Quetiapine is not an inhibitor or inducer of any major CYP enzymes. Risk for gastrointestinal adverse events in the form of obstipation, dyspepsia and vomiting motivates vigilance against insufficient intake of food, especially of carbohydrate.

A dibenzothiazepine derivative.

Quetiapine is indicated for the treatment of schizophrenia. 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 obstipation, dyspepsia and vomiting.

Quetiapine is a substrate of CYP3A4 (FDA and SPC). In vitro data indicates that the metabolism of quetiapine is mainly by CYP3A4. The metabolite nor-quetiapine is formed and eliminated by CYP3A4 (SPC). Other studies indicates that CYP2D6 is also involved (Lin 2004). Half-life elimination for quetiapine and nor-quetiapine are 7 and 12 hours, respectively. Quetiapine and several of its metabolites are weak inhibitors of CYP1A2, CYP2C9, CYP2C19, CYP2D6 and CYP3A4 in vitro. This is however only seen at concentrations 5-50 fold higher than those observed at a dose range of 300-800 mg/day in humans. Based on these in vitro results, it is unlikely that co-administration of quetiapine with other drugs will result in clinically significant drug inhibition of CYP450 mediated metabolism of the other drug (SPC). A drug-drug interaction showed that quetiapine does not have any significant effect on the pharmacokinetics of antipyrine. Antipyrine is metabolised by CYP1A2, CYP2B6, CYP2C8, CYP2C9 and CYP3A4 (DeVane 2001) and the data therefore indicates that quetiapin is not an inhibitor or inducer of any major CYP enzymes (DeVane 2001 and Nemeroff 2002).

Uneventful use reported in 1 patient with acute porphyria.