Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (752 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
An analgesic and antipyretic that has been given by mouth and as ear drops. Antipyrine is often used in testing the effects of other drugs or diseases on drug-metabolizing enzymes in the liver. (From Martindale, The Extra Pharmacopoeia, 30th ed, p29)
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Phenazone; Anodynin; Pyramidone.
Where it fits in the MeSH classification
- Broader topics
- Pyrazolones
- Narrower topics
- Edaravone
Research landscape
PubMed indexes 5,087 records tagged with the MeSH heading “Antipyrine” (counts retrieved 2026-10-31). 500 of them (9.8%) were published from 2020 onward, and the busiest period so far is through 1999 with 3,331 records.
Reviews account for 232 records (4.6%) and meta-analyses for 25. Randomized controlled trials number 153 (3.0%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 3,331 |
| 2000-2009 | 607 |
| 2010-2019 | 649 |
| 2020 onward | 500 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 232 | 4.6% |
| Meta-analyses | 25 | 0.5% |
| Randomized controlled trials | 153 | 3.0% |
Method: PubMed query "Antipyrine"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Edaravone, a Free Radical Scavenger, Delayed Symptomatic and Pathological Progression of Motor Neuron Disease in the Wobbler Mouse | 2015 | Research article Design not recorded in structured metadata | 63 | cc by PMID 26469273 · DOI · PMC4607459 |
| Edaravone guards dopamine neurons in a rotenone model for Parkinson's disease | 2011 | Research article Design not recorded in structured metadata | 60 | cc by PMID 21677777 · DOI · PMC3108992 |
| Edaravone protects against hyperosmolarity-induced oxidative stress and apoptosis in primary human corneal epithelial cells | 2017 | Research article Design not recorded in structured metadata | 43 | cc by PMID 28346481 · DOI · PMC5367814 |
| Differential Protective Effects of Edaravone in Cerebellar and Hippocampal Ischemic Injury Models | 2025 | Research article Design not recorded in structured metadata | 4 | cc by PMID 39964549 · DOI · PMC11835913 |
Edaravone, a Free Radical Scavenger, Delayed Symptomatic and Pathological Progression of Motor Neuron Disease in the Wobbler Mouse [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Edaravone, a free radical scavenger is used widely in Japanese patients with acute cerebral infarction.
- Closing excerpt
- This drug seems to be worth performing the clinical trial in ALS patients in the United States of American and Europe, in addition to Japan.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (256 words)
Edaravone, a free radical scavenger is used widely in Japanese patients with acute cerebral infarction. This antioxidant could have therapeutic potentials for other neurological diseases. Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease that affects the upper and the lower motor neuron, leading to death within 3-5 years after onset. A phase III clinical trial of edaravone suggested no significant effects in ALS patients. However, recent 2nd double-blind trial has demonstrated therapeutic benefits of edaravone in definite patients diagnosed by revised El Escorial diagnostic criteria of ALS. Two previous studies showed that edaravone attenuated motor symptoms or motor neuron degeneration in mutant superoxide dismutase 1-transgenic mice or rats, animal models of familial ALS. Herein we examined whether this radical scavenger can retard progression of motor dysfunction and neuropathological changes in wobbler mice, sporadic ALS-like model. After diagnosis of the disease onset at the postnatal age of 3-4 weeks, wobbler mice received edaravone (1 or 10 mg/kg, n = 10/group) or vehicle (n = 10), daily for 4 weeks by intraperitoneal administration. Motor symptoms and neuropathological changes were compared among three groups. Higher dose (10 mg/kg) of edaravone treatment significantly attenuated muscle weakness and contracture in the forelimbs, and suppressed denervation atrophy in the biceps muscle and degeneration in the cervical motor neurons compared to vehicle. Previous and the present studies indicated neuroprotective effects of edaravone in three rodent ALS-like models. This drug seems to be worth performing the clinical trial in ALS patients in the United States of American and Europe, in addition to Japan.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 26469273 · DOI · PMC4607459
Edaravone guards dopamine neurons in a rotenone model for Parkinson's disease [2]
Abstract reading summary — source excerpts
- Opening excerpt
- 3-methyl-1-phenyl-2-pyrazolin-5-one (edaravone), an effective free radical scavenger, provides neuroprotection in stroke models and patients.
- Closing excerpt
- Collectively, edaravone may provide novel clinical therapeutics for PD.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (99 words)
3-methyl-1-phenyl-2-pyrazolin-5-one (edaravone), an effective free radical scavenger, provides neuroprotection in stroke models and patients. In this study, we investigated its neuroprotective effects in a chronic rotenone rat model for Parkinson's disease. Here we showed that a five-week treatment with edaravone abolished rotenone's activity to induce catalepsy, damage mitochondria and degenerate dopamine neurons in the midbrain of rotenone-treated rats. This abolishment was attributable at least partly to edaravone's inhibition of rotenone-induced reactive oxygen species production or apoptotic promoter Bax expression and its up-regulation of the vesicular monoamine transporter 2 (VMAT2) expression. Collectively, edaravone may provide novel clinical therapeutics for PD.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 21677777 · DOI · PMC3108992
Edaravone protects against hyperosmolarity-induced oxidative stress and apoptosis in primary human corneal epithelial cells [3]
Abstract reading summary — source excerpts
- Opening excerpt
- An increase in the osmolarity of tears induced by excessive evaporation of the aqueous tear phase is a major pathological mechanism behind dry eye.
- Closing excerpt
- Mechanistically, we found that edaravone augmented the expression of Nrf2 and its target genes, such as HO-1, GPx-1, and GCLC.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (169 words)
An increase in the osmolarity of tears induced by excessive evaporation of the aqueous tear phase is a major pathological mechanism behind dry eye. Exposure of epithelial cells on the surface of the human eye to hyperosmolarity leads to oxidative stress, mitochondrial dysfunction, and apoptosis. Edaravone, a hydroxyl radical scavenging agent, is clinically used to reduce neuronal damage following ischemic stroke. In this study, we found that treatment with hyperosmotic media at 400 and 450 mOsM increased the levels of ROS and mitochondrial oxidative damage, which were ameliorated by edaravone treatment in a dose-dependent manner. We also found that edaravone could improve mitochondrial function in HCEpiCs by increasing the levels of ATP and mitochondrial membrane potential. MTT and LDH assays indicated that edaravone could attenuate hyperosmolarity-induced cell death. It was found that edaravone prevented apoptosis by decreasing the level of cleaved caspase-3, and attenuating the release of cytochrome C. Mechanistically, we found that edaravone augmented the expression of Nrf2 and its target genes, such as HO-1, GPx-1, and GCLC.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 28346481 · DOI · PMC5367814
Differential Protective Effects of Edaravone in Cerebellar and Hippocampal Ischemic Injury Models [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Ischemic stroke is a leading cause of mortality and disability, with cerebellar strokes posing severe complications such as herniation and brainstem compression.
- Closing excerpt
- Further in vivo studies are required to assess its full clinical potential.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (228 words)
Ischemic stroke is a leading cause of mortality and disability, with cerebellar strokes posing severe complications such as herniation and brainstem compression. Edaravone, a radical scavenger known for reducing oxidative stress, has shown neuroprotective effects in cerebral strokes, but its impact on cerebellar strokes remains unclear. This study investigates Edaravone's protective properties in organotypic slice cultures of rat cerebellum and hippocampus, employing an oxygen-glucose deprivation (OGD) model to simulate ischemic stroke. The hippocampus served as comparative structure due to its high hypoxia sensitivity. Our results confirmed effective hypoxic induction with increases in HIF-1α and HIF-2α expression. Edaravone significantly reduced lactate dehydrogenase (LDH) levels, indicating diminished cellular damage, with cerebellar tissues showing greater vulnerability. Additionally, Edaravone reduced reactive oxygen species (ROS) in both tissues, though its efficacy may be limited by higher oxidative stress in cerebellar cultures. Seahorse XF analysis revealed that Edaravone preserved mitochondrial respiration and tissue integrity in cerebellar and hippocampal slice cultures. However, Edaravone was more effective in preserving mitochondrial respiration in hippocampal slices, suggesting that OGD-induced damage is more severe in cerebellar tissue. In conclusion, Edaravone demonstrates significant cell protective effects in both cerebellar and hippocampal tissues under OGD conditions, preserving tissue integrity and enhancing mitochondrial function in a tissue-dependent manner. These findings suggest Edaravone as a promising therapeutic candidate for cerebellar stroke. Further in vivo studies are required to assess its full clinical potential.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39964549 · DOI · PMC11835913
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Riluzole and edaravone: A tale of two amyotrophic lateral sclerosis drugs [5]
- Research article Neuroprotective effects of edaravone: a novel free radical scavenger in cerebrovascular injury [6]
- Research article Retinal Diseases Associated with Oxidative Stress and the Effects of a Free Radical Scavenger (Edaravone) [7]
- Research article A critical assessment of edaravone acute ischemic stroke efficacy trials: is edaravone an effective neuroprotective therapy? [8]
- Research article Clinical efficacy of edaravone for the treatment of amyotrophic lateral sclerosis [9]
- Research article Edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one), a novel free radical scavenger, for treatment of cardiovascular diseases [10]
References
- Ikeda K, Iwasaki Y. Edaravone, a Free Radical Scavenger, Delayed Symptomatic and Pathological Progression of Motor Neuron Disease in the Wobbler Mouse. . 2015. PMID 26469273 · DOI · PMC4607459
- Xiong N, Xiong J, Khare G, Chen C, Huang J, Zhao Y, et al.. Edaravone guards dopamine neurons in a rotenone model for Parkinson's disease. . 2011. PMID 21677777 · DOI · PMC3108992
- Li Y, Liu H, Zeng W, Wei J. Edaravone protects against hyperosmolarity-induced oxidative stress and apoptosis in primary human corneal epithelial cells. . 2017. PMID 28346481 · DOI · PMC5367814
- Dickmeiß J, Henning Y, Stahlke S, Weber T, Theiss C, Matschke V. Differential Protective Effects of Edaravone in Cerebellar and Hippocampal Ischemic Injury Models. . 2025. PMID 39964549 · DOI · PMC11835913
- Jaiswal MK. Riluzole and edaravone: A tale of two amyotrophic lateral sclerosis drugs. Med Res Rev. 2019. PMID 30101496 · DOI
- Yoshida H, Yanai H, Namiki Y, Fukatsu-Sasaki K, Furutani N, Tada N. Neuroprotective effects of edaravone: a novel free radical scavenger in cerebrovascular injury. CNS Drug Rev. 2006. PMID 16834755 · DOI · PMC6741743
- Masuda T, Shimazawa M, Hara H. Retinal Diseases Associated with Oxidative Stress and the Effects of a Free Radical Scavenger (Edaravone). Oxid Med Cell Longev. 2017. PMID 28194256 · DOI · PMC5286467
- Lapchak PA. A critical assessment of edaravone acute ischemic stroke efficacy trials: is edaravone an effective neuroprotective therapy?. Expert Opin Pharmacother. 2010. PMID 20491547 · DOI · PMC2891515
- Sawada H. Clinical efficacy of edaravone for the treatment of amyotrophic lateral sclerosis. Expert Opin Pharmacother. 2017. PMID 28406335 · DOI
- Higashi Y, Jitsuiki D, Chayama K, Yoshizumi M. Edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one), a novel free radical scavenger, for treatment of cardiovascular diseases. Recent Pat Cardiovasc Drug Discov. 2006. PMID 18221078 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.