A Phase IIa, Randomized, Double-Blind, Placebo-Controlled Study Evaluating the Safety, Tolerability, Pharmacokinetics, and Efficacy of INS018_055 Administered Orally to Subjects With Idiopathic Pulmonary Fibrosis (IPF)

The goal of this clinical trial is to learn about INS018_055 in adults with Idiopathic Pulmonary Fibrosis (IPF).
The primary objective is to evaluate the safety and tolerability of INS018_055 orally administered for up to 12 weeks in adult subjects with IPF compared to placebo.

开始日期2024-02-08

申办/合作机构

英矽智能(香港)有限公司初创企业

NCT05938920 / Completed临床2期

开始日期2023-06-19

申办/合作机构

英矽智能(香港)有限公司初创企业

CTR20230776 / Completed临床2期

一项评价INS018_055口服给药用于治疗特发性肺纤维化（IPF）受试者的安全性、耐受性、药代动力学和有效性的随机、双盲、安慰剂对照、IIa期研究

主要目的：评价与安慰剂相比，成人IPF受试者口服INS018_055长达12周的安全性和耐受性。次要目的评价IPF受试者口服INS018_055后的药代动力学 (PK) 评价与安慰剂相比，成人IPF受试者口服INS018_055长达12周在FVC下降方面的有效性评价与安慰剂相比，口服INS018_055治疗长达12周在改善生活质量（QoL）和功能指标方面的有效性评价与安慰剂相比，INS018_055口服给药对IPF急性加重的影响探索性目的为： ● 探索口服INS018_055对血液中IPF疾病相关的生物标志物的影响 ● 用高通量蛋白组学探索INS018_055在IPF病人血液蛋白质组中的潜在作用机制

开始日期2023-05-15

申办/合作机构

英矽智能科技（上海）有限公司

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100 项与 INS018_055 相关的临床结果

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100 项与 INS018_055 相关的专利（医药）

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251

项与 INS018_055 相关的文献（医药）

2024-11-01·BIOORGANIC & MEDICINAL CHEMISTRY

N-substituted-4-(pyridin-4-ylalkyl)piperazine-1-carboxamides and related compounds as Leishmania CYP51 and CYP5122A1 inhibitors

Article

作者: Lin, Zhihong ; Li, Junan ; Moitra, Samrat ; Basu, Somrita ; Qin, Lingli ; Werbovetz, Karl A. ; La Rosa, Chris ; Jin, Yiru ; Junaid Dar, M ; Wu, Meng ; Junaid Dar, M. ; Uchenik, Dmitriy ; Roy, Anuradha ; Kendall, Allie ; Werbovetz, Karl A ; Zhang, Kai ; Zhuo Wang, Michael ; Sharma, Pankaj

CYP5122A1, an enzyme involved in sterol biosynthesis in Leishmania, was recently characterized as a sterol C4-methyl oxidase. Screening of a library of compounds against CYP5122A1 and CYP51 from Leishmania resulted in the identification of two structurally related classes of inhibitors of these enzymes. Analogs of screening hit N-(3,5-dimethylphenyl)-4-(pyridin-4-ylmethyl)piperazine-1-carboxamide (4a) were generally strong inhibitors of CYP51 but were less potent against CYP5122A1 and typically displayed weak inhibition of L. donovani promastigote growth. Analogs of screening hit N-(4-(benzyloxy)phenyl)-4-(2-(pyridin-4-yl)ethyl)piperazine-1-carboxamide (18a) were stronger inhibitors of both CYP5122A1 and L. donovani promastigote proliferation but also remained selective for inhibition of CYP51. Two compounds in this series, N-(4-((3,5-bis(trifluoromethyl)benzyl)oxy)phenyl)-4-(2-(pyridin-4-yl)ethyl)piperazine-1-carboxamide (18e) and N-(4-((3,5-di-tert-butylbenzyl)oxy)phenyl)-4-(2-(pyridin-4-yl)ethyl)piperazine-1-carboxamide (18i) showed modest selectivity for inhibiting L. donovani promastigote proliferation compared to J774 macrophages and were effective against intracellular L. donovani with EC₅₀ values in the low micromolar range. Replacement of the 4-pyridyl ring present in 18e with imidazole resulted in a compound (4-(2-(1H-imidazol-1-yl)ethyl)-N-(4-((3,5-bis(trifluoromethyl)benzyl)oxy)phenyl)piperazine-1-carboxamide, 18p) with approximately fourfold selectivity for CYP5122A1 over CYP51 that inhibited both enzymes with IC₅₀ values ≤ 1 µM, although selective potency against L. donovani promastigotes was lost. Compound 18p also inhibited the proliferation of L. major promastigotes and caused the accumulation of 4-methylated sterols in L. major membranes, indicating that this compound blocks sterol demethylation at the 4-position in Leishmania parasites. The molecules described here may therefore be useful for the future identification of dual inhibitors of CYP51 and CYP5122A1 as potential antileishmanial drug candidates and as probes to shed further light on sterol biosynthesis in Leishmania and related parasites.

2024-04-01·Heliyon

A novel GSK3β inhibitor 5n attenuates acute kidney injury

Article

作者: Cai, Yu-Ting ; Li, Zeng ; Ma, Qiu-Ying ; Li, Chao ; Wang, Yue-Yue

Acute kidney injury (AKI) is a clinical syndrome with high morbidity and mortality caused by various factor. The specific strategies for AKI are still lacking. GSK3β is widely expressed in the kidneys. In acute models of injury, GSK3β promotes the systemic inflammatory response, increases the proinflammatory release of cytokines, induces apoptosis, and alters cell proliferation. We screened a series of 3-(4-pyridyl)-5-(4-sulfamido-phenyl)-1,2,4-oxadiazole derivatives which are recognized as new GSK3β inhibitors, and found that 5n had the least toxicity and the best cell protection. We then tested the anti-inflammatory and reno-protective effect of 5n in cisplatin-treated tubular epithelial cells. 5n had anti-inflammation effect indicated by phosphor-NF-κB detection. Finally, we found that 5n ameliorated renal injury and inflammation in cisplatin-induced AKI mouse model. Silencing GSK3β inhibited cell injury and inflammation induced by cisplatin. We found that GSK3β interacted with PP2Ac to modulate the activity of NF-κB. In conclusion, 5n, the novel GSK3β inhibitor, protects against AKI via PP2Ac-dependent mechanisms which may provide a potential strategy for the treatment of AKI in clinic.

2023-12-01·Journal of Taibah University Medical Sciences

Molecular properties and In silico bioactivity evaluation of (4-fluorophenyl)[5)-3-phen-(4-nitrophenyl yl-4,5-dihydro-1H-pyrazol-1-yl]methanone derivatives: DFT and molecular docking approaches

Article

作者: Banjo, Semire ; Ayobami, Odunola O ; Felix, Latona D ; Kolawole, Oyebamiji A ; Omotayo, Ibrahim A ; Olasegun, Abdulsalami I ; Emmanuel, Oladuji T ; Dele, Owonikoko A ; Dasola, Adeoye M

Objectives:

Molecular structures, spectroscopic properties, charge distributions, frontier orbital energies, nonlinear optical (NLO) properties and molecular docking simulations were analyzed to examine the bio-usefulness of a series of (4-fluorophenyl)[5-(4-nitrophenyl)-3-phenyl-4,5-dihydro-1H-pyrazol-1-yl]methanone derivatives.

Methods:

The compounds were studied through computational methods. Equilibrium optimization of the compounds was performed at the B3LYP/6-31G(d,p) level of theory, and geometric parameters, frequency vibration, UV-vis spectroscopy and reactivity properties were predicted on the basis of density functional theory (DFT) calculations.

Results:

The energy gap (ΔEg), electron donating/accepting power (ω-/ω+) and electron density response toward electrophiles/nucleophiles calculated for M1 and M2 revealed the importance of substituent positioning on compound chemical behavior. In addition, ω-/ω+ and ΔEn/ΔEe indicated that M6 is more electrophilic because of the presence of two NO₂ groups, which enhanced its NLO properties. The hyperpolarizability (β₀) of the compounds ranged from 5.21 × 10^-30 to 7.26 × 10^-30 esu and was greater than that of urea; thus, M1-M6 were considered possible candidates for NLO applications. Docking simulation was also performed on the studied compounds and targets (PDB ID: 5ADH and 1RO6), and the calculated binding affinity and non-bonding interactions are reported.

Conclusion:

The calculated ω^- and ω⁺ indicated the electrophilic nature of the compounds; M6, a compound with two NO₂ groups, showed enhanced effects. Molecular electrostatic potential (MEP) analysis indicated that amide and nitro groups on the compounds were centers of electrophilic attacks. The magnitude of the molecular hyperpolarizability suggested that the entire compound had good NLO properties and therefore could be explored as a candidate NLO material. The docking results indicated that these compounds have excellent antioxidant and anti-inflammatory properties.

项与 INS018_055 相关的新闻（医药）

2024-10-24

·研发客

MNC投入逾百亿，海外AI制药势头有多猛？| AI

// • 2024年前三季度，跨国药企的AI相关合作交易数为21笔，总金额达到129.32亿美元； • 海外融资额超过1亿美元的AI制药企业在2024年上半年有6家； • 剂泰医药赖才达认为，国内AI制药公司的估值比较合理； • 英矽智能任峰认为，国内的AI技术基本可以比肩全球，但算法的优化和数据的积累稍显落后。拿下诺贝尔化学奖，仅仅是对AI的众多认可之一。“未来AI会是大势所趋，这已成为制药行业的共识，用AI的公司数量会超越不用的公司，慢慢实现产业界全面拥抱AI。”英矽智能联合首席执行官兼首席科学官任峰如是评价。事实上，跨国药企已开始拥抱AI技术。2023年，跨国药企的AI相关合作交易数仅为11笔。而2024年前三季度，这一交易数为21笔（见下图），总金额达到129.32亿美元。艾伯维更是以2.125亿美元收购了一家AI小分子公司Landos Biopharma，这也是跨国药企首次收购一家AI制药公司。跨国药企还建立内部AI团队。在今年诺贝尔化学奖公布的前一天，礼来任命了首任首席人工智能官（CAIO）这一新的职位，领导从药物发现、临床试验至制造等多个领域的AI 项目。此前8月，辉瑞也任命了首席AI官。在更早的2023年，赛诺菲宣布了“All in”人工智能战略，首席执行官Paul Hudson透露“赛诺菲在小分子药物发现的预测准确率超过80%，通过人工智能和机器学习化合物设计的小分子项目达到75%”。拓展阅读投资人如何看AI在医药行业的应用 MNC强势拥抱AI的同时，海外AI制药资本市场也正掀起热潮。2024年以来，大量的风险投资流入AI。如，超10亿美元融资的Xaira Therapeutics，创下今年以来生物医药领域的最高额融资，创始人团队里就有今年获得诺贝尔化学奖的David Baker教授。海外火热，国内呢？ 2024年上半年，海外融资额超过1亿美元的AI制药企业就有6家，其中不乏知名投资机构a16z、ARCH Venture Partners、红杉资本，以及礼来、安进、赛诺菲等MNC。其中Formation Bio在6月完成的3.72亿美元的D轮融资，就是由a16z领投，赛诺菲、红杉资本、Thrive Capital等跟投。正如BMS的首席数字与技术官Greg Meyers所说，“可能一些公司还没有很好的产品或技术平台契合市场，但只要GenAI（生成式人工智能）这个词出现在宣传平台中，就会融到钱。” 相比下，今年前三季度共有19家国内AI制药公司完成融资，其中披露融资额的14家企业，其总融资额约2.63亿美元。对此，剂泰医药联合创始人&CEO赖才达评论到，近期美国市场股价波动非常大，所以有一些泡沫的可能性，中国的资本市场相对冷静一些，估值也比较合理。的确，国内整体面临资本寒冬的情况下，AI制药领域同样难免遇到困难。不过也有好消息，晶泰科技于6月登录港交所挂牌上市，英矽智能在3月再一次向港交所递交招股书，拟香港主板IPO上市，剂泰医药完成了1亿美元的C轮融资。产品开发也有积极信息传出，9月，英矽智能的首个AI创新药物ISM001-055获得了临床2a期的积极结果。从技术端看，赖才达认为，国内外不存在太大差异，几乎是平行时间起步，可能海外的优势体现在与大药企的合作能够更快地推进内部管线和优化平台，而国内企业在出海时要花更多精力。任峰也表示，国内的AI技术基本可以比肩全球，但算法的优化和数据的积累稍显落后。“对AI制药公司而言，这两方面是主要壁垒。其一，目前企业大多使用的是公开数据，数据如何清洗并保证质量，这需要企业通过时间的积累和人员的培养积累达到。其二，算法需要不断经过项目验证，淘汰成功率低、优化成功率高的算法，才能提高最终由算法组合搭建产品的成功率。” 例如近期刚获得A轮融资的分子之心，创始人许锦波开创的深度学习算法RaptorX-Contact启发了后来的AlphaFold，被誉为“AI预测蛋白质结构第一人”。并购趋势初显新生代AI制药在资本市场火热的同时，初代AI制药企业已开始报团取暖。 8月，两家AI制药龙头公司Recursion和Exscientia宣布达成最终协议合并。两家公司都诞生于2013年最初的AI制药萌芽期，且在合并前Exscientia经历了不小的动荡。 5月Exscientia宣布裁员20%至25%，其CEO在2月被解雇，去年10月停止了一项核心产品EXS-21546的1/2期研究。 Recursion在合并前虽未有失败产品，但在合并一个月后的9月8日首次公布研究数据，主要药物REC-994的2期研究疗效有限，股价下跌超过16%。赖才达认为，AI制药行业正面临着产品进入后期阶段的瓶颈期，在资本市场中难免遇到困境，对Exscientia来说合并是当下合适的时机。不过Recursion背后有英伟达支持，并且Recursion和Exscientia的技术和管线并不重合，整合后能强强联合、优势互补。 “两家公司是生物学能力和化学能力的结合。”赖才达解释，“Recursion的强项是生物学能力，将蛋白组学、基因组学、表观组学的数据串联起来，理清靶点跟疾病的关系，Excientia强项在小分子结构设计，在知道一个靶点口袋后，设计出达到成药需求的小分子，且从药化角度解决传统制药的问题。结合后能打通制药环节的上下游，将高通量的上游细胞数据与下游的分子设计结合在一起，进一步梳理和整合两家的管线产品，节约研发与转化的成本。” 结合新生代AI企业Xaira来分析，赖才达认为利用AI技术解决研发流程中的某一关键问题、且是传统药物研发无法解决的问题，达到足够优势，成功的概率会更大一些。 “Xaira就是依托传统制药流程，在其中某一研发环节，AI能最大限度发挥作用，利用大模型解决抗体轻链端的设计，这是很大的突破点。而Excientia和Recursion在成立之初就想做全链条的AI制药研发，从而替代传统制药的流程。”赖才达说。 Xaira与Recursion、Excientia的不同选择路径，或许可以给全球AI制药行业的生物技术公司带来一些思考和借鉴。无论融资如何火热，最终获得市场认可仍需要产品来说话。英矽智能的TNIK抑制剂近期将临床研究推进到2期，这让我们增加了对AI制药的期待。下一篇，我们将关注那些可能最早冲线的在研产品。编辑 | 姚嘉 yao.jia@PharmaDJ.com 总第2229期访问研发客网站，深度报道和每日新闻抢鲜看 www.PharmaDJ.com

并购生物类似药

2024-09-29

·新药前沿

2款特发性肺纤维化First-In-Class药物取得突破

特发性肺纤维化(IPF)是一种难治性肺部疾病，有“不是癌症的癌症”之称，目前的治疗药物无法阻止其进展。近日，勃林格殷格翰和英矽智能（Insilico Medicine）分别报告了各自开发First-In-Class特发性肺纤维化新药在临床试验的积极数据。特发性肺纤维化临床试验领域获得了难得的双重好消息。试验结果表明，这两家公司的特发性肺纤维化候选药物可能能够阻止或逆转肺功能下降，这是目前任何治疗药物都无法做到的。不过业内分析人士指出，数据披露的细节尚不明确，还需要更多信息以准确评估。特发性肺纤维化无法治愈，目前的治疗旨在尽量减少症状、维持生活质量和减缓病情进展。主要治疗药物包括勃林格殷格翰的Ofev（尼达尼布）和罗氏的Esbriet（吡非尼酮），这两种药物都是抗纤维化药物，同时还有肺功能改善作用。然而，这两种药物的耐受性都不是很好，而且只能减缓用力肺活量(FVC)的下降，而用力肺活量是特发性肺纤维化患者肺功能的一个关键指标。延伸阅读：IPF也疯狂：新药开发“三剑客”突围 PDE4B抑制剂nerandomilast 勃林格殷格翰磷酸二酯酶4B（PDE4B）抑制剂nerandomilast靶向于与肺部纤维化和炎症有关的PDE4B酶，在Ⅲ期FIBRONEER-IPF研究中达到了顶线结果，nerandomilast可以显著改善特发性肺纤维化患者的肺功能。与安慰剂相比，nerandomilast在52周时显著改善了用力肺活量。勃林格殷格翰将利用FIBRONEER-IPF的研究结果，支持nerandomilast向FDA和全球其他监管机构提交的药物上市申请。勃林格殷格翰在其声明中没有提供具体数据。该公司预计将在2025年上半年提供FIBRONEER-IPF的完整数据和分析。 nerandomilast通过优先靶向和抑制PDE4B来治疗特发性肺纤维化，该酶在肺部高度表达，被认为与纤维化和炎症过程有关。nerandomilast的作用是破坏这些通路，对肺部产生抗纤维化和抗炎作用，而且副作用比抑制多种酶的药物要小。延伸阅读：PDE4B抑制剂fast-follow者海思科和人福，紧追勃林格殷格翰 TNIK抑制剂ISM001-055 英矽智能（Insilico Medicine）宣布了其ISM001-055的IIa期临床试验亦取得了积极的初步结果。ISM001-055是靶向于TNIK（Traf2和Nck相互作用激酶）的同类首创小分子药物，利用生成式AI设计用于治疗特发性肺纤维化。该研究既达到了其在所有剂量水平上均达到了安全性和耐受性的主要终点。也达到了其次要疗效终点，其中观察到剂量依赖性用力肺活量改善，其中接受60毫克QD ISM001-055治疗的患者用力肺活量改善最为显著。 Insilico专有的AI平台促进了ISM001-055的靶标识别和分子设计。在2024年3月的《自然生物技术》论文中进行了描述，该论文详细介绍了TNIK作为特发性肺纤维化新型治疗靶点的识别以及ISM001-055的后续设计。在特发性肺纤维化中，TNIK的激活会导致肺部病理性纤维化，从而导致肺功能逐渐下降。通过抑制TNIK，ISM001-055旨在阻止或逆转纤维化过程，为特发性肺纤维化患者提供改善病情的治疗方法。本文由「新药前沿」微信公众号根据公开资料整理编辑，欢迎个人转发至朋友圈。媒体或机构转载授权请在「新药前沿」微信公众号留言公众号名称，审核通过后开通白名单获取转载授权，转载请标识来源。免责声明：本文仅作信息交流之目的，非投资建议或者治疗方案推荐，「新药前沿」微信公众号不对任何主体因使用本文内容而导致的任何损失承担责任。限于作者水平和专业知识所限，如有谬误，欢迎指正！

临床3期优先审批临床2期申请上市临床结果

2024-09-24

·BioSpace

Boehringer, Insilico Appear to Break Through Against IPF

iStock/ Mihaela Rosu Clinical trial results shared by Boehringer Ingelheim and Insilico Medicine showed improvement in idiopathic pulmonary fibrosis, an intractable lung disease for which current treatment options fail to stop progression, but the data were limited, leaving experts wanting. Patients with idiopathic pulmonary fibrosis got a double helping of good news in the clinical trials arena last week as Boehringer Ingelheim and Insilico Medicine each reported positive data from their respective trials. The results indicate that both companies’ idiopathic pulmonary fibrosis (IPF) drug candidates might be able to stop or reverse decline in lung function—something no current treatments can offer. But experts cautioned that the data drops were light on the details and that more information is needed before either asset can be accurately evaluated. A progressive interstitial lung disease disproportionately affecting older adults, IPF is characterized by lung scarring, inflammation, fatigue and shortness of breath. It ultimately leads to respiratory failure and death within 3–5 years of diagnosis. As its name suggests, the origin of IPF is unknown. “IPF is a very complex, multifactorial and very idiopathic process,” Insilico co-CEO Alex Zhavoronkov told BioSpace . There is no cure for IPF and current treatment is designed to minimize symptoms, maintain quality-of-life and slow progression, Allison Reiss, an associate professor at NYU Grossman Long Island School of Medicine, told BioSpace in an email. She added that “mainstay treatment” consists of Boehringer’s Ofev (nintedanib) and Roche’s Esbriet (pirfenidone), both antifibrotic drugs, along with pulmonary rehabilitation. However, Zhavoronkov said, “neither of these drugs are extremely well tolerated,” and they only slow down decline in forced vital capacity (FVC), a key measure of lung function in IPF. “Usually, you see the decline on the standard of care.” Insilico, Boehringer See Improvements in Key IPF Indicator On Sept. 16, Boehringer reported that its IPF drug candidate nerandomilast elicited a significant improvement in FVC at 52 weeks versus placebo in the Phase III FIBRONEER-IPF trial of 1,177 patients. FIBRONEER-IPF “is the first IPF Phase III trial in a decade to meet its primary endpoint,” Ioannis Sapountzis, Boehringer’s head of global therapeutic areas, said in a statement. Reiss said she would like further specifics in regard to that endpoint. “[Boehringer Ingelheim] said [the study] met the endpoint, which means that those on the drug performed better on the forced vital capacity test, but on both doses or one of the doses? And how much better?” Trial participants were given either 9 mg or 18 mg of nerandomilast twice a day or a placebo for at least 52 weeks. Additionally, Reiss is seeking more information on the secondary endpoints: time to an IPF exacerbation, first hospitalization for respiratory cause, or death. She noted, however, that nerandomilast’s mechanism of action is promising. By preferentially blocking the phosphodiesterase 4B enzyme, she explained, “PDE4B inhibitors interfere with the function of a very specific form of the phosphodiesterase enzyme so that this class of drugs may be able to reduce inflammation and fibrosis in IPF with less side effects than a drug that would inhibit multiple forms of the enzyme.” In an emailed statement, a Boehringer spokesperson told BioSpace the company has a strong focus on IPF, given the high unmet need. The company plans to present full data and analyses from FIBRONEER-IPF in the first half of 2025. Insilico, meanwhile, reported similarly positive results on its much smaller Phase IIa trial of 60 patients with IPF. Specifically, the company released results the day after Boehringer showing that its ISM001-055 met the primary endpoint of safety and secondary efficacy endpoints, demonstrating a dose-dependent improvement in FVC over 12 weeks. Zhavoronkov acknowledged that the study is “not powered enough for me to go out and make super big claims . . . but when you see the chart, it’s very clear that you see that the drug is working.” Insilico is currently awaiting the results of a second, parallel Phase IIa trial. Next, Zhavoronkov said the company expects to run a Phase IIb study but added that the team wants to meet with regulators to understand the regulatory pathway. He suggested there could be potential for the candidate to be fast-tracked. “If you see the improvements in forced vital capacity, and it’s strong enough evidence to convince the regulators, maybe patients should be on the drug right now,” he told BioSpace . ISM001-055—which was wholly designed using Insilico’s generative AI engine referencing millions of data including patents, research publications, grants and clinical trial databases—targets Traf2- and NCK- interacting kinase (TNIK). Zhavoronkov explained that, due to the prevalence of IPF in people 65 years and older, Insilico was looking for targets that were also “very strongly implicated” in aging, Zhavoronkov said. “We were looking for a dual-purpose target.” TNIK scored high in six hallmarks of aging, and there was significant overlap in hallmarks of IPF, he said. However, Reiss said she is “pretty skeptical” about the approach. She noted that while TNIK is present in the lungs and “does regulate transforming growth factor-β signaling, which is important in IPF,” it is mostly found in the gastrointestinal system. Reiss added that the duration of the study was too short and the number of subjects was too small to draw any conclusions about ISM001-055’s efficacy. “[We’ll] have to wait and see,” she said.

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100 项与 INS018_055 相关的药物交易

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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	中国	上海合全医药有限公司	2023-05-15
炎症	临床前	中国	英矽智能(香港)有限公司初创企业	2024-03-08

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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


Biospace 人工标引	N/A	特发性肺纤维化	-	ISM001-055	積鑰鹹衊廠膚網窪窪範(積醖簾膚鏇遞廠製鹽願) = its ISM001-055 met the primary endpoint of safety. 壓憲網蓋製齋觸餘憲範 (選選顧選製壓觸範積膚 ) 达到更多	积极	2024-09-24
NCT05154240 (GlobeNewswire) 人工标引	临床1期	特发性肺纤维化	78	INS018_055	繭齋構齋鏇窪淵壓夢艱(積夢蓋膚選淵積範製餘) = not reported 鏇艱鹹繭觸膚夢獵鬱製 (艱繭衊淵淵醖獵醖艱壓 ) 更多	积极	2023-01-10