Amisulpride is mainly excreted unchanged in urine and feces. Pharmacokinetic studies suggest the absence of inducing or inhibiting effects on hepatic microsomal enzyme activity. No clinical reports of CYP-related drug-drug interactions. Side effects such as nausea and vomiting may be potentially porphyrinogenic through reduction in caloric intake.

Amisulpride is a substituted benzamide.

Amisulpride is an atypical antipsychotic used mainly in the management of psychoses such as schizophrenia, but in some countries it has also been tried in depression. Administered orally or as an intramuscular injection. Common adverse reactions of amisulpride that can be confused with an acute porphyric attack are constipation, nausea, vomiting, anxiety, and agitation. Side effects such as nausea and vomiting may be potentially porphyrinogenic through reduction in caloric intake.

Absolute bioavailability of amisulpride is 48%. Amisulpride undergoes only minimal metabolic transformation (Rosenzweig, 2002; Spina, 2007). Two inactive metabolites, accounting for approximately 4% of the dose, have been identified. Most of a dose appears in the urine as unchanged drug.(Spina, 2007). Antipyrine half-life is not altered after repeated administration, which suggests the absence of inducing or inhibiting effects on hepatic microsomal enzyme activity. (Rosenzweig, 2002). Because of its negligible metabolic elimination, amisulpride is almost devoid of clinically relevant metabolic interactions (Spina, 2007). There are no clinical reports that amisulpride influences the blood concentrations of other CYP metabolized drugs. A high-carbohydrate high-fluid meal almost halves the already low oral bioavailability of this drug (Caccia, 2000).