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Inhibition of Human Platelet Function in Vivo with a Monoclonal Antibody: With Observations on the Newly Dead as Experimental Subjects

Barry S. Coller, MD; Lesley E. Scudder, BS; Harvey J. Berger, MD; and John D. Iuliucci, PhD
[+] Article, Author, and Disclosure Information

Grant Support: Grant 19278 from the National Heart, Lung, and Blood Institute, the National Institutes of Health.

Requests for Reprints: Barry S. Coller, MD, Division of Hematology, HSC T-15/040, State University of New York at Stony Brook, Stony Brook, NY 11794.

Current Author Addresses: Dr. Coller and Ms. Scudder: Division of Hematology, State University of New York at Stony Brook, Stony Brook, NY 11794.

Drs. Berger and Iuliucci: Centocor Corporation, Malvern, PA 10355.

© 1988 American College of PhysiciansAmerican College of Physicians

Ann Intern Med. 1988;109(8):635-638. doi:10.7326/0003-4819-109-8-635
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The F(ab′)2 fragment of a monoclonal antibody to the platelet glycoprotein IIb/IIIa receptor (7E3) is a potent inhibitor of both in-vitro platelet aggregation and in-vivo platelet thrombus formation in animal studies. As a first step in assessing the potential of 7E3-F(ab′)2 as an antithrombotic agent for use in humans, we administered 7E3-F(ab′)2 intravenously at increasing doses to a person who had just died and was being maintained on a respirator (neomort). At 0.1 and at 0.2 mg/kg body weight, 74% and 92% of the glycoprotein IIb/IIIa receptors were blocked, respectively; adenosine-diphosphate-induced platelet aggregation was inhibited by 84% and 100% at these same doses. Platelet glycoprotein Ib function remained intact, even at 0.6 mg/kg. Acute hemodynamic or hemorrhagic toxicity was not noted. This antibody fragment, a potent, immediate-acting inhibitor of platelet aggregation, may be of benefit in vaso-occlusive and thromboembolic disorders.





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