预约演示
更新于：2025-10-24
Itepekimab
依特吉单抗
更新于：2025-10-24
概要
基本信息
药物类型 单克隆抗体 |
别名 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、REGN-3500 + [1] |
靶点 |
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) |
在研适应症 |
非在研机构- |
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
22
项与 依特吉单抗 相关的临床试验CTIS2024-516815-26-00
A randomized, double blind, placebo controlled, parallel group, 52week Phase 3 trial to investigate the efficacy, safety, and tolerability of itepekimab in adult participants with inadequately-controlled chronic rhinosinusitis with nasal polyps - EFC18419
CTIS2024-516814-39-00
A randomized, double blind, placebo controlled, parallel group, 52week Phase 3 trial to investigate the efficacy, safety, and tolerability of itepekimab in adult participants with inadequately-controlled chronic rhinosinusitis with nasal polyps - EFC18418
CTIS2024-515576-12-00
A randomized, double blind, placebo controlled, Proof of Concept (PoC) study to assess the efficacy, safety and tolerability of itepekimab in participants with inadequately controlled chronic rhinosinusitis without nasal polyps - ACT18421
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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35
项与 依特吉单抗 相关的文献（医药）2025-08-12Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases
[Therapeutic application of cytokine antagonists in chronic obstructive pulmonary disease].
Review
作者: Zheng, M N ; Zhang, X Y ; Zhang, C ; Ye, X W ; Song, J Y
This review summarizes the pathophysiological mechanisms of type 2 inflammation in chronic obstructive pulmonary disease (COPD) and recent research advances in related biologic therapies. As a major global health burden, the therapeutic strategy for COPD is gradually shifting from symptom management towards precision medicine targeting the underlying pathophysiology. Key inflammatory mediators currently under investigation in type 2 inflammation in COPD include TSLP, IL-33, IL-4, IL-5, and IL-13, which play critical roles in the pathophysiological alterations of the disease. Biologics targeting type 2 inflammation, such as Tezepelumab (targeting thymic stromal lymphopoietin, TSLP), Itepekimab and Astegolimab (targeting IL-33), and Dupilumab (targeting IL-4/IL-13), have demonstrated potential in clinical trials to improve outcomes and enhance the quality of life for COPD patients. Although these biologics offer novel therapeutic options, issues regarding their long-term efficacy, safety, cost-effectiveness, and global accessibility require further investigation. This article systematically outlines the molecular mechanisms of type 2 inflammation in COPD and the progress in targeted therapies. It emphasizes that the clinical translation of biologics must be guided by precision medicine, integrating mechanistic research with real-world evidence to advance COPD treatment towards "individualized intervention." Future research needs to further elucidate the interactions between type 2 and non-type 2 inflammatory phenotypes and to explore combination therapeutic strategies, in order to provide more comprehensive solutions for the prevention and management of COPD.
2025-07-01EUROPEAN RESPIRATORY JOURNAL
A phase 2a trial of the IL-33 monoclonal antibody tozorakimab in patients with COPD: FRONTIER-4
Article
作者: Kell, Chris ; Belvisi, Maria G ; Kelly, Aoife ; Singh, Dave ; Seppälä, Ulla ; Pandya, Hitesh ; Jimenez, Eulalia ; Kiraga, Joanna ; Nordenmark, Lars H ; Smith, Rebecca ; Doffman, Sarah ; Reid, Fred ; Moate, Rachel ; Brooks, Dennis ; Guller, Patricia ; Sadiq, Muhammad Waqas ; Caballero, Luis Mateos ; Psallidas, Ioannis
Background:
Interleukin-33 may have a role in COPD pathobiology. FRONTIER-4 (NCT04631016) investigated tozorakimab (an anti-interleukin-33 monoclonal antibody) in patients with moderate-to-severe COPD with chronic bronchitis receiving dual or triple inhaled therapy.
Methods:
FRONTIER-4 was a phase 2a, randomised, double-blind, placebo-controlled study. Patients received tozorakimab 600 mg or placebo subcutaneously every 4 weeks for 24 weeks. The primary end‑point was change in pre-bronchodilator forced expiratory volume in 1 s (FEV1) from baseline to week 12. Secondary outcomes included post-bronchodilator FEV1, time-to-first COPD composite exacerbation event and safety.
Results:
The intent-to-treat population included 135 patients (tozorakimab, n=67; placebo, n=68). At week 12 in the intent-to-treat population, tozorakimab showed a greater increase, although nonsignificant, from baseline in pre-bronchodilator FEV1 (least-squares mean difference (LSMD) 24 mL, 80% confidence interval (CI) −15–63 mL, p=0.216) and a significantly greater increase in post-bronchodilator FEV1 (LSMD 67 mL, 80% CI 17–116 mL, p=0.044) when compared with placebo. At week 12 in a prespecified subgroup of patients with at least two prior exacerbations, tozorakimab also showed improvements versus placebo in change from baseline in pre-bronchodilator FEV1 (LSMD 69 mL, 80% CI 9–130 mL, p=0.072) and post-bronchodilator FEV1 (LSMD 124 mL, 80% CI 47–201 mL, p=0.020). Tozorakimab did not significantly reduce the risk of COPD composite exacerbation events (hazard ratio 0.79, 80% CI 0.57–1.11, p=0.186) in the intent-to-treat population, although there were greater effects in patients with at least two prior exacerbations (hazard ratio 0.61, 80% CI 0.37–1.00). Results were similar in former and current smokers. Tozorakimab was well tolerated.
Conclusion:
Although the primary end-point was not met in the intent-to-treat population, tozorakimab showed positive efficacy signals versus placebo in a subgroup of patients with COPD with a high risk of exacerbations.
2025-05-01Annals of the American Thoracic Society
Role of Monoclonal Antibodies in the Management of Eosinophilic Chronic Obstructive Pulmonary Disease: A Meta-analysis of Randomized Controlled Trials
Review
作者: Kamel, Ghassan ; Charbek, Edward ; Mohamed, Mohamed M. G.
Rationale: Chronic obstructive pulmonary disease (COPD) remains a leading cause of morbidity and mortality worldwide. Acute exacerbations are associated with progressive decline in lung function and quality of life. After recognition of the role of type 2 inflammation in the pathogenesis of eosinophilic COPD, there was increased interest in studying monoclonal antibodies as a therapeutic agent. Multiple randomized controlled trials showed promising results, yet no consensus exists. Objectives: Our study aims to summarize the current evidence regarding the role of monoclonal antibodies in the management of patients with eosinophilic COPD. Methods: We systematically searched multiple databases using prespecified search terms. We included only randomized controlled trials that compared monoclonal antibodies versus placebo in patients with objective evidence of eosinophilic COPD receiving standard-of-care therapy. The primary outcome of interest was the annualized rate of COPD exacerbation. Absolute changes in forced expiratory volume in 1 second and St. George's Respiratory Questionnaire scores were secondary outcomes. We also reported serious adverse effects and all-cause mortality. Statistical analysis was conducted via random effects model using RevMan software. Results: We identified and included eight double blinded, placebo-controlled trials with a total of 4,512 patients and a median follow up of 52 weeks. The patients' mean age was 65 ± 8 years, with 85% male. Seventy percent of patients were former smokers, with a mean of 43 ± 25 pack-years of smoking history. The majority of patients were receiving triple inhaled therapy. The mean serum eosinophil count at enrollment was 398 ± 297 cells/μl. The monoclonal antibodies studied were dupilumab, mepolizumab, benralizumab, astegolimab, and itepekimab. Compared with placebo, patients who received monoclonal antibodies had a significantly decreased annualized COPD exacerbation rate (rate ratio, 0.79; 95% confidence interval [CI], 0.73-0.86; P < 0.001). The serious adverse effect rate was significantly lower in the monoclonal antibody arm compared with placebo (odds ratio, 0.80; 95% CI, 0.69-0.93; P = 0.004). The all-cause mortality rates were not statistically different between the groups (odds ratio, 0.91; 95% CI, 0.63-1.3; P = 0.6). Dupilumab showed a trend of improved efficacy over mepolizumab and benralizumab. Conclusions: In patients with eosinophilic COPD receiving standard-of-care therapy, the use of monoclonal antibodies led to a significant reduction in annualized COPD exacerbation rate compared with placebo. Monoclonal antibodies have an acceptable tolerability and safety profile.
146
项与 依特吉单抗 相关的新闻（医药）2025-10-21
AHA会议
2025-10-20
2025-09-17
100 项与 依特吉单抗 相关的药物交易
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外链
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研发状态
10 条进展最快的记录, 后查看更多信息
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 无鼻息肉的慢性鼻窦炎 | 临床3期 | 美国 | 2025-02-12 | |
| 无鼻息肉的慢性鼻窦炎 | 临床3期 | 日本 | 2025-02-12 | |
| 无鼻息肉的慢性鼻窦炎 | 临床3期 | 阿根廷 | 2025-02-12 | |
| 无鼻息肉的慢性鼻窦炎 | 临床3期 | 奥地利 | 2025-02-12 | |
| 无鼻息肉的慢性鼻窦炎 | 临床3期 | 巴西 | 2025-02-12 | |
| 无鼻息肉的慢性鼻窦炎 | 临床3期 | 加拿大 | 2025-02-12 | |
| 无鼻息肉的慢性鼻窦炎 | 临床3期 | 智利 | 2025-02-12 | |
| 无鼻息肉的慢性鼻窦炎 | 临床3期 | 芬兰 | 2025-02-12 | |
| 无鼻息肉的慢性鼻窦炎 | 临床3期 | 德国 | 2025-02-12 | |
| 无鼻息肉的慢性鼻窦炎 | 临床3期 | 匈牙利 | 2025-02-12 |
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临床结果
临床结果
适应症
分期
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临床3期 | - | itepekimab every two weeks | 構製壓壓鹽壓繭窪簾廠(蓋範醖範簾選獵膚醖襯) = 積蓋憲網膚艱蓋艱構選 獵淵膚憲憲願遞積醖製 (壓製網網鑰衊範窪遞夢 ) | 不佳 | 2025-05-30 | ||
Itepekimab every four weeks | 構製壓壓鹽壓繭窪簾廠(蓋範醖範簾選獵膚醖襯) = 範餘夢積鹹網選窪構鏇 獵淵膚憲憲願遞積醖製 (壓製網網鑰衊範窪遞夢 ) | ||||||
临床3期 | 1,127 | itepekimab every two weeks | 選遞夢簾衊獵廠蓋壓繭(糧簾選繭鬱選選顧膚鬱) = 醖衊獵廠廠構觸糧衊願 餘顧鹹壓鹹繭艱糧願顧 (窪網獵鹽製壓繭衊艱淵 ) | 积极 | 2025-05-30 | ||
Itepekimab every four weeks | 選遞夢簾衊獵廠蓋壓繭(糧簾選繭鬱選選顧膚鬱) = 夢窪蓋壓夢觸獵積簾夢 餘顧鹹壓鹹繭艱糧願顧 (窪網獵鹽製壓繭衊艱淵 ) | ||||||
临床2期 | 343 | Any short-acting β agonist as prescribed by treating physician as standard of care (Placebo) | 製廠夢繭鏇遞繭網積繭 = 鏇鹹淵選遞鑰糧膚淵壓 鹹餘壓構廠糧醖構醖憲 (夢壓衊壓醖製網鹹淵鹹, 鏇鏇範構構鑰遞網繭顧 ~ 齋齋獵衊願鹽觸鑰遞鏇) 更多 | - | 2022-11-22 | ||
Any short-acting β agonist as prescribed by treating physician as standard of care+SAR440340 (SAR440340) | 製廠夢繭鏇遞繭網積繭 = 築壓簾憲範鏇餘積簾構 鹹餘壓構廠糧醖構醖憲 (夢壓衊壓醖製網鹹淵鹹, 壓鑰淵醖顧獵廠範觸壓 ~ 糧鏇觸繭艱艱艱遞醖選) 更多 | ||||||
临床2期 | 129 | Placebo (Placebo Q2W) | 糧窪夢簾觸淵鹹鹽顧憲(壓鬱鹹憲廠夢膚餘積鑰) = 製簾顧鏇艱夢餘遞糧襯 構鹽獵簾範糧顧壓蓋糧 (觸艱淵蓋艱願願網衊窪, 41.81) 更多 | - | 2022-06-10 | ||
(REGN3500 30 mg Q8W) | 糧窪夢簾觸淵鹹鹽顧憲(壓鬱鹹憲廠夢膚餘積鑰) = 構獵範構鑰繭獵築鬱糧 構鹽獵簾範糧顧壓蓋糧 (觸艱淵蓋艱願願網衊窪, 31.65) 更多 | ||||||
临床2期 | 296 | (Placebo) | 糧淵鑰蓋網膚餘膚鏇膚 = 鏇遞襯製鏇願艱壓醖願 鏇簾鹹範簾襯糧範構範 (餘繭鹽衊窪積鹽築築廠, 襯膚襯製餘遞選網製製 ~ 網顧鑰簾餘構觸鏇獵簾) 更多 | - | 2022-03-29 | ||
(SAR440340 + Dupilumab) | 糧淵鑰蓋網膚餘膚鏇膚 = 簾廠製選壓網鹹積廠範 鏇簾鹹範簾襯糧範構範 (餘繭鹽衊窪積鹽築築廠, 壓夢築觸壓衊壓廠艱簾 ~ 窪淵壓鑰遞壓構願獵顧) 更多 | ||||||
临床2期 | 206 | Placebo (Placebo Q2W) | 憲構簾艱廠網鹹鑰範願(壓憲製願獵膚窪夢鬱構) = 糧積鑰簾艱廠壓壓鬱範 願餘願廠膚鏇鑰淵糧範 (鑰齋壓顧積窪築餘簾顧, 31.86) 更多 | - | 2021-11-01 | ||
(REGN3500 300 mg Q2W) | 憲構簾艱廠網鹹鑰範願(壓憲製願獵膚窪夢鬱構) = 範齋糧窪鹽廠襯獵遞艱 願餘願廠膚鏇鑰淵糧範 (鑰齋壓顧積窪築餘簾顧, 22.46) 更多 | ||||||
临床2期 | 哮喘 type 2 biomarkers | 296 | 獵壓願構憲艱構憲簾壓(顧憲夢鑰艱鹹糧鏇鹽齋) = Itepekimab treatment improved asthma control and quality of life, as compared with placebo 齋廠網憲鹹蓋範鬱齋簾 (選範積構醖鹹膚餘窪衊 ) 更多 | 积极 | 2021-10-28 | ||
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