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Platelet Protective Effect of TAK‐029, A Novel Glycoprotein IIb/IIIa Antagonist: An In Vitro Study
Author(s) -
Kawahito Koji,
Fujimura Akio,
Kobayashi Eiji,
Misawa Yoshio,
Fuse Katsuo
Publication year - 1998
Publication title -
artificial organs
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.684
H-Index - 76
eISSN - 1525-1594
pISSN - 0160-564X
DOI - 10.1046/j.1525-1594.1998.06050.x
Subject(s) - in vitro , antagonist , pharmacology , platelet membrane glycoprotein , chemistry , platelet , glycoprotein , medicine , biochemistry , immunology , receptor
Previous studies have indicated that exposure of fibrinogen receptors associated with the glycoprotein IIb/IIIa complex contributes to platelet loss during cardiopulmonary bypass. TAK‐029 is a newly developed reversible, nonpeptide inhibitor of platelet glycoprotein IIb/IIIa receptors. In this study, we tested the platelet preserving effect of TAK‐029 in an in vitro model. The methods included the comparison of the release of β‐thromboglobulin (β‐TG) between a TAK‐029 group (n = 5) and a control group (n = 5) in a mock circulation under a shear force generated by a centrifugal pump. To evaluate the degree of β‐TG release, Δβ‐ TG /Δ T was calculated where Δβ‐ TG is the increase in β TG and Δ T is the time. The results showed that the value of Δβ‐ TG /Δ T in the TAK‐029 group was significantly lower than it was in the control group (4.22 ± 0.27 × 10 2 ng/ml vs. 7.33 ± 0.66 × 10 2 ng/ml, respectively). In conclusion, TAK‐029 reduced the platelet activation under the shear forces of an in vitro model, suggesting that TAK‐029 is a potential candidate for platelet protection during cardiopulmonary bypass.