Disclosed are methods of treating an individual, for example, a human individual, or more particularly a pediatric individual, having a disease characterized by liver fibrosis, comprising administering a therapeutically effective amount of one or both of a Complement Factor B inhibitor and a Complement Factor P (“CFP” or “properdin”) inhibitor, e.g., anti-CFP antibody and/or anti-CFB antibody or the respective antigen-binding fragment(s) thereof. Exemplary disease states include, but are not limited to, biliary atresia and post-Kasai biliary atresia.

Disclosed are methods of treating an individual, for example, a human individual, or more particularly a pediatric individual, having a disease characterized by liver fibrosis, comprising administering a therapeutically effective amount of one or both of a Complement Factor B inhibitor and a Complement Factor P (“CFP” or “properdin”) inhibitor, e.g., anti-CFP antibody and/or anti-CFB antibody or the respective antigen-binding fragment(s) thereof. Exemplary disease states include, but are not limited to, biliary atresia and post-Kasai biliary atresia.

The present disclosure provides novel and improved IL-15 fusion proteins for use in the treatment of cancer and other disorders. In various embodiments, the fusion proteins of the invention have two functional domains: an IL-15/IL-15RαSushi domain (also referred to herein as an “IL-15/IL-15RαSushi complex”) and an antibody domain, each of which can take different forms, and configured such that the IL-15 is fused to the C-terminal of the antibody domain and co-expressed and non-covalently complexed with IL-15RαSushi. Importantly, the fusions proteins of the present invention address several of the limitations observed with the IL-15 therapeutics evaluated to date; specifically, the fusion proteins demonstrate extended the half-life of IL-15 in vivo, and demonstrate optimized preclinical activity compared to rIL-15 or related cytokine therapeutics.

Antibodies and antigen-binding fragments thereof that bind C1s and inhibit C1s activity and modulate the activity of at least one component in the classical pathway (CP) of complement activation, and methods for treating complement-mediated disorders using anti-C1s antibodies and fragments, are provided.

Antibodies and antigen-binding fragments thereof that bind C1s and inhibit C1s activity and modulate the activity of at least one component in the classical pathway (CP) of complement activation, and methods for treating complement-mediated disorders using anti-C1s antibodies and fragments, are provided.

The present invention relates to an assay for detecting Tumstatin, and its use in evaluating lung cancers, such as non-small cell lung cancer (NSCLC), chronic kidney disease (CKD), such as CKD resulting from diabetes, lupus nephritis (LN) and systemic lupus erythematosus (SLE).

The present invention relates to an assay for detecting Tumstatin, and its use in evaluating lung cancers, such as non-small cell lung cancer (NSCLC), chronic kidney disease (CKD), such as CKD resulting from diabetes, lupus nephritis (LN) and systemic lupus erythematosus (SLE).

An embodiment provides a method for treating a body fluid of a patient with Alzheimer's Disease, including: removing the body fluid from a patient; applying a treatment to the body fluid, wherein the treatment comprises an antibody that joins with an Alzheimer's targeted antigen (TA) in the body fluid to form an antibody-TA complex, wherein the antibody comprises a radiofrequency absorption enhancer; removing the antibody-TA complex from the body fluid using a radiofrequency source; and returning the body fluid to the patient. Other aspects are described and claimed.

Described are peptides and peptide conjugates comprising CN binding motifs (CNBM) which inhibit the CN-NFAT interaction. In some embodiments, the peptides comprise: (i) CNBM; (ii) a hydrophobic, non-peptidic moiety (RH) which interacts with the hydrophobic pocket on a CN protein; (iii) a sequence -AAU1-AAU2-AAU3-AAU4-AAU5-AAU6-, wherein each of AAU2, AAU3, AAU4, AAU5, and AAU6, is, independently, optional, and each of AAU1, AAU2, AAU3, AAU4, AAU5, and AAU6 when present is independently an amino acid as defined herein; or (iv) combinations thereof. In some embodiments, RH is conjugated to the N- or C-terminus of the CNBM. In some embodiments, the sequence -AAU1-AAU2-AAU3-AAU4-AAU5-AAU6- is conjugated to the N- or C terminus of the CNBM. In some embodiments, the peptides comprise: CNBM and RH. In some embodiments. In some embodiments, the peptides comprise: CNBM and AAU1-AAU2-AAU3-AAU4-AAU5-AAU6-. In some embodiments, the peptides of the disclosure CNBM and RH.

Disclosed herein are polynucleic acid molecules, pharmaceutical compositions, and methods for treating muscle atrophy or myotonic dystrophy.