Proteins that bind IL-1α and IL-1β are described along with their use in compositions and methods for treating, preventing, and diagnosing IL-1-related disorders and for detecting IL-1α and IL-1β in cells, tissues, samples, and compositions.

The present invention relates to guanidine compounds for inhibiting mitochondrial oxidative phosphorylation (OXPHOS) and use thereof. More specifically, the present invention relates to a pharmaceutical composition for preventing or treating a OXPHOS-related disease, particularly cancer, by inhibiting mitochondrial oxidative phosphorylation and reprogramming cellular metabolism.

The present invention relates to guanidine compounds for inhibiting mitochondrial oxidative phosphorylation (OXPHOS) and use thereof. More specifically, the present invention relates to a pharmaceutical composition for preventing or treating a OXPHOS-related disease, particularly cancer, by inhibiting mitochondrial oxidative phosphorylation and reprogramming cellular metabolism.

Compositions and methods are provided for generating islet-like cell clusters. The methods include culturing a whole non-islet pancreatic cell discard or cells sorted therefrom with an effective amount of a molecule having Bone Morphogenetic Protein (BMP) activity (e.g., a BMP polypeptide). The effective amount of said molecule having BMP activity (e.g., BMP polypeptide) is sufficient to induce the formation of islet-like cell clusters. The methods further include treating or attenuating insulin-deficiency disorders, including type 1 diabetes. In one non-limiting embodiment, an insulin-deficiency disorder in a subject is treated or attenuated by culturing a whole non-islet pancreatic cell discard or cells sorted therefrom with an effective amount of a molecule having BMP activity (e.g., a BMP polypeptide) such that tho formation of islet-like cell clusters occurs. A therapeutically effective amount of the islet-like cell clusters which produce insulin are then transplanted into a subject in need to treat the insulin-deficiency disorder.

Compositions and methods are provided for generating islet-like cell clusters. The methods include culturing a whole non-islet pancreatic cell discard or cells sorted therefrom with an effective amount of a molecule having Bone Morphogenetic Protein (BMP) activity (e.g., a BMP polypeptide). The effective amount of said molecule having BMP activity (e.g., BMP polypeptide) is sufficient to induce the formation of islet-like cell clusters. The methods further include treating or attenuating insulin-deficiency disorders, including type 1 diabetes. In one non-limiting embodiment, an insulin-deficiency disorder in a subject is treated or attenuated by culturing a whole non-islet pancreatic cell discard or cells sorted therefrom with an effective amount of a molecule having BMP activity (e.g., a BMP polypeptide) such that tho formation of islet-like cell clusters occurs. A therapeutically effective amount of the islet-like cell clusters which produce insulin are then transplanted into a subject in need to treat the insulin-deficiency disorder.

Disclosed herein are methods, compositions, kits, and agents useful for inducing β cell maturation, and isolated populations of SC-β cells for use in various applications, such as cell therapy.

The present invention relates to the compositions comprising 15-HEPE and methods of treatment relating to same.

The invention relates to the treatment or prevention of one or more conditions selected from type 1 diabetes mellitus, type 2 diabetes mellitus, impaired glucose tolerance and hyperglycemia using a SGLT-2 inhibitor. In addition the present invention relates to methods for preventing or treating of metabolic disorders and related conditions.

The present invention relates to peroxiredoxin 6 or a synthetic analogue thereof for use as a hypoglycaemic agent, for example in the treatment of diabetes, such as type 1 diabetes mellitus and type 2 diabetes mellitus.

One or more SGLT2 inhibitors or pharmaceutically acceptable forms thereof are provided for use in the treatment and/or prevention of a metabolic disorder in a feline animal, preferably where the metabolic disorder is one or more selected from the group consisting of ketoacidosis, pre-diabetes, diabetes mellitus type 1 or type 2, insulin resistance, obesity, hyperglycemia, impaired glucose tolerance, hyperinsulinemia, dyslipidemia, dysadipokinemia, subclinical inflammation, systemic inflammation, low grade systemic inflammation, hepatic lipidosis, atherosclerosis, inflammation of the pancreas, neuropathy and/or Syndrome X (metabolic syndrome) and/or loss of pancreatic beta cell function and/or where the remission of the metabolic disorder, preferably diabetic remission, is achieved and/or maintained.