Cu(II)GTSM

Names

[ Name ]:
Cu(II)GTSM

Biological Activity

[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]:

Signaling Pathways >> Stem Cell/Wnt >> GSK-3

Research Areas >> Neurological Disease

Signaling Pathways >> PI3K/Akt/mTOR >> GSK-3

[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.

Chemical & Physical Properties

[ Molecular Formula ]:
C₆H₁₀CuN₆S₂

[ Molecular Weight ]:
293.86

Related Compounds

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