Component

Menaquinone-4 / MK-4 / menatetrenone

Menaquinone-4 / MK-4 / menatetrenone. Species, exposure and limitations are retained in each linked claim.

14 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. Adding menatetrenone to calcium did not significantly reduce new vertebral fractures in the full analysis set; the clinical-fracture secondary difference was also nonsignificant.

    Menaquinone-4 / MK-4 / menatetrenone → New vertebral fracture incidence source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/k2-research/19082528.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6d29b8f43348d8acd6ee85d4f65bb0cdd1352dd6f5113f58d7e58d7196bd96f5", "start_char": 0, "end_char": 1657, "text_sha256": "6d29b8f43348d8acd6ee85d4f65bb0cdd1352dd6f5113f58d7e58d7196bd96f5"}
    experimental_model
    Randomized open-label trial with blinded endpoint evaluation
    exposure
    Calcium alone versus calcium plus menatetrenone; 36-month primary and 48-month secondary endpoints
    limitations
    Full-analysis null result; advanced-osteoporosis subgroup signals are exploratory and do not replace the overall endpoint.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    4378 osteoporotic postmenopausal women
    plain_language
    A large trial did not establish a general fracture-prevention benefit from adding MK-4.
    primary_references
    [k2-p19082528] Randomized controlled study on the prevention of osteoporotic fractures (OF study): a phase IV clinical study of 15-mg menatetrenone capsules. (2009). https://pubmed.ncbi.nlm.nih.gov/19082528/ DOI: 10.1007/s00774-008-0008-8
    tissue_or_cell_type
    Vertebral and clinical fractures

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 1111–1122

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized open-label trial with blinded endpoint evaluation · source_derived_draft · unverified_draft

    ### k2-mk4-fractures-null Adding menatetrenone to calcium did not significantly reduce new vertebral fractures in the full analysis set; the clinical-fracture secondary difference was also nonsignificant. Condition category: normal nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A large trial did not establish a general fracture-prevention benefit from adding MK-4. organism: 4378 osteoporotic postmenopausal women tissue_or_cell_type: Vertebral and clinical fractures experimental_model: Randomized open-label trial with blinded endpoint evaluation limitations: Full-analysis null result; advanced-osteoporosis subgroup signals are exploratory and do not replace the overall endpoint. exposure: Calcium alone versus calcium plus menatetrenone; 36-month primary and 48-month secondary endpoints evidence_span: {"source_cache": "artifacts/k2-research/19082528.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6d29b8f43348d8acd6ee85d4f65bb0cdd1352dd6f5113f58d7e58d7196bd96f5", "start_char": 0, "end_char": 1657, "text_sha256": "6d29b8f43348d8acd6ee85d4f65bb0cdd1352dd6f5113f58d7e58d7196bd96f5"} [k2-p19082528] Randomized controlled study on the prevention of osteoporotic fractures (OF study): a phase IV clinical study of 15-mg menatetrenone capsules. (2009). https://pubmed.ncbi.nlm.nih.gov/19082528/ DOI: 10.1007/s00774-008-0008-8
    Complete structured claim and evidence

  2. Vitamin K2 entered mitochondria but restored neither respiratory electron flow nor ATP synthesis in CoQ-deficient human cells and yeast; CoQ4 did restore function.

    Menaquinone-4 / MK-4 / menatetrenone → Mitochondrial respiratory electron transfer source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/k2-research/31024065.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "23cca3c157b598de639355c855be4221ce916ee9a338e2b59923fc980614281e", "start_char": 0, "end_char": 943, "text_sha256": "23cca3c157b598de639355c855be4221ce916ee9a338e2b59923fc980614281e"}
    experimental_model
    Cellular uptake and respiratory rescue comparisons
    exposure
    MK-4 versus CoQ4
    limitations
    Different organism and deficiency model from the fly study; failure here is a boundary to extrapolation, not a clerical error in either experiment.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    Human CoQ10-deficient cell lines and CoQ6-deficient yeast
    plain_language
    Getting into the organelle did not make MK-4 a functional substitute for CoQ.
    primary_references
    [k2-p31024065] Vitamin K2 cannot substitute Coenzyme Q10 as electron carrier in the mitochondrial respiratory chain of mammalian cells. (2019). https://pubmed.ncbi.nlm.nih.gov/31024065/ DOI: 10.1038/s41598-019-43014-y
    tissue_or_cell_type
    Mitochondrial respiratory chain
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 877–888

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cellular uptake and respiratory rescue comparisons · source_derived_draft · unverified_draft

    ### k2-mk4-not-coq Vitamin K2 entered mitochondria but restored neither respiratory electron flow nor ATP synthesis in CoQ-deficient human cells and yeast; CoQ4 did restore function. Condition category: machinery_impairment nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Getting into the organelle did not make MK-4 a functional substitute for CoQ. organism: Human CoQ10-deficient cell lines and CoQ6-deficient yeast tissue_or_cell_type: Mitochondrial respiratory chain experimental_model: Cellular uptake and respiratory rescue comparisons limitations: Different organism and deficiency model from the fly study; failure here is a boundary to extrapolation, not a clerical error in either experiment. exposure: MK-4 versus CoQ4 evidence_span: {"source_cache": "artifacts/k2-research/31024065.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "23cca3c157b598de639355c855be4221ce916ee9a338e2b59923fc980614281e", "start_char": 0, "end_char": 943, "text_sha256": "23cca3c157b598de639355c855be4221ce916ee9a338e2b59923fc980614281e"} [k2-p31024065] Vitamin K2 cannot substitute Coenzyme Q10 as electron carrier in the mitochondrial respiratory chain of mammalian cells. (2019). https://pubmed.ncbi.nlm.nih.gov/31024065/ DOI: 10.1038/s41598-019-43014-y
    Complete structured claim and evidence

  3. MK-4 was not detected in serum after the tested 420-microgram dose and serum MK-4 did not increase with the seven-day 60-microgram regimen.

    Menaquinone-4 / MK-4 / menatetrenone → Serum menaquinone-4 concentration source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/k2-research/23140417.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e72bb9c0cc5800cba0605d7abba2c4e6c113dda5fa0e9b4a3afff898b23a97c4", "start_char": 0, "end_char": 1328, "text_sha256": "e72bb9c0cc5800cba0605d7abba2c4e6c113dda5fa0e9b4a3afff898b23a97c4"}
    experimental_model
    Single-dose and seven-day nutritional-dose comparison
    exposure
    420 micrograms single dose or 60 micrograms/day for seven days; MK-4 versus MK-7
    limitations
    Small parallel groups; equal mass is not equal molar dose. Undetectable serum MK-4 does not prove absent absorption, absent tissue delivery or clinical ineffectiveness.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    Healthy young Japanese women
    plain_language
    The blood test behaved differently for MK-4; that does not tell us that none reached tissues.
    primary_references
    [k2-p23140417] Comparison of menaquinone-4 and menaquinone-7 bioavailability in healthy women. (2012). https://pubmed.ncbi.nlm.nih.gov/23140417/ DOI: 10.1186/1475-2891-11-93
    tissue_or_cell_type
    Serum vitamin K concentrations

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 279–290

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Single-dose and seven-day nutritional-dose comparison · source_derived_draft · unverified_draft

    ### k2-mk4-serum MK-4 was not detected in serum after the tested 420-microgram dose and serum MK-4 did not increase with the seven-day 60-microgram regimen. Condition category: normal nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The blood test behaved differently for MK-4; that does not tell us that none reached tissues. organism: Healthy young Japanese women tissue_or_cell_type: Serum vitamin K concentrations experimental_model: Single-dose and seven-day nutritional-dose comparison limitations: Small parallel groups; equal mass is not equal molar dose. Undetectable serum MK-4 does not prove absent absorption, absent tissue delivery or clinical ineffectiveness. exposure: 420 micrograms single dose or 60 micrograms/day for seven days; MK-4 versus MK-7 evidence_span: {"source_cache": "artifacts/k2-research/23140417.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e72bb9c0cc5800cba0605d7abba2c4e6c113dda5fa0e9b4a3afff898b23a97c4", "start_char": 0, "end_char": 1328, "text_sha256": "e72bb9c0cc5800cba0605d7abba2c4e6c113dda5fa0e9b4a3afff898b23a97c4"} [k2-p23140417] Comparison of menaquinone-4 and menaquinone-7 bioavailability in healthy women. (2012). https://pubmed.ncbi.nlm.nih.gov/23140417/ DOI: 10.1186/1475-2891-11-93
    Complete structured claim and evidence

What acts on it

  1. Purified CYP4F11 catalyzed MK-4 terminal side-chain hydroxylation in vitro.

    Human cytochrome P450 4F11 → Menaquinone-4 / MK-4 / menatetrenone source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/k2-research/24138531.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bcb3784026ddabfeb55257cddc84ffd1001d6eb4fb04ba2e9daf8ade8de770fb", "start_char": 0, "end_char": 1608, "text_sha256": "bcb3784026ddabfeb55257cddc84ffd1001d6eb4fb04ba2e9daf8ade8de770fb"}
    experimental_model
    Purified enzymes, liver microsomes and genotyping
    exposure
    MK-4 oxidation and common enzyme variants
    limitations
    Catabolism assay; no assumption that all long-chain menaquinones have identical kinetics.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    Human CYP4F2/CYP4F11 and human liver microsomes
    plain_language
    An enzyme begins breaking down MK-4 by modifying the end of its side chain.
    primary_references
    [k2-p24138531] Cytochrome P450-dependent catabolism of vitamin K: ω-hydroxylation catalyzed by human CYP4F2 and CYP4F11. (2013). https://pubmed.ncbi.nlm.nih.gov/24138531/ DOI: 10.1021/bi401208m
    tissue_or_cell_type
    MK-4 catabolism

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 331–342

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified enzymes, liver microsomes and genotyping · source_derived_draft · unverified_draft

    ### k2-cyp4f11-mk4 Purified CYP4F11 catalyzed MK-4 terminal side-chain hydroxylation in vitro. Condition category: normal nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: An enzyme begins breaking down MK-4 by modifying the end of its side chain. organism: Human CYP4F2/CYP4F11 and human liver microsomes tissue_or_cell_type: MK-4 catabolism experimental_model: Purified enzymes, liver microsomes and genotyping limitations: Catabolism assay; no assumption that all long-chain menaquinones have identical kinetics. exposure: MK-4 oxidation and common enzyme variants evidence_span: {"source_cache": "artifacts/k2-research/24138531.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bcb3784026ddabfeb55257cddc84ffd1001d6eb4fb04ba2e9daf8ade8de770fb", "start_char": 0, "end_char": 1608, "text_sha256": "bcb3784026ddabfeb55257cddc84ffd1001d6eb4fb04ba2e9daf8ade8de770fb"} [k2-p24138531] Cytochrome P450-dependent catabolism of vitamin K: ω-hydroxylation catalyzed by human CYP4F2 and CYP4F11. (2013). https://pubmed.ncbi.nlm.nih.gov/24138531/ DOI: 10.1021/bi401208m
    Complete structured claim and evidence

  2. Purified CYP4F2 catalyzed MK-4 terminal side-chain hydroxylation in vitro.

    Human cytochrome P450 4F2 → Menaquinone-4 / MK-4 / menatetrenone source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/k2-research/24138531.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bcb3784026ddabfeb55257cddc84ffd1001d6eb4fb04ba2e9daf8ade8de770fb", "start_char": 0, "end_char": 1608, "text_sha256": "bcb3784026ddabfeb55257cddc84ffd1001d6eb4fb04ba2e9daf8ade8de770fb"}
    experimental_model
    Purified enzymes, liver microsomes and genotyping
    exposure
    MK-4 oxidation and common enzyme variants
    limitations
    Catabolism assay; no assumption that all long-chain menaquinones have identical kinetics.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    Human CYP4F2/CYP4F11 and human liver microsomes
    plain_language
    An enzyme begins breaking down MK-4 by modifying the end of its side chain.
    primary_references
    [k2-p24138531] Cytochrome P450-dependent catabolism of vitamin K: ω-hydroxylation catalyzed by human CYP4F2 and CYP4F11. (2013). https://pubmed.ncbi.nlm.nih.gov/24138531/ DOI: 10.1021/bi401208m
    tissue_or_cell_type
    MK-4 catabolism

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 318–329

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified enzymes, liver microsomes and genotyping · source_derived_draft · unverified_draft

    ### k2-cyp4f2-mk4 Purified CYP4F2 catalyzed MK-4 terminal side-chain hydroxylation in vitro. Condition category: normal nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: An enzyme begins breaking down MK-4 by modifying the end of its side chain. organism: Human CYP4F2/CYP4F11 and human liver microsomes tissue_or_cell_type: MK-4 catabolism experimental_model: Purified enzymes, liver microsomes and genotyping limitations: Catabolism assay; no assumption that all long-chain menaquinones have identical kinetics. exposure: MK-4 oxidation and common enzyme variants evidence_span: {"source_cache": "artifacts/k2-research/24138531.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bcb3784026ddabfeb55257cddc84ffd1001d6eb4fb04ba2e9daf8ade8de770fb", "start_char": 0, "end_char": 1608, "text_sha256": "bcb3784026ddabfeb55257cddc84ffd1001d6eb4fb04ba2e9daf8ade8de770fb"} [k2-p24138531] Cytochrome P450-dependent catabolism of vitamin K: ω-hydroxylation catalyzed by human CYP4F2 and CYP4F11. (2013). https://pubmed.ncbi.nlm.nih.gov/24138531/ DOI: 10.1021/bi401208m
    Complete structured claim and evidence

  3. Cells lacking both GPX4 and FSP1 required higher K1/MK-4 concentrations to prevent ferroptosis than cells lacking GPX4 alone.

    FSP1 / AIFM2 → Menaquinone-4 / MK-4 / menatetrenone source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/k2-research/35922516.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a75e4881732cbe87173197db393b42d49fc6e8110df919fed8d63b16c9877da6", "start_char": 16083, "end_char": 16259, "text_sha256": "942e81f7fca3a59aecc9d6cfcdc008e88931de54074e63eeb96c71af3d236eec"}
    experimental_model
    Enzyme/liposome chemistry, knockout cells and warfarin-exposed mice
    exposure
    MK-4/K1, NAD(P)H, FSP1 loss and inhibitors
    limitations
    Preclinical experiments; not a demonstrated oral MK-7 treatment for ferroptosis-related disease or a self-treatment regimen for anticoagulant poisoning.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    Human recombinant FSP1, mammalian cells and mice
    plain_language
    The FSP1 pathway and selenium-dependent GPX4 defense are connected but not the same mechanism.
    primary_references
    [k2-p35922516] A non-canonical vitamin K cycle is a potent ferroptosis suppressor. (2022). https://pubmed.ncbi.nlm.nih.gov/35922516/ DOI: 10.1038/s41586-022-05022-3
    tissue_or_cell_type
    Lipid peroxidation and vitamin K reduction
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 812–823

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Enzyme/liposome chemistry, knockout cells and warfarin-exposed mice · source_derived_draft · unverified_draft

    ### k2-fsp1-gpx4-parallel Cells lacking both GPX4 and FSP1 required higher K1/MK-4 concentrations to prevent ferroptosis than cells lacking GPX4 alone. Condition category: machinery_impairment nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The FSP1 pathway and selenium-dependent GPX4 defense are connected but not the same mechanism. organism: Human recombinant FSP1, mammalian cells and mice tissue_or_cell_type: Lipid peroxidation and vitamin K reduction experimental_model: Enzyme/liposome chemistry, knockout cells and warfarin-exposed mice limitations: Preclinical experiments; not a demonstrated oral MK-7 treatment for ferroptosis-related disease or a self-treatment regimen for anticoagulant poisoning. exposure: MK-4/K1, NAD(P)H, FSP1 loss and inhibitors evidence_span: {"source_cache": "artifacts/k2-research/35922516.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a75e4881732cbe87173197db393b42d49fc6e8110df919fed8d63b16c9877da6", "start_char": 16083, "end_char": 16259, "text_sha256": "942e81f7fca3a59aecc9d6cfcdc008e88931de54074e63eeb96c71af3d236eec"} [k2-p35922516] A non-canonical vitamin K cycle is a potent ferroptosis suppressor. (2022). https://pubmed.ncbi.nlm.nih.gov/35922516/ DOI: 10.1038/s41586-022-05022-3
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. CYP4F2, but not CYP4F11, supported sequential MK-4 oxidation to the omega-acid without apparent release of the aldehyde intermediate.

    Human cytochrome P450 4F2 → Menaquinone-4 omega-carboxylic acid source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/k2-research/24138531.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bcb3784026ddabfeb55257cddc84ffd1001d6eb4fb04ba2e9daf8ade8de770fb", "start_char": 0, "end_char": 1608, "text_sha256": "bcb3784026ddabfeb55257cddc84ffd1001d6eb4fb04ba2e9daf8ade8de770fb"}
    experimental_model
    Purified enzymes, liver microsomes and genotyping
    exposure
    MK-4 oxidation and common enzyme variants
    limitations
    Catabolism assay; no assumption that all long-chain menaquinones have identical kinetics.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    Human CYP4F2/CYP4F11 and human liver microsomes
    plain_language
    The two enzymes did not perform every later breakdown step equally.
    primary_references
    [k2-p24138531] Cytochrome P450-dependent catabolism of vitamin K: ω-hydroxylation catalyzed by human CYP4F2 and CYP4F11. (2013). https://pubmed.ncbi.nlm.nih.gov/24138531/ DOI: 10.1021/bi401208m
    tissue_or_cell_type
    MK-4 catabolism

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 344–355

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified enzymes, liver microsomes and genotyping · source_derived_draft · unverified_draft

    ### k2-cyp4f2-acid CYP4F2, but not CYP4F11, supported sequential MK-4 oxidation to the omega-acid without apparent release of the aldehyde intermediate. Condition category: normal nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The two enzymes did not perform every later breakdown step equally. organism: Human CYP4F2/CYP4F11 and human liver microsomes tissue_or_cell_type: MK-4 catabolism experimental_model: Purified enzymes, liver microsomes and genotyping limitations: Catabolism assay; no assumption that all long-chain menaquinones have identical kinetics. exposure: MK-4 oxidation and common enzyme variants evidence_span: {"source_cache": "artifacts/k2-research/24138531.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bcb3784026ddabfeb55257cddc84ffd1001d6eb4fb04ba2e9daf8ade8de770fb", "start_char": 0, "end_char": 1608, "text_sha256": "bcb3784026ddabfeb55257cddc84ffd1001d6eb4fb04ba2e9daf8ade8de770fb"} [k2-p24138531] Cytochrome P450-dependent catabolism of vitamin K: ω-hydroxylation catalyzed by human CYP4F2 and CYP4F11. (2013). https://pubmed.ncbi.nlm.nih.gov/24138531/ DOI: 10.1021/bi401208m
    Complete structured claim and evidence

  2. FSP1 reduced vitamin K quinones to radical-trapping hydroquinones using NAD(P)H.

    FSP1 / AIFM2 → Reduced vitamin K hydroquinone family source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/k2-research/35922516.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3bd5750fd2d12a754ad4237018851391c6b5b80bac6ad58307321fb7c3042c5a", "start_char": 0, "end_char": 1403, "text_sha256": "3bd5750fd2d12a754ad4237018851391c6b5b80bac6ad58307321fb7c3042c5a"}
    experimental_model
    Enzyme/liposome chemistry, knockout cells and warfarin-exposed mice
    exposure
    MK-4/K1, NAD(P)H, FSP1 loss and inhibitors
    limitations
    Preclinical experiments; not a demonstrated oral MK-7 treatment for ferroptosis-related disease or a self-treatment regimen for anticoagulant poisoning.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    Human recombinant FSP1, mammalian cells and mice
    plain_language
    A niacin-derived electron donor helps regenerate the reduced antioxidant form.
    primary_references
    [k2-p35922516] A non-canonical vitamin K cycle is a potent ferroptosis suppressor. (2022). https://pubmed.ncbi.nlm.nih.gov/35922516/ DOI: 10.1038/s41586-022-05022-3
    tissue_or_cell_type
    Lipid peroxidation and vitamin K reduction

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 773–784

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Enzyme/liposome chemistry, knockout cells and warfarin-exposed mice · source_derived_draft · unverified_draft

    ### k2-fsp1-k-reduction FSP1 reduced vitamin K quinones to radical-trapping hydroquinones using NAD(P)H. Condition category: normal nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A niacin-derived electron donor helps regenerate the reduced antioxidant form. organism: Human recombinant FSP1, mammalian cells and mice tissue_or_cell_type: Lipid peroxidation and vitamin K reduction experimental_model: Enzyme/liposome chemistry, knockout cells and warfarin-exposed mice limitations: Preclinical experiments; not a demonstrated oral MK-7 treatment for ferroptosis-related disease or a self-treatment regimen for anticoagulant poisoning. exposure: MK-4/K1, NAD(P)H, FSP1 loss and inhibitors evidence_span: {"source_cache": "artifacts/k2-research/35922516.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3bd5750fd2d12a754ad4237018851391c6b5b80bac6ad58307321fb7c3042c5a", "start_char": 0, "end_char": 1403, "text_sha256": "3bd5750fd2d12a754ad4237018851391c6b5b80bac6ad58307321fb7c3042c5a"} [k2-p35922516] A non-canonical vitamin K cycle is a potent ferroptosis suppressor. (2022). https://pubmed.ncbi.nlm.nih.gov/35922516/ DOI: 10.1038/s41586-022-05022-3
    Complete structured claim and evidence

  3. FSP1 knockout diminished MK-4 and K1 protection; wild-type FSP1 rescued protection while its myristoylation-defective G2A mutant did not.

    FSP1 / AIFM2 → Ferroptosis source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/k2-research/35922516.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a75e4881732cbe87173197db393b42d49fc6e8110df919fed8d63b16c9877da6", "start_char": 15449, "end_char": 16082, "text_sha256": "689a74e99dd668d48baef5232109dbf2898ba3adca2999a83a7bb24b321420c0"}
    experimental_model
    Enzyme/liposome chemistry, knockout cells and warfarin-exposed mice
    exposure
    MK-4/K1, NAD(P)H, FSP1 loss and inhibitors
    limitations
    Preclinical experiments; not a demonstrated oral MK-7 treatment for ferroptosis-related disease or a self-treatment regimen for anticoagulant poisoning.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    Human recombinant FSP1, mammalian cells and mice
    plain_language
    Providing the quinone did not fully substitute for an appropriately located working reductase.
    primary_references
    [k2-p35922516] A non-canonical vitamin K cycle is a potent ferroptosis suppressor. (2022). https://pubmed.ncbi.nlm.nih.gov/35922516/ DOI: 10.1038/s41586-022-05022-3
    tissue_or_cell_type
    Lipid peroxidation and vitamin K reduction
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 799–810

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Enzyme/liposome chemistry, knockout cells and warfarin-exposed mice · source_derived_draft · unverified_draft

    ### k2-fsp1-loss FSP1 knockout diminished MK-4 and K1 protection; wild-type FSP1 rescued protection while its myristoylation-defective G2A mutant did not. Condition category: machinery_impairment nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Providing the quinone did not fully substitute for an appropriately located working reductase. organism: Human recombinant FSP1, mammalian cells and mice tissue_or_cell_type: Lipid peroxidation and vitamin K reduction experimental_model: Enzyme/liposome chemistry, knockout cells and warfarin-exposed mice limitations: Preclinical experiments; not a demonstrated oral MK-7 treatment for ferroptosis-related disease or a self-treatment regimen for anticoagulant poisoning. exposure: MK-4/K1, NAD(P)H, FSP1 loss and inhibitors evidence_span: {"source_cache": "artifacts/k2-research/35922516.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a75e4881732cbe87173197db393b42d49fc6e8110df919fed8d63b16c9877da6", "start_char": 15449, "end_char": 16082, "text_sha256": "689a74e99dd668d48baef5232109dbf2898ba3adca2999a83a7bb24b321420c0"} [k2-p35922516] A non-canonical vitamin K cycle is a potent ferroptosis suppressor. (2022). https://pubmed.ncbi.nlm.nih.gov/35922516/ DOI: 10.1038/s41586-022-05022-3
    Complete structured claim and evidence

  4. UBIAD1 synthesized MK-4 using GGPP as the isoprenyl side-chain source.

    Human UBIAD1 prenyltransferase → Geranylgeranyl diphosphate / GGPP source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/k2-research/25874989.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bbd73607ba2570aa383c81c189b29dd19f1cbd7bf7acdd8343ecf3ee7dc5faf8", "start_char": 24159, "end_char": 24399, "text_sha256": "b680e2031495b2fee24a56c799e8cb2f64bbac3c6a3cb0d33592051f2cf41b9f"}
    experimental_model
    Microsomal enzyme assays and mutagenesis
    exposure
    Prenyl donors, reductant, magnesium and lipophilic statins
    limitations
    In-vitro substrate and assay context. Residual microsomal magnesium prevents concluding that synthesis is magnesium-independent; no human supplementation effect was tested.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    Human UBIAD1 expressed in Sf9 insect cells
    plain_language
    MK-4 production needs a side-chain donor as well as the vitamin K ring.
    primary_references
    [k2-p25874989] Functional characterization of the vitamin K2 biosynthetic enzyme UBIAD1. (2015). https://pubmed.ncbi.nlm.nih.gov/25874989/ DOI: 10.1371/journal.pone.0125737
    tissue_or_cell_type
    Microsomal prenylation

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 201–212

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Microsomal enzyme assays and mutagenesis · source_derived_draft · unverified_draft

    ### k2-ggpp-sidechain UBIAD1 synthesized MK-4 using GGPP as the isoprenyl side-chain source. Condition category: normal nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: MK-4 production needs a side-chain donor as well as the vitamin K ring. organism: Human UBIAD1 expressed in Sf9 insect cells tissue_or_cell_type: Microsomal prenylation experimental_model: Microsomal enzyme assays and mutagenesis limitations: In-vitro substrate and assay context. Residual microsomal magnesium prevents concluding that synthesis is magnesium-independent; no human supplementation effect was tested. exposure: Prenyl donors, reductant, magnesium and lipophilic statins evidence_span: {"source_cache": "artifacts/k2-research/25874989.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bbd73607ba2570aa383c81c189b29dd19f1cbd7bf7acdd8343ecf3ee7dc5faf8", "start_char": 24159, "end_char": 24399, "text_sha256": "b680e2031495b2fee24a56c799e8cb2f64bbac3c6a3cb0d33592051f2cf41b9f"} [k2-p25874989] Functional characterization of the vitamin K2 biosynthetic enzyme UBIAD1. (2015). https://pubmed.ncbi.nlm.nih.gov/25874989/ DOI: 10.1371/journal.pone.0125737
    Complete structured claim and evidence

  5. Rat tracer experiments identified menadione derived from oral phylloquinone as a circulating precursor of tissue MK-4.

    Phylloquinone → Menadione / vitamin K3 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/k2-research/24085302.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a0197882d517aa2bd4d9b2919e72c588383ad183064f1a2bf8f64f5152d28386", "start_char": 0, "end_char": 1653, "text_sha256": "a0197882d517aa2bd4d9b2919e72c588383ad183064f1a2bf8f64f5152d28386"}
    experimental_model
    Stable-isotope cannulation and recombinant-enzyme product analysis
    exposure
    Oral labeled phylloquinone; MS and NMR analysis
    limitations
    Rat tracing defines a precursor route; no exact human conversion fraction or advice to ingest menadione is inferred.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    Rats and recombinant UBIAD1
    plain_language
    K1 and K2 metabolism connect through a precursor; they are not completely separate nutritional systems.
    primary_references
    [k2-p24085302] Menadione (vitamin K3) is a catabolic product of oral phylloquinone (vitamin K1) in the intestine and a circulating precursor of tissue menaquinone-4 (vitamin K2) in rats. (2013). https://pubmed.ncbi.nlm.nih.gov/24085302/ DOI: 10.1074/jbc.m113.477356
    tissue_or_cell_type
    Intestine, circulation and tissue synthesis

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 175–186

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Stable-isotope cannulation and recombinant-enzyme product analysis · source_derived_draft · unverified_draft

    ### k2-k1-menadione Rat tracer experiments identified menadione derived from oral phylloquinone as a circulating precursor of tissue MK-4. Condition category: normal nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: K1 and K2 metabolism connect through a precursor; they are not completely separate nutritional systems. organism: Rats and recombinant UBIAD1 tissue_or_cell_type: Intestine, circulation and tissue synthesis experimental_model: Stable-isotope cannulation and recombinant-enzyme product analysis limitations: Rat tracing defines a precursor route; no exact human conversion fraction or advice to ingest menadione is inferred. exposure: Oral labeled phylloquinone; MS and NMR analysis evidence_span: {"source_cache": "artifacts/k2-research/24085302.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a0197882d517aa2bd4d9b2919e72c588383ad183064f1a2bf8f64f5152d28386", "start_char": 0, "end_char": 1653, "text_sha256": "a0197882d517aa2bd4d9b2919e72c588383ad183064f1a2bf8f64f5152d28386"} [k2-p24085302] Menadione (vitamin K3) is a catabolic product of oral phylloquinone (vitamin K1) in the intestine and a circulating precursor of tissue menaquinone-4 (vitamin K2) in rats. (2013). https://pubmed.ncbi.nlm.nih.gov/24085302/ DOI: 10.1074/jbc.m113.477356
    Complete structured claim and evidence

  6. Product analysis identified reduced menadione, rather than its quinone form, as an intermediate in UBIAD1-mediated MK-4 formation.

    Human UBIAD1 prenyltransferase → Menadiol / reduced menadione source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/k2-research/24085302.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a0197882d517aa2bd4d9b2919e72c588383ad183064f1a2bf8f64f5152d28386", "start_char": 0, "end_char": 1653, "text_sha256": "a0197882d517aa2bd4d9b2919e72c588383ad183064f1a2bf8f64f5152d28386"}
    experimental_model
    Stable-isotope cannulation and recombinant-enzyme product analysis
    exposure
    Oral labeled phylloquinone; MS and NMR analysis
    limitations
    Rat tracing defines a precursor route; no exact human conversion fraction or advice to ingest menadione is inferred.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    Rats and recombinant UBIAD1
    plain_language
    The precursor must also be in the right redox state.
    primary_references
    [k2-p24085302] Menadione (vitamin K3) is a catabolic product of oral phylloquinone (vitamin K1) in the intestine and a circulating precursor of tissue menaquinone-4 (vitamin K2) in rats. (2013). https://pubmed.ncbi.nlm.nih.gov/24085302/ DOI: 10.1074/jbc.m113.477356
    tissue_or_cell_type
    Intestine, circulation and tissue synthesis

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 188–199

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Stable-isotope cannulation and recombinant-enzyme product analysis · source_derived_draft · unverified_draft

    ### k2-reduced-precursor Product analysis identified reduced menadione, rather than its quinone form, as an intermediate in UBIAD1-mediated MK-4 formation. Condition category: normal nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The precursor must also be in the right redox state. organism: Rats and recombinant UBIAD1 tissue_or_cell_type: Intestine, circulation and tissue synthesis experimental_model: Stable-isotope cannulation and recombinant-enzyme product analysis limitations: Rat tracing defines a precursor route; no exact human conversion fraction or advice to ingest menadione is inferred. exposure: Oral labeled phylloquinone; MS and NMR analysis evidence_span: {"source_cache": "artifacts/k2-research/24085302.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a0197882d517aa2bd4d9b2919e72c588383ad183064f1a2bf8f64f5152d28386", "start_char": 0, "end_char": 1653, "text_sha256": "a0197882d517aa2bd4d9b2919e72c588383ad183064f1a2bf8f64f5152d28386"} [k2-p24085302] Menadione (vitamin K3) is a catabolic product of oral phylloquinone (vitamin K1) in the intestine and a circulating precursor of tissue menaquinone-4 (vitamin K2) in rats. (2013). https://pubmed.ncbi.nlm.nih.gov/24085302/ DOI: 10.1074/jbc.m113.477356
    Complete structured claim and evidence

  7. UBIAD1 G186R significantly impaired both MK-4 biosynthesis and vitamin K-dependent reporter carboxylation.

    Human UBIAD1 prenyltransferase → Vitamin K-dependent protein gamma-carboxylation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/k2-research/34813684.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f533947abd5f26101d1bf1e2548d37b98d16bb72c470dcdfaf2b2f2625c5e206", "start_char": 0, "end_char": 1777, "text_sha256": "f533947abd5f26101d1bf1e2548d37b98d16bb72c470dcdfaf2b2f2625c5e206"}
    experimental_model
    CRISPR reporter cells with UBIAD1 variants
    exposure
    UBIAD1 N102S, G186R and other variants
    limitations
    Cell-specific residual activity differs between variants; a UBIAD1 mutation is not automatically global vitamin K failure.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    Human HEK293 reporter cells
    plain_language
    A different variant impaired both supply and use in the same assay.
    primary_references
    [k2-p34813684] Naturally occurring UBIAD1 mutations differentially affect menaquinone biosynthesis and vitamin K-dependent carboxylation. (2022). https://pubmed.ncbi.nlm.nih.gov/34813684/ DOI: 10.1111/febs.16291
    tissue_or_cell_type
    MK-4 production and protein carboxylation
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 253–264

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · CRISPR reporter cells with UBIAD1 variants · source_derived_draft · unverified_draft

    ### k2-ubiad1-g186r UBIAD1 G186R significantly impaired both MK-4 biosynthesis and vitamin K-dependent reporter carboxylation. Condition category: machinery_impairment nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A different variant impaired both supply and use in the same assay. organism: Human HEK293 reporter cells tissue_or_cell_type: MK-4 production and protein carboxylation experimental_model: CRISPR reporter cells with UBIAD1 variants limitations: Cell-specific residual activity differs between variants; a UBIAD1 mutation is not automatically global vitamin K failure. exposure: UBIAD1 N102S, G186R and other variants evidence_span: {"source_cache": "artifacts/k2-research/34813684.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f533947abd5f26101d1bf1e2548d37b98d16bb72c470dcdfaf2b2f2625c5e206", "start_char": 0, "end_char": 1777, "text_sha256": "f533947abd5f26101d1bf1e2548d37b98d16bb72c470dcdfaf2b2f2625c5e206"} [k2-p34813684] Naturally occurring UBIAD1 mutations differentially affect menaquinone biosynthesis and vitamin K-dependent carboxylation. (2022). https://pubmed.ncbi.nlm.nih.gov/34813684/ DOI: 10.1111/febs.16291
    Complete structured claim and evidence

  8. Human UBIAD1 expression supported conversion of labeled vitamin K precursors to MK-4, identified by deuterium NMR.

    Human UBIAD1 prenyltransferase → Menaquinone-4 biosynthesis source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/k2-research/20953171.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b8786e664d3b32db7b0cca72c710e24f1546e14f0a69c031908400731174cea3", "start_char": 0, "end_char": 2006, "text_sha256": "b8786e664d3b32db7b0cca72c710e24f1546e14f0a69c031908400731174cea3"}
    experimental_model
    Gene knockdown, heterologous expression, isotope conversion and NMR
    exposure
    Labeled vitamin K precursors, UBIAD1 knockdown and expression
    limitations
    Identifies a biosynthetic enzyme, not a clinical requirement to supplement MK-4. K1-derived MK-4 synthesis does not make humans independent of external vitamin K precursors.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    Human UBIAD1 in human and insect-cell systems; mouse localization
    plain_language
    Cells have an enzyme that can make MK-4 from vitamin K precursors.
    primary_references
    [k2-p20953171] Identification of UBIAD1 as a novel human menaquinone-4 biosynthetic enzyme. (2010). https://pubmed.ncbi.nlm.nih.gov/20953171/ DOI: 10.1038/nature09464
    tissue_or_cell_type
    MK-4 synthesis

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 136–147

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Gene knockdown, heterologous expression, isotope conversion and NMR · source_derived_draft · unverified_draft

    ### k2-ubiad1-synthesis Human UBIAD1 expression supported conversion of labeled vitamin K precursors to MK-4, identified by deuterium NMR. Condition category: normal nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Cells have an enzyme that can make MK-4 from vitamin K precursors. organism: Human UBIAD1 in human and insect-cell systems; mouse localization tissue_or_cell_type: MK-4 synthesis experimental_model: Gene knockdown, heterologous expression, isotope conversion and NMR limitations: Identifies a biosynthetic enzyme, not a clinical requirement to supplement MK-4. K1-derived MK-4 synthesis does not make humans independent of external vitamin K precursors. exposure: Labeled vitamin K precursors, UBIAD1 knockdown and expression evidence_span: {"source_cache": "artifacts/k2-research/20953171.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b8786e664d3b32db7b0cca72c710e24f1546e14f0a69c031908400731174cea3", "start_char": 0, "end_char": 2006, "text_sha256": "b8786e664d3b32db7b0cca72c710e24f1546e14f0a69c031908400731174cea3"} [k2-p20953171] Identification of UBIAD1 as a novel human menaquinone-4 biosynthetic enzyme. (2010). https://pubmed.ncbi.nlm.nih.gov/20953171/ DOI: 10.1038/nature09464
    Complete structured claim and evidence

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