Clomipramine is not an inhibitor or an inducer of any major CYP enzymes. Risk for gastrointestinal adverse events in the form of nausea, constipation, diarrhoea, fatigue, vomiting, abdominal disorders and decreased appetite motivates vigilance against insufficient intake of food, especially of carbohydrate.

Chlorinated imipramine (Chloro dibenzazepine propyl methylamine hydrochloride)

Clomipramine is indicated for the treatment of depression, obsessional and phobic states and adjunctive treatment of cataplexy associated with narcolepsy. 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, constipation and fatigue. Other common side effects are vomiting, abdominal disorders, diarrhoea, decreased appetite, headache, paraesthesia and muscle hypertonia.

Probably significant.

Clomipramine is metabolised by CYP3A4, CYP2C19, CYP2D6 and CYP1A2 (SPC). N-desmethylclomipramine is an active metabolite. Half-life eliminations of clomipramine and N-desmethylclomipramine are around 21 hours and 36 hours, respectively. Clomipramine is a weak inhibitor of CYP2D6 in vivo (Isoherranen 2009 and SPC). No drug-drug interactions with clomipramine as a perpetrator are observed (SPC), which indicate that clomipramine is not an inhibitor or inducer of any major CYP enzymes.

Andersson; patient inquiry: used without ill effects (n=1).

Clomipramine is listed with conflicting experimental evidence of porphyrinogenicity and is therefore listed as unsafe for use in acute porphyria (Moore 1997).

Uneventful use reported in 3 patients with acute porphyria.