|
|
||||||||||
Research Articles |
OBJECTIVE: To review the scientific literature on the pharmacology and clinical uses of abciximab. DATA SOURCES: MEDLINE, Index Medicus, and bibliographic literature searches of English-language articles pertaining to abciximab, 7E3, m7E3, and c7E3 were performed. Eli Lilly also provided unpublished results of the Evaluation of 7E3 for the Prevention of Ischemic Complications trial. DATA SELECTION: The selection of data presented focused on controlled trials using abciximab at doses currently approved by the Food and Drug Administration. DATA SYNTHESIS: Abciximab is a humanized chimeric Fab fragment of 7E3. 7E3 is a murine antibody directed against the integrin glycoprotein IIb)/IIIa receptor (GPIIb/IIIa) located on platelets. These receptors play an integral part in platelet aggregation by allowing fibrinogen to bind to them and interconnect platelets. When administered intravenously, abciximab binds to GPIIb/IIIa and hinders platelet aggregation. Bleeding times and activated clotting times are increased and the platelets' response to adenosine diphosphate is reduced with the use of abciximab. Clinical trials have indicated that abciximab can reduce the incidence of abrupt closure and restenosis associated with percutaneous transluminal coronary angioplasty (PTCA) performed in high-risk patients. Clinical trials also suggest that abciximab may have a role in the treatment of unstable angina and the acute therapy of myocardial infarctions. Complications associated with abciximab include bleeding and thrombocytopenia. The thrombocytopenia is likely related to immunologic mechanisms. In addition, the production of antimurine antibodies has been demonstrated with abciximab use. Abciximab is currently approved for the prevention of abrupt coronary closure associated with PTCA in patients at high risk for this event. CONCLUSIONS: Abciximab is effective in preventing platelet aggregation and has been proven to be of clinical benefit in selected high-risk patients receiving PTCA.
This article has been cited by other articles:
![]() |
T. Abumiya, R. Fitridge, C. Mazur, B. R. Copeland, J. A. Koziol, J. F. Tschopp, M. D. Pierschbacher, G. J. del Zoppo, and P. D. Hurn Integrin {alpha}IIb{beta}3 Inhibitor Preserves Microvascular Patency in Experimental Acute Focal Cerebral Ischemia Editorial Comment Stroke, June 1, 2000; 31(6): 1402 - 1410. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. R. Phillips, W. Teng, A. Arfsten, L. Nannizzi-Alaimo, M. M. White, C. Longhurst, S. J. Shattil, A. Randolph, J. A. Jakubowski, L. K. Jennings, et al. Effect of Ca2+ on GP IIb-IIIa Interactions With Integrilin : Enhanced GP IIb-IIIa Binding and Inhibition of Platelet Aggregation by Reductions in the Concentration of Ionized Calcium in Plasma Anticoagulated With Citrate Circulation, September 2, 1997; 96(5): 1488 - 1494. [Abstract] [Full Text] |
||||
![]() |
J. J. Cook, G. R. Sitko, M. A. Holahan, M. T. Stranieri, J. D. Glass, B. C. Askew, C. J. McIntyre, D. A. Claremon, J. J. Baldwin, G. D. Hartman, et al. Nonpeptide Glycoprotein IIb/IIIa Inhibitors. 15. Antithrombotic Efficacy of L-738,167, a Long-Acting GPIIb/IIIa Antagonist, Correlates with Inhibition of Adenosine Diphosphate-Induced Platelet Aggregation but not with Bleeding Time Prolongation J. Pharmacol. Exp. Ther., May 1, 1997; 281(2): 677 - 689. [Abstract] [Full Text] |
||||