Description |
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[1][2].
|
Related Catalog |
|
Target |
GSK3β
Amyloid-β oligomers
|
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%[2]. Western Blot Analysis[2] Cell 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[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.
|
References |
[1]. Andres SA, et al. Synthesis, Characterization, and Biological Activity of Hybrid Thiosemicarbazone-Alkylthiocarbamate Metal Complexes. Inorg Chem. 2020;59(7):4924-4935. [2]. Crouch PJ, et al. Increasing Cu bioavailability inhibits Abeta oligomers and tau phosphorylation. Proc Natl Acad Sci U S A. 2009;106(2):381-386.
|