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The purpose of the study is to evaluate the effectiveness of Elocta compared to conventional factor products in the prophylactic treatment of patients with haemophilia A over a 24-month prospective period. Data will also be collected for a 12 month retrospective period.
Observational Model: Cohort, Time Perspective: Prospective
efmoroctocog alfa, Factor VIII
Swedish Orphan Biovitrum Reserach site
Swedish Orphan Biovitrum
Published on BioPortfolio: 2016-11-30T15:45:17-0500
The ability of a new recombinant porcine coagulation factor VIII, B-domain deleted (called "OBI-1"), to control the non-life- or limb-threatening bleeding episodes patients with hemophilia...
Hemophilia A is a genetic deficiency of factor VIII that causes blood to clot too slowly. The disease is classified based on how much factor VIII is in the blood. People with mild or moder...
The purpose of this study is to determine the immunologic and overall safety associated with long-term use of Alphanate in subjects diagnosed with severe hemophilia A (Factor VIII:C less t...
The purpose of this study is to compare the pharmacokinetic parameters and safety of Advate rAHF-PFM versus Recombinate rAHF in well described previously treated patients with severe hemop...
The purpose of this study is to compare the safety and efficacy of continuous infusion versus intermittent bolus infusion employing rAHF-PFM, a recombinant antihemophilic factor manufactur...
Hemophilia A is a hereditary X-linked recessive disease caused by mutations in the gene encoding factor VIII (FVIII), occurring in 1 out of 10,000 persons. Life expectancy and quality of life have dra...
Animals with hemophilia are models for gene therapy, factor replacement, and inhibitor development in humans. We have actively sought dogs with severe hemophilia A that have novel factor VIII mutation...
The mainstay of treatment of hemophilia A and B is the replacement of the congenitally deficient coagulation factor through the intravenous infusion of specific concentrates (factor VIII, FVIII, in he...
Hemophilia A animal models have helped advance our understanding of factor VIII deficiency. Previously, factor VIII deficient mouse models were reported to have a normal life span without spontaneous ...
Bleeding phenotype in mild and moderate hemophilia A (MHA) is inversely associated with the residual plasma concentration of factor VIII (FVIII:C). Within a group of patients with the same F8 missense...
The classic hemophilia resulting from a deficiency of factor VIII. It is an inherited disorder of blood coagulation characterized by a permanent tendency to hemorrhage.
Storage-stable blood coagulation factor acting in the intrinsic pathway. Its activated form, IXa, forms a complex with factor VIII and calcium on platelet factor 3 to activate factor X to Xa. Deficiency of factor IX results in HEMOPHILIA B (Christmas Disease).
Blood-coagulation factor VIII. Antihemophilic factor that is part of the factor VIII/von Willebrand factor complex. Factor VIII is produced in the liver and acts in the intrinsic pathway of blood coagulation. It serves as a cofactor in factor X activation and this action is markedly enhanced by small amounts of thrombin.
Activated form of factor VIII. The B-domain of factor VIII is proteolytically cleaved by thrombin to form factor VIIIa. Factor VIIIa exists as a non-covalent dimer in a metal-linked (probably calcium) complex and functions as a cofactor in the enzymatic activation of factor X by factor IXa. Factor VIIIa is similar in structure and generation to factor Va.
A hereditary deficiency of blood coagulation factor XI (also known as plasma thromboplastin antecedent or PTA or antihemophilic factor C) resulting in a systemic blood-clotting defect called hemophilia C or Rosenthal's syndrome, that may resemble classical hemophilia.