PLATELET PROTECTIVE EFFECT OF TAK-029, A NOVEL GLYCOPROTEIN IIB IIIA ANTAGONIST - AN IN-VITRO STUDY/

Previous studies have indicated that exposure of fibrinogen receptors associated with the glycoprotein IIb/IIIa complex contributes to plate let loss during cardiopulmonary bypass. TAK-029 is a newly developed r eversible, nonpeptide inhibitor of platelet glycoprotein IIb/IIIa rece ptors. In this study, we tested the platelet preserving effect of TAK- 029 in an in vitro model. The methods included the comparison of the r elease of beta-thromboglobulin (beta-TG) between a TAK-029 group (n = 5) and a control group (n = 5) in a mock circulation under a shear for ce generated by a centrifugal pump. To evaluate the degree of beta-TG release, Delta beta-TG/Delta T was calculated where Delta beta-TG is t he increase in beta-TG and Delta T is the time. The results showed tha t the value of Delta beta-TG/Delta T in the TAK-029 group was signific antly lower than it was in the control group (4.22 +/- 0.27 x 10(2) ng /ml vs. 7.33 +/- 0.66 x 10(2) ng/ml, respectively). In conclusion, TAK -029 reduced the platelet activation under the shear forces of an in v itro model, suggesting that TAK-029 is a potential candidate for plate let protection during cardiopulmonary bypass.