ArticleScientific reports2015
Drug-Drug Interaction Potentials of Tyrosine Kinase Inhibitors via Inhibition of UDP-Glucuronosyltransferases.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 56 citations in OpenAlex.
- Clinical Implications ofPharmaceutics · 2026Review
- Roles of Uridine Diphosphoglucuronosyltransferase 2B Enzymes in Cancer Susceptibility and Treatment: A Review.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Sesamin exhibits potential food-drug interactions through the inhibition of cytochrome P450s and human UDP-glucuronosyltransferasesRSC advances · 2026Article
- Unveiling the role of UGT enzymes in chemoresistance: a path to enhanced cancer pharmacotherapy.Cancer drug resistance (Alhambra, Calif.) · 2026Article
- Computational drug repurposing: approaches, evaluation of in silico resources and case studies.Nature reviews. Drug discovery · 2025Review
- Predicting in vivo cannabinoid-drug interactions mediated via inhibition of UDP-glucuronosyltransferases using in vitro studies and physiologically based pharmacokinetic modeling and simulations.Drug metabolism and disposition: the biological fate of chemicals · 2025Article
- Kinase Inhibitors FDA Approved 2018-2023: Drug Targets, Metabolic Pathways, and Drug-Induced Toxicities.Drug metabolism and disposition: the biological fate of chemicals · 2024Review
- Review
- Avapritinib Carries the Risk of Drug InteractionCurrent drug metabolism · 2024Article
- Prediction of Drug-Drug Interaction Between Dabrafenib and Irinotecan via UGT1A1-Mediated Glucuronidation.European journal of drug metabolism and pharmacokinetics · 2022Article
- Cabozantinib Carries the Risk of Drug-Drug InteractionsCurrent drug metabolism · 2022Article
- Potential Assessment of UGT2B17 Inhibition by Salicylic Acid in Human Supersomes In Vitro.Molecules (Basel, Switzerland) · 2021Article
- Detoxication versus Bioactivation Pathways of Lapatinib In Vitro: UGT1A1 Catalyzes the Hepatic Glucuronidation of Debenzylated Lapatinib.Drug metabolism and disposition: the biological fate of chemicals · 2021Article
- Drug-drug interaction of atazanavir on UGT1A1-mediated glucuronidation of molidustat in human.Basic & clinical pharmacology & toxicology · 2021Article
- Emerging roles for UDP-glucuronosyltransferases in drug resistance and cancer progression.British journal of cancer · 2020Review
- In Vitro Inhibitory Effects of APINACA on Human Major Cytochrome P450, UDP-Glucuronosyltransferase Enzymes, and Drug Transporters.Molecules (Basel, Switzerland) · 2019Article
- Recent progress and challenges in screening and characterization of UGT1A1 inhibitors.Acta pharmaceutica Sinica. B · 2019Review
- Comparative review of drug-drug interactions with epidermal growth factor receptor tyrosine kinase inhibitors for the treatment of non-small-cell lung cancer.OncoTargets and therapy · 2019Review
- The concomitant use of lapatinib and paracetamol - the risk of interaction.Investigational new drugs · 2018Article
- Quantitative characterization of UDP-glucuronosyltransferase 2B17 in human liver and intestine and its role in testosterone first-pass metabolism.Biochemical pharmacology · 2018Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Tyrosine kinase inhibitors (TKIs) are anticancer drugs that may be co-administered with other drugs. The aims of this study are to investigate the inhibitory effects of TKIs on UDP-glucuronosyltransferase (UGT) activities, and to quantitatively evaluate their potential to cause drug-drug interactions (DDIs). Inhibition kinetic profiles of a panel of UGT enzymes (UGT1A1, 1A3, 1A4, 1A6, 1A7, 1A8, 1A9, 1A10, 2B4, 2B7, 2B15, and 2B17) by four TKIs (axitinib, imatinib, lapatinib and vandetanib) were characterized by using hepatic microsomes and recombinant proteins. Lapatinib exhibited potent competitive inhibition against UGT1A1 activity with a Ki of 0.5 μM. Imatinib was found to exhibit broad inhibition on several UGTs, particularly potent competitive inhibition against UGT2B17 with a Ki of 0.4 μM. The TKIs also exerted intermediate inhibition against several UGTs (i.e., UGT1A7 by lapatinib; UGT1A1 by imatinib; UGT1A4, 1A7 and 1A9 by axitinib; and UGT1A9 by vandetanib). Results from modeling for the quantitative prediction of DDI risk indicated that the coadministration of lapatinib or imatinib at clinical doses could result in a significant increase in AUC of drugs primarily cleared by UGT1A1 or 2B17. Lapatinib and imatinib may cause clinically significant DDIs when co-administered UGT1A1 or 2B17 substrates.
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