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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.
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Quality Control

Batch: Purity: 99.89%
99.89

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

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In vivo
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Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )

Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

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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 Solutions are unstable. Prepare fresh or purchase small, pre-packaged sizes. Repackage upon receipt.
Synonyms MCI-186 SMILES CC1=NN(C(=O)C1)C2=CC=CC=C2

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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.
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. 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. 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.
References
  • [4] https://pubmed.ncbi.nlm.nih.gov/15921675/

Clinical Trial Information

(data from https://clinicaltrials.gov, updated on 2026-05-22)

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT07604350 NOT_YET_RECRUITING
Post-stroke Epilepsy; Post-stroke Seizure
First Affiliated Hospital of Wenzhou Medical University
2026-06 PHASE3
NCT07682922 NOT_YET_RECRUITING
Acute Ischemic Stroke
Xinqiao Hospital of Chongqing
2026-07-01 PHASE4
NCT07454473 RECRUITING
Chemo Brain
Chuansheng Zhao
2026-03-02 PHASE4
NCT07692399 NOT_YET_RECRUITING
CADASIL
Huashan Hospital
2026-07 PHASE2
NCT07801976 NOT_YET_RECRUITING
Healthy Volunteer
St. Jude Children's Research Hospital
2026-10 EARLY_PHASE1
NCT06674460 RECRUITING
Cerebral Small Vessel Disease; Ischemic Stroke
Peking Union Medical College Hospital
2025-08-01 PHASE3

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