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• W1993428106 abstract "We investigated the antiplatelet mechanisms of TA-993 [(−)-cis-3-acetoxy-5-(2-(dimethylamino)ethyl)-2,3-dihydro-8-methyl-2-(4-methylphenyl)-1,5-benzothiazepin-4(5H)-one maleate] and its metabolite MB3 (deacetyl and N-monomethyl TA-993) in human platelets stimulated by ADP in vitro. TA-993 and MB3 concentration-dependently inhibited fibrinogen binding to the ADP-stimulated platelets as well as inhibiting platelet aggregation. The antiplatelet effect of MB3 was about 300 times more potent than those of TA-993 and a glycoprotein IIb/IIIa receptor antagonist, Arg-Gly-Asp-Ser (RGDS). Aggregation of ADP-treated fixed platelets caused by the addition of fibrinogen was inhibited by RGDS but not by TA-993 and MB3. TA-993 and MB3 inhibited ADP-induced polymerization of actin filaments. Neither TA-993 nor MB3 affected cyclic AMP and cyclic GMP levels in resting platelets, and nor suppressed the increase in intracellular Ca2+ concentration induced by ADP. These results suggest that the antiplatelet mechanisms of TA-993 and MB3 may involve inactivation of glycoprotein IIb/IIIa receptors via inhibition of the polymerization of actin." @default.
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• W1993428106 date "2000-07-01" @default.
• W1993428106 modified "2023-09-27" @default.
• W1993428106 title "Antiplatelet mechanisms of TA-993 and its metabolite MB3 in ADP-induced platelet aggregation" @default.
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• W1993428106 doi "https://doi.org/10.1016/s0014-2999(00)00352-6" @default.
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