19 results about "Type i diabetes" patented technology

The present invention relates to a method for improving glucose homeostasis and / or lowering plasma glucose levels by administering a SIRT6 activator. The present invention also provides a method for treating hyperglycemia, prediabetes, and diabetes, including type I diabetes, type II diabetes, or gestational diabetes, by administering a SIRT6 activator.

The present disclosure is generally directed to the use of biomaterial scaffolds engineered with SA-FasL for the transplantation of stem cell derived β-cells as a treatment for Type I diabetes. Early engraftment post-transplantation and subsequent maturation of these β-cells may be limited by the initial inflammatory response, which impacts the ability to sustain normoglycemia at long times. The survival and development of immature hPSC-derived β-cells transplanted on poly(lactide-co-glycolide) (PLG) microporous scaffolds into the peritoneal fat, a site being considered for clinical translation, was investigated. The scaffolds were modified with biotin for binding of a streptavidin-FasL (SAFasL) chimeric protein to modulate the local inflammatory microenvironment. The presence of FasL impacted infiltration of monocytes and neutrophils and altered their phenotypic response. Conditioned media generated from scaffolds explanted at day 4 did not impact hPSC-derived β-cell survival and maturation in vitro, which was not observed with unmodified scaffolds. Following transplantation, β-cell viability and differentiation were improved with SA-FasL modification. A sustained increase in insulin positive cell ratio was observed with SA-FasL modified relative to unmodified scaffolds. These results demonstrate that SA-FasL-modified scaffolds can mitigate initial inflammatory response and enhance β-cell engraftment and differentiation.

Recent studies indicate that sIL7R is involved in the development of autoimmune diseases. The present invention provides methods and compositions for a novel antibody therapeutic against the soluble isoform of the interleukin 7 receptor (sIL7R), a potent driver of self-destructive immune responses that cause autoimmune diseases including multiple sclerosis, lupus nephritis, type I diabetes, rheumatoid arthritis, systemic lupus erythematosus, and many other autoimmune diseases. The present invention includes antibodies specific for sIL7R that inhibit SIL7R, a driver of autoimmunity, without inhibiting mIL7R, thereby reducing the severity of or preventing autoimmunity without activating immunosuppressive mechanisms.

Provided herein are methods related to delivery of stem cell-derived cell therapies, including stem cell derived islet cell therapies, and related compositions, uses and articles of manufacture. In particular embodiments, the methods relate administering stem cell-derived islet cells. In some embodiments, the subject has a beta cell related disorder, such as diabetes (e.g. Type I diabetes).

To provide an agent for inhibiting the production of CCL20 and / or the migration of Th17 cells. The present invention also provides a composition for treating, preventing, or improving psoriasis, rheumatoid arthritis, type I diabetes, or systemic lupus erythematosus.SOLUTION: An agent for inhibiting CCL20 production and / or migration of Th17 cells, the agent comprising a fermented plant extract, wherein the fermented plant extract comprises yeasts capable of surviving in pH2 and sporulating in a complete medium, and a composition for treating, preventing, or ameliorating systemic lupus erythematosis, the composition comprising a fermented plant extract, wherein the fermented plant extract comprises yeasts capable of surviving in pH2 and sporulating in a complete medium.SELECTED DRAWING: None

Provided herein are methods of administering engineered islet cells, including functionally modified beta cells containing one or more modifications (such as genetic modifications). In some embodiments, the engineered pancreatic islets are low immunogen cells. In some embodiments, the one or more modifications reduce or eliminate the expression of one or more MHC class I and / or MHC class II human leukocyte antigens, while increasing the expression of one or more tolerogenic factors, such as CD47. In some embodiments, the subject has a beta cell related condition, such as diabetes (e.g., type I diabetes).

The present application relates to the field of medicine synthesis, disclose a long-acting dual agonist compound. The tirzepatide derivative described in the application is used for preparing a pharmaceutical composition for treating diseases, the use of the pharmaceutical composition in the preparation of a medicine for treating at least one of the following diseases, the diseases include type II diabetes, impaired glucose tolerance, type I diabetes, obesity, hypertension, metabolic syndrome, dyslipidemia, cognitive impairment, atherosclerosis, myocardial infarction, coronary heart disease, cardiovascular disease, stroke, inflammatory bowel syndrome and / or indigestion or gastric ulcer, liver fibrosis disease and pulmonary fibrosis disease.

Described herein are FasL-engineered biomaterials, as well as methods of making and using such FasL-engineered biomaterials, such as for immunomodulation, such as for inducing immunosuppression and specific immune tolerance, such as for preventing or reducing the risks of rejection of cellular or tissue grafts and / or the treatment of autoimmune disorders such as Type I diabetes. In specific embodiments, the FasL-engineered biomaterials are biotinylated microgels bound to SA-FasL.

Disclosed are: an agent for suppressing the production of CCL20 and / or the migration of Th17 cells, the agent containing a plant fermentation extract, wherein the plant fermentation extract contains yeast that can survive under conditions having a pH value of 2 and that is capable of forming spores in a complete culture medium; and a composition for treating, preventing or ameliorating psoriasis, rheumatoid arthritis, type I diabetes, or systemic lupus erythematosus, the composition containing a plant fermentation extract, wherein the plant fermentation extract contains yeast that can survive under conditions having a pH value of 2 and that is capable of forming spores in a complete culture medium.

Provided herein are anti-OVA-serine proteinase inhibitor (serpin) B13 monoclonal antibodies and antigen-binding antibody fragments that selectively and specifically bind to an epitope of serpin B13, compositions containing these antibodies and antibody fragments, and methods of using these antibodies and antibody fragments. These antibodies and antigen-binding fragments thereof are useful for inhibiting serpin B13 and for treating serpin B13-related diseases, e.g., type I diabetes.

Provided herein are methods of dosing engineered islet cells that include functional modified beta cell containing one or more modifications, such as genetic modifications. In some embodiments, the engineered islets are hypoimmunogenic cells. In some embodiments, the one or more modifications reduce or eliminate expression of one or more MHC class I and / or MHC class II human leukocyte antigens and also increase expression of one or more tolerogenic factors, such as CD47. In some embodiments, the subject has a beta cell related disorder, such as diabetes (e.g. Type I diabetes).

The invention provides a polypeptide with GLP-1 (glucagon-like peptide-1) R / GIPR / GCGR triple receptor agonistic activity or a pharmaceutically acceptable salt thereof, and the polypeptide or the pharmaceutically acceptable salt thereof has obvious triple receptor agonistic activity of glucagon-like peptide-1 (GLP-1), gastric inhibitory polypeptide (GIP) and glucagon (GCG) and an anti-DPP-IV enzyme digestion effect. The compound can be used for preparing pharmaceutical compositions for preventing or treating metabolic diseases such as type I diabetes mellitus, type II diabetes mellitus, gestational diabetes mellitus, obesity, non-alcoholic fatty liver disease (NAFLD), obesity, hyperlipidemia and the like.

The present disclosure relates to sequence selective deoxyribonucleic acid (DNA) binding compounds comprising a polyamide moiety configured to bind a DNA sequence. The invention also relates pharmaceutical compositions comprising the compounds, and methods of using the compounds for restoring expression of autoimmune regulator (AIRE) gene. The invention further relates to pharmaceutical compositions comprising the compounds, and methods of using the compounds for and treating an autoimmune disease (e.g., Addison disease, Celiac disease, dermatomyositis. Graves disease, Hashimoto thyroiditis, inflammatory bowel disease, multiple sclerosis (MS), myasthenia gravis, pernicious anemia, reactive arthritis, Sjogren syndrome, systemic lupus erythematosus, and type I diabetes). This abstract is intended as a scanning tool for purposes of searching in the particular art and is not intended to be limiting of the present invention.

This invention discloses a Cbl-b inhibitor compound as shown in formula (I), its uses, and pharmaceutical compositions containing it. This type of inhibitor is a potential tumor immunotherapy agent and autoimmune disease treatment agent. This invention also discloses the use of this type of compound in the treatment of tumors, type I diabetes, Graves' disease, systemic lupus erythematosus, and multiple sclerosis.

Provided herein are methods related to the delivery of stem cell-derived cell therapies, including stem cell-derived islet cell therapies, and related compositions, uses, and articles of manufacture. In particular embodiments, the methods involve administering stem cell-derived islet cells. In some embodiments, the subject has a beta cell related condition, such as diabetes (e.g., type I diabetes).

The present invention relates to compounds for the formulae (I) to (IV); as well as to structurally related specific (1H-indol-3-yl)(pyridin-2-yl) methanone derivatives not encompassed by any of these formulae. Said compounds are hydrocarbon receptor (AHR) agonists for the treatment of e.g. inflammatory, autoimmune, metabolic or proliferative diseases, such as e.g. metabolic syndrome, type I diabetes, steatosis, colitis (in particular ulcerative colitis), inflammatory bowel disease, Crohn's disease, rheumatoid arthritis, multiple sclerosis, psoriasis, dermatitis, pancreatitis, insulitis, atherosclerosis, graft versus host disease, or cancer.

Provided herein are methods of dosing engineered islet cells that include functional modified beta cell containing one or more modifications, such as genetic modifications. In some embodiments, the engineered islets are hypoimmunogenic cells. In some embodiments, the one or more modifications reduce or eliminate expression of one or more MHC class I and / or MHC class II human leukocyte antigens and also increase expression of one or more tolerogenic factors, such as CD47. In some embodiments, the subject has a beta cell related disorder, such as diabetes (e.g. Type I diabetes).

The present invention relates to the field of autoimmune disease. More specifically, the present invention provides compositions and methods useful for treating or preventing Type I diabetes and other autoimmune diseases. In one aspect, the present invention provides isolated antibodies or antigen-binding fragments thereof. In a specific embodiment, an isolated antibody or antigen-binding fragment thereof comprises a variable heavy chain (VH) comprising the amino acid sequence as set forth in SEQ ID NO:28 and a variable light chain (VL) comprising the amino acid sequence as set forth in SEQ ID NO:30 or 32. In certain embodiments, the antibody comprises immunoglobulin G (IgG). In more specific embodiments, the antibody or antigen-binding fragment thereof is secreted as the IgG or IgM isotype.

A computer-implemented method for treating a patient suffering from Type I Diabetes (T1D). The method can include quantifying physical activity (PA) of the patient; calculating an accumulated PA periodically based on the quantified PA, the accumulated PA indicating an aggregate of the PA; and generating an activity informed insulin bolus by adjusting a prevalent functional insulin therapy bolus with a previous activity component, wherein the previous activity component is based on the accumulated daily PA, an activity profile, and an activity factor of the patient. The method can include determining an additional glucose uptake within a time period, the additional glucose uptake being caused by a PA; translating the additional glucose uptake into a number of insulin units with a same BG lowering impact; and generating an activity informed insulin bolus by adjusting a prevalent functional insulin therapy bolus with the insulin units.