RESEARCH MONOGRAPH · KDC-MN-372

Edaravone

May 9, 2026 Kodiac biolabs Research Revised May 30, 2026 2 min read

Our opinion on this compound

67/100

Pyrazolone-class free radical scavenger with niche but interesting ALS and stroke applications, mechanism is messier than the marketing

Edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one, MCI-186) is one of those drugs where the development arc through Japan in the early 2000s was mostly about stroke, and the Western-market approval through Mitsubishi Tanabe / MT Pharma was about amyotrophic lateral sclerosis. The pharmacology and clinical evidence sit somewhat awkwardly between those use cases.

Mechanistically edaravone is described as a free radical scavenger, particularly active against hydroxyl radicals and peroxynitrite. The pyrazolone keto-enol tautomerism allows electron donation to reactive species, and the cell-permeable structure means it can act intracellularly and in the mitochondrial compartment. The Watanabe and Tabata work on mechanism is the original source material. Beyond pure ROS scavenging, edaravone has some effects on lipid peroxidation, NO metabolism, and apoptotic signaling that may or may not be downstream of the scavenging activity. Cleaner accounts of mechanism have been hard to pin down.

The clinical evidence is regionally split. In Japan, edaravone has been approved for acute ischemic stroke since 2001 and the Japanese cohort data shows modest functional improvements when administered within 24 hours of stroke onset. The Western stroke trials never replicated the Japanese signal as cleanly, and edaravone never achieved a major Western approval for stroke.

The ALS story is the bigger Western development. The MCI186-19 phase 3 trial in a defined subset of ALS patients (early disease, preserved respiratory function, specific functional rating scale criteria) showed modest reduction in ALSFRS-R decline over 24 weeks. Approved by FDA in 2017 (Radicava). The effect size is genuinely modest and the trial enrichment design has been controversial, but it's one of the few ALS approvals in decades and the oral formulation (Radicava ORS) extended access in 2022.

Sourcing as a research chemical is straightforward. Standard small molecule, pyrazolone scaffold, the IV formulation is the clinical product but pure edaravone is available from research vendors. HPLC characterization is routine.

What we like for research is edaravone as a probe for hydroxyl radical and peroxynitrite biology, particularly in CNS injury and neurodegeneration models.

What we dont love is the inconsistency between regional clinical evidence bases and the modesty of the effect size in ALS.

Evidence: 65
Mechanism: 65
Reliability: 60
Safety: 80
Sourcing: 78
Value: 60
Signal: 60
Staying power: 65

Plain-language summary Intrigue 70 / 100

Edaravone is a small molecule that mops up free radicals (reactive oxygen species that damage neurons during stress). Mitsubishi-Tokyo developed it in Japan, where it was approved in 2001 for acute ischemic stroke. The FDA later approved it in 2017 for ALS based on a Japanese phase 3 trial showing slowed functional decline in early-stage patients with preserved breathing capacity. The benefit is real but modest, and only a subset of ALS patients qualify. An oral version arrived in 2022, replacing the original IV-only protocol. Edaravone is the canonical free-radical scavenger drug in neurology research. Not stocked by Kodiac. This monograph is provided for research and educational reference.

Intrigue 0–100 blends mechanism novelty, evidence strength, and translational potential. Kodiac editorial, not peer-reviewed.

Free radical scavenger

A pyrazolone free radical scavenger; approved in Japan and the US for amyotrophic lateral sclerosis (ALS) and acute ischemic stroke.

Abstract

Edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one; CAS 89-25-8; molecular formula C10H10N2O; molecular weight 174.20) is a pyrazolone free radical scavenger developed at Mitsubishi-Tokyo Pharmaceuticals. Originally approved in Japan in 2001 for acute ischemic stroke (Radicut), and in 2017 approved by the FDA for amyotrophic lateral sclerosis (Radicava). Mechanism: edaravone scavenges peroxyl, hydroxyl, and other reactive oxygen species, reducing oxidative damage to neurons and the surrounding glia in the affected region. The ALS approval was supported by a Japanese phase 3 trial (MCI186-19) demonstrating slowed functional decline (ALSFRS-R score) in a subset of patients with early disease and preserved respiratory function. Initially IV-only; an oral formulation (Radicava ORS) was approved in 2022. Plasma half-life is approximately 4.5 hours. Used as the canonical free radical scavenger in neurology research.

Mechanism of action

Pyrazolone free radical scavenger; quenches peroxyl, hydroxyl, and other reactive oxygen species in CNS tissue.

Reported research dose ranges

Clinical IV 60 mg over 60 minutes for 14 days, then 14-day off cycles. Oral 105 mg.

References

Abe K, et al. Safety and efficacy of edaravone in well defined patients with amyotrophic lateral sclerosis. Lancet Neurol 2017.
Yoshida H, et al. Edaravone: a novel free radical scavenger. CNS Drug Rev 2006.
Brooks BR, et al. Edaravone in amyotrophic lateral sclerosis: real-world evidence. Amyotroph Lateral Scler Frontotemporal Degener 2022.

Read the full monograph

The full reference document is available as a research-use-only PDF download. Note: PDFs for newly added compounds may take a few hours to propagate after this article was published.

KDC-MN-372

The full reference document is provided strictly for research use only. It reports research dose ranges from the published literature, not instructions for use in humans or animals.

Download PDF →

FOR RESEARCH USE ONLY. Not for medical, diagnostic, or therapeutic purposes. Not for human consumption. All information is provided for research and educational purposes only.

Kodiac sells research compounds for investigative use only.

Edaravone

Abstract

Mechanism of action

Reported research dose ranges

References

Read the full monograph

Quick actions

Categories

Help and policies

Abstract

Mechanism of action

Reported research dose ranges

References

Read the full monograph

Adjacent monographs