The goal of this study is to evaluate the effect of mepolizumab on patients with COPD using MRI and CT imaging as well as breathing tests. The study will evaluate the response to this medication after 24 and 48 weeks of treatment. The main questions it aims to answer are:
1. Does mepolizumab improve ventilation defect percent as measured on 129-Xenon MRI in adults with COPD.
2. Does mepolizumab improve the amount of mucus plugs in the lungs as measured by lung CT in adults with COPD.
Participants will:
1. Take mepolizumab by subcutaneous injection every 4 weeks for the duration of the study.
2. Visit Robarts 4 times over 48 weeks for tests and imaging.

开始日期2026-10-01

申办/合作机构

University of Western Ontario

ISRCTN17701271

/ Not yet recruitingN/AIIT

Airway Dysfunction, Occlusions and RemodEling: COPD Patients and Mepolizumab (ADORE)

开始日期2026-09-15

申办/合作机构

Western University

ChiCTR2600125076

/ Not yet recruitingN/AIIT

The effects of biological agents targeting type 2 inflammation in stable phase bronchiectasis patients with type 2 inflammation

开始日期2026-05-27

申办/合作机构-

100 项与美泊利珠单抗相关的临床结果

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100 项与美泊利珠单抗相关的转化医学

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100 项与美泊利珠单抗相关的专利（医药）

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1,778

项与美泊利珠单抗相关的文献（医药）

2026-12-31·ANNALS OF MEDICINE

Beyond biomarkers: the role of clinical factors associated with biologic therapy response in severe asthma

Article

作者: Lopez-Rodríguez, Raquel ; Cañas, José Antonio ; Rial, Manuel Jorge ; Mahíllo-Fernández, Ignacio

BACKGROUND:

Severe asthma carries a high burden and often requires biologic therapy targeting type 2 (T2) inflammation. However, treatment response is heterogeneous, and traditional biomarkers, such as blood eosinophils, fractional exhaled nitric oxide (FeNO), and total serum IgE, may not fully explain this variability .

OBJECTIVE:

To evaluate clinical and inflammatory characteristics associated with response to biologic therapies in a real-world cohort of severe asthma patients.

METHODS:

A single-center, ambispective observational study was conducted in the Allergology Department of A Coruña, Spain. Sixty-seven patients with severe uncontrolled asthma and treated with omalizumab, mepolizumab, benralizumab, dupilumab, or tezepelumab, were included. Patients were followed for ≥12 months. Clinical variables and inflammatory biomarkers were assessed at baseline, 4-6 months, and 12 months. Comparisons between biologic subgroups and logistic regression analyses were performed to identify factors associated with response.

RESULTS:

Female sex, nasal polyposis, elevated blood eosinophils, and frequent exacerbations were associated with better response to biologics. Clinical factors such as nasal polyposis and aspirin-exacerbated respiratory disease (AERD) showed a stronger association with treatment response than standard biomarkers (FeNO, blood eosinophils). The mean diagnostic delay was 12.1 years, suggesting a potential influence on therapeutic results.

CONCLUSION:

Beyond traditional biomarkers, clinical factors particulary nasal polyposis and AERD may play a key role in understanding response patterns to biologics. Incorporating these variables into clinical assessment may help support a more personalized management approach in severe asthma.

2026-12-31·COPD-Journal of Chronic Obstructive Pulmonary Disease

Number Needed to Treat with Biologics in Type-2 Inflammation COPD: A Systematic Review and Meta-Analysis

Review

作者: Wang, Qinqin ; Ma, Qianli

In moderate‑to‑severe chronic obstructive pulmonary disease (COPD), the number needed to treat (NNT) quantifies therapeutic benefit but remains underused for type-2-targeted biologics. This meta-analysis quantified the NNT for type-2-targeted biologics in moderate-to-severe COPD and incorporated the recent evidence on exacerbations, lung function, symptoms, health status, and responder outcomes. We searched PubMed, Embase and Web of Science through July 2025 for phase 2 or 3 RCTs of type-2targeted biologics in adults with COPD. The primary outcome was NNT for moderate-to-severe exacerbations; secondary outcomes included pre-bronchodilator forced expiratory volume in 1 s (FEV₁), St. George's Respiratory Questionnaire (SGRQ), Evaluating Respiratory Symptoms in COPD (E-RS-COPD), and responder proportions. Pooled ratios and mean differences were synthesized using fixed‑ or random‑effects models. Patient-based NNT was derived from cumulative incidence, event‑based NNT was derived from annualized exacerbation rates. Pooled NNTs were estimated under selected baseline‑risk scenarios. Under three baseline‑risk scenarios, pooled patient‑based NNTs for reducing moderate‑to‑severe COPD exacerbations were 12-17 for dupilumab and 11-16 for mepolizumab, benralizumab showed no clear reduction. Event-based NNTs at a baseline annual exacerbation rate of 1.055 per year were 3 for dupilumab and 5 for mepolizumab. Dupilumab was associated with improvements in pre-bronchodilator FEV₁, SGRQ, and E-RS-COPD. For mepolizumab, evidence across these non‑exacerbation outcomes was not consistently observed. In conclusion, pooled patient-based and event-based analyses suggest that both dupilumab and mepolizumab consistently reduce moderate-to-severe exacerbations in eosinophilic or type 2 inflammatory COPD, while improvements in lung function and patient-reported outcomes remain less consistent across biologics and warrant further validation. These findings derive from separate placebo‑controlled trials and should not be interpreted as establishing a comparative efficacy hierarchy among biologics.

2026-10-01·AUTOIMMUNITY REVIEWS

ANCA-associated vasculitis: From immunopathogenesis to diagnosis and toward precision therapy

Review

作者: Borges, Henrique ; Silvestre-Teixeira, Vítor ; Jerónimo, Teresa M ; Domingos, Tomás G

Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) comprises a group of rare, potentially life-threatening autoimmune disorders characterized by necrotizing inflammation of small vessels. Over recent decades, remarkable advances have been made in unraveling its immunopathogenesis, emphasizing the interplay between genetic predisposition, environmental triggers, loss of immune tolerance, neutrophil extracellular trap formation, and complement-mediated neutrophil activation. This review provides an integrative synthesis of recent mechanistic and clinical insights into AAV, bridging fundamental immunology with translational and therapeutic advances. Based on an extensive literature search of PubMed and Scopus, studies were selected according to methodological quality and clinical relevance. Distinct ANCA specificities, proteinase 3 (PR3) and myeloperoxidase (MPO), define overlapping yet prognostically divergent subsets, with PR3-ANCA linked to relapsing multisystem disease and MPO-ANCA to renal involvement and progression to kidney failure. Therapeutic paradigms have evolved from cyclophosphamide-based induction toward rituximab-centered and glucocorticoid-sparing regimens, with mepolizumab further improving efficacy and safety profiles. Despite five-year survival rates exceeding 85%, long-term morbidity persists, driven by relapse and treatment-related toxicity. However, precision therapy in AAV remains incomplete, as current treatment selection is still guided mainly by disease severity, organ involvement, relapse risk, comorbidities, renal histology, and risk of glucocorticoid-toxicity rather than by validated molecular biomarkers. Emerging data on complement activation, urinary inflammatory biomarkers, B-cell kinetics, and tissue-based transcriptomic profiling may refine disease endotyping and individualized monitoring. Collectively, these advances herald a transition from empirical immunosuppression toward biologically informed, precision-oriented care in vasculitis.

1,245

项与美泊利珠单抗相关的新闻（医药）

2026-08-28

·同花顺投顾平台

国信证券-医药生物行业创新药盘点系列报告（28）——重度哮喘生物制剂还有哪些升级空间？-260828

重度哮喘以T2炎症驱动为主，但不同患者的疾病驱动通路存在明显异质性，生物标志物分层决定现有疗法的疗效天花板。EOS、FeNO及allergicsensitization可从不同维度反映T2炎症，其中EOS更接近IL-5/eosinophil axis，FeNO主要反映IL-4/IL-13 epithelial signaling，而IgE相关指标更适合作为allergic phenotype及用药eligibility marker，单独预测疗效的能力相对有限。我们估计美国重度哮喘人群中EOS+FeNO双高约占33%、EOS-dominant及FeNO-dominant分别约21%/20%，其余包括IgE-only及triple-low等患者。现有生物制剂在EOS+FeNO双高患者中的AAER降幅最高可达约75%~80%，而EOS-only或FeNO-only患者约为50%，EOS/FeNO双低患者疗效则进一步下降，提示不同endotype仍存在程度不一的残余疾病风险。下一代单靶药物的核心升级来自“长效化”，成熟靶点有望通过减少注射频率提升依从性及扩大生物制剂渗透率。IL-5赛道已率先完成半年一次给药的商业化验证，Exdensur（Depemokimab）通过Q6M给药实现对Nucala的产品迭代；TSLP则成为长效化竞争最激烈的靶点，多个Q3M~Q6M产品进入中后期临床。我们认为，凭借高亲和力及Fc/PK优化，Q3MTSLP单抗达到Tezspire相近疗效具有较高可行性，而Q6M方案对持续trough target coverage提出更高要求，因此其差异化主要体现为convenience而非提升疗效上限。 Multi-target策略有望突破单靶疗效天花板。TSLP位于上游，可覆盖allergen、viral infection及epithelial injury诱导的多条T2启动通路；IL-13直接影响FeNO、mucus、goblet-cell metaplasia、AHR及airway remodeling，两者联合可同时获得pathway breadth和downstream depth。Sanofi的TSLPxIL-13双抗Lunsekimig已在Ph1b中显示对FeNO、EOS、IL-5、eotaxin-3、TARC及IgE的同步PD抑制，并在Ph2b AIRCULES研究中达到AAER主要终点及FEV1关键次要终点，首次完成multi-target asthma临床PoC；CM512、Tilrekimig及IBI3002等后续产品亦陆续进入临床。 Multi-target产品的商业价值主要来自对现有单靶生物制剂的升级替代。基于主要产品销售额及适应症拆分，我们估计2025年美国asthma biologics市场约66亿美元、对应约21万年用药患者，bio-eligible患者渗透率约19%~23%。我们预计multi-target产品首先在EOS+FeNO及FeNO-driven患者中获得1L份额，并承接部分TSLP、IL-4Rα及IL-5/5R partial responder形成的2L switch需求；基准情形下，假设首款产品2030年前后上市，至2040年multi-target class有望达到约20%的美国生物制剂患者份额，对应~7.5万患者及~30亿美元市场规模；若后续临床研究证实能够将现有75%~80%的AAER reduction进一步提升至85%~90%，同时证明更高zero-exacerbation/clinical remission比例并获得较好的payer access，远期患者份额有望进一步达到25%~30%。风险提示：市场竞争加剧的风险、产品临床失败或有效性低于预期的风险、产品商业化不达预期的风险、技术升级迭代风险等。

2026-08-28

·南山呼吸

EOS Talk 嗜酸性粒细胞组织驻留与原位生成：破解重度哮喘“血象缓解症状未控”之谜

引言临床实践中，部分重度嗜酸性粒细胞性哮喘患者经靶向生物制剂治疗后，外周血嗜酸性粒细胞（EOS）虽已明显下降甚至接近正常范围，但哮喘症状仍控制不佳，甚至急性发作。这一看似矛盾的现象，暴露出仅依赖外周血EOS评估哮喘炎症的局限性，提示我们需要重新审视EOS在气道局部的生物学效应。在即将召开的欧洲呼吸学会年会（ERS）上，哮喘免疫机制与精准治疗被列为核心议题，全球学者将研究视野向EOS髓外原位生成等前沿方向受到关注。在“EOS Talk——嗜酸性粒细胞增多相关疾病”栏目中，我们从临床痛点出发，深度剖析“血EOS指标改善与症状不一致”背后的病理根源，探讨重度哮喘治疗策略的革新。机制之源：组织驻留与原位生成共同维持气道EOS负荷 1.组织驻留导致EOS在局部形成“炎症储备” EOS来源于骨髓，由造血祖细胞经共同髓系祖细胞、粒-单核系祖细胞、EOS祖细胞（EoP）等阶段，最终分化为成熟的EOS[1]。其中，白介素（IL）-5是EOS的分化、增殖、募集和存活的重要调控因子[2]。成熟的EOS通过整合素和选择素介导进入血液，仅停留8~18小时，随后迁移至多种组织中，尤其是呼吸道、胃肠道等黏膜屏障部位。进入组织后的EOS不再回到循环，其在组织内的寿命只有3-4天。但在炎症微环境中，IL-5、IL-13及粒细胞-巨噬细胞集落刺激因子（GM-CSF）等细胞因子可延缓其凋亡，延长其存活时间[2]。当大量的EOS在气道聚集浸润，一方面可持续释放主要碱性蛋白质（MBP）等颗粒蛋白，及转化生长因子-β（TGF-β）等多种细胞因子，引发气道损伤、气道高反应、黏液过度分泌，导致不可逆的气道重塑；另一方面通过释放IL-4、IL-13、白三烯等炎症介质，激活中性粒细胞、肥大细胞、T细胞、B细胞，放大炎症级联反应[3-5]。因此，即便外周血EOS下降，组织驻留的EOS仍可作为“炎症储备库”维持局部病理效应。图1 EOS介导的哮喘气道炎症网络[5] 2.原位生成为气道EOS提供持续补给传统观念认为，气道内的EOS完全由骨髓生成后经血液循环迁徙而来。然而，不断有研究提出并证实，EOS还可在气道组织内“就地生产”[6]。 2017年发表于Nature的一项研究发现，小鼠肺脏血管外间质中存在大量造血祖细胞，提示肺脏具备一定的髓外造血潜能，可独立完成髓系细胞的分化成熟过程[7]。这一发现为EOS原位生成提供了组织学基础。生理状态下，这些造血祖细胞处于低活性；而在炎症、损伤等病理刺激下，可被快速激活，并驱动EOS的局部分化。具体而言，过敏原、病毒感染等刺激可导致气道上皮屏障被破坏，受损的上皮细胞快速释放胸腺基质淋巴细胞生成素（TSLP）、IL-33、IL-25等上皮预警素，增强2型先天性淋巴样细胞（ILC2）等2型免疫通路的活化，诱导IL-5、IL-13和GM-CSF等因子上调，构建局部持续的炎症微环境[6,8,9]。在局部IL-5的驱动下，CD34⁺IL-5Rα⁺造血祖细胞可在气道组织内分化为成熟EOS；IL-13进一步介导造血祖细胞向气道部位募集与归巢；GM-CSF则与IL-5协同作用，增强EOS祖细胞的增殖，最终在气道局部完成从祖细胞到成熟EOS的全过程[6,8,9]。图2 气EOS道原位生成机制示意[6] 临床研究为这一机制提供了直接证据。研究发现，尽管外周血中EOS水平与轻度哮喘患者相当，但重度泼尼松依赖性哮喘患者的痰液中CD34⁺造血祖细胞、EoP及成熟EOS数量均显著升高，且其EoP对IL-5的反应性更强，能更高效地分化为成熟EOS[10]。这表明，在重度哮喘患者的气道中，存在一个过度活跃的“原位EOS生成微环境”，其活跃程度与外周血EOS水平并不平行。肺/气道EOS可能来自两条途径，一为骨髓生成后迁徙而至；此外，肺脏局部的造血祖细胞通过炎症诱导分化也会产生一定量的成熟的EOS。肺/气道已不再仅仅是炎症的被动“受害者”，更成为不断输出EOS的“原位兵工厂”。由上可见，组织驻留让EOS形成“存量储备”，原位生成又不断提供新的“增量”，二者共同解释了“血象改善而症状未控”背后的原因。更深一步看，在EOS介导的气道炎症中，组织EOS才是驱动和维持炎症的根本。外周血EOS的水平仅是局部病理状态的间接反映，单纯降低外周血EOS并不能完全等同于控制了气道炎症，临床需将视线从“血象”转向“组织”。评估之殇：外周血EOS指标与气道真实炎症的脱节正如第一部分所阐述，气道局部EOS负荷在重度哮喘的病理生理中扮演着核心角色，因此，直接检测气道组织中的EOS，能更准确地反映局部炎症的真实情况。但在临床实操层面，由于诱导痰技术、实验室的要求、周转时长等因素，目前痰EOS的应用受限[11]，部分基层医疗机构难以常规开展。而外周血EOS凭借其检测操作简便、快捷、成本相对较低的优势，被推荐为评估气道EOS的良好替代指标，成为目前指导分型和生物制剂选择的常用手段。目前一些生物医药企业正在研发EOS相关生物标志物的快速检测技术，有望进一步弥补诱导痰EOS检测在基层难以开展的短板。综合上述机制不难看出，外周血EOS水平升高，提示组织存在EOS高负荷。但血EOS正常或偏低，组织EOS水平未必低，不能排除气道局部EOS浸润的可能性，仍需保持对气道炎症的警惕性，继续动态监测、连续评估。破局之道：精准靶向EOS，重塑治疗格局如何有效降低气道局部EOS负荷，成为重度哮喘治疗的关键问题。精准靶向EOS的生物制剂，为此提供了新的路径。目前靶向EOS的生物制剂主要有抗IL-5单抗（美泊利珠单抗）与抗IL-5Rα单抗（本瑞利珠单抗）。二者作用机制各有侧重。美泊利珠单抗的策略偏于“阻断信号”，它通过与游离IL-5结合，从而阻断IL-5信号对EOS的生物作用，抑制EOS生物活性并使其数量降低至较低水平[12]。一项III期临床研究显示，美泊利珠单抗治疗SEA患者，较安慰剂降低急性发作率达65%，支气管扩张剂前一秒用力呼气容积（pre-BD FEV1）较安慰剂组多改善137mL[13]。而本瑞利珠单抗的策略则是“源头清除”。一方面，直接与EOS表面的IL-5Rα结合，阻断EOS激活、分化、成熟、迁移；另一方面，与EOS结合后，可募集自然杀伤细胞，通过细胞毒作用快速降低EOS水平。这种双重机制，使本瑞利珠单抗能实现外周血、气道组织中EOS的深度消耗竭[14]。研究显示，本瑞利珠单抗治疗重度哮喘患者，较安慰剂可降低年急性发作率达74%，且pre-BD FEV1较安慰剂提高250mL[15]。结语气道EOS组织驻留与原位生成机制的揭示，不仅解答了外周血指标与临床症状割裂的迷局，更指明了治疗策略升级的方向。未来，随着气道局部炎症评估技术的标准化和生物制剂的精准应用，我们有望实现对重度哮喘的突破性治疗，显著改善患者的长期预后。【调研小问题】答案：E 点击查看答案参考文献 [1] 中华医学会呼吸病学分会哮喘学组,等.中华医学杂志,2022,102(1):21-35. [2] Di Gioacchino M, et al. UpToDate on eosinophils. Explor Asthma Allergy. 2026;4:1009111. [3] Jacobsen EA, et al. Annu Rev Immunol. 2021;39:719-757. [4] McBrien CN, et al. Front Med (Lausanne). 2017;4:93. [5] Choi Y, et al. Korean J Intern Med. 2020;35(4):823-833. [6] Brittany M Salter, et al. Cells. 2021 Feb 16;10(2):412. [7] Lefrançais E, et al. Nature. 2017;544(7648):105-109. [8] Salter BM, et al. Chest. 2017;152(1):75-84. [9] Mukherjee M, et al. Immunol Allergy Clin N Am, 2018;38(4):639-654. [10] Sehmi R, et al. Clin Exp Allergy. 2016;46(6):793-802. [11]中华医学会呼吸病学分会哮喘学组.中华结核和呼吸杂志,2020.43(12):1023-1048. [12]Jackson DJ, et al. Eur Respir Rev. 2022; 31: 210150. [13] Chen R,et al. ERJ Open Res. 2024 May 20;10(3):00750-2023. [14]Dagher R, et al. Eur Respir J. 2022; 59:2004306. [15] Lai K, et al. Respir Med. 2024 Apr 1107611. 欢迎投稿至：nanshanhuxi_2018@163.com 转载请联系学术助手微信：KVOPR183 ↓ ↓ ↓ 点击下方名片即刻关注南山呼吸

2026-08-28

·谦铖临研健康

【国际哮喘4期临床招募】德莫奇单抗国内已获批上市，免费提供3年面向存在发作风险的2型哮喘人群探索早期干预的长期获益

【MODIFY研究：一项评估Depemokimab早期干预有风险的成人和青少年2型哮喘患者对急性发作率、临床治愈、肺功能下降和安全性的影响的为期最长156周、IIIb/IV期、随机、双盲、安慰剂对照、多中心研究。】一免费创新药 Depemokimab：是英国葛兰素史克 GSK研发的 IL‑5人源化IgG1单克隆抗体，带有YTE‑Fc改造，实现超长效半衰期，每26周（半年）皮下注射1次。【作用机制】 IL‑5是2型炎症核心细胞因子，驱动嗜酸性粒细胞成熟、存活、组织浸润，是嗜酸型哮喘急性发作的关键推手。德莫奇单抗特异性结合并中和游离IL‑5，阻断信号传导，快速、持续降低血液、气道嗜酸性粒细胞数量，减轻气道2型炎症，减少哮喘急性加重。 Fc段YTE氨基酸突变，提升和FcRn受体结合能力，大幅拉长体内半衰期，实现一年仅2针给药，区别于美泊利珠单抗每月一次的方案。【既往核心临床数据】 1. 年化哮喘急性发作率较安慰剂平均下降54%；SWIFT‑1下降58%，SWIFT‑2下降48%，达主要终点。 2. 持续耗竭血嗜酸粒细胞，疗效维持满52周。 3. 肺功能FEV1、生活质量获得改善；整体安全性和其他抗IL‑5单抗相近，常见：上呼吸道感染、头痛、注射部位反应，严重不良事件发生率低。目前国内已经获批：重度嗜酸性哮喘、慢性鼻窦炎伴鼻息肉适应症。二报名条件 1.年龄： 18 周岁及以上 2.哮喘确诊：符合 GINA 哮喘诊断标准，具备可查阅的病历记录。急性发作史：筛选前 12 个月内至少 2 次哮喘急性发作；筛选前至少 3 个月接受中高剂量 ICS‑LABA 维持治疗。用药基线：筛选期稳定接受中 / 高剂量 ICS‑LABA 治疗至少 3 个月；受试者入组前可接受最低剂量 ICS‑LABA，占总受试者最多 40%。生物标志物：筛选外周血 EOS 计数达标；满足 RINC‑1/T2 型哮喘判定；需存在过敏性发作风险；入组时 CRSwNP 可纳入。【排除标准】 1.筛选前 1 年内发生≥3 次哮喘急性发作。 2.使用 OCS 持续治疗，或高剂量 ICS‑LABA 仍无法控制哮喘。 3.除哮喘外，存在临床显著肺部基础疾病（感染、支气管扩张、肺纤维化等）；排除慢阻肺受试者。 4.可致 EOS 升高的其他疾病（高嗜酸粒细胞综合征、嗜酸性肉芽肿性多血管炎等）。 5.筛选期出现哮喘急性发作，需距离发作结束至少 4 周才可重新筛选。 6.筛选前 6 个月存在活动性寄生虫感染，未治愈者排除。 7.免疫缺陷病史；因哮喘接受 ICOS 治疗者除外。 8.近 12 个月存在恶性肿瘤病史；已完全切除的局部皮肤癌除外。 9.未经规范控制的心、内分泌、自身免疫、神经、精神、肝肾、血液系统等全身性疾病。 10.当前确诊血管炎，入组前必须排除活动性血管炎。 11.既往接受过本药或同类 mAb 生物制剂。 12.给药前 2 周内使用过活疫苗 / 减毒活疫苗。 13.近 52 周使用过任何免疫抑制剂（口服 / 注射激素除外）。 14.预判依从性差，无法遵从研究者指令。三患者获益 1.哮喘程度和资料审核通过者，免费挂号、免费全身体检、体检合格免费领药（免费体检包含：传染病检查、血常规、血生化、尿常规、心电图、、超声、CT等） 2.为期3年，访视18‑24次访趟，并有相应交通补助和采血补助；【具体以三甲医院知情同意书为准】四研究医院覆盖国家/城市北京市北京市浙江省杭州市浙江省杭州市湖南省长沙市湖南省长沙市四川省成都市河南省郑州市江苏省徐州市上海市上海市湖北省武汉市北京市北京市上海市上海市福建省福州市广东省广州市天津市天津市湖北省武汉市河南省郑州市重庆市重庆市山东省济南市河北省廊坊市新疆维吾尔自治区乌鲁木齐市广东省广州市广东省广州市 United States Nebraska University of Nebraska Medical Center United States New York Northwell Health, LLC United States Iowa University of Iowa Health Care United States Massachusetts Brigham and Women's Hospital United States Michigan University of Michigan United States Florida Envision Trials LLC United States New York Montefiore Medical Center (MMC) United States Florida VAMC Gainesville United States Florida Innovative Research of West Florida, Inc. United States Ohio Bernstein Clinical Research Center, LLC United States California Woodland Clinic United States Tennessee Clinical Trials Center of Middle Tennessee United States Montana Montana Medical Research, Inc. United States Florida University of Florida United States Michigan AA MRC LLC Ahmed Arif Medical Research Center United States Iowa Integrated Clinical Trial Services, Inc. United States Florida Synergy Healthcare, LLC United States Texas Epic Medical Research Bedford United States Oklahoma Legacy Clinical Trials of Oklahoma City United States Alabama Cullman Clinical Trials United States Arizona ORSO Health United States California 3Sync Research United States California 3Sync Research United States California ORSO Health United Kingdom Strathclyde Gartnavel General Hospital United Kingdom Avon Southmead Hospital United Kingdom Cambridgeshire Addenbrooke's Hospital United Kingdom Leicestershire Glenfield Hospital United Kingdom Hampshire Queen Alexandra Hospital United Kingdom Greater London Guy's Hospital United Kingdom Hertfordshire Lister Hospital United Arab Emirates Abu Dhabi Sheikh Shakbout Medical City United Arab Emirates Abu Dhabi Sheikh Khalifa Medical City United Arab Emirates Abu Dhabi Tawam Hospital Spain Valencia Hospital Universitari i Politecnic La Fe Spain Alcorcon Hospital Universitario Fundacion Alcorcon Spain Pamplona Hospital Universitario de Navarra Spain Badalona Hospital Universitari Germans Trias i Pujol Spain Santander Hospital Universitario Marques de Valdecilla Spain Madrid Hospital Universitario 12 de Octubre Spain Barcelona Hospital Clinic de Barcelona Spain Granada Hospital Universitario Virgen de las Nieves Spain Lugo Hospital Universitario Lucus Augusti Spain Madrid FutureMeds ES Viamed Madrid Spain Esplugues de Llobregat Hospital Sant Joan de Deu Spain Benalmádena Hospital Vithas Xanit Internacional Spain Barcelona Pectus Respiratory Health Girona Spain Barcelona Hospital del Mar Spain Palma de Mallorca Hospital Universitari Son Espases Spain Madrid Hospital Universitario de La Princesa Spain Zaragoza Hospital Universitario Miguel Servet Spain Sevilla Hospital Universitario Virgen Macarena Spain Madrid Hospital Universitario Infanta Leonor Spain Logrorio Hospital Universitario San Pedro Spain Pozuelo de Alarcón Hospital Memorial Publio Cordon Saudi Arabia Riyadh King Fahad Medical City Saudi Arabia Riyadh King Saud University Medical City Saudi Arabia Makkah King Abdulaziz University Hospital Romania Brasov S.C Centrul Medical de Diagnostic si Tratament Ambulator Neomed S.R.L Romania Brasov Theramed Healthcare SRL Romania Brasov S.C Policlinica de Diagnostic Rapid S.A Romania Craiova Spitalul Clinic de Boli Infectioase si Pneumoftiziologie Victor Babes Craiova Romania Bucuresti Institutul de Pneumoftiziologie Romania Bucuresti Delta Health Care S.R.L Romania Brasov Centrul Medical Unirea S.R.L Korea, Republic of Gyeonggi-do Seoul National University Bundang Hospital Korea, Republic of Seoul Asan Medical Center Korea, Republic of Seoul Seoul National University Hospital Korea, Republic of Gyeonggi-do Ajou University Hospital Korea, Republic of Seoul Samsung Medical Center Korea, Republic of Seoul Konkuk University Medical Center Korea, Republic of Daegu Yeungnam University Hospital Italy Ancona Azienda Ospedaliero Universitaria delle Marche Italy Varese Fondazione Salvatore Maugeri - Clinica Del Lavoro E Della Riabilitazione IRCCS - Istituto Scientific Italy Genova IRCCS Ospedale Policlinico San Martino Italy Verona Centro Ricerche Cliniche di Verona s.r.l. Italy Bari Azienda Ospedaliero Universitaria Consorziale Policlinico di Bari Italy Catanzaro Azienda Ospedaliero Universitaria Renato Dulbecco Italy Firenze Azienda Ospedaliera Universitaria Careggi Italy Roma Azienda Ospedaliera Universitaria Policlinico Umberto I - Università di Roma La Sapienza Italy Roma Fondazione Policlinico Universitario Agostino Gemelli IRCCS Italy Brescia Azienda Socio Sanitaria Territoriale degli Spedali Civili di Brescia (Presidio Spedali Civili) Italy Catania Azienda Ospedaliero Universitaria Policlinico “Gaspare Rodolico - San Marco” (Presidio G. Rodolico) Italy Cagliari Università di Cagliari-Presidio Policlinico Monserrato Italy Milano Istituto Clinico Humanitas Italy Ancona Azienda Ospedaliero Universitaria delle Marche Ireland Cork Cork University Hospital Ireland Louth Our Lady of Lourdes Ireland Dublin Connolly Hospital - Blanchardstown Ireland Dublin Beaumont Hospital Ireland Dublin Tallaght University Hospital Ireland Westmeath Midland Regional Hospital Mullingar Germany Sachsen Praxis fuer Pneumologie und Allergologie Germany Sachsen POIS Sachsen GmbH Germany Rheinland Pfalz IKF Pneumologie Mainz Germany Berlin Pneumologisches Studienzentrum MVZ Germany Rheinland Pfalz KPPK Studienzentrum Germany Berlin MECS GmbH Germany Hessen Studienzentrum Dr. Keller Germany Niedersachsen Klinische Forschung Hannover-Mitte GmbH - Pratia Germany France Alpes Maritimes CH de Cannes France Bouches-du-Rh？ne Centre Hospitalier du Pays d'Aix France Bas Rhin CHU de Strasbourg - Nouvel Hopital Civil France Finistere CHRU de Brest - H？pital Morvan France Bouches-du-Rh？ne H0pital Nord - CHU Marseille France Isere CHU de Grenoble - Hopital Nord France Paris Hopital Cochin France Finistere CHU de Brest - Hopital de la Cavale Blanche Czech Republic South Moravian Fakultni nemocnice Brno Czech Republic South Bohemian MediTrial s.r.o Czech Republic South Moravian MUDr. Ilona Pavlisova s.r.o. Canada Alberta CARe Clinic Canada Ontario Dynamic Drug Advancement Canada Quebec C.I.C. Saint Laurent Canada Quebec Jewish General Hospital Bulgaria Ruse SHATPPD Bulgaria Varna Medical Centre Pratia Clinic EOOD Bulgaria Sofia Medical Center Hera EOOD Bulgaria Sofia Medical Center Iskar EOOD Bulgaria Sofia DCC Bulgaria Varna Haelan Care 4 Medical Center EOOD Bulgaria Ruse Medical Center- Prolet Ltd Belgium Antwerp AZ Sint-Maarten Belgium Antwerp UZA Belgium Namur Pneumocare Belgium Brussels Capital Region Cliniques Universitaires Saint-Luc Belgium Liège CENTRE HOSPITALIER UNIVERSITAIRE DE LIEGE Belgium Brussels Capital Region HUB Erasme Belgium Hainaut De Meulemeester, Marc Australia New South Wales Canopy Clinical Northern Beaches Australia New South Wales Canopy Clinical Sutherland Shire Australia Western Australia TrialsWest Mandurah Australia Victoria Paratus Clinical Melbourne Australia Queensland University of the Sunshine Coast Clinical Trials Centre Australia Victoria Canopy Clinical Altona North Australia Victoria Emeritus Research, Melbourne Australia Queensland Queensland Allergy Services Australia Queensland The Prince Charles Hospital 全国共161家三甲医院开展，国内: 71人；国际: 456人； END 更多疾病临床招募，免费用创新药如果你或家人被疾病困扰，想免费用前沿创新药，全国各省三甲医院临床招募患者中… 病情和资料审核通过者，可免费挂号、免费全身体检，体检合格免费用药，三甲医院团队全程监护。有意向可私信，会发所有适配项目，并协助收集报名所需资料，让你省心高效，提高报名成功率！扫码咨询报名/合作，联系临床招募小谦：1520 163 6492（同微信）本文仅作临床试验信息传达，不构成诊疗建议，内容均取自公开信息。如有不适，请线下就医并遵医嘱，祝早日康复~

100 项与美泊利珠单抗相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D04923	美泊利珠单抗	R03DX09	DB06612

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
慢性阻塞性肺疾病	美国	GSK Plc	2025-05-22
哮喘	日本	GlaxoSmithKline KK	2020-03-25
慢性鼻窦炎伴鼻息肉	欧盟	GlaxoSmithKline Trading Services Ltd.	2015-12-01
慢性鼻窦炎伴鼻息肉	冰岛	GlaxoSmithKline Trading Services Ltd.	2015-12-01
慢性鼻窦炎伴鼻息肉	列支敦士登	GlaxoSmithKline Trading Services Ltd.	2015-12-01
慢性鼻窦炎伴鼻息肉	挪威	GlaxoSmithKline Trading Services Ltd.	2015-12-01
Churg-Strauss综合征	欧盟	GlaxoSmithKline Trading Services Ltd.	2015-12-01
Churg-Strauss综合征	冰岛	GlaxoSmithKline Trading Services Ltd.	2015-12-01
Churg-Strauss综合征	列支敦士登	GlaxoSmithKline Trading Services Ltd.	2015-12-01
Churg-Strauss综合征	挪威	GlaxoSmithKline Trading Services Ltd.	2015-12-01
嗜酸性粒细胞性哮喘	欧盟	GlaxoSmithKline Trading Services Ltd.	2015-12-01
嗜酸性粒细胞性哮喘	冰岛	GlaxoSmithKline Trading Services Ltd.	2015-12-01
嗜酸性粒细胞性哮喘	列支敦士登	GlaxoSmithKline Trading Services Ltd.	2015-12-01
嗜酸性粒细胞性哮喘	挪威	GlaxoSmithKline Trading Services Ltd.	2015-12-01
高嗜酸性粒细胞综合征	欧盟	GlaxoSmithKline Trading Services Ltd.	2015-12-01
高嗜酸性粒细胞综合征	冰岛	GlaxoSmithKline Trading Services Ltd.	2015-12-01
高嗜酸性粒细胞综合征	列支敦士登	GlaxoSmithKline Trading Services Ltd.	2015-12-01
高嗜酸性粒细胞综合征	挪威	GlaxoSmithKline Trading Services Ltd.	2015-12-01
重度哮喘	美国	GlaxoSmithKline LLC	2015-11-04

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
肺嗜酸性粒细胞增多	申请上市	中国	葛兰素史克（中国）投资有限公司	2023-03-14
哮喘，鼻息肉和阿司匹林不耐受	临床3期	日本	GSK Plc	2021-02-08
嗜酸粒细胞增多症	临床3期	英国	GSK Plc	2020-09-07
鼻息肉	临床3期	-	GSK Plc	2017-05-25
嗜酸性肉芽肿	临床3期	比利时	GSK Plc	2013-11-12
肉芽肿伴多血管炎	临床3期	比利时	GSK Plc	2013-11-12
中枢神经系统血管炎	临床3期	比利时	GSK Plc	2013-11-12
鼻病毒感染	临床3期	荷兰	GSK Plc	2012-01-01
吞咽障碍	临床2期	美国	GSK Plc	2019-03-20
中度特应性皮炎	临床2期	美国	GSK Plc	2017-03-21

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临床结果

适应症

分期

评价

查看全部结果

研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


EULAR2026	N/A	Churg-Strauss综合征	587	Mepolizumab 100 mg/4 weeks	鬱餘衊範簾壓鬱範衊醖(願襯鏇遞觸鏇積衊廠選) = 願積廠廠糧鬱顧製夢願積遞淵網廠鏇膚糧艱獵 (壓顧簾醖鬱廠餘餘構襯 ) 更多	积极	2026-06-11
				Mepolizumab 300 mg/4 weeks	鬱餘衊範簾壓鬱範衊醖(願襯鏇遞觸鏇積衊廠選) = 艱觸壓鹽鹽製壓築製壓積遞淵網廠鏇膚糧艱獵 (壓顧簾醖鬱廠餘餘構襯 ) 更多
NCT02020889 (MIRRA, EULAR2026)	临床3期	Churg-Strauss综合征 \| 慢性鼻窦炎伴鼻息肉	56	Mepolizumab	鹽積膚遞構壓壓鏇鹽顧(醖醖膚壓壓遞衊膚鏇繭): OR = 0.33 (95.0% CI, 0.1 ~ 1.03), P-Value = 0.057 更多	积极	2026-06-11
				Placebo
EULAR2026	N/A	Churg-Strauss综合征	587	Mepolizumab 100 mg	簾觸壓築齋築醖網鹹艱(簾構構憲簾構鹽蓋簾簾) = 壓網獵鹽鏇淵築範簾艱築夢遞範顧鬱憲淵築築 (觸鹹糧夢淵築齋獵艱糧 ) 更多	积极	2026-06-11
				Mepolizumab 300 mg	簾觸壓築齋築醖網鹹艱(窪鑰簾範衊蓋選積鹹構) = 鬱網壓齋衊築夢顧網淵選鬱鑰網淵齋鑰構鹹糧 (憲顧衊齋鹹簾築網簾壓 ) 更多
EULAR2026	N/A	高嗜酸性粒细胞综合征 \| Churg-Strauss综合征	50	Mepolizumab	齋襯廠鏇範積鏇鏇憲壓(憲衊範築鏇網鑰衊網夢) = 遞製觸憲鹽糧觸壓選膚壓衊廠蓋艱醖繭鬱鑰構 (構壓衊觸餘鏇顧夢襯願, 55 ~ 215) 更多	积极	2026-06-11
NCT02105948 (METREX, ATS2026)	临床3期	慢性阻塞性肺疾病	1,146	Mepolizumab 100 mg	衊淵顧壓製窪鑰築繭鬱(鬱積襯遞壓窪構壓簾顧) = 築獵鏇艱窪襯構膚鑰齋製夢鹹製醖夢構構繭網 (簾糧製鹹齋醖繭選觸鹽 ) 更多	积极	2026-05-15
				Placebo	衊淵顧壓製窪鑰築繭鬱(鬱積襯遞壓窪構壓簾顧) = 鹹構願淵築鑰襯顧鹹衊製夢鹹製醖夢構構繭網 (簾糧製鹹齋醖繭選觸鹽 ) 更多
TYREX (ATS2026)	N/A	重度哮喘	446	Mepolizumab (patients with CRSwNP)	夢繭鹽獵鏇構醖鹽窪醖(繭範糧觸鹹網觸淵鑰選) = improved in both groups, with numerically greater gains in the CRSwNP group 顧築齋製鑰夢鏇壓鏇鬱 (構醖餘獵築鑰艱壓構鑰 ) 更多	积极	2026-05-15
				Mepolizumab (patients without CRSwNP)
ATS2026	N/A	慢性阻塞性肺疾病	1,945	Mepolizumab 100 mg	蓋齋醖窪糧餘製糧糧範(積齋願獵鹹夢選憲範窪) = Mepolizumab demonstrated a safe profile, with no difference in the risk of any adverse event compared with placebo. 廠衊繭壓製糧繭膚製艱 (觸鏇網範鹽選醖鹽壓艱 ) 更多	积极	2026-05-15
				Placebo
ATS2026	N/A	慢性阻塞性肺疾病 \| 哮喘-慢性阻塞性肺疾病重叠综合征	900,144	Mepolizumab or Dupilumab	築簾夢獵醖窪夢願繭簾(築夢齋遞醖選夢構襯鑰) = 製廠鬱網鏇鹽選窪鏇醖餘製餘廠窪獵鬱繭遞鑰 (觸網醖衊鏇網窪衊網蓋 ) 更多	积极	2026-05-15
				Never received either medication	築簾夢獵醖窪夢願繭簾(築夢齋遞醖選夢構襯鑰) = 窪鏇衊淵憲範憲窪壓觸餘製餘廠窪獵鬱繭遞鑰 (觸網醖衊鏇網窪衊網蓋 ) 更多
ATS2026	N/A	Churg-Strauss综合征 MPO-ANCA \| p-ANCA+	1	Mepolizumab	鹽窪齋製鬱鹹鹹齋壓網(繭構壓膚顧鹽選築壓築) = Asymptomatic on 5 mg prednisone at 3 months 齋衊襯網繭獵鹽繭鹽願 (壓簾糧製觸鹽鏇齋築鬱 )	积极	2026-05-15
NCT02105948 (METREX, ATS2026)	临床3期	慢性阻塞性肺疾病	2,089	Mepolizumab 100 mg	構廠網淵網製餘壓繭鹽(製觸遞襯構選壓窪醖選): RR = 0.77 (95.0% CI, 0.6 ~ 0.99), P-Value = 0.044 更多	积极	2026-05-15
				Placebo