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MedChemExpress - Model Glycoursodeoxycholic acid - 64480-66-6
Glycoursodeoxycholic acid, a acyl glycine and a bile acid-glycine conjugate, is a metabolite of ursodeoxycholic acid.MCE products for research use only. We do not sell to patients.
Glycoursodeoxycholic acid
MCE China:Glycoursodeoxycholic acid
Brand:MedChemExpress (MCE)
Cat. No.HY-N1424
CAS:64480-66-6
Synonyms:Ursodeoxycholylglycine
Purity:98.0%
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.
Description:Glycoursodeoxycholic acid, a acyl glycine and a bile acid-glycine conjugate, is a metabolite of ursodeoxycholic acid.
In Vitro:The antioxidant compound glycoursodeoxycholic acid (GUDCA) fully abrogates UCB-induced cytochrome c oxidase inhibition and significantly prevents oxidative stress, metabolic alterations, and cell demise[1].GUDCA has shown therapeutic efficacy in neurodegenerative models and diseases. Increased cytosolic SOD1 inclusions were observed in 4 DIV NSC-34/hSOD1(G93A) cells together with decreased mitochondria viability, caspase-9 activation, and apoptosis[2]. Glycoursodeoxycholic acid shows preventive and restorative effects against unconjugated bilirubin -induced blood-brain barrier disruption and damage to human brain microvascular endothelial cells[3].
IC50 & Target:Microbial Metabolite Human Endogenous Metabolite
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References:
[1]. Vaz AR, et al. Bilirubin selectively inhibits cytochrome c oxidase activity and induces apoptosis in immature cortical neurons: assessment of the protective effects of glycoursodeoxycholic acid. J Neurochem. 2010 Jan;112(1):56-65. [Content Brief]
[2]. Vaz AR, et al. Glycoursodeoxycholic acid reduces matrix metalloproteinase-9 and caspase-9 activation in a cellular model of superoxide dismutase-1 neurodegeneration. [Content Brief]
[3]. Palmela I, et al. Hydrophilic bile acids protect human blood-brain barrier endothelial cells from disruption by unconjugated bilirubin: an in vitro study. Front Neurosci. 2015 Mar 13;9:80. [Content Brief]
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