A method of treating fibrosis in a subject in need thereof is provided. The method comprising administering to the subject a polypeptide comprising a propeptide of lysyl oxidase (LOX), the polypeptide being devoid of LOX catalytic activity, thereby treating the fibrosis in the subject, wherein the method does not comprise administration of D-penicillamine. Also provided are polypeptide compositions for use in therapy.

A method of treating fibrosis in a subject in need thereof is provided. The method comprising administering to the subject a polypeptide comprising a propeptide of lysyl oxidase (LOX), the polypeptide being devoid of LOX catalytic activity, thereby treating the fibrosis in the subject, wherein the method does not comprise administration of D-penicillamine. Also provided are polypeptide compositions for use in therapy.

The present invention has an object of providing a novel drug inhibiting formation of leukocyte extracellular traps. The present invention provides a lactoferrin-containing inhibitor of formation of leukocyte extracellular traps, and a lactoferrin-containing composition for treating a disease associated with the formation of the leukocyte extracellular traps.

The present invention has an object of providing a novel drug inhibiting formation of leukocyte extracellular traps. The present invention provides a lactoferrin-containing inhibitor of formation of leukocyte extracellular traps, and a lactoferrin-containing composition for treating a disease associated with the formation of the leukocyte extracellular traps.

Novel antibodies, such as single domain antibodies (sdAbs), or antigen-binding fragments thereof that specifically bind a transferrin are described. Compositions, methods and systems for increasing the half-life of a target protein in a serum using an antibody or fragment thereof against a transferrin are also described.

The invention refers to a human lactoferrin derived peptide for use as an antigen masking agent in the production of a pharmaceutical composition for delivery of a biological active substance in a mammalian organism, where the biological active substance is able to induce an undesired immune response by the mammalian organism, where the pharmaceutical composition comprises a supramolecular aggregate of the biological active substance and the human lactoferrin derived peptide, with the effect that after delivery of pharmaceutical composition to the mammalian organism, there is no or only a diminished induction of the undesired immune response against the biological active substance.

The invention refers to a human lactoferrin derived peptide for use as an antigen masking agent in the production of a pharmaceutical composition for delivery of a biological active substance in a mammalian organism, where the biological active substance is able to induce an undesired immune response by the mammalian organism, where the pharmaceutical composition comprises a supramolecular aggregate of the biological active substance and the human lactoferrin derived peptide, with the effect that after delivery of pharmaceutical composition to the mammalian organism, there is no or only a diminished induction of the undesired immune response against the biological active substance.

The present invention relates to a fusion protein in which transferrin is peptide-bonded to a terminal of a granulocyte-colony stimulating factor (G-CSF) protein or a G-CSF mutant protein in which the 116.sup.th threonine is substituted with cysteine in the amino acid sequence of the G-CSF. Specifically, the granulocyte-colony stimulating factor (G-CSF) mutant protein of the present invention or the transferrin fusion protein thereof displays a significantly increased specific activity and blood stability, compared with the conventional human G-CSF, and has a higher purification efficiency than the conventional PEGylated G-CSF characterized by the extended half-life, so that it can be advantageously used for preventing or treating ischemic diseases or neutropenia.

The present invention relates to a fusion protein in which transferrin is peptide-bonded to a terminal of a granulocyte-colony stimulating factor (G-CSF) protein or a G-CSF mutant protein in which the 116.sup.th threonine is substituted with cysteine in the amino acid sequence of the G-CSF. Specifically, the granulocyte-colony stimulating factor (G-CSF) mutant protein of the present invention or the transferrin fusion protein thereof displays a significantly increased specific activity and blood stability, compared with the conventional human G-CSF, and has a higher purification efficiency than the conventional PEGylated G-CSF characterized by the extended half-life, so that it can be advantageously used for preventing or treating ischemic diseases or neutropenia.

The present invention generally relates to the detection, treatment or prevention of disease states. Specifically, the present invention relates to the detection, treatment or prevention of amyloidosis or amyloid-associated diseases. The present invention further comprises methods and compositions comprising therapeutic vaccines, antisera and molecular constructs, comprising expression vectors and fusion proteins encoded therein.