Rivanicline does not antagonize nicotine-stimulated muscle or ganglionic nAChR function (IC50 >1 mM). Chronic exposure of M10 cells to Rivanicline (10 microM) results in an up-regulation of high-affinity nAChRs phenomenologically similar to that seen with nicotine. At concentrations up to 1 mM, Rivanicline does not significantly activate nAChRs in PC12 cells, muscle type nAChRs, or muscarinic receptors. Dose-response curves for agonist-induced ileum contraction indicate that Rivanicline is less than one-tenth as potent as nicotine with greatly reduced efficacy [1].

Rivanicline significantly improved passive avoidance retention after scopolamine-induced amnesia and enhanced both working and reference memory in rats with ibotenic acid lesions of the forebrain cholinergic projection system in an 8-arm radial maze paradigm. By comparison, Rivanicline was 15 to 30-fold less potent than nicotine in decreasing body temperature, respiration, Y-maze rears, and crosses, and acoustic startle response. Metanicotine was about 5-fold less potent than nicotine in the tail-flick test after s.c administration, but slightly more potent after central administration [2][3].