Cu(II)GTSM, a cell-permeable copper-complex, effectively inhibits GSK3β and shows inhibitory effects against Amyloid-β oligomers (AβOs) while reducing tau phosphorylation. Additionally, Cu(II)GTSM decreases the abundance of Amyloid-β trimers. With its potential as an anticancer and antimicrobial agent, Cu(II)GTSM exhibits promising therapeutic capabilities.

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%[2]. Western Blot Analysis[2]Cell Line: SH-SY5Y cells Concentration: 25 μM Incubation Time: 2 hours Result: Inhibits GSK3β and decreases Tau phosphorylation.

Cu(II)GTSM decreases brain Aβ trimer levels in AD mice, and can reverse cognitive deficits in APP/PS1 transgenic AD mice[2]. Animal Model: AD mice (K670N, M671L; 5-6 months old)[2]Dosage: 10 mg/kg Administration: Daily; p.o. Result: Restores cognitive performance of the AD mice to levels expected for healthy, cognitively normal mice.