Institute of Medical Sciences, University of Aberdeen, Foresterhill, Scotland, UK.
Curr Med Chem. 2010;17(14):1360-81. doi: 10.2174/092986710790980050.
It is widely accepted that non-endogenous compounds that target CB(1) and/or CB(2) receptors possess therapeutic potential for the clinical management of an ever growing number of disorders. Just a few of these disorders are already treated with Delta(9)-tetrahydrocannabinol or nabilone, both CB(1)/CB(2) receptor agonists, and there is now considerable interest in expanding the clinical applications of such agonists and also in exploiting CB(2)-selective agonists, peripherally restricted CB(1)/CB(2) receptor agonists and CB(1)/CB(2) antagonists and inverse agonists as medicines. Already, numerous cannabinoid receptor ligands have been developed and their interactions with CB(1) and CB(2) receptors well characterized. This review describes what is currently known about the ability of such compounds to bind to, activate, inhibit or block non-CB(1), non- CB(2) G protein-coupled receptors such as GPR55, transmitter gated channels, ion channels and nuclear receptors in an orthosteric or allosteric manner. It begins with a brief description of how each of these ligands interacts with CB(1) and/or CB(2) receptors.
人们普遍认为,靶向 CB(1) 和/或 CB(2) 受体的非内源性化合物具有治疗越来越多疾病的潜力。已经有一些疾病用 Delta(9)-四氢大麻酚或纳布啡(均为 CB(1)/CB(2) 受体激动剂)进行治疗,现在人们对扩大此类激动剂的临床应用以及开发 CB(2)-选择性激动剂、外周受限的 CB(1)/CB(2) 受体激动剂和 CB(1)/CB(2) 拮抗剂和反向激动剂作为药物有很大的兴趣。已经开发了许多大麻素受体配体,并且它们与 CB(1) 和 CB(2) 受体的相互作用已经得到很好的描述。这篇综述描述了目前已知的这些化合物以正位或变构方式与非 CB(1)、非 CB(2)G 蛋白偶联受体(如 GPR55)、递质门控通道、离子通道和核受体结合、激活、抑制或阻断的能力。它首先简要描述了每种配体如何与 CB(1) 和/或 CB(2) 受体相互作用。