A Phase 2, Randomized, Double-Blind, Placebo-Controlled, Multicenter Study to Evaluate the Efficacy, Safety, and Tolerability of Oral PIPE 791 in Subjects With Idiopathic Pulmonary Fibrosis

This is a Ph 2, randomized, double-blind, placebo-controlled global multicenter study to evaluate the efficacy, safety, tolerability, and pharmacokinetics (PK) of PIPE-791 in participants with a diagnosis of Idiopathic Pulmonary Fibrosis (IPF) with or without background treatment.

开始日期2026-01-08

申办/合作机构

Contineum Therapeutics, Inc.

NCT06810245

/ Completed临床1期

A Phase 1b, Randomized, Double-Blind, Placebo-Controlled, Crossover Multicenter Study to Explore the Safety and Efficacy of Oral PIPE-791 as Treatment in Subjects With Chronic Osteoarthritis Pain (COAP) or Chronic Low Back Pain (CLBP)

The primary goal of this clinical trial is to learn if PIPE-791 is safe and well-tolerated in adults with chronic osteoarthritis pain (COAP) or chronic low back pain (CLBP). The study will also explore whether PIPE-791 lowers pain in people with COAP or CLBP.
Subjects will:
* Complete a washout period to stop their current pain medications.
* Take a daily dose of PIPE-791 or placebo for 4 weeks, then reverse treatment assignment for another 4 weeks.
* Record pain levels and track dosing in a daily e-diary.
* Visit the clinic for checkups and lab tests throughout the study.
* Complete phone assessments during the treatment periods.

开始日期2025-02-04

申办/合作机构

Contineum Therapeutics, Inc.

NCT06683612

/ Completed临床1期

A Phase 1b, Open-label Study of PIPE-791 to Determine Brain and Lung Lysophosphatidic Acid Receptor 1 (LPA1) Occupancy, by [18F] PIPE-497 PET Imaging in Healthy Volunteers, Volunteers With Progressive Multiple Sclerosis, and Volunteers With Idiopathic Pulmonary Fibrosis

This is a study of PIPE-791, an investigational study drug to treat progressive multiple sclerosis (MS) and idiopathic pulmonary fibrosis (IPF). The purpose of this study is to find out how much of the study drug gets into the brain and lung, and what the side effects and blood levels of the study drug are in healthy volunteers and patients.
Participants will:
* Take a single dose of the study drug
* Give many samples of blood and urine
* Have multiple PET scans

开始日期2024-12-09

申办/合作机构

Contineum Therapeutics, Inc.

100 项与 PIPE-791 相关的临床结果

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100 项与 PIPE-791 相关的转化医学

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100 项与 PIPE-791 相关的专利（医药）

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项与 PIPE-791 相关的文献（医药）

2026-07-09·JOURNAL OF MEDICINAL CHEMISTRY

Discovery of PIPE-791 , A Potent and Brain-Penetrant Lysophosphatidic Acid Receptor 1 Antagonist with Slow Tight Binding Characteristics for the Treatment of Neuroinflammatory Disorders

Article

作者: Xiong, Yifeng ; Broadhead, Alexander ; Lorrain, Daniel S. ; Valdez, Lino ; Poon, Michael M. ; Baccei, Jill ; Lorrain, Kym I. ; Baccei, Christopher ; Stebbins, Karin J. ; Schrader, Thomas O. ; Roppe, Jeffrey ; Chen, Austin

We describe the discovery and characterization of PIPE-791, a potent and brain-penetrant lysophosphatidic acid receptor 1 (LPAR1) antagonist with slow association and dissociation kinetics. SAR studies initiated from a literature lead (13) led to the identification of compound 21 that possessed a unique urea scaffold responsible for slow but tight binding to LPAR1. Further optimizations that improved PK and metabolic profiles led to the discovery of PIPE-791. PIPE-791 efficiently traversed the BBB in multiple preclinical species and was efficacious in preclinical models of neuroinflammatory disorders. PIPE-791 possessed excellent ADME properties and was well-tolerated in 28 day GLP (Good Laboratory Practice) toxicity studies in rats and minipigs at doses up to 1000 mg/kg/day. Based on these results and a comprehensive first-in-human enabling preclinical data package, PIPE-791 was advanced into clinical development, including an ongoing trial in subjects with chronic osteoarthritis pain or chronic lower back pain (NCT6810245).

2026-01-08·Translational Vision Science & Technology

Pharmacological Blockade of LPAR1 Does Not Provide Neuroprotection in a Rat Model of Ocular Hypertensive Glaucoma

Article

作者: Lorrain, Daniel S. ; Nicol, Alan ; Kocherlakota, Sai ; Stebbins, Karin J. ; Tribble, James R. ; Locri, Filippo ; Williams, Pete A.

Purpose:

Current treatment strategies for glaucoma, the leading cause of irreversible blindness, only target intraocular pressure (IOP) but not the underlying retinal ganglion cell degeneration. IOP management is not always effective, necessitating neuroprotective strategies. Lysophosphatidic acid (LPA) is an extracellular signaling molecule implicated in modulating inflammation. It exerts its signaling effects through its receptors (LPAR1-6). Here we test the efficacy of PIPE-791, an LPAR1-selective antagonist, in conferring neuroprotection and modulating neuroinflammation in glaucoma.

Methods:

A bead-induced rat ocular hypertension (OHT) model of glaucoma was used to test PIPE-791 (administered intraperitoneally at 3 mg/kg dosing). We monitored IOP through tonometry and evaluated PIPE-791's neuroprotective capacity by studying retinal ganglion cell survival using cell counting and its effects on retinal vasculature, immune cell numbers and cytokine profile.

Results:

PIPE-791 had no effect on IOP in normotensive (NT) or OHT rat eyes. It also did not have any neuroprotective effect on retinal ganglion cell survival, nor did it normalize the changes in retinal vasculature observed in OHT retinas. Although PIPE-791 treatment increased microglial numbers in NT retinas, there was no effect in OHT retinas. Cytokine array profiling also revealed no significant effects for PIPE-791 on the cytokine changes between the NT and OHT retinas. These lack of changes could potentially be explained by the fact that LPAR1 protein levels are decreased in OHT retinas.

Conclusions:

Our data suggests that targeting LPAR1 through pharmacological means does not provide neuroprotection or modulate neuroinflammation favorably in glaucoma.

Translational Relevance:

Our study provides evidence that pharmacological targeting of LPAR1 as a potential therapeutic avenue in glaucoma may not be beneficial.

2025-12-01·NEUROPHARMACOLOGY

Reduced activation of pain-related brain regions with lysophosphatidic acid receptor subtype-1 antagonist PIPE-791 in a nonhuman primate model of chronic peripheral neuropathy

Article

作者: Hama, Aldric ; Okamoto, Ken ; Poon, Michael ; Baccei, Christopher ; Takamatsu, Hiroryuki ; Stebbins, Karin ; Itani, Yoshitaka ; Nozawa, Kenya ; Matsushita, Mayumi ; Chen, Austin ; Lorrain, Daniel S ; Natsume, Takahiro ; Kosugi, Tae

Lysophosphatidic acid (LPA) has been suggested to be a key mediator of painful peripheral neuropathy and blocking its action on LPA receptors could reduce symptoms by decreasing the neuroinflammatory cascade underlying neuropathic pain. The current study examined the effect of PIPE-791, a novel and potent LPA subtype-1 receptor (LPA1R) antagonist which has previously been shown to block demyelination in rodent preclinical models, on regional brain activation in response to non-noxious mechanical stimulation of the foot in male macaques with a unilateral right sciatic nerve injury. Thirteen days after nerve injury, stimuli that did not previously lead to activation in naïve macaques activated the anterior cingulate cortex (ACC) and contralateral insular/secondary somatosensory cortex (Ins/SII). Beginning two weeks after nerve injury, macaques were treated for 28 days with daily oral administration of PIPE-791 by gavage. Six weeks after nerve injury (one day after the last dose of PIPE-791) activation of the contralateral Ins/SII was reduced. Eight weeks after nerve injury (15 days after the last dose), activation of the ipsilateral thalamus, as well as activation of the ACC and contralateral thalamus and Ins/SII was observed. An overall pattern of elevated LPA species following nerve injury and decline with treatment was observed. Evoked brain activation could be related to painful peripheral neuropathy and reduced brain activation could be a direct indicator of reduced pain perception following treatment. The current findings suggest decreasing neuroinflammation by blocking LPA1Rs could be a novel approach to the management chronic painful peripheral neuropathy.

项与 PIPE-791 相关的新闻（医药）

2026-09-18

·格宁生物

LPAR1：从靶点到药物PIPE‑791的研发之路

溶血磷脂酸受体1（Lysophosphatidic Acid Receptor 1，LPAR1）是内源性溶血磷脂酸（LPA）信号系统中的关键GPCR，广泛表达于肺、脑、皮肤、血管、肾与骨等组织器官，其信号异常与纤维化、神经炎症等多种疾病密切相关，是重要的药物靶点。 📖 阅读导览 01 LPAR1 靶点简介 02 LPAR1 药物研发困境 03 PIPE-791 发展历程 04 格宁生物助力 LPAR1 药物筛选 01LPAR1 靶点简介 LPAR1是A类GPCR，约370个氨基酸，7次跨膜，与其配体LPA结合后激活 Gαi、Gαq、Gα12/13 和 β-arrestin，参与细胞迁移、增殖、分化、炎症、纤维化等功能。 LPAR1 之所以成为热门药物靶点，主要基于以下几点： 1.表达广：中枢见于神经元、胶质细胞等；外周见于肺、肝、肾、血管、骨等。 2.病理功能多样：参与组织重塑、纤维化、神经炎症和细胞迁移。 3.疾病关联明确：LPA-LPAR1异常升高与多发性硬化、脑外伤、IPF、肿瘤、肾衰竭等相关。 4.治疗价值高：中枢与外周双重分布，具双重治疗潜力。 💡 药物开发难点这种"多重G蛋白偶联"既是它生理功能丰富的根源，也是药物开发中的难点：理想拮抗剂应当尽量"全面阻断"，但不能阻断到把所有的LPAR1信号都关掉——那样会影响基础生理活动。目前临床关注度最高的四个适应症：适应症LPAR1 角色代表临床阶段特发性肺纤维化 IPF 促进成纤维细胞活化、ECM 沉积 Admiparant Ph3 (BMS); PIPE-791 Ph2 (Contineum) 系统性硬化症相关 ILD 皮肤/肺纤维化双重驱动 Admiparant 拓展中进展型多发性硬化 PrMS 抑制 OPC 分化、促神经炎症 PIPE-791 Ph1b PET 完成神经病理性疼痛 / 骨关节痛外周敏化、脊髓背根 LPAR1 上调 PIPE-791 Ph1 (已完成) 🧬 靶点类型：A类GPCR📍 表达：肺 · 脑 · 皮肤 · 血管 · 肾 · 骨🎯 适应症：纤维化 · 神经炎症 · 疼痛 02LPAR1 药物研发困境由于LPA-LPAR1信号在多种疾病中异常升高，开发LPAR1拮抗剂是很好的治疗手段。但已有拮抗剂的开发仍面临多重挑战： Admilarant 脑穿透弱难以作用于中枢，限制了其在神经炎症等中枢相关适应症中的应用。 BMS-986020 肝胆毒性 II期临床显示有效，但因肝胆毒性终止开发。 🎯 核心目标开发一款：口服 + 强效 + 穿透血脑屏障 + 药代良好 + 无肝胆毒性的LPAR1拮抗剂，是众多研究者的核心目标。最终通过持续优化发现了 PIPE-791。 03PIPE-791 发展历程 PIPE-791是强效、可穿透血脑屏障的LPAR1拮抗剂，具备慢结合、慢解离的慢-紧结合动力学特性。研究以酰胺化合物13为起点，经SAR研究获得含独特尿素骨架的化合物21；进一步优化PK和代谢性质后，最终发现PIPE-791。图1 | PIPE-791 结构优化历程化合物13 → 化合物21 → PIPE-791 (47)，逐步优化结合动力学与ADME性质临床前研究显示，PIPE-791具备以下特征：药效：在神经炎症疾病模型中显示有效； ADME：具有优异的ADME性质；安全性：在大鼠和小型猪28天GLP毒性试验中，最高1000 mg/kg/天剂量下耐受性良好。 📌 临床进展基于完整的首次人体试验临床前数据包，PIPE-791已推进至临床开发，目前正在开展针对慢性骨关节炎疼痛和慢性下背痛的临床试验。 04格宁生物助力 LPAR1 药物筛选格宁生物可为LPAR1靶点提供全套体外药理筛选与机制评价服务，助力筛选LPAR1先导候选化合物。 LPAR1参考数据如下： 🧪 服务：体外药理筛选 · 机制评价📈 平台：GPCR 钙流 · 拮抗剂评价🎯 目标：筛选 LPAR1 先导化合物关于我们 · 联系我们上海格宁生物科技有限公司（ScreeNingBio）成立于2020年，位于上海市浦江高科技园，专业提供生物医药研发外包服务，服务内容涵盖小分子和大分子药物研发早期阶段的多个方面，包括功能细胞株、药物筛选、高通量筛选、选择性和安全性评价、体外模型开发与验证、药物作用机理等。格宁生物不断自主开发新的药物靶点细胞株（如GPCR, Ion Channel）及各种药物筛选模型，全力打造筛选模型丰富、实验操作严谨、结果可信的药物筛选平台，为国内外医药企业提供优质高效的技术服务。 📞 联系方式电话：400-863-1023 邮箱：info@screeningbio.com 地址：上海市闵行区联航路1188号24号楼4层 📚 参考文献 Chen A, Baceei C, Baceei J, et al. Discovery of PIPE-791, A Potent and Brain-Penetrant Lysophosphatidic Acid Receptor 1 Antagonist with Slow Tight Binding Characteristics for the Treatment of Neuroinflammatory Disorders. J Med Chem. 2026 Jul 9;69(13):15888-15927. Geraldo LHM, Spohr TCLS, Amaral RFD, et al. Role of lysophosphatidic acid and its receptors in health and disease: novel therapeutic strategies. Signal Transduct Target Ther. 2021 Feb 1;6(1):45. Volkmann ER, Denton CP, Kolb M, et al. Lysophosphatidic acid receptor 1 inhibition: a potential treatment target for pulmonary fibrosis. Eur Respir Rev. 2024 Jun 12;33(172):240015. 格宁生物 · GPCR 药物早期发现服务从靶点验证到药效评价 · 赋能创新药物研发

2026-09-17

·Ben笔记

10亿美金BD项目二度折戟！强生合作M1受体拮抗剂PIPE‑307抑郁症II期临床宣告失败

2026‑09‑14，Contineum Therapeutics官方公告，MOONLIGHT‑1 II期研究未达主要终点。在神经精神领域，快速起效抗抑郁药物一直是全球药企追逐的热门赛道。 2023年，强生豪掷5000万美元首付款，最高可达10亿美元里程碑，引进选择性M1毒蕈碱受体拮抗剂PIPE‑307（JNJ‑5120），押注这一全新机制，布局重度抑郁症、多发性硬化两大适应症。然而短短10个月之内，该候选药物连续两项II期临床失利。继复发缓解型多发性硬化（RRMS）II期VISTA试验失败之后，MOONLIGHT‑1重度抑郁症II期概念验证研究再次未能达成主要疗效终点，给这个备受期待的BD重磅项目蒙上巨大阴影。 MOONLIGHT‑1试验详情：主要终点未达标，安全性尚可 MOONLIGHT‑1是一项随机、双盲、多中心、安慰剂对照II期概念验证临床试验，一共入组107例成人重度抑郁症（MDD）患者，受试者随机分配接受两种不同方案的PIPE‑307或者安慰剂干预。 ✅ 主要终点：第5天MADRS（蒙哥马利‑Å斯伯格抑郁评定量表）总分较基线的改善程度。试验结果显示，对比安慰剂，PIPE‑307没有展现出统计学意义的抑郁症状改善，主要疗效终点未达到。安全性数据方面，PIPE‑307整体耐受性良好，试验中没有观察到全新的安全性风险信号。值得注意：本次公告仅披露了“未达终点”的定性结论；公司没有对外公开疗效差值、P值、完整不良事件发生率等关键量化数据，也没有明确说明项目将继续开展、修改还是直接终止，完整数据集的披露时间尚未确定。药物机制：M1受体拮抗，挑战快速抗抑郁新路径 PIPE‑307是一款高选择性M1毒蕈碱型乙酰胆碱受体拮抗剂。其抗抑郁理论假说：人体胆碱能系统过度激活、胆碱能张力升高，参与抑郁状态的发生发展；通过阻断M1受体，有望调节大脑情绪环路、改善认知与抑郁相关症状，期待实现快速起效抗抑郁效果。 2023年强生（杨森）与Pipeline Therapeutics（后更名为Contineum Therapeutics）达成全球授权合作：强生拿到PIPE‑307全球独家开发权益，拥有MDD、MS及其他适应症后续开发的唯一决定权；交易包含5000万美金首付款，临床、监管、商业化里程碑最高合计可达10亿美元，另附加分级销售特许权使用费。同靶点赛道全景：M1拮抗剂抗抑郁，为何集体遇冷？ M1毒蕈碱受体通路是精神领域非常矛盾的靶点：M1激动剂已经实现药物获批，但高选择性M1拮抗剂用于抑郁症的临床转化却举步维艰。 1、东莨菪碱（Scopolamine）：非选择性M1拮抗剂，学术热，无商业化推进东莨菪碱是经典非选择性毒蕈碱受体拮抗剂，可阻断包括M1在内的多种毒蕈碱亚型。早期小样本临床观察到静脉给药后可产生快速抗抑郁效应，曾是M1拮抗抗抑郁假说最重要的临床依据，机制假说为阻断GABA中间神经元M1受体，上调谷氨酸释放，激活mTOR通路，产生快速抗抑郁效果。但局限十分突出： 1）属于非选择性拮抗剂，同时作用M1‑M5，外周抗胆碱副作用显著（口干、视力模糊、认知损害、幻觉）； 2）后期部分大样本对照研究无法重复早期阳性结果，疗效不稳定； 3）无药企商业化开发MDD适应症，仅停留在学术研究，没有推进II/III期注册性试验，没有合适口服脑穿透高选择性分子推进临床开发。 2、临床前分子VU0255035：工具化合物，止步基础研究 VU0255035是科研用高选择性M1拮抗剂，动物模型中可复制快速抗抑郁相关的分子与行为学改变。但该分子药代性质差，不适合人体给药，仅作为实验室工具药，从未进入人体临床试验，没有向临床候选药物推进。 3、全球在研：几乎无其他选择性M1拮抗剂进入抗抑郁II期截至2026年9月，PIPE‑307是全球唯一一款推进至II期概念验证的高选择性中枢M1受体拮抗剂（抑郁症适应症）。全球管线中，没有其他同类分子进入MDD的II期及以后阶段。注意区分：KarXT（Cobenfy）是M1/M4受体激动剂，已经FDA获批用于精神分裂症，机制完全相反，不属于拮抗剂，代表胆碱能通路“激动方向”的成功，和PIPE‑307“阻断M1”的治疗逻辑恰好相反。从管线现状可以看出：动物实验上“阻断M1可以抗抑郁”的假说很漂亮，但缺少其他II期候选药物交叉验证；PIPE‑307连续两次II期失利，直接削弱了“选择性M1受体拮抗治疗抑郁症”这一假说的临床可信度。到底是靶点假说本身存在缺陷，还是分子剂量、入组人群、试验时间窗口设计问题，目前行业仍有争论。 10个月两次II期失利，项目命运悬而未决这已经是PIPE‑307第二次II期临床失败。早在2025年11月，针对复发缓解型多发性硬化（RRMS）的II期VISTA试验，该药同样未能达到预设主要、次要疗效终点，仅安全性可接受。短短10个月，两大适应症II期全部折戟。行业分析师指出：连续两项II期概念验证研究失利，意味着PIPE‑307整个分子管线极有可能走向终结。公告披露之后，资本市场快速做出反应：Contineum（NASDAQ:CTNM）盘后股价下跌约10%。周一收盘报14.82美元，盘后下探至约13.30美元，创下该公司被纳入罗素2000、罗素3000价值指数之后的新低；在此之前5个交易日，该股已经累计下跌11.26%。 PIPE‑307项目受挫，直接威胁来自强生的后续里程碑付款，也挤压了公司其余管线的资金空间。下一步何去何从：强生评估探索性终点，公司重心转向LPA1R项目PIPE‑791 根据官方新闻稿，强生团队仍在完整复盘MOONLIGHT‑1全部数据集，对预设的探索性终点开展分析，综合评估全部研究结果之后，才会决定PIPE‑307后续开发走向，是继续推进、调整方案还是彻底终止该项目，目前暂无定论。对于Contineum公司自身，PIPE‑307受挫之后，管线重心或将全面转移到全资拥有的LPA1受体拮抗剂PIPE‑791。该分子为脑穿透性小分子，当前主要开发适应症为特发性肺纤维化（IPF）与慢性疼痛，处于II期临床阶段。不少分析师认为，PIPE‑791或将成为Contineum当前阶段最核心价值资产。公司表示后续会择机对外发布MOONLIGHT‑1完整II期数据集以及项目更新，但是目前没有确定的公开披露时间表。思考：神经领域新药研发，假说与临床转化之间巨大鸿沟神经、精神类药物一直是新药研发的“死亡谷”：靶点假说成立于临床前模型，进入人体临床之后，常常无法转化为临床终点获益。 M1通路非常典型：激动M1已经实现药物获批（KarXT），但阻断M1的治疗假说至今没有选择性分子在II期获得确证。即便拿到Big‑Pharma大额BD背书，也不能为项目临床成功兜底。PIPE‑307连续两次II期失败，再次印证神经创新药从靶点假说走到临床获益之间巨大的鸿沟。后续重点关注：强生对PIPE‑307的最终决策、MOONLIGHT‑1完整数据集、PIPE‑791的II期临床读出结果。参考文献 [1] Contineum Therapeutics. Contineum Therapeutics Reports Phase 2 Results for JNJ‑5120/PIPE‑307 for the Treatment of Major Depressive Disorder[EB/OL]. Press Release, Sep 14, 2026. [2] Contineum Therapeutics. Top‑line results from Phase 2 VISTA trial of PIPE‑307 in relapsing‑remitting multiple sclerosis[EB/OL]. Press Release, Nov 20, 2025. [3] Psychiatric Times. Phase 2 Failure: JNJ‑5120/PIPE‑307 for the Treatment of Major Depressive Disorder[EB/OL]. Sep 15,2026. [4] Pipeline Therapeutics. Janssen and Pipeline Therapeutics Announce Global Licensing Agreement for PIPE‑307[EB/OL]. Apr 17,2023. [5] 快速起效抗抑郁药物研究进展[J]. 中国药理学通报,2025. [6] Citeline. Phase II Depression Failure May Close Door On Contineum/J&J’s M1 Antagonist[EB/OL]. Sep 16,2026.

2026-09-15

·FierceBiotech

J&J’s Contineum-partnered depression drug flunks another phase 2 test

A phase 2 trial of Johnson & Johnson’s JNJ-5120 has missed its primary endpoint, denting the prospects of the Contineum Therapeutics-partnered depression drug candidate. In 2023, J&J paid Pipeline Therapeutics $50 million upfront and committed up to $1 billion in milestones for global rights to the M1 receptor antagonist, which is also called PIPE-307. Pipeline, which rebranded as Contineum later in 2023, had completed two phase 1 trials of the drug candidate, teeing J&J up to run midphase studies in relapsing-remitting multiple sclerosis (MS) and major depressive disorder (MDD). Ten months after disclosing the failure of the MS trial, Contineum reported that the MDD study missed its primary endpoint. Investigators randomized 107 people with MDD to receive one of two JNJ-5120 regimens or placebo. At Day 5, patients receiving JNJ-5120 performed no better on a depression scale than those on placebo, causing the trial to miss its primary endpoint. William Blair analysts removed JNJ-5120 from their model in response to the setback, extinguishing hopes of success that they had put at 35% before the readout. “We had always viewed the study as risky, especially considering the risky nature of placebo-controlled studies in MDD, where placebo responses have eroded effect sizes and patient heterogeneity can lead to volatility in patient response rates on active drug,” the analysts said. J&J has yet to give up on the asset. The Big Pharma continues to evaluate the results, including data on prespecified exploratory endpoints, Contineum said. J&J’s review of the totality and clinical relevance of its findings will inform the next steps. Investors appeared sanguine about the setback, sending Contineum’s share price down just 3.5% to $14.30 in after-hours trading. The muted response aligns with the assessment of William Blair analysts, who said most of Contineum’s value is tied to the LPAR1 antagonist, PIPE-791, which the company is developing in idiopathic pulmonary fibrosis. PIPE-791, a potential rival to Bristol Myers Squibb’s admilparant, is in phase 2 development. The next key catalyst for Contineum's shares is readthrough from phase 3 data on admilparant, which BMS is expected to share early in the fourth quarter, the analysts said.

临床2期临床结果

100 项与 PIPE-791 相关的药物交易

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研发状态

10 条进展最快的记录,

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适应症	最高研发状态	国家/地区	公司	日期
特发性肺纤维化	临床2期	阿根廷	Contineum Therapeutics, Inc.	2026-01-08
特发性肺纤维化	临床2期	澳大利亚	Contineum Therapeutics, Inc.	2026-01-08
特发性肺纤维化	临床2期	加拿大	Contineum Therapeutics, Inc.	2026-01-08
特发性肺纤维化	临床2期	智利	Contineum Therapeutics, Inc.	2026-01-08
特发性肺纤维化	临床2期	法国	Contineum Therapeutics, Inc.	2026-01-08
特发性肺纤维化	临床2期	希腊	Contineum Therapeutics, Inc.	2026-01-08
特发性肺纤维化	临床2期	以色列	Contineum Therapeutics, Inc.	2026-01-08
特发性肺纤维化	临床2期	新西兰	Contineum Therapeutics, Inc.	2026-01-08
特发性肺纤维化	临床2期	秘鲁	Contineum Therapeutics, Inc.	2026-01-08
特发性肺纤维化	临床2期	波兰	Contineum Therapeutics, Inc.	2026-01-08