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Ticlopidine hydrochloride (T), 5-[(2-chlorophenyl) methyl]-U,5»6,7-tetrahydrothieno [3,2-c] pyridine hydro­ chloride, is a potent antiplatelet agent of unknown mech­ anism of action. T does not inhibit human platelet low Km, cAMP phosphodiesterase (PDE) in vitro, (ICso» 1 0 ~ 3M), but does have some activity versus the low Km, cGMP-PDE (IC 5 o 3-tacl Equivalent values for theophylline, a weak PDE inhibitor, are 1.6x10”^ and l*.2xlO”**M, respec­ tively. T has no synergistic effect in vitro on plate­ let aggregation inhibited by PGEi. PDE inhibitors do show synergism with PGEi and other antiaggregatory PGs. Ex vivo in humans and animals, T inhibits ADP-induced aggre­ gation. This inhibition is not altered by addition of SQ-22536 (f.c.-10-,*M), a purported inhibitor of adenylate cyclase activity, whereas drugs whose platelet inhibitory activity depend on elevation of platelet cAMP, e.g., PGEi, adenosine and dipyridamole, have this inhibition partial­ ly reversed by SQ-22536.

Role Of Platelet cAMP And Prostaglandin Synthesis In Platelet Aggregation Inhibition By Ticlopidine Hydrochloride