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^[1][2].

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].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cu(II)GTSM decreases brain Aβ trimer levels in AD mice, and can reverse cognitive deficits in APP/PS1 transgenic AD mice^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

293.86

C₆H₁₀CuN₆S₂

68341-14-0

Solid

Light brown to brown

CNC1=N[N]2=CC=[N]3N=C(NC)[S-][Cu+2]23[S-]1

Room temperature in continental US; may vary elsewhere.

• [1]. Andres SA, et al. Synthesis, Characterization, and Biological Activity of Hybrid Thiosemicarbazone-Alkylthiocarbamate Metal Complexes. Inorg Chem. 2020;59(7):4924-4935.  [Content Brief]

  [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.  [Content Brief]