AIM: To observe the oral anti-platelet efficacy and the potential action mechanism of polyaspartoyl L-arginine (PDR), a new L-arginine rich compound. METHODS: Platelet aggregation was conducted by Born’s method; bleeding time was determined using tail’s bleeding time in mice; platelet adhesion was carried out with glass bottle method; nitric oxide (NO) was tested with Griess’ method; and cAMP, thromboxane B2 (TXB2) and 6-keto-PGF1α were assessed with commercial kits. RESULTS: The inhibition by PDR (15-60 mg/kg ig or 10 mg/kg iv) of platelet aggregation induced by adenosine diphosphate (ADP), collagen or thrombin at 1 h after oral administration or at 20 min after iv injection for rats (P<0.01), and its (15 mg/kg, ig) inhibition of ADP-induced platelet aggregation for rabbits during 6 h after administration were observed. PDR (15-60 mg/kg) prolonged the bleeding time of mice (P<0.05) and (30 mg/kg) increased NO concentration in plasma. On the other hand PDR did not change the contents of cAMP in platelet and TXB2 or 6-keto-PGF1α in plasma. CONCLUSION: PDR is a novel, oral effective platelet aggregation inhibitor and its action mechanism possibly related to increasing NO generation. AIM: To observe the oral anti-platelet efficacy and the potential action mechanism of polyaspartoyl L-arginine (PDR), a new L-arginine rich compound. METHODS: Platelet aggregation was conducted by Born’s method; bleeding time was determined using tail’s bleeding time in mice; platelet adhesion was carried out with glass bottle method; nitric oxide (NO) was tested with Griess’ method; and cAMP, thromboxane B2 (TXB2) and 6-keto-PGF1α were assessed with commercial kits. PDR (15-60 mg / kg ig or 10 mg / kg iv) of platelet aggregation induced by adenosine diphosphate (ADP), collagen or thrombin at 1 h after oral administration or at 20 min after iv injection for rats (P <0.01) (15 mg / kg, ig) inhibition of ADP-induced platelet aggregation for rabbits during 6 h after administration were observed. PDR (15-60 mg / kg) prolonged the bleeding time of mice (P < 30 mg / kg) increased NO concentration in plasma. On the other hand PDR did not change the contents of cAMP in platelet and TXB2 or 6-keto-PGF1α in plasma. CONCLUSION: PDR is a novel, oral effective platelet aggregation inhibitor and its action mechanism may related to increasing NO generation.