product name EUK 134
Description: EUK 134, a synthetic superoxide dismutase (SOD)/catalase mimetic, exhibits potent antioxidant activities, and 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.
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.
416.74
Formula
C18H18ClMnN2O4
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
Solubility (In vivo)
Synonyms
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19401063
| 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). Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | EUK 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 model | Rat model in stroke. |
| Formulation & Dosage | Dissolved in 0.9% saline; 2.5 mg/kg; i.v. injection |
| 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. |
Related Posts
product name EUK 134
Description: EUK 134, a synthetic superoxide dismutase (SOD)/catalase mimetic, exhibits potent antioxidant activities, and 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.
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.
416.74
Formula
C18H18ClMnN2O4
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
Solubility (In vivo)
Synonyms
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19401063
| 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). Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | EUK 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 model | Rat model in stroke. |
| Formulation & Dosage | Dissolved in 0.9% saline; 2.5 mg/kg; i.v. injection |
| 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. |