The C-Jun N-Terminal Kinases Inhibition: A New Approach to the Regulation of Venlafaxine Pharmacokinetics
DOI:
https://doi.org/10.35516/jjps.v16i3.718Keywords:
Metabolism, Pharmacokinetics, Antidepressant Therapy, Intracellular Signal Transduction, JNKAbstract
The effect of the c-Jun N-terminal kinases (JNK) inhibitor 'IQ-1' on the pharmacokinetics of the antidepressant venlafaxine was studied. An acceleration of the metabolism of this psychotropic agent was revealed when a modifier of intracellular signal transduction was administered to experimental animals in vivo. The JNK blockade was accompanied by a decrease in the plasma level of the antidepressant without changes in the concentration of the pharmacologically active metabolite O-desmethylvenlafaxine. The results obtained indicate a modification of the pattern of venlafaxine biotransformation, involving a change in metabolic pathways with an increase in the formation of other metabolites, or a correction of its distribution in the body. The revealed properties of the JNK inhibitor can be used to develop fundamentally new approaches to improve the effectiveness of antidepressant therapy with venlafaxine within the framework of implementing the 'Strategy for Targeted Regulation of Xenobiotic Metabolism and Drug Pharmacokinetics'.
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