Buspirone is not an inhibitor or an inducer of CYP3A4 or CYP1A2. Risk for gastrointestinal adverse events in the form of nausea, abdominal pain, diarrhoea, obstipation and vomiting motivates vigilance against insufficient intake of food, especially of carbohydrate.

Buspirone is a serotonin agonist, but has also effects on dopamine receptors.

Buspirone is indicated for the treatment of anxiety disorders. 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, abdominal pain, diarrhoea, obstipation and vomiting. Other common side effects are nervousness, insomnia, depression, confusion, paraesthesia, tremor, tachycardia, chest pain musculoskeletal pain and fatigue.

Buspirone is metabolised via CYP3A4 (SPC). Metabolites include 5-hydroxy-buspirone which is inactive and 1-pyrimidinylpiperazine which is 1 to 20% as potent as buspirone (Gammans 1986). The elimination half-life is 2-11 hours. Buspirone did not have any statistical significant effect on the AUC of diazepam, a CYP3A4 and CYP2C19 substrate (SPC), when they were co-administered (Gammans 1986 and SPC). When co-administered with haloperidol, a CYP1A2, CYP2D6 and CYP3A4 substrate (Cheng 2010), buspirone did not affect the pharmacokinetics of haloperidol significantly (Huang 1996). These data indicate that buspirone is not an inhibitor or an inducer of CYP3A4 or CYP1A2. It is also listed as an unlikely major perpetrator of CYP3A (Polasek 2011).

Uneventful use of buspiron in a patient with documented acute intermittent porphyria (Holroyd 1999).