Abciximab inhibits release of platelet granule constituents

Mascelli, Mary Ann; Marciniak, Stanley J.; Lance, Ellen T.; Jordan, Robert E.

doi:10.1016/s0735-1097(98)80758-4

“…The total number of platelets contained in the aggregates as shown by electron microscopy may be limited compared with those being depleted from the circulation by adhesion. The substantial reduction of the fluid-phase platelet activation-marker BTG with Reopro is consistent with a report from a human study [22]. It should, however, be emphasized that Reopro inhibits aggregation but not specifically the release reaction from the platelets.…”

Section: Effects Of Reopto On Platelet Activation Markers and Formatisupporting

confidence: 89%

Inhibition of platelet aggregation by the GPIIb/IIIa antagonist Reopro does not significantly prolong xenograft survival in an ex vivo model

Fiane¹,

Videm

²

,

Mollnes

³

et al. 1999

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Effects on hyperacute re-better preservation of morphology jection were studied in a discordant model with the platelet GPIIb/IIIa antagonist Reopro. Pig kidneys perfused with human blood survived median 118 min in the Reopro group and 103 min in the controls (P = 0.22). Platelet and leukocyte counts decreased, whereas plasma thrombospondin and soluble as well as platelet membrane P-selectin increased significantly in both groups without significant intergroup differences. P-Thromboglobulin and myeloperoxidase increased significantly more in the control group than in the Reopro group ( P = 0.009 and P = 0.02, respectively). The classical complement pathway was substantially and similarly activated in both groups. Light and electron microscopy revealed arterial thrombi and numerous glomerular platelet aggregates in the control group in contrast to the Reopro group. In conclusion, Reopro reduced platelet aggregation, and platelet and leukocyte activation to some extent, but had no effect on complement activation and did not significantly prolong xenograft survival, even though was shown.

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“…Abciximab exerts a dose-dependent inhibitory effect on the release of platelet granule constituents (38). At a dose that produced 100% inhibition of platelet aggregation, abciximab resulted in 81 % inhibition of the release of adenosine triphosphate (ATP) from dense platelet granules.…”

Section: Inhibition Of Granule Releasementioning

confidence: 99%

Abciximab: The First Platelet Glycoprotein IIb/IIIa Receptor Antagonist

Jordan¹,

Nakada²,

Weisman³

1999

Biopharmaceuticals, an Industrial Perspective

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Abstract:Platelet aggregation plays Q crucial role in the development of the lifethreatening thrombosis responsible for such acute coronary syndromes as myocardial infarction and unstable angina pectoris. Although aspirin has traditionally been the mainstay of antiplatelet therapy, it is neither potent nor specific enough to provide adequate protection against thrombosis. The identification of glycoprotein (GP) IIblIIla as the key platelet receptor in the fmal common pathway of platelet aggregation and the development of therapeutic agents that block this receptor have opened up an entirely new dimension in cardiovascular medicine.Abciximab is the first of an innovative new class of cardiovascular drugs, the GP IIblIIIa receptor antagonists. As sUch, it is the fIrst agent that specifically blocks the fimction of a cellular adhesion molecule, thereby interfering with the adhesion of platelets and inhibiting platelet aggregation.This chapter will review the development of the first murine IgGj antibody directed against the GP IIblIIla receptor and describe how it was genetically engineered to become the less immunogenic but equally effective human/chimeric antibody fragment c7E3 Fab, or abciximab. The extensive studies that elucidated the mechanisms of action and binding characteristics of the new agent, as well as the pharmacology and toxicology studies that confirmed the safety and antithrombotic efficacy of antiplatelet therapy with an antibody fragment will be discussed. Finally, the chapter will explore in depth the

show abstract

Inhibition of platelet aggregation by the GPIIb/IIIa antagonist Reopro does not significantly prolong xenograft survival in an ex vivo model

Fiane

¹

,

Videm

²

,

Mollnes

³

et al. 1999

Transplant International

View full text Add to dashboard Cite

Effects on hyperacute re-better preservation of morphology jection were studied in a discordant model with the platelet GPIIb/IIIa antagonist Reopro. Pig kidneys perfused with human blood survived median 118 min in the Reopro group and 103 min in the controls (P = 0.22). Platelet and leukocyte counts decreased, whereas plasma thrombospondin and soluble as well as platelet membrane P-selectin increased significantly in both groups without significant intergroup differences. P-Thromboglobulin and myeloperoxidase increased significantly more in the control group than in the Reopro group ( P = 0.009 and P = 0.02, respectively). The classical complement pathway was substantially and similarly activated in both groups. Light and electron microscopy revealed arterial thrombi and numerous glomerular platelet aggregates in the control group in contrast to the Reopro group. In conclusion, Reopro reduced platelet aggregation, and platelet and leukocyte activation to some extent, but had no effect on complement activation and did not significantly prolong xenograft survival, even though was shown.

show abstract

Abciximab inhibits release of platelet granule constituents

Cited by 3 publications

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Inhibition of platelet aggregation by the GPIIb/IIIa antagonist Reopro does not significantly prolong xenograft survival in an ex vivo model

Inhibition of platelet aggregation by the GPIIb/IIIa antagonist Reopro does not significantly prolong xenograft survival in an ex vivo model

Abciximab: The First Platelet Glycoprotein IIb/IIIa Receptor Antagonist

Inhibition of platelet aggregation by the GPIIb/IIIa antagonist Reopro does not significantly prolong xenograft survival in an ex vivo model

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