SSR180711 hydrochloride is an orally active, selective and reversible α7 acetylcholine nicotinic receptor (n-AChRs) partial agonist. SSR180711 hydrochloride can act on rat α7 n-AChR (Ki=22 nM; IC50=30 nM) and human α7 n-AChR (Ki=14 nM; IC50=18 nM). SSR180711 hydrochloride increases glutamatergic neurotransmission, ACh release and long-term potentiation (LTP) in the hippocampus.IC50 & Target: IC50: 30 nM (rat α7 n-AChR) and 18 nM (human α7 n-AChR)
Ki: 22 nM (rat α7 n-AChR) and 14 nM (human α7 n-AChR)In Vitro: SSR180711 hydrochloride is selective for the α7 receptor subtype compared to α4β2, α3β2, α3β4, and α1β1γδ human n-AChR subtypes (IC50>5?μM). SSR180711 hydrochloride (10?μM) has no inhibition (lower than 50%) for the ionic channels, neurotransmitter, or peptide receptors.
SSR180711 hydrochloride (0.01-10000 μM) is a potent partial agonist at human α7 n-AChRs expressed in Xenopus oocytes or GH4C1 cells and elicits typical concentration-dependent inward currents with an EC50 value of 4.4?μM (2.5-7.8?μM).
In Vivo: SSR180711 hydrochloride rapidly penetrates into the brain (ID50=8?mg/kg; p.o.). SSR180711 hydrochloride dose-dependently inhibits the specific [3H]α-BTX binding in the mouse brain (ID50=8.3 and 7.5?mg/kg for p.o. and i.p., respectively).
SSR180711 hydrochloride (1-10?mg/kg for i.p.; 10-30 mg/kg for p.o.) dose-dependently increases extracellular acetylcholine (ACh) levels in the hippocampus and prefrontal cortex of freely moving rats.
SSR180711 hydrochloride (0.1, 0.3, 1?mg/kg; i.v.) dose-dependently increases firing rate.