Chenodeoxycholic Acid-d4

Chenodeoxycholic Acid-d4 is the deuterium labeled Chenodeoxycholic Acid. Chenodeoxycholic Acid is a hydrophobic primary bile acid that activates nuclear receptors (FXR) involved in cholesterol metabolism.

Product Specifications

CAS Number

[99102-69-9]

Product Name Alternative

CDCA-d4

UNSPSC

12352211

Hazard Statement

H302, H315, H319, H335

Target

Autophagy; Endogenous Metabolite; FXR

Type

Isotope-Labeled Compounds

Related Pathways

Autophagy; Metabolic Enzyme/Protease

Field of Research

Metabolic Disease; Cancer

Purity

99.93

Solubility

DMF : ≥ 30mg/mL|DMSO : ≥ 20mg/mL|Ethanol : ≥ 20mg/mL

Smiles

O[C@@H]1C([2H])(C[C@]2([C@@]([H])(C1([2H])[2H])C[C@H]([C@@]3([C@@]2(CC[C@]4([C@]3(CC[C@@]4([C@@H](CCC(O)=O)C)[H])[H])C)[H])[H])O)C)[2H]

Molecular Formula

C24H36D4O4

Molecular Weight

396.60

Precautions

H302, H315, H319, H335

References & Citations

[1]Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53 (2) :211-216. |[2]Casaburi I, et al. Chenodeoxycholic acid through a TGR5-dependent CREB signaling activation enhances cyclin D1 expression and promotes human endometrial cancer cell proliferation. Cell Cycle. 2012 Jul 15;11 (14) :2699-710|[3]Stauffer AT, et al. Chenodeoxycholic acid and deoxycholic acid inhibit 11 beta-hydroxysteroid dehydrogenase type 2 and cause cortisol-induced transcriptional activation of the mineralocorticoid receptor. J Biol Chem. 2002 Jul 19;277 (29) :26286-92|[4]Kawabe Y, et al. The molecular mechanism of the induction of the low density lipoprotein receptor by chenodeoxycholic acid in cultured human cells. Biochem Biophys Res Commun. 1995 Mar 8;208 (1) :405-11.|[5]Ao M, et al. Chenodeoxycholic acid stimulates Cl (-) secretion via cAMP signaling and increases cystic fibrosis transmembrane conductance regulator phosphorylation in T84 cells. Am J Physiol Cell Physiol. 2013 Aug 15;305 (4) :C447-56|[6]Noh K, et al. Farnesoid X receptor activation by chenodeoxycholic acid induces detoxifying enzymes through AMP-activated protein kinase and extracellular signal-regulated kinase 1/2-mediated phosphorylation of CCAAT/enhancer binding protein β. Drug Metab