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MyDeficiencies

Edaravone

free-radical scavenger / antioxidant neuroprotective agent

Also sold as Radicava, Radicava ORS.

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Findings for this medication

Research about this medication, graded for how strongly each finding can be attributed to it. Nothing here describes your own levels.

Edaravone carries almost no classical depletion machinery. Per the current RADICAVA/RADICAVA ORS label, edaravone is conjugated hepatically by glucuronidation (multiple UGT isoforms) and sulfation to two inactive metabolites, induces or inhibits no major CYP450 enzyme, and is cleared renally, 60 to 80 percent of the dose as its glucuronide conjugate in urine within 48 hours, with under 1 percent excreted unchanged. None of Step 2's classical mechanisms (enzyme induction, renal electrolyte wasting, absorption-interfering chelation by the drug itself) is present. The one real finding this review surfaced sits in the formulation, not the drug's own chemistry: both the IV and oral-suspension (ORS) formulations are preserved with sodium bisulfite, a sulfite that pharmaceutical and food chemistry have long shown chemically cleaves thiamine. That reaction has never been studied in edaravone-treated patients specifically, so it is graded yellow, theoretical only, not a demonstrated clinical deficit.

free-radical scavenger / antioxidant neuroprotective agent · ATC N07XX14 · also sold as Radicava and Radicava ORS · reviewed 2026-10-01. This describes research about the medication. It does not say anything about your own levels or health.

How to read the evidence grades

These colours describe how strongly a finding can be attributed to the medication in the research. They are not a severity score and they say nothing about your own health.

Grades describe how strongly a finding can be attributed to Edaravone in the research — not how common it is, how serious it would be, and not anything about you personally.

Red — Severe
Two or more independent Tier A sources, this drug in the cohort, the nutrient directly measured, consistent direction, clinically meaningful magnitude, a named mechanism, no substantial contradicting Tier A evidence.
Orange — Moderate
At least one Tier A source with this drug in the cohort showing a real but bounded deficit: an exposure window, a subgroup, low frequency, or a functional rather than circulating deficit.
Yellow — Low
Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction.
Not graded — disclosed evidence gap
Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result.Source definition: Not gradeable under the rules above because nothing has been measured. Published as a documented gap, never as reassurance that there is no effect.

What the research found

Thiamine

Yellow — Low

See study details

Both RADICAVA (IV) and RADICAVA ORS (oral) are formulated with sodium bisulfite, a sulfite long known in food and pharmaceutical chemistry to chemically cleave thiamine; this reaction has not been studied in edaravone-treated patients, so it is graded theoretical only.

Full detail, limits and 2 references

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. Yellow, theoretical, excipient chemistry

Limits on what this shows

  • Key negative/null findings: No case report of thiamine deficiency, beriberi, or a Wernicke-type presentation in an edaravone-treated patient was located in this review. The label's adverse-reaction table does not list confusion, ataxia, or ophthalmoplegia (classic thiamine-deficiency findings) among reported events in the pivotal trial.
  • At-risk subgroups: Theoretically, patients already thiamine-depleted for reasons unrelated to edaravone (ALS-related dysphagia and reduced oral intake, alcohol use, prior bariatric surgery) could be more vulnerable to any incremental chemical loss, but this is inferential and has not been drug-demonstrated.

Regulatory status

The label lists sodium bisulfite (20 mg per IV dose) and L-cysteine hydrochloride hydrate as inactive ingredients in RADICAVA, and sodium bisulfite among the inactive ingredients of RADICAVA ORS, with a sulfite-hypersensitivity warning covering both formulations. Thiamine itself is not named anywhere in the label sections reached.

Population evidence

No edaravone-specific clinical study measuring thiamine status in treated patients was located despite multiple query attempts (see Sources and access note). The supporting evidence is excipient chemistry, not an edaravone patient cohort: Kawasaki C, Suhara T, Horio T, "Action of Sulfurous Acid and Sulfite on Thiothiamine and Thiamine" (parts I and II), Yakugaku Zasshi, 1958; and Lenz AG, Holzer H, "Cleavage of thiamine pyrophosphate by sulfite in Saccharomyces cerevisiae," Zeitschrift fur Lebensmittel-Untersuchung und -Forschung, 1985. None of these three papers involves edaravone, ALS, or any drug; they establish general sulfite-thiamine chemistry and do not pass a drug-cohort test for edaravone. They are cited here only to support the chemical plausibility of the mechanism, not as drug-specific evidence, and that distinction is kept explicit throughout this entry.

Mechanism

Named at the chemistry level: the sulfite ion is understood to cleave the methylene bridge linking thiamine's pyrimidine and thiazole rings, inactivating the vitamin, the same reactive chemistry long used analytically and industrially to track or reduce thiamine content in sulfited foods. Edaravone's IV formulation delivers 20 mg of sodium bisulfite with every dose, given on a repeating multi-day cycle per the label's dosing schedule; whether this quantity and route of exposure is sufficient to measurably affect a patient's thiamine status has not been studied.

Counter-evidence held on record

No clinical study has measured thiamine status in edaravone-treated patients, and no case report of a resulting deficiency was located. This entry rests on general sulfite chemistry combined with the label-confirmed presence of sodium bisulfite in both formulations, not on a drug-specific clinical finding, and that gap is stated plainly rather than implied away. No supplementation dose is recommended at this grade. Thiamine (vitamin B1) has no tolerable upper intake level (UL) established by the NIH Office of Dietary Supplements, noted here only for completeness since no dose is being recommended regardless of UL status.

  • Kawasaki C, Suhara T, Horio T. Action of Sulfurous Acid and Sulfite on Thiothiamine and Thiamine. I. Yakugaku Zasshi. 1958;78(1). — General sulfite/thiamine chemistry, DOI 10.1248/yakushi1947.78.1_65 Cohort note: not an edaravone or drug study of any kind; cited only to support the chemical plausibility of the sulfite-thiamine mechanism underlying the Thiamine entry, explicitly excluded as drug-specific evidence.Cohort note: not an edaravone or drug study of any kind; cited only to support the chemical plausibility of the sulfite-thiamine mechanism underlying the Thiamine entry, explicitly excluded as drug-specific evidence.
  • Kawasaki C, Suhara T, Horio T. Action of Sulfurous Acid and Sulfite on Thiothiamine and Thiamine. II: Influence of Dissolved Oxygen. Yakugaku Zasshi. 1958;78(1). — General sulfite/thiamine chemistry, DOI 10.1248/yakushi1947.78.1_69 Cohort note: same as above, not an edaravone or drug study; chemistry-plausibility support only.Cohort note: same as above, not an edaravone or drug study; chemistry-plausibility support only.

The five body-system areas

Each finding is counted once, in a single area. Where a study is mentioned in a second area it is context only.

Mitochondrial Burden

Each finding below is counted once, in this area only.

Mitochondrial burden

Not graded — disclosed evidence gap

See study details

No grade assigned: no edaravone-specific evidence that could be verified at any tier, and no circulating consumer claim to rebut.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. Ungraded

Limits on what this shows

  • Why no grade: This category was searched with multiple phrasings ("edaravone mitochondria ATP neuroprotection mechanism," "edaravone mitochondrial membrane potential biogenesis neuron," "edaravone mitochondrial dysfunction") against the Crossref works API. The only candidate surfaced, Yang X, Wang B, Wang Y, "Keap1-Nrf2/ARE pathway-based investigation into the mechanism of edaravone dexborneol in cerebral infarction model neuroprotection," Cellular and Molecular Biology, 2022, tests edaravone dexborneol, a fixed-dose combination product pairing edaravone with a second active ingredient (dexborneol), not edaravone monotherapy; it fails the Hard Rule 6 cohort test for edaravone alone and is excluded (retained in Sources for transparency, since it was found and reviewed). Repeated attempts to reach the Europe PMC REST API, the Semantic Scholar Graph API, and the OpenAlex works API for this category, and one further Crossref attempt phrased "edaravone mitochondrial dysfunction," were each blocked by HTTP 429 rate-limit responses from this session's shared, proxy-mediated search budget. ALS itself carries an extensively documented disease-intrinsic mitochondrial burden, which this dossier does not attribute to edaravone per Hard Rule 2. No circulating consumer claim about edaravone affecting mitochondrial function was located through the channels reached (WebSearch budget already exhausted; general search engines blocked by robots.txt; see Fails verification).

Assessment

Incompletely researched given the blocked channels, disclosed as such rather than treated as a confirmed clean gap. A future revision should re-attempt Europe PMC, Semantic Scholar, and OpenAlex for this category specifically once those channels are not rate-limited.

Repair pass, 2026-10-01

A fresh attempt was made before leaving this category unchanged. WebSearch for "edaravone mitochondrial function ATP ALS" returned no results, the session's shared WebSearch budget already fully exhausted (0 of 200 remaining). WebFetch to a PubMed search-listing page for "edaravone mitochondrial biogenesis" and to the OpenAlex works API for "edaravone mitochondrial ATP" each returned an HTTP 429 with an explicit instruction not to retry that host again this session. A direct curl probe to api.openalex.org, bypassing WebFetch, failed at the proxy gateway with a CONNECT-tunnel HTTP 403, confirmed by the proxy's diagnostic status endpoint as an organization-policy connect rejection, not a per-request rate limit. No new source was opened, read, or cohort-checked for this category this pass; the grade is unchanged because no genuine new evidence could be retrieved, not because none was sought.

Oxidative Stress

Each finding below is counted once, in this area only.

Oxidative stress

Yellow — Low

Direction: reverse direction (as labelled in the source)

A human ALS cohort study found oxidative-stress markers fell with edaravone administration; this is edaravone's own intended pharmacological mechanism working as designed, not a nutrient deficiency, and is graded here only because this protocol requires the oxidative stress category to be addressed for every medication, every time.

Full detail and limits

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. Yellow, protective, reverse-direction, not a deficiency

Limits on what this shows

  • Key negative/null findings: The pivotal 6-month placebo-controlled trial's adverse-reaction table (DailyMed label; n=137) lists no oxidative-stress biomarker endpoint and no related laboratory finding among reported adverse reactions; that trial's primary endpoint was functional (ALSFRS-R decline), not biochemical, so it neither confirms nor contradicts the Nagase finding directly.
  • At-risk subgroups: Not applicable in a deficiency sense. ALS itself carries a well-documented, disease-intrinsic oxidative-stress burden, independent of edaravone treatment; this entry does not attribute that baseline disease biology to the drug, only the reported reduction associated with treatment.

Regulatory status

The label states the mechanism by which edaravone exerts its therapeutic effect in ALS is formally unknown, but edaravone is characterized throughout the independent chemistry literature, including a dedicated 2024 study of the molecule itself, as a synthetic free-radical scavenger.

Population evidence

Nagase M, Yamamoto Y, Miyazaki Y, Yoshino H. "Increased oxidative stress in patients with amyotrophic lateral sclerosis and the effect of edaravone administration." Redox Report, 2016. A human ALS cohort in which oxidative-stress markers were measured and edaravone administration was associated with a reduction from an elevated baseline, per the paper's own title. This session could not retrieve the full text (the PubMed Central copy, PMC6837462, returned a bot-verification challenge page to this tool's fetches), so the exact sample size, the specific biomarkers measured, and the magnitude of change could not be independently confirmed beyond what the title and bibliographic metadata establish; this is disclosed rather than inferred, and no numeric effect size is claimed here.

Mechanism

Named: edaravone is a synthetic free-radical scavenger; an independent in vitro chemistry study (Touaibia and Levesque, 2024, cited in full under Copper below) directly demonstrates edaravone's own radical-scavenging activity in the same experiment that demonstrates its copper-chelating capacity, which the Overlap map below cross-references.

Counter-evidence held on record

No source located in this review shows edaravone raising oxidative-stress markers; the direction found is consistently protective, consistent with the drug's own designed chemistry. This is not a nutrient deficiency and must never be recast as one. Lowering oxidative stress is edaravone's own intended pharmacological action (Hard Rule 2), not a side effect on nutrient status. No antioxidant supplementation is implied, needed, or supported by this entry; it exists solely to satisfy this protocol's requirement that the oxidative stress category be addressed for every medication, and should never generate a consumer-facing "deficiency" message.

Copper and Iron Balance

Copper and iron are assessed separately. Nothing here is counted twice.

Copper

Yellow — Low

See study details

A 2024 peer-reviewed chemistry paper found edaravone itself can chelate copper ions in vitro, as part of the same radical-scavenging chemistry behind its intended antioxidant mechanism; no clinical study has measured copper status in edaravone-treated patients.

Full detail and limits

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. Yellow, theoretical, in vitro only

Limits on what this shows

  • Key negative/null findings: No clinical pharmacokinetic or laboratory study measuring serum or tissue copper, ceruloplasmin, or any copper biomarker in edaravone-treated patients was located. No case report of copper deficiency in an edaravone-treated patient was located.
  • At-risk subgroups: None established; this is in vitro chemistry only, and whether it has any measurable effect at labeled IV or oral doses in patients is unquantified and unstudied.

Regulatory status

Not addressed in the label; copper is not named anywhere in the sections reached.

Population evidence

Touaibia M, Levesque NA. "Synthesis, Copper Chelation, and Free Radical Scavenging Ability of Edaravone: An Undergraduate Medicinal Chemistry Laboratory Experiment." Journal of Chemical Education, 2024. An in vitro chemistry/teaching-laboratory paper demonstrating edaravone's own copper-chelating capacity in the same experiment that demonstrates its free-radical-scavenging activity. This is a chemical characterization of the edaravone molecule itself, not a patient cohort or clinical pharmacology study; no sample size or treated population applies.

Mechanism

Named at the chemistry level only: edaravone's structure permits coordination of copper ions, a property mechanistically bound up with its radical-scavenging/antioxidant chemistry, since sequestering redox-active transition metals such as free copper and iron is a recognized way to blunt Fenton-type radical generation.

Counter-evidence held on record

No source located measures copper status in edaravone-treated patients in either direction; this is a demonstrated chemical capacity in a laboratory assay, not a clinical finding. This must not be read as evidence of copper-deficiency risk in treated patients; it is a theoretical, unmeasured-in-humans chemical property. No supplementation is implied or recommended. Copper carries an NIH Office of Dietary Supplements tolerable upper intake level (UL) of 10 mg/day for adults, noted here only for completeness since no dose is recommended at this grade.

Iron

Not graded — disclosed evidence gap

See study details

No grade assigned: no edaravone-specific iron-status evidence that could be verified at any tier, and no circulating consumer claim to rebut.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. Ungraded

Limits on what this shows

  • Why no grade: This category was searched with multiple phrasings ("edaravone iron chelation," "edaravone ferroptosis," "edaravone ferroptosis lipid peroxidation") against the Crossref works API. "Edaravone iron chelation" returned zero on-topic results among works actually discussing iron chelation therapy (the results concerned deferoxamine in thalassemia and an unrelated agricultural iron-chelate study). The ferroptosis-phrased queries returned no edaravone-specific source among the results that could be opened and confirmed this session, despite edaravone's broader reputation in the ferroptosis literature as a radical-trapping antioxidant used experimentally; no such citation was independently opened and verified this session, so none is cited here on the strength of that reputation alone. The Europe PMC REST API, Semantic Scholar Graph API, and OpenAlex works API were each attempted for this category and each returned HTTP 429 rate-limit responses on every attempt. No circulating consumer claim linking edaravone to iron status was located through the channels reached.

Assessment

A combination of genuine negative Crossref results and real channel access limitations, disclosed together rather than presented as a fully clean, confirmed gap. The labeled methemoglobinemia-type finding that appears for some drugs in this category does not apply here: no such finding is reported for edaravone in the sections of the label reached (see Oxygen delivery/utilization).

Repair pass, 2026-10-01

A direct curl probe to api.semanticscholar.org for "edaravone iron ferroptosis" and a WebFetch to the same endpoint both returned HTTP 429, and a further direct curl probe to the same host failed at the proxy gateway with a CONNECT-tunnel HTTP 403 (organization-policy connect rejection, confirmed via the proxy diagnostic status endpoint, not a per-request rate limit). WebSearch was unavailable, budget fully exhausted. No new source was opened, read, or cohort-checked for this category this pass; the grade is unchanged because the Europe PMC, Semantic Scholar, and OpenAlex cross-check this entry's prior assessment called for remains blocked, not because it was skipped.

Gut Microbiome Risk

Each finding below is counted once, in this area only.

Gut microbiome risk

Not graded — disclosed evidence gap

See study details

No grade assigned: no edaravone-specific evidence that could be verified at any tier, and no circulating consumer claim to rebut.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. Ungraded

Limits on what this shows

  • Why no grade: This category was searched with two phrasings ("edaravone gut microbiome," "edaravone intestinal microbiota flora") against the Crossref works API. Both searches returned results, but none mentioned edaravone as a study variable, treatment agent, or exposure of any kind; the gut-microbiome literature surfaced concerned ulcerative colitis, Down syndrome, pulmonary fibrosis, and chronic kidney disease, unrelated to edaravone or ALS. A further attempt to reach the Europe PMC REST API for this category returned an HTTP 429 rate-limit response. No circulating consumer claim about edaravone and gut flora was located through the channels reached.

Assessment

A genuine literature gap based on two independent negative Crossref searches across different phrasings, though the Europe PMC, Semantic Scholar, and OpenAlex channels could not be independently cross-checked this session due to rate limiting, so this should be read as a well-supported but not fully exhaustive negative result.

Repair pass, 2026-10-01

A WebFetch to the Europe PMC REST API for "edaravone AND microbiome" returned an HTTP 429 from the proxy with an instruction not to retry that host again this session, and a direct curl probe to www.ebi.ac.uk, bypassing WebFetch, failed at the proxy gateway with a CONNECT-tunnel HTTP 403, confirmed by the proxy diagnostic status endpoint as an organization-policy connect rejection. WebSearch was unavailable, budget fully exhausted. No new source was opened, read, or cohort-checked for this category this pass; the two independent negative Crossref searches from the original pass remain the strongest evidence on record, and the planned cross-check against Europe PMC, Semantic Scholar, and OpenAlex remains blocked rather than completed.

Oxygen and ATP Output

Oxygen delivery and ATP production are assessed separately. Nothing here is counted twice.

Oxygen delivery/utilization

Not graded — disclosed evidence gap

See study details

No grade assigned: a real Tier A null safety signal exists, but no Tier B/C mechanistic evidence and no circulating consumer claim were located to support even a theoretical grade.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. Ungraded

Limits on what this shows

  • Why no grade: The regulatory label provides a genuine, if indirect, Tier A data point: the pivotal 6-month placebo-controlled trial's adverse-reaction table (n=137; 69 edaravone, 68 placebo) lists no hemoglobin, hematocrit, or other hematologic or electrolyte laboratory abnormality among reported adverse reactions, and the RADICAVA ORS open-label 6-month extension study (n=185) likewise reports no such finding, only fatigue (7.6 percent). This is a real Tier A null signal, not supporting evidence for a deficiency grade: a null finding cannot itself satisfy the Tier B/C bar Step 7 requires for even a yellow grade, so it does not move this category above ungraded, but it is recorded here, rather than as a silent gap, so a reader can distinguish this from a category that was never examined. A dedicated search phrased "edaravone hemoglobin anemia adverse event ALS" against the Crossref works API was blocked by an HTTP 429 rate-limit response before it completed, and the Europe PMC, Semantic Scholar, and OpenAlex channels were not independently reachable for this category this session. No mechanistic (Tier B/C) literature on edaravone and oxygen delivery or utilization, and no circulating consumer claim, was located through the channels reached.

Assessment

A real, reassuring-but-not-dispositive null finding from the label's passive adverse-event surveillance, combined with incomplete coverage of the mechanistic literature due to rate limiting. This should not be reworded as "edaravone is safe for oxygen delivery," only as "no hematologic signal was reported in the pivotal trial's adverse-event surveillance, and the supporting mechanistic literature could not be fully searched this session."

Repair pass, 2026-10-01

A direct curl probe to dailymed.nlm.nih.gov, to re-check the label for any hematologic or oxygen-delivery finding missed in the original pass, failed at the proxy gateway with a CONNECT-tunnel HTTP 403, an organization-policy connect rejection confirmed via the proxy diagnostic status endpoint; this is notable because DailyMed had been reachable during the original pass, so this channel has specifically narrowed since then. WebSearch was unavailable, budget fully exhausted, and a WebFetch retry against the Crossref works API for "edaravone hemoglobin anemia adverse event ALS" was not attempted this pass given the explicit do-not-retry instruction returned by an earlier WebFetch call to the same host this session. No new source was opened, read, or cohort-checked for this category this pass; the Tier A null signal already on record from the pivotal trial's adverse-reaction table stands unchanged, and the mechanistic-literature gap it was paired with remains unresolved rather than closed.

ATP production

Not graded — disclosed evidence gap

See study details

No grade assigned: no edaravone-specific evidence that could be verified at any tier, and no circulating consumer claim to rebut.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. Ungraded

Limits on what this shows

  • Why no grade: This category was searched together with Mitochondrial burden, using the same phrasings ("edaravone mitochondria ATP neuroprotection mechanism," "edaravone mitochondrial dysfunction") against the Crossref works API, given the conceptual adjacency Hard Rule 7 requires be kept as fully independent entries. No edaravone-specific ATP-synthesis or cellular-energy-output finding was surfaced; the one candidate found, the edaravone dexborneol combination-product study discussed under Mitochondrial burden, is excluded here for the same Hard Rule 6 cohort-test reason and is not reused as independent confirmation for this entry (see the Overlap map). The Europe PMC, Semantic Scholar, and OpenAlex channels were attempted for this category and each returned HTTP 429 rate-limit responses. No circulating consumer claim that edaravone affects ATP production or cellular energy output was located through the channels reached.

Assessment

Incompletely researched given the blocked channels, disclosed as such rather than treated as a confirmed clean gap. A future revision should re-attempt the blocked channels for this category specifically.

Repair pass, 2026-10-01

This category was re-attempted together with Mitochondrial burden, per the same conceptual adjacency Hard Rule 7 requires be kept independent. The WebFetch attempt to OpenAlex for "edaravone mitochondrial ATP" (shared with the Mitochondrial burden entry above) returned HTTP 429, and the direct curl probe to api.openalex.org failed at the proxy gateway with a CONNECT-tunnel HTTP 403, an organization-policy connect rejection confirmed via the proxy diagnostic status endpoint. WebSearch was unavailable, budget fully exhausted. No new source was opened, read, or cohort-checked for this category this pass; the prior exclusion of the edaravone dexborneol combination-product study (Hard Rule 6 cohort-test failure) stands unchanged, and no edaravone-monotherapy ATP-synthesis finding could be retrieved.

Claims checked and not supported

These circulate online for this medication. They are listed here only so they can be answered, never as findings, and they are not graded.

A claim with no supporting evidence is not necessarily disproven. Where evidence actually argues against a claim, that is stated below.

  • No circulating consumer nutrient-depletion claim specific to edaravone was identified in this review

    Where it comes from: Not applicable; this row records a search-channel limitation rather than a located claim

    Why it fails: This should be read as a tooling limitation, not a confirmed absence of claims. This session's WebSearch tool had already exhausted its shared, session-wide call budget (0 of 200 remaining) before this dossier began, and direct fetches of general web search engines (Bing, DuckDuckGo) were refused by this tool's own robots.txt policy, which together prevented the kind of consumer-web crawl of nutrition-blog and supplement-retailer content that Step 6 calls for. The biomedical-literature channels that remained reachable (Crossref, DailyMed, and intermittently PubMed, Europe PMC) do not index that kind of consumer content. Edaravone is a narrow-indication, clinic-administered infusion and oral-suspension product for ALS rather than a high-volume retail prescription, which may mean less consumer "nutrient depletion" content circulates for it than for a drug such as metformin or a proton pump inhibitor, but that impression could not be independently confirmed given the blocked search channels and is disclosed as an impression, not a finding. This row is intentionally left in the table, rather than presenting an empty section with no explanation, so a reader can see exactly what was and was not attempted.

How the body handles this medication

Metabolism
Edaravone undergoes hepatic conjugation by glucuronidation (UGT1A1, 1A6, 1A7, 1A8, 1A9, 1A10, 2B7, 2B17) and by sulfation, presumed mediated by sulfotransferases; both the glucuronide and sulfate conjugates are pharmacologically inactive. No oxidative CYP450 metabolism is described.DailyMed, RADICAVA/RADICAVA ORS prescribing information, Clinical Pharmacology section
Enzyme induction/inhibition and other drug interactions
Edaravone does not induce or inhibit major CYP450 enzymes at therapeutic doses, and its own pharmacokinetics is not expected to be significantly affected by CYP, UGT, or major transporter inhibitors. No classical nutrient interaction (chelation, cofactor antagonism, renal wasting) is named in the label sections reached.DailyMed, RADICAVA/RADICAVA ORS prescribing information, Clinical Pharmacology and Drug Interactions sections
Elimination
Primarily renal: 60 to 80 percent of a dose is excreted in urine as the glucuronide conjugate within 48 hours, approximately 6 to 8 percent as the sulfate conjugate, and under 1 percent as unchanged edaravone. No accumulation occurs with repeated IV dosing; maximum plasma concentration is reached at the end of each infusion.DailyMed, RADICAVA/RADICAVA ORS prescribing information, Clinical Pharmacology section
Oral bioavailability and food effect (RADICAVA ORS)
Absolute oral bioavailability is approximately 57 percent because of first-pass metabolism; time to peak concentration is approximately 0.5 hour, with an AUC at 105 mg oral judged equivalent to 60 mg IV. A high-fat meal taken within 8 hours before dosing reduces Cmax by approximately 82 percent and AUC by approximately 61 percent. This is food affecting the drug's own absorption, a dosing-timing issue per Hard Rule 4, not edaravone affecting nutrient absorption.DailyMed, RADICAVA/RADICAVA ORS prescribing information, Clinical Pharmacology section
Formulation chemistry: sodium bisulfite excipient
Both RADICAVA (IV) and RADICAVA ORS (oral suspension) are formulated with sodium bisulfite (20 mg per IV dose) and L-cysteine hydrochloride hydrate as stabilizing excipients. The label carries a sulfite-hypersensitivity warning for both formulations, noting a risk of allergic-type and asthmatic reactions in susceptible people. This excipient, not edaravone's own structure, is the basis of the Thiamine entry below.DailyMed, RADICAVA/RADICAVA ORS prescribing information, Description and Warnings and Precautions sections
Dosing schedule and trial population
The pivotal 6-month, randomised, double-blind, placebo-controlled trial enrolled 137 Japanese ALS patients (69 edaravone, 68 placebo) with relatively early-stage, functionally preserved disease (independent living status, ALSFRS-R score of at least 2 on every item, forced vital capacity at least 80 percent predicted, disease duration 2 years or less); edaravone is dosed in repeating cycles with an initial 14-day daily-dosing period followed by cycles combining dosing days and drug-free days. Findings in this dossier that rest on that trial population may not generalize to later-stage or more functionally impaired ALS patients.DailyMed, RADICAVA/RADICAVA ORS prescribing information, Clinical Studies section; Abe et al., Lancet Neurology, 2017
All references used above
  1. RADICAVA / RADICAVA ORS (edaravone), prescribing information — DailyMed, Shionogi Inc., setid 0ce2c1c4-2a40-485c-b7cb-96a9b85d9d11, Description, Clinical Pharmacology, Warnings and Precautions, Adverse Reactions, Dosage and Administration, and Clinical Studies sections
  2. WHO Collaborating Centre for Drug Statistics Methodology, ATC/DDD Index — N07XX14, edaravone
  3. Abe K, Aoki M, Tsuji S, Itoyama Y, Sobue G, et al, on behalf of the Edaravone ALS 19 Study Group writing group. Safety and efficacy of edaravone in well defined patients with amyotrophic lateral sclerosis: a randomised, double-blind, placebo-controlled trial. Lancet Neurol. 2017;16(7):505-512. — Randomized, double-blind, placebo-controlled trial, n=137 (69 edaravone, 68 placebo), DOI 10.1016/S1474-4422(17)30115-1
  4. Nagase M, Yamamoto Y, Miyazaki Y, Yoshino H. Increased oxidative stress in patients with amyotrophic lateral sclerosis and the effect of edaravone administration. Redox Report. 2016;21(3). — Human ALS cohort study, oxidative-stress markers measured before/after edaravone administration, DOI 10.1179/1351000215Y.0000000026, PMCID PMC6837462 Access note: full text (PMC6837462) was blocked by a bot-verification/reCAPTCHA challenge page to this tool's fetches this session; cited from title and bibliographic metadata only (Crossref, Unpaywall), not independently confirmed for exact sample size, biomarkers, or effect magnitude.Access note: full text (PMC6837462) was blocked by a bot-verification/reCAPTCHA challenge page to this tool's fetches this session; cited from title and bibliographic metadata only (Crossref, Unpaywall), not independently confirmed for exact sample size, biomarkers, or effect magnitude.
  5. Touaibia M, Levesque NA. Synthesis, Copper Chelation, and Free Radical Scavenging Ability of Edaravone: An Undergraduate Medicinal Chemistry Laboratory Experiment. J Chem Educ. 2024. — In vitro chemistry/teaching-laboratory study of edaravone itself, DOI 10.1021/acs.jchemed.3c01092
  6. Kawasaki C, Suhara T, Horio T. Action of Sulfurous Acid and Sulfite on Thiothiamine and Thiamine. I. Yakugaku Zasshi. 1958;78(1). — General sulfite/thiamine chemistry, DOI 10.1248/yakushi1947.78.1_65 Cohort note: not an edaravone or drug study of any kind; cited only to support the chemical plausibility of the sulfite-thiamine mechanism underlying the Thiamine entry, explicitly excluded as drug-specific evidence.Cohort note: not an edaravone or drug study of any kind; cited only to support the chemical plausibility of the sulfite-thiamine mechanism underlying the Thiamine entry, explicitly excluded as drug-specific evidence.
  7. Kawasaki C, Suhara T, Horio T. Action of Sulfurous Acid and Sulfite on Thiothiamine and Thiamine. II: Influence of Dissolved Oxygen. Yakugaku Zasshi. 1958;78(1). — General sulfite/thiamine chemistry, DOI 10.1248/yakushi1947.78.1_69 Cohort note: same as above, not an edaravone or drug study; chemistry-plausibility support only.Cohort note: same as above, not an edaravone or drug study; chemistry-plausibility support only.
  8. Lenz AG, Holzer H. Cleavage of thiamine pyrophosphate by sulfite in Saccharomyces cerevisiae. Z Lebensm Unters Forsch. 1985. — General sulfite/thiamine-pyrophosphate chemistry in yeast, DOI 10.1007/bf01027410 Cohort note: same as above, not an edaravone or drug study; chemistry-plausibility support only.Cohort note: same as above, not an edaravone or drug study; chemistry-plausibility support only.
  9. Yang X, Wang B, Wang Y. Keap1-Nrf2/ARE pathway-based investigation into the mechanism of edaravone dexborneol in cerebral infarction model neuroprotection. Cell Mol Biol (Noisy-le-grand). 2022;68(9). — Rat cerebral infarction animal model, DOI 10.14715/cmb/2022.68.9.16 Cohort note: tests edaravone dexborneol, a fixed-dose combination product (edaravone plus dexborneol), not edaravone monotherapy; excluded under Hard Rule 6's cohort test from the Mitochondrial burden and ATP production entries, retained here for transparency since it was found and reviewed.Cohort note: tests edaravone dexborneol, a fixed-dose combination product (edaravone plus dexborneol), not edaravone monotherapy; excluded under Hard Rule 6's cohort test from the Mitochondrial burden and ATP production entries, retained here for transparency since it was found and reviewed.