Warfarin

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

The drug blocks vitamin K recycling, but that is a different enzyme step from making MK-4.

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 162–173

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-warfarin Warfarin did not inhibit UBIAD1-mediated MK-4 biosynthesis in the reported experiments. Condition category: normal nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The drug blocks vitamin K recycling, but that is a different enzyme step from making MK-4. 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

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/k2-research/17848178.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d2d79c43cc8142d6dc8f1eab4ac99b05ceb01e50e5afb41f5ca75aec732cba27", "start_char": 0, "end_char": 1745, "text_sha256": "d2d79c43cc8142d6dc8f1eab4ac99b05ceb01e50e5afb41f5ca75aec732cba27"}

experimental_model

Human vascular-cell calcification and synthetic-peptide assays

exposure

Elevated calcium, warfarin, K1 and modified MGP peptides

limitations

Vitamin K1 intervention in cells; K2-specific efficacy and human arterial reversal were not tested.

nutrient_topic

Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family

organism

Human vascular smooth muscle cells

plain_language

Changing the vitamin K cycle changed the protein state and the mineral-deposition outcome in these cells.

primary_references

[k2-p17848178] Post-translational modifications regulate matrix Gla protein function: importance for inhibition of vascular smooth muscle cell calcification. (2007). https://pubmed.ncbi.nlm.nih.gov/17848178/ DOI: 10.1111/j.1538-7836.2007.02758.x

tissue_or_cell_type

Extracellular matrix and vesicle-like surfaces

trigger_kind

machinery_impairment Imported condition classification; unverified.

Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 539–550

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human vascular-cell calcification and synthetic-peptide assays · source_derived_draft · unverified_draft

### k2-warfarin-mgp Warfarin-treated vascular cells produced uncarboxylated MGP and accumulated more calcium salts than controls. Condition category: machinery_impairment nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Changing the vitamin K cycle changed the protein state and the mineral-deposition outcome in these cells. organism: Human vascular smooth muscle cells tissue_or_cell_type: Extracellular matrix and vesicle-like surfaces experimental_model: Human vascular-cell calcification and synthetic-peptide assays limitations: Vitamin K1 intervention in cells; K2-specific efficacy and human arterial reversal were not tested. exposure: Elevated calcium, warfarin, K1 and modified MGP peptides evidence_span: {"source_cache": "artifacts/k2-research/17848178.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d2d79c43cc8142d6dc8f1eab4ac99b05ceb01e50e5afb41f5ca75aec732cba27", "start_char": 0, "end_char": 1745, "text_sha256": "d2d79c43cc8142d6dc8f1eab4ac99b05ceb01e50e5afb41f5ca75aec732cba27"} [k2-p17848178] Post-translational modifications regulate matrix Gla protein function: importance for inhibition of vascular smooth muscle cell calcification. (2007). https://pubmed.ncbi.nlm.nih.gov/17848178/ DOI: 10.1111/j.1538-7836.2007.02758.x

evidence_span

{"source_cache": "artifacts/k2-research/14765195.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "32f373fc0363ed079e580b2d47a3cb36c82b46871860fc6740b0285e23936496", "start_char": 0, "end_char": 1385, "text_sha256": "32f373fc0363ed079e580b2d47a3cb36c82b46871860fc6740b0285e23936496"}

experimental_model

siRNA identification and recombinant expression

exposure

Gene silencing, enzyme expression and warfarin sensitivity

limitations

Gene-discovery experiments; later structural understanding supersedes the original minimal topology description.

nutrient_topic

Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family

organism

Human VKORC1 and insect-cell expression

plain_language

An anticoagulant acts on cofactor recycling, which changes protein maturation downstream.

primary_references

[k2-p14765195] Identification of the gene for vitamin K epoxide reductase. (2004). https://pubmed.ncbi.nlm.nih.gov/14765195/ DOI: 10.1038/nature02254

tissue_or_cell_type

Vitamin K recycling enzyme

Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 448–459

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · siRNA identification and recombinant expression · source_derived_draft · unverified_draft

### k2-warfarin-vkor Recombinantly expressed VKORC1 activity was sensitive to warfarin. Condition category: normal nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: An anticoagulant acts on cofactor recycling, which changes protein maturation downstream. organism: Human VKORC1 and insect-cell expression tissue_or_cell_type: Vitamin K recycling enzyme experimental_model: siRNA identification and recombinant expression limitations: Gene-discovery experiments; later structural understanding supersedes the original minimal topology description. exposure: Gene silencing, enzyme expression and warfarin sensitivity evidence_span: {"source_cache": "artifacts/k2-research/14765195.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "32f373fc0363ed079e580b2d47a3cb36c82b46871860fc6740b0285e23936496", "start_char": 0, "end_char": 1385, "text_sha256": "32f373fc0363ed079e580b2d47a3cb36c82b46871860fc6740b0285e23936496"} [k2-p14765195] Identification of the gene for vitamin K epoxide reductase. (2004). https://pubmed.ncbi.nlm.nih.gov/14765195/ DOI: 10.1038/nature02254

evidence_span

{"source_cache": "artifacts/coumarin-research/9143352.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dca3f4253c2977d47070bb95696634ee2e06fa9a28a3d76ac9790ce695ed6f09", "start_char": 0, "end_char": 2723, "text_sha256": "dca3f4253c2977d47070bb95696634ee2e06fa9a28a3d76ac9790ce695ed6f09"}

experimental_model

Human microsomal and recombinant CYP2A6 inhibitor screen

exposure

Coumarin 0.5–50 micromolar; 47 inhibitor/substrate probes

limitations

In vitro inhibition thresholds are not demonstrated clinical interactions at food exposure.

nutrient_topic

Coumarin research collection; topical membership is not evidence of a direct dietary effect. · Coumarin

organism

Human

plain_language

Warfarin is a separate molecule with a different principal target.

primary_references

[coumarin-p9143352] Inhibition of coumarin 7-hydroxylase activity in human liver microsomes. (1997). https://pubmed.ncbi.nlm.nih.gov/9143352/ DOI: 10.1006/abbi.1997.9964

tissue_or_cell_type

Liver enzyme preparations

Coumarin: metabolism, signaling and nutrient connections (2026-09-17) · lines 592–603

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human microsomal and recombinant CYP2A6 inhibitor screen · source_derived_draft · unverified_draft

### coumarin-warfarin-inhibition-null Warfarin showed little or no CYP2A6 inhibition in this assay, with Ki above 200 micromolar. Condition category: normal nutrient_topic: Coumarin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Warfarin is a separate molecule with a different principal target. organism: Human tissue_or_cell_type: Liver enzyme preparations experimental_model: Human microsomal and recombinant CYP2A6 inhibitor screen limitations: In vitro inhibition thresholds are not demonstrated clinical interactions at food exposure. exposure: Coumarin 0.5–50 micromolar; 47 inhibitor/substrate probes evidence_span: {"source_cache": "artifacts/coumarin-research/9143352.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dca3f4253c2977d47070bb95696634ee2e06fa9a28a3d76ac9790ce695ed6f09", "start_char": 0, "end_char": 2723, "text_sha256": "dca3f4253c2977d47070bb95696634ee2e06fa9a28a3d76ac9790ce695ed6f09"} [coumarin-p9143352] Inhibition of coumarin 7-hydroxylase activity in human liver microsomes. (1997). https://pubmed.ncbi.nlm.nih.gov/9143352/ DOI: 10.1006/abbi.1997.9964

evidence_span

{"source_cache": "artifacts/coq10-research/9621803.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "510d412753fc2f3ff7e974beda97125c6112e530d6379145495e56fa01adb498", "start_char": 0, "end_char": 752, "text_sha256": "510d412753fc2f3ff7e974beda97125c6112e530d6379145495e56fa01adb498"}

experimental_model

Case report with supplement withdrawal

exposure

CoQ10 exposure then discontinuation

limitations

Single case; temporal association is not proof of mechanism or interaction frequency. Chemical similarity does not establish vitamin K activity.

nutrient_topic

Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system

organism

72-year-old woman taking warfarin

plain_language

A possible drug interaction was reported, but one case cannot determine how often it occurs.

primary_references

[coq10-p9621803] [Interaction between warfarin and coenzyme Q10]. (1998). https://pubmed.ncbi.nlm.nih.gov/9621803/

tissue_or_cell_type

Anticoagulant response

Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 1256–1267

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Case report with supplement withdrawal · source_derived_draft · unverified_draft

### coq10-warfarin-case The case report described reduced warfarin responsiveness during CoQ use and recovery after withdrawal. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A possible drug interaction was reported, but one case cannot determine how often it occurs. organism: 72-year-old woman taking warfarin tissue_or_cell_type: Anticoagulant response experimental_model: Case report with supplement withdrawal limitations: Single case; temporal association is not proof of mechanism or interaction frequency. Chemical similarity does not establish vitamin K activity. exposure: CoQ10 exposure then discontinuation evidence_span: {"source_cache": "artifacts/coq10-research/9621803.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "510d412753fc2f3ff7e974beda97125c6112e530d6379145495e56fa01adb498", "start_char": 0, "end_char": 752, "text_sha256": "510d412753fc2f3ff7e974beda97125c6112e530d6379145495e56fa01adb498"} [coq10-p9621803] [Interaction between warfarin and coenzyme Q10]. (1998). https://pubmed.ncbi.nlm.nih.gov/9621803/

evidence_span

{"source_cache": "artifacts/coq10-research/12772396.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0c668036863182db6c07a131179cd78f773088609808e320fdee5fe34d2d9d14", "start_char": 0, "end_char": 1260, "text_sha256": "0c668036863182db6c07a131179cd78f773088609808e320fdee5fe34d2d9d14"}

experimental_model

Randomized double-blind placebo-controlled crossover trial

exposure

CoQ10 100 mg/day for four weeks; separate ginkgo and placebo periods

limitations

Small short trial with dose adjustment to maintain INR. Same trial was reported in a 2002 letter; not independent replication.

nutrient_topic

Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system

organism

24 stable warfarin-treated outpatients; three withdrawals

plain_language

A small controlled study did not demonstrate the interaction reported in cases.

primary_references

[coq10-p12772396] [Effect of Coenzyme Q10 and Ginkgo biloba on warfarin dosage in patients on long-term warfarin treatment. A randomized, double-blind, placebo-controlled cross-over trial]. (2003). https://pubmed.ncbi.nlm.nih.gov/12772396/

tissue_or_cell_type

INR and adjusted weekly warfarin dose

Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 1269–1280

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind placebo-controlled crossover trial · source_derived_draft · unverified_draft

### coq10-warfarin-trial INR remained stable and mean warfarin dose did not change significantly during CoQ versus placebo periods. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A small controlled study did not demonstrate the interaction reported in cases. organism: 24 stable warfarin-treated outpatients; three withdrawals tissue_or_cell_type: INR and adjusted weekly warfarin dose experimental_model: Randomized double-blind placebo-controlled crossover trial limitations: Small short trial with dose adjustment to maintain INR. Same trial was reported in a 2002 letter; not independent replication. exposure: CoQ10 100 mg/day for four weeks; separate ginkgo and placebo periods evidence_span: {"source_cache": "artifacts/coq10-research/12772396.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0c668036863182db6c07a131179cd78f773088609808e320fdee5fe34d2d9d14", "start_char": 0, "end_char": 1260, "text_sha256": "0c668036863182db6c07a131179cd78f773088609808e320fdee5fe34d2d9d14"} [coq10-p12772396] [Effect of Coenzyme Q10 and Ginkgo biloba on warfarin dosage in patients on long-term warfarin treatment. A randomized, double-blind, placebo-controlled cross-over trial]. (2003). https://pubmed.ncbi.nlm.nih.gov/12772396/

evidence_span

{"source_cache": "artifacts/k2-research/36788244.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5fda09197d386351a1b1d261c9b385db36e02eab0c238bf18599d7086b501f93", "start_char": 0, "end_char": 1359, "text_sha256": "5fda09197d386351a1b1d261c9b385db36e02eab0c238bf18599d7086b501f93"}

experimental_model

Genome-wide CRISPR screen and reporter biochemistry

exposure

FSP1 knockout/inhibition and DHODH comparison

limitations

Supports cycle biochemistry; a different ferroptosis defense enzyme need not share the same vitamin K function.

nutrient_topic

Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family

organism

Human vitamin K-dependent reporter cells

plain_language

The antioxidant enzyme also helps supply cofactor for protein modification.

primary_references

[k2-p36788244] A genome-wide CRISPR-Cas9 knockout screen identifies FSP1 as the warfarin-resistant vitamin K reductase. (2023). https://pubmed.ncbi.nlm.nih.gov/36788244/ DOI: 10.1038/s41467-023-36446-8

tissue_or_cell_type

Warfarin-resistant quinone reduction

Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 825–836

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Genome-wide CRISPR screen and reporter biochemistry · source_derived_draft · unverified_draft

### k2-fsp1-carboxylation A CRISPR screen independently identified FSP1 as the warfarin-resistant vitamin K reductase; FSP1 inhibition impaired vitamin K-dependent carboxylation. Condition category: normal nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The antioxidant enzyme also helps supply cofactor for protein modification. organism: Human vitamin K-dependent reporter cells tissue_or_cell_type: Warfarin-resistant quinone reduction experimental_model: Genome-wide CRISPR screen and reporter biochemistry limitations: Supports cycle biochemistry; a different ferroptosis defense enzyme need not share the same vitamin K function. exposure: FSP1 knockout/inhibition and DHODH comparison evidence_span: {"source_cache": "artifacts/k2-research/36788244.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5fda09197d386351a1b1d261c9b385db36e02eab0c238bf18599d7086b501f93", "start_char": 0, "end_char": 1359, "text_sha256": "5fda09197d386351a1b1d261c9b385db36e02eab0c238bf18599d7086b501f93"} [k2-p36788244] A genome-wide CRISPR-Cas9 knockout screen identifies FSP1 as the warfarin-resistant vitamin K reductase. (2023). https://pubmed.ncbi.nlm.nih.gov/36788244/ DOI: 10.1038/s41467-023-36446-8

evidence_access

Primary full text

experimental_model

Albumin fluorescence and ultrafiltration assays.

limitations

Not demonstrated displacement toxicity or a change in patient anticoagulation.

nutrient_topic

Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin

plain_language

Carrier binding changes the freely available fraction.

primary_references

Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021

Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 124–130

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Albumin fluorescence and ultrafiltration assays. · source_derived_draft · unverified_draft

## myricetin-parent-albumin Carrier binding changes the freely available fraction. The parent bound human serum albumin with high affinity and moderately displaced the Site I marker warfarin in vitro. Model: Albumin fluorescence and ultrafiltration assays. Limitations: Not demonstrated displacement toxicity or a change in patient anticoagulation. Evidence access: Primary full text Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021

evidence_access

Primary full text

experimental_model

Albumin fluorescence and ultrafiltration assays.

limitations

Not demonstrated displacement toxicity or a change in patient anticoagulation.

nutrient_topic

Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin

plain_language

Carrier binding changes the freely available fraction.

primary_references

Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021

Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 172–178

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Albumin fluorescence and ultrafiltration assays. · source_derived_draft · unverified_draft

## myricetin-sulfate-albumin Carrier binding changes the freely available fraction. The sulfate bound human serum albumin with high affinity and moderately displaced the Site I marker warfarin in vitro. Model: Albumin fluorescence and ultrafiltration assays. Limitations: Not demonstrated displacement toxicity or a change in patient anticoagulation. Evidence access: Primary full text Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes, and organic anion-transporting polypeptides (OATP1B1 and OATP2B1). · 2024 · https://pubmed.ncbi.nlm.nih.gov/39344282/ · DOI 10.1002/prp2.70021

dose

Warfarin 25 mg once; ginger product at recommended study dose, exact herbal amount not in accessed abstract

duration

Ginger for 7 days before and 7 days after warfarin

evidence_access

Primary PubMed abstract.

evidence_scope

literature_reviewed; model-specific source-derived curation, not universally established human effects

experimental_model

12 healthy men in an open randomized three-way crossover study

limitations

Whole ginger rather than purified gingerols; a small healthy-volunteer null result cannot exclude interactions during chronic anticoagulation.

nutrient_topic

Gingerols collection; each molecular form and experimental preparation remains explicit. · Gingerols

organism

12 healthy men in an open randomized three-way crossover study

plain_language

Co-administered ginger product did not significantly change the INR response to a single warfarin dose in healthy men.

primary_references

Effect of ginkgo and ginger on the pharmacokinetics and pharmacodynamics of warfarin in healthy subjects. (2005). https://pubmed.ncbi.nlm.nih.gov/15801937/ DOI: 10.1111/j.1365-2125.2005.02322.x

route

Oral co-exposure

tissue

Plasma and coagulation measurements

Gingerols: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 558–567

Original AI-assisted curation of thirteen primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · 12 healthy men in an open randomized three-way crossover study · source_derived_draft · unverified_draft

## gingerols-ginger-warfarin-inr-null Co-administered ginger product did not significantly change the INR response to a single warfarin dose in healthy men. Model/species: 12 healthy men in an open randomized three-way crossover study Tissue: Plasma and coagulation measurements Exposure: Warfarin 25 mg once; ginger product at recommended study dose, exact herbal amount not in accessed abstract Route: Oral co-exposure Duration: Ginger for 7 days before and 7 days after warfarin Limits: Whole ginger rather than purified gingerols; a small healthy-volunteer null result cannot exclude interactions during chronic anticoagulation. Primary reference: Effect of ginkgo and ginger on the pharmacokinetics and pharmacodynamics of warfarin in healthy subjects. (2005). https://pubmed.ncbi.nlm.nih.gov/15801937/ DOI: 10.1111/j.1365-2125.2005.02322.x Access: Primary PubMed abstract.

dose

Warfarin 25 mg once; ginger product at recommended study dose, exact herbal amount not in accessed abstract

duration

Ginger for 7 days before and 7 days after warfarin

evidence_access

Primary PubMed abstract.

evidence_scope

literature_reviewed; model-specific source-derived curation, not universally established human effects

experimental_model

12 healthy men in an open randomized three-way crossover study

limitations

Whole ginger rather than purified gingerols; a small healthy-volunteer null result cannot exclude interactions during chronic anticoagulation.

nutrient_topic

Gingerols collection; each molecular form and experimental preparation remains explicit. · Gingerols

organism

12 healthy men in an open randomized three-way crossover study

plain_language

Co-administered ginger product did not significantly change apparent clearance of either warfarin enantiomer in the crossover study.

primary_references

Effect of ginkgo and ginger on the pharmacokinetics and pharmacodynamics of warfarin in healthy subjects. (2005). https://pubmed.ncbi.nlm.nih.gov/15801937/ DOI: 10.1111/j.1365-2125.2005.02322.x

route

Oral co-exposure

tissue

Plasma and coagulation measurements

Gingerols: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 569–578

Original AI-assisted curation of thirteen primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · 12 healthy men in an open randomized three-way crossover study · source_derived_draft · unverified_draft

## gingerols-ginger-warfarin-pk-null Co-administered ginger product did not significantly change apparent clearance of either warfarin enantiomer in the crossover study. Model/species: 12 healthy men in an open randomized three-way crossover study Tissue: Plasma and coagulation measurements Exposure: Warfarin 25 mg once; ginger product at recommended study dose, exact herbal amount not in accessed abstract Route: Oral co-exposure Duration: Ginger for 7 days before and 7 days after warfarin Limits: Whole ginger rather than purified gingerols; a small healthy-volunteer null result cannot exclude interactions during chronic anticoagulation. Primary reference: Effect of ginkgo and ginger on the pharmacokinetics and pharmacodynamics of warfarin in healthy subjects. (2005). https://pubmed.ncbi.nlm.nih.gov/15801937/ DOI: 10.1111/j.1365-2125.2005.02322.x Access: Primary PubMed abstract.