Cu(II)GTSM

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

No numbering system information yet

No physical and chemical property information yet

No safety information yet

No production method and use information yet

No upstream information yet

No downstream information yet

No related product information yet