艾加莫德α(Efgartigimod Alfa) - 药物靶点：FcRn_在研适应症：慢性炎症性脱髓鞘性多发性神经病，慢性特发性血小板减少性紫癜，免疫性血小板减少症_专利_临床

概要

基本信息

药物类型

Fc片段

别名

Efgartigimod、Efgartigimod alfa、Efgartigimod Alfa (Genetical Recombination)

+ [9]

靶点

FcRn

作用方式

拮抗剂、调节剂

作用机制

FcRn拮抗剂(IgG受体FcRn大亚基p51拮抗剂)、免疫调节剂

治疗领域

肿瘤免疫系统疾病神经系统疾病+ [13]

在研适应症

慢性炎症性脱髓鞘性多发性神经病慢性特发性血小板减少性紫癜免疫性血小板减少症+ [24]

非在研适应症

原研机构

在研机构

+ [6]

非在研机构-

权益机构

argenx SEGenpharm, Inc.

Medison Pharma Ltd.

+ [6]

最高研发阶段批准上市

首次获批日期

美国 (2021-12-17),

重症肌无力

最高研发阶段(中国)批准上市

特殊审评优先审评 (美国)、快速通道 (美国)、孤儿药 (美国)、孤儿药 (欧盟)、突破性疗法 (中国)、孤儿药 (日本)、孤儿药 (韩国)、儿科研究计划 (欧盟)、潜力创新药 (英国)、优先审评 (中国)

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结构/序列

Sequence Code 18457995

来源: *****

关联

70

项与艾加莫德α 相关的临床试验

NCT07072988

/ Not yet recruiting临床4期IIT

A Multicenter, Prospective, Observational, Open-label Study to Evaluate the Benefit of Corticoid Sparing in Elderly With Generalized AntiRAch Myasthenia Gravis Treated With IV or SC Efgartigimod

Generalized Myasthenia Gravis (gMG) is a rare chronic autoimmune disorder causing muscle weakness and fatigue, primarily due to autoantibodies that disrupt neuromuscular junction function. The most common antibodies target nicotinic acetylcholine receptors (AChR), with others such as anti-MuSK and anti-LRP4 being less prevalent. The conventional gMG treatments include acetylcholinesterase inhibitors, corticosteroids, immunosuppressant and, in case of myasthenic crisis, plasma exchange (PLEX) and intravenous immunoglobulins (IVIG). Treatment aims to achieve minimal manifestation status (MMS), but many patients face persistent symptoms or side effects. Corticosteroids, while effective, carry significant risks, especially for long-term use, such as, increased infection and cardiovascular risks, chronic conditions like hypertension, diabetes, and osteoporosis and quality of life impacts, including weight gain and mood changes. Elderly patients, who form the majority of the gMG population, are particularly vulnerable due to age-related comorbidities, which limit treatment options and prolong corticosteroid reliance. This contributes to increased mortality, disability, and dependency. Efgartigimod (EFG), a novel therapeutic targeting the neonatal Fc receptor (FcRn), accelerates degradation of pathogenic IgG antibodies, including anti-AChR. Clinical trials (Phase 2, ADAPT, and ADAPT-SC) demonstrated its efficacy and safety in reducing antibody levels, improving muscle strength, and enhancing quality of life. Both intravenous (IV) and subcutaneous (SC) forms are effective and well tolerated. Approved in the United States (2021) and subsequently in Japan and Europe (2022), EFG became available in France in 2023. The present multicenter observational study aims to evaluate the real-life impact of EFG in elderly gMG patients struggling with corticosteroid side effects or comorbidity exacerbations. The objectives of this study include the assessing EFG's ability to enable corticosteroid reduction and monitoring improvements in gMG symptoms, quality of life, comorbidities, and overall health.
This approach highlights a shift towards targeted therapies that balance efficacy with reduced treatment-related burdens for vulnerable gMG populations.

开始日期2025-09-01

申办/合作机构

Centre Hospitalier Universitaire de Nice

NCT07025330

/ Not yet recruiting临床2期IIT

A Phase IIa, Single-Site, Open-Label Study of Efgartigimod in Patients With IgG4-Related Disease

The goal of this clinical trial is to learn if efgartigimod can treat IgG4-related disease in adults. The main questions it aims to answer are:
In patients with IgG4-related disease, does treatment with efgartigimod reduce the volume of the:
* lacrimal gland(s) and/or
* salivary gland(s) and/or
* pancreas
Participants will:
* Receive efgartigimod once weekly for up to 12 weeks
* Visit the clinic every one to six weeks for checkups and tests
* Be asked to complete questionnaires to see how they feel on efgartigimod

开始日期2025-07-15

申办/合作机构

Stanford University

NCT07011589

/ Not yet recruiting临床1/2期IIT

Targeting Collagen VII Antibodies in Bullous Diseases Using Efgartigimod IV (VYVGART)

The study objective is to see if IV Efgartigimod and Vyjuvek treatment in Recessive Dystrophic Epidermolysis Bullosa (RDEB) and IV Efgartigimod treatment in Epidermolysis Bullosa Acquisita (EBA) improves wound healing and affects the levels of C7 antibody levels in serum.
Fewer wounds, more rapidly healing wounds, and decreased C7 antibodies could improve quality of life.

开始日期2025-07-01

申办/合作机构

Stanford University

[+1]

100 项与艾加莫德α 相关的临床结果

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100 项与艾加莫德α 相关的转化医学

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100 项与艾加莫德α 相关的专利（医药）

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213

项与艾加莫德α 相关的文献（医药）

2025-12-31·Human Vaccines & Immunotherapeutics

Impact of FcRn antagonism on vaccine-induced protective immune responses against viral challenge in COVID-19 and influenza mouse vaccination models

Article

作者: Vanhoenacker, Peter ; Baumeister, Judith ; Wouters, Heidi ; Schotsaert, Michael ; Laghlali, Gabriel ; Ulrichts, Peter ; Singh, Gagandeep ; Chang, Lauren A ; Binazon, Ornella ; Warang, Prajakta ; Moshir, Mahan ; Augustynková, Kateřina ; Elhemdaoui, Nadia ; Steeland, Sophie ; Notebaert, Margo

Antagonism of the neonatal Fc receptor through an engineered antibody Fc fragment, such as efgartigimod, results in a decrease in immunoglobulin G levels. This approach is being evaluated as a therapeutic strategy for the treatment of IgG-mediated autoimmune diseases. Our goal was to evaluate the impact of mFc-ABDEG, a mouse-adapted antibody Fc fragment with a mode of action highly similar to efgartigimod, on vaccine-induced protective immune responses against viral infections. Therefore, mouse vaccination models for COVID-19 and influenza were employed, utilizing an mRNA COVID-19 vaccine (COMIRNATY) and an adjuvanted, inactivated quadrivalent influenza vaccine (Seqirus+AddaVax), respectively. In both models, vaccination induced robust humoral responses. As expected, animals treated with mFc-ABDEG had lower levels of virus-specific IgG, while virus-specific IgM responses remained unaffected. The COVID-19 vaccine induced a strong Th1-type T cell response irrespective of mFc-ABDEG treatment. Influenza vaccination resulted in a poor T cell induction, regardless of mFc-ABDEG treatment, due to the Th2-biased response that inactivated influenza vaccines typically induce. Importantly, mFc-ABDEG treatment had no effect on protective immunity against live viral challenges in both models. Vaccinated animals treated with mFc-ABDEG were equally protected as the non-treated vaccinated controls. These non-clinical data demonstrate that FcRn antagonism with mFc-ABDEG did not affect the generation of vaccine-induced protective humoral and cellular responses, or protection against viral challenges. These data substantiate the clinical observations that, although IgG titers were reduced, FcRn antagonism with efgartigimod did not impair the ability to generate new specific IgG responses, regardless of the timing of vaccination.

2025-09-01·INTERNATIONAL IMMUNOPHARMACOLOGY

FcRn inhibition with efgartigimod ameliorates muscle weakness and modulates dendritic cell subsets in an experimental autoimmune myasthenia gravis mouse model

Article

作者: Liang, Xiaole ; Xie, Shenxia ; Mo, Xuean ; Liang, Manli ; Lu, Ting ; Wu, Yu ; Shi, Danli ; Huang, Wen ; Huang, Yanzhen ; Que, Xianting

BACKGROUND:

Myasthenia gravis (MG) is an IgG-mediated autoimmune neuromuscular disorder characterized by exercise-induced skeletal muscle weakness. Reducing circulating IgG levels is a critical therapeutic strategy. Here, we evaluated efgartigimod, a novel neonatal Fc receptor (FcRn) inhibitor that lowers IgG levels, in an experimental autoimmune myasthenia gravis (EAMG) mouse model.

METHODS:

EAMG was induced in mice by immunization with recombinant acetylcholine receptor (AChR). Serum anti-R97-116 IgG titers were quantified by ELISA. Electromyography assessed compound muscle action potentials (CMAPs) in the gastrocnemius muscle using repetitive nerve stimulation. The EAMG+EF group (n = 12) received intraperitoneal efgartigimod (10 mg/kg/week) starting after the third immunization and continuing for 4 weeks, while the EAMG group (n = 12) remained untreated. Control mice (n = 12) underwent mock immunization with CFA. Clinical assessments included body weight, grip strength, and inverted grid test. The proportion of cDC1s, cDC2s, and pDCs, along with their antigen-presenting and co-stimulatory molecules, was analyzed with flow cytometry.

RESULTS:

Compared with controls, repetitive nerve stimulation in EAMG mice revealed a > 10 % reduction in gastrocnemius muscle response, accompanied by elevated anti-R97-116 IgG titers and aggravated myasthenia symptoms, confirming successful AChR peptide-induced EAMG. Efgartigimod treatment improved disease severity, significantly decreasing anti-R97-116 IgG levels, mitigating weight loss, enhancing grip strength, and partially restoring performance on the inverted screen test. Additionally, EAMG mice exhibited a significant increase in the cDC1 subset and a decrease in the cDC2 subset compared to controls. The expression of MHCII was reduced in the cDC1 subset, and the expression of MHCII and CD86 were downregulated in cDC2s in EAMG mice. Efgartigimod treatment normalized cDC1 and cDC2 proportions, restoring MHCII expression to control levels in cDC1s and cDC2s. Furthermore, it significantly upregulated CD80, CD86, and CD40 expression on cDC2s compared to EAMG mice. These findings indicate that efgartigimod modulates the frequencies of dendritic cell subsets as well as their surface expression of antigen presentation (via MHCII) and co-stimulatory signaling molecules (CD40/CD80/CD86).

CONCLUSION:

It is indicated that efgartigimod not only alleviates MG symptoms but also exerts immunomodulatory effects on different dendritic cell subsets.

2025-09-01·CYTOKINE

FcRn inhibitors in immune thrombocytopenia: A comprehensive review of therapeutic advances and clinical outcomes

Review

作者: Abdollahi Namanloo, Mahdi ; Heidari, Nazila ; Nilforoushzadeh, Mohammad Ali ; Heidari, Amirhossein ; Ghotbi, Negar ; Hosseini, Seyedayin

Immune thrombocytopenia (ITP) is an autoimmune disorder characterized by low platelet counts, leading to bleeding risks. Despite existing treatments, many patients with chronic or refractory ITP remain inadequately managed. Fc-receptors, including neonatal Fc receptor (FcRn), play a crucial role in the ITP pathogenesis by activating antibody-dependent cell-mediated cytotoxicity and antibody-dependent cell-mediated phagocytosis, leading to platelet destruction. In addition, recent insights highlight cytokine dysregulation, particularly involving interleukin (IL)-17, IL-6, and Interferon-gamma (IFN-γ), as contributing to disease persistence and immune dysfunction. We sought to evaluate the efficacy and safety of FcRn inhibitors for chronic or persistent ITP treatment. PubMed/Medline, Scopus, and Web of Science databases were systematically searched until January 16th, 2025. Preclinical and clinical studies with available full-text in English were included. Efgartigimod significantly improved platelet counts and reduced Immunoglobulin G (IgG) levels in refractory as well as chronic patients with minimal adverse effects. Rozanolixizumab also showed favorable outcomes in terms of platelet count elevation and IgG reduction in Phase 2 and Phase 3 clinical trials in cases who were unresponsive to ≥2 standard-of-care ITP treatments. These immunotherapeutic agents can effectively increase platelet counts and reduce IgG serum levels, addressing a critical need in patients who do not respond to corticosteroids, thrombopoietin receptor agonists (TPO-RAs), and rituximab. Further long-term studies are warranted to confirm these findings and explore their broader clinical implications.

690

项与艾加莫德α 相关的新闻（医药）

2025-07-25

·生物制品圈

阿斯利康纳米抗体III期告捷重症肌无力治疗添新选

摘要：阿斯利康近日宣布，其靶向补体 C5 的纳米抗体药物 gefurulimab 在重症肌无力（gMG）的 III 期 PREVAIL 试验中达到所有主要和次要终点，为这一罕见自身免疫性疾病带来新的治疗希望。尽管具体数据尚未披露，但该药物的每周皮下自我给药优势，有望挑战现有市场格局。业内预计，详细结果可能于 10 月的医学会议上公布，届时将进一步揭示其与同类药物的竞争力。一、试验突破：纳米抗体展现临床价值Gefurulimab 的 III 期胜利聚焦于抗乙酰胆碱受体（AChR）抗体阳性的全身性重症肌无力患者 —— 这一人群占所有重症肌无力病例的 85%。试验采用 MG-ADL 量表（重症肌无力日常生活活动量表）评估疗效，阿斯利康称药物实现了 “具有统计学意义和临床意义的基线改善”。威廉・布莱尔分析师指出，MG-ADL 量表的最小临床重要差异为≥2 分，而目前已上市的 UCB 药物 Zilbrysq 在 III 期试验中实现了 4.39 分的降低，这为 gefurulimab 的疗效对比提供了参考基准。作为补体 C5 抑制剂，gefurulimab 通过纳米抗体技术精准阻断补体系统过度激活，从而减少神经肌肉接头的损伤，其作用机制与已获批的同类药物相似，但纳米抗体的分子更小，组织穿透性更强，或为其带来差异化优势。二、市场格局：三强争霸即将开启当前重症肌无力治疗市场由两款药物主导：argenx 的 Vyvgart（2023 年 6 月获批）和 UCB 的 Zilbrysq（首款皮下注射制剂）。其中，Vyvgart 凭借两年的先发优势，已占据约 60% 的市场份额，2024 年销售额突破 12 亿美元；Zilbrysq 则以皮下给药便利性快速抢占约 25% 市场。Gefurulimab 的加入将使市场竞争更趋激烈。与 Vyvgart（每两周静脉输注）和 Zilbrysq（每周皮下注射，需医护协助）相比，gefurulimab 的 “每周自我皮下注射” 设计更贴合患者需求，有望提升长期依从性。分析师预测，若其疗效不劣于现有药物，上市后可能在 3-5 年内夺取 15%-20% 的市场份额，年销售额峰值或达 8-10 亿美元。三、技术亮点：纳米抗体的差异化潜力Gefurulimab 的核心优势在于其纳米抗体结构。传统单克隆抗体分子量约 150kDa，而纳米抗体仅为 15kDa，更小的尺寸使其更容易穿透病变组织，且生产工艺更简单，成本相对较低。此外，纳米抗体的半衰期经过优化，支持每周一次给药，避免了频繁注射的负担。阿斯利康在补体系统靶向药物开发上经验丰富，其已上市的长效 C5 抑制剂 Soliris 和 Ultomiris 在罕见病领域表现强劲。此次 gefurulimab 的推进，进一步巩固了公司在补体调控领域的地位。有业内人士推测，该药物可能与阿斯利康的其他自身免疫管线形成协同，拓展至更多补体介导的疾病领域。四、阿斯利康的 “喜忧参半” 周Gefurulimab 的利好消息为阿斯利康近期的研发动态增添了亮色。就在一周前，该公司的淀粉样变性药物 anselamimab 因未能改善患者生存或减少住院率，在 III 期试验中失利。而本周初，阿斯利康宣布在美国投资 500 亿美元扩建生产基地，其中弗吉尼亚州的工厂将专注于代谢疾病（包括心血管和肥胖）药物的生产，显示其在巩固现有优势领域的同时，持续押注新治疗领域。这种 “得失交织” 的研发节奏，反映了大型药企在罕见病和复杂疾病领域的投入策略。重症肌无力虽为罕见病（全球患者约 70 万），但现有疗法价格高昂（年治疗费超 10 万美元），且仍有 30% 的患者对现有药物响应不佳，这为 gefurulimab 留下了市场空间。五、未来展望：数据细节成关键阿斯利康表示，将在即将召开的医学会议上公布 PREVAIL 试验的详细数据，威廉・布莱尔分析师推测可能在 10 月 29 日美国神经肌肉与电诊断医学协会（AANEM）年会上披露。届时，药物的具体疗效数值、亚组分析（如对难治性患者的效果）以及安全性数据，将成为评估其市场潜力的核心依据。对于患者而言，gefurulimab 的上市有望增加治疗选择，推动市场竞争并可能降低治疗成本。而对阿斯利康来说，若能顺利获批，该药物将成为其自身免疫管线的重要补充，与肿瘤、心血管等核心领域形成协同增长。这场由纳米抗体引发的治疗变革，或将为重症肌无力患者的生活质量带来实质性改善。参考来源：https://www.biospace.com/drug-development/astrazenecas-claims-piii-win-with-nanobody-treatment-for-myasthenia-gravis识别微信二维码，添加生物制品圈小编，符合条件者即可加入生物制品微信群！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。

临床3期上市批准临床成功临床结果

2025-07-24

·E药经理人

重症肌无力诊疗指南时隔5年再更新，艾加莫德获高等级推荐

时隔5年，《中国重症肌无力诊断和治疗指南》（下称指南）终于迎来更新。7月22日，由中华医学会神经病学分会神经免疫学组编写的《指南（2025版）》正式发布。5年里，除了传统的激素、免疫抑制剂，多款新型生物制剂获批、进入国家医保目录，也得以在此次指南更新中得到体现。作为国内首款获批的FcRn拮抗剂，艾加莫德首次被纳入指南，被推荐用于治疗AChR-MG患者（证据等级：Ⅰa级，推荐等级：A级）。新指南还推荐了艾加莫德在维持治疗中的长期用药，至少使用三个治疗周期。此外，艾加莫德被推荐用于各类人群的快速达标治疗以及巩固维持治疗。新指南还对MG治疗目标进行了更新，明确了疗效和安全性“双达标”的重要性并将MSE作为疗效“达标”与否的金标准，首次推荐了MG-ADL作为疾病严重程度及疗效的核心评估工具。01艾加莫德长期用药地位得以明确近年来多款重症肌无力的创新药物获批上市。2024年，艾加莫德、依库珠单抗被纳入国家医保目录。今年3月底，第二款FcRn拮抗剂罗泽利昔珠单抗在国内获批，5月底，泰它西普的重症肌无力适应证也获批上市。选择更多的同时，疑惑也随之而来：什么类型的患者适合用靶向生物制剂、怎么用、用多久？新指南中，艾加莫德在维持治疗中的长期用药地位得以明确。指南指出，可根据患者个体状态及医疗中心的实际情况选择每两周一次（Q2W）或固定周期方案，至少使用3个周期，3个周期后可考虑逐渐增加周期间隔。对于肌无力患者来说，周期性维持治疗的好处不少。可以避免病情反复加重，治疗效果不佳。对于这些急性发作的患者，症状改善出院后的一年内仍处于复发高危期，至少3个周期的巩固治疗能降低复发风险。过去，激素和免疫抑制剂是治疗主力，但长期使用副作用大，比如激素会导致“满月脸”、骨质疏松。在今年6月发布的《重症肌无力治疗满意度调研报告》中，约四成患者将减轻治疗副作用列为当下最主要的治疗目标。而维持治疗可以让患者少吃甚至停用激素，重回正常生活。纵观指南不难发现，除了被推荐作为周期性使用的维持治疗手段，艾加莫德还被推荐用于各类人群的快速达标治疗以及巩固维持治疗。02明确“双达标”治疗目标，MSE成衡量疗效“达标”的金标准最大程度地实现症状控制，同时降低药物治疗副作用，这是每个重症肌无力患者的心愿。此次，新指南强调了疗效和安全性“双达标”的治疗目标，同时引入了一个更量化、更贴近患者感受的目标——MSE（最小症状表达，MG-ADL评分0或1分）来衡量疗效是否“达标”。只有达到最小症状或无症状，患者才能真正意义上地回归生活。换而言之，MSE是衡量gMG治疗的金标准。此次中国版指南将MSE的概念引入，标志着国内肌无力治疗理念的转变——从“症状控制”转向“追求更快更好地回归正常生活”。艾加莫德“短期达标”和“长期达标”的数据上均有亮眼的表现——在ADAPT研究的首个周期，40%的患者达到MSE，而传统治疗对照组仅11%。艾加莫德中国真实世界多中心研究显示，多周期治疗9个月MSE累计可达73.3%。03重磅药物或成为再鼎未来业绩重要增长锚点作为一种罕见病中的常见病，重症肌无力的特点之一就是症状容易波动、时好时坏。高盛在今年4月的一份报告中指出，维持治疗或成为 MG 药物市场未来的竞争焦点。高盛引用的临床数据表明，艾加莫德的两种治疗模式在 21 周内展现出良好的安全性和持续疗效。这表明艾加莫德可以作为一种可靠的维持治疗方案。此外，高盛还指出，艾加莫德在美国和中国的真实世界使用数据表明，快速起效的特性使其在急性、难治性gMG 患者群体中被广泛采用。这可能成为未来竞争格局中推动艾加莫德市场份额扩大的重要因素。今年4月11日，艾加莫德预充式皮下注射剂型获FDA批准，这一剂型每次注射仅需20-30秒，由患者、照护人员或医疗卫生专业人士操作。患者在接受皮下注射的指导后可自我给药。这进一步提高了药物使用的便利性。未来艾加莫德将具有三种剂型，以满足不同患者和临床场景的需求。艾加莫德2024年全球销售超过22亿美元，作为纳入医保的首个完整商业化年度，其国内销售额6.3亿人民币，预期国内销售峰值超过30亿-50亿人民币。国盛证券预测，艾加莫德在国内销售峰值有望达到69.39亿人民币（约合9.46亿美元）。一审| 黄佳二审| 李芳晨三审| 李静芝

上市批准临床结果临床3期

2025-07-24

·BioSpace

AstraZeneca’s Claims PIII Win With Nanobody Treatment for Myasthenia Gravis

iStock, Robert Way The company didn’t share specific data for the molecule, gefurulimab, but said it hit all endpoints in the Phase III PREVAIL trial and promised to share more at an upcoming scientific meeting. AstraZeneca’s investigational myasthenia gravis treatment gefurulimab cleared a Phase III trial, meeting all primary and secondary endpoints, the company announced Thursday. The company did not release specific numerical data, only noting that gefurulimab “demonstrated a statistically significant and clinically meaningful improvement from baseline” using the Myasthenia Gravis Activities of Daily Living (MG-ADL) scale, a validated measurement tool for symptoms of myasthenia gravis. Analysts at William Blair said in a note Thursday morning on the news that investors should keep in mind “the minimal clinically important difference on the MG-ADL scale is considered to be ≥2 points from baseline.” A comparable approved daily treatment, UCB’s Zilbrysq, got a 4.39-point reduction using that scale in its Phase III trial, the group wrote. Gefurulimab is a complement C5 inhibiting nanobody, a fragment of a normal antibody. The molecule is being tested in the Phase III PREVAIL trial in adults with anti-acetylcholine receptor (AChR) antibody-positive (Ab+) generalized myasthenia gravis, an autoimmune condition that breaks down communications between the brain and muscles. According to AstraZeneca, 85% of patients with myasthenia gravis have this version of the disease. More detailed information will be presented at a future medical meeting, according to AstraZeneca. The William Blair analysts speculated that that presentation could be at the Myasthenia Gravis Foundation of America (MFGA)’s sessions at the American Association of Neuromuscular & Electrodiagnostic Medicine (AANEM) Annual Meeting on Oct. 29. Zilbrysq is the only FDA-approved subcutaneous treatment for gMG. Gefurulimab could compete with Zilbrysq given that it is a self-administered weekly drug. However, the William Blair analysts cautioned that argenx’s Vyvgart still leads in the $20 billion myasthenia gravis market, given its two-year head-start, having received FDA approval in June 2023. Both AstraZeneca’s and argenx’s stock prices were up about 1.2% in morning trading following the news. The PREVAIL announcement follows a week of newsmaking for AstraZeneca. The company stumbled last week in another rare disease setting after its antibody anselamimab failed to improve survival or hospitalization in patients with amyloidosis. Earlier this week the company also announced a new $50 billion manufacturing push in the U.S., led by a plant in Virginia that will create the company’s metabolic drugs aimed at cardiovascular conditions and obesity.

临床3期临床结果上市批准

100 项与艾加莫德α 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
-	艾加莫德α	-	DB15270

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
慢性炎症性脱髓鞘性多发性神经病	欧盟	argenx US, Inc.	2025-06-20
慢性炎症性脱髓鞘性多发性神经病	冰岛	argenx US, Inc.	2025-06-20
慢性炎症性脱髓鞘性多发性神经病	列支敦士登	argenx US, Inc.	2025-06-20
慢性炎症性脱髓鞘性多发性神经病	挪威	argenx US, Inc.	2025-06-20
慢性特发性血小板减少性紫癜	日本	argenx SE	2024-03-26
免疫性血小板减少症	日本	argenx SE	2024-03-26
重症肌无力	美国	argenx BV	2021-12-17

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
原发性干燥综合征	临床3期	美国	argenx SE	2025-01-15
原发性干燥综合征	临床3期	日本	argenx SE	2025-01-15
原发性干燥综合征	临床3期	奥地利	argenx SE	2025-01-15
原发性干燥综合征	临床3期	比利时	argenx SE	2025-01-15
原发性干燥综合征	临床3期	保加利亚	argenx SE	2025-01-15
原发性干燥综合征	临床3期	加拿大	argenx SE	2025-01-15
原发性干燥综合征	临床3期	爱沙尼亚	argenx SE	2025-01-15
原发性干燥综合征	临床3期	法国	argenx SE	2025-01-15
原发性干燥综合征	临床3期	格鲁吉亚	argenx SE	2025-01-15
原发性干燥综合征	临床3期	德国	argenx SE	2025-01-15

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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


NCT05817669 (rho, CTgov)	临床2期	脊髓小脑性共济失调 \| 原发性干燥综合征	34	Efgartigimod (Efgartigimod)	製繭積鏇膚顧網淵鑰繭 = 網壓糧蓋繭衊糧遞艱獵範選蓋淵鹹鑰積簾選鹽 (襯齋選壓廠鏇獵構簾襯, 顧醖簾鹹鹹網構糧廠齋 ~ 築觸衊壓選鏇衊餘積網) 更多	-	2025-07-18
				placebo+efgartigimod (Placebo)	製繭積鏇膚顧網淵鑰繭 = 膚蓋衊製憲夢願窪蓋遞範選蓋淵鹹鑰積簾選鹽 (襯齋選壓廠鏇獵構簾襯, 餘鹹鏇膚鑰獵鏇築鬱淵 ~ 鹽夢鹹膚淵窪遞積夢淵) 更多
NCT05633407 (POTS, CTgov)	临床2期	体位性心动过速综合征 \| 新冠肺炎后遗症	53	Efgartigimod (Efgartigimod)	鹽遞醖鹹夢觸蓋淵選衊(壓築觸顧獵壓憲窪衊窪) = 鹽鬱鏇遞願膚遞艱膚夢餘憲範淵構廠醖選襯願 (艱鹹衊網鬱遞廠簾廠鏇, 15.2541) 更多	-	2025-05-23
				Placebo (Placebo)	鹽遞醖鹹夢觸蓋淵選衊(壓築觸顧獵壓憲窪衊窪) = 廠艱鬱鹹願觸獵廠鏇蓋餘憲範淵構廠醖選襯願 (艱鹹衊網鬱遞廠簾廠鏇, 17.2963) 更多
NCT04188379 (ADVANCE IV, EHA2025)	临床3期	免疫性血小板减少症维持	131	Efgartigimod IV 10 mg/kg	醖壓廠繭鹽蓋齋繭淵範(築範觸選夢鹹餘襯鹹範) = 鑰範醖蓋衊餘製齋鏇糧蓋膚糧糧蓋膚製壓蓋簾 (鹽齋醖蓋齋遞鏇膚蓋壓, ±3.8) 更多	积极	2025-05-14
				Placebo	醖壓廠繭鹽蓋齋繭淵範(築範觸選夢鹹餘襯鹹範) = 糧願鹽淵獵築繭範淵範蓋膚糧糧蓋膚製壓蓋簾 (鹽齋醖蓋齋遞鏇膚蓋壓, ±2.0) 更多
NCT04980495 (ADAPT NXT, Neurology \| AAN2025) 人工标引	临床3期	重症肌无力	69	efgartigimod fixed-cycle(4 once-weekly infusions, 4 weeks between cycles) (Part A)	築蓋憲顧願範遞製範鏇(衊顧夢鹹糧憲網糧獵襯) = 鏇選糧餘築觸願襯積構艱鹹廠淵淵齋製鏇壓願 (壓遞窪襯壓願獵壓醖餘, -6.5 ~ -3.8) 更多	积极	2025-04-07
				efgartigimod Q2W (Part A)	築蓋憲顧願範遞製範鏇(衊顧夢鹹糧憲網糧獵襯) = 遞繭願蓋範餘網網鬱醖艱鹹廠淵淵齋製鏇壓願 (壓遞窪襯壓願獵壓醖餘, -5.4 ~ -3.8) 更多
P7-11.026 (AAN2025)	N/A	重症肌无力 \| 肌肉无力 AChR antibody positive	16	Efgartigimod 10 mg/kg	醖壓築鑰蓋鹽廠鬱壓夢(蓋積襯願鏇製積遞顧窪) = An 89-year-old female with thymoma and multiple comorbidities developed diarrhea, UTIs, respiratory infections, and failure postoperatively. She was reintubated on POD 21, and died of multiple organ failure on POD 43. 遞觸鑰淵蓋齋醖衊憲選 (製壓齋齋窪簾築窪糧齋 )	积极	2025-04-07
AAN2025	N/A	重症肌无力	25	Efgartigimod	齋襯蓋鏇艱範鹹衊壓網(製網積構鹽積膚鹽觸蓋) = Only one patient experienced transient vomiting and diarrhea; no serious adverse reactions reported 淵鏇網夢膚顧繭遞鬱願 (築鹹夢簾鬱積膚膚製構 )	积极	2025-04-07
P4-8.003 (AAN2025)	N/A	重症肌无力 anti-acetylcholine receptor antibody-positive	4	Efgartigimod	壓膚艱廠願觸壓製鏇獵(衊蓋衊觸製鏇積顧膚鑰) = 衊觸鹹鑰鑰窪觸艱膚齋鬱壓窪蓋獵鹽鏇網積憲 (鑰鑰願鹽選醖窪鬱夢壓 )	积极	2025-04-07
				Ravulizumab	壓膚艱廠願觸壓製鏇獵(衊蓋衊觸製鏇積顧膚鑰) = 積網廠糧壓醖簾壓製齋鬱壓窪蓋獵鹽鏇網積憲 (鑰鑰願鹽選醖窪鬱夢壓 )
P1-11.001 (AAN2025)	N/A	重症肌无力 anti-acetylcholine receptor antibody-positive (AChR-Ab+)	152	Ravulizumab	觸憲願鹹憲觸艱網夢鏇(蓋糧觸膚鹹蓋蓋醖壓範) = 簾繭構蓋憲壓構鑰衊築鬱襯獵鑰廠選餘遞襯艱 (繭遞醖築鏇鑰膚淵憲餘 )	积极	2025-04-07
				Efgartigimod	構鬱鏇淵艱積壓鹹艱餘(鑰製齋憲淵衊鏇衊醖鹹) = 艱範鏇齋獵積顧鬱鹽蓋願獵鑰糧範淵繭製鑰顧 (簾鏇積繭鏇顧夢範鑰鹹 ) 更多
NCT04188379 (ADVANCE \| ADVANCE IV, CTgov)	临床3期	免疫性血小板减少症	131	efgartigimod (Efgartigimod)	廠獵壓鏇選觸製膚鏇膚 = 鏇鏇艱選觸鑰鬱顧夢壓壓夢鏇積蓋衊艱衊鏇窪 (顧鏇艱鹹襯選齋鬱淵齋, 積製鑰繭夢構糧選膚鹹 ~ 壓醖蓋夢壓遞願築鏇艱) 更多	-	2025-03-13
				Placebo (Placebo)	廠獵壓鏇選觸製膚鏇膚 = 鑰蓋鏇範膚艱觸顧壓餘壓夢鏇積蓋衊艱衊鏇窪 (顧鏇艱鹹襯選齋鬱淵齋, 顧醖餘顧鏇壓廠獵窪餘 ~ 窪夢艱鑰鑰製網鏇憲遞) 更多
NCT04687072 (ADVANCE SC, CTgov)	临床3期	免疫性血小板减少症	207	Efgartigimod PH20 SC (Efgartigimod PH20 SC)	齋醖廠襯鹹製糧鹽廠憲 = 簾積艱積構壓夢積簾簾觸膚選願鹽壓網選壓憲 (鑰鏇觸鏇襯鏇鹹艱積鏇, 築餘衊窪鑰餘積獵蓋窪 ~ 壓繭鑰蓋積蓋繭鹽獵艱) 更多	-	2024-10-31
				Placebo PH20 SC (Placebo PH20 SC)	齋醖廠襯鹹製糧鹽廠憲 = 蓋網製餘觸衊選網鹽壓觸膚選願鹽壓網選壓憲 (鑰鏇觸鏇襯鏇鹹艱積鏇, 襯繭簾獵遞鑰糧繭鬱鬱 ~ 願艱網選窪遞鹽餘餘蓋) 更多