product name Edaravone
Description: Edaravone is a novel potent free radical scavenger that has been clinically used to reduce the neuronal damage following ischemic stroke. Edaravone inhibits MMP-9-related brain hemorrhage in rats treated with tissue plasminogen activator. It was approved by FDA in May 5th 2017 for the treatment of amyotrophic lateral sclerosis (ALS). Edaravone reduces apoptosis and necrosis caused by glutamate. Pretreatment of edaravone (500 μM) reverses these changes to approximately normal levels.
References: CNS Drug Rev. 2006 Spring;12(1):9-20; Stroke. 2005 Oct;36(10):2220-5.
174.2
Formula
C10H10N2O
CAS No.
89-25-8
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 35 mg/mL (200.9 mM)
Water: <1 mg/mL
Ethanol: 35 mg/mL (200.9 mM)
Solubility (In vivo)
Synonyms
MCI-186
other peoduct :
| In Vitro |
In vitro activity: Edaravone exerts neuroprotective effects by inhibiting endothelial injury and by ameliorating neuronal damage in brain ischemia. Edaravone provides the desirable features of NOS: it increases eNOS (beneficial NOS for rescuing ischemic stroke) and decreases nNOS and iNOS (detrimental NOS). Edaravone, which inhibits oxidation and enhances NO production derived from increased eNOS expression, may improve and conserve cerebral blood flow without peroxynitrite generation during reperfusion. Kinase Assay: Cell Assay: Cell viability is quantified by MTT assay and trypan blue staining. MTT (5 mg/mL, 20 μL) is added to each well and incubated for 4 h at 37°C after the drug treatments. The medium is removed and the cell pellet is dissolved in DMSO. Then, the optical density (OD) values are measured at 570 nm using an ELISA reader. |
|---|---|
| In Vivo | Edaravone significantly reduces the infarct volume and improves the neurological deficit scores at 24 hours after reperfusion in mice brain. Edaravone markedly suppresses the accumulation of HNE-modified protein and 8-OHdG at the penumbra area during the early period after reperfusion and reduces microglial activation, iNOS expression, and nitrotyrosine formation at the late period. Edaravone attenuates renal function and pathologic findings significantly in rat kidney. Edaravone significantly reduces the generation of free radicals in the tubular cells indicated by dichlorodihydrofluorescein. Edaravone-treated animals shows significantly improved neurological outcome. Edaravone-treatment provides a significant reduction in the number of TUNEL-positive apoptotic cells, a decrease in Bax immunoreactivity and an increase in Bcl-2 expression within the peri-infarct area. Edaravone shows an excellent neuroprotective effect against ischemia/reperfusion brain injury through a Bax/Bcl-2 dependent anti-apoptotic mechanism. |
| Animal model | |
| Formulation & Dosage | |
| References | CNS Drug Rev. 2006 Spring;12(1):9-20; Stroke. 2005 Oct;36(10):2220-5. |
