Reversing External-beam Radiotherapy-associated Fibrosis Syndrome: an Interventional Bayesian Adaptive Randomized-controlled Orphan Drug Platform Trial for Orodental Sequelae (Reverse-fibrose)

To find out if adding medication can help treat or prevent lymphedema and/or fibrosis related to radiation therapy, in survivors of head and neck cancer. Researchers will compare these drugs to find the most effective therapy for preventing or limiting these side effects.

开始日期2025-09-18

申办/合作机构-

NCT06241560

/ Not yet recruiting临床2期

An Open-label, Single-group Trial to Evaluate the Effect of Pirfenidone on the Pharmacokinetics of a Single Oral Dose of BI 1015550

This study is open to adults with idiopathic pulmonary fibrosis (IPF) who are 40 years and older. The purpose of this study is to find out whether a medicine called pirfenidone changes the amount of a medicine called BI 1015550 in the blood. Some people may take more than one medicine at a time. Therefore, it is important to understand how different medicines influence one another.
Participants take one dose of BI 1015550 as a tablet. Participants then take one tablet of pirfenidone 3 times a day for one week. The dose is then increased to 2 tablets 3 times a day for the second week. In the third week the dose is increased further to 3 tablets 3 times a day. Participants then take another dose of BI 1015550 as a tablet.
Participants are in the study for a little over 1 month. During this time, they visit the study site 15 times. Two of the visits include overnight stays at the study site. The study staff also contacts the participants by phone. During the visits, the doctors collect information about participants' health and take blood samples from the participants. They compare the amount of pirfenidone and BI 1015550 in the blood. Doctors also regularly check participants' health and take note of any unwanted effects.

开始日期2025-06-06

申办/合作机构

Boehringer Ingelheim GmbH

NCT07015398

/ Not yet recruiting临床1期

A Phase 1, Two-Part, Open-Label Drug-Drug Interaction Study to Evaluate the Steady State Pharmacokinetics and Safety Following Co-Administration of Nalbuphine Extended-Release Tablets (NAL ER), and Pirfenidone or Nintedanib in Healthy Adult Subjects

The primary purpose of this study is to evaluate the effect of NAL ER on the steady-state pharmacokinetics (PK) of pirfenidone or nintedanib and the effect of pirfenidone or nintedanib on the steady-state PK of NAL ER in healthy participants.

开始日期2025-06-01

申办/合作机构

Trevi Therapeutics, Inc.

100 项与吡非尼酮相关的临床结果

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100 项与吡非尼酮相关的转化医学

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100 项与吡非尼酮相关的专利（医药）

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2,680

项与吡非尼酮相关的文献（医药）

2025-08-01·TOXICOLOGY AND APPLIED PHARMACOLOGY

3,4-Dimethoxycinnamic acid from coffee silverskin biowaste ameliorates bleomycin-induced pulmonary fibrosis via modulating caveolin-1-dependent activation of NF-κB, TGF-β1/Smad3, and ERK1/2 signaling pathways

Article

作者: Khalil, Ibrahim T ; Althobaiti, Musaad M ; Hamdi, Abdelrahman ; Haikal, Abdullah ; Arafa, El-Shaimaa A ; Elshal, Mahmoud ; Arab, Hany H

The aim of the current study was to explore the potential beneficial effect of 3,4-dimethoxycinnamic acid (DMCA), obtained from coffee silverskin (CS) biowaste, on bleomycin-induced lung fibrosis in rats and elucidate its possible underlying mechanisms. Lung fibrosis was induced in rats by a single intratracheal administration of bleomycin. DMCA (25 and 50 mg/kg) and pirfenidone (50 mg/kg) were orally administered. Our results showed that DMCA markedly reduced lactate dehydrogenase activity, total protein content, and total and differential inflammatory cell counts in the bronchoalveolar lavage fluid. DMCA also inhibited oxidative stress and nuclear factor kappa B (NF-κB)-mediated tumor necrosis factor and interleukin-1β production. Furthermore, DMCA markedly downregulated the pulmonary levels of transforming growth factor beta 1 (TGF-β1), SMAD family member 3 (Smad3), and extracellular signal-regulated kinase 1/2 (ERK1/2), concurrently with a marked reduction in collagen-1 expression in the lung. Contrarily, DMCA upregulated lung caveolin-1 expression. These findings were concomitantly accompanied by remarkable improvement in the lung histopathology. In conclusion, DMCA effectively mitigates bleomycin-induced lung fibrosis in rats, which is comparable to pirfenidone, through antioxidant, anti-inflammatory, and anti-fibrotic effects. These beneficial effects are mainly mediated through boosting caveolin-1 expression that halts NF-κB, TGF-β1/smad3, and ERK1/2 signaling pathways.

2025-08-01·COLLOIDS AND SURFACES B-BIOINTERFACES

Enhanced skin adhesion of transdermal drug delivery system a semi-IPN strategy: / evaluation and drug release mechanism

Article

作者: Zhang, Yimeng ; Li, Maojian ; Xie, Daoxuan ; Zhao, Nanxi ; Luo, Zheng ; Chen, Guixue ; Liu, Yanan ; Li, Man

Pressure-sensitive adhesives (PSAs) used for transdermal patches often present mechanical issues that lead to cold flow phenomena, patch shifting, and disrupt dose precision while creating an unwanted "dark ring" effect. Semi-interpenetrating network (semi-IPN) PSAs were synthesized in this study, which enhanced cohesion and reduced cold flow by integrating a cross-linked network into a linear polymer matrix to enhance structural integrity. Meanwhile, rivastigmine, etodolac, ketoprofen, propranolol, pirfenidone, and zolmitriptan were used to evaluate drug release rates from the semi-IPN PSA. The skin adhesion properties of the semi-IPN PSA were outstanding. Its cohesion was significantly higher than two commercially available PSAs: over 1000-fold greater than DURO-TAK® 87-2287 and 75.9 times greater than DURO-TAK® 87-4098. Drug release rates were comparable between traditional and semi-IPN PSAs. The release rates of different drugs were negatively correlated with drug polarizability, suggesting dipole-dipole interactions as the key mechanism. In summary, the semi-IPN strategy offers a robust solution for high-performance transdermal patches by improving adhesion without compromising drug release.

2025-08-01·PHARMACOLOGY & THERAPEUTICS

Post-COVID pulmonary sequelae: Mechanisms and potential targets to reduce persistent fibrosis

Review

作者: Pillay, Janesh ; Vreeman, Emma C A ; Burgess, Janette K

After the severe acute respiratory syndrome (SARS) coronavirus 2 (SARS-CoV-2) pandemic, the emergence of long-term sequelae post-infection poses a new healthcare challenge. Following initial infection with SARS-CoV-2, approximately 1 in 10 people experience post-acute sequelae of COVID-19 (PASC), also known as long COVID. PASC can affect the entire body, with the airways and lungs being a primary target of the initial viral infection. Many post-COVID symptoms have been associated with fibrotic lung lesions and diminished respiratory function. The reversibility, persistence, or progression of post-COVID-19 pulmonary fibrosis is still a topic of debate. We aimed to compare current findings and examined similar viral infections from the past, to increase understanding of prevalence, persistence and possible pharmacological targets of post-COVID-19 pulmonary fibrosis. Recent studies have documented PASC symptoms persisting up to 3 years post-recovery, and lung impairments present after 15 years after infection with the similar SARS-CoV virus in 2003. These findings suggest the potential for long-term pulmonary fibrosis following SARS-CoV-2 infection, highlighting the need for new anti-fibrotic treatments capable of reversing pulmonary fibrosis. Besides the approved anti-fibrotics, pirfenidone and nintedanib, other promising treatments include histone deacetylase inhibitors, angiotensin receptor blockers and mesenchymal stem cells. The pathophysiological mechanisms underlying post-COVID-19 pulmonary fibrosis are still incompletely understood, necessitating future research to clarify the development of persistent post-COVID-19 pulmonary fibrosis following SARS-CoV-2 infection. Given the widespread transmission of SARS-CoV-2, even a low prevalence of persistent post-COVID-19 pulmonary fibrosis would represent a significant public health concern for which therapeutic strategies are essential to identify.

289

项与吡非尼酮相关的新闻（医药）

2025-06-04

·药时空

国产新锐，PDE4 抑制剂授权海外biotech

近日，苏州璞正医药（Suzhou Intragrand Pharma）与美国Transpire Bio联合宣布，双方就研究性 PDE4 抑制剂 “ITG-1052（通用名：Lenamilast）” 达成独家许可协议。Transpire Bio 将获得除中国以外全球范围内的开发、生产及商业化权利，标志着这款靶向特发性肺纤维化（IPF）的创新药物正式进入国际化开发阶段。根据协议，苏州璞正医药保留中国地区权益，而 Transpire Bio 将负责全球（除中国）的临床开发与商业化。双方未披露具体交易金额。将开发为吸入制剂。苏州璞正医药是一家专注于全球领先的小分子呼吸道新药吸入剂开发的初创型公司。公司管理层拥有多年企业管理、新药研发、临床医学研究经验，致力于攻破疾病药物靶点难成药的差异化药物一体化设计创新，形成了创新吸入剂靶向呼吸道为特色的产品管线。ITG-1052 是该公司继雄激素受体拮抗剂普克鲁胺后，在呼吸系统疾病领域推出的又一重点品种。此次合作标志着璞正医药从 “本土研发” 向 “全球创新网络” 的重要跨越。Transpire Bio专注于吸入疗法在肺部及全身性疾病中的应用，其技术平台覆盖干粉吸入制剂（DPI）、软雾吸入制剂（SMI）和定量吸入气雾剂（MDI）三大主流剂型，具备从药物递送系统设计到工业化生产的全链条能力。公司现有管线包括针对慢性阻塞性肺疾病（COPD）、特发性肺纤维化（IPF）和过敏性哮喘的多个创新品种，此次引入 ITG-1052 是其继 2024 年获得 β2 受体激动剂 T-007 的全球权益后，再次通过外部合作扩充吸入制剂管线。目前，市场上治疗特发性肺纤维化 (IPF) 的药物，例如勃林格殷格翰的Ofev和罗氏的Esbriet，虽然能延缓纤维化进展，但并不能阻止甚至逆转疾病。这正是PDE4抑制剂被寄予厚望的原因。对于药物研发人员而言，此次合作的技术细节（如吸入制剂的处方优化、跨区域临床开发策略、PDE4 亚型选择性抑制的安全性平衡）值得持续关注。据悉，Transpire Bio 计划于 2025 年下半年启动 ITG-1052 的全球 Ⅱ 期临床试验，重点评估其在 IPF 和慢性支气管炎中的疗效与安全性。本文综合自药融圈info、新药说、吸入制剂.识别微信二维码，可添加药时空小编请注明：姓名+研究方向！

临床2期引进/卖出申请上市

2025-06-04

·生物世界

Nature Medicine：AI赋能研发原创新药2a期临床数据积极，肺纤维化患者迎来新希望

撰文丨王聪编辑丨王多鱼排版丨水成文人工智能（AI）正迅速变革制药行业，从靶点发现到精准医疗，全方位重塑行业格局，为加速药物研发与上市带来了前所未有的机遇。然而，尽管 AI 技术应用日益广泛，但由 AI 赋能研发并真正进入临床试验阶段的药物，仍然寥寥无几，实现临床概念验证的更是少之又少。2025 年 6 月 3 日，英矽智能（Insilico Medicine）联合北京协和医院徐作军教授团队，在国际顶尖医学期刊 Nature Medicine 发布了题为：A generative AI-discovered TNIK inhibitor for idiopathic pulmonary fibrosis: a randomized phase 2a trial 的研究论文。该研究发布了全球首个完全由人工智能发现药物靶点并设计生成的肺纤维化新药 Rentosertib（ISM001-055）2a 期临床试验的安全性和有效性数据，结果显示，Rentosertib 安全且耐受性良好，显示出改善患者肺活量的效果，具有潜在的抗纤维化及抗炎作用，值得在更大规模、更长时间的临床试验中进一步研究。这款由中国团队主导，使用生成式人工智能设计生成的创新药物，有望改写特发性肺纤维化无有效治疗药物的历史。这项 2a 期多中心、双盲、随机、安慰剂对照临床试验的数据显示：接受每天一次 60 毫克 Rentosertib 治疗的特发性肺纤维化（IPF）患者，用力肺活量（FVC）平均改善幅度最大，FVC 均值增加 98.4 毫升，而对照组 FVC 均值下降 20.3 毫升；进一步探索性生物标志物分析，验证了通过人工智能方法发现的新颖靶点 TNIK 的生物学机制，研究结果支持了 Rentosertib 具有潜在的抗纤维化及抗炎作用。传统药物研发之痛：十年磨一剑，百亿打水漂新药研发历来是场高风险豪赌，开发周期越来越长，开发成本越来越高，90% 的候选药物倒在了临床试验的路上。据估计，平均需要花费 20-30 亿美元，耗时 10-15 年，才能将一款新药从实验室推向市场。特发性肺纤维化（IPF）是一种年龄相关的进行性肺部疾病，其特征为间质性肺炎、呼吸困难和咳嗽，组织学上表现为成纤维细胞增生和细胞外基质重塑，全世界范围内有数百万患者。尽管抗纤维化靶向疗法已广泛普及，但特发性肺纤维化患者确诊后的中位生存期仍仅为 2-4 年，这凸显了研发新型有效疗法以治疗该病的迫切需求。目前，治疗特发性肺纤维化的标准疗法方案包括使用尼达尼布（一种广谱受体酪氨酸激酶抑制剂）或吡非尼酮（一种 TGF-β 介导的成纤维细胞向肌成纤维细胞转化的抑制剂）。然而，这两种药物只能减缓疾病进展，对生存期的益处尚不明确，因此，开发能够恢复肺功能并逆转疾病进展的有效疗法成为当务之急。AI 破局：18 个月创造新药研发奇迹人工智能（AI）的进步已证明其概念创新性，并展现出在药物研发的各个阶段加速进程和降低成本的潜力，这得益于其在疾病相关靶点优先级排序、化合物设计与优化以及临床试验表现方面的促进作用。将药物研发中耗费时间、材料和人力的步骤更多地转移到 AI 平台上，能够更迅速地发现候选化合物，更全面地探索可能的化学空间，同时减少人工筛选，从而让更多的临床前候选化合物进入临床试验，最终应用于临床实践。英矽智能（Insilico Medicine）团队使用其 AI 驱动的靶点发现平台 PandaOmics，通过分析海量生物学数据，锁定了抗纤维化靶点——TNIK，然后使用其生成式 AI 药物设计平台 Chemstry42，设计并生成了靶向 TNIK 的小分子抑制剂，该抑制剂可通过口服、吸入或局部给药，在体内不同器官中表现出理想的药物样特性和抗纤维化活性，除了具有抗纤维化特性外，还具有抗炎作用。2024 年 3 月 8 日，英矽智能（Insilico Medicine）在 Nature Biotechnology 期刊发表了这款 TNIK 抑制剂的临床前和 1 期临床试验数据【2】，这也是首次报道 TNIK 抑制剂的临床试验数据，显示出对健康个体安全且耐受性良好，且表现出良好的药代动力学特征。值得一提的是，这是首次报道通过 AI 平台发现疾病相关靶点及针对该靶点设计生成候选药物的实例。通过使用生成式人工智能方法，英矽智能仅耗时 18 个月就完成了从靶点发现到提名临床前候选药物，从靶点发现到完成 1 期临床试验耗时不到 30 个月，这标志着药物研发流程的革命性转变。2 期临床试验数据解读：曙光初现该论文报道了这项多中心、双盲、随机、安慰剂对照的 2a 期临床试验数据，该试验旨在评估特发性肺纤维化（IPF）患者使用不同剂量的 Rentosertib，在长达 12 周内的安全性、耐受性、药代动力学，以及对用力肺活量（FVC）的影响。主要终点为安全性，该试验还设计了次要终点和探索性终点及分析，以进一步衡量 Rentosertib 治疗及反应相关的肺功能、生活质量（QOL）指标和细胞表型。在 22 个中心共入组了 71 例 IPF 患者，他们被随机分配接受安慰剂（17人）、每天一次 30 毫克 Rentosertib（18人）、每天两次 30 毫克 Rentosertib（18人）或每天一次 60 毫克 Rentosertib（18人）。主要终点指标为至少出现一次治疗相关不良事件的患者比例，结果显示，各治疗组间情况相似，每天一次 30 毫克 Rentosertib 组为 72.2%（13/18），每天两次 30 毫克 Rentosertib组为 83.3%（15/18），每天一次 60 毫克 Rentosertib组为 83.3%（15/18），安慰剂组为 70.6%（12/17）。治疗相关的严重不良事件发生率较低，且各治疗组间发生率相当，导致治疗中断的最常见事件与肝酶升高或腹泻有关。次要终点包括药代动力学指标，以及通过用力肺活量、一氧化碳弥散量、1 秒用力呼气量测定的肺功能变化，Leicester 咳嗽问卷评分变化、6 分钟步行距离变化以及特发性肺纤维化急性加重的次数和住院时长。结果显示，每天一次 60 毫克 Rentosertib 组中，患者的用力肺活量（FVC）有所增加，平均增加 98.4 毫升，而安慰剂组则下降 20.3 毫升，两组之间拉开了 120 毫升的差距。每天一次 60 毫克 Rentosertib组中那些没有使用标准疗法的患者，FVC 更是增加了 187.8 毫升。Rentosertib治疗12周后用力肺活量（FVC）变化值及其95%置信区间相比基线的变化情况。（左图）FVC绝对变化值及其95%置信区间；（中图）基于采用随机缺失（MAR）假设的多重插补方法完成的ANCOVA模型，显示FVC的绝对变化值及其95%置信区间；（右图）治疗12周后FVC变化值及其95%置信区间，分析中排除了两个患者数据：一个为安慰剂组的患者，另一个为Rentosertib 30 mg QD组的患者。这两名患者筛查与基线肺活量测量值之间的差异超过600 mL，导致其基线FVC值存在不确定性。这些结果表明，使用 Rentosertib 靶向 TNIK，安全且耐受性良好的，显示出改善患者肺活量的效果，具有潜在的抗纤维化及抗炎作用，值得在更大规模、更长时间的临床试验中进一步研究。探索性研究：AI 药物如何逆转纤维化研究团队进一步通过血液蛋白质组学分析，以揭示 Rentosertib 的作用机制，结果显示，在经过 12 周治疗后，IPF 患者的血清蛋白水平和用力肺活量（FVC）均出现了剂量和时间依赖性的变化，进一步支持了 Rentosertib 的抗纤维化和抗炎作用。具体来说，高剂量组中——关键蛋白下调：COL1A1（胶原蛋白）、MMP10（基质金属蛋白酶）、FAP（成纤维活化蛋白）等促纤维化因子显著降低；信号通路抑制：细胞外基质重组通路活性下降；生物标志物发现：PTPRZ1 等蛋白变化与肺功能改善强相关。这些发现与临床前研究结果一致，为开展下一步临床验证的剂量选择和生物标志物识别提供了宝贵的指导。这些发现也印证了 TNIK 靶点在纤维化中的核心地位——它像指挥家一样同时调控多条促纤维化通路。未来展望：AI制药新时代来临近年来，人工智能（AI）在药物研发领域取得了实质性进展，但还很少有 AI 发现或设计的药物进入人体临床试验。此次 Rentosertib 的 2a 期临床数据的发布，具有里程碑意义——首次证实了 AI 的全流程能力：从靶点发现，到分子设计，再到临床验证的闭环；中国创新力量的崛起：Rentosertib 由中国团队主导开发并完成关键临床试验；药物研发范式革新：生成式人工智能将成药物发现的“新引擎”。随着这一全球首款生成式 AI 设计的抗纤维化药物进入临床后期，让特发性肺纤维化患者看到了逆转病情的曙光。而更深远的意义在于——生成式人工智能的持续突破，正在曾重写“制药界摩尔定律”。论文链接：1. https://www.nature.com/articles/s41591-025-03743-22. https://www.nature.com/articles/s41587-024-02143-0设置星标，不错过精彩推文开放转载欢迎转发到朋友圈和微信群微信加群为促进前沿研究的传播和交流，我们组建了多个专业交流群，长按下方二维码，即可添加小编微信进群，由于申请人数较多，添加微信时请备注：学校/专业/姓名，如果是PI/教授，还请注明。点在看，传递你的品味

临床2期临床结果

2025-06-04

·PRNewswire

Daewoong Pharmaceutical Presents Phase 2 Clinical Trial Poster on 'Bersiporocin' at ATS 2025, Highlights Global Patient Demographics

- Ongoing Phase 2 study enrolling 102 patients in the U.S. and South Korea, with more than 50% of participants identified as Asian - Selectively inhibits collagen synthesis via PRS targeting, aiming to suppressing fibrosis progression SEOUL, June 3, 2025 /PRNewswire/ -- Daewoong Pharmaceutical (Co-CEOs Seongsoo Park and Chang-Jae Lee) announced that it presented interim results from a global Phase 2 clinical trial of its investigational idiopathic pulmonary fibrosis (IPF) treatment candidate Bersiporocin (DWN12088) at the 2025 American Thoracic Society (ATS) International Conference, held from May 16 to 21 in San Francisco. The scientific poster was presented during the official ATS session titled "WHAT'S NEW IN ILD DIAGNOSIS, MONITORING, AND TREATMENT" on May 18, by Dr. Jinwoo Song, Professor of Pulmonology at Asan Medical Center, who also serves as the trial's global Coordinating Investigator and principal investigator. The interim analysis highlighted key baseline demographic and clinical characteristics of enrolled participants, including racial distribution and antifibrotic medication use. Approximately 70% of participants were receiving Bersiporocin in combination with approved antifibrotic therapies (nintedanib or pirfenidone), while the remaining 30% participated without any background treatment. Notably, more than half of the enrolled patients are Asian— enabling exploratory assessment of treatment responses across ethnic subgroups, in contrast to prior IPF studies which were predominantly limited to White populations. The ongoing randomized, double-blind, placebo-controlled Phase 2 study is being conducted at 30 sites in the U.S. and South Korea, targeting 102 IPF patients. Participants receive 150 mg of Bersiporocin or placebo twice daily for 24 weeks, with efficacy and safety assessed based on changes in forced vital capacity (FVC) and other clinical endpoints. As of April 2025, 80 patients (approximately 80% of target enrollment) had completed registration. Bersiporocin is a first-in-class oral antifibrotic drug candidate developed by Daewoong Pharmaceutical. It selectively inhibits Prolyl-tRNA Synthetase (PRS), a key enzyme in proline activation and collagen biosynthesis. This targeted mechanism aims to interrupt the fibrotic cascade at its origin, potentially delivering more effective disease control with fewer off-target effects—positioning Bersiporocin as a next-generation therapeutic. The drug was granted Orphan Drug Designation by both the U.S. FDA and the European Medicines Agency (EMA) in 2019, and has also received Fast Track designation from the FDA—affirming its potential as a globally significant treatment option for IPF. "This trial not only offers hope for a new treatment option, but also allows us to assess responses across a racially diverse patient population, including Asian patients," said Professor Jinwoo Song. "We look forward to providing safer and more effective treatment options for patients with IPF." Seongsoo Park, CEO of Daewoong Pharmaceutical, added, "Bersiporocin represents a breakthrough in antifibrotic therapy by targeting the root cause of fibrosis through PRS inhibition. We are committed to advancing this program to help redefine the global IPF treatment paradigm." SOURCE Daewoong Pharmaceutical Co., Ltd. WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

孤儿药临床2期临床结果快速通道

100 项与吡非尼酮相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D01583	吡非尼酮	L04AX05	DB04951

研发状态

批准上市

10 条最早获批的记录,

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适应症	国家/地区	公司	日期
特发性肺纤维化	日本	Shionogi & Co., Ltd.	2008-10-16

未上市

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适应症	最高研发状态	国家/地区	公司	日期
系统性硬化相关的间质性肺病	临床3期	中国	GNI Group Ltd.	2023-05-29
煤肺病	临床3期	-	北京康蒂尼药业股份有限公司	2022-04-15
尘肺病	临床3期	-	北京康蒂尼药业股份有限公司	2022-04-15
矽肺	临床3期	-	北京康蒂尼药业股份有限公司	2022-04-15
皮肌炎	临床3期	中国	北京康蒂尼药业股份有限公司	2018-06-01
间质性肺疾病	临床3期	中国	北京康蒂尼药业股份有限公司	2017-10-31
硬化肼胝症	临床3期	中国	北京康蒂尼药业股份有限公司	2017-10-31
进展性肺纤维化	临床2期	美国	Avalyn Pharma, Inc.	2024-04-03
进展性肺纤维化	临床2期	阿根廷	Avalyn Pharma, Inc.	2024-04-03
进展性肺纤维化	临床2期	澳大利亚	Avalyn Pharma, Inc.	2024-04-03

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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


ASCO2025	N/A	特发性肺纤维化	4,529	Pirfenidone	淵餘繭廠選鹽襯顧蓋餘(襯願鬱構醖窪齋齋齋壓) = 壓遞範鬱鹽餘醖築醖艱壓製繭醖範鹽獵鹽夢艱 (構觸遞壓築顧窪鏇顧繭 )	积极	2025-05-30
				Non-Pirfenidone	淵餘繭廠選鹽襯顧蓋餘(襯願鬱構醖窪齋齋齋壓) = 繭範蓋構衊鑰築衊糧鹹壓製繭醖範鹽獵鹽夢艱 (構觸遞壓築顧窪鏇顧繭 )
ATS2025	N/A	-	-	CXN-8	築齋鬱遞鏇鏇夢廠顧憲(選襯壓艱醖淵簾壓製網) = 淵鹽鹹繭鑰襯襯獵鹽獵餘簾網範鑰齋觸構築淵 (鬱觸顧蓋糧襯鹹觸鏇鬱 ) 更多	-	2025-05-16
ATLAS Phase 1b Trial (ATS2025)	临床1期	特发性肺纤维化	64	Nebulised AP01 50mg QD	構觸廠築淵醖願齋淵製(淵繭鹹齋製繭淵夢獵獵) = 蓋範鏇鏇顧築廠廠範齋選繭壓壓夢願窪壓願蓋 (積獵網獵醖製淵憲糧淵 ) 更多	积极	2025-05-16
				Nebulised AP01 100mg BID	構觸廠築淵醖願齋淵製(淵繭鹹齋製繭淵夢獵獵) = 壓壓衊糧醖壓鏇艱願糧選繭壓壓夢願窪壓願蓋 (積獵網獵醖製淵憲糧淵 ) 更多
AP01-002 (ATLAS) (ATS2025)	N/A	-	91	50 mg AP01 once daily	鏇齋鹹夢鬱憲憲繭壓憲(醖鹹艱鬱衊醖選觸鹽鬱) = 淵衊齋鬱襯膚壓窪製構膚鏇壓壓選餘鹽艱餘窪 (廠廠蓋襯淵鏇鏇構範壓 )	积极	2025-05-16
				100 mg AP01 twice daily	鏇齋鹹夢鬱憲憲繭壓憲(醖鹹艱鬱衊醖選觸鹽鬱) = 壓製膚膚壓顧鬱齋簾遞膚鏇壓壓選餘鹽艱餘窪 (廠廠蓋襯淵鏇鏇構範壓 ) 更多
ATS2025	N/A	进展性肺纤维化	33	Pirfenidone	構築鏇夢鑰齋憲襯襯壓(艱構衊願衊鬱膚鑰夢範) = 21.2% 衊衊膚鹹齋鏇壓獵淵鏇 (繭積繭淵憲壓襯簾衊窪 ) 更多	积极	2025-05-16
ASTRO2024	临床2期	辐射损伤	134	Pirfenidone plus standard therapy	廠願憲蓋齋醖衊鹹蓋範(願夢艱艱簾築淵蓋夢廠) = 壓壓觸範壓鹽艱艱範築範蓋繭鏇選鏇築憲積鑰 (壓艱範鏇壓製製鹹網遞 ) 更多	积极	2024-10-01
WCLC2024	临床2期	肺损伤 PD-1 inhibitors	14	Pirfenidone	鹽鑰遞夢繭範願廠壓齋(鹽糧廠築構選襯襯糧醖) = Pirfenidone-related adverse events (≤ grade 2) occurred in 7 patients, including six gastrointestinal reactions and one photosensitivity reaction 艱獵鏇壓醖鹽憲願積鹹 (鑰窪蓋鏇網壓餘艱選夢 )	积极	2024-09-07
				Immune Checkpoint Inhibitors
ATS2024	N/A	-	-	50mg AP01 once daily	衊齋憲齋選膚鹹鬱壓糧(顧範膚衊蓋獵蓋襯網網) = AE were present in 93.3% of patients overall, with AE frequencies similar across cohorts 醖選糧憲觸壓觸遞艱淵 (糧糧蓋窪觸獵醖糧醖鑰 )	-	2024-05-19
				100mg AP01 twice daily
ATS2024	N/A	疾病进展	-	AP01 100 mg BID	顧遞蓋憲齋廠鹽蓋簾憲(願憲窪鑰艱願窪醖範淵) = 鑰艱衊膚願齋膚選網簾衊鏇衊願繭齋膚積簾膚 (鹹範簾網衊鏇淵糧夢糧 )	-	2024-05-19
				AP01 50 mg QD	顧遞蓋憲齋廠鹽蓋簾憲(願憲窪鑰艱願窪醖範淵) = 襯齋鬱繭衊觸糧積鑰廠衊鏇衊願繭齋膚積簾膚 (鹹範簾網衊鏇淵糧夢糧 )
ATS2024	N/A	特发性肺纤维化	-	Fybro® 400 mg	獵壓築膚衊淵蓋鬱選積(網選衊選鬱膚齋膚範繭) = 16.5% 構積廠鏇鹽積鏇餘鏇選 (憲淵鑰構簾鹽膚廠觸齋 ) 更多	-	2024-05-19