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Maprotiline metabolism appears to co‐segregate with the genetically‐ determined CYP2D6 polymorphic hydroxylation of debrisoquine.
Author(s) -
Firkusny L,
Gleiter CH
Publication year - 1994
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1111/j.1365-2125.1994.tb04293.x
Subject(s) - maprotiline , debrisoquine , cyp2d6 , bronchoconstriction , pharmacology , medicine , endocrinology , pharmacogenetics , chemistry , metabolism , antidepressant , biochemistry , cytochrome p450 , asthma , genotype , gene , hippocampus
The plasma concentrations of the tetracyclic antidepressant maprotiline and its effect on histamine‐induced bronchoconstriction were measured after single (50 mg) and multiple (50 mg twice daily) oral doses in healthy subjects. Histamine‐induced bronchoconstriction was abolished after a single dose of maprotiline and this effect persisted throughout multiple dose treatment. The mean Cmax of maprotiline in six poor metabolisers (PM) of debrisoquine was 2.7‐fold greater than that in six extensive metabolisers (EM) and the mean AUC(0,48 h) was 3.5 times higher. The duration of the pulmonary effect of maprotiline after cessation of multiple dose treatment in EM was less than 3 weeks compared with at least 4 weeks in PM.