MedChemExpress LLC (MCE)

MedChemExpress - Model Glycochenodeoxycholic acid - 640-79-9

Glycochenodeoxycholic acid (Chenodeoxycholylglycine) is a relatively toxic bile salt generated in the liver from chenodeoxycholic acid and glycine. Glycochenodeoxycholic acid inhibits Autophagosome formation and impairs lysosomal function by inhibiting lysosomal proteolysis and increasing lysosomal pH in human normal liver cells, leading to the Apoptosis of human hepatocyte cells. Glycochenodeoxycholic acid induces stemness and chemoresistance via activating STAT3 signaling pathway in hepatocellular carcinoma cells (HCC). Glycochenodeoxycholic acid is promising for research in the field of cholestasis desease, hepatocellular carcinoma and primary sclerosing cholangitis (PSC)[1][2][3][4].

Glycochenodeoxycholic acid

MCE China：Glycochenodeoxycholic acid

Brand：MedChemExpress (MCE)

Cat. No.HY-N2334

CAS：640-79-9

Synonyms：Chenodeoxycholylglycine

Purity：99.25%

Storage：Powder -20°C 3 years 4°C 2 years In solvent -80°C 2 years -20°C 1 year

Shipping：Room temperature in continental US; may vary elsewhere.

Description：Glycochenodeoxycholic acid (Chenodeoxycholylglycine) is a relatively toxic bile salt generated in the liver from chenodeoxycholic acid and glycine. Glycochenodeoxycholic acid inhibits Autophagosome formation and impairs lysosomal function by inhibiting lysosomal proteolysis and increasing lysosomal pH in human normal liver cells, leading to the Apoptosis of human hepatocyte cells. Glycochenodeoxycholic acid induces stemness and chemoresistance via activating STAT3 signaling pathway in hepatocellular carcinoma cells (HCC). Glycochenodeoxycholic acid is promising for research in the field of cholestasis desease, hepatocellular carcinoma and primary sclerosing cholangitis (PSC).

In Vitro：Glycochenodeoxycholic acid (0-100 μM, 6 h) significantly increases the amount of dead cells and decreases in LC3, ATG5 and BECN1 expression in human normal liver cells, leading to Autophagosome formation inhibition[1]. Glycochenodeoxycholic acid (5–500 μM, 24 h) exerts no induction or reduction of TGF-β mRNA expression in KMBC cells and LX-2 cells[2]. Glycochenodeoxycholic acid (200 μM, 24 h and 48 h) enhances stemness and chemoresistance of hepatocellular carcinoma cells (HCC) by activating the STAT3 signaling pathway, suppressing the expression of apoptotic genes (Bcl10, Caspase 3, Caspase 4, Tp53, BAD) and increasing the expression of anti-apoptotic genes (Bcl2, Bcl-xl and IL10)[4].

IC50 & Target：Microbial Metabolite Human Endogenous Metabolite

References：

[1]. Lan W, et al. Glycochenodeoxycholic acid impairs transcription factor E3 -dependent autophagy-lysosome machinery by disrupting reactive oxygen species homeostasis in L02 cells[J]. Toxicol Lett. 2020 Oct 1;331:11-21. [Content Brief]

[2]. Wang A, et al. Glycochenodeoxycholic Acid Does Not Increase Transforming Growth Factor-Beta Expression in Bile Duct Epithelial Cells or Collagen Synthesis in Myofibroblasts[J]. J Clin Exp Hepatol. 2017 Dec;7(4):316-320. [Content Brief]

[3]. Gonzalez B, et al. Glycochenodeoxycholic acid (GCDC) induced hepatocyte apoptosis is associated with early modulation of intracellular PKC activity. Mol Cell Biochem. 2000 Apr;207(1-2):19-27. [Content Brief]

[4]. Shi C, et al. Glycochenodeoxycholic acid induces stemness and chemoresistance via the STAT3 signaling pathway in hepatocellular carcinoma cells[J]. Aging (Albany NY). 2020 Aug 3;12(15):15546-15555. [Content Brief]

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