Figure 2.
Effect of PKa inhibition on contact pathway–initiated TG in FXII-sufficient and -deficient WB. Representative curves of silica-initiated TG in F12+/+ (A) and F12–/– (B) mouse WB in the presence of increasing concentrations of the PKa inhibitor (PKai) berotralstat or vehicle control. Quantification of TG lag time (C) and peak TG (D) in F12+/+ or F12–/– WB in the presence of 8 μM berotralstat or vehicle control (n = 3 per group). (E) Representative curves of silica-initiated TG in F12–/– mouse WB in the presence of increasing concentrations of the inhibitory anti-PKa antibody lanadelumab or IgG control. Quantification of TG lag time (F) and peak TG (G) in F12–/– WB in the presence of 400 μg/mL lanadelumab or IgG control (n = 3 per group). Data presented as individual values with mean ± standard deviation (SD). Data analyzed with paired Student t tests comparing samples with and without inhibitor; ∗P < .05; ∗∗P < .01. Bero, berotralstat; Lana, lanadelumab; ns, not significant; Veh, vehicle.

Effect of PKa inhibition on contact pathway–initiated TG in FXII-sufficient and -deficient WB. Representative curves of silica-initiated TG in F12+/+ (A) and F12/ (B) mouse WB in the presence of increasing concentrations of the PKa inhibitor (PKai) berotralstat or vehicle control. Quantification of TG lag time (C) and peak TG (D) in F12+/+ or F12/ WB in the presence of 8 μM berotralstat or vehicle control (n = 3 per group). (E) Representative curves of silica-initiated TG in F12/ mouse WB in the presence of increasing concentrations of the inhibitory anti-PKa antibody lanadelumab or IgG control. Quantification of TG lag time (F) and peak TG (G) in F12/ WB in the presence of 400 μg/mL lanadelumab or IgG control (n = 3 per group). Data presented as individual values with mean ± standard deviation (SD). Data analyzed with paired Student t tests comparing samples with and without inhibitor; ∗P < .05; ∗∗P < .01. Bero, berotralstat; Lana, lanadelumab; ns, not significant; Veh, vehicle.

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