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This trial is conducted in Africa, Asia, Europe, South America, and the United States of America (USA).
The purpose of this study is to evaluate the effectiveness of secondary prophylactic treatment with NovoSeven® in haemophilia A and B patients with inhibitors.
Allocation: Randomized, Control: Uncontrolled, Endpoint Classification: Efficacy Study, Intervention Model: Parallel Assignment, Masking: Double Blind (Subject, Investigator), Primary Purpose: Treatment
activated recombinant human factor VII
Novo Nordisk Clinical Trial Call Center
Published on BioPortfolio: 2014-08-27T03:53:25-0400
This trial is conducted in Asia, Europe, Japan and North America. The aim of this clinical trial is to investigate the safety and the efficacy of a prophylactic treatment option with long ...
In this postmarketing study, the safety of Nonafact® (human coagulation factor IX) is evaluated in previous treated and untreated patients with severe, moderate or mild haemophilia B.
This study is conducted in the United States of America (USA). The aim of this study is to investigate the at-home-administration of bypassing agents for treatment of bleeding episodes in ...
This study is conducted in Europe. The primary objective of this registry is to observe the use of single dose and multi-dose use of NovoSeven® and to compare short-term outcomes, includi...
This NON INTERVENTIONAL OBSERVATIONAL STUDY is conducted in Europe. The primary aim is to observe the haemostatic efficacy of NovoSeven® treatment during routine practice in German clinic...
The thrombomodulin (TM)/activated protein C (APC) system is a key regulator of haemostasis, limiting amplification and propagation of the formed blood clot to the injury site. Dampening APC's inhibiti...
Monitoring recombinant activated factor VII (rFVIIa) treatment outcomes remains challenging. Thromboelastography (TEG) and the thrombin generation assay (TGA), measure coagulation dynamics over time a...
One of the most challenging issues facing us in the treatment of haemophilia is the development of alloantibodies against infused factor VIII (FVIII) or factor IX (FIX). Inhibitors render factor repla...
As the pharmacokinetics (PK) of factor VIII (FVIII) is individualized in children with haemophilia A (HA), PK parameters may be indicators of patients' bleeding phenotype and instruction for their per...
Activated form of factor XI. In the intrinsic pathway, Factor XI is activated to XIa by factor XIIa in the presence of cofactor HMWK; (HIGH MOLECULAR WEIGHT KININOGEN). Factor XIa then activates factor IX to factor IXa in the presence of calcium.
A hemostatic disorder characterized by a poor anticoagulant response to activated protein C (APC). The activated form of Factor V (Factor Va) is more slowly degraded by activated protein C. Factor V Leiden mutation (R506Q) is the most common cause of APC resistance.
Heat- and storage-stable plasma protein that is activated by tissue thromboplastin to form factor VIIa in the extrinsic pathway of blood coagulation. The activated form then catalyzes the activation of factor X to factor Xa.
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).
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.
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