EUK 134 is a manganese-salen subordinate that displays powerful cancer prevention agent exercises. EUK is a superoxide dismutase (SOD) that hinders amyloid fibril arrangement, including islet amyloid polypeptide (IAPP), β-amyloid and lysozyme amyloid total. It is ideal for experimentation on stimulants
- Product Name: EUK
- Molecular Formula: C24H27MnN2O8
- Appearance: Crystalline solid and powder
- Application: Research purposes
EUK 134, a synthetic superoxide dismutase (SOD)/catalase mimetic, has exhibited potent antioxidant activities and inhibited the formation of β-amyloid and related amyloid fibril.
In vitro: Salen-manganese complex, showed potent catalase and cytoprotective activities and SOD activity. After middle cerebral artery occlusion, administration at 3 hr significantly reduced brain infarct size, with the highest dose apparently preventing further infarct growth. Administration of EUK 134 (20 μM) prevented Aβ-induced microglial proliferation in vitro. In human neuroblastoma cell line SK-N-MC, pre-treatments with EUK134 protected cells against H2O2-induced oxidative stress through inhibition of MAPK pathway in a dose-dependent manner.EUK134 also decreased the expression of pro-apoptotic genes p53 and Bax and enhanced expression of the anti-apoptotic Bcl-2 gene . Incubation of human amylin with significantly inhibited amyloid formation at two molar ratios of 1:1 and 5:1 (chemical to protein).
- Availability: In Stock
- Packaging: Aluminum foil bag package done by an expert
- Purity: 99.9%
- Origin: China
- Minimum order: 10 Grams
- Production Capacity: 100KG/WEEK
- Transportation: Delivery done by EMS, DHL, FEDEX, UPS and TNT
In vivo: Compared to the vehicle-injected rats, the EUK-134-treated group at doses of 0.5 and 5.0 μmol/kg (0.25 and 2.5 mg/kg, respectively) exhibited infarct volumes that were significantly lower than those of vehicle-injected rats. At 5.0 μmol/kg, EUK-134 reduced the infarct volume by 90% when compared with that of the vehicle controls.Protected most of the vulnerable neurons from excitotoxic cell death.Significantly reduced (P< 0.05) KA-induced neuronal damage in CA1 (22% of total neurons), almost complete protection in CA3 (7%), and piriform cortex (14%), indicating that prevented most but not all neuronal damage resulting from KA-induced seizure activity .