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This study will determine the efficacy of human-cl rhFVIII in previously treated patients with severe hemophilia A during prophylactic treatment, treatment of bleeding episodes and in surgical prophylaxis.
Allocation: Non-Randomized, Control: Uncontrolled, Endpoint Classification: Efficacy Study, Intervention Model: Single Group Assignment, Masking: Open Label, Primary Purpose: Prevention
Severe Hemophilia A
recombinant Factor VIII
Published on BioPortfolio: 2014-07-23T21:09:03-0400
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...
Efficacy, Safety and Pharmacokinetics Study of a rFVIII in Chinese subjects with Hemophilia A.To assess efficacy and safety of rFVIII administered as treatment and as on-demand therapy in ...
The purpose of this study is to determine the safety and tolerability of the factor VIII gene transfer treatment with BAY 2599023 (DTX201) in individuals with severe hemophilia A.
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...
Patients with hemophilia A are defined as "severe" if they present
Emicizumab is a bispecific monoclonal antibody that bridges activated factor IX and factor X to replace the function of missing activated factor VIII, thereby restoring hemostasis. In a phase 3, multi...
Prophylactic injections of factor VIII reduce the incidence of bleeds and slow the development of joint damage in people with hemophilia. The aim of this study was to identify optimal person-specific ...
Factor VIII inhibitor development is currently the most serious complication of the treatment of haemophilia A. Differences in manufacturing and the molecular structure of brands of recombinant factor...
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.