The invention relates to a protein material includes angiogenin and/or angiogenin hydrolysate in an amount of 2 to 15 mg/100 mg, and lactoperoxidase and/or lactoperoxidase hydrolysate, in the mass ratio to angiogenin and/or angiogenin hydrolysate of 0.3 to 20.

The present invention relates to a biocompatible peptide inhibiting the aggregation of a β-amyloid protein, and more particularly, to a biocompatible peptide derived from superoxide dismutase 1 (SOD1) and specifically binding to β-amyloid, a β-amyloid aggregation inhibitor including the peptide, and a pharmaceutical composition for treating a β-amyloid aggregation-associated disease. The peptide of the present invention has a strong binding strength to β-amyloid, inhibits the formation of a β-amyloid protein aggregate, and prevents neural cell death, thereby treating a neurodegenerative disease such as Alzheimer's disease. In addition, since the peptide of the present invention does not have cytotoxicity, it has no side effect of disturbing an immune system.

The present invention comprises methods and compositions for the reduction of oxalate in humans, and methods for the purification and isolation of recombinant oxalate reducing enzyme proteins. The invention provides methods and compositions for the delivery of oxalate-reducing enzymes in particle compositions. The compositions of the present invention are suitable in methods of treatment or prevention of oxalate-related conditions.

The present disclosure provides methods of treating plasma protein imbalances or depletion (e.g., plasma protein imbalances or depletion caused by hemorrhagic shock or other clinical conditions), in particular by administering protein compositions derived from plasma or plasma isolates.

The present disclosure provides methods of treating plasma protein imbalances or depletion (e.g., plasma protein imbalances or depletion caused by hemorrhagic shock or other clinical conditions), in particular by administering protein compositions derived from plasma or plasma isolates.

The present invention provides a means for transferring a therapeutic gene of interest into a nervous system cell by a highly-efficient and simpler means. More specifically, the present invention provides a recombinant vector that uses an adeno-associated virus (AAV), a method for manufacturing the recombinant vector, and a method for using the recombinant vector. More specifically, recombinant adeno-associated virus virions, which are capable of passing through the brain-brain barrier, for transferring a therapeutic genes of interest into a nervous system cell in a highly-efficient manner, a drug composition containing the recombinant adeno-associated virus virions, a method for manufacturing the recombinant adeno-associated virus virions, and a kit or the like are provided.

The disclosure provides methods of treating gout in patients comprising administering a PEGylated uricase. Also provided are methods of treating gout in patients comprising co-administering a PEGylated uricase and methotrexate (MTX). Also provided are methods of reducing immunogenicity of a PEGylated uricase and prolonging the urate lowering effect comprising co-administration of the PEGylated uricase and MTX.

The disclosure provides methods of treating gout in patients comprising administering a PEGylated uricase. Also provided are methods of treating gout in patients comprising co-administering a PEGylated uricase and methotrexate (MTX). Also provided are methods of reducing immunogenicity of a PEGylated uricase and prolonging the urate lowering effect comprising co-administration of the PEGylated uricase and MTX.

The present invention is directed to methods and compositions of treating cardiovascular disease or disorder in a subject in need thereof, comprising steps of determining and identifying the haptoglobin phenotype of the subject and thereby selecting the course of treatment with an agent capable of raising HDL.

The present invention provides a method form making a composition of nanoparticles comprising a biological mimetic base component that forms the structure of the nanoparticle. By interacting with the functional groups of the base component, the half-life of a bioactive molecule is extended.