Clopidogrel inhibits the action of ADP at the platelet P2Y12 receptor. Drug effects may be measured by evaluating ADP-induced platelet aggregation. We hypothesize that PlateletMappingTM using the thrombelastograph (TEG®) is able to quantify the degree of platelet inhibition in dogs given clopidogrel. PlateletMappingTM uses heparinized blood, ADP, and a reptilase-based activator. Six dogs were given clopidogrel at doses of 0.5 and 1 mg/kg PO, and blood samples were analyzed every 20 minutes for one hour and hourly to 3 hours. Platelet function was assessed using PlateletMappingTM, and compared with impedance aggregometry in three dogs at each dose. The maximum amplitude (MA) of the TEG® tracing was compared to baseline to determine the degree of clopidogrel-induced platelet inhibition. Most dogs displayed partial (40-60%) inhibition by 1 hour, and by 3 hours after the initial dose, MA had decreased to a mean of 20% of baseline, regardless of dose (p <0.001 vs. baseline). Correcting for the effect of thrombin activation on the TEG® tracing, the 3-hour MA values indicated near 100% inhibition of ADP-induced platelet aggregation. Impedance aggregometry showed a rapid decrease in ADP-induced platelet aggregation, decreasing to zero in most dogs by 2 hours (p < 0.001 vs. baseline). One dog at 0.5 mg/kg did not show a change in ADP-stimulated platelet aggregation measured by aggregometry, but did show a decrease when evaluated with PlateletMappingTM. PlateletMappingTM appears to be a viable test, and demonstrates clopidogrel to be an effective, rapidly acting drug for inhibition of ADP-induced platelet aggregation in the dog.