American Society of Hematology

Figure 2.

PRN1008 and PRN473 inhibit CLEC-2– and GPVI–mediated platelet aggregation. Healthy donor–washed platelets (2 × 108/mL) were incubated with vehicle (0.02% DMSO) or indicated concentration (50, 200, 500, or 2000 nM) of Btk inhibitors PRN1008 and PRN473 for 1 hour before platelet aggregation to snake venom toxin rhodocytin 100 (A) and 300 nM collagen (B); 3 (C) and 10 μg/mL CRP (D); 1 (E) and 3 μg/mL (F) or thrombin (0.04 U/mL) and thromboxane A2 mimetic U46619 (3 μM) (G) were measured by lumi-aggregometry. Representative traces (i) and quantification (ii). Mean ± SEM (n = 6). OD, optical density; Rhodo, rhodocytin; Veh, vehicle.

PRN1008 and PRN473 inhibit CLEC-2– and GPVI–mediated platelet aggregation. Healthy donor–washed platelets (2 × 10⁸/mL) were incubated with vehicle (0.02% DMSO) or indicated concentration (50, 200, 500, or 2000 nM) of Btk inhibitors PRN1008 and PRN473 for 1 hour before platelet aggregation to snake venom toxin rhodocytin 100 (A) and 300 nM collagen (B); 3 (C) and 10 μg/mL CRP (D); 1 (E) and 3 μg/mL (F) or thrombin (0.04 U/mL) and thromboxane A2 mimetic U46619 (3 μM) (G) were measured by lumi-aggregometry. Representative traces (i) and quantification (ii). Mean ± SEM (n = 6). OD, optical density; Rhodo, rhodocytin; Veh, vehicle.

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