Chenodeoxycholic acid-13C

Chenodeoxycholic acid-13C is the 13C-labeled Chenodeoxycholic Acid. Chenodeoxycholic Acid is a hydrophobic primary bile acid that activates nuclear receptors (FXR) involved in cholesterol metabolism.

Product Specifications

CAS Number

[52918-92-0]

Product Name Alternative

CDCA-13C

UNSPSC

12352211

Target

Autophagy; Endogenous Metabolite; FXR

Type

Isotope-Labeled Compounds

Related Pathways

Autophagy; Metabolic Enzyme/Protease

Applications

Metabolism-sugar/lipid metabolism

Field of Research

Metabolic Disease; Cancer

Assay Protocol

https://www.medchemexpress.com/chenodeoxycholic-acid-13c.html

Purity

98.0

Solubility

DMSO : 125mg/mL (ultrasonic)

Smiles

C[C@@]12[C@](CC[C@]2([H])[C@H](C)CC[13C](O)=O)([H])[C@@]3([H])[C@@](CC1)([H])[C@@]4([C@](C[C@@H](CC4)O)([H])C[C@H]3O)C

Molecular Formula

C23 13CH40O4

Molecular Weight

393.56

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