Figure 5.
AnVWF rescues murine FVIII and exhibits reduced clearance in vivo. (A) VWF antigen (blue bars) and FVIII (red bars) activity was determined by ELISA and chromogenic assay, respectively, following hydrodynamic infusion of AnVWF plasmid DNA (n = 4) or saline (n = 9). Mice administered An88-VWF plasmid possessed significantly increased (*) FVIII activity (P = .0412; Dunnett’s ANOVA) despite reduced VWF present in circulation (P = .013; Dunnett’s ANOVA). (B) Molar ratios of VWF and FVIII were calculated. Molar excess of An84-, An63-, An70-, and An88-VWF was significantly reduced compared with cohVWF (*P < .05; Dunnett’s ANOVA). (C) Male VWF-deficient mice were administered 20 μg recombinant AnVWF. VWF antigen levels were determined by ELISA normalized to the initial dose via 2-phase decay, n = 3 per time point.

AnVWF rescues murine FVIII and exhibits reduced clearance in vivo. (A) VWF antigen (blue bars) and FVIII (red bars) activity was determined by ELISA and chromogenic assay, respectively, following hydrodynamic infusion of AnVWF plasmid DNA (n = 4) or saline (n = 9). Mice administered An88-VWF plasmid possessed significantly increased (*) FVIII activity (P = .0412; Dunnett’s ANOVA) despite reduced VWF present in circulation (P = .013; Dunnett’s ANOVA). (B) Molar ratios of VWF and FVIII were calculated. Molar excess of An84-, An63-, An70-, and An88-VWF was significantly reduced compared with cohVWF (*P < .05; Dunnett’s ANOVA). (C) Male VWF-deficient mice were administered 20 μg recombinant AnVWF. VWF antigen levels were determined by ELISA normalized to the initial dose via 2-phase decay, n = 3 per time point.

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