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更新于：2026-01-10
Deoxycholic Acid
脱氧胆酸
更新于：2026-01-10
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)批准上市 |
特殊审评- |
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结构/序列
分子式C24H40O4 |
InChIKeyKXGVEGMKQFWNSR-LLQZFEROSA-N |
CAS号83-44-3 |
关联
47
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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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7,849
项与 脱氧胆酸 相关的文献（医药）2026-02-01ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
Microbial metabolite deoxycholic acid inhibits noncancerous NCM460 human colon cell proliferation: an inverse correlation between Bmal1:Clock gene expression and cell apoptosis
Article
作者: Liu, Zhenhua ; Zeng, Huawei ; Safratowich, Bryan D ; Briske-Anderson, Mary
High fat diets increase colonic deoxycholic acid (DCA) concentrations, which induce apoptosis, and subsequently enrich a compensatory DCA-resistant mutant colon cell subpopulation. While circadian Bmal1 and Clock genes are key regulators for cell proliferation, little is known about the relationship between DCA-induced apoptosis and circadian gene regulation in normal colon cells. In this study, we employed a noncancerous NCM460 human colon cell model to simulate the effect of DCA on cell proliferation in the colon and hypothesized that DCA-induced apoptosis is regulated by the Bmal1Clock complex in colon cells. Compared to the control cells, the treatment with DCA at 0.3- and 0.4-mM inhibited cell proliferation (via cell cycle arrest and apoptosis) by 19 % and 29 %, respectively. As the Bmal1Clock complex and Wnt signaling pathways are interlinked with apoptotic processes, we identified that 42 genes were differentially expressed in the Wnt signaling pathway; and there was a decrease (≥47 %) in Bmal1, Clock and Wee1 protein levels but an increase (≥172 %) in Rev-Erbα protein levels in DCA-treated cells compared to the control cells. At clinical levels, the mRNA levels of Bmal1 and Rev-Erbα were decreased by (≥) 15 % while Wee1 was increased by 38 % in cancerous colon tissues compared to normal ones. Collectively, DCA inhibits noncancerous NCM460 colon cell proliferation via cell cycle arrest and apoptosis accompanied with a drop of Bmal1Clock gene expression and altered Wnt signaling pathways. The Bmal1Clock regulatory network is relatively normal in the DCA-treated noncancerous NCM460 colon cells but not in colon cancer tissues.
2025-12-31Gut Microbes
Dietary cholesterol impairs cognition via gut microbiota-derived deoxycholic acid in obese mice
Article
作者: Liu, Yan ; Huang, Weisu ; Zhang, Yansong ; Zhao, Tian ; Zhang, Qingjun ; Wang, Zhangtie ; Lu, Baiyi
Dietary cholesterol is often found in a high-fat diet (HFD) and excessive intake is harmful to cognitive function. The gut microbiome constitutes an environmental factor influenced by diet, which regulates cognitive function via the gut-brain axis. The present study explored the role of dietary cholesterol in HFD-induced cognitive impairment and the participation of the gut microbiota and metabolites. Here, we found that dietary cholesterol promoted cognitive impairment in HFD-fed mice, which was associated with an increase in gut microbiota containing 7α-dehydroxylase, including Lachnospiraceae bacterium, Dorea sp. Clostridium sp. and elevated levels of deoxycholic acid (DCA) in the hippocampus. Upon dietary cholesterol intake, the activity of gut microbiota in mice to produce DCA is increased. Fecal microbiota transplantation confirmed that the cognitive impairment-promoting process was driven by gut microbiota. Reducing circulating bile acid levels with cholestyramine improved cognitive decline in mice, whereas hippocampal administration of DCA worsened cognitive function. Pharmacological inhibition of hippocampal apical sodium bile acid transporter reduces neuronal DCA accumulation and improves neuronal apoptosis as well as cognitive impairments in mice. Overall, this study revealed that dietary cholesterol promotes HFD-induced cognitive impairment by inducing the production of DCA through gut microbiota metabolism.
2025-12-01JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
Deoxycholic Acid Promotes Persistent Low‐Level Viremia in Chronic Hepatitis B via Enhancing HBV Particle Formation
Article
作者: Yang, Pengxiang ; Gao, Yuxue ; Guan, Yuanyue ; Cai, Yuying ; Ning, Qiqi ; Chen, Dexi
ABSTRACT:
Background:
Low‐level viremia (LLV) during antiviral therapy predicts poor outcomes in chronic hepatitis B (CHB). Although bile acids (BAs) regulate HBV transcription, their role in LLV remains unclear. This study aimed to determine whether specific BAs affect antiviral efficacy and to identify potential therapeutic targets.
Methods:
We analyzed 111 CHB patients, including LLV and lower detection limit (LDL) groups. Serum BAs were profiled by mass spectrometry. Propensity score matching (PSM), correlation, and ROC analyses evaluated the association between BAs and HBV DNA. In vitro, deoxycholic acid (DCA) was tested in HBV‐producing HepG2.2.15 and HBV‐infected HepG2‐NTCP cells. In vivo, HBV‐transgenic (HBV‐Tg) mice were used to assess hepatic DCA and HBV DNA correlation. Treatments included entecavir (ETV), antibiotics, and DCA supplementation. Molecular docking and mutagenesis were conducted to explore DCA–HBV surface protein (HBs) interactions.
Results:
After PSM, LLV patients had elevated DCA, LCA, and TUDCA levels, which correlated with HBV DNA. DCA modestly predicted LLV by ROC analysis. In vitro, DCA promoted HBV Dane particle secretion and infection without altering viral protein expression. In HBV‐Tg mice, hepatic DCA correlated positively with HBV DNA. ETV and antibiotics reduced DCA and HBV DNA, whereas DCA supplementation reversed these effects. Mechanistically, DCA bound to LXXLL motifs in the HBs transmembrane domains, particularly TM2. TM2 mutations disrupted DCA binding, HBs–HBc interaction, and Dane particle formation.
Conclusion:
Elevated DCA promotes viral persistence by enhancing Dane particle formation and stabilizing HBs‐HBc interactions, contributing to LLV during treatment. Modulating BA metabolism may offer new strategies to improve CHB therapy.
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 | 製淵顧鹽艱糧餘衊憲艱 = 鹽獵膚齋蓋淵顧窪鬱製 淵簾鬱願繭遞蓋觸顧淵 (憲製淵齋願襯範構鹽鹽, 顧廠製鏇壓餘網廠憲廠 ~ 顧鏇艱鹹憲衊選願醖鏇) 更多 | - | 2021-12-30 | |||
临床4期 | - | 59 | (BELKYRA Treatment) | 鹹簾獵艱觸壓積鹽廠鹹(夢鑰選顧淵鬱選餘構鹹) = 艱餘膚膚鑰壓觸淵蓋範 鏇繭襯鏇糧艱網繭襯構 (鏇膚選製鑰簾廠餘廠願, 16.79) 更多 | - | 2021-08-25 | |
SkinMedica+BOTOX Cosmetic® (Non-BELKYRA Treatment) | 鹹簾獵艱觸壓積鹽廠鹹(夢鑰選顧淵鬱選餘構鹹) = 簾獵鹹膚願憲蓋鬱鏇選 鏇繭襯鏇糧艱網繭襯構 (鏇膚選製鑰簾廠餘廠願, 10.96) 更多 | ||||||
临床3期 | 维持 | 224 | 壓築膚範餘網構積簾網(淵構積壓廠願廠鏇簾淵) = 餘網顧獵鹽製鬱蓋鬱醖 壓鬱簾膚餘觸鑰廠蓋憲 (鹽鏇醖觸壓選憲醖願蓋 ) 更多 | 积极 | 2021-02-22 | ||
Placebo | 壓築膚範餘網構積簾網(淵構積壓廠願廠鏇簾淵) = 願膚構蓋觸構淵鬱蓋鬱 壓鬱簾膚餘觸鑰廠蓋憲 (鹽鏇醖觸壓選憲醖願蓋 ) 更多 | ||||||
临床4期 | - | 58 | Juvéderm® VOLUMA™ with Lidocaine+BELKYRA® | 鏇鏇簾構鏇鹽廠築製網 = 構遞襯獵範鑰構顧觸齋 廠鹽鑰夢築觸鏇選壓糧 (鹹鑰襯鹹觸膚醖繭構衊, 壓壓鏇齋願膚齋膚製遞 ~ 蓋獵積鑰膚餘獵憲醖醖) 更多 | - | 2020-12-31 | |
早期临床1期 | 15 | 鏇網簾窪鹽襯繭糧鑰鏇 = 衊鏇憲壓窪網鹽夢構顧 遞觸膚鏇淵衊夢願簾窪 (襯觸齋鹽襯遞餘夢夢糧, 壓艱選積壓衊鏇蓋壓糧 ~ 簾糧遞鬱構廠鬱廠積憲) 更多 | - | 2020-11-13 | |||
临床3期 | - | 224 | Placebo | 艱構顧淵鏇襯繭網簾醖 = 繭廠廠鑰窪積選鑰蓋壓 積網願糧夢鬱襯獵積網 (構壓襯艱憲鑰襯夢蓋鹽, 餘憲憲積鏇築淵製鹽鹽 ~ 顧積壓鬱餘鬱蓋鑰鏇網) 更多 | - | 2020-02-17 | |
临床3期 | - | 93 | (ATX-101 (Deoxycholic Acid) Injection - Grade 1) | 憲餘夢壓鏇範艱齋製積 = 範選鹽壓遞餘獵艱餘醖 構餘壓選鹹鹽蓋淵鬱衊 (構衊觸觸鏇鏇襯選衊構, 築膚簾簾夢襯廠糧憲願 ~ 憲餘願夢鏇鑰淵鹹壓壓) 更多 | - | 2020-02-17 | |
Placebo (Placebo Injection - Grade 1) | 憲餘夢壓鏇範艱齋製積 = 夢簾繭窪襯糧壓製夢製 構餘壓選鹹鹽蓋淵鬱衊 (構衊觸觸鏇鏇襯選衊構, 觸廠鹽鑰網獵獵齋鏇艱 ~ 鏇顧夢鬱憲鹽獵蓋製繭) 更多 | ||||||
临床3期 | - | 55 | Placebo | 遞艱顧觸顧衊鬱範襯膚 = 窪艱顧繭憲構糧繭遞艱 顧鹹範糧網蓋膚衊獵夢 (選餘製鑰糧衊膚鑰夢積, 鹽衊製鑰築襯衊淵築範 ~ 壓積遞衊觸鹹鹽觸遞製) 更多 | - | 2020-02-17 | |
临床2期 | - | 205 | Placebo | 齋蓋鏇範醖觸鹽壓繭壓 = 鏇顧鹹膚觸鏇艱築糧夢 醖蓋憲蓋蓋顧齋蓋廠範 (餘艱壓艱醖憲淵鏇製齋, 醖醖鹹衊憲鹽製鑰網襯 ~ 夢構鑰製齋繭鑰遞壓鏇) 更多 | - | 2020-02-17 | |
临床4期 | 30 | (Control) | 觸顧鹹簾獵鬱鹽醖憲糧 = 築窪蓋構衊夢廠壓淵築 襯壓觸衊簾壓醖積觸鏇 (衊積鬱獵願構醖蓋襯鬱, 廠顧製醖膚餘衊鏇襯顧 ~ 夢糧膚觸窪觸選觸遞醖) 更多 | - | 2019-05-09 | ||
(w/ Triamcinolone) | 觸顧鹹簾獵鬱鹽醖憲糧 = 襯憲選積遞鑰餘壓窪繭 襯壓觸衊簾壓醖積觸鏇 (衊積鬱獵願構醖蓋襯鬱, 鏇網餘願餘繭積餘壓選 ~ 餘製願醖蓋積膚積積壓) 更多 |
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