Abstract: The invention also relates to antigen binding proteins and related fragments thereof for binding Von Willebrand factor (VWF) and uses thereof. In one aspect, the present invention provides an antigen binding protein comprising an antigen binding domain that binds to or specifically binds to Von Willebrand factor (VWF) under shear gradient conditions. Preferably, the antigen binding protein comprises an antigen binding domain that does not bind to VWF under constant shear conditions.

Abstract: The present invention relates to oral controlled-release formulations of 5-(pyridinyl)-2(1H)-pyridinone compounds and their use in the treatment of a subject with heart failure, a stage, class or manifestation of heart failure, or at risk of developing or exhibiting symptoms of heart failure. The formulations of the invention release the compounds in the range of between 0.1 ?g/kg body weight/minute and 20 ?g/kg body weight/minute.

Abstract: The present invention relates to methods of treating subjects having heart failure with preserved ejection fraction (HFpEF) with a sustained-delivery formulation of cardiotonic 5-(pyridinyl)-2(1H)-pyridinone compounds.

Abstract: Described herein are vectors, such as adeno-associated virus (AAV) vectors, and recombinant AAV expressing Smad7. The disclosed AAV vectors and rAAV can be used for therapeutic applications in the treatment and amelioration of muscle wasting, cardiac and/or skeletal muscle wasting associated with cancer cachexia.

Abstract: The specification relates generally to the post-genomic identification of therapeutic targets and agents. In particular the specification relates to PSMD9 inhibitors and methods for preventing or treating metabolic disorders such as fatty liver disease that are associated with dysregulation of lipid homeostasis.

Abstract: The present invention relates generally to a method of therapeutically or prophylactically treating ischaemia-induced myocardial tissue damage, in particular ischaemia-reperfusion-induced myocardial tissue damage. More particularly, the present invention relates to a method of reducing the extent of ischaemia-induced myocardial tissue damage in a mammal by selectively upregulating FPR1-mediated ERK signalling. The method of the present invention is useful, inter alia, in reducing the extent and/or severity of myocardial tissue damage associated with conditions characterized by myocardial ischaemia or myocardial ischaemia and reperfusion, such as acute myocardial infarction caused by atherosclerotic artery occlusion or blood clot-induced artery occlusion.

Abstract: Described herein are vectors, such as adeno-associated virus (AAV) vectors, and recombinant AAV expressing Smad7. The disclosed AAV vectors and rAAV can be used for therapeutic applications in the treatment and amelioration of muscle wasting, cardiac and/or skeletal muscle wasting associated with cancer cachexia.