Abstract: The present invention provides a method of treating a subject in need thereof comprising classifying the subject into functional group FG1, FG2 or FG3, wherein i) when the subject is classified into the FG1 functional group, (A) the level of OPN or the activity of OPN in said subject is increased; (B) the subject is not treated with a brace; or (C) a combination of (A) and (B); and ii) when the subject is classified into the FG2 or FG3 functional group, (A) the level of OPN or the activity of OPN in said subject is decreased; (B) the subject is treated with a brace; or (C) a combination of (A) and (B).

Abstract: The present disclosure provides compositions and methods for repairing cartilage defects.

Abstract: In certain aspects, the disclosure provides compositions and methods for treating spinal muscular atrophy. For example, in some embodiments, the disclosure provides ALK4:ActRIIB antagonists that may be used to treat spinal muscular atrophy, particularly treating one or more complications of spinal muscular atrophy including, for example, increasing muscle mass muscle strength, and bone mineral density.

Abstract: Disclosed are methods and compositions for treating, inhibiting, and/or preventing heterotopic ossification in a subject in need thereof. Particularly disclosed are methods for treating, inhibiting, and/or preventing heterotopic ossification in a subject in need thereof by administering to the subject a therapeutic agent such as an immune checkpoint inhibitor and/or Fetuin-A or a variant thereof. Also disclosed are pharmaceutical compositions and pharmaceutical kits comprising an immune checkpoint inhibitor and/or Fetuin-A or a variant thereof for treating, inhibiting, and/or preventing heterotopic ossification in a subject in need thereof.

Abstract: Provided herein are proteins, antibodies, assays and methods useful for modulating growth factor levels and/or activities. In some embodiments, such growth factors are members of the TGF-? superfamily of proteins.

Abstract: The present inventors have found that HMGB1 fragment peptides having a particular amino acid sequence exhibit the effects of improvement of cardiac function, inhibition of cardiomyocyte hypertrophy, inhibition of myocardial fibrosis, and promotion of angiogenesis in an animal model of dilated cardiomyopathy, that the particular HMGB1 fragment peptides also exhibit the effects of improvement of cardiac function, inhibition of cardiomegaly, inhibition of cardiomyocyte hypertrophy, inhibition of myocardial fibrosis, and promotion of angiogenesis in an animal model of ischemic cardiomyopathy caused by old myocardial infarction, and that the particular HMGB1 fragment peptides exhibit the effects of inhibition of cardiomyocyte hypertrophy and inhibition of myocardial fibrosis in an animal model of hypertensive cardiomyopathy.

Abstract: Provided herein are methods of treating diseases associated with vascular calcification and/or cardiovascular disease in a subject by using the level of a biomarker, in particular, snail homolog 1 (Snai1), phosphosmad2, phosphosmad3, urinary protein, dickkopf homolog 1 (Dkk1), collagen type 1 alpha 1 (Col1a1), activin (e.g., free activin), runt-related transcription factor 2 (Runx2), alkaline phosphatase (Alp), bone-specific alkaline phosphatase (BSAP), C-terminal type 1 collagen telopeptide (CTX), osterix, Klotho, alpha-smooth muscle actin (alpha-SMA), myocardin (MYOCD), activin receptor type 2A (ActRIIA), axis inhibition protein 2 (Axin2), and/or smooth muscle protein 22-alpha (Sm22-alpha), as an indicator(s) of responsiveness of the subject to the treatment, efficacy of the treatment, or appropriate dosage for the treatment with an activin type II receptor signaling inhibitor.

Abstract: Methods of treating and preventing metabolic disease through inhibiting interleukin 11 (IL-11)-mediated signalling are disclosed, as well as agents for use in such methods.

Abstract: The present invention provides a method of promoting local bone growth by administering a therapeutic amount of a Sost antagonist to a mammalian patient in need thereof. Preferably, the Sost antagonist is an antibody or FAB fragment selectively recognizing any one of SEQ ID NOS: 1-23. The Sost antagonist may be coadministered together or sequentially with a matrix conducive to anchoring new bone growth. Orthopedic and Periodontal devices comprising an implantable portion adapted to be permanently implanted within a mammalian body and bearing an external coating of a Sost antagonist are also disclosed, as it a method of increasing bone density by administering to a mammalian patient a therapeutic amount of a Sost antagonist together with an antiresorptive drug.

Abstract: This invention provides an NBP158 recombinant protein, a recombinant or synthetic NBP158 mutant protein, a pharmaceutical compositions comprising the NBP158 recombinant protein, and a method for treating metabolic disorders and conditions using such a pharmaceutical composition.

Abstract: In a non-limiting embodiment, there is provided a pharmaceutical composition for prevention and/or treatment of atopic dermatitis comprising an IL-31 antagonist as an active ingredient, wherein the IL-31 antagonist is repeatedly administered in equal amounts at the same dosing interval to a subject with or potentially with atopic dermatitis, at 0.1 to 1000 mg/body/1 day to 12 weeks, preferably at 0.1 to 1000 mg/body/2 weeks, 0.1 to 1000 mg/body/4 weeks, or 0.1 to 1000 mg/body/8 weeks.

Abstract: Provided are therapies, including combination therapies, for the treatment of lung inflammation, including interstitial lung diseases (ILDs), which include the use of at least one histidyl-tRNA synthetase (HRS) polypeptide or an expressible polynucleotide that encodes the HRS polypeptide, alone or in combination with at least one immunomodulatory agent.

Abstract: The present invention relates to monoclonal anti-human-GDF-15 antibodies. The antibodies include chimeric antibodies and humanized antibodies. The invention also relates to monoclonal anti-human-GDF-15 antibodies including murine anti bodies, chimeric antibodies and humanized antibodies for use in methods for the treatment of cancer cachexia and also for the treatment of cancer. The invention also provides pharmaceutical compositions, kits, methods and uses and cell lines capable of producing the monoclonal antibodies of the invention.

Abstract: Methods of treating patients having inflammatory bowel disease (IBD) or primary sclerosing cholangitis (PSC) are provided herein.

Abstract: GDF15 polypeptides, constructs comprising GDF15, and mutants thereof are provided. In various embodiments the GDF15 polypeptides, constructs comprising GDF15, and mutants thereof, can be of use in the treatment or ameliorating a metabolic disorder. In various embodiments the metabolic disease or disorder is type 2 diabetes, obesity, dyslipidemia, elevated glucose levels, elevated insulin levels and diabetic nephropathy.

Abstract: The present invention provides isolated IL-33 proteins, active fragments thereof and antibodies, antigen binding fragments thereof, against IL-33 proteins. Also provided are methods of modulating cytokine activity, e.g., for the purpose of treating immune and inflammatory disorders.

Abstract: The present invention provides methods for treating a stiffened joint in a subject that comprise administering relaxin, e.g., a PEGylated relaxin-2, to the subject. The relaxin may be administered intra-articularly as a sustained release formulation. The present invention also provides sustained release formulations in the form of a hydrogel for administering polypeptides that are covalently attached to a polymer, e.g., PEG.

Abstract: Monoclonal antibodies that bind and inhibit the activity of human GDF15 are disclosed. The antibodies can be used to treat body weight loss, including cachexia, associated with the over-expression of human GDF15.

Abstract: Compositions and methods relating to antibodies that specifically bind to TGF-beta binding proteins are provided. These methods and compositions relate to altering bone mineral density by interfering with the interaction between a TGF-beta binding protein sclerostin and a TGF-beta superfamily member, particularly a bone morphogenic protein. Increasing bone mineral density has uses in diseases and conditions in which low bone mineral density typifies the condition, such as osteopenia, osteoporosis, and bone fractures.

Abstract: The invention provides compositions and methods for treating optic neuropathic disorders.