1. Metabolic Enzyme/Protease
  2. FXR

Chenodeoxycholic Acid (Synonyms: CDCA)

Cat. No.: HY-76847 Purity: >98.0%
Data Sheet SDS Handling Instructions

Chenodeoxycholic Acid is a hydrophobic primary bile acid that activates nuclear receptors (FXR) involved in cholesterol metabolism.

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Chenodeoxycholic Acid Chemical Structure

Chenodeoxycholic Acid Chemical Structure

CAS No. : 474-25-9

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  • Biological Activity

  • Protocol

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Description

Chenodeoxycholic Acid is a hydrophobic primary bile acid that activates nuclear receptors (FXR) involved in cholesterol metabolism.

In Vitro

Chenodeoxycholic acid (CDCA) and Deoxycholic acid (DCA) both inhibit 11 beta HSD2 with IC50 values of 22 mM and 38 mM, respectively and causes cortisol-dependent nuclear translocation and increases transcriptionalactivity of mineralocorticoid receptor (MR)[1]. Chenodeoxycholic acid is able to stimulate Ishikawa cell growth by inducing a significant increase in Cyclin D1 protein and mRNA expression through the activation of the membrane G protein-coupled receptor (TGR5)-dependent pathway[2]. Chenodeoxycholic acid (CDCA) induces LDL receptor mRNA levels approximately 4 fold and mRNA levels for HMG-CoA reductase and HMG-CoA synthase two fold in a cultured human hepatoblastoma cell line, Hep G2[3]. Chenodeoxycholic acid-induced Isc is inhibited (≥67%) by Bumetanide, BaCl2, and the cystic fibrosis transmembrane conductance regulator (CFTR) inhibitor CFTRinh-172. Chenodeoxycholic acid-stimulated Isc is decreased 43% by the adenylate cyclase inhibitor MDL12330A and Chenodeoxycholic acid increases intracellular cAMP concentration[4]. Chenodeoxycholic acid treatment activates C/EBPβ, as shown by increases in its phosphorylation, nuclear accumulation, and expression in HepG2 cells. Chenodeoxycholic acid enhances luciferase gene transcription from the construct containing -1.65-kb GSTA2 promoter, which contains C/EBP response element (pGL-1651). Chenodeoxycholic acid treatment activates AMP-activated protein kinase (AMPK), which leads to extracellular signal-regulated kinase 1/2 (ERK1/2) activation, as evidenced by the results of experiments using a dominant-negative mutant of AMPKα and chemical inhibitor[5].

Clinical Trial
NCT Number Sponsor Condition Start Date Phase
NCT01069653 Shiga University|Human Genome Center, Institute of Medical Science, University of Tokyo Small Cell Lung Cancer February 2010 Phase 1
NCT01069575 Shiga University|Human Genome Center, Institute of Medical Science, University of Tokyo Non-Small Cell Lung Cancer February 2010 Phase 1
NCT01950156 Shiga University|Tokyo University Non-small Cell Lung Cancer September 2011 Phase 1|Phase 2
NCT01225471 Iwate Medical University|Human Genome Center, Institute of Medical Science, University of Tokyo Prostate Cancer June 2009 Phase 1|Phase 2
NCT01259505 Tokyo Medical University|Tokyo University|Saint Luca International Hospital Metastatic Breast Cancer December 2009 Phase 1
NCT00874588 Fukushima Medical University|Human Genome Center, Institute of Medical Science, University of Tokyo Non Small Cell Lung Cancer March 2009 Phase 1
NCT01674946 University Hospital, Basel, Switzerland Echolocation September 2011 Phase 1
NCT03168555 Zealand University Hospital Bile Acid Malabsorption|Cholelithiasis June 22, 2017 Phase 4
NCT03059537 Lars Kristian Munck|Zealand University Hospital Bile Acid Malabsorption March 13, 2017 Phase 4
NCT00018694 VA Office of Research and Development Cerebrotendinous Xanthomatosis October 1999
NCT00465751 University Hospital, Basel, Switzerland Metabolic Syndrome|Familial Hypertriglyceridemia|Familial Combined Hyperlipidemia October 2004 Early Phase 1
NCT00004346 National Center for Research Resources (NCRR)|Oregon Health and Science University Cerebrotendinous Xanthomatosis January 1996 Phase 2
NCT02340247 Hvidovre University Hospital|University of Copenhagen Severe Obesity November 2014 Phase 4
NCT02876484 Hvidovre University Hospital|University of Copenhagen Severe Obesity June 2016 Phase 4
NCT02952963 Hvidovre University Hospital|University of Copenhagen Severe Obesity October 2016 Phase 4
NCT00004442 University of Cincinnati|Children's Hospital Medical Center, Cincinnati|FDA Office of Orphan Products Development Infantile Refsum's Disease|Zellweger Syndrome|Bifunctional Enzyme Deficiency|Adrenoleukodystrophy
NCT01666223 University Hospital, Gentofte, Copenhagen Type 2 Diabetes|Obesity November 2012
NCT01069653 Shiga University|Human Genome Center, Institute of Medical Science, University of Tokyo Small Cell Lung Cancer February 2010 Phase 1
NCT01069575 Shiga University|Human Genome Center, Institute of Medical Science, University of Tokyo Non-Small Cell Lung Cancer February 2010 Phase 1
NCT01950156 Shiga University|Tokyo University Non-small Cell Lung Cancer September 2011 Phase 1|Phase 2
NCT01225471 Iwate Medical University|Human Genome Center, Institute of Medical Science, University of Tokyo Prostate Cancer June 2009 Phase 1|Phase 2
NCT01259505 Tokyo Medical University|Tokyo University|Saint Luca International Hospital Metastatic Breast Cancer December 2009 Phase 1
NCT00874588 Fukushima Medical University|Human Genome Center, Institute of Medical Science, University of Tokyo Non Small Cell Lung Cancer March 2009 Phase 1
NCT01674946 University Hospital, Basel, Switzerland Echolocation September 2011 Phase 1
NCT03168555 Zealand University Hospital Bile Acid Malabsorption|Cholelithiasis June 22, 2017 Phase 4
NCT03059537 Lars Kristian Munck|Zealand University Hospital Bile Acid Malabsorption March 13, 2017 Phase 4
NCT00018694 VA Office of Research and Development Cerebrotendinous Xanthomatosis October 1999
NCT00465751 University Hospital, Basel, Switzerland Metabolic Syndrome|Familial Hypertriglyceridemia|Familial Combined Hyperlipidemia October 2004 Early Phase 1
NCT00004346 National Center for Research Resources (NCRR)|Oregon Health and Science University Cerebrotendinous Xanthomatosis January 1996 Phase 2
NCT02340247 Hvidovre University Hospital|University of Copenhagen Severe Obesity November 2014 Phase 4
NCT02876484 Hvidovre University Hospital|University of Copenhagen Severe Obesity June 2016 Phase 4
NCT02952963 Hvidovre University Hospital|University of Copenhagen Severe Obesity October 2016 Phase 4
NCT00004442 University of Cincinnati|Children's Hospital Medical Center, Cincinnati|FDA Office of Orphan Products Development Infantile Refsum's Disease|Zellweger Syndrome|Bifunctional Enzyme Deficiency|Adrenoleukodystrophy
NCT01666223 University Hospital, Gentofte, Copenhagen Type 2 Diabetes|Obesity November 2012
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References
Preparing Stock Solutions
Concentration Volume (DMSO) Mass 1 mg 5 mg 10 mg
1 mM 2.5473 mL 12.7366 mL 25.4732 mL
5 mM 0.5095 mL 2.5473 mL 5.0946 mL
10 mM 0.2547 mL 1.2737 mL 2.5473 mL
Kinase Assay
[1]

Briefly, transfected HEK-293 cells, incubated in charcoal-treated Dulbecco's modified Eagle's medium for 24 h, are washed once with Hanks' solution and resuspended in a buffer containing 100 mM NaCl, 1 mM MgCl2, 1 mM EDTA, 1 mM EGTA, 250 mMsucrose, 20 mM Tris-HCl, pH 7.4. Cells are lysed by freezing in liquid nitrogen. Dehydrogenase activity is measured in a final volume of 20 μL containing the appropriate concentration of bile acid, 30 nCi of [3H]cortisol, and unlabeled cortisol to a final concentrations of 50 nM. The reaction is started by mixing cell lysate with the reaction mixture. Alternatively, endoplasmic reticulum microsomes are prepared from transfected HEK-293 cells and incubated with reaction mixture containing various concentrations of cortisol and CDCA. Incubation proceeded for 20 min, and the conversion of cortisol to cortisone is determined by thin layer chromatography (TLC). Because of the inaccuracy of the TLC method at low conversion rates and the end-product inhibition of 11βHSD2 at conversion rates higher than 60-70%, only conversion rates between 10 and 60% are considered for calculation. The inhibitory constant IC50 is evaluated using the curve-fitting program. Results are expressed as means±S.E. and consist of at least four independent measurements. MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Assay
[1]

The cell viability is analyzed by incubating transfected HEK-293 cells and CHO cells for 1 h with the corresponding concentration of bile acid and staining with trypan blue. The toxicity of bile acids is analyzed using the tetrazolium salt MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) according to the cell proliferation kit I. No significant differences between control and bile acid-treated cells are obtained in both tests. MCE has not independently confirmed the accuracy of these methods. They are for reference only.

References
Molecular Weight

392.57

Formula

C₂₄H₄₀O₄

CAS No.

474-25-9

Storage
Powder -20°C 3 years
  4°C 2 years
In solvent -80°C 6 months
  -20°C 1 month
Shipping

Room temperature in continental US; may vary elsewhere

Solvent & Solubility

DMSO: ≥ 3.6 mg/mL

* "<1 mg/mL" means slightly soluble or insoluble. "≥" means soluble, but saturation unknown.

Purity: >98.0%

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Product Name:
Chenodeoxycholic Acid
Cat. No.:
HY-76847
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