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Edaravone Antioxidant chemical

Cat.No.S1326

Edaravone (MCI-186) is a novel potent free radical scavenger that has been clinically used to reduce the neuronal damage following ischemic stroke.
Edaravone Antioxidant chemical Chemical Structure

Chemical Structure

Molecular Weight: 174.2

Quality Control

Chemical Information, Storage & Stability

Molecular Weight 174.2 Formula

C10H10N2O

Storage (From the date of receipt) 3 years -20°C powder (seal)
CAS No. 89-25-8 Download SDF Storage of Stock Solutions

Synonyms MCI-186 Smiles CC1=NN(C(=O)C1)C2=CC=CC=C2

Solubility

In vitro
Batch:

DMSO : 35 mg/mL (200.91 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Ethanol : 4 mg/mL

Water : Insoluble

Molarity Calculator

Mass Concentration Volume Molecular Weight

In vivo
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Mechanism of Action

In vitro
Edaravone exerts neuroprotective effects by inhibiting endothelial injury and by ameliorating neuronal damage in brain ischemia. This compound provides the desirable features of NOS: it increases eNOS (beneficial NOS for rescuing ischemic stroke) and decreases nNOS and iNOS (detrimental NOS). This chemical, 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. This compound 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] It attenuates renal function and pathologic findings significantly in rat kidney. This chemical significantly reduces the generation of free radicals in the tubular cells indicated by dichlorodihydrofluorescein. [3] Treated animals shows significantly improved neurological outcome. This 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. It shows an excellent neuroprotective effect against ischemia/reperfusion brain injury through a Bax/Bcl-2 dependent anti-apoptotic mechanism. [4]
References

Clinical Trial Information

(data from https://clinicaltrials.gov, updated on 2024-05-22)

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT06107205 Completed
Healthy Adult Subjects
Auzone Biological Technology Pty Ltd
November 7 2023 Phase 1
NCT05953103 Recruiting
Subjects With Cerebral Hemorrhage
Simcere Pharmaceutical Co. Ltd
July 3 2023 Phase 2
NCT05410457 Recruiting
Ischemic Stroke
Nanjing First Hospital Nanjing Medical University
May 24 2022 --
NCT04776135 Completed
Healthy Adult Subjects
Mitsubishi Tanabe Pharma Corporation
February 26 2021 Phase 1
NCT04254913 Completed
Japanese Patients With ALS
Mitsubishi Tanabe Pharma Corporation
January 24 2020 Phase 1
NCT05342597 Completed
Healthy Adult Subjects
Mitsubishi Tanabe Pharma Corporation
June 10 2019 Phase 1

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