Ursocholic acid
(Synonyms: 熊果胆酸) 目录号 : GC33799
A bile acid
Cas No.:2955-27-3
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Ursocholic acid (UCA) is a bile acid and the 7β-hydroxyepimer of cholic acid .1 Dietary administration of UCA (0.25%) decreases gallbladder cholesterol, phospholipid, and bile acid levels and the occurrence of gallstones in male mice fed a lithogenic diet.
1.Uchida, K., Akiyoshi, T., Igmi, H., et al.Differential effects of ursodeoxycholic acid and ursocholic acid on the formation of biliary cholesterol crystals in miceLipids26(7)526-530(1991)
| Cas No. | 2955-27-3 | SDF | |
| 别名 | 熊果胆酸 | ||
| Canonical SMILES | C[C@H](CCC(O)=O)[C@H]1CC[C@@]2([H])[C@]3([H])[C@@H](O)C[C@]4([H])C[C@H](O)CC[C@]4(C)[C@@]3([H])C[C@H](O)[C@]12C | ||
| 分子式 | C24H40O5 | 分子量 | 408.57 |
| 溶解度 | DMSO : 100 mg/mL (244.76 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.4476 mL | 12.2378 mL | 24.4756 mL |
| 5 mM | 0.4895 mL | 2.4476 mL | 4.8951 mL |
| 10 mM | 0.2448 mL | 1.2238 mL | 2.4476 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Metabolism of Ursocholic acid in humans: conversion of Ursocholic acid to deoxycholic acid
Hepatology 1992 Apr;15(4):645-50.PMID:1551642DOI:10.1002/hep.1840150415.
To study the metabolism of Ursocholic acid, control subjects were injected with radiolabeled cholic and ursocholic acids before and after 1 wk of 900 mg/day oral Ursocholic acid. Daily samples of bile were obtained, and biliary bile acids were extracted and purified to determine bile acid kinetics. During Ursocholic acid therapy Ursocholic acid became the principal bile acid (35% +/- 3% of total bile acids, mean +/- S.E.M.), and the percentage of biliary cholic and chenodeoxycholic acids decreased (p less than 0.05). Cholic acid production fell from 190 +/- 15 mg/day to 135 +/- 20 mg/day (p = 0.078). The total bile acid pool was increased twofold (p less than 0.05), whereas the deoxycholic acid pool was enlarged from 440 +/- 170 mg to 1,175 +/- 90 mg (p less than 0.02). As much as 28% of the fed Ursocholic acid was excreted in the urine, 85% as the free acid and 15% as the glycine conjugate. During treatment, Ursocholic acid became the source for 69% +/- 11% of biliary deoxycholic acid. The time course of the deoxycholic acid specific activity was modeled as a single pool precursor-product system with a variable time delay for the C-7-dehydroxylation of cholic and ursocholic acids (mean delay 0.86 +/- 0.11 days, p less than 0.001 vs. zero delay). Most of this delay probably arises from a slow process of bacterial C-7-dehydroxylation within the colon. These results demonstrate that during Ursocholic acid therapy the synthesis of primary bile acids continues whereas the formation of secondary bile acids is greatly increased.
Differential effects of ursodeoxycholic acid and Ursocholic acid on the formation of biliary cholesterol crystals in mice
Lipids 1991 Jul;26(7):526-30.PMID:1943496DOI:10.1007/BF02536598.
The preventive effect of 3 alpha, 7 beta, 12 alpha-trihydroxy-5 beta-cholanoic acid (Ursocholic acid) and ursodeoxycholic acid on the formation of biliary cholesterol crystals was studied in mice. Cholesterol crystals developed with 80% incidence after feeding for five weeks a lithogenic diet containing 0.5% cholesterol and 0.25% sodium cholate. When 0.25% Ursocholic acid or ursodeoxycholic acid was added to the lithogenic diet, the incidence as well as the grade (severity) of the gallstones were reduced. Plasma and liver cholesterol levels were decreased by ursodeoxycholic acid but not by Ursocholic acid. Gallbladder cholesterol and phospholipid levels were decreased by both bile acids. The biliary bile acid level was decreased by Ursocholic acid but not by ursodeoxycholic acid. After feeding Ursocholic acid, its level in the bile was about 25% and the levels of cholic acid and beta-muricholic acid decreased. Fecal sterol excretion was not changed by Ursocholic acid, but was increased by ursodeoxycholic acid. After feeding Ursocholic acid, fecal excretion of deoxycholic acid, cholic acid, and Ursocholic acid increased. No differences were found between mice, with or without gallstones, in plasma and liver cholesterol levels, biliary phospholipid and bile acid levels, fecal sterol and bile acid levels, and biliary and fecal bile acid composition. The results suggest that the lower incidence of crystal formation after treatment with Ursocholic acid is probably by a different mechanism than with ursodeoxycholic acid. In the mouse model, ursodeoxycholic acid exerts its effect at least partially, by decreasing cholesterol absorption. Ursocholic acid is well absorbed and excreted into bile and transformed into deoxycholic acid by the intestinal microflora in mice.
Effect of Ursocholic acid on bile lipid secretion and composition
Gastroenterology 1986 Apr;90(4):865-74.PMID:3949116DOI:10.1016/0016-5085(86)90862-0.
To further clarify the relationship between physical-chemical characteristics of bile acids and biliary lipid secretion, we investigated the effect of Ursocholic acid, the 7 beta-hydroxyepimer of cholic acid, on bile lipid secretion and composition. The study included acute duodenal infusion (1 g/h for 5 h) of Ursocholic acid contrasted with a less hydrophilic bile acid, ursodeoxycholic acid, in 3 T-tube patients and short-term oral administration (2 wk) of Ursocholic acid (10-15 mg/kg X day) to 10 gallstone patients. Following acute infusion, Ursocholic acid, similarly to ursodeoxycholic acid, accounted for greater than 80% of the biliary bile acids. However, Ursocholic acid induced (per micromole of secreted bile acid) a significantly lower (p less than 0.01) secretion of cholesterol (0.013 mumol) and phospholipids (0.054 mumol) than that induced by ursodeoxycholic acid (0.034 mumol of cholesterol and 0.138 mumol of phospholipids). Biliary alkaline phosphatase activity during Ursocholic acid administration was significantly lower (p less than 0.01) than during ursodeoxycholic acid administration. After short-term oral administration, Ursocholic acid, undetectable before treatment, constituted 20.50% +/- 8.60% of the biliary bile acids. The percentage of deoxycholic acid increased from 32.35% +/- 18.79% to 47.53% +/- 16.19% (p less than 0.05). Mean saturation index decreased from a pretreatment value of 1.23 +/- 0.22 to 0.99 +/- 0.17 (p less than 0.05), but only in 4 of 10 subjects did bile become undersaturated. It is concluded that Ursocholic acid, due to its higher hydrophilicity, stimulates a lower cholesterol and phospholipid output than ursodeoxycholic acid. Consequently, despite the low enrichment of the biliary bile acids with Ursocholic acid, oral administration of Ursocholic acid induces a reduction of bile cholesterol saturation.
Gut microbiota and metabolites associate with outcomes of immune checkpoint inhibitor-treated unresectable hepatocellular carcinoma
J Immunother Cancer 2022 Jun;10(6):e004779.PMID:35738801DOI:10.1136/jitc-2022-004779.
Background: Immune checkpoint inhibitors (ICIs) are promising agents for unresectable hepatocellular carcinoma (uHCC), but lack effective biomarker to predict outcomes. The gut microbiome can modulate tumor response to immunotherapy, but its effect on HCC remains unclear. Methods: From May 2018 to February 2020, patients receiving ICI treatment for uHCC were prospectively enrolled; their fecal samples were collected before treatment. The fecal microbiota and metabolites were analyzed from 20 patients with radiology-proven objective responses (OR) and 21 randomly selected patients with progressive disease (PD). After March 2020, 33 consecutive Child-Pugh-A patients were recruited as a validation cohort. Additionally, feces from 17 healthy volunteers were collected for comparison of background microbes. Results: A significant dissimilarity was observed in fecal bacteria between patients with OR and patients with PD before immunotherapy. Prevotella 9 was enriched in patients with PD, whereas Lachnoclostridium, Lachnospiraceae, and Veillonella were predominant in patients with OR. Ursodeoxycholic acid and Ursocholic acid were significantly enriched in the feces of patients with OR and strongly correlated with the abundance of Lachnoclostridium. The coexistence of Lachnoclostridium enrichment and Prevotella 9 depletion significantly predicted better overall survival (OS). In the validation cohort, better progression-free survival (PFS) and OS were noted in patients who had a preferable microbial signature in comparison with counter-group (PFS: 8.8 months vs 1.8 months; OS: not reached vs 6.5 months, both p<0.001). Conclusions: Fecal microbiota and bile acids were associated with outcomes of immunotherapy for uHCC. These findings highlight the potential role of gut microbiota and metabolites as biomarkers to predict outcomes of ICI-treated HCC.
Ursocholic acid: bile acid and bile lipid dose response and clinical studies in patients with gall stones
Gut 1989 Jan;30(1):97-103.PMID:2920932DOI:10.1136/gut.30.1.97.
The biliary bile acid and bile lipid responses to six weeks treatment with approximately 5, 10, and 15 mg/kg/day of Ursocholic acid (UCA) were studied in 11 gall stone patients. Maximum enrichment of bile with UCA (24 (SE) 4.9%) occurred with 15 mg UCA/kg/day. The maximum reduction in biliary cholesterol saturation was seen with the 10 mg/kg/day dose when the moles % cholesterol fell from 14 (2.4)% before treatment to 5.6 (0.83)% (p less than 0.02) and the saturation index fell from 1.4 (0.23) to 0.77 (0.13) (p less than 0.05). Clinical studies of the safety and efficacy of UCA in dissolving gall stones were carried out in 13 patients treated for up to two years with a dose of approximately 10 mg/kg/day. Diarrhoea caused withdrawal of treatment in three patients. There were no significant changes in liver function or haematology tests but fasting serum cholesterol tended to rise during treatment. Of nine patients treated for greater than 6 months, only one showed complete gall stone dissolution. As UCA may cause diarrhoea and hypercholesterolaemia, has only a modest effect on biliary cholesterol saturation and low gall stone dissolution efficacy, it is unlikely to replace existing forms of gall stone dissolution therapy.