Lidocaine metabolism (WP2646)

Homo sapiens

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Lidocaine is primarily metabolized by CYP1A2 but minor involvement of CYP3A4 is observed too. Based on [http://www.genome.jp/kegg-bin/show_pathway?hsa00982 KEGG]

Authors

Egon Willighagen and Kristina Hanspers

Activity

last edited

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Cited In

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Organisms

Homo sapiens

Communities

Annotations

Pathway Ontology

phase I biotransformation pathway via cytochrome P450 xenobiotic metabolic pathway

Participants
Query Drugst.One

Label Type Compact URI Comment
2,6-xylidine Metabolite chebi:28738
3-hydroxymonoethylglycinexylidide Metabolite kegg.compound:C16572
glycinexylidide Metabolite chebi:357241
Lidocaine Metabolite hmdb:HMDB0014426
2-amino-3-methylbenzoate Metabolite pubchem.compound:4161142
monoethylglycinexylidide Metabolite pubchem.compound:24415
3-hydroxylidocaine Metabolite pubchem.compound:161824
4-hydroxy-2,6-dimethylaniline Metabolite chebi:55545
CYP3A4 GeneProduct ensembl:ENSG00000160868
CYP1A2 GeneProduct ensembl:ENSG00000140505

References

  1. Fluvoxamine is a more potent inhibitor of lidocaine metabolism than ketoconazole and erythromycin in vitro. Wang JS, Backman JT, Wen X, Taavitsainen P, Neuvonen PJ, Kivistö KT. Pharmacol Toxicol. 1999 Nov;85(5):201–5. PubMed Europe PMC Scholia
  2. Cytochrome P450 1A2 is a major determinant of lidocaine metabolism in vivo: effects of liver function. Orlando R, Piccoli P, De Martin S, Padrini R, Floreani M, Palatini P. Clin Pharmacol Ther. 2004 Jan;75(1):80–8. PubMed Europe PMC Scholia
  3. Effect of fluvoxamine and erythromycin on the pharmacokinetics of oral lidocaine. Isohanni MH, Neuvonen PJ, Olkkola KT. Basic Clin Pharmacol Toxicol. 2006 Aug;99(2):168–72. PubMed Europe PMC Scholia