ABSTRACT
Receptors ...................................................................................... 236 13.4.2 Morphine ...................................................................................... 236 13.4.3 Fentanyls ....................................................................................... 236 13.4.4 MOR-Selective Peptide and Peptidomimetic Agonists ................ 237 13.4.5 DOR Agonists............................................................................... 238 13.4.6 KOR Agonists ............................................................................... 238
13.5 Opioid Ligands Deprived of Some Pharmacophores ................................. 239 13.5.1 Derivatization or Deletion of Tyr1 ................................................ 239 13.5.2 The Case of Salvinorin ................................................................. 241 13.5.3 The Case of Cycloendomorphins ................................................. 242
13.6 Conclusions .................................................................................................246 Acknowledgments ..................................................................................................246 References ..............................................................................................................246
Opioids are widely utilized as analgesics for sedating acute pain (Heitz, Witkowski, and Viscusi 2009) or for prolonged treatment of chronic pain caused by cancer, nerve damage, arthritis, and other diseases (Przewlocki and Przewlocka 2001; Bountra, Munglani, and Schmidt 2003; Gentilucci 2004; Manchikanti et al. 2010). The mechanisms involved in the transition from acute to chronic pain are complex, with the involvement of interacting receptor systems and intracellular ion ux, second messenger systems, new synaptic connections, and apoptosis (Vadivelu and Sinatra 2005).
