Cilostazol is mainly metabolized by CYP3A4. It is possibly an inhibitor of CYP3A4, but is not listed as a mechanism-based inhibitor or an inducer. Side effects that can be potentially porphyrinogenic through reduction in carbohydrate intake are diarrhoea, nausea and vomiting.

Cyclohexyl-tetrazol quinolinone

Cilostazol is indicated for the improvement of the maximal and pain-free walking distances in patients with intermittent claudication, who do not have rest pain and who do not have evidence of peripheral tissue necrosis (peripheral arterial disease Fontaine stage II). Side effects that can be potentially porphyrinogenic through reduction in carbohydrate intake are diarrhoea, nausea and vomiting. Other common side effects that can be confused with an acute porphyria attack are tachycardia, dyspepsia, abdominal pain and chest pain.

Cilostazol is metabolized by CYP3A4 and to a lesser extent by CYP2C19 and CYP1A2. It is 95-98% protein bound (SPC). In vitro studies have indicated that cilostazol has a very low affinity for inhibiting CYP3A4 (Mallikaarjun 1999 and Abbas 2000). There are on the other hand conflicting in vivo studies indicating that cilostazol do (Bramer 1999) and do not inhibit CYP3A4 (Chapman 2003). Cilostazol has been shown to increase the AUC of lovastatin (substrate for CYP3A4) and its β-hydroxy acid by 70% (SPC). There are no data indicating induction of hepatic microsomal enzymes. Cilostrazol is not listed as a mechanism-based inhibitor. The elimination half-life is 10.5 hours.