Zuclopenthixol is a substrate of CYP2D6 and CYP3A4. It is not listed as inducer or inhibitor of any major CYP enzymes. Risk for gastrointestinal adverse events in the form of obstipation, vomiting, dyspepsia and diarrhoea motivates vigilance against insufficient intake of food, especially of carbohydrate.

Zuclopenthixol is indicated for the treatment of schizophrenia and other psychoses. 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, vomiting, dyspepsia and diarrhoea. Another common side effect is myalgia. Less common side effects are abdominal pain and nausea. Abrupt discontinuation of zuclopenthixol may be accompanied by withdrawal symptoms. The most common symptoms are nausea, vomiting, anorexia, diarrhoea, rhinorrhoea, sweating, myalgias, paraesthesias, insomnia, restlessness, anxiety, and agitation. Patients may also experience vertigo, alternate feelings of warmth and coldness, and tremor. Symptoms generally begin within 1 to 4 days of withdrawal and abate within 7 to 14 days (SPC).

Zuclopenthixol is metabolised by CYP2D6 (Dahl 2002 and SPC) to inactive metabolites (Norsk legemiddelhåndbok). In vitro data indicates that zuclopenthixol is metabolised by CYP2D6 and CYP3A4 (Davies 2010). A therapeutic drug monitoring study also suggested the same (Davies 2010). Zuclopenthixol is not listed as an inducer or inhibitor or any major CYP enzymes (Isoherranen 2009 and Pelkonen 2008).

Zuclopenthixol is listed as unsafe because it has been shown to be porphyrinogenic in animals or in vitro systems (Moore 1997).