Inhibition of platelet aggregation by monoclonal antibodies against glycoprotein IIb–IIIa complex |
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Authors: | T V Byzova T N Vlasik A V Mazurov |
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Institution: | (1) Institute of Experimental Cardiology, Cardiology Research Center, Russian Academy of Medical Sciences, Moscow |
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Abstract: | Monoclonal antibodies CRC64 are obtained against Ca2+-dependent glycoprotein IIb–IIIa complex of the platelet membrane which possess the ability to inhibit completely fibrinogen-dependent
platelet aggregation. CRC64 is directed against the epitope formed by the glycoprotein IIb–IIIa complex and does not interact
with proteins isolated after platelets are treated with ethylenediamine tetraacetate. Complete, reproducible blockade of platelet
aggregation caused by 5 μM adenosine diphosphate is noted in an MCA concentration of 3 μg/ml, while in the case of a stronger
inductor, namely 1 U/ml thrombin, platelet aggregation is inhibited in a concentration of 5 μg/ml. F(ab′)2 fragments are also able to inhibit platelet aggregation completely and are usually effective in concentrations lower than
native monoclonal antibodies.
Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 118, N
o
10, pp. 402–405, October, 1994
Presented by V. N. Smirnov, Member of the Russian Academy of Medical Sciences |
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Keywords: | monoclonal antibodies platelets aggregation glycoprotein IIb– IIIa complex |
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