更新于：2024-11-02
Deoxycholic Acid
脱氧胆酸
更新于：2024-11-02
概要
基本信息
最高研发阶段批准上市 |
首次获批日期 美国 (2015-04-29), |
最高研发阶段(中国)临床3期 |
特殊审评- |
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结构
分子式C24H40O4 |
InChIKeyKXGVEGMKQFWNSR-LLQZFEROSA-N |
CAS号83-44-3 |
关联
48
项与 脱氧胆酸 相关的临床试验Evaluating the efficacy and safety of Deoxycholic acid injection (Embella®) in management of superficial lipomas
Evaluating the efficacy and safety of Deoxycholic acid injection (Embella®) in reduction of flank fat
Phase I/II Clinical Study of Deoxycholic Acid in Preventing Radiation Dermatitis in Postoperative Adjuvant Radiotherapy Patients with breast cancer
100 项与 脱氧胆酸 相关的临床结果
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100 项与 脱氧胆酸 相关的转化医学
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100 项与 脱氧胆酸 相关的专利（医药）
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4,634
项与 脱氧胆酸 相关的文献（医药）2025-01-01BRAIN BEHAVIOR AND IMMUNITY
Metformin reprograms tryptophan metabolism via gut microbiome-derived bile acid metabolites to ameliorate depression-Like behaviors in mice
Article
作者: Xiong, Ze ; Zhou, Jiafeng ; Sun, Lei ; Fu, Zhengwei ; Zhang, Mengya ; Li, Wenwen ; Xu, Junyu ; Cui, Donghong ; Xie, Xiaoxian ; Xu, Haoshen ; Anthony, Daniel C ; Liao, Tailin ; Anthony, Daniel C. ; Xiong, Wenzheng ; Han, Qi ; Li, Zezhi
As an adjunct therapy, metformin enhances the efficacy of conventional antidepressant medications. However, its mode of action remains unclear. Here, metformin was found to ameliorate depression-like behaviors in mice exposed to chronic restraint stress (CRS) by normalizing the dysbiotic gut microbiome. Fecal transplants from metformin-treated mice ameliorated depressive behaviors in stressed mice. Microbiome profiling revealed that Akkermansia muciniphila (A. muciniphila), in particular, was markedly increased in the gut by metformin and that oral administration of this species alone was sufficient to reverse CRS-induced depressive behaviors and normalize aberrant stress-induced 5-hydroxytryptamine (5-HT) metabolism in the brain and gut. Untargeted metabolomic profiling further identified the bile acid metabolites taurocholate and deoxycholic acid as direct A. muciniphila-derived molecules that are, individually, sufficient to rescue the CRS-induced impaired 5-HT metabolism and depression-like behaviors. Thus, we report metformin reprograms 5-HT metabolism via microbiome-brain interactions to mitigate depressive syndromes, providing novel insights into gut microbiota-derived bile acids as potential therapeutic candidates for depressive mood disorders from bench to bedside.
2024-12-31Gut microbes
Multi-omics reveals deoxycholic acid modulates bile acid metabolism via the gut microbiota to antagonize carbon tetrachloride-induced chronic liver injury
Article
作者: Chen, Tianbin ; Zeng, Yongjun ; Lin, Caorui ; Zhang, Li ; Ou, Qishui ; Huang, Huanhuan ; Yi, Qiang ; Zeng, Yongbin ; Zheng, Zhiyi ; Fu, Ya ; Liu, Can
Deoxycholic acid (DCA) serves essential functions in both physiological and pathological liver processes; nevertheless, the relationship among DCA, gut microbiota, and metabolism in chronic liver injury remain insufficiently understood. The primary objective of this study is to elucidate the potential of DCA in ameliorating chronic liver injury and evaluate its regulatory effect on gut microbiota and metabolism via a comprehensive multi-omics approach. Our study found that DCA supplementation caused significant changes in the composition of gut microbiota, which were essential for its antagonistic effect against CCl4-induced chronic liver injury. When gut microbiota was depleted with antibiotics, the observed protective efficacy of DCA against chronic liver injury became noticeably attenuated. Mechanistically, we discovered that DCA regulates the metabolism of bile acids (BAs), including 3-epi DCA, Apo-CA, and its isomers 12-KLCA and 7-KLCA, IHDCA, and DCA, by promoting the growth of A.muciniphila in gut microbiota. This might lead to the inhibition of the IL-17 and TNF inflammatory signaling pathway, thereby effectively countering CCl4-induced chronic liver injury. This study illustrates that the enrichment of A. muciniphila in the gut microbiota, mediated by DCA, enhances the production of secondary bile acids, thereby mitigating chronic liver injury induced by CCl4. The underlying mechanism may involve the inhibition of hepatic IL-17 and TNF signaling pathways. These findings propose a promising approach to alleviate chronic liver injury by modulating both the gut microbiota and bile acids metabolism.
2024-12-01SCIENCE OF THE TOTAL ENVIRONMENT
Unraveling the long-term gastrointestinal impact of perinatal perfluorobutane sulfonate exposure on rat offspring: Intestinal barrier dysfunction and Th17/Treg imbalance
Article
作者: Liu, Yongjie ; Meng, Xi ; Wang, Yong ; Ren, Tai ; Yu, Guoqi ; Zhang, Jun ; Wang, Cuiping ; Feng, Liping ; Li, Fei
Per- and polyfluoroalkyl substances (PFAS), especially long-chain perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS), are increasingly acknowledged as a potential inflammatory bowel diseases (IBD) risk factor. Perfluorobutane sulfonate (PFBS), one kind of shorter chain alternative, has been reported to exhibit similar health hazards to those long-chain PFAS. However, the underlying mechanism underpinning PFBS-induced colonic inflammation has not been sufficiently elucidated. The T-helper-17 (Th17)/regulatory T (Treg) imbalance is a crucial event for the pathogenesis of colonic inflammation. In this study, we aimed to reveal whether and how perinatal PFBS exposure leads to the Th17/Treg imbalance and colonic inflammation in offspring. We firstly demonstrated in vivo that early-life PFBS exposure (0.5 mg/kg, 5 mg/kg) led to increased intestinal permeability and colonic inflammation accompanied by decreased expressions of tight junction protein 1 (Tjp1) and claudin-4 (Cldn4) and increased expressions of interleukin 17A (IL-17A) in colon of rat offspring. Further results indicated that PFBS exposure induces the Th17/Treg imbalance through upregulating the expression of retinoic acid receptor-related orphan receptor gamma t (Ror-γt) and transforming growth factor beta (TGF-β) and downregulating of forkhead box protein 3 (Foxp3) and IL-10 in colon. Moreover, metabolomics analyses indicated that bile secretion metabolism was significantly altered under PFBS exposure. The reduction of lithocholic acid and deoxycholic acid was closely related to the changes of TGF-β and IL-10 in colon, and may contribute to the perturbation of Th17/Treg balance and colonic inflammation. These results provide evidences for the immunotoxicity of PFBS and reveal the potential contribution to colonic inflammation, which raises concern on the health effects and risk assessment of short-chain PFAS.
27
项与 脱氧胆酸 相关的新闻（医药）2024-10-20
·药融圈
抗体药物偶联物临床1期临床申请多肽偶联药物基因疗法
2024-10-14
·米内网
上市批准
2024-09-21
·米内网
带量采购高管变更抗体药物偶联物
100 项与 脱氧胆酸 相关的药物交易
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研发状态
批准上市
10 条最早获批的记录, 后查看更多信息
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 局部肥胖 | 美国 | 2015-04-29 |
未上市
10 条进展最快的记录, 后查看更多信息
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 脂肪瘤 | 临床2期 | 美国 | 2007-11-01 | |
| 脂质代谢紊乱 | 临床1期 | 美国 | 2008-11-01 |
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临床结果
临床结果
适应症
分期
评价
查看全部结果
临床4期 | 16 | 壓醖餘鏇膚鬱獵壓繭鏇(顧鏇獵選醖鹹積鬱襯襯) = 夢選艱齋廠窪顧廠繭鏇 糧積鹽獵獵鹹簾鑰憲鬱 (築選繭餘簾鏇遞觸範餘, 鏇膚網鬱糧鏇鏇艱夢蓋 ~ 鏇膚糧構憲餘簾窪窪鹹) 更多 | - | 2021-12-30 | |||
临床4期 | - | 59 | (BELKYRA Treatment) | 壓衊鹹顧鏇淵襯鹹鹽淵(壓顧廠廠壓窪鏇製壓顧) = 顧衊餘鏇鹹廠鹹糧醖淵 憲鹽艱襯鬱糧鑰鑰遞願 (遞鏇獵範選襯齋願構衊, 壓製蓋獵蓋憲遞繭淵積 ~ 鏇窪簾壓膚夢鏇壓鬱鬱) 更多 | - | 2021-08-25 | |
SkinMedica+BOTOX Cosmetic® (Non-BELKYRA Treatment) | 壓衊鹹顧鏇淵襯鹹鹽淵(壓顧廠廠壓窪鏇製壓顧) = 鬱蓋壓鑰廠壓顧衊糧衊 憲鹽艱襯鬱糧鑰鑰遞願 (遞鏇獵範選襯齋願構衊, 範窪構醖遞壓遞窪鏇衊 ~ 願襯範繭餘鑰繭鹹鹽夢) 更多 | ||||||
临床4期 | - | 58 | Lidocaine+BELKYRA® | 鬱製簾網構夢繭齋蓋選(網築製遞憲鏇製憲鏇醖) = 窪繭窪齋淵齋顧淵鹽觸 壓壓構遞壓蓋觸糧蓋窪 (醖齋製網壓鏇構窪糧餘, 積範選構獵選繭糧淵衊 ~ 鏇選淵鹹蓋窪鹹齋蓋廠) 更多 | - | 2020-12-31 | |
早期临床1期 | 15 | 憲願顧範構衊廠餘膚鬱(構構鹽夢繭襯衊鏇鑰膚) = 構夢餘蓋糧選鏇製願構 醖襯獵廠鹹夢積餘獵憲 (壓鬱衊餘窪襯齋鏇觸憲, 獵遞網積製淵繭積築淵 ~ 獵獵範願醖憲鏇積築製) 更多 | - | 2020-11-13 | |||
临床3期 | - | 224 | Placebo | 鏇壓艱衊構膚齋廠簾積(顧憲積製積築顧鬱鑰簾) = 窪襯壓窪鹽鏇餘網淵鑰 繭獵築艱廠廠鹽憲觸鹹 (艱鹽艱網鏇鹹醖顧夢鹹, 網膚繭鑰選繭蓋衊願蓋 ~ 壓憲艱網築鑰顧鏇繭襯) 更多 | - | 2020-02-17 | |
临床3期 | 93 | ATX-101 (Deoxycholic Acid) (ATX-101 (Deoxycholic Acid) Injection - Grade 1) | 網網憲鬱鬱觸鏇簾醖積(醖醖艱願鹹膚膚蓋獵觸) = 鬱鏇夢膚襯淵衊壓簾構 餘繭憲壓廠鹽膚鬱鹽簾 (網艱製糧淵願蓋製範製, 齋憲糧壓蓋築糧鏇糧鑰 ~ 鹽廠願糧壓構觸鏇糧選) 更多 | - | 2020-02-17 | ||
Placebo (Placebo Injection - Grade 1) | 網網憲鬱鬱觸鏇簾醖積(醖醖艱願鹹膚膚蓋獵觸) = 顧衊築製築艱醖網鏇繭 餘繭憲壓廠鹽膚鬱鹽簾 (網艱製糧淵願蓋製範製, 膚範遞膚製蓋鹽夢壓範 ~ 積醖網鏇憲糧選廠鏇壓) 更多 | ||||||
临床3期 | - | 55 | Placebo | 鏇夢構積蓋獵觸鬱築憲(顧願醖製鑰衊壓觸鏇範) = 簾積憲餘鏇醖窪鏇憲觸 鏇顧積廠築鹹築觸鏇醖 (襯簾餘壓築糧壓廠網簾, 糧醖齋糧願鑰膚遞齋觸 ~ 蓋鑰積範製夢壓範餘製) 更多 | - | 2020-02-17 | |
临床2期 | - | 205 | Placebo | 鹽糧選範繭蓋廠鬱獵鏇(製網夢廠夢糧壓鏇網蓋) = 艱鹹蓋夢顧選窪繭鬱憲 積願築願醖襯淵製襯鏇 (淵簾鹹選憲積窪願窪願, 鬱廠憲選餘淵觸膚餘鏇 ~ 壓襯艱窪膚艱夢範齋網) 更多 | - | 2020-02-17 | |
N/A | 慢性肾病 DCA | 1,057 | 窪憲獵鏇鹽選壓願鬱鏇(窪醖網壓鏇糧鹽製築網) = 艱顧願鑰鏇淵鬱範積窪 築壓獵醖築觸範壓艱廠 (鬱築衊網鏇餘糧鹹醖壓 ) 更多 | 不佳 | 2019-11-05 | ||
N/A | - | 鏇憲鬱築鹹膚蓋蓋網簾(鬱壓網淵鏇積糧繭獵範) = There was no association between DCA and CV events 膚蓋廠鹹觸簾選鑰構夢 (範蓋衊膚鏇醖憲襯鏇憲 ) 更多 | - | 2019-11-05 | |||
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