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Formula | C10H10N2O |
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Molecular Weight | 174.2 | CAS No. | 89-25-8 | ||||
Solubility (25°C)* | In vitro | DMSO | 35 mg/mL (200.91 mM) | ||||
Ethanol | 4 mg/mL (22.96 mM) | ||||||
Water | Insoluble | ||||||
In vivo (Add solvents to the product individually and in order) |
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* <1 mg/ml means slightly soluble or insoluble. * Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations. * Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.) |
Description | Edaravone (MCI-186) is a novel potent free radical scavenger that has been clinically used to reduce the neuronal damage following ischemic stroke. |
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In vitro | 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. [1] |
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. [2] 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. [3] 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. [4] |
Spinal cord tissue engineering via covalent interaction between biomaterials and cells [ Sci Adv, 2023, 9(6):eade8829] | PubMed: 36753555 |
Edaravone Attenuated Particulate Matter-Induced Lung Inflammation by Inhibiting ROS-NF-κB Signaling Pathway [ Oxid Med Cell Longev, 2022, 2022:6908884] | PubMed: 35502210 |
High replication stress and limited Rad51-mediated DNA repair capacity, but not oxidative stress, underlie oligodendrocyte precursor cell radiosensitivity [ NAR Cancer, 2022, 4(2):zcac012] | PubMed: 35425901 |
Paeoniflorin ameliorates ischemic injury in rat brain via inhibiting cytochrome c/caspase3/HDAC4 pathway [ Acta Pharmacol Sin, 2021, 10.1038/s41401-021-00671-y] | PubMed: 33976387 |
Bioactive Flavonoids Icaritin and Icariin Protect against Cerebral Ischemia-Reperfusion-Associated Apoptosis and Extracellular Matrix Accumulation in an Ischemic Stroke Mouse Model [ Biomedicines, 2021, 9(11)1719] | PubMed: 34829948 |
Dysfunctional Oxidative Phosphorylation Shunts Branched-Chain Amino Acid Catabolism Onto Lipogenesis in Skeletal Muscle [ EMBO J, 2020, 3;e103812] | PubMed: 32488939 |
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SHIPPING AND STORAGE
Selleck products are transported at room temperature. If you receive the product at room temperature, please rest assured, the Selleck Quality Inspection Department has conducted experiments to verify that the normal temperature placement of one month will not affect the biological activity of powder products. After collecting, please store the product according to the requirements described in the datasheet. Most Selleck products are stable under the recommended conditions.
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