Ziprasidone is not an inhibitor or inducer of CYP3A4 in vivo. Risk for gastrointestinal adverse events in the form of nausea, vomiting and obstipation motivates vigilance against insufficient intake of food, especially of carbohydrate.

Ziprasidone is indicated for the treatment of schizophrenia. It is an antagonist of serotonin type 2A and dopamine type 2 receptors. 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.

Ziprasidone is metabolised to S-methyldihydro ziprasidone, ziprasidone sulphoxide, ziprasidone sulphone, oxindole acetic acid (Prakash 2000 and SPC), benzisothiazole piperidine sulphoxide and benzisothiazole piperidine sulfone (Urichuk 2008). Aldehyde oxidase is the enzyme responsible for most of the metabolism (Urichuk 2008). It is also metabolised via oxidative metabolism primarily via CYP3A4, with potentially contribution by CYP1A2 (SPC). In vitro data indicates that ziprasidone can be a moderate inhibitor of CYP2D6 and CYP3A4 (SPC). In vitro data also indicates that CYP1A2, CYP2C9, CYP2C19 and CYP2D6 do not contribute significantly to ziprasidone metabolism (Prakash 2000). Ziprasidone was shown to have no effect on the pharmacokinetics of ethinyl estradiol and levonorgestrel, CYP3A4 substrates, when co-administered (Muirhead 2000 and SPC). This indicates that ziprasidone is not an inhibitor or inducer of CYP3A4.