Effect of PKa inhibition on contact pathway–initiated TG in FXII-deficient PRP and RBC-reconstituted PRP. Representative curves of silica-initiated TG in F12^–/– PRP (A) and F12^–/– PRP reconstituted with RBCs (PRP+RBCs) (B) in the presence of the PKa inhibitor berotralstat or vehicle control. Quantification of TG lag time (C) and peak TG (D) in F12^–/– PRP and PRP with RBCs (n = 4 per group). Data presented as mean ± SD with paired t tests comparing samples with and without inhibitor; ∗∗P < .01; ∗∗∗P < .001. Bero, berotralstat; ns, not significant; Veh, vehicle.