Monograph
N06AA21 - Maprotiline |
Propably not porphyrinogenic |
PNP |
Rationale
Maprotiline is not listed as an inhibitor or an inducer of any major CYP enzymes.
Risk for gastrointestinal adverse events in the form of nausea, vomiting and obstipation motivates vigilance against insufficient intake of food, especially of carbohydrate.
Chemical description
Maprotiline is a tricyclic antidepressant.
Therapeutic characteristics
Maprotiline is indicated for the treatment of depression.
Very common side effects that can be potentially porphyrinogenic through reduction in carbohydrate intake and that also can be confused with an acute porphyria attack are nausea, vomiting and obstipation. Other common side effects are fatigue, dizziness and headache.
Metabolism and pharmacokinetics
In vitro data indicate that maprotiline is metabolised extensively by CYP2D6 and to a minor degree by CYP1A2 to its major active metabolite desmethylmaprotiline (Brachtendorf 2002 and Wang 2009). Maprotiline is listed as a substrate of CYP2D6 (Hisaka 2010).
Half-life elimination is between 27-58 hours.
Maprotiline is not listed as an inducer or inhibitor of any major CYP enzymes (FDA, Hisaka 2010, Isoherranen 2009 and Pelkonen 2008) and no drug-drug interaction with maprotiline as a perpetrator has been reported in the literature.
Published experience
Maprotiline is listed to be unsafe for use in acute porphyria because it has been shown to be porphyrinogenic in animals or in vitro (Moore 1997).
Two observations of safe use (Kauppinen 1992).
References
| # | Citation details | PMID |
|---|---|---|
| * | Scientific articles | |
| 1. | Cytochrome P450 enzymes contributing to demethylation of maprotiline in man.
Brachtendorf L, Jetter A, et al. Pharmacol Toxicol. 2002 Mar;90(3):144-9. |
12071336 |
| 2. | Prediction of pharmacokinetic drug-drug interaction caused by changes in cytochrome P450 activity using in vivo information.
Hisaka A, Ohno Y, et al. Pharmacol Ther. 2010 Feb;125(2):230-48. |
|
| 3. | Qualitative analysis of the role of metabolites in inhibitory drug-drug interactions: literature evaluation based on the metabolism and transport drug interaction database.
Isoherranen N, Hachad H, et al. Chem Res Toxicol. 2009 Feb;22(2):294-8. |
|
| 4. | Prognosis of acute porphyria: occurrence of acute attacks, precipitating factors, and associated diseases. Medicine (Baltimore). 1992 Jan;71(1):1-13.
Kauppinen R, Mustajoki P. |
1549056 |
| 5. | Drugs in the acute porphyrias--toxicogenetic diseases. Cell Mol Biol (Noisy-le-grand). 1997 Feb;43(1):89-94.
Moore MR, Hift RJ. |
9074793 |
| 6. | Inhibition and induction of human cytochrome P450 enzymes: current status.
Pelkonen O, Turpeinen M, et al. Arch Toxicol. 2008 Oct;82(10):667-715. |
18618097 |
| 7. | Synthetic and natural compounds that interact with human cytochrome P450 1A2 and implications in drug development.
Wang B, Zhou SF. Curr Med Chem. 2009;16(31):4066-218. |
19754423 |
| * | Government bodies | |
| 8. | U.S Food and Drug Administration (FDA).
|
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| * | Other sources | |
| 9. | Swedish National Formulary. FASS. Ludiomil. www.fass.se
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