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AR-R 17779 is a selective agonist of α7 nicotinic acetylcholine receptor (α7-nAChR) [1] with an EC50 of 21 μM to rat α7-nAChRs expressed in Xenopus oocytes [2].

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 [3].

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 [4].

Cholesterol is necessary for the homeostasis of acetylcholine receptor (AChR) levels for ion translocation and at the plasmalemma [5]. 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) [1].

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