Cu(II)GTSM, a cell-permeable copper-complex, effectively inhibits GSK3β, reduces tau phosphorylation, and shows inhibitory effects against Amyloid-β oligomers (AβOs) and trimers. Additionally, Cu(II)GTSM exhibits promising therapeutic capabilities as an anticancer and antimicrobial agent.

Cu(II)GTSM activates the kinase protein kinase B (Akt), which in turn stimulates GSK3β phosphorylation at serine-9 (ser9) and increases the phosphorylation of associated extracellular signal-related kinase 1/2 (ERK1/2) in SH-SY5Y cells. Additionally, it reduces tau phosphorylation at ser404 by 64%[2] in cells treated with CuII(gtsm). Through Western Blot Analysis[2] on the SH-SY5Y cell line, with a concentration of 25 μM and an incubation time of 2 hours, it was demonstrated that Cu(II)GTSM inhibits GSK3β and decreases tau phosphorylation.

Cu(II)GTSM reduces Aβ trimer levels in the brains of AD mice and can reverse cognitive deficits in APP/PS1 transgenic AD mice[2]. In an animal model using AD mice (K670N, M671L; 5-6 months old)[2] at a dosage of 10 mg/kg administered daily by oral route, results showed a restoration of cognitive performance in AD mice to that of healthy, cognitively normal mice.