<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Giraudo, Alessandro</style></author><author><style face="normal" font="default" size="100%">Tae, Han-Shen</style></author><author><style face="normal" font="default" size="100%">Hung, Andrew</style></author><author><style face="normal" font="default" size="100%">Richter, Katrin</style></author><author><style face="normal" font="default" size="100%">Shivankar, Bhavana</style></author><author><style face="normal" font="default" size="100%">Armano, Edoardo</style></author><author><style face="normal" font="default" size="100%">Grau, Veronika</style></author><author><style face="normal" font="default" size="100%">Pallavicini, Marco</style></author><author><style face="normal" font="default" size="100%">Adams, David J.</style></author><author><style face="normal" font="default" size="100%">Bolchi, Cristiano</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Dual agonist/antagonist modulation of α9-containing nicotinic acetylcholine receptors by 2-ammoniumethyl ethers of stilbenol and stilbenol analogues</style></title><secondary-title><style face="normal" font="default" size="100%">Journal of Medicinal Chemistry</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2025</style></year><pub-dates><date><style  face="normal" font="default" size="100%">DEC </style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">68</style></volume><pages><style face="normal" font="default" size="100%">26099-26120</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;
	2-(Cyclohexyldimethylammoniumethyl)ether of 4-stilbenol (2), and its styryl-modified analogues 21 and 22, were identified as lead compounds from a series targeting human alpha 9 alpha 10, alpha 9, and alpha 7 nicotinic acetylcholine receptors (nAChRs). Compounds 2 and 21 exhibited potent, and subtype-selective modulation of alpha 9-containing receptors, with low nanomolar IC50 values and dual agonist/antagonist activity in a concentration-dependent manner. In contrast, compound 22 acted as a selective, pure antagonist. Molecular dynamics (MD) simulations of compound 21 supported a concentration-dependent allosteric mechanism, with orthosteric binding at low concentrations and vestibular site interaction at higher levels. In a human monocytic cell line, all three compounds inhibited ATP-induced IL-1 beta release at nanomolar concentrations. These findings identify alpha 9 alpha 10-selective ligands as promising scaffolds for the development of nonopioid analgesics and immunomodulators, with favorable selectivity over alpha 7 nAChRs to minimize CNS-related side effects.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">24</style></issue><work-type><style face="normal" font="default" size="100%">Article</style></work-type><custom3><style face="normal" font="default" size="100%">&lt;p&gt;
	Foreign&lt;/p&gt;
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	7.2&lt;/p&gt;
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