Format

Send to

Choose Destination
Pharmacol Res. 2016 Oct;112:49-57. doi: 10.1016/j.phrs.2016.01.031. Epub 2016 Feb 2.

Recent updates on GPCR biased agonism.

Author information

1
Department of Pharmacology, Instituto de Biociências, UNESP, Botucatu, SP, Brazil. Electronic address: aspupo@ibb.unesp.br.
2
Department of Biochemistry and Immunology, Faculty of Medicine at Ribeirão Preto, University of São Paulo, 14049-900 Ribeirão Preto, SP, Brazil.
3
Department of Pharmacology, Instituto de Biociências, UNESP, Botucatu, SP, Brazil; Department of Biochemistry and Immunology, Faculty of Medicine at Ribeirão Preto, University of São Paulo, 14049-900 Ribeirão Preto, SP, Brazil.
4
Department of Biochemistry and Immunology, Faculty of Medicine at Ribeirão Preto, University of São Paulo, 14049-900 Ribeirão Preto, SP, Brazil. Electronic address: claudio@fmrp.usp.br.

Abstract

G protein-coupled receptors (GPCRs) are the most important targets for drug discovery and not surprisingly ∼40% of all drugs currently in the market act on these receptors. Currently, one of the most active areas in GPCRs signaling is biased agonism, a phenomenon that occurs when a given ligand is able to preferentially activate one (or some) of the possible signaling pathways. In this review, we highlight the most recent findings about biased agonism, including an extension of this concept to intracellular signaling, allosterism, strategies for assessment and interpretation, and perspectives of therapeutic applications for biased agonists.

KEYWORDS:

7TMR; Functional selectivity; GPCR

PMID:
26836887
DOI:
10.1016/j.phrs.2016.01.031
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center