Cholic Acid-d4
(Synonyms: 胆酸 d4) 目录号 : GC47086An internal standard for the quantification of cholic acid
Cas No.:116380-66-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Cholic acid-d4 is intended for use as an internal standard for the quantification of cholic acid by GC- or LC-MS. Cholic acid is a primary bile acid.1 It is formed from cholesterol via a multistep process catalyzed by the cytochrome P450 (CYP) isoforms CYP7A1, CYP8B1, and CYP27A1. Cholic acid is conjugated to glycine or taurine by bile acid-CoA:amino acid N-acyltransferase (BAAT) to produce glycocholic acid and taurocholic acid , respectively, in the liver, and is transformed into the secondary bile acid deoxycholic acid by intestinal microbiota.1,2,3 It induces C. difficile colony formation in an agar dilution assay when used at a concentration of 0.1% w/v.4 Dietary administration of cholic acid (0.4% w/w) increases serum cholesterol levels, biliary phospholipid secretion, and fecal DCA levels in rats.5
1.šarenac, T.M., and Mikov, M.Bile acid synthesis: From nature to the chemical modification and synthesis and their applications as drugs and nutrientsFront. Pharmacol.9939(2018) 2.Hunt, M.C., Siponen, M.I., and Alexson, S.E.H.The emerging role of acyl-CoA thioesterases and acyltransferases in regulating peroxisomal lipid metabolismBiochim. Biophys. Acta1822(9)1397-1410(2012) 3.Staley, C., Weingarden, A.R., Khoruts, A., et al.Interaction of gut microbiota with bile acid metabolism and its influence on disease statesAppl. Microbiol. Biotechnol.101(1)47-64(2017) 4.Sorg, J.A., and Sonenshein, A.L.Bile salts and glycine as cogerminants for Clostridium difficile sporesJ. Bacteriol.190(7)2505-2512(2008) 5.Uchida, K., Nomura, Y., and Takeuchi, N.Effects of cholic acid, chenodeoxycholic acid, and their related bile acids on cholesterol, phospholipid, and bile acid levels in serum, liver, bile, and feces of ratsJ. Biochem.87(1)187-194(1980)
| Cas No. | 116380-66-6 | SDF | |
| 别名 | 胆酸 d4 | ||
| Canonical SMILES | O[C@@H]1C([2H])([2H])C[C@@]2(C)[C@@](C[C@@H](O)[C@]3([H])[C@]2([H])C[C@H](O)[C@@]4(C)[C@@]3([H])CC[C@]4([H])[C@H](C)CCC(O)=O)([H])C1([2H])[2H] | ||
| 分子式 | C24H36D4O5 | 分子量 | 412.6 |
| 溶解度 | DMF: 30 mg/ml,DMF:PBS(pH 7.2)(1:1): 0.5 mg/ml,DMSO: 20 mg/ml,Ethanol: 20 mg/ml | 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 | 2.4237 mL | 12.1183 mL | 24.2365 mL |
| 5 mM | 0.4847 mL | 2.4237 mL | 4.8473 mL |
| 10 mM | 0.2424 mL | 1.2118 mL | 2.4237 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。
Determination of cholic acid and chenodeoxycholic acid pool sizes and fractional turnover rates by means of stable isotope dilution technique, making use of deuterated cholic acid and chenodeoxycholic acid
Clin Chim Acta 1988 Jul 15;175(2):143-55.PMID:3044647DOI:10.1016/0009-8981(88)90004-6.
A procedure is described for the simultaneous determination of cholic acid and chenodeoxycholic acid pool sizes and fractional turnover rates. After oral administration of known amounts of 11,12-dideuterated chenodeoxycholic acid and 2,2,4,4-tetradeuterated cholic acid, the ratios of chenodeoxycholic acid-D2/chenodeoxycholic acid and Cholic Acid-d4/cholic acid are measured in consecutive serum samples, after which fractional turnover rates and pool sizes of chenodeoxycholic acid and cholic acid are determined arithmetically. In 7 healthy volunteers pool sizes for chenodeoxycholic acid and cholic acid were 22.9 +/- 7.8 and 24.1 +/- 11.7 mumol/kg, respectively. The corresponding values for the fractional turnover rates were 0.23 +/- 0.10 and 0.29 +/- 0.12/day. After oral administration of the labelled bile acids in capsule, the obtained pool sizes were significantly higher than after administration in a bicarbonate solution. Bile acid kinetics were also performed in a patient suffering from a cholesterol synthesis deficiency and in a patient very likely suffering from a bile acid synthesis deficiency. Furthermore, the kinetics of the intestinal absorption and hepatic clearance of unconjugated bile acids have been investigated in 2 healthy subjects.
Use of a Bile Salt Export Pump Knockdown Rat Susceptibility Model to Interrogate Mechanism of Drug-Induced Liver Toxicity
Toxicol Sci 2019 Jul 1;170(1):180-198.PMID:30903168DOI:10.1093/toxsci/kfz079.
Inhibition of the bile salt export pump (BSEP) may be associated with clinical drug-induced liver injury, but is poorly predicted by preclinical animal models. Here we present the development of a novel rat model using siRNA knockdown (KD) of Bsep that displayed differentially enhanced hepatotoxicity to 8 Bsep inhibitors and not to 3 Bsep noninhibitors when administered at maximally tolerated doses for 7 days. Bsep KD alone resulted in 3- and 4.5-fold increases in liver and plasma levels, respectively, of the sum of the 3 most prevalent taurine conjugated bile acids (T3-BA), approximately 90% decrease in plasma and liver glycocholic acid, and a distinct bile acid regulating gene expression pattern, without resulting in hepatotoxicity. Among the Bsep inhibitors, only asunaprevir and TAK-875 resulted in serum transaminase and total bilirubin increases associated with increases in plasma T3-BA that were enhanced by Bsep KD. Benzbromarone, lopinavir, and simeprevir caused smaller increases in plasma T3-BA, but did not result in hepatotoxicity in Bsep KD rats. Bosentan, cyclosporine A, and ritonavir, however, showed no enhancement of T3-BA in plasma in Bsep KD rats, as well as Bsep noninhibitors acetaminophen, MK-0974, or clarithromycin. T3-BA findings were further strengthened through monitoring TCA-d4 converted from Cholic Acid-d4 overcoming interanimal variability in endogenous bile acids. Bsep KD also altered liver and/or plasma levels of asunaprevir, TAK-875, TAK-875 acyl-glucuronide, benzbromarone, and bosentan. The Bsep KD rat model has revealed differences in the effects on bile acid homeostasis among Bsep inhibitors that can best be monitored using measures of T3-BA and TCA-d4 in plasma. However, the phenotype caused by Bsep inhibition is complex due to the involvement of several compensatory mechanisms.