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  • 鹅去氧胆酸; 鹅脱氧胆酸

    Chenodeoxycholic acid

    鹅去氧胆酸; 鹅脱氧胆酸
    产品编号 CFN90478
    CAS编号 474-25-9
    分子式 = 分子量 C24H40O4 = 392.57
    产品纯度 >=98%
    物理属性 Cryst.
    化合物类型 Steroids
    植物来源 From the bile.
    ChemFaces的产品在影响因子大于5的优秀和顶级科学期刊中被引用
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    产品名称 产品编号 CAS编号 包装 QQ客服
    鹅去氧胆酸; 鹅脱氧胆酸 CFN90478 474-25-9 10mg QQ客服:215959384
    鹅去氧胆酸; 鹅脱氧胆酸 CFN90478 474-25-9 20mg QQ客服:215959384
    鹅去氧胆酸; 鹅脱氧胆酸 CFN90478 474-25-9 50mg QQ客服:215959384
    鹅去氧胆酸; 鹅脱氧胆酸 CFN90478 474-25-9 100mg QQ客服:215959384
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    ChemFaces的产品在许多优秀和顶级科学期刊中被引用

    Cell. 2018 Jan 11;172(1-2):249-261.e12.
    doi: 10.1016/j.cell.2017.12.019.
    IF=36.216(2019)

    PMID: 29328914

    Cell Metab. 2020 Mar 3;31(3):534-548.e5.
    doi: 10.1016/j.cmet.2020.01.002.
    IF=22.415(2019)

    PMID: 32004475

    Mol Cell. 2017 Nov 16;68(4):673-685.e6.
    doi: 10.1016/j.molcel.2017.10.022.
    IF=14.548(2019)

    PMID: 29149595

    ACS Nano. 2018 Apr 24;12(4): 3385-3396.
    doi: 10.1021/acsnano.7b08969.
    IF=13.903(2019)

    PMID: 29553709

    Nature Plants. 2016 Dec 22;3: 16206.
    doi: 10.1038/nplants.2016.205.
    IF=13.297(2019)

    PMID: 28005066

    Sci Adv. 2018 Oct 24;4(10): eaat6994.
    doi: 10.1126/sciadv.aat6994.
    IF=12.804(2019)

    PMID: 30417089
    我们的产品现已经出口到下面的研究机构与大学,并且还在增涨
  • Harvard University (USA)
  • University of the Basque Country (Spain)
  • Copenhagen University (Denmark)
  • University of Bordeaux (France)
  • Kazusa DNA Research Institute (Japan)
  • Lodz University of Technology (Poland)
  • Sanford Burnham Prebys Medical Discovery Institute (USA)
  • University of Melbourne (Australia)
  • Wageningen University (Netherlands)
  • Research Unit Molecular Epigenetics (MEG) (Germany)
  • University of Illinois (USA)
  • Universidad de La Salle (Mexico)
  • University of British Columbia (Canada)
  • Pennsylvania State University (USA)
  • More...
  • 国外学术期刊发表的引用ChemFaces产品的部分文献
  • Phytomedicine.2022, 100:154085.
  • Compounds.2023, 3(1), 169-179.
  • J Nat Prod.2015, 78(6):1339-4
  • Int J Anal Chem.2017, 2017:1254721
  • Front Pharmacol.2020, 11:566490.
  • Molecules.2023, 28(19):6775.
  • Front Plant Sci.2020, 10:1705
  • Elife.2021, 10:e68058.
  • Biochem Biophys Res Commun.2018, 505(4):1148-1153
  • Evid Based Complement Alternat Med.2019, 2019:2135351
  • J Agric Food Chem.2021, 69(14):4210-4222.
  • J Funct Foods2019, 54:449-456
  • Molecules.2016, 21(6)
  • Front Pharmacol.2022, 13:883475.
  • Molecules.2023, 28(9):3685.
  • Neuropharmacology.2018, 131:68-82
  • Front Microbiol.2021, 12:736780.
  • Front Plant Sci.2021, 12: 648426.
  • HIV Med.2021, 22(8):690-704.
  • Drug Dev Res.2022, 83(7):1673-1682.
  • Food Res Int.2017, 96:40-45
  • Journal of Third Military Medical University2018, 40(12):1073-1078
  • Sci Rep.2023, 13(1):7475.
  • ...
  • 生物活性
    Description: Chenodeoxycholic acid is a hydrophobic primary bile acid that activates nuclear receptors (FXR) involved in cholesterol metabolism. Chenodeoxycholic acid could reverse obesity in cHF-fed mice, mainly in response to the reduction in food intake.
    Targets: IL Receptor | p38MAPK | PKA
    In vitro:
    J Gastroenterol Hepatol. 2013 May;28(5):823-8.
    Acidic deoxycholic acid and chenodeoxycholic acid induce interleukin-8 production through p38 mitogen-activated protein kinase and protein kinase A in a squamous epithelial model.[Pubmed: 23425072]
    Immune-mediated mucosal inflammation characterized by the production of interleukin (IL)-8 is associated with the development of gastroesophageal reflux disease. The effects of bile acids, which are major components of reflux fluid, on the production of IL-8 and related mechanisms remain unclear. This study aimed to address these questions using an esophageal stratified squamous epithelial model.
    METHODS AND RESULTS:
    Normal human esophageal epithelial cells were seeded on the Transwell inserts and cultured with the air-liquid interface system to establish the model. Bile acids under different pH conditions were added to the apical compartment to examine their effects on IL-8 production and the underlying cellular signaling. Conjugated bile acids under a neutral or acidic condition did not induce IL-8 production, and unconjugated bile acids, deoxycholic acid (DCA), and chenodeoxycholic acid (CDCA) all significantly induced IL-8 production, dose- and time-dependently, only under weakly acid conditions. Inhibition of p38 mitogen-activated protein kinase (p38 MAPK) and protein kinase A (PKA) attenuated the production of IL-8 induced by acidic DCA and CDCA. Inhibition of PKA did not block the bile acid-induced p38 MAPK activation.
    CONCLUSIONS:
    Compared with conjugated bile acids, the unconjugated bile acids DCA and CDCA are more likely to induce IL-8 production in vivo, especially under weakly acid conditions. This process involves two independent signaling pathways, p38 MAPK and PKA.
    In vivo:
    J Inherit Metab Dis. 2014 Sep;37(5):851-61.
    Liver disease in infancy caused by oxysterol 7 α-hydroxylase deficiency: successful treatment with chenodeoxycholic acid.[Pubmed: 24658845]
    A child of consanguineous parents of Pakistani origin developed jaundice at 5 weeks and then, at 3 months, irritability, a prolonged prothrombin time, a low albumin, and episodes of hypoglycaemia. Investigation showed an elevated alanine aminotransferase with a normal γ-glutamyl-transpeptidase.
    METHODS AND RESULTS:
    Analysis of urine by electrospray ionisation tandem mass spectrometry (ESI-MS/MS) showed that the major peaks were m/z 480 (taurine-conjugated 3β-hydroxy-5-cholenoic acid) and m/z 453 (sulphated 3β-hydroxy-5-cholenoic acid). Analysis of plasma by gas chromatography-mass spectrometry (GC-MS) showed increased concentrations of 3β-hydroxy-5-cholenoic acid, 3β-hydroxy-5-cholestenoic acid and 27-hydroxycholesterol, indicating oxysterol 7 α-hydroxylase deficiency. The patient was homozygous for a mutation (c.1249C>T) in CYP7B1 that alters a highly conserved residue in oxysterol 7 α-hydroxylase (p.R417C) - previously reported in a family with hereditary spastic paraplegia type 5. On treatment with ursodeoxycholic acid (UDCA), his condition was worsening, but on chenodeoxycholic acid (CDCA), 15 mg/kg/d, he improved rapidly. A biopsy (after 2 weeks on CDCA), showed a giant cell hepatitis, an evolving micronodular cirrhosis, and steatosis. The improvement in liver function on CDCA was associated with a drop in the plasma concentrations and urinary excretions of the 3β-hydroxy-Δ5 bile acids which are considered hepatotoxic. At age 5 years (on CDCA, 6 mg/kg/d), he was thriving with normal liver function. Neurological development was normal apart from a tendency to trip. Examination revealed pes cavus but no upper motor neuron signs.
    CONCLUSIONS:
    The findings in this case suggest that CDCA can reduce the activity of cholesterol 27-hydroxylase - the first step in the acidic pathway for bile acid synthesis.
    J Clin Endocrinol Metab. 2013 Aug;98(8):3351-8.
    Effects of chenodeoxycholic acid on the secretion of gut peptides and fibroblast growth factors in healthy humans.[Pubmed: 23783097]
    We hypothesized that intraduodenal infusions of Chenodeoxycholic acid (CDCA) would stimulate FGF and gut peptide secretion, thereby positively influencing glucose homeostasis.
    METHODS AND RESULTS:
    This randomized, double-blind, placebo-controlled, crossover trial included 12 healthy volunteers who received intraduodenal infusions (2.0 mL/min for 180 minutes) of saline, Chenodeoxycholic acid (5 or 15 mmol/L), and a fatty acid (sodium oleate), either alone or with 5 mmol/L Chenodeoxycholic acid. After 60 minutes, an oral glucose tolerance test (oGTT) was performed. Within the first 60 minutes, high-concentration Chenodeoxycholic acid induced a small but significant increase in GLP-1 and CCK secretion (P = .016 and P =.011), whereas plasma C-peptide, insulin, and glucose were not affected. Attenuated C-peptide and insulin release was observed after the oGTT with 15 mmol/L CDCA (P = .013 and P =.011). Plasma BA and FGF19 levels significantly increased after Chenodeoxycholic acid administration (P = .001 and P < .001).
    CONCLUSIONS:
    Chenodeoxycholic acid modulates GLP-1 and CCK secretion; the effect is small and does not influence glucose levels. The marked increase in plasma BAs and the attenuated insulin release after the oGTT indicate the role of BAs in glycemic control, independent of the incretin axis, and suggest involvement of farnesoid X receptor activation pathways.
    制备储备液(仅供参考)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 2.5473 mL 12.7366 mL 25.4732 mL 50.9463 mL 63.6829 mL
    5 mM 0.5095 mL 2.5473 mL 5.0946 mL 10.1893 mL 12.7366 mL
    10 mM 0.2547 mL 1.2737 mL 2.5473 mL 5.0946 mL 6.3683 mL
    50 mM 0.0509 mL 0.2547 mL 0.5095 mL 1.0189 mL 1.2737 mL
    100 mM 0.0255 mL 0.1274 mL 0.2547 mL 0.5095 mL 0.6368 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    部分图片展示
    产品名称 产品编号 CAS编号 分子式 = 分子量 位单 联系QQ
    胆酸钠; Sodium cholate CFN96673 361-09-1 C24H39NaO5 = 430.55 5mg QQ客服:3257982914
    甘氨脱氧胆酸; Glycodeoxycholic acid CFN96947 360-65-6 C26H43NO5 = 449.63 20mg QQ客服:1457312923
    甘氨熊去氧胆酸; Glycoursodeoxycholic acid CFN89075 64480-66-6 C26H43NO5 = 449.63 20mg QQ客服:1457312923
    牛磺胆酸; Taurocholic acid CFN96646 81-24-3 C26H45NO7S = 515.70 5mg QQ客服:3257982914
    牛磺熊去氧胆酸 ; Tauroursodeoxycholic acid CFN96645 14605-22-2 C26H45NO6S = 499.70 5mg QQ客服:1413575084
    牛磺鹅去氧胆酸钠; Sodium taurochenodeoxycholate CFN80241 6009-98-9 C26H44NNaO6S = 521.68 5mg QQ客服:3257982914
    熊去氧胆酸; Ursodeoxycholic acid CFN96464 128-13-2 C24H40O4 = 392.58 20mg QQ客服:1457312923
    鹅去氧胆酸; 鹅脱氧胆酸; Chenodeoxycholic acid CFN90478 474-25-9 C24H40O4 = 392.57 20mg QQ客服:1413575084
    胆酸; Cholic acid CFN99796 81-25-4 C22H40O5 = 408.57 20mg QQ客服:1457312923
    猪胆酸; Hyocholic acid CFN91626 547-75-1 C24H40O5 = 408.6 5mg QQ客服:1457312923

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