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UDP-glucuronosyltransferase family 1 member A10 (UGT1A10)
- Target
- UGT1A10
- Molecular classification
- Enzyme, Transferase, Glycosyltransferase, UDP-glucuronosyltransferase, EC 2.4.1.17
01
Overview
UDP-glucuronosyltransferase family 1 member A10 (UGT1A10) is an enzyme responsible for catalyzing Phase II glucuronidation reactions, conjugating lipophilic molecules—including drugs, endogenous hormones, and xenobiotics—with glucuronic acid to facilitate their excretion. This enzyme plays a critical role in the metabolism and detoxification of estrogens, bilirubin, arachidonic acid metabolites, coumarins, and certain antihypertensive drugs, as well as natural dietary isoflavones and other exogenous compounds. Genetic variation or altered expression of UGT1A10 can impact drug metabolism, disease susceptibility, and risk of adverse events, making it both a functional metabolic enzyme and a potential pharmacological target or biomarker
- Other names
- UGT1A10UDP-glucuronosyltransferase 1A10UGT1JUDP-glucuronosyltransferase 1-10UDP-glucuronosyltransferase 1-JGNT1UDP-glucuronosyltransferase family 1 member A10UGT1-10UGT1.10UGT-1JUDP glycosyltransferase 1 family, polypeptide A10UGT1UGT-1AUGT1AhUG-BR1EC 2.4.1.17
02
Mechanism of action
Glucuronidation/conjugation: drugs or endogenous substrates are chemically conjugated to glucuronic acid via UGT1A10, increasing water solubility and facilitating excretion into urine or bile. Detoxification: elimination/inactivation of biologically active or toxic compounds.
03
Biological functions
Drug metabolism (Phase II metabolism; biotransformation)Detoxification (conversion of lipophilic molecules to water-soluble metabolites for excretion)Glucuronidation of estrogens (estradiol, estrone, estriol)Glucuronidation of drugs (e.g., angiotensin receptor antagonists, mycophenolic acid, coumarins, quinolines)Glucuronidation of endogenous compounds (bilirubin, steroids, hormones, arachidonic acid-derived eicosanoids, phytoestrogens)
04
Disease associations
HyperbilirubinemiaCrigler-Najjar syndrome type ITransient familial neonatal hyperbilirubinemiaIndirectly implicated in drug-induced liver injury, cancer, and cardiovascular disease via metabolism of drugs/endogenous molecules
05
Safety considerations
Drug-drug interactions: altered UGT1A10 activity can affect clearance and toxicity of drugs metabolized by glucuronidationGenetic polymorphisms: variation affects individual response/adverse reactions to metabolized drugsHyperbilirubinemia or risk of drug-induced liver injury: impaired function can lead to accumulation of toxic substrates
06
Interacting drugs
Losartan (and other angiotensin II receptor antagonists: caderastan, zolarsatan)
5 more in the full profile.
07
Biomarkers
UGT1A10 expression or activity in tissues may serve as a biomarker for drug metabolism capacity, hyperbilirubinemia risk, response to isoflavones, or susceptibility to drug toxicity/efficacy
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