In vitro and in vivo effects of an anti-human VWFA1 monoclonal antibody in the H1HA mouse strain. (A) Response to ristocetin (1.5 mg/mL) in PRP from 4 mouse strains; platelet aggregation is evident only in H1HA mice. (B) Dose-response of H1HA PRP to the indicated ristocetin concentrations. (C) The anti-human VWFA1 monoclonal antibody NMC-4 (5 μg/mL; 1 minute incubation), but not 5 μg/mL of nonimmune control immunoglobulin G (IgG), completely blocked ristocetin-induced platelet aggregation in H1HA mouse PRP. (D) Treatment of H1HA mice with NMC-4 (0.8 mg/kg injected IV 7 minutes before the start of the test procedure [n = 6]) prolonged the tail bleeding time to >10 minutes as compared with <3 minutes in mice treated with control IgG (n = 6). (E) The same dose of NMC-4 prevented carotid artery occlusion in H1HA mice after a 9% FeCl₃–induced lesion (n = 10 for both treated and control mice). (A-C) Platelet aggregation is shown as a time-dependent increase in light transmittance through PRP. (D-E) Individual data are shown with median and interquartile range. Statistical analysis was performed with the Mann-Whitney nonparametric U test. **P < .01; ***P < .001.