198 results about "Autoimmunity" patented technology

The present application provides a variety of salts of 25HC3S, including crystalline salts of 25HC3S. Provided herein are pharmaceutical formulations of the salts of the invention, and methods of treating or preventing diseases therewith, the diseases such as non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), alcoholic hepatitis, acute kidney injury (AKI), psoriasis, atherosclerosis, hypercholesterolemia, hypertriglyceridemia, alcoholic fatty liver disease (AFLD), alcoholic steatohepatitis (ASH), leptin resistance, leptin deficiency, diabetic conditions, autoimmune conditions, inflammatory conditions, and the like. Nervous system disorders, EB virus related growth, and disorders associated with fat accumulation and inflammation. Methods of making the salts of the present application are also provided.

The present invention relates to a multiplex immunoassay method for diagnosing autoimmune nodopathy and, more specifically, to a multiplex immunoassay method, comprising the steps of: (1) binding CNTN1, Caspr1, NF155, and NF186 proteins each to microspheres having different color codes; (2) mixing the microspheres having different color codes to which the proteins are each bound; (3) treating the mixed microspheres with a biological sample to induce an antigen-antibody reaction; (4) adding a detection antibody; and (5) reading fluorescence information of the microspheres to measure the presence or absence of anti-CNTN1 antibody, anti-Caspr1 antibody, anti-NF155 antibody, or anti-NF186 antibody in the biological sample and quantify amounts thereof, thereby enabling simultaneous testing of four antibodies for rapid diagnosis of autoimmune nodopathy.

The disclosure features chemical entities (e.g., compounds or pharmaceutically acceptable salts thereof) that degrade the protooncogene VAV 1 protein (VAV1). These chemical entities are useful, for example, in the treatment of subjects suffering from inflammatory or autoimmune disorders (e.g., human subjects).

25HC3S choline and crystalline 25HC3S choline are described in the present application. Further disclosed herein are pharmaceutical formulations of 25HC3S choline (e.g., containing crystalline 25HC3S choline) and methods of using the pharmaceutical formulations to treat or prevent diseases such as non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), alcoholic hepatitis, acute kidney injury (AKI), psoriasis, atherosclerosis, hypercholesteremia, hypertriglyceridemia, and the like. Methods of treating fatty liver disease (AFLD), alcoholic steatohepatitis (ASH), leptin resistance, leptin deficiency, diabetic conditions, autoimmune conditions, inflammatory conditions, neurological conditions, Epstein-Barr virus associated growth, and conditions associated with fat accumulation and inflammation are provided. Also provided herein are methods of making 25HC3S, including crystalline 25HC3S choline.

This invention provides a kit for detecting anti-peroxidase-1-IgG antibodies, comprising the antigen protein peroxiredoxin-1 (peroxidase-1), a solid-phase carrier, labeled antibody, antigen dilution buffer, sample dilution buffer, antibody dilution buffer, substrate chromogenic agent, washing buffer, standards, positive control, and negative control. This kit utilizes an indirect reaction principle combined with magnetic microparticle chemiluminescence immunoassay to detect anti-peroxidase-1-IgG antibodies in the serum of the test sample. This invention is the first to identify autoantibodies against the target antigen peroxidase-1 in the serum of patients with autoimmune nephrotic syndrome. The provided kit provides a basis for domestic and international research on the molecular mechanisms and clinical diagnosis and treatment of autoimmune nephrotic syndrome related to peroxidase-1 and peroxidase-1-IgG autoantibodies.

The present invention provides novel drug-linker conjugates and antibody-drug conjugates of imidazo quinoline amine derivatives, which have agonistic activity against Toll-like receptors (TLRs), in particular TLR7 and / or TLR8, also provided are pharmaceutical compositions and methods of treatment against certain diseases or conditions mediated by or associated with TLR7 and / or TLR8 (e.g., graft rejection, autoimmunity, inflammation, allergy, asthma, infection, sepsis, cancer, and immunodeficiency).

Disclosed herein is a method for treating, preventing, and / or slowing the progression of various chronic inflammatory condition groups including: (1) the Type 2 Diabetes group (Metabolic Syndrome (MET), obesity, hyperglycemia); (2) ARDS (Acute Respiratory Distress Syndrome); (3) chronic autoimmune inflammatory conditions (Rheumatoid Arthritis (RA), Lupus, and Psoriasis); (4) inflammatory bowel diseases (IBD), such as Crohn's disease and ulcerative colitis; (5) metabolite group-mediated diseases (atherosclerosis, hypertension, and congestive heart failure); and (6) eating disorders, such as Prader-Willi Syndrome and other monogenic and symptomatic obesity disorders including leptin pathway defects, each method comprising orally administering a pharmaceutical composition comprising a denatonium salt. The present disclosure is based on the results of a series of studies that tracked biomarker cluster levels to track mediators of inflammatory conditions and mediators of gut signaling hormones in response to orally administered denatonium salts.

The present disclosure relates to collagen binding modification engineering of anti-inflammatory agents using collagen binding peptides (CBP) and vWF A3 to achieve targeted therapy of inflammatory diseases. Accordingly, embodiments of the present disclosure relate to compositions comprising an anti-inflammatory agent operably linked to an extracellular matrix (ECM) affinity peptide. Also disclosed are cytokines and anti-inflammatory agents, such as CD200, linked to serum proteins and / or ECM affinity peptides. Other aspects of the present disclosure relate to methods for treating an autoimmune or inflammatory disorder in a subject comprising administering to the subject a composition of the present disclosure.

Cyclopropyl N-[(S)-[3-[1-(2,2-difluoropropylcarbamoyl)-3-hydroxy-3-methyl- cyclobutyl]imidazo[1,2-b][1,2,4]triazin-6-yl]-[4- (trifluoromethyl)cyclohexyl]methyl]carbamate, or a pharmaceutically acceptable salt thereof, being a potent modulator of human IL-17 activity, is accordingly of benefit in the treatment and / or prevention of various human ailments, including inflammatory and autoimmune disorders.

This disclosure features chemical entities (e.g., a compound or a pharmaceutically acceptable salt thereof) that degrade and / or otherwise modulate (e.g., inhibit) NIMA Related Kinase 7 (NEK7). Said chemical entities are useful, e.g., for treating a subject (e.g., a human subject) having one or more disorders or diseases associated with NLRP3 inflammasome activation. Said disorders or diseases include but are not limited to, autoinflammatory and autoimmune disorders (e.g., gout, inflammatory bowel disease, rheumatoid arthritis, multiple sclerosis), neurodegenerative diseases (e.g., Alzheimer's disease, Parkinson's disease), cardiovascular and metabolic disorders (eg. pericarditis, atherosclerosis, Type 2 diabetes, obesity, and metabolic syndrome), fibrotic disorders (e.g. interstitial lung disease, chronic kidney disease), hematology (eg, anemia of inflammation) and eye disorders (eg. macular degeneration). In embodiments, and while not wishing to be bound by theory, it is believed that the chemical entities described herein directly target (e.g., directly bind to) NEK7, thereby altering (e.g., attenuating) the inflammatory response modulated by the NLRP3 inflammasome. This disclosure also features compositions containing the same as well as methods of using and making the same.

The present invention relates to gene therapy agents for the treatment of pulmonary alveolar proteinosis (PAP), particularly autoimmune PAP (aPAP). In particular, the present invention relates to gene therapy vectors which drive transient and / or low-level expression of granulocyte-macrophage colony-stimulating factor (GM-CSF), which provide a therapeutic effect without therapy-associated toxicity. The invention further relates to related products and an animal model of aPAP.

Provided herein are bispecific antibodies and antibody fragments that bind to both human TNFRSF25 and Α4Β7. Methods of treating or preventing diseases or disorders associated with inflammation and / or autoimmunity are provided, comprising administering to a patient in need thereof an effective amount of a human TNFRSF25- and Α4Β7-binding bispecific antibody.

Described herein are compounds that are useful in treating a TYK2-mediated disorder. In some embodiments, the TYK2-mediated disorder is an autoimmune disorder, an inflammatory disorder, a proliferative disorder, an endocrine disorder, a neurological disorder, or a disorder associated with transplantation.

Disclosed herein are methods of treating autoimmune, allergic, and / or inflammatory diseases in a subject in need thereof, comprising administering a therapeutic agent comprising one or more antigen-binding sites on a cell involved in the autoimmune, allergic, and / or inflammatory diseases and depleting the cell.

N-[(S)-[3-[1-(2,2-difluoropropylcarbamoyl)-3-hydroxy-3-methyl- cyclobutyl]imidazo[1,2-b][1,2,4]triazin-6-yl]-[4-(trifluoromethyl)cyclohexyl]methyl]-4-5 methyl-1,2,5-oxadiazole-3-carboxamide, or a pharmaceutically acceptable salt and / or solvate thereof, being a potent modulator of human IL-17 activity, is accordingly of benefit in the treatment and / or prevention of various human ailments, including inflammatory and autoimmune disorders.

The present invention relates to methods and compositions for the treatment of autoimmune diseases and of excessive hair shedding or hair loss in a subject or for promoting hair growth in a subject wherein the subject has an autoimmune hair loss disorder, such as alopecia areata. The methods and compositions comprise the administration of a janus kinase inhibitor, such as tofacitinib, wherein the inhibitor is predominantly absorbed through the oral mucosal routes such as the sublingual mucosa.

This disclosure features chemical entities (e.g., a compound or a pharmaceutically acceptable salt thereof) that degrade and / or otherwise modulate (e.g., inhibit) NIMA Related Kinase 7 (NEK7). Said chemical entities are useful, e.g., for treating a subject (e.g., a human subject) having one or more disorders or diseases associated with NLRP3 inflammasome activation. Said disorders or diseases include but are not limited to, autoinflammatory and autoimmune disorders (e.g., gout, inflammatory bowel disease, rheumatoid arthritis, multiple sclerosis), neurodegenerative diseases (e.g., Alzheimer's disease, Parkinson's disease), cardiovascular and metabolic disorders (eg. pericarditis, atherosclerosis, Type 2 diabetes, obesity, and metabolic syndrome), fibrotic disorders (e.g. interstitial lung disease, chronic kidney disease), hematology (eg. anemia of inflammation) and eye disorders (eg. macular degeneration). In embodiments, and while not wishing to be bound by theory, it is believed that the chemical entities described herein directly target (e.g., directly bind to) NEK7, thereby altering (e.g., attenuating) the inflammatory response modulated by the NLRP3 inflammasome. This disclosure also features compositions containing the same as well as methods of using and making the same.

The utility model relates to a detection kit of autoimmune nervous system disease, including box and with box rotation connection's box cover, the inside position adjustable of box is provided with a plurality of baffle, the both sides of each baffle upper portion respectively symmetry is provided with a plurality of clamping block, moves the baffle, makes the clamping block between adjacent two baffles clamp test tube, each baffle top is equipped with the limiting structure for fixing its position, the inside one side of box evenly interval is provided with a plurality of card slot, the baffle one side has opened first recess, and the baffle upside has opened the second recess with first recess intercommunication, the limiting structure includes the clamping block for with first recess sliding fit and with clamping block vertical connection's operating block, the operating block is away from the inner wall between second recess between clamping block one side and first recess and is equipped with the compression spring. The detection kit of autoimmune nervous system disease can clamp test tube of different diameter size, and the scope of application is wider.

Provided herein are, among other things, methods for treating a patient suffering from an autoimmune disease.

The present invention relates to antigen-binding proteins, related fragments thereof, for binding to CD80, and their use for treating various conditions such as inflammation and autoimmunity.

The present invention provides a compound of Formula (I) or a pharmaceutically acceptable salt thereof. Also disclosed are methods of using such compounds and pharmaceutical compositions comprising such compounds. These compounds are useful in treating disorders and diseases including inflammatory diseases, autoimmune disorders, cancer / oncologic disorders, or autoimmune disorders.

This invention relates to MASP isotypes as inhibitors of complement activation. It also relates to novel ficolin-related peptides and peptides derived from these ficolin-related peptides for the treatment of conditions associated with inflammation, apoptosis, autoimmunity, coagulation, thrombosis, or coagulopathy, and for use as biomarkers. Furthermore, this invention relates to antibodies recognizing the novel ficolin-related peptides and peptides derived therefrom, nucleic acid molecules encoding the peptides, vectors for producing the peptides, and host cells.

The invention discloses a pig IFNAR2 protein mutant, which is characterized in that the 399th site in the amino acid sequence of the pig IFNAR2 protein is mutated from glycine to alanine, and the amino acid sequence of the pig IFNAR2 protein is as shown in SEQ ID NO. 1. The invention provides a specific cleavage site of ASFV protease pS273R, and the site is mutated through a gene editing technology so as to block the cleavage of pig IFNAR2 by the pS273R and improve the ability of pigs to resist African swine fever virus infection. By blocking ASFV from damaging type I IFN mediated JAK-STAT signal activation, on the basis of retaining pig autoimmune performance, higher specificity and higher efficiency are achieved, negative effects of genetic engineering on pig growth performance and reproductive performance can be greatly reduced, and biosafety is higher.

Provided herein are methods for generating extracellular vesicles (EVs) from massively cultured polarized DCs, as well as additional operations of separating CTLA-4 + EV and CTLA-4-EV from each other and recovering the two EV populations in a physically and functionally intact state; also provided is a composition comprising the EV obtained by the method. In addition, the use of CTLA-4-EV in the treatment of cancer, as well as the use of CTLA-4 + EV in the treatment of GVHD and other T cell mediated autoimmune conditions, is also provided.

The present application relates to a compound of formula (I) or formula (II), wherein L, R1, R2, R3 and R4 are as defined in the claims. The compounds of formula (I) or formula (II) are useful as medicaments for modulating SIK activity in autoimmune disorders, inflammation and other disorders. (I) and (II).

The present invention relates to a genetically modified cell wherein a nucleic acid encoding a Stefin A protein variant that specifically binds to TNFR2 and / or a fusion protein comprising the protein variant is introduced into a host cell, a conditioned cell culture medium thereof, a pharmaceutical formulation of the genetically modified cell, and a method for preparing the genetically modified cell. And the use of the genetically modified cells in the treatment of immune diseases, including inflammation, autoimmunity and cancer.

Materials and methods are provided herein for detecting the presence of an autoantibody specific for PDE10A to identify the mammal as having an autoimmune neurological disorder as well as methods and materials for treating an autoimmune neurological disorder. Materials and methods also are provided herein for treating cancer and / or neurological autoimmunity in a mammal using an immune checkpoint inhibitor and detecting the presence of an autoantibody specific for PDE10A to monitor for the development of neurologic complications in the mammal.

The invention discloses application of a reagent for detecting an SLC17A7 autoantibody in diagnosis of nervous system diseases. By comparing different fluorescence modes of autoimmune antibodies related to IgG of healthy people in mouse brain tissue slices of patients with nervous system diseases, it is found that fluorescence signals only exist in the patients with nervous system diseases and do not exist in the healthy people, and it is prompted that the patients possibly have the autoimmune antibodies. According to the invention, IgG specific protein related to nervous system diseases is sought through a co-immunoprecipitation technology, a specific SLC17A7 autoantibody is found through cell immunofluorescence (CBA) detection, verification is carried out in cerebrospinal fluid, and finally it is determined that the SLC17A7 autoantibody can be used as a specific marker for diagnosis of nervous system autoimmune diseases. The SLC17A7 is taken as a detection antigen, detection of the expression of the SLC17A7 autoantibody can be applied to a kit for detecting the SLC17A7 autoantibody, the kit can be applied to detection of nervous system diseases, markers for identifying the nervous system diseases are enriched, and the detection accuracy of nervous system related diseases is improved.

N-[(S)-(4, 4-difluorocyclohexyl) {3-[1-(2, 2-difluoropropylcarbamoyl)-3-hydroxy-3-methylcyclobutyl] imidazo [1, 2-b] [1, 2, 4] triazin-6-yl} methyl]-4-methyl-1, 2, 5-oxadiazole-3-carboxamide, or a pharmaceutically acceptable salt thereof, is a potent modulator of human IL-17 activity, and is therefore of benefit in the treatment and / or prevention of a variety of human diseases, such as, for example, human IL-17. Inflammatory and autoimmune disorders are included.