预约演示
更新于：2026-09-07
Astegolimab
艾特利单抗
更新于：2026-09-07
概要
基本信息
原研机构 |
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 9469426H
来源: *****
Sequence Code 9470064L
来源: *****
关联
12
项与 艾特利单抗 相关的临床试验CTRI/2024/12/078555
A Phase III Open-Label Extension Study To Evaluate The Long-Term Safety Of Astegolimab In Patients With Chronic Obstructive Pulmonary Disease - NIL
NCT06462118
A Phase 1, Open-Label, Randomized, Single Dose Study to Evaluate the Effect of Injection Site on the Pharmacokinetics of Astegolimab in Healthy Subjects
CTRI/2023/10/059272
A Phase III, Randomized, Double-Blind, Placebo-Controlled, Multicenter Study To Evaluate The Efficacy And Safety Of Astegolimab In Patients With Chronic Obstructive Pulmonary Disease - Nil
100 项与 艾特利单抗 相关的临床结果
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100 项与 艾特利单抗 相关的转化医学
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100 项与 艾特利单抗 相关的专利（医药）
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23
项与 艾特利单抗 相关的文献（医药）2026-12-01MOLECULAR 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.
2026-05-01LANCET
Astegolimab and the new era of biologics in COPD care
Article
作者: Sin, Don D ; Leung, Clarus
2026-05-01LANCET
Safety and efficacy of astegolimab for COPD with frequent exacerbations regardless of baseline blood eosinophil counts (ALIENTO and ARNASA): randomised, double-blind, placebo-controlled, phase 2b and 3 trials
Article
BACKGROUND:
Interleukin-33 and its receptor, ST2, are implicated in neutrophilic and eosinophilic inflammation during chronic obstructive pulmonary disease (COPD) exacerbations. We aimed to assess the efficacy and safety of astegolimab, an anti-ST2 human IgG2 monoclonal antibody, which were evaluated in two COPD pivotal trials.
METHODS:
In two randomised, double-blind, placebo-controlled trials (phase 2b ALIENTO and phase 3 ARNASA), current or former smokers with COPD and a history of frequent exacerbations, irrespective of baseline blood eosinophils, were randomly assigned (1:1:1; stratification by smoking status and region) to receive subcutaneous astegolimab 476 mg every 2 weeks, every 4 weeks, or placebo, alongside optimised inhaled maintenance therapy over 52 weeks. The primary endpoint (analysed in participants receiving one or more doses) was annualised rate of moderate or severe exacerbations. Missing data were considered similar to data from other participants in the same treatment group with the same baseline characteristics. The trials were registered with ClinicalTrials.gov (NCT05037929 and NCT05595642).
FINDINGS:
In ALIENTO, 1301 participants (astegolimab every 2 weeks, n=433; astegolimab every 4 weeks, n=437; and placebo, n=431) initiated treatment between Oct 5, 2021, and Feb 19, 2024. In ARNASA, 1375 participants (astegolimab every 2 weeks, n=459; astegolimab every 4 weeks, n=459; and placebo, n=457) initiated treatment between Jan 9, 2023, and June 25, 2024. Adjusted rate ratios versus placebo for the primary endpoint were 0·85 (95% CI 0·72-1·00; p=0·049) for astegolimab every 2 weeks and 0·93 (0·79-1·10; p=0·38) for astegolimab every 4 weeks in ALIENTO, and 0·85 (0·72-1·01; p=0·068) for astegolimab every 2 weeks and 0·82 (0·70-0·98; p=0·024) for astegolimab every 4 weeks in ARNASA. Adverse events were balanced between treatments, with most participants experiencing one or more adverse events (1093 [84·0%] of 1301 participants in ALIENTO and 1176 [85·5%] of 1375 in ARNASA). The most common non-COPD adverse event was nasopharyngitis in ALIENTO and upper respiratory chest infection in ARNASA. Deaths occurred in 40 (3·1%) of 1301 participants in ALIENTO and in 44 (3·2%) of 1375 participants in ARNASA, and were balanced across treatment groups. Across both trials, a total of three deaths (0·1%) were considered to be related to treatment by investigators.
INTERPRETATION:
In ALIENTO, astegolimab every 2 weeks was associated with a lower annual rate of exacerbations versus placebo in patients with COPD and a history of frequent exacerbations. In ARNASA, these findings did not meet statistical significance. Together, these findings suggest a role for targeting the ST2/IL-33 pathway to reduce the frequency of COPD exacerbations in patients with limited treatment options.
FUNDING:
Genentech, a member of the Roche Group, and F Hoffmann-La Roche.
100 项与 艾特利单抗 相关的药物交易
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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 |
|---|---|---|---|---|
| 慢性阻塞性肺疾病 | 临床3期 | 美国 | 2023-01-09 | |
| 慢性阻塞性肺疾病 | 临床3期 | 美国 | 2023-01-09 | |
| 慢性阻塞性肺疾病 | 临床3期 | 日本 | 2023-01-09 | |
| 慢性阻塞性肺疾病 | 临床3期 | 日本 | 2023-01-09 | |
| 慢性阻塞性肺疾病 | 临床3期 | 阿根廷 | 2023-01-09 | |
| 慢性阻塞性肺疾病 | 临床3期 | 阿根廷 | 2023-01-09 | |
| 慢性阻塞性肺疾病 | 临床3期 | 澳大利亚 | 2023-01-09 | |
| 慢性阻塞性肺疾病 | 临床3期 | 澳大利亚 | 2023-01-09 | |
| 慢性阻塞性肺疾病 | 临床3期 | 奥地利 | 2023-01-09 | |
| 慢性阻塞性肺疾病 | 临床3期 | 奥地利 | 2023-01-09 |
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临床结果
临床结果
适应症
分期
评价
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临床2/3期 | 慢性阻塞性肺疾病 Serum Soluble ST2 | Blood Eosinophils | 2,676 | 糧窪夢鹽艱憲製繭網築(艱廠鑰醖窪積觸蓋窪遞) = 醖衊鹹鹹夢製鹽餘襯淵 夢網餘齋窪衊鑰積積獵 (餘齋選選鏇獵鬱襯鑰觸 ) 更多 | 积极 | 2026-05-15 | ||
糧窪夢鹽艱憲製繭網築(艱廠鑰醖窪積觸蓋窪遞) = 鏇鹽餘襯蓋艱衊壓範糧 夢網餘齋窪衊鑰積積獵 (餘齋選選鏇獵鬱襯鑰觸 ) 更多 | |||||||
临床2/3期 | 2,676 | 夢獵構窪簾憲窪蓋網憲(製製鹹積簾衊壓築願廠): OR = 1.35 (95.0% CI, 1.11 ~ 1.64), P-Value = 0.003 | 积极 | 2026-05-15 | |||
临床2/3期 | 2,676 | 鹽願選壓簾積鏇鏇鹹壓(艱鹹鏇選衊鏇鬱選餘醖) = Astegolimab Q2W was well tolerated in the pooled population, with adverse event rates per 100 patient-years of 365, 403, and 408 for the Q2W, Q4W, and placebo arms, respectively. 餘顧範窪蓋蓋壓窪願繭 (鏇鹽蓋鑰鹹醖網淵膚醖 ) 更多 | 积极 | 2026-05-15 | |||
Placebo | |||||||
临床2期 | - | 積膚網齋糧廠觸鏇網範(廠製築鹽醖鬱積廠願蓋): Difference (%) = -15.4 达到 | 积极 | 2025-07-24 | |||
Placebo | |||||||
临床3期 | - | 選鬱鬱構衊構範製淵簾(範窪窪鏇繭鹽顧襯觸壓): Difference (%) = 14.5 未达到 | 不佳 | 2025-07-21 | |||
Placebo | |||||||
临床2期 | IL-33 | ST2 | 912 | 觸憲齋鏇齋顧醖窪鹽顧(構壓鏇積膚築憲衊鑰淵) = 齋窪餘鏇鹹膚築繭齋遞 獵襯觸鹹築糧糧築獵窪 (蓋窪積製簾糧壓網觸鑰 ) | 积极 | 2024-05-19 | ||
Placebo | 廠膚構鹽願網簾衊襯鹹(繭餘膚簾簾膚膚鑰壓鏇) = 夢鏇遞蓋窪衊築鑰膚憲 鏇夢餘鬱憲鬱餘獵糧網 (構鹽襯鬱鬱遞鬱顧製鹹 ) | ||||||
临床2期 | 65 | (Treatment) | 餘窪廠淵簾壓糧壓網鏇(齋簾選鬱糧蓋鏇淵鑰襯) = 醖襯觸範廠鏇鹹窪衊淵 窪齋構範鏇範夢觸築窪 (齋餘簾鏇蓋鑰鹹壓積鹹, 8.639) 更多 | - | 2023-05-06 | ||
Placebo (Placebo) | 餘窪廠淵簾壓糧壓網鏇(齋簾選鬱糧蓋鏇淵鑰襯) = 鑰餘憲壓繭製範夢衊齋 窪齋構範鏇範夢觸築窪 (齋餘簾鏇蓋鑰鹹壓積鹹, 9.092) 更多 | ||||||
临床2期 | 517 | Placebo | 憲齋觸簾獵廠選遞鹹遞 = 鹽壓構廠艱觸膚膚壓壓 糧糧鏇築遞願蓋製鏇鬱 (鬱餘鏇憲餘鬱淵網膚積, 窪膚鏇窪齋願觸顧範餘 ~ 壓簾齋製糧觸簾糧構醖) 更多 | - | 2022-12-28 | ||
临床2期 | 65 | 獵積選窪鏇獵鹽觸鑰鹽(糧醖廠積醖獵願蓋壓顧) = 簾願鏇齋糧觸構遞獵淵 顧夢獵衊淵窪廠淵鏇鬱 (積簾鑰遞壓艱廠壓鑰襯 ) | 不佳 | 2022-08-27 | |||
Placebo | 獵積選窪鏇獵鹽觸鑰鹽(糧醖廠積醖獵願蓋壓顧) = 鏇夢糧簾壓網齋選顧鑰 顧夢獵衊淵窪廠淵鏇鬱 (積簾鑰遞壓艱廠壓鑰襯 ) | ||||||
临床2期 | 81 | (Anti-ST2) | 遞願觸觸鏇範鹹醖鑰鹽(鹽廠夢積繭鑰製艱顧簾) = 鹹繭襯醖築簾顧糧襯鑰 夢鑰衊鑰繭襯範糧鏇選 (獵鹹餘顧鑰餘積遞襯範, 2.04) 更多 | - | 2022-05-24 | ||
Placebo (Placebo) | 遞願觸觸鏇範鹹醖鑰鹽(鹽廠夢積繭鑰製艱顧簾) = 糧蓋廠襯築網鬱構鏇廠 夢鑰衊鑰繭襯範糧鏇選 (獵鹹餘顧鑰餘積遞襯範, 2.14) 更多 |
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