Effects of receptor-directed platelet inhibitors on TG. TG was measured in parallel in the WB (A) and autologous PRP (B). Samples were preincubated with vehicle medium or inhibitor at 5 increasing concentrations: vorapaxar (Vora; 0.04, 0.16, 0.63, 2.5, or 10 μM; PAR1 antagonist), atopaxar (Ato, idem), BMS-986120 (BM, idem; PAR4 antagonist), aptamer 1 (Apt1, 0.50, 1.75, 3, 9, or 15 μM; thrombin exosite-1 antagonist), aptamer 2 (Apt2, idem exosite-2), aptamer 1+2 (Apt1+2, idem exosite 1+2), tirofiban (0.31, 0.63, 1.25, 2.5, or 5 μg/mL; integrin αIIbβ3 antagonist), or PRT-060318 (PRT, 0.02, 0.08, 0.4, 2, or 10 μM; Syk antagonist), for 10 minutes at 37°C. TG parameters were compared relative to the vehicle condition (set at 100%). Heatmap presentation of % treatment effect at increasing dose on lagtime (left, 6 rows), thrombin peak levels (middle, 6 rows), and ETP (area under the curve; right, 6 rows). Color code showing increase (red) or decrease (green) in comparison with the vehicle control condition (black, 100%). Each condition was measured 3 times. Significance from vehicle controls, ∗P < .05; ∗∗P < .01; ∗∗∗P < .001; ∗∗∗∗P < .0001 (paired t test).