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

Regeneron Pharmaceuticals, Inc.

Sanofi

+ [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-

登录后查看时间轴

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, Yue ; Wang, Xinquan

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.

332

项与依特吉单抗相关的新闻（医药）

2026-08-25

·东方九紫

9年烧了52亿，迈威生物凭什么是"稀缺"？

如果在 A 股创新药里选一只"争议股"，迈威生物（688062.SH / 02493.HK）无疑榜上有名。一边是刺眼的数字：成立 9 年，累计研发投入烧掉 50 多亿，直到 2024 年归母净利润仍为 -10.44 亿元；另一边也是数字：2025 年营收 6.63 亿元、同比翻超两倍，对外授权（BD）潜在里程碑总额超过 20 亿美元，核心产品 9MW2821 在 Nectin-4 ADC 这条赛道上，是本土企业中进度领先、全球范围内仅次于 Padcev 的存在。同一家公司，两种叙事。今天这篇文章，我们不做情绪站队，只回答一个很实在的问题：迈威生物到底是不是龙头？它的稀缺性，是真的还是包装的？一、先看清它是谁：一家"全链条"的创新药企迈威生物成立于 2017 年，创始人、CEO 为刘大涛。2022 年 1 月登陆科创板（688062），2026 年 4 月又登陆港交所（02493），成为"A+H"两地上市的创新药企。和很多"只懂研发、卖货靠外包"的 Biotech 不同，迈威从一开始就在搭"全产业链"：前端发现：自动化、高通量的抗体工程与成药性评价平台；中端开发：工艺开发、质量研究，快速推进 IND；后端产能：江苏泰州基地符合 NMPA、美国 FDA、欧盟 EMA 的 GMP 标准，已通过欧盟 QP 审计、哥伦比亚 INVIMA 检查；上海金山大规模基地在建；商业网络：国内已覆盖 327 个城市、8000+ 医院；海外组建了专业 BD 团队。目前公司管线约 15 个重点品种：4 款已上市、1 款在审评、2 款处于 III 期关键注册临床。已上市的四款里，既有阿达木单抗（君迈康）、地舒单抗（迈利舒 / 迈卫健）、阿柏西普眼内注射溶液这类生物类似药，也有 2025 年 5 月刚获批、全球率先采用白蛋白长效融合技术开发的 G-CSF（迈粒生）。一句话画像：它既是烧钱的 Biotech，也在努力长成能自我造血的 Pharma。二、核心之问：它是"龙头"吗？直接给结论——分两层看，结论不一样。放在整个创新药行业版图上，它不是严格意义上的龙头。论营收体量、论净利润、论全球化商业化能力，恒瑞医药、百济神州才是真正的头部。迈威 2025 年 6.63 亿营收里，还有 4.09 亿来自授权首付款/里程碑，自身"卖药"收入（2.50 亿）仍然偏小，且大半来自竞争激烈、毛利承压的生物类似药。但放在"Nectin-4 ADC"这条细分赛道上，它是实打实的国内进度领先、全球唯二。这才是理解迈威的关键：它不靠"综合领先"取胜，而靠"在少数高价值靶点上的卡位领先"。用投资里的说法，它不是宽基龙头，而是细分赛道里的卡位型龙头。三、稀缺性解剖：到底藏在哪里？迈威的稀缺性，不是一句口号，可以拆成四块硬资产。 1）王牌 9MW2821：Nectin-4 ADC 的"国产代表队" Nectin-4 是一种在膀胱癌、宫颈癌、乳腺癌等多种实体瘤高表达的靶点。全球目前只有一款上市产品——安斯泰来 / 辉瑞的 Padcev，2025 年销售额约 24 亿美元、同比增长约 45%，证明了这条赛道的天花板。迈威的 9MW2821 卡位相当精准：维度 9MW2821 的卡位国内进度本土企业同靶点中进度领先，全球仅次 Padcev 宫颈癌全球率先进入关键 III 期的 Nectin-4 ADC 临床规模已布局 4 项 III 期关键注册临床监管认可 3 项 FDA 快速通道（FTD）、1 项孤儿药（ODD）、2 项 CDE 突破性疗法疗效信号二线尿路上皮癌 ORR 54.1%，优于 Padcev 的 37.5%；一线联合特瑞普利单抗 ORR 达 87.5% 更关键是它的差异化路径：Padcev 主要吃透尿路上皮癌，而 9MW2821 在宫颈癌、三阴性乳腺癌（TNBC）上做"全球首发"式推进——宫颈癌 III 期已启动、TNBC III 期已完成首例给药，且基于 Nectin-4 高表达，不强制做生物标志物筛查，覆盖全人群。2026 年预计递交 pre-BLA。 2）9MW1911：全球第 2 款 ST2 单抗，COPD 上的潜在 Best-in-Class 很多人只盯 ADC，忽略了迈威在自免 / 慢病上的卡位。9MW1911 是全球第 2 款进入临床的 ST2 单抗，针对慢阻肺（COPD）——全球第三大健康威胁。其 2a 期数据显示，在 RP2D 剂量下，中重度急性加重年化发生率下降超 30%、重度下降超 40%，优于已公布三期数据的赛诺菲 Itepekimab、罗氏 / 安进 Astegolimab。这是一个被严重低估的稀缺资产。 3）9MW3811（IL-11）与双靶点 siRNA：用"出海"验证稀缺稀缺性的另一面，是别人愿不愿意为真金白银买单：9MW3811（抗 IL-11）：病理性瘢痕 2a 期全球率先，2025 年授权给 Calico，获 2500 万美元首付 + 上限 5.71 亿美元里程碑 + 销售分成，总额近 6 亿美元；双靶点 siRNA：通过 NewCo 模式授权 Kalexo，潜在里程碑上限 10 亿美元；9MW3011（抗 TMPRSS6）：授权 Disc，潜在里程碑上限 4.125 亿美元。合计对外授权潜在里程碑超过 20 亿美元——国际买方用钱投票，反向印证了管线的全球竞争力。 4）底层技术平台：别人抄不走的"内功" 迈威围绕 ADC 自研了四大技术：定点偶联工艺 DARfinity、定点连接子 IDconnect、新型载荷 Mtoxin、稳定连接结构 LysOnly；在 TCE（T 细胞衔接抗体）上则用"空间位阻遮蔽"降低 CRS 相关不良反应。平台型能力意味着它不是"一款药赌一把"，而是可持续产出差异化分子的工厂——这才是稀缺性的根基。四、安全边际：不是只会烧钱看一家 Biotech，光看管线不够，还要看"活着的能力"。现金弹药：2025 年末现金及等价物 15.26 亿元，较 2024 年底增加约 3 亿元；收入曲线：营收从 2024 年约 2.0 亿增至 2025 年 6.63 亿（+231.6%），商业化产品持续放量；BD 闭环：授权收入改善短期现金流，又保留长期销售分成；产能与认证：泰州基地通过欧盟 QP 审计，地舒单抗已向海外商业化发货，生物类似药在巴基斯坦、印尼等多国获批；A+H 平台：双融资通道，为海外临床与注册提供资本弹性。换句话说，迈威用"biosimilar 现金流 + BD 首付款 + 全产业链"三条腿，给自己争取了把核心管线"养大"的时间窗口。五、必须正视的三道风险迈威的稀缺性真实，但风险同样高： 1、盈利拐点未至：2025 年仍处亏损，年研发投入近 10 亿，现金消耗与融资节奏高度绑定； 2、商业化以类似药为主：已上市产品中 biosimilar 占比高，集采与同质化竞争会持续压制毛利； 3、临床与竞争双重不确定性：9MW2821 的 BLA 尚未获批；Nectin-4 ADC 赛道正涌入石药（SYS6002 / CRB-701）、恒瑞、科伦等国产玩家，Padcev 的先发与品牌优势短期难撼。所以，迈威的稀缺性是"用时间换空间"的稀缺——故事成立，但兑现需要耐心。六、结语：它是什么？回到开头的问题。迈威生物并非严格意义上的"龙头"，但它是细分赛道里的卡位龙头，是一只同时具备"全球及本土率先布局的资产 + 自研技术平台 + A+H 全产业链 + BD 闭环"多重稀缺性的创新药企。它的稀缺，不在口号，而在：Nectin-4 ADC 的国内进度领先、ST2 单抗的潜在 Best-in-Class、IL-11 与 siRNA 的全球化授权、以及一套别人短期抄不走的 ADC / TCE 平台。对读者而言，重要的不是"现在买不买"，而是先看懂：一家还在亏损的公司，凭什么被市场反复讨论——答案，就藏在这份稀缺性里。 ⚠️ 风险提示与免责：本文基于公开资料梳理，仅供研究与交流，不构成任何投资建议。创新药研发与商业化存在重大不确定性，投资有风险，决策需谨慎。

抗体药物偶联物临床3期引进/卖出生物类似药

2026-08-24

·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

2026-08-20

·泓博医药人工智能药物设计平台

今日生物医药快讯-2026.08.20

本期快讯摘要临床方面，Moderna 与默克个性化癌症疫苗在黑色素瘤 III 期临床取得显著疗效，联合 Keytruda 降低复发风险；Enveda 口服肥胖候选药物 ENV-308 完成 I 期试验，展现胃肠道安全性优势；公司动态方面，诺和诺德口服 GLP-1 药物 Wegovy 销售额远超礼来 Foundayo，巩固市场领先地位；FDA获批方面，武田首款 Orexin 药物 Orzeyful 获批治疗发作性睡病，或重塑该领域治疗格局；Regeneron 针对 FOP 的疗法 Pasatru 获批，为罕见病治疗提供新选择。本文多维度解读全球生物医药产业新变化，助力读者高效洞察行业趋势。 01 专题板块临床试验 4 条 01Moderna 与默克联合开发的个性化癌症疫苗在黑色素瘤中取得关键临床进展 Moderna 与默克（Merck）联合开发的个性化癌症疫苗 intismeran（V940/MRNA-4157）在一项 III 期临床试验中达到主要终点，显示出在黑色素瘤术后辅助治疗中能够显著延缓疾病复发并阻止其扩散。该疫苗基于 mRNA 技术，可识别患者肿瘤细胞中多达 34 个新抗原，实现个体化治疗。在 II 期试验中，intismeran 联合 Keytruda 相较 Keytruda 单药治疗，将死亡或复发的相对风险降低了 44%。尽管 III 期试验未公布详细数据，但独立数据监测委员会已确认其具有统计学和临床意义的改善。该结果被视为癌症疫苗领域的重要里程碑，分析师预计其在黑色素瘤市场的年销售额可达数十亿美元。Moderna 正在进一步评估该疫苗在肺癌、肾癌和膀胱癌中的疗效。 ModernaKeytrudaintismeran癌症疫苗 02Enveda口服肥胖候选药物ENV-308完成I期临床试验，胃肠道安全性突出 Enveda宣布其口服肥胖候选药物ENV-308在健康志愿者中的I期临床试验中展现出“卓越”的胃肠道安全性，为后续临床试验奠定了基础。ENV-308旨在模拟运动后升高的激素N-lactoyl-phenylalanine（Lac-Phe），该激素在动物研究中被发现可抑制摄食和肥胖。尽管该试验未直接评估体重变化，但通过生物标志物显示，ENV-308可显著降低瘦素（leptin）水平，这一结果与动物研究一致，初步验证了其作用机制。基于积极结果，Enveda计划启动II期临床试验，探索ENV-308是否能在停止GLP-1治疗的患者中维持体重减轻和代谢益处。该试验是ENV-308更广泛开发计划的一部分，未来可能拓展至偏头痛、炎症性肠病等运动有益的疾病领域。Enveda此前已完成5.17亿美元融资，为其推进ENV-308及其他候选药物（如ENV-294和ENV-6946）提供了充足资金支持。 EnvedaENV-308肥胖Lac-Phe 03Amylyx Phase 3试验成功，GLP-1拮抗剂avexitide有望提交FDA申请 Amylyx Pharmaceuticals的GLP-1受体拮抗剂avexitide在治疗术后低血糖症（PBH）的Phase 3临床试验LUCIDITY中取得积极结果，显著减少中度和重度低血糖事件。试验数据显示，在16周治疗期内，avexitide使PBH患者的2级和3级低血糖复合事件发生率降低了55%，这一结果高度统计学显著。目前尚无获批的PBH治疗药物，Amylyx计划于2026年底提交新药申请，并预计该药物全球峰值销售额可达17亿美元。与现有GLP-1激动剂不同，avexitide通过抑制GLP-1受体来调节过度的胰岛素反应，为PBH患者提供新的治疗机制。该试验结果不仅为Amylyx带来商业化机会，也凸显了GLP-1靶点在罕见病治疗中的新潜力。 AmylyxavexitideGLP-1Phase 3 04Regeneron因安全性问题终止抗炎抗体REGN7041治疗非感染性葡萄膜炎的临床试验 Regeneron近日宣布终止其针对非感染性葡萄膜炎的Phase 1/2临床试验，试验药物为靶向CD3的抗炎抗体REGN7041。公司表示，该决定基于对药物风险-获益评估的更新，源于试验中观察到的安全事件。尽管未披露具体不良事件细节，但Regeneron已对事件进行了深入调查，目前尚无法明确其原因。REGN7041作为首个靶向CD3治疗葡萄膜炎的候选药物，其终止标志着Regeneron在免疫炎症疾病领域遭遇又一挫折。此前，该公司曾因Dupixent后续药物itepekimab在COPD试验中的失败，以及一项黑色素瘤联合疗法在Phase 3中输给Merck的Keytruda而备受关注。尽管如此，Regeneron仍表示对外部合作机会持开放态度，并在近期与Telix及Parabilis Medicines达成多笔合作，以拓展其创新药物管线。该事件对Regeneron的免疫疾病研发战略和投资者预期可能产生一定影响。 RegeneronREGN7041CD3非感染性葡萄膜炎 02 专题板块公司动态 4 条 01诺和诺德在口服GLP-1药物市场竞争中领先，但分析师认为领先优势难以持久诺和诺德的口服GLP-1药物Wegovy在2026年第二季度的销售额达到4.96亿美元，远高于礼来口服减肥药Foundayo的9800万美元。这一领先主要得益于Wegovy延续了其注射剂品牌，利用了医生和患者已有的认知基础。尽管Wegovy在72周内实现16.6%的体重减轻，优于Foundayo的11.2%，但礼来在口服药物的使用便利性方面占据优势，Foundayo无需特定服用方式，而Wegovy则需配合水服用并避免30分钟内摄入其他食物或饮料。分析师认为，礼来在注射剂领域曾凭借tirzepatide超越诺和诺德，未来在口服市场也可能凭借Foundayo的便利性和全球商业化能力实现反超。此外，礼来正在推进其三重G受体靶向药物retatrutide的开发，预计将在2027年提交FDA审批，并可能在2028年后重新夺回市场主导地位。诺和诺德礼来GLP-1口服药物 02LEO Pharma 4.35亿美元收购罕见病药物 Dersimelagon，拓展皮肤科管线 LEO Pharma 宣布以 4.35 亿美元收购日本田边制药（Tanabe Pharma）开发的处于后期阶段的罕见病药物 Dersimelagon，用于治疗光敏感性皮肤病 EPP（红细胞生成性原卟啉症）和 XLP（X 连锁原卟啉症）。该药物为每日一次的口服 MC1R 激动剂，已完成 III 期临床试验，并于 2026 年 6 月向 FDA 提交了两项适应症的上市申请。在 III 期 INSPIRE 试验中，Dersimelagon 显著延长了患者平均日晒时间，12 至 16 周期间平均增加 23 分钟，补充分析显示至第 16 周时可延长至 29 分钟，并能减少疼痛事件。该药物已获得 FDA 的快速通道和孤儿药认定，若获批将成为该领域首个上市疗法。LEO 表示，此次收购是其近期在皮肤科领域一系列交易中的第三项，旨在强化其在医疗皮肤科领域的领导地位。 LEO PharmaDersimelagonMC1REPP 03阿斯利康肺癌组合疗法获关键临床数据，有望成为首个口服方案阿斯利康宣布其肺癌靶向药物Tagrisso与和记黄埔医药的Orpathys联合使用，在EGFR阳性且携带MET突变的非小细胞肺癌患者中展现出优于化疗的疗效。该联合疗法不仅显著延缓了疾病进展，还延长了患者的总生存期。阿斯利康表示，这一结果支持其开发首个针对该生物标志物的全口服治疗方案的目标。Tagrisso已在欧美等主要市场获批，而Orpathys则在中国和瑞士获批。此次数据为肺癌治疗领域的重要进展，尤其在精准医疗和靶向治疗方向上具有行业示范意义。阿斯利康TagrissoOrpathysMET突变 04BioMarin 2.75 亿美元收购 Alesta，强化骨骼与肌肉疾病管线 BioMarin Pharmaceutical 宣布以 2.75 亿美元收购私营公司 Alesta Therapeutics，后者拥有针对罕见骨代谢疾病低磷酸酯酶症（hypophosphatasia）的候选药物 ALE1。此次交易包括 2.75 亿美元预付款和最高 2.15 亿美元的开发与监管里程碑付款。ALE1 目前处于 Phase 1/2 临床试验阶段，通过靶向降低无机焦磷酸盐水平，有望成为 BioMarin 面向最大患者群体的治疗药物。该药物将加入 BioMarin 现有的骨骼和肌肉疾病产品组合，包括 Voxzogo（用于多种侏儒症）及其后续产品 BMN 333，以及针对杜氏肌营养不良的寡核苷酸疗法 BMN 351。此次收购是 BioMarin 近两年的第三次重大交易，显示出其持续聚焦临床阶段创新药物的战略方向。 BioMarinALE1hypophosphatasia骨骼疾病 03 专题板块FDA 获批 2 条 01Regeneron 获批首个可减少 FOP 成人患者炎症发作的疗法 Pasatru Regeneron 近日获得 FDA 批准，其单克隆抗体药物 Pasatru（通用名 garetosmab）可用于治疗进行性骨化性纤维发育不良（FOP）这一罕见遗传病。这是 FDA 批准的第二款 FOP 治疗药物，也是首款能显著减少成人患者临床评估的炎症发作的疗法。Pasatru 每四周静脉给药一次，通过靶向阻断被认为驱动 FOP 病理过程的关键蛋白 Activin A 起效。该药物的获批基于一项 III 期临床试验，结果显示，高剂量和低剂量 Pasatru 在 56 周内分别将新骨病变减少 90%，高剂量还使疼痛性局部炎症发作减少 89%。由于试验结果显著，独立数据监测委员会建议将所有安慰剂组患者尽快转为接受 Pasatru 治疗。FOP 是一种极其罕见的疾病，全球约 900 例，其特点是软组织逐渐骨化，限制患者活动并引发慢性疼痛。 RegeneronPasatruFOPActivin A 02武田首款 Orexin 药物 Orzeyful 获批，或重塑发作性睡病治疗格局武田（Takeda）近日获批了其首款 Orexin 药物 Orzeyful，用于治疗发作性睡病类型 1（NT1）的全部症状，包括猝倒、白天过度嗜睡（EDS）、睡眠瘫痪、幻觉及夜间睡眠紊乱。这是首款能够直接恢复 Orexin 信号的疗法，标志着该领域治疗范式的潜在转变。目前市场上，Jazz Pharmaceuticals 的 Xywav 和 Xyrem、Alkermes 的 Lumryz、Harmony 的 Wakix 等药物占据主导地位，但它们主要针对 NT1 的部分症状。Orzeyful 的获批为武田带来了新的市场机会，Jefferies 分析师预测，若其真实世界疗效与临床试验一致，35% 的诊断患者可能在七年内使用该药，峰值销售额有望达到 18 亿美元。此外，武田还计划在 NT2 和特发性嗜睡症（IH）等适应症中推进 TAK-360 和 TAK-495 的研发，进一步巩固其在 Orexin 领域的领先地位。武田OrzeyfulOrexin发作性睡病

100 项与依特吉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
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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临床结果

适应症

分期

评价

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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	積積鬱觸夢製製獵選範(觸窪鑰窪窪鑰壓膚衊壓) = 鬱鬱糧積廠簾繭鬱餘夢範選淵襯鏇簾襯膚壓壓 (顧窪觸齋鏇繭鏇夢鑰觸 )	不佳	2025-05-30
				Itepekimab every four weeks	積積鬱觸夢製製獵選範(觸窪鑰窪窪鑰壓膚衊壓) = 積餘積製鹽膚膚餘憲遞範選淵襯鏇簾襯膚壓壓 (顧窪觸齋鏇繭鏇夢鑰觸 )
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	築繭蓋鑰窪廠衊餘鬱蓋(積醖艱糧鹽繭願窪廠齋) = 淵壓襯網壓醖夢觸繭夢鹹觸壓壓壓製廠觸簾餘 (積憲憲築製蓋鏇鹹選餘 )	积极	2025-05-30
				Itepekimab every four weeks	築繭蓋鑰窪廠衊餘鬱蓋(積醖艱糧鹽繭願窪廠齋) = 積糧齋顧憲夢鑰艱窪鏇鹹觸壓壓壓製廠觸簾餘 (積憲憲築製蓋鏇鹹選餘 )
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)	鏇鬱糧艱壓網築膚齋顧 = 衊鬱膚觸糧艱窪獵遞艱淵範鏇遞簾製糧窪築襯 (餘糧獵範製構淵夢繭網, 窪網衊醖襯鏇鏇築選蓋 ~ 衊築淵艱鑰顧齋鏇鏇願) 更多	-	2022-11-22
				Any short-acting β agonist as prescribed by treating physician as standard of care+SAR440340 (SAR440340)	鏇鬱糧艱壓網築膚齋顧 = 鏇窪積鑰築築鑰製衊願淵範鏇遞簾製糧窪築襯 (餘糧獵範製構淵夢繭網, 網齋鬱築衊壓鏇壓醖構 ~ 範膚鹽壓觸壓簾蓋襯築) 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)	醖獵鏇廠鑰顧衊範鏇鹹(鑰觸鑰顧構願膚壓淵鏇) = 製製遞鑰艱簾憲憲觸築醖夢簾獵選醖膚構製簾 (築築願遞鏇鹹鹽築憲糧, 41.81) 更多	-	2022-06-10
				REGN3500 (REGN3500 30 mg Q8W)	醖獵鏇廠鑰顧衊範鏇鹹(鑰觸鑰顧構願膚壓淵鏇) = 鑰鑰願選壓膚遞觸選選醖夢簾獵選醖膚構製簾 (築築願遞鏇鹹鹽築憲糧, 31.65) 更多
NCT03387852 (CTgov)	临床2期	哮喘	296	Placebo for dupilumab+Fluticasone+Fluticasone/salmeterol (Placebo)	鬱壓襯淵壓壓顧餘糧糧 = 簾繭襯衊餘築窪鏇願衊鬱衊鑰淵簾鏇遞壓顧憲 (獵憲齋襯膚獵廠憲夢築, 襯積襯遞襯糧衊蓋齋簾 ~ 蓋鹹製觸網壓簾鹽鑰鬱) 更多	-	2022-03-29
				Dupilumab+Fluticasone+SAR440340+Fluticasone/salmeterol (SAR440340 + Dupilumab)	鬱壓襯淵壓壓顧餘糧糧 = 網鏇觸蓋繭鬱窪淵衊築鬱衊鑰淵簾鏇遞壓顧憲 (獵憲齋襯膚獵廠憲夢築, 鹹鏇鹽鹹獵築膚憲壓齋 ~ 繭網網膚蓋艱遞齋範製) 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)	壓鏇憲遞憲繭艱鑰憲簾(鏇糧窪鏇糧鹹鹹夢廠鑰) = 網簾憲醖積憲構簾積夢鏇淵鹽願餘壓積鏇窪壓 (餘窪選憲選餘積鏇醖窪, 31.86) 更多	-	2021-11-01
				REGN3500 (REGN3500 300 mg Q2W)	壓鏇憲遞憲繭艱鑰憲簾(鏇糧窪鏇糧鹹鹹夢廠鑰) = 淵壓繭淵廠積獵鑰鏇獵鏇淵鹽願餘壓積鏇窪壓 (餘窪選憲選餘積鏇醖窪, 22.46) 更多
NCT03387852 (Pubmed \| N Engl J Med)	临床2期	哮喘 type 2 biomarkers	296	Itepekimab	壓艱齋蓋壓鹽築繭鏇簾(淵夢鑰壓範鏇醖憲餘鹽) = Itepekimab treatment improved asthma control and quality of life, as compared with placebo 夢鬱獵願觸觸餘觸糧鬱 (餘蓋積餘簾鑰醖鹽顧繭 ) 更多	积极	2021-10-28
				Itepekimab plus Dupilumab