Human UGT2B4
Based on 1 Customer Validation
Human UGT2B4 is a UDP-glucuronosyltransferase. UGT2B4 catalyzes the glucuronidation of bile acids, Carvedilol (HY-B0006) and 6-hydroxylated bile acids to form glucuronide derivatives. UGT2B4 participates in the inactivation of endogenous and exogenous substances, including catechol estrogens, C19 steroids, phenols and monoterpenoids. Human UGT2B4 can be used in the research of hypertension, angina pectoris, chronic heart failure and intrahepatic cholestasis.
For research use only. We do not sell to patients.
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
IC50 & Target
[1]|
UGT2B4 |
In Vitro
Human UGT2B4 (expressed in insect cell microsomes) catalyzes the formation of carvedilol (HY-B0006) glucuronides G1 and G2, with a higher catalytic efficiency for G1 production (Vmax/Km = 0.33 μl/min/mg protein) than for G2 production (Vmax/Km = 0.12 μl/min/mg protein)[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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SMILES
[Human UGT2B4]
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Research Protocol for Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
Purity & Documentation
References
[1]. Monaghan G, et al. Structure of the human UGT2B4 gene encoding a bile acid UDP-glucuronosyltransferase. Mamm Genome. 1997 Sep;8(9):692-4. [Content Brief]
[2]. Ohno A, et al. Involvement of human hepatic UGT1A1, UGT2B4, and UGT2B7 in the glucuronidation of carvedilol. Drug metabolism and disposition: the biological fate of chemicals. 2004 Feb;32(2):235-9. [Content Brief]
[3]. Barbier O, et al. FXR induces the UGT2B4 enzyme in hepatocytes: a potential mechanism of negative feedback control of FXR activity. Gastroenterology. 2003 Jun;124(7):1926-40. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Human UGT2B4 Related Classifications
HY-E72116 Related Classifications
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