σ1 agonist (IC50 = 860 nM); also displays affinity for muscarinic M1-M4 receptors (Ki values < 500 nM), but not for σ2 receptors. Exhibits neuroprotective effects, prevents tau hyperphosphorylation, and attenuates scopolamine- and (+)-MK 801-induced learning deficits in a mouse model of amyloid toxicity.
Pre-administration of Blarcamesine HCl results in a dose-dependent attenuation of scopolamine-induced alternation deficits, significant at doses of 1 and 3 mg/kg. Blarcamesine HCl pretreatment can mitigate the damage to step-through latency, showing dose-dependency and significance at doses above 0.3 mg/kg[1]. Blarcamesine HCl treatment dose-dependently blocks recognition memory deficits, with significant effects observed at a dose of 1 mg/kg. One day post-injection, Blarcamesine HCl at doses of 0.1 and 1 mg/kg significantly weakens the reduction of Akt phosphorylation induced by Aβ25-35. Seven days post-injection, Blarcamesine HCl at 0.3 and 1 mg/kg can attenuate the peptide-induced decrease in Ser9 phosphorylation. Blarcamesine HCl treatment dose-dependently prevents the increase in Aβ1-42 levels induced by Aβ25-35, with significant effects at the highest tested dose[2].
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