Cu(II)GTSM, a cell-permeable Cu-complex, significantly inhibits GSK3β. Cu(II)GTSM inhibits Amyloid-β oligomers (AβOs) and decreases tau phosphorylation. Cu(II)GTSM also decreases the abundance of Amyloid-β trimers. Cu(II)GTSM is a potential anticancer and antimicrobial agent. In Vitro Cu(II)GTSM induces GSK3β phosphorylation at serine-9 (ser9) via its upstream kinase, protein kinase B (Akt), and aslo increases the phosphorylation of the associated extracellular signal-related kinase 1/2 (ERK1/2) in SH-SY5Y cells. Tau phosphorylation at ser404 was decreased in CuII(gtsm)-treated cells by 64%. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Western Blot AnalysisCell Line: SH-SY5Y cells Concentration: 25 μM Incubation Time: 2 hours Result: Inhibits GSK3β and decreases Tau phosphorylation. In Vivo Cu(II)GTSM decreases brain Aβ trimer levels in AD mice, and can reverse cognitive deficits in APP/PS1 transgenic AD mice. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: AD mice (K670N, M671L; 5-6 months old)Dosage: 10 mg/kg Administration: Daily; p.o. Result: Restores cognitive performance of the AD mice to levels expected for healthy, cognitively normal mice. Form:Solid