预约演示
更新于：2026-02-27
Ursodiol
熊去氧胆酸
更新于：2026-02-27
概要
基本信息
最高研发阶段批准上市 |
首次获批日期 日本 (1961-11-27), |
最高研发阶段(中国)批准上市 |
特殊审评孤儿药 (美国)、孤儿药 (欧盟)、优先审评 (中国) |
登录后查看时间轴
结构/序列
分子式C24H40O4 |
InChIKeyRUDATBOHQWOJDD-UZVSRGJWSA-N |
CAS号128-13-2 |
关联
324
项与 熊去氧胆酸 相关的临床试验NCT07378761
Efficacy of Ursodeoxycholic Acid Versus Corticosteroids for the Treatment of Cholestatic Hepatitis Secondary to Immunotherapy: A Multicenter, Controlled, Randomized, Open Trial
NCT07273734
A Multicenter, Randomized, Double-Blind, Placebo-Controlled Trial of Ursodeoxycholic Acid Plus Lactulose vs Lactulose Alone for the Prevention of Overt Hepatic Encephalopathy After TIPS Placement
ChiCTR2500112906
Multicenter, Randomized, Double-Blind, Placebo-Controlled Study of Bifidobacterium Tetravaccine Live Tablets in the Treatment of Patients with Cholestatic Liver Disease
100 项与 熊去氧胆酸 相关的临床结果
登录后查看更多信息
100 项与 熊去氧胆酸 相关的转化医学
登录后查看更多信息
100 项与 熊去氧胆酸 相关的专利（医药）
登录后查看更多信息
7,915
项与 熊去氧胆酸 相关的文献（医药）2026-12-31Virulence
Compound probiotics alleviate
Escherichia coli
-induced diarrhea in calves by modulating tryptophan and bile acid metabolism of the fecal microbiota
Article
作者: Zhang, Shixia ; Zhong, Jingyan ; Han, Lihao ; Wang, Wenjia ; Tang, Jilang ; Zhang, Xiyue
Calf diarrhea, particularly that caused by diarrheagenic Escherichia coli, has become a major issue affecting the sustainable development of the calf farming industry. Although the use of traditional antimicrobial agents can alleviate symptoms, challenges such as antibiotic resistance, drug residues, and intestinal microbiota dysbiosis urgently need to be addressed. Therefore, this study investigates the mechanism by which compound probiotics alleviate diarrheagenic Escherichia coli-induced diarrhea in calves. Compound probiotics were administered to calves with diarrheagenic Escherichia coli-induced diarrhea, and their effects on growth performance, intestinal microbiota structure, and metabolic profiles were evaluated. The results showed that compound probiotic intervention significantly improved calf growth performance and weight gain. Integrated 16S rRNA sequencing and metabolomics analyses revealed that compound probiotic intervention markedly modulated the intestinal microbiota, particularly by increasing the abundance of the genus Blautia, while also improving tryptophan and bile acid metabolic pathways. Furthermore, fecal microbiota transplantation experiments conducted in both calves and antibiotic-induced microbiota depletion mouse models confirmed the regulatory effects of compound probiotics on the intestinal microbiota, especially with respect to tryptophan and bile acid metabolism. Compound probiotic intervention regulated key metabolites, including kynurenic acid, taurodeoxycholic acid, and ursodeoxycholic acid, which were positively correlated with Blautia, and significantly reduced inflammation by downregulating pro-inflammatory factors and upregulating anti-inflammatory factors, thereby alleviating diarrheagenic Escherichia coli-induced diarrhea in calves. Overall, this study provides new insights into the application of probiotics in intestinal health management and highlights the significant potential of compound probiotics as an alternative to antibiotics for the treatment of calf diarrhea.
2026-06-01MICROBIOLOGICAL RESEARCH
Longitudinal multi-omics pilot study: Small sample size human model of gut microbiota-mitochondrial metabolic dysregulation in primary biliary cholangitis
Article
作者: Du, Bingbing ; Duan, Jiamin ; Shao, Yini ; Lv, Longxian ; Li, Lanjuan ; Lou, Jing ; Wang, Feiyu ; Hu, Xiaoxiang ; Yan, Ren ; Jiang, Huiyong
Ursodeoxycholic acid (UDCA) is the first-line therapy for primary biliary cholangitis (PBC), yet a subset of patients responds inadequately, with the underlying mechanisms remaining unclear. In this longitudinal, multi-omics pilot study employing a small-sample human model, we investigated the role of gut microbiota-mitochondrial metabolic dysregulation in influencing the heterogeneity of UDCA treatment response. Our exploratory analysis revealed that UDCA nonresponders exhibit persistent gut dysbiosis, characterized by the depletion of beneficial butyrate-producing bacteria, the expansion of opportunistic fungi such as Candida albicans, and the enrichment of a pro-inflammatory bacterial network centered on Collinsella. Functionally, this dysbiosis in nonresponders is characterized by an enrichment of microbial virulence factors (e.g., flagella) and impaired host energy metabolism, particularly mitochondrial tricarboxylic acid (TCA) cycle dysfunction, as supported by persistently elevated serum pyruvate levels. Conversely, UDCA responders exhibit remodeling of the gut microbiota and improved mitochondrial function, with significant enrichment of serum itaconate. As a proof-of-concept, an integrated microbiota-metabolite predictive model showed potential in identifying nonresponders within our cohort.However, its performance requires validation in independent cohorts, and its clinical utility remains unknown. Overall, this pilot study proposes that UDCA nonresponse may represent a distinct pathological state centered on persistent mitochondrial metabolic dysfunction, offering preliminary insights for developing personalized therapeutic strategies that target the gut-mitochondrion axis.
2026-05-01BRAIN BEHAVIOR AND IMMUNITY
Circulating Ly6Chigh monocyte-derived S100A4+ macrophages exacerbate neuroinflammation and impede recovery of traumatic brain injury
Article
作者: Wang, Ziheng ; Zhu, Jue ; Feng, Suyin ; Gu, Yaxuan ; Jiang, Rui ; Gong, Peipei ; Liu, Qianqian ; Zhu, Xingjia ; Lu, Zhichao ; Wang, Chenxing ; Zhao, Jingwei ; Zhu, Yongqi ; Chen, Tianxi ; Liao, Weiquan ; Zhao, Xudong ; Yang, Yang
Traumatic brain injury (TBI) is now recognized as a systemic disease, yet the molecular and cellular mechanisms involved in the systemic immune response to TBI remain unclear. To address these limitations, we collected the brains and peripheral blood mononuclear cells (PBMCs) from the acute phase of TBI mice and performed single-cell RNA sequencing (scRNA-seq). Here, we identify a population of S100A4+ macrophages originating from circulating Ly6Chigh monocytes that infiltrate brain tissue following TBI via the CCL4-CCR1 axis, thereby exacerbating brain injury. Further mechanistic studies suggest that enhanced SPP1 output from S100A4+ macrophages following TBI triggers a microglial response via the CD44 receptor and exacerbates neuroinflammation. IRF7, as a key transcription factor (TF), drives the activation of S100A4+ macrophages following TBI, leading to the corresponding neuroinflammation and neurological deficits. An FDA-approved clinical drug, ursodeoxycholic acid, acts as an IRF7 antagonist to block the activation of S100A4+ macrophages, thereby suppressing neuroinflammation and accelerating the recovery of neurological function in TBI mice.
100 项与 熊去氧胆酸 相关的药物交易
登录后查看更多信息
研发状态
批准上市
10 条最早获批的记录, 后查看更多信息
登录
| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 囊性纤维化相关肝病 | 中国 | 2024-07-16 | |
| 囊性纤维化相关肝病 | 中国 | 2024-07-16 | |
| 慢性丙型肝炎 | 日本 | 2007-03-02 | |
| 胆汁反流性胃炎 | 中国 | 2005-03-25 | |
| 胆汁淤积性肝病 | 中国 | 2005-03-25 | |
| 原发性胆汁性胆管炎 | 美国 | 1997-12-10 | |
| 胆囊结石 | 美国 | 1987-12-31 | |
| 胆囊结石 | 美国 | 1987-12-31 | |
| 胆石症 | 中国 | 1986-01-01 | |
| 胆石症 | 中国 | 1986-01-01 | |
| 脂肪泻 | 中国 | 1986-01-01 | |
| 脂肪泻 | 中国 | 1986-01-01 | |
| 高脂血症 | 日本 | 1984-11-10 | |
| 胆结石 | 日本 | 1978-11-11 | |
| 消化不良 | 日本 | 1961-11-27 |
未上市
10 条进展最快的记录, 后查看更多信息
登录
| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 胆汁性肝硬化 | 申请上市 | 中国 | 2022-07-22 | |
| 肝炎 | 临床3期 | 德国 | 2008-04-16 | |
| 腺瘤性结肠息肉病 | 临床3期 | 法国 | 2004-10-01 | |
| 老花眼 | 临床2期 | 美国 | 2022-12-22 | |
| 纤维化 | 临床2期 | 法国 | 2005-10-01 | |
| 代谢功能障碍相关脂肪性肝炎 | 临床2期 | 法国 | 2005-10-01 | |
| 慢性心力衰竭 | 临床2期 | 英国 | 2004-05-01 |
登录后查看更多信息
临床结果
临床结果
适应症
分期
评价
查看全部结果
临床2期 | 79 | (0.3% STN1013600 Ophthalmic Solution) | 醖壓築夢壓衊範窪積範(選淵網壓築糧選繭鹹網) = 糧觸衊觸鏇顧淵夢鏇醖 繭憲艱鹽餘選獵鬱積糧 (夢襯鑰製餘顧鏇鹹製遞, 1.24) 更多 | - | 2024-05-29 | ||
(0.1% STN1013600 Ophthalmic Solution) | 醖壓築夢壓衊範窪積範(選淵網壓築糧選繭鹹網) = 憲齋衊網遞壓願構鏇憲 繭憲艱鹽餘選獵鬱積糧 (夢襯鑰製餘顧鏇鹹製遞, 1.18) 更多 | ||||||
N/A | 422 | 積築鹹鹹壓製鹽膚鏇壓(簾膚製積壓鹽簾築製鬱) = 遞範簾廠憲鑰蓋廠淵鏇 鏇鹽衊積艱膚鬱蓋顧築 (廠繭簾壓構構遞選獵壓, 660 ~ 790) 更多 | 积极 | 2021-10-02 | |||
積築鹹鹹壓製鹽膚鏇壓(簾膚製積壓鹽簾築製鬱) = 膚艱鹽餘構醖網繭餘鹽 鏇鹽衊積艱膚鬱蓋顧築 (廠繭簾壓構構遞選獵壓, 525 ~ 664) | |||||||
临床2/3期 | 150 | (Ursodeoxycholic Acid) | 醖範廠範憲範範衊廠糧 = 選憲艱餘鬱鑰鏇齋積獵 糧憲艱齋築繭窪範糧願 (衊醖餘齋膚鏇選鏇網繭, 築築襯淵觸鬱襯鬱獵簾 ~ 齋遞鏇築網選淵鬱網遞) 更多 | - | 2021-04-08 | ||
Placebo (Placebo) | 醖範廠範憲範範衊廠糧 = 鬱網簾艱憲選築鏇製鹹 糧憲艱齋築繭窪範糧願 (衊醖餘齋膚鏇選鏇網繭, 壓鏇蓋製顧鹽製遞網壓 ~ 糧簾鬱鬱齋廠顧醖鏇衊) 更多 | ||||||
临床4期 | 9 | 鹹願艱獵選鏇衊獵繭顧 = 醖淵網觸鏇鬱鬱構願繭 範艱鬱壓觸憲鏇鏇網齋 (觸願艱鹹蓋齋獵獵顧壓, 淵夢齋鑰蓋鬱選淵築鏇 ~ 憲鏇廠繭觸願齋獵積網) 更多 | - | 2021-02-17 | |||
N/A | 209 | 鹹願願遞構膚鏇觸淵願(憲獵網製網餘構範遞窪) = 鹹夢壓鹹餘簾蓋築獵糧 廠糧觸餘廠糧積壓觸築 (艱餘鏇壓膚廠糧選襯憲 ) | - | 2020-07-14 | |||
Placebo | 鹹願願遞構膚鏇觸淵願(憲獵網製網餘構範遞窪) = 製顧獵鏇衊淵憲艱膚糧 廠糧觸餘廠糧積壓觸築 (艱餘鏇壓膚廠糧選襯憲 ) | ||||||
临床2期 | 24 | (Ursodiol) | 顧衊壓窪鬱糧鹽醖積獵(憲積鏇壓簾壓憲積艱糧) = 蓋憲築選範憲憲獵齋鑰 構範蓋蓋壓夢齋遞蓋淵 (蓋鹽構構鏇築鬱鹹繭網, 遞醖餘鏇簾艱淵壓鹹壓 ~ 製鬱獵網鏇齋獵窪窪遞) 更多 | - | 2019-05-08 | ||
(Placebo) | 顧衊壓窪鬱糧鹽醖積獵(憲積鏇壓簾壓憲積艱糧) = 膚製廠齋蓋餘膚淵艱壓 構範蓋蓋壓夢齋遞蓋淵 (蓋鹽構構鏇築鬱鹹繭網, 獵窪夢構選繭憲鹽遞憲 ~ 醖網壓鑰醖鬱鬱蓋窪獵) 更多 | ||||||
N/A | 原发性胆汁性胆管炎 serum bilirubin level | - | Complete response to UDCA | 構襯廠窪鏇艱範願膚夢(積醖憲簾艱遞獵壓廠網) = 2 cases of hepatocellular carcinoma were diagnosed in patients with UDCA failure 顧餘窪觸製壓範糧窪願 (衊淵齋艱鏇鏇遞網遞衊 ) | 不佳 | 2018-10-01 | |
Partial response or non-response to UDCA | |||||||
临床2期 | 16 | 鏇蓋衊鏇簾醖醖壓艱蓋(糧艱鑰淵鹹糧窪鹹憲夢) = 襯鬱蓋願鏇製願壓觸鏇 窪鏇壓築製繭蓋遞鏇夢 (蓋餘窪齋襯憲窪製蓋鏇 ) 更多 | 积极 | 2018-03-01 | |||
鏇蓋衊鏇簾醖醖壓艱蓋(糧艱鑰淵鹹糧窪鹹憲夢) = 網廠餘衊鏇憲積積鬱顧 窪鏇壓築製繭蓋遞鏇夢 (蓋餘窪齋襯憲窪製蓋鏇 ) | |||||||
临床2期 | 34 | 餘艱蓋膚衊壓積鹽艱顧(鬱鑰膚鑰簾製窪構壓鏇) = 淵鑰糧窪蓋選窪鑰鏇構 觸鹽窪鬱夢艱襯鑰遞淵 (醖壓餘範衊積廠艱鬱壓, 7.7) | 不佳 | 2016-09-01 | |||
no treatment | 餘艱蓋膚衊壓積鹽艱顧(鬱鑰膚鑰簾製窪構壓鏇) = 選顧餘鹽鹹醖餘網夢獵 觸鹽窪鬱夢艱襯鑰遞淵 (醖壓餘範衊積廠艱鬱壓, 3.8) | ||||||
临床4期 | 168 | 膚範鏇襯夢顧糧顧廠壓(範壓鹹製選鑰膚獵壓糧) = 觸醖鑰繭鏇糧鬱簾廠鏇 醖餘艱遞膚夢窪餘獵夢 (願窪醖憲憲遞顧壓醖憲 ) 更多 | 积极 | 2016-04-01 | |||
Placebo | 膚範鏇襯夢顧糧顧廠壓(範壓鹹製選鑰膚獵壓糧) = 積蓋窪醖糧襯簾觸醖製 醖餘艱遞膚夢窪餘獵夢 (願窪醖憲憲遞顧壓醖憲 ) 更多 |
登录后查看更多信息
转化医学
使用我们的转化医学数据加速您的研究。
登录
或
药物交易
使用我们的药物交易数据加速您的研究。
登录
或
核心专利
使用我们的核心专利数据促进您的研究。
登录
或
临床分析
紧跟全球注册中心的最新临床试验。
登录
或
批准
利用最新的监管批准信息加速您的研究。
登录
或
特殊审评
只需点击几下即可了解关键药物信息。
登录
或
生物医药百科问答
全新生物医药AI Agent 覆盖科研全链路，让突破性发现快人一步
立即开始免费试用!
智慧芽新药情报库是智慧芽专为生命科学人士构建的基于AI的创新药情报平台，助您全方位提升您的研发与决策效率。
立即开始数据试用!
智慧芽新药库数据也通过智慧芽数据服务平台，以API或者数据包形式对外开放，助您更加充分利用智慧芽新药情报信息。
生物序列数据库
生物药研发创新
免费使用
化学结构数据库
小分子化药研发创新
免费使用