Component

N1-methyl-2-pyridone-5-carboxamide (2PY)

N1-methyl-2-pyridone-5-carboxamide (2PY). The model and exposure of each linked claim define its scope.

3 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What it acts on

  1. Higher serum 2PY was associated with three-year major adverse cardiovascular events in both validation cohorts.

    N1-methyl-2-pyridone-5-carboxamide (2PY) → Major cardiovascular event incidence source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    cross_nutrient
    Niacin precursor form and the measured endpoint are separate graph entities.
    evidence_span
    {"source_cache": "artifacts/niacin-clinical-sources/ferrell2024.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "09530c87779c7a8db8507c847dcb29ae3b7e439967c9271dec5f7cbda6c33d19", "start_char": 0, "end_char": 2066, "text_sha256": "09530c87779c7a8db8507c847dcb29ae3b7e439967c9271dec5f7cbda6c33d19"}
    experimental_model
    Prospective stable cardiac patient cohorts with three-year event follow-up
    exposure
    Discovery cohort 1,162; US validation 2,331 and European validation 832; three-year cardiovascular follow-up; physiological-level mouse metabolite exposure
    limitations
    Human metabolite associations are not randomized effects of niacin intake. Renal handling and other determinants of levels matter. Mouse exposure results do not prove dietary niacin or supplements caused human events.
    nutrient_topic
    Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
    organism
    Homo sapiens
    plain_language
    A breakdown-product measurement tracked risk; that does not identify dietary niacin as the cause.
    primary_references
    [nia-clin-ferrell2024] A terminal metabolite of niacin promotes vascular inflammation and contributes to cardiovascular disease risk. (2024). https://pubmed.ncbi.nlm.nih.gov/38374343/ DOI: 10.1038/s41591-023-02793-8
    tissue_or_cell_type
    Serum metabolites and clinical cardiovascular outcomes
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1557–1569

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Prospective stable cardiac patient cohorts with three-year event follow-up · source_derived_draft · unverified_draft

    ### nia-clin-2py-risk Higher serum 2PY was associated with three-year major adverse cardiovascular events in both validation cohorts. Condition category: biomarker_context nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A breakdown-product measurement tracked risk; that does not identify dietary niacin as the cause. organism: Homo sapiens tissue_or_cell_type: Serum metabolites and clinical cardiovascular outcomes experimental_model: Prospective stable cardiac patient cohorts with three-year event follow-up limitations: Human metabolite associations are not randomized effects of niacin intake. Renal handling and other determinants of levels matter. Mouse exposure results do not prove dietary niacin or supplements caused human events. exposure: Discovery cohort 1,162; US validation 2,331 and European validation 832; three-year cardiovascular follow-up; physiological-level mouse metabolite exposure cross_nutrient: Niacin precursor form and the measured endpoint are separate graph entities. evidence_span: {"source_cache": "artifacts/niacin-clinical-sources/ferrell2024.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "09530c87779c7a8db8507c847dcb29ae3b7e439967c9271dec5f7cbda6c33d19", "start_char": 0, "end_char": 2066, "text_sha256": "09530c87779c7a8db8507c847dcb29ae3b7e439967c9271dec5f7cbda6c33d19"} [nia-clin-ferrell2024] A terminal metabolite of niacin promotes vascular inflammation and contributes to cardiovascular disease risk. (2024). https://pubmed.ncbi.nlm.nih.gov/38374343/ DOI: 10.1038/s41591-023-02793-8
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Physiological-level 4PY exposure, unlike structural isomer 2PY, induced vascular VCAM-1 expression and leukocyte adherence in mice.

    N1-methyl-4-pyridone-3-carboxamide (4PY) → Mouse endothelial Vcam1 expression source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Mouse vascular cell adhesion molecule 1 / Vcam1 (induced_protein); Leukocyte adherence to vascular endothelium (measured_consequence); N1-methyl-2-pyridone-5-carboxamide (2PY) (negative_comparator)
    evidence_span
    {"source_cache": "artifacts/niacin-clinical-sources/ferrell2024.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "09530c87779c7a8db8507c847dcb29ae3b7e439967c9271dec5f7cbda6c33d19", "start_char": 0, "end_char": 2066, "text_sha256": "09530c87779c7a8db8507c847dcb29ae3b7e439967c9271dec5f7cbda6c33d19"}
    experimental_model
    Prospective cardiac cohorts, genetic associations, and separate mouse metabolite exposures
    exposure
    Discovery cohort 1,162; US validation 2,331 and European validation 832; three-year cardiovascular follow-up; physiological-level mouse metabolite exposure
    limitations
    Human metabolite associations are not randomized effects of niacin intake. Renal handling and other determinants of levels matter. Mouse exposure results do not prove dietary niacin or supplements caused human events.
    nutrient_topic
    Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
    organism
    Mus musculus
    plain_language
    In mice, one breakdown product directly promoted a vessel-wall adhesion response; its close chemical relative did not.
    primary_references
    [nia-clin-ferrell2024] A terminal metabolite of niacin promotes vascular inflammation and contributes to cardiovascular disease risk. (2024). https://pubmed.ncbi.nlm.nih.gov/38374343/ DOI: 10.1038/s41591-023-02793-8
    tissue_or_cell_type
    Circulating metabolites and mouse vascular endothelium

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1585–1597

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Prospective cardiac cohorts, genetic associations, and separate mouse metabolite exposures · source_derived_draft · unverified_draft

    ### nia-clin-4py-mouse-vcam Physiological-level 4PY exposure, unlike structural isomer 2PY, induced vascular VCAM-1 expression and leukocyte adherence in mice. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: In mice, one breakdown product directly promoted a vessel-wall adhesion response; its close chemical relative did not. organism: Mus musculus tissue_or_cell_type: Circulating metabolites and mouse vascular endothelium experimental_model: Prospective cardiac cohorts, genetic associations, and separate mouse metabolite exposures limitations: Human metabolite associations are not randomized effects of niacin intake. Renal handling and other determinants of levels matter. Mouse exposure results do not prove dietary niacin or supplements caused human events. exposure: Discovery cohort 1,162; US validation 2,331 and European validation 832; three-year cardiovascular follow-up; physiological-level mouse metabolite exposure cross_nutrient: Mouse vascular cell adhesion molecule 1 / Vcam1 (induced_protein); Leukocyte adherence to vascular endothelium (measured_consequence); N1-methyl-2-pyridone-5-carboxamide (2PY) (negative_comparator) evidence_span: {"source_cache": "artifacts/niacin-clinical-sources/ferrell2024.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "09530c87779c7a8db8507c847dcb29ae3b7e439967c9271dec5f7cbda6c33d19", "start_char": 0, "end_char": 2066, "text_sha256": "09530c87779c7a8db8507c847dcb29ae3b7e439967c9271dec5f7cbda6c33d19"} [nia-clin-ferrell2024] A terminal metabolite of niacin promotes vascular inflammation and contributes to cardiovascular disease risk. (2024). https://pubmed.ncbi.nlm.nih.gov/38374343/ DOI: 10.1038/s41591-023-02793-8
    Complete structured claim and evidence

  2. Urinary 2PY below 1.2 mg/day tracked the lowest intake; the urinary 2PY-to-methyl-nicotinamide ratio performed less well than individual metabolite outputs and missed the 10.1-NE/day restriction.

    Niacin (vitamin B3) → Urinary 2PY excretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    N1-methyl-2-pyridone-5-carboxamide (2PY) (measured_metabolite)
    evidence_span
    {"source_cache": "artifacts/niacin-clinical-sources/jacob1989.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "749fc69d8d6cb1ba79a0b17e38e9300611713e3939224ba9ac809cef91c7a64c", "start_char": 0, "end_char": 1463, "text_sha256": "749fc69d8d6cb1ba79a0b17e38e9300611713e3939224ba9ac809cef91c7a64c"}
    experimental_model
    Controlled metabolic-unit feeding of young men for 11 weeks
    exposure
    6.1–32 NE/day; oral nicotinamide test doses
    limitations
    Small controlled male metabolic-unit study. Erythrocytes are not every tissue; historical adequate intake is not a current recommendation. Jacob and Fu reports may describe related participants and are not counted as independent trials. Historical NMN abbreviation means N1-methylnicotinamide, not nicotinamide mononucleotide. Urinary output is not a universal diagnostic cutoff.
    nutrient_topic
    Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
    organism
    Homo sapiens
    plain_language
    Individual urine measurements were more informative than assuming their ratio was a better marker.
    primary_references
    [nia-clin-jacob1989] Biochemical markers for assessment of niacin status in young men: urinary and blood levels of niacin metabolites. (1989). https://pubmed.ncbi.nlm.nih.gov/2522982/ DOI: 10.1093/jn/119.4.591
    tissue_or_cell_type
    Urine and plasma
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1163–1175

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Controlled metabolic-unit feeding of young men for 11 weeks · source_derived_draft · unverified_draft

    ### nia-clin-urine-2py-restriction Urinary 2PY below 1.2 mg/day tracked the lowest intake; the urinary 2PY-to-methyl-nicotinamide ratio performed less well than individual metabolite outputs and missed the 10.1-NE/day restriction. Condition category: nutrient_deficiency nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Individual urine measurements were more informative than assuming their ratio was a better marker. organism: Homo sapiens tissue_or_cell_type: Urine and plasma experimental_model: Controlled metabolic-unit feeding of young men for 11 weeks limitations: Small controlled male metabolic-unit study. Erythrocytes are not every tissue; historical adequate intake is not a current recommendation. Jacob and Fu reports may describe related participants and are not counted as independent trials. Historical NMN abbreviation means N1-methylnicotinamide, not nicotinamide mononucleotide. Urinary output is not a universal diagnostic cutoff. exposure: 6.1–32 NE/day; oral nicotinamide test doses cross_nutrient: N1-methyl-2-pyridone-5-carboxamide (2PY) (measured_metabolite) evidence_span: {"source_cache": "artifacts/niacin-clinical-sources/jacob1989.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "749fc69d8d6cb1ba79a0b17e38e9300611713e3939224ba9ac809cef91c7a64c", "start_char": 0, "end_char": 1463, "text_sha256": "749fc69d8d6cb1ba79a0b17e38e9300611713e3939224ba9ac809cef91c7a64c"} [nia-clin-jacob1989] Biochemical markers for assessment of niacin status in young men: urinary and blood levels of niacin metabolites. (1989). https://pubmed.ncbi.nlm.nih.gov/2522982/ DOI: 10.1093/jn/119.4.591
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

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