Animal experiment:

Male mice aged 7-9 weeks and weighing 32±2 g are used. Drugs (including AVex-73 hydrochloride) are brought up to each dose by dilution and injected in a volume of 100 μL/20 g body weight. Animals are used between days 1 and 9 after i.c.v. injections for behavioral testing or killed before biochemical measures[2].

AVex-73 hydrochloride is a Sigma-1 Receptor agonist with an IC50 of 860 nM.

The pre-administration of AVex-73 hydrochloride (ANAVEX2-73) leads to a dose-dependent attenuation of the scopolamine induced alternation deficit, significant at 1 and 3 mg/kg. The pre-treatment with AVex-73 hydrochloride attenuates the impairments of step-through latency, dose dependently and significantly at doses higher than 0.3 mg/kg[1]. The AVex-73 hydrochloride treatment dose-dependently blocks the recognition memory deficit, with a significant effect measured at 1 mg/kg. One day after injections, the significant Aβ25-35-induced decrease in Akt phosphorylation is significantly attenuated by AVex-73 hydrochloride at 0.1 and 1 mg/kg dose. Seven days after injections,AVex-73 hydrochloride attenuates the decrease in Ser9 phosphorylation induced by the peptide at 0.3 and 1 mg/kg. The AVex-73 hydrochloride treatment dose-dependently prevents the Aβ25-35-induced increase in Aβ1-42 content, with a significant effect at the highest dose tested[2].

References:
[1]. Villard V, et al. Anti-amnesic and neuroprotective potentials of the mixed muscarinic receptor/sigma 1 (σ1) ligand ANAVEX2-73, a novel aminotetrahydrofuran derivative. J Psychopharmacol. 2011 Aug;25(8):1101-17.
[2]. Valentine Lahmy, et al. Blockade of Tau Hyperphosphorylation and Aβ1-42 Generation by the Aminotetrahydrofuran Derivative ANAVEX2-73, a Mixed Muscarinic andσ1 Receptor Agonist, in a Nontransgenic Mouse Model of Alzheimer's Disease. Neuropsychopharmacology. 2013 Aug; 38(9): 1706-1723.