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MyDeficiencies

Naratriptan

Also sold as Amerge.

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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.

Naratriptan has essentially no classical nutrient-depletion machinery. Of the nine mechanism classes screened (absorption interference, accelerated catabolism via enzyme induction, renal wasting, cofactor antagonism, mitochondrial/conjugation loss, dilutional or hormonal disturbance, microbiome disruption, changed intake, increased metabolic demand), none test positive. Naratriptan is 70% orally bioavailable with no food effect, is cleared predominantly by the kidney (50% unchanged, 30% as metabolites in urine, renal clearance exceeding glomerular filtration rate consistent with active tubular secretion), is metabolized across "a wide range" of unnamed cytochrome P450 isoenzymes rather than one dominant, named pathway, does not induce any CYP450 enzyme, is "a poor inhibitor of P450," and, unlike its sister triptans sumatriptan and rizatriptan, is not a monoamine oxidase substrate. No mineral, electrolyte, or vitamin interaction of any kind is named anywhere in the FDA label. Zero classical nutrients are carried forward from the mechanism screen, a valid and clinically informative null result in its own right, not a gap in this review.

ATC N02CC02 · also sold as Amerge (generic naratriptan tablets) · 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 Naratriptan 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.

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, triptan-class extrapolation only, not naratriptan-specific

Yellow — Low

See study details

No naratriptan-specific mitochondrial evidence exists at any tier; two other triptans in the same drug class, sumatriptan and rizatriptan, each have a drug-specific Tier B preclinical hepatotoxicity study showing mitochondrial dysfunction, graded yellow here only as explicit class extrapolation.

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

Limits on what this shows

  • Key negative/null findings: Dedicated PubMed searches, "naratriptan mitochondria" and "naratriptan apoptosis," each returned an explicit, completed zero-result negative. A full-text scan of the current FDA label found no mention of mitochondria anywhere in the document. These are genuine drug-specific negatives, not merely unsearched gaps.
  • At-risk subgroups: Not established for naratriptan specifically.
  • Counter-evidence on record: The zero-result PubMed negatives above function as the counter-evidence: no naratriptan-specific mitochondrial signal, positive or negative in direction, was found to confirm or refute the class extrapolation.

Regulatory status

Not addressed anywhere in the naratriptan label; no mitochondrial, hepatic, or related hematologic/laboratory warning is listed.

Population evidence

Tier C, class extrapolation: Khalili Fard J, Hamzeiy H, Sattari M, Eghbal MA. Protective Roles of N-acetyl Cysteine and/or Taurine against Sumatriptan-Induced Hepatotoxicity. Adv Pharm Bull 2016. In vitro hepatocyte study, sumatriptan named specifically, measuring mitochondrial membrane potential decline alongside oxidative-stress markers. PMID 28101470, DOI 10.15171/apb.2016.077. Fard JK, Hamzeiy H, Sattari M, Eftekhari A, Ahmadian E, Eghbal MA. Triazole rizatriptan Induces Liver Toxicity through Lysosomal/Mitochondrial Dysfunction. Drug Res (Stuttg) 2016. In vitro/animal hepatotoxicity model, rizatriptan named specifically. PMID 27399851, DOI 10.1055/s-0042-110178. Naratriptan was confirmed absent from both studied cohorts (both are single-drug, drug-named-in-title preclinical models of a different triptan).

Mechanism

Extrapolated only: if naratriptan's hepatic CYP450-mediated metabolism produced mitochondrial stress similar to its sister triptans, a comparable signal could theoretically occur. This is not confirmed for naratriptan by any drug-specific source; naratriptan's metabolic pathway ("a wide range" of unnamed CYP450 isoenzymes) has not itself been characterized at the enzyme level in any located study, which further limits how far the extrapolation can be pressed.

Counter-evidence held on record

This entry exists to satisfy the mandatory seven-category review and to make the triptan-class extrapolation explicit, not because naratriptan itself has been shown to affect mitochondrial function. Do not present this as naratriptan-specific evidence. No mitochondrial-support supplementation (CoQ10, carnitine, or similar) is indicated on this basis.

Oxidative Stress

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

Oxidative stress, same triptan-class hepatotoxicity models, not naratriptan-specific

Yellow — Low

See study details

No naratriptan-specific oxidative-stress evidence exists at any tier; the same two sumatriptan and rizatriptan hepatotoxicity studies cited for Mitochondrial burden also measured oxidative-stress markers directly, graded yellow here only as explicit class extrapolation (see Overlap map).

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

Limits on what this shows

  • Key negative/null findings: Dedicated PubMed searches returned explicit zero-result negatives for "naratriptan oxidative stress" and "naratriptan apoptosis"; "naratriptan antioxidant" returned a single result (a general menstrual-migraine review, unrelated to oxidative-stress biomarkers) confirmed irrelevant on review. A full-text label scan found no mention of oxidative stress, antioxidant, or reactive oxygen species anywhere in the document.
  • At-risk subgroups: Not established for naratriptan specifically.
  • Counter-evidence on record: The zero/irrelevant-result searches above are the counter-evidence located; no naratriptan-specific redox signal in either direction was found.

Regulatory status

Not addressed anywhere in the naratriptan label; no oxidative-stress or antioxidant-related warning is listed.

Population evidence

Tier C, class extrapolation, same two sources as Mitochondrial burden: Khalili Fard J et al. 2016 (sumatriptan, PMID 28101470) directly measured oxidative-stress markers in hepatocytes alongside mitochondrial membrane potential, in a design testing N-acetyl cysteine and taurine as protective agents against sumatriptan-induced hepatotoxicity. Fard JK et al. 2016 (rizatriptan, PMID 27399851) implicated CYP450-mediated oxidative stress in the cytotoxicity mechanism. Naratriptan was confirmed absent from both cohorts.

Mechanism

Extrapolated only: naratriptan's CYP450-mediated metabolism could theoretically generate reactive intermediates by the same general logic proposed for sumatriptan and rizatriptan; not demonstrated for naratriptan by any drug-specific source.

Counter-evidence held on record

This entry exists to satisfy the mandatory seven-category review and to make the triptan-class extrapolation explicit, not because naratriptan itself has been shown to raise oxidative stress. Do not present this as naratriptan-specific evidence. No antioxidant supplementation is indicated on this basis.

Copper and Iron Balance

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

Copper

Not graded — disclosed evidence gap

See study details

No naratriptan-specific or triptan-class evidence of an effect on copper status was located anywhere this session.

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: Both Step 7 conditions hold: no Tier B/C evidence (drug-specific or class-level) and no circulating claim to rebut. Mechanistically, naratriptan's elimination is predominantly renal (50% unchanged) with the remainder cleared by unnamed, non-induced CYP450 isoenzymes, none of which is documented as copper-dependent, which further reduces prior plausibility. A residual tooling-limited component remains: direct connections to Europe PMC, NCBI eutils, the Crossref API, the Semantic Scholar API, and the OpenAlex API each returned HTTP 403 policy-denial rejections at the network-policy layer this session (confirmed against the live proxy status log, fresh timestamps 2026-10-01 10:40-10:41 UTC), and WebFetch-routed PubMed queries repeatedly returned HTTP 429 rate-limit rejections requiring 30-90 second pacing between attempts; the WebSearch tool's session-wide query budget (200 of 200 calls) was exhausted partway through this review, closing off general web search as a supplementary discovery channel. Judged, on balance, a genuine literature gap rather than primarily a tooling artifact, since the Crossref bibliographic search and the FDA label full-text scan, both of which did complete, returned clean, reviewed negatives; a future revision with unblocked Europe PMC/eutils/Semantic Scholar/OpenAlex-search access should still re-check.

Channels tried

FDA prescribing information, full-text scanned for copper and ceruloplasmin (neither term appears anywhere in the document; the only "iron" hit is the inactive excipient "iron oxide yellow" dye in the 2.5 mg tablet, not a biological finding). PubMed search-listing queries: "naratriptan copper OR iron OR ferritin" (via WebSearch, before budget exhaustion; no drug-specific result, only generic biochemistry pages) and, separately, "naratriptan AND (hemoglobin OR hematocrit OR anemia OR copper)" via PubMed search-listing (attempted, see Channels blocked). Crossref API bibliographic search, query "naratriptan copper iron hemoglobin": 7 results reviewed individually, all generic nutrition-science papers (hemoglobin/iron/copper interactions in rats, chicks, and pregnant women), none mentioning naratriptan, triptans, or any migraine drug at all, a clean completed negative.

Circulating claim

None found; see Fails verification. The drugs.com consumer interaction checker for naratriptan (106 drug interactions, 2 food/alcohol, 5 disease interactions) lists no copper- or mineral-related entry.

Iron

Not graded — disclosed evidence gap

See study details

No naratriptan-specific or triptan-class evidence of an effect on iron status was located anywhere this session.

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: Both Step 7 conditions hold. Naratriptan's absorption mechanism (70% oral bioavailability, no documented food effect, no named transporter) has no documented chelation, gastric-pH, or mucosal-injury component that would plausibly interfere with iron absorption, which further reduces prior plausibility. The same tooling constraints disclosed under Copper applied here: HTTP 403 policy-denial rejections at the network-policy layer for Europe PMC, eutils, Crossref, Semantic Scholar, and OpenAlex when attempted directly, HTTP 429 rate-limit rejections on repeated WebFetch-routed PubMed attempts (several queries, including a combined "naratriptan AND (hemoglobin OR hematocrit OR anemia OR copper)" query, had to be abandoned after repeated 429 rejections despite pacing of 30-90 seconds between attempts), and an exhausted WebSearch budget partway through the review. The single completed, clean "naratriptan iron" PubMed zero-result negative, together with the Crossref negative and the full label-text scan, support treating this as a genuine literature gap rather than primarily a tooling artifact, though the hemoglobin/hematocrit/anemia PubMed queries specifically could not be completed this session (rate-limited before returning) and are flagged for re-check on a future revision with working access to those channels.

Channels tried

FDA prescribing information, full-text scanned for iron, hemoglobin, hematocrit, and anemia (the only "iron" hit anywhere in the document is the inactive excipient "iron oxide yellow" dye in the 2.5 mg tablet; hemoglobin, hematocrit, and anemia do not appear at all, and no hematologic laboratory abnormality is listed in Adverse Reactions). PubMed search-listing query "naratriptan iron" completed cleanly: zero results, an explicit "No results were found." Crossref API bibliographic search, query "naratriptan copper iron hemoglobin": 7 results reviewed, all generic nutrition-science papers on rats, chicks, and pregnant women, none mentioning naratriptan or any triptan, a clean completed negative.

Circulating claim

None found; see Fails verification. The drugs.com consumer interaction checker lists no iron- or anemia-related entry for naratriptan.

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 naratriptan-specific or triptan-class evidence of a gut microbiome effect was located anywhere this session.

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: Both Step 7 conditions hold. Naratriptan's acute, as-needed dosing pattern (not a chronic daily medication) further limits plausibility of a sustained microbiome effect compared with a chronic daily drug, and no antimicrobial or motility mechanism is documented in the label. The same network-policy-layer HTTP 403 rejections (Europe PMC, eutils, Crossref direct, Semantic Scholar, OpenAlex) and WebFetch-routed HTTP 429 rate limiting disclosed under Copper and Iron applied to this category as well; a dedicated PubMed search-listing query specifically for "naratriptan microbiome" or "naratriptan microbiota" could not be completed this session after repeated 429 rejections, so this category relies on the WebSearch-era and Crossref results above rather than a PubMed-confirmed zero. Judged a genuine literature gap, consistent across all four triptan dossiers in this batch, but with a real residual tooling-limited component specific to the PubMed channel that a future revision should close.

Channels tried

FDA prescribing information, full-text scanned for microbiome, microbiota, intestinal flora, and gastrointestinal flora: none of these terms appear anywhere in the document, and no antimicrobial, pH-altering, or motility-disrupting mechanism is documented. PubMed search-listing query "naratriptan gut microbiome" (via WebSearch, before budget exhaustion): no naratriptan-specific or triptan-specific result, only generic gut-microbiota review articles and unrelated Wikipedia pages. Crossref API bibliographic search, query "naratriptan microbiome microbiota gut": 6 results reviewed individually (skin microbiome, nasopharyngeal microbiome, general gut-microbiota function and fecal-transplant reviews), none mentioning naratriptan or any triptan drug, a clean completed negative. This dossier's companion triptan dossiers in the same batch series (sumatriptan, rizatriptan, zolmitriptan) independently reached the same ungraded conclusion for this category, with no class-level evidence found for any of them either, consistent with this result rather than carried forward from it.

Circulating claim

None found; see Fails verification.

Oxygen and ATP Output

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

Oxygen delivery/utilization, drug's own vasoconstrictive mechanism, bounded by a null coronary-diameter finding

Yellow — Low

See study details

Naratriptan produces a measurable, non-ischemic reduction in myocardial blood flow and rise in coronary vascular resistance at the therapeutic dose in migraineurs without ischemic heart disease, while a separate human study found no significant change in epicardial coronary artery diameter at the same dose; this is naratriptan's own intended 5-HT1B/1D vasoconstrictive pharmacology, not a nutrient-mediated oxygen-delivery deficiency.

Full detail, limits and 4 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

Limits on what this shows

  • Key negative/null findings: Hood 1999 found no statistically significant change in epicardial coronary artery diameter despite a clear systemic and pulmonary vasopressor effect at the same dose, dissociating naratriptan's systemic vasoconstriction from any measurable epicardial coronary narrowing. Gnecchi-Ruscone 2000 found no significant effect on coronary vasodilator reserve and no ischemic symptoms in migraineurs without underlying coronary disease.
  • At-risk subgroups: Patients with the drug's labeled contraindications (ischemic coronary artery disease, peripheral vascular disease, ischemic bowel disease, uncontrolled hypertension) were excluded from the studies above and were not themselves studied here. Separately, a single published case report (Gergaud S, Lermite E, Butel F, Soltner C, Lasocki S. Extended mesenteric ischemia associated with excessive naratriptan and grapefruit juice intake. Ann Fr Anesth Reanim 2012;31:472-474, PMID 22465646) describes a patient who developed extensive mesenteric ischemia requiring small bowel resection and colectomy after naratriptan overuse combined with grapefruit juice, a probable CYP-mediated exposure interaction; this is an overdose/misuse scenario, Tier B, not typical labeled dosing, and is carried in the Monitoring panel rather than used to upgrade this entry's tier.
  • Counter-evidence on record: Hood 1999's null epicardial coronary-diameter finding, above, is the principal counter-evidence bounding this entry; it was deliberately sought and is reported here even though it weakens the magnitude of the signal.

Regulatory status

Labeled class-wide risk of vasospastic reactions, including coronary artery vasospasm/Prinzmetal's angina, myocardial infarction, and other ischemic events; naratriptan is contraindicated in ischemic coronary artery disease or coronary artery vasospasm, peripheral vascular disease, ischemic bowel disease, uncontrolled hypertension, and within 24 hours of another 5-HT1 agonist or ergot-type medication.

Population evidence

Tier A, naratriptan-specific: Gnecchi-Ruscone T, Bernard X, Pierre P, et al. Effect of naratriptan on myocardial blood flow and coronary vasodilator reserve in migraineurs. Neurology 2000;55:95-99. Randomized, double-blind, placebo-controlled crossover PET study ([15O]water), 34 migraine patients without ischemic heart disease, subcutaneous naratriptan 1.5 mg versus placebo at rest and during hyperemia. Myocardial blood flow fell 13% versus placebo and coronary vascular resistance rose 19%; coronary vasodilator reserve was not significantly affected; no ischemic symptoms occurred. PMID 10891912. Hood S, Birnie DH, Swan L, Murray LS, Whitehouse H, Winter P, Hillis WS. Effects of subcutaneous naratriptan on systemic and pulmonary haemodynamics and coronary artery diameter in humans. J Cardiovasc Pharmacol 1999;34:89-94. Cardiac catheterization study, 10 patients, naratriptan 1.5 mg subcutaneous versus placebo. Coronary artery diameter change was not statistically significant (95% CI -0.27 to 0.11 mm, p=0.37) despite a significant rise in systolic arterial pressure (p=0.0015), systemic vascular resistance (p=0.003), pulmonary vascular resistance (p=0.025), and pulmonary artery wedge pressure (p=0.009). PMID 10413073. MaassenVanDenBrink A, Reekers M, Bax WA, Ferrari MD, Saxena PR. Coronary side-effect potential of current and prospective antimigraine drugs. Circulation 1998;98:25-30. Ex vivo human isolated coronary artery segments; naratriptan named among the triptans tested, contracting coronary tissue with low intrinsic efficacy (Emax <25% of K+-induced contraction) despite higher potency (lower EC50) than sumatriptan. PMID 9665056.

Mechanism

Named: 5-HT1B receptor-mediated vasoconstriction of vascular smooth muscle, naratriptan's labeled therapeutic mechanism for cranial vasoconstriction in migraine, also measurably active, to a lesser and non-ischemic degree at therapeutic dosing, in coronary and systemic/pulmonary vasculature.

Counter-evidence held on record

This is naratriptan's own intended pharmacologic mechanism (5-HT1B/1D receptor-mediated vasoconstriction), not a nutrient-mediated oxygen-delivery deficiency, per Hard Rule 2. No iron, antioxidant, or other supplementation is indicated on this basis. The single mesenteric-ischemia case report reflects overuse combined with a CYP-exposure-altering substance, not standard dosing, and should not be read as typical-dose risk.

ATP production, triptan-class extrapolation only, not naratriptan-specific

Yellow — Low

See study details

No naratriptan-specific energy-metabolism evidence exists; graded yellow only via triptan-class extrapolation from a sumatriptan-specific human muscle-energy-metabolism study, with naratriptan confirmed absent from that study's cohort.

Full detail, limits and 1 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

Limits on what this shows

  • Key negative/null findings: No naratriptan-specific energy-metabolism study, positive or negative, was located to confirm or refute the extrapolation either way; a full-text label scan found no mention of ATP or energy metabolism anywhere in the document.
  • At-risk subgroups: Not established for naratriptan specifically.

Regulatory status

Not addressed anywhere in the naratriptan label; no energy-metabolism or ATP-related finding is listed.

Population evidence

Tier C, class extrapolation: Boska MD, Welch KM, Schultz L, Nelson J. Effects of the anti-migraine drug sumatriptan on muscle energy metabolism: relationship to side-effects. Cephalalgia 2000. Human 31P-MRS study; cohort was sumatriptan-treated migraine patients. PMID 10817445. Naratriptan was not in the studied cohort.

Mechanism

Extrapolated only: if naratriptan's vasoconstrictive action reduced local tissue perfusion the way sumatriptan's does (see Oxygen delivery/utilization; mechanism shared, sources distinct, disclosed in the Overlap map), a similar transient muscle energy-metabolism signal could theoretically follow. Not confirmed for naratriptan by any drug-specific source.

Counter-evidence held on record

This entry exists to satisfy the mandatory seven-category review and to make the class extrapolation explicit, not because naratriptan itself has been shown to affect ATP production. Do not present this as naratriptan-specific evidence. No energy-support supplementation (CoQ10, carnitine, creatine, or similar) is indicated on this basis.

How the body handles this medication

Metabolism
Metabolized in vitro by "a wide range of cytochrome P450 isoenzymes" into a number of inactive metabolites; no single enzyme is named in the label, and naratriptan is not a monoamine oxidase substrate, unlike sumatriptan and rizatriptan.FDA prescribing information (AMERGE), Clinical Pharmacology 12.3
CYP450 induction or inhibition
Naratriptan "does not inhibit monoamine oxidase (MAO) enzymes and is a poor inhibitor of P450." No enzyme induction is documented anywhere in the label.FDA prescribing information (AMERGE), Clinical Pharmacology 12.3
Elimination
Renal elimination predominates: 50% of the dose recovered unchanged and 30% as metabolites in urine. Systemic clearance 6.6 mL/min/kg; renal clearance 220 mL/min exceeds glomerular filtration rate, consistent with active renal tubular secretion (specific transporter not named in the label). Mean elimination half-life 6 hours (11 hours, range 7-20, in moderate renal impairment). No accumulation with repeat dosing at normal renal/hepatic function.FDA prescribing information (AMERGE), Clinical Pharmacology 12.3
Absorption
About 70% oral bioavailability; Tmax 2-3 hours (3-4 hours during a migraine attack). Food does not affect the pharmacokinetics of naratriptan. No transporter-mediated absorption mechanism is named.FDA prescribing information (AMERGE), Clinical Pharmacology 12.3
Renal and hepatic impairment
Mild-to-moderate renal impairment (creatinine clearance 18-39 mL/min) reduces clearance by about 50% and raises Cmax by about 40%; mild-to-moderate hepatic impairment (Child-Pugh A/B) reduces clearance by about 30% and raises half-life by about 40%. Maximum dose capped at 2.5 mg per 24 hours (1 mg starting dose) in either case; severe renal or hepatic impairment is contraindicated.FDA prescribing information (AMERGE), Dosage and Administration 2.3, Use in Specific Populations 8.6-8.7
Documented drug and lifestyle interactions
Oral contraceptives reduce naratriptan clearance by about 32%. Smoking increases clearance by about 30%. Fluoxetine, beta-blockers, tricyclic antidepressants, and alcohol show no substantial effect on naratriptan clearance. No mineral, electrolyte, or vitamin interaction, and no renal-tubular electrolyte/water-handling effect, is documented anywhere in the label.FDA prescribing information (AMERGE), Clinical Pharmacology 12.3, Drug Interactions 7
All references used above
  1. FDA prescribing information, AMERGE (naratriptan hydrochloride) tablets — Regulatory label. NDA 020763, supplement s011, approved 2016. Full text scanned for pharmacokinetic, mechanism-screen, and all seven Step 3 category terms.
  2. DailyMed, NARATRIPTAN tablet (multiple ANDA holders: Bionpharma, Heritage/Avet, Hikma, Asclemed) — Confirms current generic naratriptan labels indexed in DailyMed, consistent with the AMERGE reference label above.
  3. Gnecchi-Ruscone T, Bernard X, Pierre P, Anderson D, Legg NJ, Enahoro H, Winter PD, Crisp A, Melin JA, Camici PG. Effect of naratriptan on myocardial blood flow and coronary vasodilator reserve in migraineurs. Neurology. 2000;55(1):95-99. — Tier A, human randomized double-blind placebo-controlled crossover PET study, 34 migraineurs without ischemic heart disease, naratriptan named specifically. PMID 10891912. DOI 10.1212/wnl.55.1.95. Basis for the Oxygen delivery/utilization entry.Direct PubMed record page fetch was rate-limited (HTTP 429) this session; abstract reconstructed via OpenAlex single-record lookup instead.
  4. Hood S, Birnie DH, Swan L, Murray LS, Whitehouse H, Winter P, Hillis WS. Effects of subcutaneous naratriptan on systemic and pulmonary haemodynamics and coronary artery diameter in humans. J Cardiovasc Pharmacol. 1999;34(1):89-94. — Tier A, human cardiac catheterization study, 10 patients, naratriptan named specifically. PMID 10413073. DOI 10.1097/00005344-199907000-00015. Basis for the null coronary-diameter counter-evidence in the Oxygen delivery/utilization entry.Abstract reconstructed via OpenAlex single-record lookup; direct PubMed record page was not independently fetched this session.
  5. MaassenVanDenBrink A, Reekers M, Bax WA, Ferrari MD, Saxena PR. Coronary side-effect potential of current and prospective antimigraine drugs. Circulation. 1998;98(1):25-30. — Tier A, ex vivo human isolated coronary artery study, naratriptan named specifically among the triptans tested. PMID 9665056. DOI 10.1161/01.cir.98.1.25.Abstract reconstructed via OpenAlex single-record lookup; individual naratriptan-only Emax/EC50 figures were not disaggregated in the available abstract text, only the class-wide range, disclosed as a citation-completeness limitation in the entry above.
  6. Valentin JP, Bonnafous R, John GW. Contractile responses evoked by dihydroergotamine, naratriptan and sumatriptan in the canine isolated coronary artery. Fundam Clin Pharmacol. 1998;12(5):537-543. — Tier B, animal (canine) ex vivo coronary artery study, naratriptan named specifically. PMID 9565768. Identified during coronary-artery search but not separately relied on; consistent with the human ex vivo finding above.
  7. Connor HE, Feniuk W, Beattie DT, North PC, Oxford AW, Saynor DA, Humphrey PP. Naratriptan: biological profile in animal models relevant to migraine. Cephalalgia. 1997;17(5):534-542. — Tier B, animal pharmacology profile, naratriptan named specifically. PMID 9170336. Identified during coronary-artery search as background pharmacology; not separately relied on for a graded entry.
  8. Gergaud S, Lermite E, Butel F, Soltner C, Lasocki S. Extended mesenteric ischemia associated with excessive naratriptan and grapefruit juice intake [French]. Ann Fr Anesth Reanim. 2012;31(5):472-474. — Tier B, case report, naratriptan named specifically. PMID 22465646. DOI 10.1016/j.annfar.2012.01.022. Used for Monitoring panel context and as an at-risk-subgroup note in the Oxygen delivery/utilization entry; an overdose/misuse clinical outcome, not graded as a nutrient-status entry per Hard Rule 2.Abstract reconstructed via OpenAlex single-record lookup (French-language article); full text and exact dose/overuse pattern were not independently confirmed beyond the OpenAlex metadata, disclosed as a citation-completeness limitation.
  9. Khalili Fard J, Hamzeiy H, Sattari M, Eghbal MA. Protective Roles of N-acetyl Cysteine and/or Taurine against Sumatriptan-Induced Hepatotoxicity. Advanced Pharmaceutical Bulletin. 2016. — Tier B for sumatriptan, Tier C (class extrapolation) for naratriptan. In vitro hepatocyte hepatotoxicity model, sumatriptan named specifically; naratriptan confirmed absent from the cohort. PMID 28101470. DOI 10.15171/apb.2016.077. Basis for the Mitochondrial burden and Oxidative stress class-extrapolation entries (see Overlap map).
  10. Fard JK, Hamzeiy H, Sattari M, Eftekhari A, Ahmadian E, Eghbal MA. Triazole rizatriptan Induces Liver Toxicity through Lysosomal/Mitochondrial Dysfunction. Drug Research (Stuttg). 2016. — Tier B for rizatriptan, Tier C (class extrapolation) for naratriptan. In vitro/animal hepatotoxicity model, rizatriptan named specifically; naratriptan confirmed absent from the cohort. PMID 27399851. DOI 10.1055/s-0042-110178. Basis for the Mitochondrial burden and Oxidative stress class-extrapolation entries (see Overlap map).Cohort excluded naratriptan; cited only as the class-level basis for the Mitochondrial burden and Oxidative stress yellow grades, explicitly flagged as extrapolation.
  11. Boska MD, Welch KM, Schultz L, Nelson J. Effects of the anti-migraine drug sumatriptan on muscle energy metabolism: relationship to side-effects. Cephalalgia. 2000. — Tier A for sumatriptan, Tier C for naratriptan (class extrapolation only). Human 31P-MRS study; PMID 10817445. Cohort was sumatriptan-treated migraine patients; naratriptan was not in the studied cohort.Cohort excluded naratriptan; cited here only as the class-level basis for the ATP production yellow grade, per the same study's citation in the companion sumatriptan, rizatriptan, and zolmitriptan dossiers in this batch.
  12. WHO Collaborating Centre for Drug Statistics Methodology, ATC/DDD Index, code N02CC02 — Confirms ATC code N02CC02 for naratriptan and the 2.5 mg oral defined daily dose.
  13. Drugs.com interactions checker, naratriptan — Consumer-facing drug-interaction database, checked for nutrient- or vitamin-depletion listings as part of the circulating-claim audit; 106 drug interactions listed (70 major, 32 moderate, 4 minor), 2 food/alcohol interactions, 5 disease interactions. Only supplement-type entries: 5-hydroxytryptophan and St. John's Wort, both serotonergic, zero nutrient-depletion related.
  14. PubMed search-listing pages, multiple queries: "naratriptan mitochondria" (zero results); "naratriptan oxidative stress" (zero results); "naratriptan antioxidant" (one irrelevant result); "naratriptan apoptosis" (zero results); "naratriptan liver" (4 results, none naratriptan-specific hepatotoxicity); "naratriptan cytochrome" (2 results, neither a naratriptan-specific enzyme-identification study); "naratriptan coronary artery" (10 results, reviewed above); "naratriptan iron" (zero results); "naratriptan Eghbal OR naratriptan toxicity" (3 results, including the Gergaud mesenteric-ischemia case report above) — Search-listing results used to identify candidate Tier A/B sources and to document negative searches for Mitochondrial burden, Oxidative stress, and Iron. Each result count was confirmed directly from the page content, not inferred.Several queries in this family were interrupted by proxy-level rate limiting (HTTP 429) and required retry after a delay of roughly 30 to 90 seconds; a combined query, "naratriptan AND (hemoglobin OR hematocrit OR anemia OR copper)," could not be completed this session after repeated 429 rejections and was abandoned in favor of the single-term "naratriptan iron" query above and the Crossref cross-check below.
  15. Crossref API (api.crossref.org) bibliographic search, two queries: "naratriptan copper iron hemoglobin" (7 results, all generic nutrition science, zero naratriptan/triptan mentions) and "naratriptan microbiome microbiota gut" (6 results, all generic microbiome science, zero naratriptan/triptan mentions) — Used to cross-check the Copper, Iron, and Gut microbiome risk ungraded categories against a second bibliographic index beyond PubMed. Both queries completed successfully via WebFetch and returned clean, reviewed negatives.
  16. OpenAlex API (api.openalex.org), per-PMID lookups — Used throughout this review to obtain bibliographic detail and reconstructed abstracts (from abstract_inverted_index) for the Gnecchi-Ruscone 2000, Hood 1999, MaassenVanDenBrink 1998, and Gergaud 2012 records, where direct PubMed record-page fetches were rate-limited. Reliable for per-ID lookups throughout this session; its search endpoint (distinct from per-record lookup) was not successfully used.
  17. Europe PMC (www.ebi.ac.uk/europepmc), NCBI eutils (eutils.ncbi.nlm.nih.gov), Semantic Scholar API (api.semanticscholar.org), OpenAlex search endpoint (api.openalex.org/works?search=), WebSearch tool — Named evidence-retrieval channels under this protocol that were genuinely attempted this session and found unavailable or degraded.Direct proxy-level connections to Europe PMC, eutils, the Crossref API host, the Semantic Scholar API, and the OpenAlex API each returned explicit HTTP 403 policy-denial connection rejections when attempted outside WebFetch, confirmed directly against the live session proxy status log (recentRelayFailures entries for www.ebi.ac.uk:443, eutils.ncbi.nlm.nih.gov:443, api.crossref.org:443, api.semanticscholar.org:443, and api.openalex.org:443, timestamps 2026-10-01 10:40-10:41 UTC). Through WebFetch, Europe PMC's REST search endpoint and the OpenAlex search endpoint (distinct from its reliable per-record lookup) both returned HTTP 429 or 503 errors on the attempts made; PubMed's search-listing pages were reachable through WebFetch but were rate-limited (HTTP 429) on roughly half of all attempts this session, requiring repeated pacing delays. The WebSearch tool reported its session-wide query budget (200 of 200 calls) exhausted partway through this dossier's research (after three initial searches succeeded), so no general web search was available as a supplementary discovery channel for the remainder of this review; this is a session-level tooling constraint shared across concurrent dossiers in this batch, not a finding about the literature. Any future revision should re-attempt Europe PMC, eutils, Semantic Scholar, and the OpenAlex and Crossref search endpoints with a fresh WebSearch budget.