The endothelial protein C receptor enhances hemostasis of FVIIa administration in hemophilic mice in vivo
The endothelial protein C receptor enhances hemostasis of FVIIa administration in hemophilic mice in vivo
Key Points The binding of administered FVIIa to endogenous EPCR enhances its ability to bypass FVIII or FIX deficiency in vivo. EPCR modulation of function of pharmacologic FVIIa administration may be exploited in protein or gene-based FVIIa therapeutics.
- University of Pennsylvania United States
- Children's Hospital of Philadelphia United States
Male, Hemostasis, Binding Sites, Receptors, Cell Surface, CHO Cells, Factor VIIa, Hemophilia A, Binding, Competitive, Blood Coagulation Factors, Recombinant Proteins, Mice, Inbred C57BL, Kinetics, Cricetulus, Cricetinae, Animals, Humans, Amino Acids, 1-Carboxyglutamic Acid, Blood Coagulation, Protein Binding
Male, Hemostasis, Binding Sites, Receptors, Cell Surface, CHO Cells, Factor VIIa, Hemophilia A, Binding, Competitive, Blood Coagulation Factors, Recombinant Proteins, Mice, Inbred C57BL, Kinetics, Cricetulus, Cricetinae, Animals, Humans, Amino Acids, 1-Carboxyglutamic Acid, Blood Coagulation, Protein Binding
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