Beta-Arrestin Biased GPCR Agonists for Inflammation and Metabolic Disease
Tech ID: 20932 / UC Case 2009-028-0
It has been shown recently that in addition to their classical role in desensitizing G protein coupled receptors (GPCR’s), beta-arrestins can act as signaling molecules themselves. Thus, it is now widely held that GPCR’s are able to signal through parallel G-Protein and beta-arrestin pathways. Next generation GPCR therapeutics will be advanced by fine-tuning the actions along these pathways.
GPCR ligands that preferentially activate the latter pathway are called beta-arrestin “biased” agonists. Different biological responses have been observed with such beta-arrestin biased agonists, compared with traditional GPCR therapeutics designed to activate G-proteins.
UC San Diego researchers have developed screening methods for beta-arrestin biased agonist of a known GPCR. Data obtained using a model compound to activate the GPCR suggests a novel role for this GPCR in modulating inflammatory responses through the beta-arrestin pathways. Beta-arrestin biased agonists are expected to avoid the side effects mediated by G-protein signaling.
Treatment of diabetes, obesity, arthritis, IBD, and neurodegeneration
State Of Development
Demonstration of anti-inflammatory response in in-vitro cellular assays
|United States Of America||Published Application||US-2012-0295975||11/22/2012||2009-028|
- Olefsky, Jerrold M.
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