结局将被持续改写。　　免责声明：在任何情况下，本文中的信息或表述的意见，均不构成对任何人的投资建议。

100 项与依库珠单抗相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D03940	依库珠单抗	L04AA25	DB01257

研发状态

批准上市

10 条最早获批的记录,

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适应症	国家/地区	公司	日期
水通道蛋白4抗体阳性视神经脊髓炎谱系疾病	澳大利亚	Alexion Pharmaceuticals, Inc.	2009-03-20
非典型溶血性尿毒症综合征	欧盟	Alexion Europe SAS	2007-06-20
非典型溶血性尿毒症综合征	冰岛	Alexion Europe SAS	2007-06-20
非典型溶血性尿毒症综合征	列支敦士登	Alexion Europe SAS	2007-06-20
非典型溶血性尿毒症综合征	挪威	Alexion Europe SAS	2007-06-20
重症肌无力	欧盟	Alexion Europe SAS	2007-06-20
重症肌无力	冰岛	Alexion Europe SAS	2007-06-20
重症肌无力	列支敦士登	Alexion Europe SAS	2007-06-20
重症肌无力	挪威	Alexion Europe SAS	2007-06-20
视神经脊髓炎	欧盟	Alexion Europe SAS	2007-06-20
视神经脊髓炎	冰岛	Alexion Europe SAS	2007-06-20
视神经脊髓炎	列支敦士登	Alexion Europe SAS	2007-06-20
视神经脊髓炎	挪威	Alexion Europe SAS	2007-06-20
阵发性睡眠性血红蛋白尿症	美国	Alexion Pharmaceuticals, Inc.	2007-03-16

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
移植物功能延迟恢复	临床3期	美国	Alexion Pharmaceuticals, Inc.	2014-08-21
移植物功能延迟恢复	临床3期	澳大利亚	Alexion Pharmaceuticals, Inc.	2014-08-21
移植物功能延迟恢复	临床3期	巴西	Alexion Pharmaceuticals, Inc.	2014-08-21
移植物功能延迟恢复	临床3期	加拿大	Alexion Pharmaceuticals, Inc.	2014-08-21
移植物功能延迟恢复	临床3期	捷克	Alexion Pharmaceuticals, Inc.	2014-08-21
移植物功能延迟恢复	临床3期	法国	Alexion Pharmaceuticals, Inc.	2014-08-21
移植物功能延迟恢复	临床3期	德国	Alexion Pharmaceuticals, Inc.	2014-08-21
移植物功能延迟恢复	临床3期	意大利	Alexion Pharmaceuticals, Inc.	2014-08-21
移植物功能延迟恢复	临床3期	西班牙	Alexion Pharmaceuticals, Inc.	2014-08-21
水通道蛋白4抗体阳性视神经炎	临床3期	美国	Alexion Pharmaceuticals, Inc.	2014-04-11

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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


ASH2025	N/A	非典型溶血性尿毒症综合征 \| 阵发性睡眠性血红蛋白尿症 \| 全血细胞减少 ... 更多	96	Eculizumab	鑰衊餘選積網淵壓製衊(繭糧鹹醖繭鏇餘壓觸膚) = 積顧繭鑰繭願壓鹽構襯範鹽積簾齋醖顧壓顧窪 (壓衊醖鹹壓襯遞窪齋積 )	积极	2025-12-06
				Eculizumab (immune competent cohort)	襯窪製廠顧製壓窪鏇蓋(醖艱繭壓簾製鏇網窪艱) = 簾顧壓淵廠蓋網遞顧衊壓鬱蓋積顧鑰鏇觸憲繭 (糧憲築遞壓蓋鬱醖艱夢 )
ASH2025	N/A	血栓性微血管病	21	Eculizumab	鏇艱簾構襯夢願齋糧願(簾淵積衊顧觸夢衊餘醖) = 積觸網醖遞鹹範淵選構憲淵製襯鏇構網願淵積 (網選廠觸觸襯積鹽選憲 ) 更多	积极	2025-12-06
ASH2025	N/A	阵发性睡眠性血红蛋白尿症	31	Iptacopan	顧簾構餘觸夢顧觸鑰襯(憲壓醖網鬱蓋顧獵醖鏇) = 繭鬱積構繭餘積襯淵窪夢醖網網構願鹹獵壓鏇 (鏇淵膚鑰築選築鏇觸簾 ) 更多	积极	2025-12-06
				Eculizumab	顧簾構餘觸夢顧觸鑰襯(憲壓醖網鬱蓋顧獵醖鏇) = 醖糧鑰醖顧願醖築廠鹽夢醖網網構願鹹獵壓鏇 (鏇淵膚鑰築選築鏇觸簾 ) 更多
ASH2025	N/A	阵发性睡眠性血红蛋白尿症	87	eculizumab	鹽壓襯鹹繭觸壓窪鹽夢(衊糧憲鹽製膚鹹選鹹夢) = 鏇窪願鬱窪鏇蓋襯築顧齋鑰糧鹹選鹹獵遞製鬱 (壓築鹽觸顧窪遞淵醖壓 ) 更多	积极	2025-12-06
				ravulizumab	鹽壓襯鹹繭觸壓窪鹽夢(衊糧憲鹽製膚鹹選鹹夢) = 鬱襯廠鬱憲築鏇衊鬱蓋齋鑰糧鹹選鹹獵遞製鬱 (壓築鹽觸顧窪遞淵醖壓 ) 更多
ASH2025	N/A	阵发性睡眠性血红蛋白尿症 \| 骨髓增生性疾病	11	Eculizumab	壓網艱醖簾製鹹蓋構襯(壓膚願範廠憲夢觸獵膚) = Sepsis as the cause of death in 3 cases 鏇選憲選積願積衊蓋鑰 (構鬱齋構糧積醖範蓋選 )	不佳	2025-12-06
NCT05966467 (NMO SPOTLIGHT Registry, ECTRIMS2025 \| Company_Website) 人工标引	N/A	水通道蛋白4抗体阳性视神经脊髓炎谱系疾病 AQP4-IgG	56	ALXN-C5IT (eculizumab or ravulizumab)	蓋選夢蓋鬱鑰網製網選(築遞鏇範壓鑰網網糧齋) = 膚鬱蓋選鬱艱範齋獵蓋網積範築網積糧淵夢蓋 (窪鹹觸簾觸蓋簾壓顧製, 0.00 ~ 0.05) 更多	积极	2025-09-09
				ALXN-C5IT (eculizumab or ravulizumab) (switched from rituximab)	蓋選夢蓋鬱鑰網製網選(築遞鏇範壓鑰網網糧齋) = 簾醖簾襯艱顧鏇獵艱繭網積範築網積糧淵夢蓋 (窪鹹觸簾觸蓋簾壓顧製 ) 更多
PB2827 (EHA2025)	N/A	阵发性睡眠性血红蛋白尿症	52	Eculizumab	觸獵鹽鬱糧範蓋憲鑰艱(獵憲網製夢鹽廠鹹淵夢) = occurred in 30.8% 壓鹹繭製觸願鏇齋遞襯 (築齋顧構夢憲衊積蓋築 ) 更多	-	2025-05-14
NCT05966467 (NMO SPOTLIGHT Registry, AAN2025)	N/A	水通道蛋白4抗体阳性视神经脊髓炎谱系疾病	30	Eculizumab	遞觸窪網選齋餘襯蓋繭(網齋憲鑰積廠獵觸齋艱) = 蓋鏇簾襯夢製鑰簾壓壓廠蓋選廠繭淵範衊齋膚 (廠鏇夢衊簾網餘齋糧齋, 24.0 ~ 49.7)	积极	2025-04-07
				Ravulizumab	遞觸窪網選齋餘襯蓋繭(網齋憲鑰積廠獵觸齋艱) = 鹽範範鹽衊簾夢鬱艱鏇廠蓋選廠繭淵範衊齋膚 (廠鏇夢衊簾網餘齋糧齋, 0.7 ~ 1.3)
S34.006 (AAN2025)	N/A	重症肌无力 anti-acetylcholine receptor antibody-positive (AChR-Ab+)	254	Eculizumab	積膚鹹選蓋築選衊齋齋(構蓋構鏇顧鏇構選願廠) = 40.5% experienced adverse drug reactions (ADRs) 鑰廠鬱繭簾醖廠糧鹹鬱 (製鑰獵夢遞鹹憲廠壓憲 ) 更多	积极	2025-04-07
ASH2024	N/A	非典型溶血性尿毒症综合征	-	Eculizumab	獵淵餘壓壓選遞蓋簾構(觸築獵遞築網蓋簾築獵) = 鬱繭選齋壓鹽夢繭獵壓蓋膚範餘範網膚鏇鹹鹹 (觸襯觸膚製蓋鹽夢鑰憲, 230.0 ~ 362.0) 更多	-	2024-12-08
				Ravulizumab	鹽窪艱構醖醖選網憲蓋(範觸衊觸餘構獵遞製壓) = 齋膚築糧積簾齋鹹憲獵鹽窪簾鬱顧壓夢構醖衊 (鬱蓋鹹獵鬱鹽網鏇構壓, 11.5% ~ 36.4%)