Brands, Medical Use, Clinical Data
- Neuroprotective Agents
- Vasodilator Agents
- Fibrinolytic Agents
- Bronchodilator Agents
Brands / Synonyms
Cilostazol; Cilostazol [Inn:Jan]; Cilostazole; Cilostazolum [Inn-Latin]; Pletaal; Pletal; Pletal
For the reduction of symptoms of intermittent claudication (pain in the legs that occurs with walking and disappears with rest)
Cilostazol is a quinolinone derivative indicated for the reduction of symptoms of intermittent claudication, as indicated by an increased walking distance. Intermittent claudication is pain in the legs that occurs with walking and disappears with rest. The pain occurs due to reduced blood flow to the legs.
Mechanism of Action
The mechanism of the effects of Cilostazol on the symptoms of intermittent claudication is not fully understood. Cilostazol and several of its metabolites are cyclic AMP (cAMP) phosphodiesterase III inhibitors (PDE III inhibitors), inhibiting phosphodiesterase activity and suppressing cAMP degradation with a resultant increase in cAMP in platelets and blood vessels, leading to inhibition of platelet aggregation and vasodilation.
Biotrnasformation / Drug Metabolism
Cilostazol and several of its metabolites are inhibitors of phosphodiesterase III. Several drugs with this
pharmacologic effect have caused decreased survival compared to placebo in patients with class III-IV congestive
heart failure. PLETAL is contraindicated in patients with congestive heart failure of any severity.
PLETAL is contraindicated in patients with haemostatic disorders or active pathologic bleeding, such as bleeding
peptic ulcer and intracranial bleeding. PLETAL inhibits platelet aggregation in a reversible manner.
PLETAL is contraindicated in patients with known or suspected hypersensitivity to any of its components.
Since PLETAL is extensively metabolized by cytochrome P-450 isoenzymes, caution should be exercised when PLETAL is
coadministered with inhibitors of C.P.A. such as ketoconazole and erythromycin or inhibitors of CYP2C19 such as
omeprazole. Pharmacokinetic studies have demonstrated that omeprazole and erythromycin significantly increased the
systemic exposure of cilostazol and/or its major metabolites. Population pharmacokinetic studies showed higher
concentrations of cilostazol among patients concurrently treated with diltiazem, an inhibitor of C.P.A.. Pletal does
not, however, appear to cause increased blood levels of drugs metabolized by CYP3A4, as it had no effect on
lovastatin, a drug with metabolism very sensitive to C.P.A. inhibition.