|AR-R 17779 hydrochloride Selective agonist of α7 nAChRs|
Sample solution is provided at 25 µL, 10mM.
Publications citing ApexBio Products
|Cas No.||178419-42-6||SDF||Download SDF|
|Chemical Name||(1'R,3'S,4'R)-1'-azaspiro[oxazolidine-5,3'-bicyclo[2.2.2]octan]-2-one hydrochloride|
|Canonical SMILES||O=C(NC1)O[[email protected]]21[[email protected]](CC3)CC[[email protected]]3C2.Cl|
|Solubility||Soluble in DMSO > 10 mM||Storage||Desiccate at RT|
|Physical Appearance||Off-white solid||Shipping Condition||Evaluation sample solution : ship with blue ice.All other available size: ship with RT , or blue ice upon request|
|General tips||For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.|
AR-R 17779 is a selective agonist of α7 nicotinic acetylcholine receptor (α7-nAChR)  with an EC50 of 21 μM to rat α7-nAChRs expressed in Xenopus oocytes .
Nicotine enhances cognitive functions, e.g. learning, attention, retention and memory in both humans and animals, via activation of brain nicotinic acetylcholine receptors (nAChRs). These receptors are homo- or heteropentameric ligand-gated ion channels. The most common nicotinic receptors found in the brain are the α4β2-nAChR and the α7-nAChR .
The expression of CD38, CD138, and Bcl-6, was sensitive to regulation via nAChRs. Daudi cells exposed to AR-R 17779 ± methyllycaconitine (MLA) resulted in only moderate changes in the gene expression of CD38, CD138 and Bcl-6, but AR-R 17779 alone significantly (P< 0.05) increased protein levels of CD38 and CD138. That means the effect of AR-R 17779 was abolished by MLA .
Cholesterol is necessary for the homeostasis of acetylcholine receptor (AChR) levels for ion translocation and at the plasmalemma . In ApoE-deficient mice, AR-R 17779 significantly reduced atherosclerotic plaque area in the thoracic aorta, and lowered heart rate, blood pressure, serum triglyceride level and serum total cholesterol level compared with which in Ang II + HFD mice. Treatment with AR-R 17779 in mice did not result in any sickness behavior or apparent abnormalities. At the end of the experiment, the serum concentration of AR-R 17779 was 1.18 ± 0.17 μM. In ApoE-deficient mice, treatment with AR-R 17779 resulted in significantly reduced aortic diameter comparable to control mice (0.81 ± 0.11 mm, p< 0.0001 vs. Ang II + HFD) .
. Toru Hashimoto, Toshihiro Ichiki, AyaWatanabe, et al. Stimulation of α7 nicotinic acetylcholine receptor by AR-R17779 suppresses atherosclerosis and aortic aneurysm formation in apolipoprotein E-deficient mice. Vascular Pharmacology, 2014, 61:49-55.
. Rudy Schreiber, Marion Dalmus and Jean De Vry. Effects of α4/β2- and α7-nicotine acetylcholine receptor agonists on prepulse inhibition of the acoustic startle response in rats and mice. Psychopharmacology, 2002, 159:248-257.
. Marja van Kampen, Karin Selbach, Renate Schneider, et al. AR-R 17779 improves social recognition in rats by activation of nicotinic α7 receptors. Psychopharmacology, 2004, 172:375-383.
. Juan Arredondo, Denys Omelchenko, Alexander I Chernyavsky, et al. Functional role of the nicotinic arm of the acetylcholine regulatory axis in human B-cell lines. Journal of Experimental Pharmacology, 2009, 1:1-7.
. Virginia Borroni and Francisco J. Barrantes. Cholesterol Modulates the Rate and Mechanism of Acetylcholine Receptor Internalization. J. Biol. Chem., 2011, 286(19):17122-32.