Direct visualization of autophagosome accumulation using GFP-LC3B reporter construct, showing increased number of LC3-II-positive puncta
Cells. 2019 Mar 2;8(3):211
HeLa cells
10, 1, 0.1 µM
2 h
Analyze the effect of ANAVEX2-73 on autophagic activity, finding that ANAVEX2-73 significantly induces autophagic flux
Cells. 2019 Mar 2;8(3):211
Blarcamesine HCl 动物实验
Species
Animal Model
Administration
Dosage
Frequency
Description
References
Caenorhabditis elegans
GFP-LGG-1 expressing worms
Liquid culture medium
80 µM
2 hours
Analyze the effect of ANAVEX2-73 on autophagic flux, finding that ANAVEX2-73 significantly enhances autophagic flux
Cells. 2019 Mar 2;8(3):211
Mice
Alzheimer's disease model
Intraperitoneal injection
0.1-1 mg/kg
Single administration
ANAVEX2-73 significantly blocked Aβ25-35-induced hyperphosphorylation of Tau protein and reduced Aβ1-42 generation.
Neuropsychopharmacology. 2013 Aug;38(9):1706-23
Blarcamesine HCl 动物研究
Animal study
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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