Tranilast Vs. Steroids to Prevent Esophageal Stricture (TAPES) Following Circumferential Endoscopic Submucosal Dissection (cESD) for Superficial Neoplasms

The goal of this clinical trial is to learn if tranilast works to prevent esophageal stricture after circumferential endoscopic submucosal dissection (cESD) in adults. It will also help us learn more about the safety of tranilast. The main questions it aims to answer are: 1. Does tranilast reduce the occurence of esophageal stricture in participants after cESD? 2. What medical problems do participants have when taking tranilast.
Researchers will compare tranilast to prednisone (a steroid used in clinical practice with potential defects) to see if tranilast works well to prevent esophageal stricture.
Participants will: 1. Take tranilast or prednisone every day for 8 weeks. 2. Attend visit (at clinic or phone) once every 2 weeks for checkups and tests until 16 weeks. 3. Keep a diary of their symptoms and let researchers know during the 16 weeks follow up.

开始日期2025-01-01

申办/合作机构

浙江大学医学院附属第二医院（浙江省第二医院）

[+1]

ChiCTR2400092529

/ Suspended早期临床1期IIT

Study on the effectiveness of tranilast in the treatment of medium to large volume benign prostatic hyperplasia

开始日期2024-11-20

申办/合作机构-

NCT06689514

/ Not yet recruiting早期临床1期IIT

Study on the Effectiveness of Tranilast in the Treatment of Medium to Large Volume Benign Prostatic Hyperplasia

Benign prostatic hyperplasia (BPH) is one of the most common urinary and reproductive system diseases in elderly men. The preliminary research of the research group found that mast cells are cells that promote the progression of BPH, and the commonly used mast cell membrane stabilizer and TGF - β pathway inhibitor tranilast significantly inhibited the increase in prostate volume in animal experiments, which is considered to have potential applications in the treatment of BPH. This study plans to include 30 patients with medium to large volume BPH and experimentally explore the efficacy and safety of tranilast in the treatment of medium to large volume BPH.

开始日期2024-11-20

申办/合作机构

上海市第一人民医院

100 项与曲尼司特相关的临床结果

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100 项与曲尼司特相关的转化医学

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100 项与曲尼司特相关的专利（医药）

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项与曲尼司特相关的文献（医药）

2025-01-01·Journal of Lipid Research

Small molecule-driven LKB1 deacetylation is responsible for the inhibition of hepatic lipid response in NAFLD

Article

作者: Ding, Yu ; Sun, Lu ; Zheng, Xueying ; Qin, Weiwei ; Zhang, Wenhao ; Luo, Sihui ; Weng, Jianping

Nonalcoholic fatty liver disease (NAFLD) is a progressive condition characterized by ectopic fat accumulation in the liver, for which no FAD-approved drugs currently exist. Emerging evidence highlights the role of liver kinase B1 (LKB1), a key metabolic regulator, has been proposed in NAFLD, particularly in response to excessive nutrient levels. However, few agents have been identified that can prevent the progression of nonalcoholic steatohepatitis (NASH) by targeting LKB1 deacetylation. Through comprehensive screening of our in-house chemical library, we identified tranilast, a small molecule with remarkable inhibitory efficacy against lipid deposition induced by palmitic acid/oleic acid (PO). In this study, we investigated the novel biological function and mechanism of tranilast in regulating hepatic lipid response in NAFLD, focusing on its role in LKB1 deacetylation within hepatocytes. Our findings demonstrate that tranilast effectively reduced hepatic steatosis, inflammation, and fibrosis in NASH models induced by high-fat and high-cholesterol (HFHC) and methionine choline-deficient (MCD) diets. Mechanistic analysis using RNA sequencing revealed that tranilast mitigated hepatic lipid response by promoting LKB1 deacetylation and activating AMPK. Notably, in vivo experiments showed that the beneficial effects of tranilast in MCD diet-induced NASH model were reversed by the compound C (C-C), a known AMPK inhibitor, confirming that tranilast's effects on hepatic lipid response are mediated through the AMPK pathway. In summary, tranilast inhibits hepatic lipid response in NAFLD through LKB1 deacetylation, providing robust experimental evidence for the role of LKB1 in NAFLD. These findings position tranilast as a promising therapeutic candidate for the pharmacological management of metabolic diseases.

2024-12-01·Cell Biology International

Erucic acid increases the potency of cisplatin‐induced colorectal cancer cell death and oxidative stress by upregulating the TRPM2 channel

Article

作者: Nazıroğlu, Ayşenur ; Nazıroğlu, Mustafa ; Çarhan, Ahmet

AbstractErucic acid (ErA) is a source of omega‐9 monounsaturated fatty acids. ErA exhibited antitumor effects by causing apoptosis and oxidative stress in tumor cells, with the exception of the HT‐29 human colorectal cancer cell line. The apoptotic and Ca2+ signaling pathways in tumor cells are triggered when mitochondrial Ca2+ and Zn2+ accumulation produce reactive free oxygen species (ROS), which in turn activate TRPM2. ErA‐induced ROS and TRPM2 stimulation may augment the anticancer action of cisplatin (CSP). We aimed to study the effects of ErA and CSP incubations on ROS, apoptosis, and cell death in the HT‐29 cells by activating TRPM2. The cells were divided into five groups: control, ErA (200 µM for 48 h), CSP (25 µM for 24 h), and ErA + CSP + TRPM2 antagonists (200 µM carvacrol and 25 µM N‐(p‐amylcinnamoyl)anthranilic acid for 24 h). The TRPM2 antagonists reduced ErA plus CSP‐induced increases in H2O2‐induced intracellular free Ca2+ concentration ([Ca2+]c) and adenosine diphosphate‐ribose‐caused TRPM2 currents. ErA and CSP were found to cause apoptosis and cell death by raising the intracellular free Zn2+ concentration (Zn2+]c), caspase‐3, −8, and −9, mitochondrial membrane dysfunction, and ROS, while lowering reduced glutathione, cell viability, and cell number. The oxidative, apoptotic, and tumor cell death effects of CSP in the cells were enhanced by the increase of ErA‐mediated [Ca2+]c and Zn2+]c entering mitochondria through the activation of TRPM2. In conclusion, we observed that the combination of ErA and CSP was synergistic via TRPM2 activation for the treatment of HT‐29 tumor cells.

2024-12-01·Biochemical and Biophysical Research Communications

Tranilast alleviates skin inflammation and fibrosis in rosacea-like mice induced by long-term exposure to LL-37

Article

作者: Jin, Hui ; Li, Linfeng ; Zhang, Chuanxi ; Xu, Hong ; Yang, Jie ; Wu, Yiling ; Zheng, Ruiping

Rosacea, a prevalent chronic facial inflammatory condition, afflicts millions worldwide. Its multifaceted pathogenesis poses challenges for effective treatment. Tranilast (TR), an analog of a tryptophan metabolite, has demonstrated anti-inflammatory and anti-fibrotic properties across various diseases. Yet, its potential in rosacea treatment remains understudied. Here, we induced rosacea-like symptoms in mice via prolonged LL-37 injections and administered TR intervention. Our findings reveal that TR mitigated skin lesions, reduced skin thickness, and suppressed inflammatory cell infiltration within the dermis of LL-37 mice. Notably, TR downregulated the expression of rosacea-associated inflammatory cytokines (TNF-α, IL-6, IL-1β, and IL-18) and the antimicrobial peptide CAMP, while also inhibiting NLRP3 inflammasome activation and the TLR4 signaling pathway. Furthermore, TR attenuated LL-37-induced fibrosis and hindered the transforming growth factor-β1 (TGF-β1)/Smad2/3 pathway. In summary, our study underscores TR's therapeutic potential in rosacea by mitigating both skin inflammation and fibrosis, thereby offering a promising treatment avenue for this condition.

项与曲尼司特相关的新闻（医药）

2024-10-08

·生物制药小编

炎症靶点转型肥胖

NLRP3抑制剂或许能成为错过GLP-1激动剂风口公司的潜在肥胖症药物第二选择。近日，Ventyx Biosciences获得了赛诺菲的2700万投资，而此次赛诺菲的目标就是该公司的NLRP3抑制剂VTX3232，VTX3232还具有中枢神经系统渗透性，可以用于如帕金森症和阿尔兹海默症等神经退行行疾病。本文将对目前的NLRP3抑制剂的研究现状进行简单盘点。当机体出现营养过剩的情况时，超过自身能量消耗的多余热量会以甘油三酯(triacylglycerols, TGs)的形式储存在白色脂肪组织(white adipose tissue, WAT)中。而当患者肥胖时，这些白色脂肪细胞会过多增殖和存储TGs, 形成脂肪肥大。而脂肪过量积累超出负荷后, 会降解生成游离脂肪酸(free fatty acids, FFAs)，FFAs被巨噬细胞识别后会产生有毒性的神经酰胺(ceramides)。而NLRP3炎性小体能够感知脂毒性相关神经酰胺，诱导巨噬细胞和脂肪组织中的Caspase-1裂解。而长期保持肥胖状态就会导致胰岛素抵抗，脂肪功能失调，线粒体功能障碍等问题，与代谢功能障碍相关脂肪性肝病及肥胖相关慢性肾脏疾病密切相关。而NLRP3抑制剂能够精确靶向NLRP3炎症小体，抑制其组装和激活，从而减少下游炎症因子的释放，如IL-1β和IL-18。另外，临床前研究表明，NLRP3抑制剂能够显著降低与肥胖相关的心血管炎症生物标志物，如纤维蛋白原、sVCAM-1、suPAR和PCSK9。这些生物标志物的降低表明NLRP3抑制剂在改善心血管健康方面具有潜力。而这些机制的共同作用，有助于减轻体重、改善代谢异常并降低心血管风险。上文中提到的VTX3232最初就是作为一种心血管药物而开发。除了一些天然具有NLRP3抑制作用的中药和后期发现具有抗NLRP3作用的tranilast等，NLRP3小分子抑制剂的早期开发者是辉瑞。上个世纪爱尔兰的Luke A. J. O’Neill和澳大利亚的Matthew A. Cooper等研究人员发现了NLRP3的选择性抑制剂CP-456773，然后交给辉瑞开发，辉瑞就打算将其用于类风湿性关节炎。然而CP-456773存在严重肝毒性，似乎在高剂量环境下存在脱靶风险，因此不得不放弃开发。早期的临床失败一度浇灭了NLRP3抑制剂的热情，后续一系列开发以Inflazome，Jecure Therapeutics，IFM Therapeutics，NodThera等Biotech公司为主。 Inflazome开发了两款药物inzomelid和Somalix，他们打算将其用作一个罕见病——隐热蛋白相关周期综合征(CAPS)的开发，这是一种一因NLRP3激活突变引起的罕见病。而随着Inflazome在2020年被罗氏旗下的基因泰克收购，基因泰克获得Inflazome后，又在CP-456773的基础上开发了相对安全点的GDC-2394，打算用于心血管疾病，但是GDC-2394仍然存在毒性，会和他汀药物因为CYP3A4底物问题出现相互作用，而大部分心血管疾病患者都在服用他汀类药物，药物相互作用(DDI)阶段时，又两名参与者出现了4级药物性肝损伤，这导致试验中止。基因泰克放弃开发。基因泰克还收购了Jecure Therapeutics，Jecure Therapeutics同样手握大量临床前NLRP3抑制剂资产，并打算将其开发用于NASH、肝纤维化、痛风、炎症性肠病（IBD）和心血管疾病等炎症性疾病，Jecure的收购时间点要早于Inflazome（2017年），开发了一款JT002，目前处于临床前阶段，拟定用于炎症疾病。而基因泰克收购Jecure Therapeutics这个时间段，诺华也收购了另外一家手握NLRP3管线专利的公司IFM Therapeutics的分拆IFM Tre，并获得了IFM-2427（DFV-890），目前在健康受试者中，单剂量和多剂量DFV890的耐受性良好，长达14天，没有安全性或耐受性问题。 NodThera公司有诺和诺德基金和赛诺菲基金的资金支持，该公司先后开发了CP-456773的衍生物NT-0167和NT-0796。NT-0167后来似乎因为迭代到NT-0796而遭到搁置，NT-0796倒是展现出了一定减重潜力。今年6月发布的数据显示，NT-0796可有效减少患者体内C反应蛋白（CRP）水平，并造成患者体重显著减少。而此次的Ventyx Biosciences正是NLRP3抑制剂在肥胖领域的较早验证，目前临床前的数据表明，VTX3232具有一定的减重效果，但相比司美格鲁肽差距较大，与司美格鲁肽联用减重效果有一定提升。总的来说，目前NLRP3抑制剂的开发前景还不明朗，目前临床前数据表明，确实可以有一定减重效果，但需要和司美格鲁肽联用，是否联用能拓宽一些市场值得未来期待。参考来源： Tang F, Kunder R, Chu T, Hains A, Nguyen A, McBride JM, Zhong Y, Santagostino S, Wilson M, Trenchak A, Chen L, Ly J, Moein A, Lewin-Koh N, Raghavan V, Osaghae U, Wynne C, Owen R, Place D. First-in-human phase 1 trial evaluating safety, pharmacokinetics, and pharmacodynamics of NLRP3 inflammasome inhibitor, GDC-2394, in healthy volunteers. Clin Transl Sci. 2023 Sep;16(9):1653-1666. doi: 10.1111/cts.13576. Epub 2023 Jul 23. PMID: 37350225; PMCID: PMC10499406. 王哲,孙诚.NLRP3炎性体在肥胖及其代谢综合征中的研究进展[J].中国细胞生物学学报,2024,46(09):1730-1736. McBride C, Trzoss L, Povero D, Lazic M, Ambrus-Aikelin G, Santini A, Pranadinata R, Bain G, Stansfield R, Stafford JA, Veal J, Takahashi R, Ly J, Chen S, Liu L, Nespi M, Blake R, Katewa A, Kleinheinz T, Sujatha-Bhaskar S, Ramamoorthi N, Sims J, McKenzie B, Chen M, Ultsch M, Johnson M, Murray J, Ciferri C, Staben ST, Townsend MJ, Stivala CE. Overcoming Preclinical Safety Obstacles to Discover (S)-N-((1,2,3,5,6,7-Hexahydro-s-indacen-4-yl)carbamoyl)-6-(methylamino)-6,7-dihydro-5H-pyrazolo[5,1-b][1,3]oxazine-3-sulfonamide (GDC-2394): A Potent and Selective NLRP3 Inhibitor. J Med Chem. 2022 Nov 10;65(21):14721-14739. doi: 10.1021/acs.jmedchem.2c01250. Epub 2022 Oct 24. PMID: 36279149. Ambrus-Aikelin G, Takeda K, Joetham A, Lazic M, Povero D, Santini AM, Pranadinata R, Johnson CD, McGeough MD, Beasley FC, Stansfield R, McBride C, Trzoss L, Hoffman HM, Feldstein AE, Stafford JA, Veal JM, Bain G, Gelfand EW. JT002, a small molecule inhibitor of the NLRP3 inflammasome for the treatment of autoinflammatory disorders. Sci Rep. 2023 Aug 19;13(1):13524. doi: 10.1038/s41598-023-39805-z. Erratum in: Sci Rep. 2023 Nov 16;13(1):20081. doi: 10.1038/s41598-023-47251-0. PMID: 37598239; PMCID: PMC10439952. 内容来源于网络，如有侵权，请联系删除。

并购临床研究

2023-02-06

·FierceBiotech

Ex-Shire drug improves outcomes in autoimmune disease, setting Certa on path to phase 3

Certa CEO and founder Darren Kelly (Medical Research Commercialisation Fund) Certa Therapeutics’ attempt to resurrect an ex-Shire drug has delivered midphase data. Nine years after Shire paid $75 million to acquire FT011, the Australian biotech has linked the candidate to improvements in the symptoms of a rare autoimmune disease in a small clinical trial. FT011 is a derivative of tranilast, an anti-fibrotic agent used in the treatment of scars and skin disorders. By improving on the potency of tranilast, while dialing down its cellular toxicity, Australian researchers tried to create a molecule capable of treating diseases including diabetic nephropathy. The work led to the formation of Fibrotech and later its acquisition by Shire for $75 million plus milestones. Shire subsequently walked away from FT011, enabling some of the people behind Fibrotech to form Certa and have a second crack at developing the molecule. Certa picked scleroderma, a rare autoimmune disease associated with thickened areas of skin, as its lead indication and entered phase 2 in 2021. Investigators randomized 30 patients to receive one of two oral daily doses of FT011 or placebo for 12 weeks. While the primary endpoints looked at levels of two dose regimens of the molecule in plasma, Certa’s statement focused on the measures of efficacy analyzed across multiple secondary endpoints. According to Certa, 60% of patients in the high-dose arm had a “clinically meaningful improvement,” resulting in a p-value versus placebo of 0.019. Certa defined a score of 0.6 or greater on the 0 to 1 CRISS scale as clinically meaningful. Twenty percent of participants in the low-dose cohort experienced such an improvement. Three patients across the two FT011 arms scored 1.0 on the scale. Certa also reported improvements on a skin score, a disability index and the global physician assessment, leading CEO and founder Darren Kelly to give a bullish take on the data and the prospects of FT011. “These exceptional trial results demonstrate the potential of this novel treatment for patients with scleroderma,” Kelly said in a statement. “The changes seen in CRISS score, lung function and physician reported outcomes in addition to the patient reported outcomes within such a short treatment timeframe of 12 weeks, is unprecedented and paves the way for a confirmatory global phase 3 study.” The phase 3 trial will provide a sterner test of FT011. Success would position Certa to address an unmet medical need. Boehringer Ingelheim’s Ofev and Roche’s Actemra are used in the treatment of interstitial lung disease linked to scleroderma, but other therapies are needed. Horizon Therapeutics is among the other companies trying to address the unmet need.

临床结果并购临床3期临床2期

2022-08-10

·生物谷

趁热吃，会致癌，中科院广州生物院李志远团队揭示背后的分子机制

该研究首次发现瞬时受体电位离子通道香草素亚型2（TRPV2）反复受热或激动剂作用可激活HSP70/27和PI3K/Akt/mTOR信号通路。食管癌是高发的恶性肿瘤之一，严重威胁居民生命健康。据世界卫生组织国际癌症研究署（IARC）发布的2020年全球癌症负担数据，食管癌是世界年新增人数第8，年死亡人数第6的恶性肿瘤。而且，食管癌在中国尤为突出，全球每年新增和死亡的食管癌，均有超过一半在中国。已知食管癌的发病及进展与多基因异常有关，而外界环境因素特别是高温饮食被认为是引起食管鳞癌的主要风险因素之一，高温饮食往往使食管黏膜经受频繁、反复的热刺激，导致食管黏膜上皮细胞功能变异风险增加。实际上，高热刺激已被国际癌症研究署列为食管癌的二类病因之一，但目前对其内在分子机制知之甚少。近日，中国科学院广州生物医药与健康研究院李志远团队在 British Journal of Cancer 期刊发表了题为：Thermal stress involved in TRPV2 promotes tumorigenesis through the pathways of HSP70/27 and PI3K/Akt/mTOR in esophageal squamous cell carcinoma 的研究论文。该研究首次发现瞬时受体电位离子通道香草素亚型2（TRPV2）反复受热或激动剂作用可激活HSP70/27和PI3K/Akt/mTOR信号通路，在体外实验中可显著促进食管鳞癌细胞的恶性行为，在体内则可显著促进食管鳞癌的成瘤和扩散。这揭示了热敏型TRPV2通道在食管鳞癌发生发展过程中的重要作用，并为食管鳞癌的防治提出了新方向。李志远研究团队基于多年对瞬时受体电位离子通道（TRP）的研究，检测了热敏型TRPV在人食管鳞状上皮细胞的表达和功能，发现与非瘤组织相比，食管鳞癌（ESCC）细胞和临床ESCC样本中的TRPV2表达均明显上调，钙成像实验证实其功能活动相应增强。进一步研究发现，以激活TRPV2通道的热（54°C）对ESCC细胞进行短暂而频繁的刺激后，在体外实验中可明显增强ESCC细胞的增殖、侵袭和促血管生成等恶性细胞行为，而体内实验则可显著促进裸鼠皮下成瘤和尾静脉注射的肿瘤转移。研究使用TRPV2特异激活剂O1821作用于ESCC细胞后，也取得类似结果。反之，TRPV2拮抗剂Tranilast的应用或经CRISPR-Cas9方法敲除ESCC细胞的TRPV2基因后，上述的ESCC致瘤作用均显著减弱。另外，研究将TRPV2过表达于非瘤食管鳞状细胞NE2后，以热（54°C）和O1821对NE2细胞进行短暂而频繁的作用后可显著促进NE2的增殖，使其呈现侵袭性并在裸鼠皮下成瘤，说明过表达过激活的TRPV2可使非肿瘤细胞转向肿瘤化。在机制上，TRPV2在ESCC细胞经热应激激活后可上调细胞的热休克因子1（HSF1）并促进热休克蛋白70和27（HSP70/27）的转录表达，从而促进ESCC的成瘤性；同时PI3K在此过程中显著激活，进而激活其下游信号蛋白PDK1，随后PDK1上调靶蛋白AKT1和mTORC1的功能，反之，PI3K的负调控蛋白PTEN受到下调抑制，说明PI3K信号被PTEN放大，从而显著促进ESCC的成瘤性和侵袭力。激活的TRPV2还上调Akt蛋白的S473和T308位点的磷酸化水平，而p-mTOR（S2448）和效应蛋白磷酸化水平p-p70S6K（T389）和p-4EBP1（S65）均相应提升，而Tranilast的应用或TRPV2基因敲除则抑制上述作用。热应激参与TRPV2促进食管鳞状细胞癌的肿瘤发生示意图该研究还发现，pan-PI3K/mTOR激酶抑制剂VS5584和Oroxin B可显著抑制TRPV2过激活的ESCC细胞增殖，两者与Tranilast合用可进一步削弱ESCC细胞的增殖能力，提示Tranilast联合pan-PI3K/mTOR抑制剂可能可用于ESCC的治疗。多因素生存分析提示TPRV2高表达是ESCC患者预后不良的独立因素，表明TRPV2有望成为ESCC不良预后的生物标志物和新的治疗靶点。值得注意的是，该研究发现的TRPV2通道的激活温度54°C，低于许多人群中的膳食温度，也远低于国际癌症研究署建议的高温饮食风险温度（65°C），因此该研究为食管鳞癌的防治提出了新方向。

100 项与曲尼司特相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D02027	曲尼司特	R	DB07615

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
哮喘	中国	Kissei Pharmaceutical Co., Ltd.	2011-02-28
特应性皮炎	中国	Kissei Pharmaceutical Co., Ltd.	2011-02-28
变应性结膜炎	日本	ROHTO NITTEN Co., Ltd.	1995-09-29
变应性结膜炎	日本	Kissei Pharmaceutical Co., Ltd.	1995-09-29

未上市

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适应症	最高研发状态	国家/地区	公司	日期
翼状胬肉	临床3期	巴西	Faculdade de Medicina de São José do Rio Preto	2015-01-01
类风湿关节炎	药物发现	塞尔维亚	Nuon Therapeutics, Inc.	2009-03-01
类风湿关节炎	药物发现	墨西哥	Nuon Therapeutics, Inc.	2009-03-01
类风湿关节炎	药物发现	阿根廷	Nuon Therapeutics, Inc.	2009-03-01
类风湿关节炎	药物发现	英国	Nuon Therapeutics, Inc.	2009-03-01
类风湿关节炎	药物发现	德国	Nuon Therapeutics, Inc.	2009-03-01

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临床结果

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


UEGW2023	N/A	-	-	Tranilast (Irradiation Group)	(構淵衊淵範範憲廠襯顧) = 獵獵鹽顧積繭選廠積淵顧窪膚獵範餘遞製蓋襯 (糧網鹽積醖齋繭糧製壓 ) 更多	-	2023-10-15
UEGW2023	N/A	-	-	Tranilast Pre-treated Irradiation Group	(構淵衊淵範範憲廠襯顧) = 餘遞鑰製醖憲糧廠顧築顧窪膚獵範餘遞製蓋襯 (糧網鹽積醖齋繭糧製壓 ) 更多	-	2023-10-15
ACR2012	N/A	皮肌炎 TIF-g \| NXP-2	111	NXP-2 (Antibodies to TIF-g)	積願壓淵膚醖憲選蓋襯(餘製襯糧蓋蓋膚壓窪糧) = 醖構餘廠遞鑰範壓鹹膚夢鹽衊願鏇網窪鏇膚獵 (襯憲憲鑰齋繭鏇齋蓋餘 )	-	2012-11-09
ASTRO2006	N/A	辐射损伤	-	Tranilast 100mg/kg	鑰遞選蓋願膚醖衊壓鬱(齋膚襯鑰窪遞範窪觸鏇) = 襯鑰齋壓夢淵築網遞築觸鹽鬱觸壓窪醖膚鏇夢 (觸艱繭夢鏇鑰製蓋鏇鹹 )	-	2006-11-01
ASTRO2006	N/A	辐射损伤	-	Vehicle	鑰遞選蓋願膚醖衊壓鬱(齋膚襯鑰窪遞範窪觸鏇) = 繭選觸製願顧遞鏇獵壓觸鹽鬱觸壓窪醖膚鏇夢 (觸艱繭夢鏇鑰製蓋鏇鹹 )	-	2006-11-01
ARVO2006	N/A	-	4	Tranilast 12.5 µg/ml	淵選艱鹹夢簾憲選襯蓋(願壓餘醖構顧獵壓壓醖) = 築鹽衊鹽艱築遞鏇蓋構範衊築糧衊選鹹齋繭餘 (鹽遞構壓獵鹽網醖鹹鹹 )	积极	2006-05-01
NCT01003613 (Pubmed)	临床3期	-	32	Tranilast	淵簾艱網夢築積繭鹹膚(夢壓窪鹽選壓壓糧膚簾) = 艱鹽選選積醖壓蓋願醖鏇壓鏇艱遞鏇衊鬱膚鹹 (膚鹹鬱構遞膚鬱簾鹹憲 ) 更多	-	2004-03-01