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Key Documents

SML0769

Sigma-Aldrich

Cu-ATSM

≥98% (HPLC)

Synonym(e):

CuII(ATSM), Diacetylbis(N(4)-methylthiosemicarbazonato) copper(II), [[2,2′-(1,2-Dimethyl-1,2-ethanediylidene)bis[N-methylhydrazinecarbothioamidato]]] copper

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About This Item

Empirische Formel (Hill-System):
C8H14CuN6S2
CAS-Nummer:
68341-09-3
Molekulargewicht:
321.91
UNSPSC-Code:
12352200
NACRES:
NA.77

Qualitätsniveau

100

Assay

≥98% (HPLC)

Form

powder

Farbe

, brown to dark red-brown

Löslichkeit

DMSO: 0.5 mg/mL, clear (warmed)

Lagertemp.

2-8°C

Biochem./physiol. Wirkung

Cu-ATSM is an orally bioavailable, blood-brain barrier permeable complex that specifically inhibits the action of peroxynitrite on Cu,Zn superoxide dismutase (SOD1) and subsequent nitration of cellular proteins. CuII(ATSM) significantly delayed onset of disease (paralysis and prolonged lifespan) in amyotrophic lateral sclerosis (ALS) mice model. Also, Cu-ATSM was reported to lower lipid peroxidation in a model of ischemicreperfusion injury. Cu-ATSM subsequently was shown to inhibit ferroptosis with a potency similar to Liproxstatin-1.

Lagerklassenschlüssel

11 - Combustible Solids

WGK

WGK 3

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable

Analysenzertifikate (COA)

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Adam Southon et al.
British journal of pharmacology, 177(3), 656-667 (2019-10-28)
Diacetyl-bis(4-methyl-3-thiosemicarbazonato)copperII (CuII (atsm)) ameliorates neurodegeneration and delays disease progression in mouse models of amyotrophic lateral sclerosis (ALS) and Parkinson's disease (PD), yet the mechanism of action remains uncertain. Promising results were recently reported for separate Phase 1 studies in ALS
Erin J McAllum et al.
Amyotrophic lateral sclerosis & frontotemporal degeneration, 14(7-8), 586-590 (2013-08-21)
Our objective was to assess the copper(II) complex of diacetylbis(4-methylthiosemicarbazone) [Cu(II)(atsm)] for its preclinical potential as a novel therapeutic for ALS. Experimental paradigms used were designed to assess Cu(II)(atsm) efficacy relative to treatment with riluzole, as a function of dose
Erin J McAllum et al.
Neurobiology of disease, 81, 20-24 (2015-03-15)
Mutations in the metalloprotein Cu,Zn-superoxide dismutase (SOD1) cause approximately 20% of familial cases of amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disease for which effective therapeutics do not yet exist. Transgenic rodent models based on over-expression of mutant SOD1 have
Blaine R Roberts et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 34(23), 8021-8031 (2014-06-06)
Mutations in the metallo-protein Cu/Zn-superoxide dismutase (SOD1) cause amyotrophic lateral sclerosis (ALS) in humans and an expression level-dependent phenotype in transgenic rodents. We show that oral treatment with the therapeutic agent diacetyl-bis(4-methylthiosemicarbazonato)copper(II) [Cu(II)(atsm)] increased the concentration of mutant SOD1 (SOD1G37R)

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