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• W4281739791 abstract "Agonists are defined as the ligands that activate intracellular signaling and evoke cellular responses. Synthetic and endogenous agonists should bind specific amino acids to activate G protein-coupled receptor (GPCR). Agonists that induce maximal responses are full agonists. Partial agonists cannot induce full responses unlike full agonists. In definition, antagonists inhibit agonist-stimulated responses by binding to orthosteric or allosteric sites. Antagonists modulate agonist-induced responses and are often related with inverse agonist activity. However, the relationship between antagonists and partial agonists is complex. An antagonist behaves as a partial agonist when the constitutive activity of the GPCR is high. In contrast, a partial agonist with very weak intrinsic activity may be classified as an antagonist. Thus, antagonisms of the compounds are influenced by constitutive activity of GPCRs, intrinsic activity and differences in the binding sites of GPCRs. Since “antagonism” has been revealed to have multiple aspects and more complex than previously thought, it may be difficult to classify each compound as simply “agonist” or “antagonist” as before. In this review, we discuss the recent findings and perspectives on the pharmacology of GPCR-binding antagonists, inverse agonists, and signaling." @default.
• W4281739791 created "2022-06-13" @default.
• W4281739791 creator A5011925781 @default.
• W4281739791 creator A5089461702 @default.
• W4281739791 date "2022-06-01" @default.
• W4281739791 modified "2023-10-16" @default.
• W4281739791 title "Pharmacology of Antagonism of GPCR" @default.
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• W4281739791 doi "https://doi.org/10.1248/bpb.b22-00143" @default.
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