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    EUK 134
    EUK 134

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V1315
    CAS #: 81065-76-1Purity ≥98%

    Description: EUK 134 (EUK-134; EUK134), a synthetic and cell permeable superoxide dismutase (SOD)/catalase mimetic, is a novel antioxidant compound that exhibits potent antioxidant activities. It inhibits the formation of β-amyloid and related amyloid fibril. In SK-N-MC cells, EUK134 protects neuronal cells against H2O2 toxicity by attenuating oxidative stress through inhibition of MAPK pathway, and also results in decreased expression of pro-apoptotic genes p53 and Bax as well as enhanced expression of anti-apoptotic Bcl-2 gene. Pretreatment with EUK-134 (10 μM) was effective in the prevention of hypertrophic changes in H9C2 cells, reduction of oxidative stress, and prevention of metabolic shift. EUK-134 treatment improved the oxidative status of mitochondria and reversed hypertrophy-induced reduction of mitochondrial membrane potential. Supplementation with EUK-134 is therefore identified as a novel approach to attenuate cardiac hypertrophy and lends scope for the development of EUK-134 as a therapeutic agent in the management of human cardiovascular disease.

    References: J Pharmacol Exp Ther. 1998 Jan;284(1):215-21; Proc Natl Acad Sci U S A. 1999 Aug 17;96(17):9897-902;  2017 Feb 2;12(2):e0169146;  2016 Sep;420(1-2):185-94.

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    Molecular Weight (MW)416.74
    FormulaC18H18ClMnN2O4
    CAS No.81065-76-1
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 83 mg/mL (199.2 mM)
    Water: 13 mg/mL (31.2 mM)
    Ethanol: <1 mg/mL
    SMILESCOC1=C2C(C=[N]3CC[N]4=CC5=CC=CC(OC)=C5O[Mn+3]34([O-2]2)[Cl-])=CC=C1
    Synonyms EUK-134; EUK-134; EUK-134


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    In Vitro

    In vitro activity: EUK 134 shows potent catalase and SOD activities, and protects human fibroblasts against cytotoxicity by glucose and glucose oxidase. EUK 134 (20 μM) prevents Aβ-induced microglial proliferation in vitro. In SK-N-MC cells, EUK134 protects neuronal cells against H(2)O(2) toxicity by attenuating oxidative stress through inhibition of MAPK pathway, and also results in decreased expression of pro-apoptotic genes p53 and Bax as well as enhanced expression of anti-apoptotic Bcl-2 gene. EUK 134 significantly inhibits amyloid formation at two molar ratios of 1:1 and 5:1 (drugs to protein).


    Cell Assay: in SK-N-MC cells, EUK134 protects neuronal cells against H2O2 toxicity by attenuating oxidative stress through inhibition of MAPK pathway, and also results in decreased expression of pro-apoptotic genes p53 and Bax as well as enhanced expression of anti-apoptotic Bcl-2 gene. Pretreatment with EUK-134 (10 μM) was effective in the prevention of hypertrophic changes in H9C2 cells, reduction of oxidative stress, and prevention of metabolic shift. EUK-134 treatment improved the oxidative status of mitochondria and reversed hypertrophy-induced reduction of mitochondrial membrane potential. 

    In VivoEUK 134 (2.5 mg/kg), in a middle cerebral artery occlusion model, significantly reduces brain infarct size, and apparently prevents further infarct growth. EUK-134 prevents oxidative stress and attenuates rat brain damage induced by systemic administration of systemic kainic acid (KA).
    Animal modelRat model in stroke.
    Formulation & DosageDissolved in 0.9% saline; 2.5 mg/kg; i.v. injection  
    ReferencesJ Pharmacol Exp Ther. 1998 Jan;284(1):215-21; Proc Natl Acad Sci U S A. 1999 Aug 17;96(17):9897-902.


    These protocols are for reference only. InvivoChem does not independently validate these methods.

    EUK 134

    Effects of EUK-134 treatment on KA-induced neuronal damage. Proc Natl Acad Sci U S A. 1999 Aug 17;96(17):9897-902.
     

    EUK 134

    Effects of EUK-134 treatment on KA-induced changes in NF-κB- and AP-1-binding activity. Proc Natl Acad Sci U S A. 1999 Aug 17;96(17):9897-902.
     

    EUK 134

    Effects of EUK-134 treatment on KA-induced changes in nitrotyrosine immunoreactivity. Proc Natl Acad Sci U S A. 1999 Aug 17;96(17):9897-902.


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