Anti-IL-33 mAb(Regeneron Pharmaceuticals)、Immunoglobulin igg4 (230-proline), anti-(human interleukin 33) (human monoclonal regn3500 .gamma.4-chain), disulfide with human monoclonal regn3500 .kappa.-chain, dimer、伊塔特珠单抗

+ [2]

靶点

IL-33

作用方式

抑制剂

作用机制

IL-33抑制剂(白细胞介素-33抑制剂)

治疗领域

呼吸系统疾病感染耳鼻咽喉疾病

在研适应症

慢性鼻窦炎伴鼻息肉慢性支气管炎中度慢性阻塞性肺疾病+ [3]

非在研适应症

过敏性哮喘哮喘炎症+ [4]

原研机构

Regeneron Pharmaceuticals, Inc.

在研机构

Sanofi-Aventis Recherche & Développement SA

赛诺菲（中国）投资有限公司

Regeneron Pharmaceuticals, Inc.

+ [2]

非在研机构-

权益机构

Regeneron Pharmaceuticals, Inc.

Sanofi

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-

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结构/序列

Sequence Code 17746027H

来源: *****

Sequence Code 17746031L

来源: *****

关联

项与依特吉单抗相关的临床试验

NCT07484230

/ Withdrawn临床3期

A Randomized, Double-blind, Parallel-group, 52-week Trial to Investigate the Efficacy, Safety, and Tolerability of Itepekimab in Adult Japanese Participants With Inadequately-controlled Chronic Rhinosinusitis With Nasal Polyps

This is a randomized, multicenter, double-blind, Phase 3 study with 2 parallel groups. The purpose of this study is to evaluate the efficacy, safety, and tolerability of 2 different dosing regimens of itepekimab monotherapy in Japanese participants aged 18 years or older with chronic rhinosinusitis with nasal polyp(s) (CRSwNP) who are not adequately controlled despite previous surgery and/or treatment with systemic corticosteroid(s) (SCS).
The total study duration par participant is approximately 76 week, including:
* A screening period for up to 4 weeks.
* A randomized study intervention period for up to 52 weeks
* A post-intervention safety follow-up for up to 20 weeks
* The number of visits will be 9 site visits and 20 phone/home visits

开始日期2026-05-08

申办/合作机构

Sanofi

[+1]

NCT07424144

/ Active, not recruiting临床3期

A Double-blinded Extension Study to Evaluate the Long-term Safety and Tolerability of Itepekimab in Adult Participants With Inadequately Controlled Chronic Rhinosinusitis With Nasal Polyps (CRSwNP) Who Participated in Either EFC18418 or EFC18419 Clinical Studies

This is a double-blind, parallel-group, Phase 3, 2-arm study that is designed to provide additional safety information, assess the durability of treatment response, and provide additional PK and immunogenicity assessments.
The primary purpose of this study is to evaluate safety and tolerability of both new or continued treatment with itepekimab 300 mg SC high dose or itepekimab 300 mg SC low dose in participants with CRSwNP having completed the intervention period of the clinical studies EFC18418 or EFC18419. A secondary purpose of this study is to provide efficacy outcomes beyond the intervention period of the parent trials EFC18418 and EFC18419.
Study details include:
* The study duration will be up to 72 weeks.
* The intervention duration will be 52 weeks.
* A follow-up period of 20 weeks will be conducted.
* The number of visits will be 8 and the number of phone contacts will be 4.

开始日期2026-03-12

申办/合作机构

Sanofi

[+1]

NCT06834347

/ Terminated临床3期

A Randomized, Double-blind, Placebo-controlled, Parallel-group, 52-week Phase 3 Trial to Investigate the Efficacy, Safety, and Tolerability of Itepekimab in Adult Participants With Inadequately-controlled Chronic Rhinosinusitis With Nasal Polyps

EFC18418 is a multinational, randomized, double-blind, placebo-controlled, parallel-group, Phase 3 study with 3 treatment groups. The purpose of the study is to evaluate the efficacy, safety and tolerability of 2 dosing regimens of itepekimab compared to placebo as add-on therapy to intranasal corticosteroids (INCS) in male and female participants with chronic rhinosinusitis with nasal polyps (CRSwNP) aged 18 years of age and older.
Study details include:
* The study duration per participant (4-week screening, 52-week treatment, 20-week safety follow-up) will be up to 76 weeks. For participants transitioning to the LTS18420 study, the study duration will be 56 weeks.
* The treatment duration will be up to 52 weeks.
* The number of visits will be 9 site visits and 20 phone/home visits.

开始日期2025-02-12

申办/合作机构

Sanofi

[+1]

100 项与依特吉单抗相关的临床结果

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100 项与依特吉单抗相关的转化医学

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100 项与依特吉单抗相关的专利（医药）

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项与依特吉单抗相关的文献（医药）

2026-12-31·mAbs

Structures of clinical antibodies bound to IL-33 uncover two distinct epitopes underlying differential efficacy

Article

作者: Chen, Jing ; Wang, Xinquan ; Wang, Yue

Interleukin-33 (IL-33), an alarmin cytokine of the IL-1 family, drives type 2 inflammation through signaling via the ST2 and IL-1RAcP receptors, making it a critical therapeutic target for inflammatory diseases such as asthma and chronic obstructive pulmonary disease. Current therapeutic strategies have primarily focused on antibodies that target IL-33 or ST2 to disrupt their specific interaction. However, the structural mechanisms underlying antibody-mediated neutralization of IL-33 remain poorly understood. Here, we report the structures of three antibodies in clinical trial - etokimab, itepekimab, and tozorakimab - complexed with IL-33, determined by X-ray crystallography and cryo-electron microscopy. Structural analysis reveals two distinct neutralizing epitopes on IL-33, termed Epitope 1 at IL-33/ST2 binding Site 1 and Epitope 2 at IL-33/ST2 binding Site 2. Tozorakimab, which targets Epitope 1, completely blocks ST2 engagement by sterically occluding the ST2 D1-D2 domain-binding interface. In contrast, etokimab and itepekimab, which recognize Epitope 2, interfere with IL-33 recognition of the ST2 D3 domain and thereby only partially inhibit ST2 binding. These structural and biochemical findings provide a molecular explanation for the differential efficacy of the three antibodies in inhibiting IL-33 signaling in cellular assays. Collectively, our results provide valuable insights into the molecular determinants of efficacy for existing IL-33 therapeutics and offer a structural framework for the rational design of next-generation IL-33 targeted inhibitors.

2026-12-01·MOLECULAR BIOLOGY REPORTS

Epithelial alarmins TSLP, IL-33, and IL-25 in asthma pathogenesis: mechanistic roles and therapeutic implications

Review

作者: Nelson Kumar, Sadhu ; Siva Ganesh, Vakkalagadda ; Rajaram, Cuddapah ; H R, Sneha ; Dhanush, Yarava

BACKGROUND:

Asthma is a heterogeneous chronic inflammatory airway disease affecting over 300 million people worldwide. The airway epithelium serves as the primary interface with environmental stimuli and responds by releasing epithelial-derived alarmins, thymic stromal lymphopoietin (TSLP), interleukin-33 (IL-33), and interleukin-25 (IL-25), which act as upstream regulators of both innate and adaptive immune responses. Current therapies targeting downstream inflammatory mediators demonstrate limited efficacy in severe and refractory asthma, necessitating novel approaches targeting upstream pathways.

OBJECTIVE:

This narrative review examines the mechanistic roles of epithelial alarmins TSLP, IL-33, and IL-25 in asthma pathogenesis, covering their regulation, receptor signalling, downstream immune activation, and contributions to airway remodelling. Current and emerging biologic therapies targeting these alarmins are summarised, with key clinical trials tabulated.

METHODS:

A comprehensive narrative literature review was conducted. Electronic databases searched included PubMed/MEDLINE, Scopus, Web of Science, and ClinicalTrials.gov, covering publications from January 2015 to March 2025, with seminal earlier studies included where relevant. Search terms used included: "TSLP asthma," "IL-33 asthma," "IL-25 asthma," "epithelial alarmins," "thymic stromal lymphopoietin," "tezepelumab," "itepekimab," "astegolimab," "airway inflammation," "ILC2," "airway remodelling," and "biologic therapy severe asthma." Priority was given to original research articles, randomised controlled trials, and systematic reviews; review articles were included to provide mechanistic context. Studies were selected based on relevance to alarmin biology, immunological pathways, and clinical evidence in asthma.

RESULTS:

TSLP: Functions as a central amplifier of type-2 and mixed inflammatory responses through transcriptional regulation following epithelial stimulation. Activates dendritic cells, group 2 innate lymphoid cells (ILC2s), and granulocytes via the TSLPR/IL-7Rα complex, driving both eosinophilic and non-eosinophilic inflammation. Tezepelumab, an anti-TSLP monoclonal antibody, has achieved regulatory approval (FDA/EMA) for severe asthma with demonstrated exacerbation reduction across multiple endotypes (40-60% reduction in clinical trials). IL-33: Constitutively stored in epithelial cell nuclei, acts as an immediate danger signal upon cellular injury, triggering rapid innate immune activation through the ST2/IL-1RAcP receptor complex. Mediates acute exacerbations, airway hyperresponsiveness, and steroid-refractory inflammation. Anti-IL-33 agents including itepekimab, astegolimab, and tozorakimab are in Phase 2-3 clinical development with promising early efficacy data. IL-25: Predominantly produced by epithelial tuft cells, sustains chronic type-2 immunity, mucus hypersecretion, and corticosteroid-insensitive disease phenotypes through IL-17RA/IL-17RB receptor engagement. IL-25-targeted approaches demonstrate preclinical efficacy and are advancing toward clinical evaluation.

CONCLUSION:

Epithelial alarmins represent critical upstream drivers of asthma pathogenesis, orchestrating diverse inflammatory pathways that determine disease endotypes and severity. Therapeutic targeting of TSLP, IL-33, and IL-25 offers a paradigm shift from downstream cytokine inhibition to source-directed intervention, with potential to reduce exacerbations, prevent airway remodelling, and improve disease control across different asthma phenotypes. The success of anti-TSLP therapy and ongoing clinical development of IL-33 and IL-25 inhibitors validate epithelial alarmins as essential molecular targets for precision medicine approaches in severe and refractory asthma.

2026-09-01·Biochemistry and Biophysics Reports

The IL-33/ST2 pathway to modulate the inflammatory microenvironment: A new therapeutic target in chronic obstructive pulmonary disease

Review

作者: Yang, Lei ; Zhong, Jingjing ; Zheng, Gaofeng ; Shen, Hao ; Chen, Jie ; Wu, Yonghong ; Xie, Xiaoyan

The IL-33/ST2 pathway is critically implicated in the pathogenesis and progression of chronic obstructive pulmonary disease (COPD), orchestrating a complex interplay of oxidative stress, immunity, inflammation, and pulmonary injury. Clinical evidence shows that the expression levels of IL-33 and ST2 are significantly elevated in patients with COPD, which correlates strongly with disease severity, increased frequency of acute exacerbations, and negative clinical outcomes. Therapeutic strategies targeting the IL-33/ST2 pathway, including anti-IL-33 monoclonal antibodies and ST2 inhibitors, have demonstrated considerable potential in preclinical studies. These approaches have shown efficacy in mitigating inflammatory responses, enhancing lung function, and reducing the risk of acute exacerbations. Notably, the precise regulatory mechanisms of the IL-33/ST2 pathway in COPD and its crosstalk with inflammation remain incompletely understood and warrant further investigation. This review mainly elaborates the molecular biological characteristics and mechanism of IL-33/ST2, summarizes the function of IL-33/ST2 in COPD development and treatment, illustrates the application of IL-33/ST2 in patient's immune-inflammatory regulation and drug discovery, and discusses the prospects of targeting IL-33/ST2.

327

项与依特吉单抗相关的新闻（医药）

2026-08-18

·BioSpace

Regeneron ends eye disease study after antibody shows ‘unfavorable’ risk/benefit profile

iStock, Aryo Hadi The discontinuation of the uveitis study adds to Regeneron’s series of clinical setbacks, including the Phase 3 failures of the Dupixent follow-up itepekimab and an investigational combo regimen for melanoma. Regeneron has terminated a Phase 1/2 study of an investigational anti-inflammatory antibody, which was being tested for non-infectious uveitis. The decision to end the trial is due to an “unfavorable benefit-risk assessment” of the candidate, called REGN7041, according to a federal clinical trials database . BioSpace has reached out to Regeneron for more details regarding the discontinuation of the study and the company’s future plans for REGN7041. The asset is no longer listed on the pharma’s pipeline page . REGN7041 is a monoclonal antibody that targets CD3, a marker found on immune cells that drives the inflammatory cascade. Non-infectious uveitis is an eye disease characterized by inflammation of a layer of the eye. Common symptoms include redness, pain, sensitivity to light and compromised eyesight. There hasn’t yet been an anti-CD3 therapy approved for uveitis. The discontinuation of the uveitis study continues somewhat of a losing streak for Regeneron. In May last year, for instance, the pharma announced that itepekimab—an interleukin-33 blocker that many had been eyeing as a follow-up to Dupixent— failed one of two late-stage chronic obstructive pulmonary disease trials. A year later, the pharma’s investigational melanoma combo kneeled to Merck’s Keytruda in a Phase 3 trial. Earnings Regeneron’s ‘aversion’ to M&A questioned as bumper Q2 builds war chest Calls for Regeneron to step up dealmaking have intensified as the company has established an $18 billion cash pile and suffered clinical trial setbacks. July 30, 2026 · 2 min read · Nick Paul Taylor Read more In the face of these setbacks, analysts have been piling on the M&A pressure as a way for Regeneron not just to beef up its pipeline, but also make use of what BMO Capital Markets last month called the pharma’s “financial strength.” The company, for its part, has clarified that it is not “allergic to any external opportunity,” CEO Leonard Schleifer said during a second quarter investor call in July. “We look at them all, but we are pretty disciplined in trying to create value with these transactions.” While it’s true that Regeneron hasn’t signed a mega-deal in a while, the pharma has indeed been looking externally for innovation. Just in the past few months, the pharma has inked a handful of partnerships, including one with Telix in April, putting up to $4.3 billion on the line to advance radiopharmaceutical programs for several cancer indications. Shortly after, Regeneron linked up with Parabilis Medicines in a deal that could potentially reach $2.3 billion, hoping to unlock a new class of medicines called antibody-helicon conjugates to address previously undruggable targets. Deals Regeneron, Parabilis set out to create new drug class in deal worth up to $2.3B Right after reporting a major Phase 3 LAG-3 miss that has rattled analysts, Regeneron Pharmaceuticals revealed a back-loaded partnership with Parabilis Medicines aimed at adding a new drug class to its early-stage pipeline. May 18, 2026 · 2 min read · Gabrielle Masson Read more

临床3期

2026-08-18

·BioSpace

Regeneron ends eye disease study due to antibody’s safety profile

iStock, Aryo Hadi The discontinuation of the uveitis study adds to Regeneron’s series of clinical setbacks, including the Phase 3 failures of the Dupixent follow-up itepekimab and an investigational combo regimen for melanoma. Regeneron has terminated a Phase 1/2 study of an investigational anti-inflammatory antibody, which was being tested for non-infectious uveitis. The decision to end the trial is due to an “unfavorable benefit-risk assessment” of the candidate, called REGN7041, according to a federal clinical trials database . A company spokesperson confirmed the discontinuation to BioSpace via email on Tuesday morning, noting that “this decision follows an updated risk-benefit assessment for the study treatment, prompted by a thorough review of a safety event observed in the trial.” The spokesperson did not specify what the safety event was, noting only that Regeneron has conducted an investigation into the event and that the cause “has not been identified.” REGN7041 is a monoclonal antibody that targets CD3, a marker found on immune cells that drives the inflammatory cascade. Non-infectious uveitis is an eye disease characterized by inflammation of a layer of the eye. Common symptoms include redness, pain, sensitivity to light and compromised eyesight. There hasn’t yet been an anti-CD3 therapy approved for uveitis. The discontinuation of the uveitis study continues somewhat of a losing streak for Regeneron. In May last year, for instance, the pharma announced that itepekimab—an interleukin-33 blocker that many had been eyeing as a follow-up to Dupixent— failed one of two late-stage chronic obstructive pulmonary disease trials. A year later, the pharma’s investigational melanoma combo kneeled to Merck’s Keytruda in a Phase 3 trial. Earnings Regeneron’s ‘aversion’ to M&A questioned as bumper Q2 builds war chest Calls for Regeneron to step up dealmaking have intensified as the company has established an $18 billion cash pile and suffered clinical trial setbacks. July 30, 2026 · 2 min read · Nick Paul Taylor Read more In the face of these setbacks, analysts have been piling on the M&A pressure as a way for Regeneron not just to beef up its pipeline, but also make use of what BMO Capital Markets last month called the pharma’s “financial strength.” The company, for its part, has clarified that it is not “allergic to any external opportunity,” CEO Leonard Schleifer said during a second quarter investor call in July. “We look at them all, but we are pretty disciplined in trying to create value with these transactions.” While it’s true that Regeneron hasn’t signed a mega-deal in a while, the pharma has indeed been looking externally for innovation. Just in the past few months, the pharma has inked a handful of partnerships, including one with Telix in April, putting up to $4.3 billion on the line to advance radiopharmaceutical programs for several cancer indications. Shortly after, Regeneron linked up with Parabilis Medicines in a deal that could potentially reach $2.3 billion, hoping to unlock a new class of medicines called antibody-helicon conjugates to address previously undruggable targets. Deals Regeneron, Parabilis set out to create new drug class in deal worth up to $2.3B Right after reporting a major Phase 3 LAG-3 miss that has rattled analysts, Regeneron Pharmaceuticals revealed a back-loaded partnership with Parabilis Medicines aimed at adding a new drug class to its early-stage pipeline. May 18, 2026 · 2 min read · Gabrielle Masson Read more Editor’s note (Aug. 18): The story and headline have been updated to include information from a Regeneron spokesperson.

临床3期

2026-08-16

·新药心谈

靶向IL-33托雷奇单抗申报：首款冲线的慢阻肺靶向药，目标呼吸界的dupi？

*免责声明：部分资料来自网络，仅供医药专业人士参考。任何药品相关描述，都不应理解为对任何品种的处方及诊疗推荐。®标仅展示商品名，并不代表已注册。 **凡有原创标记的文章，未经授权，谢绝转载。 6月26日，阿斯利康托雷奇单抗注射液（Tozorakimab）的进口上市申请获受理。根据公开资料和临床进展，本次申报适应症指向慢性阻塞性肺疾病（COPD）。这是全球首个申报上市的IL-33靶向单抗。在慢阻肺生物制剂屡屡"挑患者"的当下，它走出了一条不一样的路。 COPD是一种进展性、致命性的呼吸系统疾病，特征是持续性气流受限和气道慢性炎症，已成为全球第三大死因（不含COVID-19）。临床上有个数据很刺眼：即使接受了优化的吸入维持治疗，高达60%的患者仍会继续经历急性加重。每一次中重度急性加重，都意味着肺功能的一次"跳水"——加速病情进展、增加住院率，甚至推高死亡风险。现有的慢阻肺生物制剂，大多在"挑患者"：度普利尤单抗（Dupilumab）等靶向IL-4/IL-13的生物制剂，主要对血嗜酸性粒细胞计数偏高（>300 cells/μL）的患者有效再生元/赛诺菲的IL-33单抗依特吉单抗（Itepekimab），二期研究显示疗效仅在既往吸烟者中显现换句话说，当前吸烟者、嗜酸性粒细胞不高、肺功能重度受损的患者，几乎没有什么靶向药可选。 IL-33是IL-1家族的警报素（alarmin）。当气道上皮和内皮细胞受到损伤、感染或环境刺激时，IL-33就会从细胞核里被释放出来，相当于拉响炎症警报。关键细节在这里——IL-33在COPD患者气道中存在两种形态，走的是两条完全不同的通路：还原型IL-33（IL-33^red）：与免疫细胞表面的ST2受体结合，启动1型、2型、3型等多种炎症表型氧化型IL-33（IL-33^ox）：构象发生改变后不再结合ST2，转而与RAGE受体结合，通过EGFR通路导致气道上皮修复障碍、黏液过度分泌氧化型IL-33这条"旁路"，恰好是慢阻肺上皮功能障碍和黏液高分泌的核心驱动。而在吸烟者、尤其是当前吸烟者的肺部氧化应激环境中，IL-33^ox反而可能是主角。这就解释了为什么只阻断IL-33^red/ST2的单抗（如依特吉单抗），疗效会受限于"既往吸烟者"这一子集。托雷奇单抗是一款高亲和力全人源IgG1单抗，它的独特之处在于：第一重阻断：以飞摩尔（femtomolar）级别的超高亲和力结合IL-33^red，完全占据ST2的结合界面，阻断炎症信号传导。晶体结构研究显示，托雷奇单抗结合在IL-33的Epitope 1位点，通过空间位阻完全遮蔽ST2的D1-D2结构域结合面——这比结合Epitope 2的依特匹单抗"部分抑制"更彻底。第二重阻断：更关键的是，它的超高亲和力和快速结合速率，能在IL-33^red被氧化之前就把它"锁住"，从源头阻止IL-33^ox的形成，进而间接阻断RAGE/EGFR通路。一款药，同时做两件事——压制炎症 + 促进上皮修复、减少黏液分泌。这是它区别于其他IL-33/ST2药物的本质差异。阿斯利康在COPD领域布局了5项III期临床（OBERON、TITANIA、MIRANDA、PROSPERO、ROMEO），目前已公布的三项均达到主要终点。 OBERON和TITANIA（2026年3月公布）：两项重复的III期试验，共纳入2306例患者，托雷奇单抗300mg皮下注射、每4周一次，在优化吸入双联或三联治疗基础上加用。主要终点为52周时既往吸烟者中重度急性加重年化率。结果：两项试验均达到主要终点，较安慰剂显著降低急性加重年化率；在包含当前吸烟者的总人群中，关键次要终点同样达成。无论血嗜酸性粒细胞计数高低、无论肺功能损伤严重度，均观察到一致获益。 MIRANDA（2026年4月公布）：采用300mg每2周一次给药方案，纳入1454例有症状COPD患者（入组前12个月内至少2次中度或1次重度急性加重，且已接受至少3个月吸入维持治疗）。结果：在既往吸烟者主要人群中达到中重度急性加重年化率显著降低的主要终点；在包含当前吸烟者的总人群中，关键次要终点同样达成。不同嗜酸性粒细胞水平、不同肺功能严重度的人群，均观察到一致的统计学和临床意义的降低。安全性方面，托雷奇单抗总体耐受性良好，不良事件特征与既往研究一致。具体不良反应谱尚未在顶线数据中披露，需等待后续医学会议公布完整结果。三项试验、不同给药间隔（每2周/每4周）、不同人群，读出的都是一致阳性——这在COPD生物制剂开发史上是罕见的。更关键的是，获益不依赖嗜酸性粒细胞水平，意味着它有可能覆盖那些被现有生物制剂"拒之门外"的患者。对临床医生而言，托雷奇单抗在华申报，意味着慢阻肺生物制剂可能进入"不挑患者"的时代。过去几年，IL-33/ST2这条通路屡遭挫折——AERIFY-2失败、罗氏等项目喜忧参半，市场对这条通路的信心一度降到冰点。托雷奇单抗三项III期连续阳性，且机制上能同时覆盖炎症和上皮修复，重新验证了IL-33作为COPD靶点的价值。对患者而言，这是首款申报上市的IL-33单抗。目前在吸入标准治疗下仍反复急性加重的患者——尤其是当前仍在吸烟、嗜酸性粒细胞不高、肺功能重度受损的那批人——终于在临床试验之外，看到了一种可能的靶向治疗选择。话说回来，托雷奇单抗目前还在审评阶段，最终能否获批、何时获批，要以CDE后续官方消息为准。PROSPERO和ROMEO两项III期试验的结果也尚未公布，前者将评估托雷奇单抗对重度急性加重（需住院或致死）的长期影响——这才是真正决定它能否改写COPD治疗格局的关键数据。全球范围内，14款IL-33靶向药已进入临床，托雷奇单抗是第一个跑到申报上市位置的。它能不能成为呼吸慢阻肺领域的度普利尤单抗，要看接下来PROSPERO的数据，也要看CDE的审评尺度。阿斯利康在呼吸领域是绝对优势，应该问题不大。 ✦ END ✦

临床结果临床2期申请上市临床3期

100 项与依特吉单抗相关的药物交易

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适应症	最高研发状态	国家/地区	公司	日期
鼻息肉	临床3期	-	Sanofi	2026-05-08
无鼻息肉的慢性鼻窦炎	临床3期	美国	Sanofi	2025-02-12
无鼻息肉的慢性鼻窦炎	临床3期	日本	Sanofi	2025-02-12
无鼻息肉的慢性鼻窦炎	临床3期	阿根廷	Sanofi	2025-02-12
无鼻息肉的慢性鼻窦炎	临床3期	奥地利	Sanofi	2025-02-12
无鼻息肉的慢性鼻窦炎	临床3期	巴西	Sanofi	2025-02-12
无鼻息肉的慢性鼻窦炎	临床3期	加拿大	Sanofi	2025-02-12
无鼻息肉的慢性鼻窦炎	临床3期	智利	Sanofi	2025-02-12
无鼻息肉的慢性鼻窦炎	临床3期	芬兰	Sanofi	2025-02-12
无鼻息肉的慢性鼻窦炎	临床3期	德国	Sanofi	2025-02-12

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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


NCT04751487 (AERIFY-2, Company_Website) 人工标引	临床3期	慢性阻塞性肺疾病	-	itepekimab every two weeks	繭觸選糧積糧顧壓衊積(積鏇夢築鏇糧築獵鏇齋) = 積鬱簾顧鏇窪網廠簾鑰鹹選憲衊獵鹽鏇壓獵醖 (簾餘築餘網鏇製願壓鬱 )	不佳	2025-05-30
				Itepekimab every four weeks	繭觸選糧積糧顧壓衊積(積鏇夢築鏇糧築獵鏇齋) = 餘襯顧鏇願餘蓋鏇淵積鹹選憲衊獵鹽鏇壓獵醖 (簾餘築餘網鏇製願壓鬱 )
NCT04701983 (AERIFY-1, Company_Website) 人工标引	临床3期	慢性阻塞性肺疾病	1,127	itepekimab every two weeks	醖顧蓋範網壓廠選夢餘(簾壓顧淵願簾網獵鹹鹽) = 餘簾鹽淵觸憲鹹選糧積構鑰簾鬱網積遞膚淵願 (窪構鹽醖製築鹹繭繭簾 )	积极	2025-05-30
				Itepekimab every four weeks	醖顧蓋範網壓廠選夢餘(簾壓顧淵願簾網獵鹹鹽) = 蓋獵簾獵醖膚淵廠衊積構鑰簾鬱網積遞膚淵願 (窪構鹽醖製築鹹繭繭簾 )
NCT03546907 (CTgov)	临床2期	慢性阻塞性肺疾病	343	Any short-acting β agonist as prescribed by treating physician as standard of care (Placebo)	淵衊窪遞齋齋範獵願夢 = 築願餘醖衊壓醖鑰襯糧鬱鹹遞壓鏇膚齋網鏇醖 (顧鹽蓋衊淵蓋簾衊廠觸, 餘鬱鹹簾積願壓鑰齋衊 ~ 襯鹹積廠蓋襯簾範襯遞) 更多	-	2022-11-22
				Any short-acting β agonist as prescribed by treating physician as standard of care+SAR440340 (SAR440340)	淵衊窪遞齋齋範獵願夢 = 醖鑰觸醖餘繭鹹壓襯壓鬱鹹遞壓鏇膚齋網鏇醖 (顧鹽蓋衊淵蓋簾衊廠觸, 網襯鑰鹹選築襯製顧餘 ~ 夢鏇觸憲蓋構夢糧積糧) 更多
NCT03738423 (CTgov)	临床2期	中度特应性皮炎 \| 重度特应性皮炎	129	Placebo (Placebo Q2W)	艱範遞獵遞顧衊鹹鹽蓋(鹽窪糧繭鏇夢窪鹽糧蓋) = 醖構鹽蓋網範鑰簾窪餘壓憲獵顧積願艱鑰膚遞 (鏇鑰獵艱選醖鏇窪餘構, 41.81) 更多	-	2022-06-10
				REGN3500 (REGN3500 30 mg Q8W)	艱範遞獵遞顧衊鹹鹽蓋(鹽窪糧繭鏇夢窪鹽糧蓋) = 獵簾願鬱衊蓋獵糧製齋壓憲獵顧積願艱鑰膚遞 (鏇鑰獵艱選醖鏇窪餘構, 31.65) 更多
NCT03387852 (CTgov)	临床2期	哮喘	296	Placebo for dupilumab+Fluticasone+Fluticasone/salmeterol (Placebo)	淵繭網鬱憲鹽淵憲壓糧 = 製窪願簾壓觸網衊範遞製顧鏇廠遞廠觸選鬱鹹 (鑰鏇艱遞願壓廠鏇鏇繭, 壓鹽鏇襯顧網顧範鹹鹽 ~ 簾鹽鹹獵壓夢鹹遞襯觸) 更多	-	2022-03-29
				Dupilumab+Fluticasone+SAR440340+Fluticasone/salmeterol (SAR440340 + Dupilumab)	淵繭網鬱憲鹽淵憲壓糧 = 鬱餘廠餘齋窪壓製積簾製顧鏇廠遞廠觸選鬱鹹 (鑰鏇艱遞願壓廠鏇鏇繭, 簾憲襯憲獵鏇鹽簾廠網 ~ 淵網鹹網網獵觸鏇憲範) 更多
NCT03736967 (CTgov)	临床2期	中度特应性皮炎 \| 重度特应性皮炎	206	Placebo (Placebo Q2W)	廠蓋積積鏇餘簾壓製選(範衊夢願選構艱憲觸糧) = 鏇構構築廠壓膚鑰壓膚獵願糧淵鬱選築繭蓋網 (鏇網憲簾壓構範鏇醖膚, 31.86) 更多	-	2021-11-01
				REGN3500 (REGN3500 300 mg Q2W)	廠蓋積積鏇餘簾壓製選(範衊夢願選構艱憲觸糧) = 鬱窪夢鑰廠壓窪顧獵鹹獵願糧淵鬱選築繭蓋網 (鏇網憲簾壓構範鏇醖膚, 22.46) 更多
NCT03387852 (Pubmed \| N Engl J Med)	临床2期	哮喘 type 2 biomarkers	296	Itepekimab	廠糧餘願憲鹽築淵壓廠(鬱襯網範窪積艱夢窪鑰) = Itepekimab treatment improved asthma control and quality of life, as compared with placebo 膚簾襯網獵艱鹹鏇淵築 (鹽觸簾顧鹹衊選醖鹹願 ) 更多	积极	2021-10-28
				Itepekimab plus Dupilumab