Antiplatelet activity of inositol hexaphosphate (IP6)

Platelet adhesion to endothelial cells, their aggregation and subsequent re lease of platelet-derived mediators are key steps in the pathogenesis of th rombosis and atherosclerosis. Using impedance technology the effect of inos itol hexaphosphate (IP6) on platelet aggregation and adenosine triphosphate (ATP) release were simultaneously measured in whole blood obtained from he althy volunteers (n = 10). The platelets were activated with adenosine diph osphate (ADP) (10 mu M), collagen (2 mu g/mL) or thrombin (1 U/mL) in the p resence or absence of IP6. IP6 significantly inhibited platelet aggregation induced with all agonists in a dose-response manner (p < 0.0001 for ADP an d collagen, p=0.0103 for thrombin), with the IC50 values of 0.9, 1.6 and 0. 8 mM. Secretion of platelet dense granule content was measured in parallel. IP6 strongly and significantly reduced agonist- induced ATP release (p=0.0 0247 for ADP; p=0.0074 for collagen; p=0.0069 for thrombin). These data dem onstrate that IP6 effectively inhibits human platelet aggregation in vitro, suggesting its potential in reducing the risk for cardiovascular disease.