A method of treating inflammatory bowel disorders, such as ulcerative colitis, comprises administering an IL-23 inhibitor, such as an anti-IL-23p19 antibody (e.g., guselkumab) and a TNFα inhibitor, such as an anti-TNFα antibody (e.g., golimumab).

The present invention relates to use of a fusion protein in the treatment of age-related macular degeneration. In particular, the present invention relates to use of a bispecific fusion protein inhibiting the activation of a complement pathway and a vascular endothelial growth factor (VEGF) pathway for the treatment of age-related macular degeneration. The present invention also relates to a pharmaceutical composition comprising the fusion protein and a method for treating age-related macular degeneration using the fusion protein.

Use of a TNFR1-FADD-caspase8-caspase3 pathway inhibitor in preparation of a medicament for treating an immune system related disease caused by autoinducer, a method for screening a medicament for treating an immune system related disease caused by autoinducer and a method for treating an immune system related disease.

Dosing regimens for the administration of complexes comprising IL-15/IL-15Ra in combination with an anti-PD-1 antibody molecule to patients are disclosed. Such dosing regimens can be used for preventing, treating and/or managing disorders such as cancer.

Dosing regimens for the administration of complexes comprising IL-15/IL-15Ra in combination with an anti-PD-1 antibody molecule to patients are disclosed. Such dosing regimens can be used for preventing, treating and/or managing disorders such as cancer.

The present application relates to novel prodrugs of IL-12. Further included in the present application are methods of making and using the novel prodrugs.

The invention relates to the formulation of pharmaceutical compositions of etanercept. The invention also relates to methods of removing buffer and of formulating pharmaceutical compositions of etanercept.

Bioactive peptides and methods for their use for preventing, treating, and/or reducing the incidence and/or symptoms of an autoimmune disease or disorder that may result from chronic inflammation, damage to β-cells of the pancreas, and other conditions that are implicated by the CD40-CD154 dyad. In particular, small peptides that are capable of interacting with CD40, thereby interfering with the ability of CD40 to interact with CD154, which impacts inflammation, autoimmunity, and disease progression. The use of such peptides in reducing diabetes mellitus, and in particular, the autoimmune inflammatory response that may be a driving factor thereof. Methods and materials for preventing and modulating diabetes mellitus and autoimmune diseases especially in dogs, cats, and horses.

The invention is relative to monoclonal anti-CD123 antibodies, or fragments thereof that specifically bind to the alpha chain of the human interleukin 3 (IL3) receptor. Further, the invention is relative to an isolated nucleic acid molecule encoding a chimeric antigen receptor (CAR), wherein the CAR comprises an antibody or an antibody fragment which includes an anti-CD123 binding domain, a transmembrane domain, and an intracellular signaling domain comprising at least a stimulatory domain, polypeptides encoded by said nucleic acid molecule as well as an isolated chimeric antigen receptor (CAR) molecules comprising such an antibody or antibody fragment. The invention is also relative to a vector comprising a nucleic acid molecule encoding a CAR, as well as a T cell comprising said vector, and to the use of a T cell expressing a CAR molecule for a treatment of a proliferative disease in a mammal, such as cancer.

Synthetic alphavirus-derived replicon expression systems comprising nucleic acid sequences encoding at least one modified nonstructural protein, and synthetic nucleic acid sequences encoding at least one heterologous protein are described. Methods of producing at least one heterologous protein in a cell, or of inducing an immune response in a subject by administering and/or expressing the synthetic alphavirus-derived replicon expression systems are provided.