Disclosed here is a novel use of a pharmaceutical composition comprising glutathione or its pharmaceutically acceptable salts or derivatives as active ingredient, in the forms of tablets, capsules, powder, spray and/or liquid, through oral administration, intervene injection, inhale and/or skin transmission, to treat and prevent gout and lead nephropathy. Embodiments of gout and lead nephropathy treatable by the pharmaceutical composition described herein include, without limitation, gout, kidney stones, tophi, hyperuricemia, blood lead, renal disease (lead nephropathy), complications thereof, as well as other conditions caused by lifestyle, genetics, medical conditions, and blood lead level. Symptoms treatable may include inflammatory arthritis, which typically involves a red, tender, hot, and swollen joint.

The present invention is drawn to novel topiramate compositions as well as methods for effecting weight loss, e.g., in the treatment of obesity and related conditions, including conditions associated with and/or caused by obesity per se. The present invention features an escalating dosing regimen adapted for the administration of topiramate and optionally a sympathomimetic agent such as phentermine or bupropion, in the treatment of obesity and related conditions.

The present disclosure relates generally to modulators of Cot (cancer Osaka thyroid) and methods of use and manufacture thereof.

The present disclosure relates to compounds that are Syk inhibitors or pharmaceutically acceptable salts or co-crystals thereof, and pharmaceutical compositions thereof, and to their use in the treatment of various disease states, including cancer and inflammatory conditions. In particular embodiments, a Syk inhibitor is a crystalline monomesylate salt of 6-(6-aminopyrazin-2-yl)-N-(4-(4-(oxetan-3-yl)piperazin-1-yl)phenyl)imidazo-[1,2-a]pyrazin-8-amine of formula 2: ##STR00001##

A method for treating a subject having a medical condition associated with inflammation and/or an unwanted immune response without an alpha1-antitrypsin (AAT) deficiency, wherein the method comprises administering genetically modified mesenchymal stem cells to the subject, wherein said genetically modified mesenchymal stem cells comprise an exogenous nucleic acid comprising (i) an Alpha-1 antitrypsin (AAT) encoding region operably linked to (ii) a promoter or promoter/enhancer combination.

The inventive subject matter provides compounds, compositions and methods for lowering serum acid (sUA) for the treatment of gout, and having reduced liver toxicity, associated with CYP2C9 metabolic pathway.

The inventive subject matter provides compounds, compositions and methods for lowering serum acid (sUA) for the treatment of gout, and having reduced liver toxicity, associated with CYP2C9 metabolic pathway.

The invention relates to a process for the preparation of colchicine 1 from colchicoside 2 which comprises enzymatic conversion of colchicoside 2 to 3-O-demethylcolchicine 3, wherein the enzyme used is a cellulase. According to another aspect of the invention, 3-O-demethylcolchicine 3 can be converted to colchicine 1 using an alkylating agent. The invention also relates to a process or enriching the colchicine 1 content of extracts from plants belonging to the Colchicaceae family containing colchicine 1, colchicoside 2 and 3-(9-demethyl colchicine 3, which comprises conversion by means of a colchicoside 2 cellulase to 3-O-demethylcolchicine 3, followed by conversion of 3-O-demethylcolchicine 3 to colchicine 1 using an alkylating agent.

The present invention is directed to antigen binding proteins and in particular to IL-1β antigen binding proteins. The present invention further provides compositions comprising the antigen binding proteins, use of the antigen binding proteins and methods for production.

The present disclosure relates to novel sulfonylurea and sulfonyl thiourea compounds and related compounds and their use in treating a disease or condition responsive to modulation of cytokines such as IL-1β and IL-18, modulation of NLRP3 or inhibition of the activation of NLRP3 or related components of the inflammatory process.