Arginine-glycine-aspartate (RGD)-containing peptides are a class of platelet function inhibitors binding to the glycoprotein (GP) IIb-IIIa on the platelet surface.The relative effectiveness of three GP IIb-IIIa peptide inhibitors, RPR 110885, RPR 109891, and RPR 109035, were assessed for their capacity to inhibit equine platelet aggregation.Sodium citrate-anticoagulated blood (30 mL) was collected from each six adult quarter horses 1-2 h before performing platelet aggregation assays.Results show that RPR 109891 and its metabolite RPR 109039 are more potent inhibitors of equine platelet aggregation compared with RPR 110885.RPR 109891 has several potential advantages when compared with RPR 110885 in that its greater potency may reduce the cost of treating adult horses and it can be both orally and i.v. given.

01 Aug 2001·British Journal of PharmacologyQ2 · MEDICINE

Antithrombotic efficacy of a novel factor Xa inhibitor, FXV673, in a canine model of coronary artery thrombolysis

Q2 · MEDICINE

Article

Author: Bentley, Ross G. ; Leadley, Robert J. ; Rebello, Sam S. ; Morgan, Suzanne R. ; Kasiewski, Charles J. ; Chu, Valeria ; Perrone, Mark H.

We compared the antithrombotic efficacy of a potent factor Xa inhibitor, FXV673, to heparin and RPR109891, a GPIIb/IIIa antagonist, when used as adjunctive therapy in a canine model of rt‐PA‐induced coronary thrombolysis.

Thrombus formation was induced by electrolytic injury to stenosed coronary artery. After thrombotic occlusion, a 135 min infusion of saline (n=8), FXV673 (10, 30 or 100 μg kg−1+1, 3, or 10 μg kg−1 min−1, respectively; n=8 per dose), heparin (60 u kg−1+0.7 u kg−1 min−1, n=8), or RPR109891 (30 μg kg−1+0.45 μg kg−1 min−1, n=8), was initiated. Aspirin (5 mg kg−1, i.v.) was administered to all animals. Fifteen minutes after the start of drug infusion, rt‐PA was administered (100 μg kg−1+20 μg kg−1 min−1 for 60 min).

The incidence of reperfusion in the high dose FXV673 (8/8, 100%) was significantly greater than that in the heparin group (4/8, 50%), with a trend to faster reperfusion (23±5 min for FXV673 versus 41±11 min for heparin). Only 2/8 (25%) of the vessels reoccluded in the high dose FXV673 group, compared to 4/4 (100%) and 5/5 (100%) vessels in the heparin and RPR109891 groups, respectively (P<0.05).

Throughout the protocol, blood flow was higher in the FXV673 treated group compared to other groups. FXV673 enhanced vessel patency in a dose‐dependent manner.

Compared to vehicle and heparin groups, the thrombus mass was decreased by 60% in the high dose FXV673. FXV673, heparin and RPR109891 increased the bleeding time by 2.7, 1.7 and 4 fold, and APTT by 2.8, 2.7 and 1.2 fold, respectively.

In conclusion, FXV673 is more effective than heparin and at least as effective as RPR109891 when used as an adjunct during rt‐PA‐induced coronary thrombolysis.

British Journal of Pharmacology (2001) 133, 1190–1198; doi:10.1038/sj.bjp.0704182

01 Aug 2001·The American Journal of CardiologyQ3 · MEDICINE

Oral glycoprotein IIb/IIIa antagonism in patients with coronary artery disease

Q3 · MEDICINE

Article

Author: FitzGerald, G. A. ; Moretti, D. ; Vigilante, G. J. ; Catella-Lawson, F. ; Ramsey, K. E. ; Rocca, B. ; Kapoor, S. ; Cucchiara, A. J. ; De Marco, S. ; Theroux, P. ; Combe, S.

Dose-finding studies and trials of interaction of oral glycoprotein IIb/IIIa antagonists with other antiplatelet agents have been limited. We hypothesized that these detailed assessments could be first performed in patients with stable coronary artery disease (CAD) and then extrapolated to the target population. To this end, we performed 2 sequential studies. The first study examined the dose-related effects on indexes of platelet and vascular function induced by the oral inhibitor RPR 109891, when given alone and in combination with aspirin, in patients (n = 100) with stable CAD. The second study (the Antagonism of the FIbrinogen Receptor after Myocardial Events trial) assessed the pharmacodynamics and safety of derived regimens in patients (n = 320) with unstable coronary syndromes. In patients with stable CAD, platelet aggregation was dose dependently inhibited by RPR 109891, and the dose-response relation was shifted to the right by the concomitant administration of aspirin (p = 0.0001). The degree of platelet inhibition induced by 3 doses of RPR 109891 (plus aspirin) was lower in patients with unstable than stable CAD. No drug-related major bleeding occurred in either study. RPR 109891 treatment was associated with acute and delayed thrombocytopenia. In conclusion, chronic treatment with an oral glycoprotein IIb/IIIa antagonist (1) induces antiplatelet effects that are potentiated by concomitant administration of aspirin, (2) may require dose adjustment in syndromes of platelet activation, (3) is associated with a low rate of clinically significant bleeding when doses inducing incomplete inhibition of platelet aggregation are used, and (4) requires frequent monitoring of platelet count unless reliable predictors of delayed thrombocytopenia become available.

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Indication	Highest Phase	Country/Location	Organization	Date
Myocardial Infarction	Phase 2	US	-	-
Myocardial Infarction	Phase 2	JP	-	-
Myocardial Infarction	Phase 2	-	Sanofi	-
Myocardial Infarction	Phase 2	-	-	-

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