Celecoxib: molecular mechanisms & dependencies

How nutrients influence it

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Human evidence only

How nutrients reach it in more than one step

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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

Where it participates (unsigned role)

Ibuprofen but not celecoxib significantly inhibited thromboxane-dependent platelet aggregation induced ex vivo by arachidonic acid, 83% against 11.9%, and reduced serum thromboxane B2 by 95% and urinary 11-dehydro thromboxane B2 by 70%, while both ibuprofen and celecoxib suppressed an index of cyclooxygenase-2 activity to a comparable degree and both suppressed urinary excretion of the prostacyclin metabolite 2,3-dinor-6-keto-prostaglandin F1 alpha, data suggesting that cyclooxygenase-2 is a major source of systemic prostacyclin biosynthesis in healthy humans.
Ibuprofen → Systemic prostacyclin biosynthesis measured as urinary 2,3-dinor-6-keto-prostaglandin F1 alpha source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/ibuprofen-research/9874808.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a643d03df8bc925866696516e7040644634dca29b4f98d39df38ea9c9ab295f4", "start_char": 0, "end_char": 1789, "text_sha256": "a643d03df8bc925866696516e7040644634dca29b4f98d39df38ea9c9ab295f4"}
experimental_model
Volunteers given celecoxib at three doses or ibuprofen, with platelet, serum and urinary indices
exposure
800 milligrams ibuprofen against 100, 400 or 800 milligrams celecoxib
limitations
Measures both isoform-specific indices in the same people, which is what allows the prostacyclin source to be assigned. Acute dosing in healthy volunteers.
nutrient_topic
Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. · Ibuprofen
organism
Human
plain_language
The enzyme these drugs are meant to spare the stomach by blocking is the one that makes the body’s main anticlotting prostaglandin.
primary_references
[ibu-p9874808] Systemic biosynthesis of prostacyclin by cyclooxygenase (COX)-2: the human pharmacology of a selective inhibitor of COX-2. (1999). https://pubmed.ncbi.nlm.nih.gov/9874808/ DOI: 10.1073/pnas.96.1.272
tissue_or_cell_type
Platelets and whole body
Ibuprofen: the enantiomer that works, the one that was called inactive, the one-way chemistry that turns one into the other, and the targets that are not cyclooxygenase (2026-09-22) · lines 526–537
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Volunteers given celecoxib at three doses or ibuprofen, with platelet, serum and urinary indices · source_derived_draft · unverified_draft
### ibu-cox2-makes-the-prostacyclin Ibuprofen but not celecoxib significantly inhibited thromboxane-dependent platelet aggregation induced ex vivo by arachidonic acid, 83% against 11.9%, and reduced serum thromboxane B2 by 95% and urinary 11-dehydro thromboxane B2 by 70%, while both ibuprofen and celecoxib suppressed an index of cyclooxygenase-2 activity to a comparable degree and both suppressed urinary excretion of the prostacyclin metabolite 2,3-dinor-6-keto-prostaglandin F1 alpha, data suggesting that cyclooxygenase-2 is a major source of systemic prostacyclin biosynthesis in healthy humans. Condition category: normal nutrient_topic: Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. plain_language: The enzyme these drugs are meant to spare the stomach by blocking is the one that makes the body’s main anticlotting prostaglandin. organism: Human tissue_or_cell_type: Platelets and whole body experimental_model: Volunteers given celecoxib at three doses or ibuprofen, with platelet, serum and urinary indices limitations: Measures both isoform-specific indices in the same people, which is what allows the prostacyclin source to be assigned. Acute dosing in healthy volunteers. exposure: 800 milligrams ibuprofen against 100, 400 or 800 milligrams celecoxib evidence_span: {"source_cache": "artifacts/ibuprofen-research/9874808.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a643d03df8bc925866696516e7040644634dca29b4f98d39df38ea9c9ab295f4", "start_char": 0, "end_char": 1789, "text_sha256": "a643d03df8bc925866696516e7040644634dca29b4f98d39df38ea9c9ab295f4"} [ibu-p9874808] Systemic biosynthesis of prostacyclin by cyclooxygenase (COX)-2: the human pharmacology of a selective inhibitor of COX-2. (1999). https://pubmed.ncbi.nlm.nih.gov/9874808/ DOI: 10.1073/pnas.96.1.272
Complete structured claim and evidence
Although ibuprofen, naproxen and celecoxib all had the potential to compete with aspirin for access to the substrate binding channel of cyclooxygenase-1 in vitro, measuring aspirin target engagement directly by mass spectrometry after a single therapeutic dose of each followed by 325 milligrams of aspirin revealed a potent drug-drug interaction between ibuprofen and aspirin and between naproxen and aspirin but not between celecoxib and aspirin.
Naproxen → Aspirin / acetylsalicylic acid source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/aspirin-research/25385584.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b2de8f18887f336c8c735f7ffbd1b72b92e5da43aa6388c229590dea120439f2", "start_char": 0, "end_char": 1242, "text_sha256": "b2de8f18887f336c8c735f7ffbd1b72b92e5da43aa6388c229590dea120439f2"}
experimental_model
Mass-spectrometric assay of cyclooxygenase-1 acetylation in platelets from volunteers given an NSAID followed by aspirin
exposure
A single therapeutic dose of ibuprofen, naproxen or celecoxib followed by 325 milligrams of aspirin
limitations
Measures target engagement directly rather than inferring it from platelet function, and separates the drugs. A single dose of each, in volunteers rather than patients.
nutrient_topic
Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. · Aspirin / acetylsalicylic acid
organism
Human
plain_language
Ibuprofen and naproxen block aspirin in people; celecoxib does not.
primary_references
[asa-p25385584] Differential impairment of aspirin-dependent platelet cyclooxygenase acetylation by nonsteroidal antiinflammatory drugs. (2014). https://pubmed.ncbi.nlm.nih.gov/25385584/ DOI: 10.1073/pnas.1406997111
tissue_or_cell_type
Platelets
trigger_kind
biomarker_context Imported condition classification; unverified.
Aspirin: the serine it acetylates, the enzyme that acetylation creates, the dose that separates platelet from vessel wall, and the metabolite that is a different drug (2026-09-22) · lines 455–466
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mass-spectrometric assay of cyclooxygenase-1 acetylation in platelets from volunteers given an NSAID followed by aspirin · source_derived_draft · unverified_draft
### asa-which-nsaids-interact Although ibuprofen, naproxen and celecoxib all had the potential to compete with aspirin for access to the substrate binding channel of cyclooxygenase-1 in vitro, measuring aspirin target engagement directly by mass spectrometry after a single therapeutic dose of each followed by 325 milligrams of aspirin revealed a potent drug-drug interaction between ibuprofen and aspirin and between naproxen and aspirin but not between celecoxib and aspirin. Condition category: biomarker_context nutrient_topic: Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. plain_language: Ibuprofen and naproxen block aspirin in people; celecoxib does not. organism: Human tissue_or_cell_type: Platelets experimental_model: Mass-spectrometric assay of cyclooxygenase-1 acetylation in platelets from volunteers given an NSAID followed by aspirin limitations: Measures target engagement directly rather than inferring it from platelet function, and separates the drugs. A single dose of each, in volunteers rather than patients. exposure: A single therapeutic dose of ibuprofen, naproxen or celecoxib followed by 325 milligrams of aspirin evidence_span: {"source_cache": "artifacts/aspirin-research/25385584.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b2de8f18887f336c8c735f7ffbd1b72b92e5da43aa6388c229590dea120439f2", "start_char": 0, "end_char": 1242, "text_sha256": "b2de8f18887f336c8c735f7ffbd1b72b92e5da43aa6388c229590dea120439f2"} [asa-p25385584] Differential impairment of aspirin-dependent platelet cyclooxygenase acetylation by nonsteroidal antiinflammatory drugs. (2014). https://pubmed.ncbi.nlm.nih.gov/25385584/ DOI: 10.1073/pnas.1406997111
Complete structured claim and evidence

The events it takes part in

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Situations it appears in

Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.

In the sources

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Open hypotheses

Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.

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

Celecoxib