A Phase 1, Open-Label, Randomized, Single Dose Study to Evaluate the Effect of Injection Site on the Pharmacokinetics of Astegolimab in Healthy Subjects

The main objective is to study how astegolimab may behave in the body when injected subcutaneously into the abdomen, thigh, or upper arm in healthy participants.

开始日期2024-06-17

申办/合作机构

Genentech, Inc.

CTRI/2023/10/059272

/ Not yet recruiting临床3期

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

开始日期2023-11-20

申办/合作机构-

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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项与艾特利单抗相关的文献（医药）

2026-04-01·Tuberculosis and Respiratory Diseases

Biologics in Chronic Obstructive Pulmonary Disease: Current Status and Future Prospects

Article

作者: Choi, Joon Young

Significant progress has been made in managing chronic obstructive pulmonary disease (COPD), yet substantial unmet needs persist due to the disease's heterogeneity and the diverse underlying inflammatory mechanisms. Recent advances have broadened our understanding of COPD beyond a single pathophysiologic model, leading to the development of biologic therapies that target specific immune pathways. This review summarizes current evidence from clinical trials involving biologics in COPD. Early efforts to inhibit non-type 2 inflammation yielded limited results, highlighting the necessity for more refined, endotype-based approaches. Subsequent phase 3 trials have shown considerable clinical benefits in specific patient subsets: dupilumab, which blocks interleukin (IL)-4 and IL-13 signaling, and mepolizumab, which targets IL-5, consistently reduced exacerbation frequency among patients with high blood eosinophil counts (≥300 cells/μL). In contrast, other biologics—such as benralizumab, tezepelumab, and IL-33/suppression of tumorigenicity 2 pathway inhibitors like itepekimab, tozorakimab, and astegolimab—have demonstrated variable efficacy, often influenced by biomarker profiles and patient characteristics. These findings emphasize the importance of precise patient stratification based on inflammatory endotypes. While biologics mark a significant advancement for select COPD populations, further research is needed to clarify long-term outcomes, refine biomarker thresholds, and broaden treatment options for non-eosinophilic COPD.

2025-10-01·CTS-Clinical and Translational Science

Safety, Pharmacokinetics, and Immunogenicity of Astegolimab, an Anti‐ST2 Monoclonal Antibody, in Randomized, Phase I Clinical Studies

Article

作者: Brooks, Logan ; Cheung, Dorothy ; Dash, Ajit ; Arjomandi, Audrey ; Fong, Alice ; Zhang, Wenhui ; Mohan, Divya ; Grimbaldeston, Michele A. ; Yang, Xiaoying ; Parnes, Jane R. ; Wong, Hansen

ABSTRACT:

Astegolimab, a fully human immunoglobulin G2 monoclonal antibody, binds with high affinity to ST2, the interleukin‐33 receptor, thereby blocking ST2/interleukin‐33 binding and subsequent inflammatory cascades involved in inflammatory diseases. Here, we present three randomized, double‐blind, placebo‐controlled, Phase I studies evaluating the safety, tolerability, pharmacokinetics, and immunogenicity of single‐ascending doses of astegolimab in healthy participants and patients with mild atopic asthma (NCT01928368), multiple‐ascending doses in healthy participants (NCT02170337), and single‐ascending doses in healthy Japanese and White adults. Overall, 152 participants were enrolled, randomized, and treated with single‐ or multiple‐ascending doses of astegolimab ( n = 112) or placebo ( n = 40) subcutaneously (2.1–560 mg) or intravenously (210 or 700 mg). No deaths, serious adverse events, or discontinuations due to adverse events occurred during the studies. No clinically meaningful differences in incidence of TEAEs were observed between treatment arms. Pharmacokinetic exposure increased more than dose proportionally over 2.1–420 mg for single‐ascending doses but were approximately dose proportional for single‐ and multiple‐ascending doses ≥ 70 mg following subcutaneous administration. No pharmacokinetic differences were observed based on ethnicity between Japanese and White participants following body weight adjustments. Incidence of antidrug antibodies to astegolimab in healthy participants in the single‐ and multiple‐ascending dose studies was 14%–23% and 33%–50% for subcutaneous and intravenous administration, respectively. Astegolimab was well tolerated in these Phase I studies with no safety concerns identified. Thus, further assessment of astegolimab in targeted patient populations was justified; the Phase IIb ALIENTO and Phase III ARNASA trials in patients with chronic obstructive pulmonary disease are ongoing.

2025-08-12·Zhonghua 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, C ; Zhang, X Y ; 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.

150

项与艾特利单抗相关的新闻（医药）

2026-04-28

·赛业生物订阅号

破局COPD！阿斯利康IL-33单抗Ⅲ期三连捷，一文解析IL-33/ST2/IL1RAP疗法突围与人源化模型赋能

4月20日，阿斯利康宣布其抗IL-33单抗Tozorakimab在COPD的Ⅲ期MIRANDA试验中达到主要终点[1]。这是继3月OBERON和TITANIA两项Ⅲ期临床告捷后，Tozorakimab取得的第三项关键胜利，标志着IL-33通路靶向治疗迎来重大突破。然而，这条赛道也曾充满坎坷 IL-33抗体：再生元/赛诺菲的Itepekimab在COPD中仅在前吸烟者或高加重风险亚组显示获益，关键Ⅲ期研究未达主要终点；AnaptysBio的Etokimab因疗效不足终止开发。 ST2抗体：罗氏的Astegolimab虽在Ⅱb期显著降低加重率（15.4%），但Ⅲ期ARNASA试验未能取得统计学显著性；GSK的Melrilimab同样因疗效不佳提前终止。值得注意的是，Tozorakimab本身在Ⅱ期FRONTIER-4（慢性支气管炎）和FRONTIER-3（哮喘）试验中也曾折戟，仅在高加重风险亚组观察到改善趋势。此次连续三项Ⅲ期成功，不仅夯实了其作为IL-33通路首个COPD生物制剂的地位，更为整个领域重新注入信心。图1 Tozorakimab又一项Ⅲ期研究成功[1] COPD：亟待破局的全球健康挑战慢性阻塞性肺疾病（COPD）是全球第三大死因，影响近4亿人。即使患者接受了双联或三联吸入剂的标准维持治疗，仍有超50%会经历中重度急性加重。首次重度加重后，仅半数患者存活时间超过3.5年［2-5］。因此，开发能够从根本上抑制炎症通路、减少急性加重的新型靶向疗法，已成为该领域的迫切需求。图2 全球COPD疾病负担统计[2] 机制解析：IL-33/ST2/IL1RAP ——炎症级联的"上游开关" IL-33作为IL-1家族成员，扮演着独特的“警报素”（Alarmin）角色。在组织机械损伤、病毒感染或过敏原刺激下，IL-33会迅速从屏障组织的细胞核释放至胞外。其生物学功能的发挥高度依赖由ST2（IL1RL1）和IL1RAP组成的异源二聚体受体复合物。IL-33作为IL-1家族成员，扮演着独特的“警报素”（Alarmin）角色。在组织机械损伤、病毒感染或过敏原刺激下，IL-33会迅速从屏障组织的细胞核释放至胞外。其生物学功能的发挥高度依赖由ST2（IL1RL1）和IL1RAP组成的异源二聚体受体复合物。图3 IL-33信号通路在多种病理状态下的关键作用[13] 当IL-33结合主受体ST2后，招募共受体IL1RAP形成三元复合体，激活MyD88-NF-κB及MAPK通路，诱发大量2型细胞因子释放，成为桥接先天免疫与适应性炎症的关键上游开关［6-7］。图4 IL-33/ST2/IL1RAP复合物结构及下游信号传导[7] 研发格局：从单一阻断到多重协同鉴于IL-33/ST2/IL1RAP在2型免疫与炎症中的枢纽地位，该轴已成为呼吸、自身免疫及肿瘤领域的战略高地。全球药企正加速从单一配体/受体中和单抗，向双特异性抗体（如IL-33×TSLP、IL-33×IL-4Rα）及多通路协同抑制剂演进。图5 IL-33/ST2主要在研管线布局以Tozorakimab为例，其独特优势在于能够同时抑制IL-33的还原型与氧化型信号传导：一方面阻断IL-33与ST2结合，抑制ST2依赖的炎症信号；另一方面阻断氧化型IL-33通过RAGE/EGFR通路引发的上皮功能障碍。这种双重机制更全面地干预COPD病理循环，为高加重风险患者带来显著获益［8］。图6 Tozorakimab的双重抑制机制[8] IL33/ST2：多疾病领域的广阔应用潜力 1、自身免疫性疾病：在类风湿关节炎、重度哮喘、特应性皮炎及溃疡性结肠炎中，IL-33/ST2轴显著上调。阻断该通路已在临床试验中展现出控制急性加重的高潜力[9-10]。 2、肿瘤免疫：该通路在肿瘤微环境中呈双重作用：在软组织肉瘤中与良好预后相关，而在急性髓系白血病（AML）中促进T细胞耗竭[11-13]。 3、代谢与心血管疾病：可溶性ST2（sST2）已获FDA批准用于心力衰竭风险分层，血清阈值>35 ng/mL提示不良心血管事件风险显著增加[14]。在肥胖及2型糖尿病患者脂肪组织中，IL-33/ST2信号可改善胰岛素敏感性，但循环sST2升高与代谢综合征严重程度独立相关[15]。 IL1RAP：多通路阻断的核心枢纽作为IL-1、IL-33和IL-36三条炎症通路的共享共受体，IL1RAP（IL1R3）不仅是IL-33信号传导的必需组分，更是极具潜力的广谱靶点。其与主受体（IL1R1、ST2、IL-36R）及配体形成三元复合体后，经TIR招募MyD88/IRAK/TRAF6，激活NF-κB/MAPK通路，驱动炎症级联与肿瘤微环境重塑。肿瘤免疫双效协同：IL1RAP在AML及多种实体瘤（胰腺癌、非小细胞肺癌）中显著过表达。靶向IL1RAP的ADCC增强型抗体（如Nadunolimab）展现"阻断炎症微环境+靶向清除肿瘤细胞"双重机制，在实体瘤和血液瘤中前景广阔［16-19］。自身免疫广谱抑制：靶向IL1RAP的Fc静默拮抗单抗（如SAR445399、CAN10）在斑块状银屑病、化脓性汗腺炎等疾病中，验证了对多条炎症通路的广谱抑制潜力及良好安全性［20-21］。图7 IL1RAP作为IL-1、IL-33、IL-36三条通路的共享共受体[16] 相较于单一通路靶向策略，IL1RAP在适应症拓展方面展现出更广阔的应用潜力，其靶向疗法在临床前研究及临床试验阶段已覆盖广泛的疾病谱：在自身免疫与炎症性疾病领域，包括斑块状银屑病（PsO）、化脓性汗腺炎（HS）、系统性硬皮病（SSc）以及急性痛风性关节炎（GA）；在肿瘤领域，则涵盖胰腺癌（PC）、三阴性乳腺癌（TNBC）、结直肠癌（CRC）以及急性髓系白血病（AML）等多种实体瘤与血液系统恶性肿瘤。图8 重要IL1RAP靶向抗体药物管线赛业生物IL-33/ST2/IL1RAP人源化小鼠模型：赋能下一代免疫疗法研发尽管IL-33/ST2/IL1RAP靶向药物研发火热，但人鼠核心蛋白在序列与构象上存在显著差异。目前多种高度特异性的人源化抗体（如Tozorakimab和Itepekimab均不与小鼠IL-33结合）难以在常规野生型小鼠中准确评估亲和力、药代动力学及体内药效。为全面赋能IL-33/ST2/IL1RAP通路疗法的临床前验证，赛业生物重磅推出涵盖三个核心靶点的人源化小鼠模型。 IL33人源化小鼠模型（产品编号：C001722）验证数据图9 IL33人源化小鼠体内中人源/鼠源IL33基因及蛋白表达检测 IL1RL1 (IL33R/ST2）人源化小鼠模型（产品编号：C001632）验证数据图10 IL1RL1 (IL33R/ST2）人源化小鼠体内中人源/鼠源IL1RL1基因及蛋白表达检测 IL1RAP人源化小鼠模型（产品编号：C001631）验证数据图11 IL1RAP小鼠体内各组织中人源/鼠源IL1RAP基因及蛋白表达检测模型总结从主导COPD炎症循环的IL-33，到介导微环境重塑的ST2与IL1RAP复合物，这一关键信号轴正深刻重塑呼吸系统疾病、自身免疫及抗肿瘤创新药的研发格局。在阿斯利康等跨国药企的持续突破为IL-33通路临床成药性注入强心剂的背景下，赛业生物紧跟前沿临床需求，推出的IL33、ST2及IL1RAP人源化模型凭借人源基因与蛋白的高保真稳定表达，实现了与临床高度契合的转化价值，不仅能全面覆盖COPD、哮喘等呼吸系统疾病拮抗型单抗的药效学评价，还可深度支持AML、PDAC等肿瘤免疫治疗的机制探索，从而有效扫清早期靶标验证向临床转化跨越的关键技术障碍。本文作者：Layne 编辑：西米审核：西米、🍑momo 参考文献： [1]AstraZeneca. (2026) Tozorakimab met primary endpoint in Phase III MIRANDA trial in patients with COPD. AstraZeneca Press Release. [2]Montes de Oca M et al. (2025) The global burden of COPD: epidemiology and effect of prevention strategies. Global Epidemiol Chronic Respir Dis. 13(18):709-724. [3]WHO. (2024) The top 10 causes of death. WHO Fact Sheet. [4][Chen S et al. (2018) Symptomatic burden of COPD for patients receiving dual or triple therapy. Int J Chron Obstruct Pulmon Dis. 13:1365-1376. [5]Singh D et al. (2024) Implications of cardiopulmonary risk for the management of COPD: a narrative review. Adv Ther. 41:2151-2167. [6]Sheng F et al. (2025) IL-33/ST2 axis in diverse diseases: regulatory mechanisms and therapeutic potential. Front Immunol. 16:1533335. [7]Riera-Martínez L et al. (2023) The role of IL-33/ST2 in COPD and its future as an antibody therapy. Int J Mol Sci. 24(10):8702. [8]England E et al. (2023) Tozorakimab (MEDI3506): an anti-IL-33 antibody that inhibits IL-33 signalling via ST2 and RAGE/EGFR to reduce inflammation and epithelial dysfunction. Sci Rep. 13(1):9825. [9]Griesenauer B et al. (2017) The ST2/IL-33 axis in immune cells during inflammatory diseases. Front Immunol. 8:475. [10]Mok MY et al. (2010) Serum levels of IL-33 and soluble ST2 and their association with disease activity in systemic lupus erythematosus. Rheumatology. 49(3):520-527. [11]Kang BH et al. (2025) Unlocking IL-33: new insights into tumor immunity. Immune Netw. 25(5):e36. [12]Che K et al. (2025) IL-33 in cancer immunotherapy: pleiotropic functions and biological strategies. Cytokine Growth Factor Rev. 85:81-92. [13]Chen H et al. (2018) Integrated expression profiles analysis reveals correlations between the IL-33/ST2 axis and CD8+ T cells, regulatory T cells, and myeloid-derived suppressor cells in soft tissue sarcoma. Front Immunol. 9:1179. [14]Chen J et al. (2022) Growth stimulation expressed gene 2 (ST2): clinical research and application in cardiovascular related diseases. Front Cardiovasc Med. 9:1007450. [15]Missous G et al. (2024) Circulating interleukin-33 levels in obesity and type 2 diabetes: a systematic review and meta-analysis. Am J Physiol Endocrinol Metab. 327(6):E686-E699. [16]Garlanda C et al. (2025) IL-1 family cytokines in inflammation and immunity. Cell Mol Immunol. 22(11):1345-1362. [17]Frenay J et al. (2022) IL-1RAP, a key therapeutic target in cancer. Int J Mol Sci. 23(23):14918. [18]Zarezadeh Mehrabadi A et al. (2024) Interleukin-1 receptor accessory protein (IL-1RAP): a magic bullet candidate for immunotherapy of human malignancies. Crit Rev Oncol Hematol. 193:104200. [19]Rydberg Millrud C et al. (2023) Blockade of IL-1α and IL-1β signaling by the anti-IL1RAP antibody nadunolimab (CAN04) mediates synergistic anti-tumor efficacy with chemotherapy. Cancer Immunol Immunother. 72(3):667-678. [20]Fields JK et al. (2024) Antibodies targeting the shared cytokine receptor IL-1 receptor accessory protein invoke distinct mechanisms to block all cytokine signaling. Cell Rep. 43(5):114099. [21]Meijs A et al. (2025) The novel, first-in-class IL-1R3 antagonist SAR445399 reduces skin inflammation in an innovative proof-of-mechanism study with dual immune challenge models and comparator drugs. Sanofi Medical Congress. 相关推荐从“快乐假象”到疾病真相：Ube3a KO小鼠揭秘天使综合征的“微笑”之殇诺华31亿重金回购FXI靶向疗法，F11“人源化”小鼠助力终结【抗凝出血】难题小身躯，大使命：挑战人体最大基因DMD的人源化小鼠靶向成纤维细胞的Col1a2-iCre小鼠（附赠工具鼠取材验证重组效率的解决方案）工具鼠系列：MerCreMer与CreERT2的诱导方式有何异同？寻找更好的动脉粥样硬化模型——B6J-Apoe KO小鼠 HFD+CCl4诱导的代谢功能障碍相关性脂肪肝炎MASH（NASH）小鼠结直肠癌（CRC）&家族性腺瘤性息肉病（FAP）研究模型——Apc KO小鼠 SKG小鼠——类风湿性关节炎（RA）和强直性脊柱炎（AS）研究好帮手点击“阅读原文” 立即咨询

2026-04-28

·allsci.com

AstraZeneca’s Breztri Aerosphere picks up US approval for asthma

The US FDA has approved Breztri Aerosphere (budesonide/glycopyrrolate/formoterol fumarate) for the maintenance treatment of asthma in adults and adolescents aged 12 years and older, marking the first approval of a single-inhaler triple therapy for asthma in the US. The approval represents a second indication for AstraZeneca’s fixed-dose combination product, which was given the nod to treat chronic obstructive pulmonary disease (COPD) in the US in 2020. Breztri Aerosphere delivers budesonide, an inhaled corticosteroid (ICS), alongside glycopyrrolate, a long-acting muscarinic antagonist (LAMA), and formoterol fumarate, a long-acting beta2-agonist (LABA), at doses of 320/18/9.6 µg per actuation. The combination adds a LAMA component to the ICS/LABA backbone that has formed the standard maintenance regimen for uncontrolled asthma, and the approval covers maintenance use only — the therapy is not indicated for acute symptom relief and does not replace a rescue inhaler. Regulatory filings for the asthma indication are under review in the EU, Japan, and China. The FDA approval was supported by data from the Phase III KALOS and LOGOS trials, replicate randomized, double-blind, double-dummy, parallel-group studies enrolling approximately 4,300 patients with asthma, with or without a recent exacerbation. Both trials ran for 24 to 52 weeks and assessed Breztri against dual ICS/LABA comparators, including Symbicort (budesonide/formoterol fumarate) and an Aerosphere formulation of budesonide/formoterol fumarate designated PT009. In the data package submitted to the FDA, the primary endpoint was change from baseline in forced expiratory volume in one second (FEV1) area under the curve from 0 to 3 hours at week 24, compared with PT009. Breztri met this endpoint with a statistically significant improvement in lung function. A key secondary endpoint showed a significant improvement from baseline in lung function within five minutes of the first dose. Results from the KALOS and LOGOS trials were published in The Lancet Respiratory Medicine in February 2026. No new safety or tolerability signals were identified relative to the established profile of the molecule. The approval enters a treatment landscape where approximately 27 million people in the US are living with asthma, according to the US Centers for Disease Control and Prevention, and where a substantial proportion of patients remain uncontrolled despite adherence to dual ICS/LABA maintenance therapy. Uncontrolled asthma is associated with persistent bronchoconstriction, exacerbations, and reduced lung function, with nearly 10 million asthma attacks occurring annually in the US. The addition of a LAMA to ICS/LABA therapy had already been validated in COPD, where triple fixed-dose combinations are standard of care, but the mechanistic rationale for LAMA use in asthma — addressing airway smooth muscle tone through muscarinic receptor antagonism alongside corticosteroid-mediated inflammation control and LABA-driven bronchodilation — had not previously translated into an approved single-inhaler product for this indication. The asthma treatment field has seen considerable activity across both inhaled and biologic modalities. Among approved biologics, dupilumab (Dupixent), mepolizumab (Nucala), benralizumab (Fasenra), and tezepelumab (Tezspire) target distinct components of type 2 inflammatory pathways and are indicated for severe or uncontrolled phenotypes. Breztri occupies a different position as an inhaled maintenance therapy applicable across a broader asthma population, including patients without the eosinophilic or allergic phenotypes that define eligibility for most biologics. The pipeline adds further complexity: GSK’s depemokimab, an extended half-life anti-IL-5 antibody with a twice-yearly dosing interval, has Phase III data in severe eosinophilic asthma [from the SWIFT-1 and SWIFT-2 trials](); Genentech’s astegolimab targets IL-33 in the SOLSTICE program; and Sanofi/Regeneron’s amlitelimab, an anti-OX40L antibody, is in Phase IIb/III development for moderate-to-severe uncontrolled asthma, with potential applicability to non-type-2 phenotypes that remain without approved biologic options. For AstraZeneca, the approval extends a molecule with an established manufacturing and prescribing infrastructure into a substantially larger patient population than COPD alone. The company has parallel respiratory assets in the biologic space, including tezepelumab (Tezspire), developed with Amgen, and benralizumab (Fasenra), creating a portfolio that spans inhaled and injectable modalities across asthma severity strata. The decision also carries relevance for triple bronchodilator and anti-inflammatory combinations outside COPD, with the KALOS and LOGOS data now underpinning a US label and formally establishing this approach in asthma. This article was generated with AI assistance and reviewed and edited by the AllSci editorial team Explore more at AllSci News: https://allsci.com/news/ Your email address will not be published. Required fields are marked * Comment * Name * Email * Website

临床3期临床结果上市批准

2026-04-26

·医学界呼吸频道

2026 ATS抢先看｜划重点！10项呼吸新药Ⅲ期数据，一文吃透

*仅供医学专业人士阅读参考 10项呼吸新药Ⅲ期试验抢先解锁。撰文 | 医学界会议报道组 2026年美国胸科学会（ATS）国际大会将于5月15日至20日在美国奥兰多举办，作为全球呼吸领域极具权威性与影响力的学术盛会，本次大会将集中公布多项呼吸领域新药Ⅲ期临床试验的成果。为帮助临床医师提前洞悉前沿动态，“医学界呼吸频道”精心梳理了10项重点研究[1-10]，涵盖危重症呼吸窘迫、慢性阻塞性肺疾病（COPD）、自身免疫性肺泡蛋白沉积症（aPAP）等罕见肺疾病，以及特发性肺纤维化（IPF）、进展性肺纤维化（PPF）等肺纤维化相关领域，带您提前解码呼吸领域诊疗新方向、新突破。 1. 抗TLR4抗体Paridiprubart在接受有创机械通气的呼吸窘迫成年患者中的Ⅲ期、多中心、双盲、安慰剂对照研究 Paridiprubart是一种Toll样受体4（TLR4）的单克隆抗体抑制剂，长期被认为参与急性呼吸窘迫综合征（ARDS）的发病机制。关键结果：结果显示，Paridiprubart组28天死亡率的调整后估计风险为39%，显著低于安慰剂组的52%（P<0.001）；60天死亡率的调整后估计风险为46%，显著低于安慰剂组的59%（P<0.005）；WHO疾病严重程度评分降低≥2分的患者比例达38%，明显高于安慰剂组的27%（P<0.05），且耐受性良好，无新增安全性风险。结论：Paridiprubart可显著改善危重症ARDS患者的预后，耐受性良好，有望成为此类患者的治疗新选择。 2. Revefenacin支气管舒张作用起效更早：来自Ⅲ期COPD试验的新分析 Revefenacin是每日一次雾化吸入的长效毒蕈碱拮抗剂（LAMA），通过松弛气道平滑肌缓解COPD患者气道阻塞，用于COPD维持治疗，本研究重点分析其首剂起效时间。关键结果：首剂给药后15分钟即出现明显支气管舒张作用，第一秒用力呼气量（FEV1）的LS均值较基线平均增加90 mL，30分钟时FEV1 LS均值改善超过基线100 mL，达132 mL；安慰剂校正后15分钟的FEV₁均值差异为114 mL，超过最小临床重要差异，置信度超92%。结论：Revefenacin起效快速，可及时缓解COPD患者气道阻塞症状，为临床灵活用药提供有力支持。 3. Astegolimab治疗有频繁急性加重史的COPD患者：Ⅲ期、随机、双盲、安慰剂对照、多中心ARNASA试验 Astegolimab是抗ST2单克隆抗体，通过抑制气道慢性炎症减少COPD急性加重，用于有频繁急性加重史的COPD患者的辅助治疗。关键结果：1375名COPD患者随机（1:1:1）接受476 mg Astegolimab皮下注射，每2周1次（Q2W）或每4周1次（Q4W）或安慰剂，为期52周。在主要终点（52周治疗期间中重度急性加重年化率）中，与安慰剂相比，Astegolimab Q2W组中重度急性加重的年化发生率降低14.5%，未达到统计学显著性。在次要终点中，Q2W剂量组重度急性加重年化率显著降低33.1%（P=0.0238）；圣乔治呼吸问卷-COPD版（SGRQ-C）总分改善≥4分（具有临床意义）的患者比例显著增加（P=0.0037）；三组不良事件发生率相当（Q2W组83.2%、Q4W组87.9%、安慰剂组85.5%）。结论：尽管ARNASA试验未达到主要终点，但Astegolimab Q2W剂量在重度急性加重及生活质量等关键次要终点上显示出具有临床意义的改善，且耐受性良好，为频繁急性加重的COPD患者提供了潜在的新选择。 4. Itepekimab在既往吸烟的COPD患者中的疗效与安全性：AERIFY-1和AERIFY-2试验 Itepekimab是一种全人源单克隆抗体，可特异性结合IL-33，阻断其信号传导，抑制气道炎症，用于治疗既往吸烟的COPD患者，通过两项Ⅲ期试验验证其疗效与安全性。关键结果：AERIFY-1研究中，Q2W、Q4W组中重度急性加重率较安慰剂分别显著降低27.1%（P=0.0019）、20.5%（P=0.0213）。在AERIFY-2研究中，Q2W、Q4W组中重度急性加重率较安慰剂分别降低1.6%、12.4%，差异无统计学意义。结论：在既往吸烟的COPD患者中，Itepekimab在AERIFY-1中显著降低了中度或重度急性加重率，但此疗效未能在AERIFY-2中复现，整体安全性可接受。 5. 莫拉司亭在自身免疫性肺泡蛋白沉积症患者中的长期疗效与安全性：IMPALA-2 Ⅲ期试验开放标签治疗期结果莫拉司亭（Molgramostim）是重组人GM-CSF吸入溶液，可补充aPAP患者体内GM-CSF，恢复肺泡巨噬细胞功能，用于治疗aPAP这一罕见慢性肺疾病，本次评估其长期治疗效果。关键结果：双盲期第48周，莫拉司亭组一氧化碳弥散量（DLco%）较基线平均增加11.6，显著高于安慰剂组的3.7（P=0.0008）；开放标签期，持续用药组DLco%持续改善，安慰剂转换组也平均增加8.8，生活质量评分同步提升，耐受性良好，无新增安全性信号。结论：莫拉司亭是aPAP患者可靠的长期治疗方案，可持续改善患者肺功能及生活质量，安慰剂转换后仍有效，为这一罕见病提供有效治疗选择。 6. Admilparant（BMS-986278）治疗特发性肺纤维化的Ⅲ期、随机、安慰剂对照ALOFT-IPF试验的患者基线特征 Admilparant是口服溶血磷脂酸受体1拮抗剂，通过抑制纤维化信号通路延缓IPF进展，其Ⅱ期试验已显示出良好的安全性和初步疗效，本次呈现其Ⅲ期试验入组患者基线情况，为后续疗效评估奠定基础。关键结果：共入组1251名IPF患者，中位年龄71岁，79.4%为男性，64.1%接受背景抗纤维化治疗，中位用力肺活量（FVC）为2710 mL，预测用力肺活量（ppFVC）为78.9%，DLco%为51.9%，人群特征与近期其他IPF Ⅲ期试验高度一致，地域分布广泛。结论：入组人群代表临床典型IPF患者，涵盖不同疾病阶段，为后续评估Admilparant最长3年的治疗影响提供可靠基础，有望为IPF患者带来新的抗纤维化治疗选择。 7. 吸入性曲前列尼尔治疗进展性肺纤维化的TETON-PPF Ⅲ期临床试验吸入性曲前列尼尔（Treprostinil）是前列环素类药物，具有扩张肺血管、抑制肺成纤维细胞增殖的抗纤维化作用，此前已在IPF患者中证实有效，本次探索其对PPF患者的治疗效果。关键结果：试验计划入组698名PPF患者，治疗周期52周，允许背景使用抗纤维化药物，主要终点为第52周绝对FVC变化；目前正在全球16个国家入组，已招募患者多为中度限制性疾病，约半数接受背景抗纤维化治疗。结论：该试验聚焦PPF这一未被充分满足的治疗领域，有望为这类进展性肺疾病患者提供新的治疗方向，丰富肺纤维化治疗格局。 8. 吸入性曲前列尼尔治疗特发性肺纤维化的TETON-1 Ⅲ期临床试验本研究是TETON-IPF项目的重要组成部分，进一步验证吸入性曲前列尼尔治疗IPF的疗效与安全性，IPF作为进展迅速、预后不良的慢性间质性肺疾病，目前治疗选择有限，亟需新型抗纤维化药物补充。关键结果：试验于2025年1月完成入组，入组患者均为FVC≥45%预计值的IPF患者，基线特征与其他IPF临床研究可比，主要终点为第52周绝对FVC变化，主要结果预计2026年上半年公布。结论：该试验将为吸入性曲前列尼尔治疗IPF提供关键数据，进一步验证其抗纤维化疗效，有望丰富IPF抗纤维化治疗选择。 9. 吸入性曲前列尼尔治疗特发性肺纤维化的TETON Ⅲ期临床试验：TETON-1与TETON-2的综合疗效和安全性结果综合两项Ⅲ期试验数据，强化吸入性曲前列尼尔治疗IPF的疗效与安全性评估，为其临床应用提供更可靠的证据支持，该药物已被证实可减缓IPF患者肺功能下降、改善临床结局。关键结果：TETON-2已完成入组并达到主要终点，曲前列尼尔组FVC下降幅度较安慰剂组显著减少95.6 mL（P<0.0001），临床恶化风险降低29%（P=0.0190），安全性与既往研究一致；TETON-1结果预计2026年上半年公布，将进一步补充数据。结论：TETON-2已证实吸入性曲前列尼尔治疗IPF的优效性，耐受性良好，两项试验综合数据将为其临床广泛应用提供更坚实的证据，助力优化IPF治疗策略。 10. SURPASS-IPF：Deupirfenidone对比吡非尼酮治疗特发性肺纤维化患者的Ⅲ期头对头试验的研究设计 Deupirfenidone是吡非尼酮的氘代衍生物，保留抗纤维化活性的同时优化药代动力学特征，目前IPF仍存在未满足的治疗需求，本研究为目前首个IPF新药与获批药物的Ⅲ期头对头试验。关键结果：计划入组约1100名IPF患者，按1:1随机接受Deupirfenidone 825 mg每日3次或吡非尼酮801 mg每日3次治疗≥52周，主要终点为第52周绝对FVC变化，同时评估临床恶化时间、生存期等次要终点及安全性。结论：该试验设计科学严谨，将直接对比两种药物的疗效与安全性，为临床医生和IPF患者提供更精准的用药参考，有望优化IPF治疗方案。小结 2026 ATS大会公布的这10项重点新药Ⅲ期研究，精准覆盖呼吸领域多个核心病种，涉及单克隆抗体、长效支气管舒张剂、抗纤维化药物等多种药物类型，多数药物展现出良好的疗效和安全性，为临床诊疗提供了新的思路与选择，也彰显了呼吸领域新药研发的蓬勃活力。下一期我们将继续梳理2026 ATS大会重磅新药研究，解锁更多呼吸领域前沿诊疗突破，敬请期待！参考文献： [1]Steiner T, et al. A Phase 3, Multicenter, Double-blind, Placebo Controlled Study of an Anti-TLR4 Antibody, Paridiprubart, in Adult Patients With Respiratory Distress on Invasive Mechanical Ventilation. 2026 ATS. [2]Moran EJ, et al. Earlier Onset of Bronchodilation With Revefenacin: New Analyses From Phase 3 COPD Trials. 2026 ATS. [3]Papi A, et al. Astegolimab for Chronic Obstructive Pulmonary Disease (COPD) in Patients With a History of Frequent Exacerbations: The Phase III, Randomized, Double-blind, Placebo-controlled, Multicenter ARNASA Trial. 2026 ATS. [4]Rabe KF, et al. Efficacy and Safety of Itepekimab in Former Smokers With Chronic Obstructive Pulmonary Disease: AERIFY-1 and AERIFY-2 Trials. 2026 ATS. [5]Trapnell BC, et al.Long-term Efficacy and Safety of Molgramostim in Patients With Autoimmune Pulmonary Alveolar Proteinosis (aPAP): Results From the IMPALA-2 Trial Open-label Treatment Period. 2026 ATS. [6]Maher TM, et al. Baseline Characteristics of Patients in the ALOFT-IPF Phase 3, Randomized, Placebo-Controlled Trial of Admilparant (BMS-986278), an Oral Lysophosphatidic Acid Receptor 1 Antagonist, in Idiopathic Pulmonary Fibrosis. 2026 ATS. [7]Nathan SD, et al. TETON-PPF Clinical Trial of Inhaled Treprostinil for the Treatment of Progressive Pulmonary Fibrosis. 2026 ATS. [8]Nathan SD, et al. TETON-1 Phase 3 Clinical Trial of Inhaled Treprostinil for the Treatment of Idiopathic Pulmonary Fibrosis. 2026 ATS. [9]Nathan SD, et al. TETON Phase 3 Clinical Trials of Inhaled Treprostinil for the Treatment of Idiopathic Pulmonary Fibrosis: Integrated Efficacy and Safety Results for TETON-1 and TETON-2. 2026 ATS. [10]Maher TM, et al. SURPASS-IPF: Study Design of a Phase 3, Head-to-head Trial of Deupirfenidone Compared to Pirfenidone in Patients With Idiopathic Pulmonary Fibrosis. 2026 ATS. 本文来源：医学界呼吸频道责任编辑：大晨 *“医学界”力求所发表内容专业、可靠，但不对内容的准确性做出承诺；请相关各方在采用或以此作为决策依据时另行核查。戳“阅读原文”，学习更多临床技能

100 项与艾特利单抗相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
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研发状态

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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	Roche Holding AG	2023-01-09
慢性阻塞性肺疾病	临床3期	日本	Roche Holding AG	2023-01-09
慢性阻塞性肺疾病	临床3期	阿根廷	Roche Holding AG	2023-01-09
慢性阻塞性肺疾病	临床3期	澳大利亚	Roche Holding AG	2023-01-09
慢性阻塞性肺疾病	临床3期	奥地利	Roche Holding AG	2023-01-09
慢性阻塞性肺疾病	临床3期	比利时	Roche Holding AG	2023-01-09
慢性阻塞性肺疾病	临床3期	巴西	Roche Holding AG	2023-01-09
慢性阻塞性肺疾病	临床3期	保加利亚	Roche Holding AG	2023-01-09
慢性阻塞性肺疾病	临床3期	加拿大	Roche Holding AG	2023-01-09
慢性阻塞性肺疾病	临床3期	智利	Roche Holding AG	2023-01-09

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适应症

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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


NCT05037929 (ALIENTO, GlobeNewswire) 人工标引	临床2期	慢性阻塞性肺疾病	-	astegolimab	鏇艱選製窪襯遞積構網(選網構鬱簾築簾製憲獵): Difference (%) = -15.4 达到	积极	2025-07-24
				Placebo
NCT05595642 (ARNASA, GlobeNewswire) 人工标引	临床3期	慢性阻塞性肺疾病	-	astegolimab	積夢鬱壓衊壓壓繭鹹顧(簾齋衊選鏇鹹糧襯簾淵): Difference (%) = 14.5 未达到	不佳	2025-07-21
				Placebo
NCT04386616 \| NCT02918019 \| NCT03615040 \| NCT03747575 (ZENYATTA \| ZARNIE \| COPD-ST2OP \| COVASTIL, ATS2024)	临床2期	IL-33 \| ST2	912	Astegolimab	蓋齋獵艱遞選構觸製繭(遞醖遞顧繭簾襯鑰鏇簾) = 淵繭廠獵遞積鬱鹽願鏇獵鹹鬱鏇構顧願餘鏇觸 (築膚艱構餘觸襯夢構齋 )	积极	2024-05-19
				Placebo	壓鑰糧餘膚膚壓餘積鏇(積膚夢壓願築製獵鏇範) = 蓋醖觸夢衊簾襯築簾積廠蓋糧獵鏇糧顧積衊鑰 (製繭淵觸壓繭鹹壓齋淵 )
NCT03747575 (CTgov)	临床2期	中度特应性皮炎 \| 重度特应性皮炎	65	MSTT1041A (Treatment)	鹹衊鹽繭窪膚遞齋膚襯(衊夢構鬱膚築築獵獵繭) = 簾廠衊襯範網廠餘鹹獵廠簾夢憲築壓鹹範夢獵 (願製鬱壓艱膚範蓋淵夢, 8.639) 更多	-	2023-05-06
				Placebo (Placebo)	鹹衊鹽繭窪膚遞齋膚襯(衊夢構鬱膚築築獵獵繭) = 鹹淵簾齋積鹹壓衊壓壓廠簾夢憲築壓鹹範夢獵 (願製鬱壓艱膚範蓋淵夢, 9.092) 更多
NCT02918019 (CTgov)	临床2期	哮喘	517	Placebo	鹹願窪遞齋糧壓廠餘鬱 = 顧獵壓觸遞簾蓋蓋鹽製蓋鏇顧夢艱簾繭範築憲 (膚艱憲蓋顧衊獵膚遞鑰, 製糧襯製範衊鹹繭廠構 ~ 積淵膚廠製淵窪糧衊製) 更多	-	2022-12-28
NCT03747575 (Pubmed) 人工标引	临床2期	特应性皮炎	65	Astegolimab	鹹艱齋鑰選選鏇鹹構繭(選範範選顧簾鹹艱範餘) = 鹹築蓋遞範鹽齋廠製齋鏇淵網衊壓獵願遞鹽製 (廠簾鹹顧顧範積觸餘選 )	不佳	2022-08-27
				Placebo	鹹艱齋鑰選選鏇鹹構繭(選範範選顧簾鹹艱範餘) = 窪鹽鑰獵繭夢窪鹹築範鏇淵網衊壓獵願遞鹽製 (廠簾鹹顧顧範積觸餘選 )
NCT03615040 (COPD-ST2OP, CTgov)	临床2期	慢性阻塞性肺疾病	81	MSTT1041A (Anti-ST2)	齋廠遞鑰觸憲齋淵夢簾(糧淵網鏇糧繭獵襯憲膚) = 蓋構鏇簾糧齋鏇壓壓廠醖壓鹹衊繭鏇遞觸築簾 (鑰範夢網襯選衊遞蓋鑰, 2.04) 更多	-	2022-05-24
				Placebo (Placebo)	齋廠遞鑰觸憲齋淵夢簾(糧淵網鏇糧繭獵襯憲膚) = 選構積鑰遞簾簾築齋餘醖壓鹹衊繭鏇遞觸築簾 (鑰範夢網襯選衊遞蓋鑰, 2.14) 更多
NCT03615040 (COPD-ST2OP, Pubmed \| Lancet Respir Med) 人工标引	临床2期	慢性阻塞性肺疾病	-	Astegolimab	艱簾顧窪築鹽獵夢窪繭(壓淵製齋鏇築膚簾觸築) = similar between group 築鹽襯夢醖糧遞選夢顧 (糧築壓齋襯鏇繭襯網積 ) 更多	积极	2022-03-24
				Placebo
NCT03615040 (COPD-ST2OP, ERS2021)	临床2期	慢性阻塞性肺疾病 blood eosinophil count	-	Astegolimab 490mg	廠襯觸顧夢積襯鹹廠遞(鏇廠範簾獵獵膚築蓋簾) = 夢餘築齋襯餘積顧繭廠選糧鏇範鬱構選選範遞 (顧蓋築鑰齋餘壓糧範獵, -10 ~ 90)	不佳	2021-09-05