ArticleThe AAPS journal2024
UGT2B10 is the Major UDP-Glucuronosyltransferase 2B Isoform Involved in the Metabolism of Lamotrigine and is Implicated in the Drug-Drug Interaction with Valproic Acid.
Article in The AAPS journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Determination of Hecogenin in Mouse Blood by UPLC-MS/MS and Applied to a Pharmacokinetic Study.Biomedical chromatography : BMC · 2026Article
- Modulatory effects of valproic acid and UGT polymorphisms on norclozapine plasma levels in clozapine-treated patients with schizophrenia.Scientific reports · 2026Article
- Drug-Metabolizing Enzymes in Human Keratinocytes and In Vitro Detection of Cytochrome P450-Mediated Phenolic Lamotrigine Metabolite.Chemical research in toxicology · 2026Article
- Age- and sex-associated variability in lamotrigine prescription patterns and clearance.Epilepsia · 2026Article
- Lamotrigine-Associated Toxic Epidermal Necrolysis in a Southeast Asian Female: A Case Report Highlighting Sex and Ancestry-Related Susceptibility.Case reports in psychiatry · 2026Article
- Flunitrazepam increases the risk of lamotrigine-induced cutaneous adverse reactions: Combined analysis of medical big data and clinical research.Psychiatry and clinical neurosciences · 2025Observational
- Development of a PBPK Model for Lamotrigine which Incorporates Metabolism by UGT2B10: Impact of UGT2B10 Poor Metabolizer Phenotype and Pregnancy.The AAPS journal · 2025Article
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Authors and funding
3 authors.
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Abstract
Lamotrigine is a phenyltriazine anticonvulsant that is primarily metabolized by phase II UDP-glucuronosyltransferases (UGT) to a quaternary N2-glucuronide, which accounts for ~ 90% of the excreted dose in humans. While there is consensus that UGT1A4 plays a predominant role in the formation of the N2-glucuronide, there is compelling evidence in the literature to suggest that the metabolism of lamotrigine is catalyzed by another UGT isoform. However, the exact identity of the UGT isoform that contribute to the formation of this glucuronide remains uncertain. In this study, we harnessed a robust reaction phenotyping strategy to delineate the identities and its associated fraction metabolized (f
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