| Patent application number | Description | Published |
|---|
| 20080199888 | Non-endogenous, constitutively activated versions of human G protein coupled receptor: FSHR - The invention disclosed in this patent document relates to transmembrane receptors, particularly to a human G protein-coupled receptor, more particularly to a follicle stimulating hormone receptor (FSHR), and most particularly to mutated (non-endogenous) versions of the human FSHR for evidence of constitutive activity. | 08-21-2008 |
| 20080199889 | Human orphan G protein-coupled receptors - The invention disclosed in this patent document relates to transmembrane receptors, more particularly to endogenous, human orphan G protein-coupled receptors. | 08-21-2008 |
| 20090076254 | NON-ENDOGENOUS, CONSTITUTIVELY ACTIVATED HUMAN SEROTONIN RECEPTORS AND SMALL MOLECULE MODULATORS THEREOF - Disclosed herein are non-endogenous, constitutively activated forms of the human 5-HT | 03-19-2009 |
| 20090117559 | Methods for Determining Probability of an Adverse or Favorable Reaction to a Niacin Receptor Agonist - The present invention relates generally to a GPR109A niacin receptor. The present invention relates more particularly to assessing a GPR109A polymorphism in an individual, wherein the GPR109A polymorphism is indicative of the subject's risk for an adverse reaction to the administration of a GPR109A receptor agonist, wherein the adverse reaction is associated with stimulation of MAP kinase activity by the GPR109A receptor agonist. More specifically, the present invention relates to assessing a GPR109A polymorphism in an individual and determining the level of risk for the subject for experiencing an adverse reaction, wherein the subject's GPR109A zygosity is predictive of the risk for a cutaneous flushing response that can be experienced following administration of a GPR109A receptor agonist. | 05-07-2009 |
| 20090313708 | GPR22 AND METHODS RELATING THERETO - Methods for generating an expression-enhanced GPR22 nucleic acid, as well as substituted GPR22 nucleic acids providing for enhanced expression of the encoded GPR22 polypeptide, are provided. In practicing the subject methods, a nucleic acid encoding a mammalian GPR22 receptor polypeptide (e.g., a wild-type nucleic acid) is expression-enhanced by identifying the various codons of the coding region for the GPR22 amino acid sequence and substituting nucleotides so as to enhance expression without changing the amino acid sequence of the encoded GPR22 polypeptide. Methods, compositions, and kits using the same for screening of modulators of GPR22 are also provided. | 12-17-2009 |
| 20090317332 | HUMAN G PROTEIN-COUPLED RECEPTOR AND MODULATORS THEREOF FOR THE TREATMENT OF OBESITY AND CONDITIONS RELATED THERETO - The present invention relates to methods of using a G protein-coupled receptor (GPCR) to screen one or more candidate compounds as a modulator of body mass or of adiposity or of percentage body fat in a subject or as a pharmaceutical agent for obesity and conditions related thereto. Inverse agonists and antagonists of the invention are useful as therapeutic agents for the prevention or treatment of obesity and conditions related thereto, including hypertension, insulin resistance, metabolic syndrome, Type 2 diabetes, dyslipidemia, atherosclerosis, coronary heart disease, and stroke. Agonists and partial agonists of the invention are useful as therapeutic agents for the prevention or treatment of disorders ameliorated by increasing body mass including, but not limited to, cachexia. | 12-24-2009 |
| 20100317046 | Non-Endogenous, Constitutively Activated Versions of Human G Protein Coupled Receptor: FSHR - The invention disclosed in this patent document relates to transmembrane receptors, particularly to a human G protein-coupled receptor, more particularly to a follicle stimulating hormone receptor (FSHR), and most particularly to mutated (non-endogenous) versions of the human FSHR for evidence of constitutive activity. | 12-16-2010 |
| 20100331238 | Human G protein-coupled receptor and modulators thereof for the treatment of atherosclerosis and atherosclerotic disease and for the treatment of conditions related to MCP-1 expression - The present invention relates to methods of using a G protein-coupled receptor (GPCR) to identify whether a candidate compound is a modulator of atherogenesis. In certain embodiments, the GPCR couples to Gi. In certain embodiments, the GPCR is human. Agonists of the invention are useful as therapeutic agents for the prevention or treatment of atherosclerosis and atherosclerotic disease, including coronary artery disease, myocardial infarction, peripheral arterial disease, and ischemic stroke. Agonists of the invention are additionally useful as therapeutic agents for the prevention or treatment of conditions related to MCP-1 expression, including but not limited to rheumatoid arthritis, Crohn's disease, and multiple sclerosis. | 12-30-2010 |
