Glycoursodeoxycholic acid 3-sulfate 

Glycoursodeoxycholic acid 3-sulfate is a glycine-conjugated sulfated bile acid 3-sulfate, which is produced by SULT2A1-mediated sulfation of glycoursodeoxycholic acid (HY-N1424) in the liver. Glycoursodeoxycholic acid 3-sulfate attenuates the anti-inflammatory effect of glycoursodeoxycholic acid and impairs the inhibitory effect on the IL-17 and NF-κB signaling pathways. Glycoursodeoxycholic acid 3-sulfate shows a significant correlation with aortic flow velocity and BNP in patients with aortic stenosis. Glycoursodeoxycholic acid 3-sulfate is mainly used in related studies such as quantitative analysis, quality control and biochemical experiments; it often serves as a reagent for metabolomics analysis and can also be applied to research related to aortic stenosis^[1][2].

Glycoursodeoxycholic acid 3-sulfate is accurately and precisely quantified in human blank urine across a concentration range of 20-2000 ng/mL via the LC/ESI-MS/MS method^[1].
Glycoursodeoxycholic acid 3-sulfate (100 μM; 24 h) does not reverse ISO-induced upregulation of IL-17 and NF-κB inflammatory pathways in human embryonic stem cell-derived cardiomyocytes, demonstrating diminished anti-inflammatory activity compared to unsulfonated Glycoursodeoxycholic acid (HY-N1424)^[2].
Glycoursodeoxycholic acid 3-sulfate (50-100 μM; 24 h) weakly inhibits ISO-induced upregulation of IL-17A, IL-6, and NF-κB p65 protein expression in human embryonic stem cell-derived cardiomyocytes, showing diminished anti-inflammatory efficacy relative to unsulfonated glycoursodeoxycholic acid^[2].
Glycoursodeoxycholic acid 3-sulfate (100 μM; 24 h) does not effectively prevent ISO-induced nuclear translocation of NF-κB p65 in human embryonic stem cell-derived cardiomyocytes, indicating impaired anti-inflammatory function relative to unsulfonated glycoursodeoxycholic acid^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Glycoursodeoxycholic acid 3-sulfate was elevated in plasma of ITAO-induced aortic stenosis in beagle dogs, linked to increased hepatic SULT2A1 expression which connects hemodynamic changes to bile acid metabolism^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

529.69

C₂₆H₄₃NO₈S

133429-88-6

O[C@@H]1[C@]2([H])[C@@](CC[C@]3([C@@]2([H])CC[C@]3([H])[C@H](C)CCC(NCC(O)=O)=O)C)([H])[C@@]4([C@](C[C@@H](CC4)OS(=O)(O)=O)([H])C1)C

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• [1]. Goto T, et al. LC/ESI-tandem mass spectrometric determination of bile acid 3-sulfates in human urine 3beta-Sulfooxy-12alpha-hydroxy-5beta-cholanoic acid is an abundant nonamidated sulfate. J Chromatogr B Analyt Technol Biomed Life Sci. 2007;846(1-2):69-77.

  [2]. Zhu M, et al. Glycoursodeoxycholic acid 3 sulfate sodium links hemodynamics and bile acid metabolism in aortic stenosis. J Adv Res. Published online September 9, 2025.