The pharmacology of cilostazol

Cilostazol (6‐[4‐(1‐cyclohexyl‐1H‐tetrazol‐5‐yl)butoxy]‐3,4‐dihydro‐2(1H)‐quinolinone; OPC‐13013) is a 2‐oxo‐quinoline derivative with antithrombotic, vasodilator, antimitogenic and cardiotonic properties. The compound is a potent inhibitor of phosphodiesterase (PDE) 3A, the isoform of PDE 3 in the...

Full description

Saved in:
Bibliographic Details
Published in:Diabetes, obesity & metabolism obesity & metabolism, 2002-03, Vol.4 (s2), p.S14-S19
Main Author: Schrör, Karsten
Format: Article
Language:English
Subjects:
Blood Flow Velocity - drug effects
cilostazol
Humans
Muscle, Smooth, Vascular - drug effects
Muscle, Smooth, Vascular - physiology
peripheral arterial disease
pharmacology
Platelet Aggregation Inhibitors - pharmacokinetics
Platelet Aggregation Inhibitors - pharmacology
Regional Blood Flow - drug effects
Tetrazoles - pharmacokinetics
Tetrazoles - pharmacology
Tetrazoles - therapeutic use
Vasodilator Agents - pharmacokinetics
Vasodilator Agents - pharmacology
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Cilostazol (6‐[4‐(1‐cyclohexyl‐1H‐tetrazol‐5‐yl)butoxy]‐3,4‐dihydro‐2(1H)‐quinolinone; OPC‐13013) is a 2‐oxo‐quinoline derivative with antithrombotic, vasodilator, antimitogenic and cardiotonic properties. The compound is a potent inhibitor of phosphodiesterase (PDE) 3A, the isoform of PDE 3 in the cardiovascular system (IC50: 0.2 µm). In addition, there is inhibition of adenosine uptake, eventually resulting in changes in cAMP levels, dependent on the type of adenosine receptors (A1 or A2). Cilostazol inhibits platelet aggregation and has considerable antithrombotic effects in vivo. The compound relaxes vascular smooth muscle and inhibits mitogenesis and migration of vascular smooth muscle cells. In the heart, cilostazol causes positive inotropic and chronotropic effects. Most, if not all, of these actions are cAMP‐mediated, including the modification of cAMP‐controlled gene expression. Cilostazol decreases levels of serum triglycerides and causes some increase in HDL‐cholesterol levels. The compound has a number of additional effects which might contribute to its overall clinical efficacy. Cilostazol undergoes intensive and finally complete hepatic metabolism via the cytochrome P450 systems. This might result in some drug interaction, i.e. with erythromycin and omeprazole. The half‐life is approximately 10 h, resulting in about 2‐fold accumulation of the drug during repeated administration.
ISSN:1462-8902
1463-1326
DOI:10.1046/j.1463-1326.2002.0040s2s14.x