Journal of thrombosis and haemostasis : JTH
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Hemophilia is characterized by abnormal thrombin generation and impaired clot stability. FXIII promotes clot stability and may be a useful adjunct treatment for hemophilia. ⋯ The effects of FXIII on clot stability and physical clot structure are seen at low concentrations of FVIII, indicating that FXIII could be a useful treatment in a variety of clinical scenarios.
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J. Thromb. Haemost. · Feb 2014
Anti-factor IXa/X bispecific antibody (ACE910): hemostatic potency against ongoing bleeds in a hemophilia A model and the possibility of routine supplementation.
We previously reported that a humanized anti-factor IXa/X bispecific antibody, hBS23, mimics the function of FVIII even in the presence of FVIII inhibitors, and has preventive hemostatic activity against bleeding in an animal model of acquired hemophilia A. After further molecular engineering of hBS23, we recently identified an improved humanized bispecific antibody, ACE910, for clinical investigation. ⋯ ACE910 may offer an alternative on-demand treatment option for patients with hemophilia A, as well as user-friendly and aggressive routine supplementation.
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J. Thromb. Haemost. · Feb 2014
Anti-factor IXa/X bispecific antibody (ACE910): hemostatic potency against ongoing bleeds in a hemophilia A model and the possibility of routine supplementation.
We previously reported that a humanized anti-factor IXa/X bispecific antibody, hBS23, mimics the function of FVIII even in the presence of FVIII inhibitors, and has preventive hemostatic activity against bleeding in an animal model of acquired hemophilia A. After further molecular engineering of hBS23, we recently identified an improved humanized bispecific antibody, ACE910, for clinical investigation. ⋯ ACE910 may offer an alternative on-demand treatment option for patients with hemophilia A, as well as user-friendly and aggressive routine supplementation.
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J. Thromb. Haemost. · Feb 2014
Antiplasmin, but not amiloride, prevents synovitis and cartilage damage following hemarthrosis in hemophilic mice.
Blood-induced joint damage is characterized by synovitis and cartilage damage. Recently, we demonstrated that joint bleeding in hemophilic mice results in elevated synovial levels of urokinase plasminogen activator (u-PA) and plasmin, and in plasmin-mediated cartilage damage. ⋯ Intra-articular treatment with antiplasmin (but not amiloride) following joint bleeding prevented synovitis and cartilage damage in hemophilic mice. These data offer promise for the use of antiplasmin as a new therapeutic intervention for patients who suffer from joint bleeds despite administration of clotting factor.