Catalog No.S1843 Synonyms: Chenodiol
Molecular Weight(MW): 392.57
Chenodeoxycholic Acid is a naturally occurring human bile acid, and inhibits production of cholesterol in the liver and absorption in the intestines.
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|Description||Chenodeoxycholic Acid is a naturally occurring human bile acid, and inhibits production of cholesterol in the liver and absorption in the intestines.|
Chenodeoxycholic acid (CDCA) and Deoxycholic acid (DCA) both inhibits 11 beta HSD2 with IC(50) values of 22 mM and 38 mM, respectively and causes cortisol-dependent nuclear translocation and increases transcriptionalactivity of mineralocorticoid receptor (MR).  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.  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.  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.  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. 
-  Stauffer AT, et al. J Biol Chem,?002, 277(29), 26286-26292.
-  Casaburi I, et al. Cell Cycle, 2012, 11(14), 2699-2710.
-  Kawabe Y, et al. Biochem Biophys Res Commun,?995, 208(1), 405-411.
|In vitro||DMSO||79 mg/mL (201.23 mM)|
|Ethanol||79 mg/mL (201.23 mM)|
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT02952963||Recruiting||Severe Obesity||Hvidovre University Hospital|University of Copenhagen||October 2016||Phase 4|
|NCT02876484||Recruiting||Severe Obesity||Hvidovre University Hospital|University of Copenhagen||June 2016||Phase 4|
|NCT02340247||Completed||Severe Obesity||Hvidovre University Hospital|University of Copenhagen||November 2014||Phase 4|
|NCT01666223||Completed||Type 2 Diabetes|Obesity||University Hospital, Gentofte, Copenhagen||November 2012||--|
|NCT01674946||Completed||Echolocation||University Hospital, Basel, Switzerland||September 2011||Phase 1|
|NCT00465751||Completed||Metabolic Syndrome|Familial Hypertriglyceridemia|Familial Combined Hyperlipidemia||University Hospital, Basel, Switzerland||October 2004||Early Phase 1|
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