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Ursocholic acid Sale

(Synonyms: 熊果胆酸) 目录号 : GC33799

A bile acid

Ursocholic acid Chemical Structure

Cas No.:2955-27-3

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10mM (in 1mL DMSO)
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5mg
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10mg
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25mg
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100mg
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产品描述

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)

Chemical Properties

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 Soluble in DMSO 储存条件 Store at -20°C
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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
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Research Update

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.