Platelet protective effect of TAK-029, a novel glycoprotein IIb/IIIa antagonist: an in vitro study

Artificial Organs
K KawahitoK Fuse

Abstract

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 beta-thromboglobulin (beta-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 beta-TG release, deltabeta-TG/deltaT was calculated where deltabeta-TG is the increase in beta-TG and deltaT is the time. The results showed that the value of deltabeta-TG/deltaT in the TAK-029 group was significantly 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 vitro model, suggesting that TAK-029 is a potential candidate for platelet protection during cardiopulmonary bypass.

References

May 1, 1990·The Annals of Thoracic Surgery·J R KappaV P Addonizio
Mar 24, 1990·Lancet·J R O'Brien
Jul 1, 1985·Seminars in Thrombosis and Hemostasis·E F MammenR F Wilson
Apr 11, 1981·Lancet·D B LongmoreW A Jones
Apr 1, 1994·The Annals of Thoracic Surgery·M J RayM O'Brien
Jan 1, 1997·The Journal of Thoracic and Cardiovascular Surgery·Y HiramatsuL H Edmunds
Apr 1, 1997·Artificial Organs·K Kawahito, Y Nosé

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Citations

Oct 4, 2003·ASAIO Journal : a Peer-reviewed Journal of the American Society for Artificial Internal Organs·Larry O ThompsonGeorge P Noon

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