| Literature DB >> 34844790 |
Dilip K Tosh1, Veronica Salmaso1, Ryan G Campbell1, Harsha Rao1, Amelia Bitant2, Eline Pottie3, Christophe P Stove3, Naili Liu4, Oksana Gavrilova4, Zhan-Guo Gao1, John A Auchampach2, Kenneth A Jacobson5.
Abstract
Following our study of 4'-truncated (N)-methanocarba-adenosine derivatives that displayed unusually high mouse (m) A3AR affinity, we incorporated dopamine-related N6 substituents in the full agonist 5'-methylamide series. N6-(2-(4-Hydroxy-3-methoxy-phenyl)ethyl) derivative MRS7618 11 displayed Ki (nM) 0.563 at hA3AR (∼20,000-fold selective) and 1.54 at mA3AR. 2-Alkyl ethers maintained A3 affinity, but with less selectivity than 2-alkynes. Parallel functional assays of G protein-dependent and β-arrestin 2 (βarr2)-dependent pathways indicate these are full agonists but not biased. Through use of computational modeling, we hypothesized that phenyl OH/OMe groups interact with polar residues, particularly Gln261, on the mA3AR extracellular loops as the basis for the affinity enhancement. Although the pharmacokinetics indicated facile clearance of parent O-methyl catechol nucleosides 21 and 31, prolonged mA3AR activation in vivo was observed in a hypothermia model, suggested potential formation of active metabolites through demethylation. Selected analogues induced mouse hypothermia following i.p. injection, indicative of peripheral A3AR agonism in vivo.Entities:
Keywords: Adenosine receptor; G protein-coupled receptor; Hypothermia; Molecular modeling; Nucleosides; Structure activity relationship
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Year: 2021 PMID: 34844790 PMCID: PMC8865922 DOI: 10.1016/j.ejmech.2021.113983
Source DB: PubMed Journal: Eur J Med Chem ISSN: 0223-5234 Impact factor: 6.514