Ibuprofen

evidence_span

{"source_cache": "artifacts/ibuprofen-research/3303291.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8609926e51d2ad349198eb5f3ad78b6b552e8f4d4fc74d07bb3a58795a86e7a7", "start_char": 0, "end_char": 1757, "text_sha256": "8609926e51d2ad349198eb5f3ad78b6b552e8f4d4fc74d07bb3a58795a86e7a7"}

experimental_model

Review of gastroduodenal defence with isolated mucosal preparations

exposure

Acetylsalicylic acid, fenclofenac, ibuprofen and indomethacin on bicarbonate transport and glycoprotein synthesis

limitations

A review of mechanisms rather than an outcome study. The claim that E-series prostaglandins reverse the effect is what ties it to cyclooxygenase.

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 and animal

plain_language

The stomach’s own defences are built by prostaglandins, so blocking them removes the coat rather than adding an acid.

primary_references

[ibu-p3303291] Gastroduodenal mucosal defence mechanisms and the action of non-steroidal anti-inflammatory agents. (1987). https://pubmed.ncbi.nlm.nih.gov/3303291/ DOI: 10.3109/00365528709090947

tissue_or_cell_type

Gastric and duodenal mucosa

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 500–511

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Review of gastroduodenal defence with isolated mucosal preparations · source_derived_draft · unverified_draft

### ibu-bicarbonate-and-mucus A range of non-steroidal anti-inflammatory agents including acetylsalicylic acid, fenclofenac, ibuprofen and indomethacin inhibit gastric bicarbonate transport in isolated mucosal preparations, effects which can be antagonised by exogenous prostaglandins of the E series, and while the secreted mucus gel overlying the epithelial surface is not affected in the short term a number of these agents inhibit glycoprotein biosynthesis by the epithelial cells, so that loss of this protective coat could be anticipated during chronic exposure as erosion by luminal shear and proteolysis would not be compensated by continued secretion. 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 stomach’s own defences are built by prostaglandins, so blocking them removes the coat rather than adding an acid. organism: Human and animal tissue_or_cell_type: Gastric and duodenal mucosa experimental_model: Review of gastroduodenal defence with isolated mucosal preparations limitations: A review of mechanisms rather than an outcome study. The claim that E-series prostaglandins reverse the effect is what ties it to cyclooxygenase. exposure: Acetylsalicylic acid, fenclofenac, ibuprofen and indomethacin on bicarbonate transport and glycoprotein synthesis evidence_span: {"source_cache": "artifacts/ibuprofen-research/3303291.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8609926e51d2ad349198eb5f3ad78b6b552e8f4d4fc74d07bb3a58795a86e7a7", "start_char": 0, "end_char": 1757, "text_sha256": "8609926e51d2ad349198eb5f3ad78b6b552e8f4d4fc74d07bb3a58795a86e7a7"} [ibu-p3303291] Gastroduodenal mucosal defence mechanisms and the action of non-steroidal anti-inflammatory agents. (1987). https://pubmed.ncbi.nlm.nih.gov/3303291/ DOI: 10.3109/00365528709090947

evidence_span

{"source_cache": "artifacts/ibuprofen-research/9060042.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2c89a26f3812060e97e7bb481126a90840282d64348fc8d4ae9d1dcc7f0a4543", "start_char": 0, "end_char": 1394, "text_sha256": "2c89a26f3812060e97e7bb481126a90840282d64348fc8d4ae9d1dcc7f0a4543"}

experimental_model

Rat cerebellar membrane preparations assayed by time-dependent loss of anandamide potency and by direct amidase assay

exposure

Ibuprofen compared against acetylsalicylic acid, sulindac, acetaminophen, ketoprofen and naproxen

limitations

The comparator set is what distinguishes this from a class effect: five other drugs failed. The concentration required is high, and the authors relate it to peak plasma levels rather than measuring them.

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

Rat

plain_language

Ibuprofen, and not the other painkillers tested, slows the destruction of the body’s own cannabis-like signal.

primary_references

[ibu-p9060042] Ibuprofen inhibits the metabolism of the endogenous cannabimimetic agent anandamide. (1997). https://pubmed.ncbi.nlm.nih.gov/9060042/ DOI: 10.1111/j.1600-0773.1997.tb00291.x

tissue_or_cell_type

Cerebellar membranes

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 448–459

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat cerebellar membrane preparations assayed by time-dependent loss of anandamide potency and by direct amidase assay · source_derived_draft · unverified_draft

### ibu-blocks-anandamide-breakdown The time-dependent reduction in potency of anandamide toward inhibition of cannabinoid agonist binding in rat cerebellar membranes was blocked by ibuprofen but not by acetylsalicylic acid, sulindac, acetaminophen or to any significant extent by ketoprofen and naproxen, a direct assay of anandamide amidase gave a half-maximal inhibitory concentration for ibuprofen of approximately 400 micromolar, and that potency was of the same order as required for inhibition of cyclooxygenase-2 in cell-free systems and as the peak plasma concentrations following a two times 200 milligram dose regimen, so following therapeutic doses the metabolism of anandamide may be affected. 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: Ibuprofen, and not the other painkillers tested, slows the destruction of the body’s own cannabis-like signal. organism: Rat tissue_or_cell_type: Cerebellar membranes experimental_model: Rat cerebellar membrane preparations assayed by time-dependent loss of anandamide potency and by direct amidase assay limitations: The comparator set is what distinguishes this from a class effect: five other drugs failed. The concentration required is high, and the authors relate it to peak plasma levels rather than measuring them. exposure: Ibuprofen compared against acetylsalicylic acid, sulindac, acetaminophen, ketoprofen and naproxen evidence_span: {"source_cache": "artifacts/ibuprofen-research/9060042.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2c89a26f3812060e97e7bb481126a90840282d64348fc8d4ae9d1dcc7f0a4543", "start_char": 0, "end_char": 1394, "text_sha256": "2c89a26f3812060e97e7bb481126a90840282d64348fc8d4ae9d1dcc7f0a4543"} [ibu-p9060042] Ibuprofen inhibits the metabolism of the endogenous cannabimimetic agent anandamide. (1997). https://pubmed.ncbi.nlm.nih.gov/9060042/ DOI: 10.1111/j.1600-0773.1997.tb00291.x

evidence_span

{"source_cache": "artifacts/ibuprofen-research/10722687.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8e9ebedd8a4d791246c951376fa2f6f07a5ca8af828bafd15836bec26c090348", "start_char": 0, "end_char": 2063, "text_sha256": "8e9ebedd8a4d791246c951376fa2f6f07a5ca8af828bafd15836bec26c090348"}

experimental_model

Product analysis and kinetics for solubilised, membrane-associated and active-site-mutant ovine cyclooxygenase-1

exposure

Arachidonate product profiling with ibuprofen as a competitive inhibitor

limitations

The identical inhibitory concentration across three different products is the informative result. The concentrations are high and the enzyme is ovine.

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

Sheep enzyme

plain_language

The drug blocks the door rather than any one position inside, which is why it stops every product equally.

primary_references

[ibu-p10722687] Different catalytically competent arrangements of arachidonic acid within the cyclooxygenase active site of prostaglandin endoperoxide H synthase-1 lead to the formation of different oxygenated products. (2000). https://pubmed.ncbi.nlm.nih.gov/10722687/ DOI: 10.1074/jbc.275.12.8501

tissue_or_cell_type

Cyclooxygenase-1

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 305–316

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Product analysis and kinetics for solubilised, membrane-associated and active-site-mutant ovine cyclooxygenase-1 · source_derived_draft · unverified_draft

### ibu-blocks-entry-not-orientation Native ovine cyclooxygenase-1 produced primarily prostaglandin G2 along with 11R-, 15S- and 15R-hydroxyeicosatetraenoic acids with different Km values for each product, establishing that arachidonate can assume at least three catalytically productive arrangements within the site, and half-maximal inhibitory concentrations for the competitive inhibitor ibuprofen were the same for every product of a given enzyme form, 175 micromolar for the native enzyme and 15 micromolar for the V349L mutant, most simply rationalised by a model in which arachidonate forms its various arrangements only after entering the cyclooxygenase active site. 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 drug blocks the door rather than any one position inside, which is why it stops every product equally. organism: Sheep enzyme tissue_or_cell_type: Cyclooxygenase-1 experimental_model: Product analysis and kinetics for solubilised, membrane-associated and active-site-mutant ovine cyclooxygenase-1 limitations: The identical inhibitory concentration across three different products is the informative result. The concentrations are high and the enzyme is ovine. exposure: Arachidonate product profiling with ibuprofen as a competitive inhibitor evidence_span: {"source_cache": "artifacts/ibuprofen-research/10722687.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8e9ebedd8a4d791246c951376fa2f6f07a5ca8af828bafd15836bec26c090348", "start_char": 0, "end_char": 2063, "text_sha256": "8e9ebedd8a4d791246c951376fa2f6f07a5ca8af828bafd15836bec26c090348"} [ibu-p10722687] Different catalytically competent arrangements of arachidonic acid within the cyclooxygenase active site of prostaglandin endoperoxide H synthase-1 lead to the formation of different oxygenated products. (2000). https://pubmed.ncbi.nlm.nih.gov/10722687/ DOI: 10.1074/jbc.275.12.8501

availability_state

biomarker_context Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/ibuprofen-research/497895.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9d0874e6d05ee46097aeebdc1f0b9024541aa1305a648d6b783c329108a0bf0f", "start_char": 0, "end_char": 1229, "text_sha256": "9d0874e6d05ee46097aeebdc1f0b9024541aa1305a648d6b783c329108a0bf0f"}

experimental_model

Circular strips of lamb ductus arteriosus from 90 to 144 days gestation studied in vitro at low and high oxygen tension

exposure

Ibuprofen applied at low oxygen tension across gestational ages, with potassium and oxygen contractions

limitations

An isolated tissue study across a developmental range, which is what reveals that the prostaglandin brake matures before term. In vitro strips rather than a treated infant.

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

Lamb

plain_language

Blocking prostaglandins closes the vessel that has to close at birth, which is why the drug is used for that on purpose.

primary_references

[ibu-p497895] Age-dependent changes in the response of the lamb ductus arteriosus to oxygen and ibuprofen. (1979). https://pubmed.ncbi.nlm.nih.gov/497895/ DOI: 10.1139/y79-126

tissue_or_cell_type

Ductus arteriosus

trigger_kind

biomarker_context Imported condition classification; unverified.

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 513–524

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Circular strips of lamb ductus arteriosus from 90 to 144 days gestation studied in vitro at low and high oxygen tension · source_derived_draft · unverified_draft

### ibu-closes-the-ductus At low oxygen tension ibuprofen produced a dose-dependent contraction of isolated lamb ductus arteriosus strips at all gestational ages and enhanced the potassium-induced contraction of the immature ductus, both effects being relatively greater in the 103 to 107 day group where ibuprofen also potentiated the oxygen-induced contraction, confirming that a prostaglandin is involved in ductus patency and indicating that the prostaglandin-relaxing mechanism becomes functional at an early stage of gestation and reaches maximal activity before term. Condition category: biomarker_context 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: Blocking prostaglandins closes the vessel that has to close at birth, which is why the drug is used for that on purpose. organism: Lamb tissue_or_cell_type: Ductus arteriosus experimental_model: Circular strips of lamb ductus arteriosus from 90 to 144 days gestation studied in vitro at low and high oxygen tension limitations: An isolated tissue study across a developmental range, which is what reveals that the prostaglandin brake matures before term. In vitro strips rather than a treated infant. exposure: Ibuprofen applied at low oxygen tension across gestational ages, with potassium and oxygen contractions evidence_span: {"source_cache": "artifacts/ibuprofen-research/497895.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9d0874e6d05ee46097aeebdc1f0b9024541aa1305a648d6b783c329108a0bf0f", "start_char": 0, "end_char": 1229, "text_sha256": "9d0874e6d05ee46097aeebdc1f0b9024541aa1305a648d6b783c329108a0bf0f"} [ibu-p497895] Age-dependent changes in the response of the lamb ductus arteriosus to oxygen and ibuprofen. (1979). https://pubmed.ncbi.nlm.nih.gov/497895/ DOI: 10.1139/y79-126

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

availability_state

biomarker_context Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/ibuprofen-research/696734.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ca9f025b68310a2b49def4e15ad6f25fb14fc900284de8d68cd80aa6a7f47139", "start_char": 0, "end_char": 949, "text_sha256": "ca9f025b68310a2b49def4e15ad6f25fb14fc900284de8d68cd80aa6a7f47139"}

experimental_model

Clinical case report of an adverse reaction in an aspirin-sensitive asthmatic

exposure

A single 400 milligram ibuprofen tablet in a 53-year-old aspirin-sensitive asthmatic with nasal polyps

limitations

A single case, but it identifies the basis of the reaction as shared pharmacology rather than immunology, which is what determines whether a substitute drug is safe.

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 reaction is not an allergy to the drug but to what the drug does, so any drug that does the same thing will do it too.

primary_references

[ibu-p696734] Cross-reactivity between aspirin and ibuprofen in an asthmatic--a case report. (1978). https://pubmed.ncbi.nlm.nih.gov/696734/ DOI: 10.1093/ajhp/35.10.1245

tissue_or_cell_type

Airway and skin

trigger_kind

biomarker_context Imported condition classification; unverified.

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 539–550

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Clinical case report of an adverse reaction in an aspirin-sensitive asthmatic · source_derived_draft · unverified_draft

### ibu-cross-reacts-pharmacologically A 53-year-old aspirin-sensitive asthmatic man with nasal polyps developed an urticarial rash, laboured breathing, laryngeal oedema and chest tightness after a 400 milligram ibuprofen tablet, requiring isoproterenol, subcutaneous epinephrine, intramuscular diphenhydramine and intravenous hydrocortisone; the reaction was not mediated immunologically but resulted from the prostaglandin synthetase inhibitor activity shared by aspirin, ibuprofen and other analgesics, so selection of an analgesic for an aspirin-sensitive patient should be based on that activity. Condition category: biomarker_context 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 reaction is not an allergy to the drug but to what the drug does, so any drug that does the same thing will do it too. organism: Human tissue_or_cell_type: Airway and skin experimental_model: Clinical case report of an adverse reaction in an aspirin-sensitive asthmatic limitations: A single case, but it identifies the basis of the reaction as shared pharmacology rather than immunology, which is what determines whether a substitute drug is safe. exposure: A single 400 milligram ibuprofen tablet in a 53-year-old aspirin-sensitive asthmatic with nasal polyps evidence_span: {"source_cache": "artifacts/ibuprofen-research/696734.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ca9f025b68310a2b49def4e15ad6f25fb14fc900284de8d68cd80aa6a7f47139", "start_char": 0, "end_char": 949, "text_sha256": "ca9f025b68310a2b49def4e15ad6f25fb14fc900284de8d68cd80aa6a7f47139"} [ibu-p696734] Cross-reactivity between aspirin and ibuprofen in an asthmatic--a case report. (1978). https://pubmed.ncbi.nlm.nih.gov/696734/ DOI: 10.1093/ajhp/35.10.1245

evidence_span

{"source_cache": "artifacts/ibuprofen-research/3088675.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ee49ae775f6c268fd63afc816cda206f0bdab5efe9ce86b4f97fd8ee6bda3a1a", "start_char": 0, "end_char": 1400, "text_sha256": "ee49ae775f6c268fd63afc816cda206f0bdab5efe9ce86b4f97fd8ee6bda3a1a"}

experimental_model

Kinetics of recovery of platelet thromboxane production after single doses, with platelets resuspended in drug-free plasma

exposure

Indomethacin and ibuprofen compared, with isolated platelets and platelet microsomes

limitations

The resuspension experiment is what separates a reversible inhibitor from a slowly reversible one. It uses indomethacin as the contrast and reports ibuprofen as the reference reversible drug.

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

Wash the drug away and the platelet enzyme is working again at once, which is the opposite of what aspirin does.

primary_references

[ibu-p3088675] Time-dependent inhibition of platelet cyclooxygenase by indomethacin is slowly reversible. (1986). https://pubmed.ncbi.nlm.nih.gov/3088675/ DOI: 10.1016/0090-6980(86)90170-x

tissue_or_cell_type

Platelets

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 279–290

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Kinetics of recovery of platelet thromboxane production after single doses, with platelets resuspended in drug-free plasma · source_derived_draft · unverified_draft

### ibu-ibuprofen-washes-straight-out When platelets were isolated and resuspended in homologous drug-free plasma, slow recovery of thromboxane production was seen after indomethacin with 50% of control activity regained in 100 minutes, whereas ibuprofen-treated platelets, exposed to a competitive inhibitor of cyclooxygenase, recovered nearly completely immediately on being resuspended in drug-free plasma. 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: Wash the drug away and the platelet enzyme is working again at once, which is the opposite of what aspirin does. organism: Human tissue_or_cell_type: Platelets experimental_model: Kinetics of recovery of platelet thromboxane production after single doses, with platelets resuspended in drug-free plasma limitations: The resuspension experiment is what separates a reversible inhibitor from a slowly reversible one. It uses indomethacin as the contrast and reports ibuprofen as the reference reversible drug. exposure: Indomethacin and ibuprofen compared, with isolated platelets and platelet microsomes evidence_span: {"source_cache": "artifacts/ibuprofen-research/3088675.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ee49ae775f6c268fd63afc816cda206f0bdab5efe9ce86b4f97fd8ee6bda3a1a", "start_char": 0, "end_char": 1400, "text_sha256": "ee49ae775f6c268fd63afc816cda206f0bdab5efe9ce86b4f97fd8ee6bda3a1a"} [ibu-p3088675] Time-dependent inhibition of platelet cyclooxygenase by indomethacin is slowly reversible. (1986). https://pubmed.ncbi.nlm.nih.gov/3088675/ DOI: 10.1016/0090-6980(86)90170-x

evidence_span

{"source_cache": "artifacts/ibuprofen-research/11755007.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "85bd65aa6bff20262f11cfa0cd26a25a327aff114898605cea3a0cc05459192b", "start_char": 0, "end_char": 1213, "text_sha256": "85bd65aa6bff20262f11cfa0cd26a25a327aff114898605cea3a0cc05459192b"}

experimental_model

Six month and three month ibuprofen treatment of APPsw Tg2576 transgenic mice with behavioural and biochemical endpoints

exposure

Ibuprofen begun at different ages, with soluble and insoluble amyloid-beta and open field behaviour measured

limitations

An in vivo test with a behavioural endpoint and two treatment durations. A transgenic model of amyloid deposition, which is not Alzheimer’s disease.

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

Mouse

plain_language

In mice bred to deposit amyloid, the drug lowered the peptide and changed their behaviour back toward normal.

primary_references

[ibu-p11755007] Ibuprofen effects on Alzheimer pathology and open field activity in APPsw transgenic mice. (2001). https://pubmed.ncbi.nlm.nih.gov/11755007/ DOI: 10.1016/s0197-4580(01)00299-8

tissue_or_cell_type

Brain

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 435–446

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Six month and three month ibuprofen treatment of APPsw Tg2576 transgenic mice with behavioural and biochemical endpoints · source_derived_draft · unverified_draft

### ibu-in-vivo-and-behavioural In APPsw transgenic mice, ibuprofen effects were not mediated by alterations in amyloid precursor protein expression or oxidative damage, six months of treatment in transgene-positive females decreased open field behaviour to values similar to transgene-negative mice and reduced caspase activation per plaque, and a shorter three month trial begun at 14 months produced a significant treatment effect on amyloid-beta levels with reductions of both soluble amyloid-beta and amyloid-beta 42 most marked in entorhinal cortex, the magnitude of the effect on soluble amyloid-beta not depending on treatment duration. 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: In mice bred to deposit amyloid, the drug lowered the peptide and changed their behaviour back toward normal. organism: Mouse tissue_or_cell_type: Brain experimental_model: Six month and three month ibuprofen treatment of APPsw Tg2576 transgenic mice with behavioural and biochemical endpoints limitations: An in vivo test with a behavioural endpoint and two treatment durations. A transgenic model of amyloid deposition, which is not Alzheimer’s disease. exposure: Ibuprofen begun at different ages, with soluble and insoluble amyloid-beta and open field behaviour measured evidence_span: {"source_cache": "artifacts/ibuprofen-research/11755007.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "85bd65aa6bff20262f11cfa0cd26a25a327aff114898605cea3a0cc05459192b", "start_char": 0, "end_char": 1213, "text_sha256": "85bd65aa6bff20262f11cfa0cd26a25a327aff114898605cea3a0cc05459192b"} [ibu-p11755007] Ibuprofen effects on Alzheimer pathology and open field activity in APPsw transgenic mice. (2001). https://pubmed.ncbi.nlm.nih.gov/11755007/ DOI: 10.1016/s0197-4580(01)00299-8

availability_state

biomarker_context Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/ibuprofen-research/6361565.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "98ef6b906f4841d1488baebb3c03c7452c98c5266ae012dd2a0eb579661dc15b", "start_char": 0, "end_char": 1550, "text_sha256": "98ef6b906f4841d1488baebb3c03c7452c98c5266ae012dd2a0eb579661dc15b"}

experimental_model

Randomised one week treatment in 20 women with chronic glomerular disease and 5 healthy women

exposure

Ibuprofen for one week, against sulindac in a parallel group

limitations

The healthy comparison group is what makes this decisive: the same suppression of renal prostacyclin produced no functional change in them. Twenty patients, one week.

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 same drop in kidney prostaglandins does nothing to a healthy kidney and takes a third of the function from a diseased one.

primary_references

[ibu-p6361565] Effects of sulindac and ibuprofen in patients with chronic glomerular disease. Evidence for the dependence of renal function on prostacyclin. (1984). https://pubmed.ncbi.nlm.nih.gov/6361565/ DOI: 10.1056/nejm198402023100502

tissue_or_cell_type

Kidney

trigger_kind

biomarker_context Imported condition classification; unverified.

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 461–472

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomised one week treatment in 20 women with chronic glomerular disease and 5 healthy women · source_derived_draft · unverified_draft

### ibu-kidney-depends-on-what-is-blocked In 10 patients with chronic glomerular disease randomly assigned to one week of ibuprofen, urinary 6-keto-prostaglandin F1 alpha and prostaglandin E2 excretion fell by 80%, serum creatinine rose by 40% and creatinine and para-aminohippurate clearances fell by 28% and 35% respectively, with the reduction in both clearances inversely related to the basal urinary excretion of 6-keto-prostaglandin F1 alpha but not of prostaglandin E2, while no functional changes were detected in five healthy women despite a similar suppression of renal prostacyclin synthesis, and one week of sulindac did not affect renal prostacyclin synthesis or renal function despite marked inhibition of extrarenal cyclooxygenase. Condition category: biomarker_context 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 same drop in kidney prostaglandins does nothing to a healthy kidney and takes a third of the function from a diseased one. organism: Human tissue_or_cell_type: Kidney experimental_model: Randomised one week treatment in 20 women with chronic glomerular disease and 5 healthy women limitations: The healthy comparison group is what makes this decisive: the same suppression of renal prostacyclin produced no functional change in them. Twenty patients, one week. exposure: Ibuprofen for one week, against sulindac in a parallel group evidence_span: {"source_cache": "artifacts/ibuprofen-research/6361565.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "98ef6b906f4841d1488baebb3c03c7452c98c5266ae012dd2a0eb579661dc15b", "start_char": 0, "end_char": 1550, "text_sha256": "98ef6b906f4841d1488baebb3c03c7452c98c5266ae012dd2a0eb579661dc15b"} [ibu-p6361565] Effects of sulindac and ibuprofen in patients with chronic glomerular disease. Evidence for the dependence of renal function on prostacyclin. (1984). https://pubmed.ncbi.nlm.nih.gov/6361565/ DOI: 10.1056/nejm198402023100502

evidence_span

{"source_cache": "artifacts/ibuprofen-research/11700559.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "eb9be6e821c04b48c65a999ac5852996bcb4f0249b8bd78b4454a256435e8267", "start_char": 0, "end_char": 1411, "text_sha256": "eb9be6e821c04b48c65a999ac5852996bcb4f0249b8bd78b4454a256435e8267"}

experimental_model

Cultured cells of several types and mutant amyloid precursor protein transgenic mice

exposure

Ibuprofen, indomethacin and sulindac sulphide, with short-term ibuprofen administration in vivo

limitations

The cyclooxygenase-independence is inferred from the fact that the effect is not shared by all inhibitors of the enzyme, rather than shown by a genetic control. Short-term dosing in a transgenic model.

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 cells and mouse

plain_language

The drug shifts where an enzyme cuts rather than stopping it, and the sticky fragment is replaced by a shorter harmless one.

primary_references

[ibu-p11700559] A subset of NSAIDs lower amyloidogenic Abeta42 independently of cyclooxygenase activity. (2001). https://pubmed.ncbi.nlm.nih.gov/11700559/ DOI: 10.1038/35102591

tissue_or_cell_type

Cultured cells and brain

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 383–394

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cultured cells of several types and mutant amyloid precursor protein transgenic mice · source_derived_draft · unverified_draft

### ibu-lowers-abeta42-not-via-cox Ibuprofen, indomethacin and sulindac sulphide preferentially decreased the highly amyloidogenic amyloid-beta 42 peptide produced by a variety of cultured cells by as much as 80%, an effect not seen with all non-steroidal anti-inflammatory drugs and seemingly not mediated by inhibition of cyclooxygenase activity, and short-term administration of ibuprofen to mice producing mutant amyloid precursor protein lowered brain amyloid-beta 42; in cultured cells the decrease was accompanied by an increase in the amyloid-beta 1-38 isoform, indicating that these drugs subtly alter gamma-secretase activity without significantly perturbing other processing pathways or Notch cleavage. 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 drug shifts where an enzyme cuts rather than stopping it, and the sticky fragment is replaced by a shorter harmless one. organism: Human cells and mouse tissue_or_cell_type: Cultured cells and brain experimental_model: Cultured cells of several types and mutant amyloid precursor protein transgenic mice limitations: The cyclooxygenase-independence is inferred from the fact that the effect is not shared by all inhibitors of the enzyme, rather than shown by a genetic control. Short-term dosing in a transgenic model. exposure: Ibuprofen, indomethacin and sulindac sulphide, with short-term ibuprofen administration in vivo evidence_span: {"source_cache": "artifacts/ibuprofen-research/11700559.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "eb9be6e821c04b48c65a999ac5852996bcb4f0249b8bd78b4454a256435e8267", "start_char": 0, "end_char": 1411, "text_sha256": "eb9be6e821c04b48c65a999ac5852996bcb4f0249b8bd78b4454a256435e8267"} [ibu-p11700559] A subset of NSAIDs lower amyloidogenic Abeta42 independently of cyclooxygenase activity. (2001). https://pubmed.ncbi.nlm.nih.gov/11700559/ DOI: 10.1038/35102591

evidence_span

{"source_cache": "artifacts/ibuprofen-research/7299691.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "217a7f084ce5301b9b357bed0af13552ba7114c56c9d2692852bd4581450a02d", "start_char": 0, "end_char": 1542, "text_sha256": "217a7f084ce5301b9b357bed0af13552ba7114c56c9d2692852bd4581450a02d"}

experimental_model

Regional vascular resistance measurement in pentobarbital-anaesthetised dogs

exposure

Indomethacin and ibuprofen given intravenously and intra-arterially, including a 50 milligram intravenous bolus

limitations

A direct head-to-head between two drugs of the same class in the same animals, with a negative result for ibuprofen. Anaesthetised dogs.

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

Dog

plain_language

One drug of this class strangles the gut circulation and the other does not, and it is not a prostaglandin effect.

primary_references

[ibu-p7299691] Differential effects of ibuprofen and indomethacin in the regional circulation of the dog. (1981). https://pubmed.ncbi.nlm.nih.gov/7299691/ DOI: 10.1016/s0022-3565(25)32861-2

tissue_or_cell_type

Mesenteric and renal circulations

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 487–498

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Regional vascular resistance measurement in pentobarbital-anaesthetised dogs · source_derived_draft · unverified_draft

### ibu-not-a-class-effect Indomethacin produced severe acute mesenteric vasoconstriction by intravenous infusion and by intra-arterial injection with rapid tachyphylaxis, whereas ibuprofen did not alter mesenteric blood flow even when a large 50 milligram bolus was rapidly injected, and the indomethacin response was not modified when prostaglandin synthesis was inhibited nor significantly mediated by alpha adrenergic agents or serotonin, while both drugs raised aortic pressure and reduced renal blood flow by small but significant amounts. 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: One drug of this class strangles the gut circulation and the other does not, and it is not a prostaglandin effect. organism: Dog tissue_or_cell_type: Mesenteric and renal circulations experimental_model: Regional vascular resistance measurement in pentobarbital-anaesthetised dogs limitations: A direct head-to-head between two drugs of the same class in the same animals, with a negative result for ibuprofen. Anaesthetised dogs. exposure: Indomethacin and ibuprofen given intravenously and intra-arterially, including a 50 milligram intravenous bolus evidence_span: {"source_cache": "artifacts/ibuprofen-research/7299691.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "217a7f084ce5301b9b357bed0af13552ba7114c56c9d2692852bd4581450a02d", "start_char": 0, "end_char": 1542, "text_sha256": "217a7f084ce5301b9b357bed0af13552ba7114c56c9d2692852bd4581450a02d"} [ibu-p7299691] Differential effects of ibuprofen and indomethacin in the regional circulation of the dog. (1981). https://pubmed.ncbi.nlm.nih.gov/7299691/ DOI: 10.1016/s0022-3565(25)32861-2

availability_state

biomarker_context Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/ibuprofen-research/6420135.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "efb8422d9d57d38da8a5cea4e37f5c6e043c527d2a59f8fee8cfe5ffcf29daf7", "start_char": 0, "end_char": 957, "text_sha256": "efb8422d9d57d38da8a5cea4e37f5c6e043c527d2a59f8fee8cfe5ffcf29daf7"}

experimental_model

Case report of acute reversible renal failure with review of non-steroidal anti-inflammatory drug nephrotoxicity

exposure

An increase in ibuprofen dose in a susceptible patient

limitations

A single case with a narrative review. The predisposing factors listed are the authors’ synthesis rather than a measured risk model.

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 kidney injury usually reverses when the drug stops, and the people at risk are the ones already leaning on prostaglandins.

primary_references

[ibu-p6420135] Reversible renal failure associated with ibuprofen: case report and review of the literature. (1984). https://pubmed.ncbi.nlm.nih.gov/6420135/ DOI: 10.1177/106002808401800103

tissue_or_cell_type

Kidney

trigger_kind

biomarker_context Imported condition classification; unverified.

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 552–563

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Case report of acute reversible renal failure with review of non-steroidal anti-inflammatory drug nephrotoxicity · source_derived_draft · unverified_draft

### ibu-renal-failure-is-reversible A probable case of acute reversible renal failure with hyperkalaemia followed an increase in ibuprofen dose, and across reviewed cases the ability of these drugs to inhibit prostaglandin synthesis may explain the various renal consequences, with possible predisposing factors including the amount of drug consumed, compromised renal blood flow, underlying renal insufficiency, nephrotoxic drug combinations and high urinary prostaglandin excretion; renal failure with these drugs is generally acute and reversible although analgesic nephropathy with papillary necrosis and chronic failure are reported. Condition category: biomarker_context 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 kidney injury usually reverses when the drug stops, and the people at risk are the ones already leaning on prostaglandins. organism: Human tissue_or_cell_type: Kidney experimental_model: Case report of acute reversible renal failure with review of non-steroidal anti-inflammatory drug nephrotoxicity limitations: A single case with a narrative review. The predisposing factors listed are the authors’ synthesis rather than a measured risk model. exposure: An increase in ibuprofen dose in a susceptible patient evidence_span: {"source_cache": "artifacts/ibuprofen-research/6420135.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "efb8422d9d57d38da8a5cea4e37f5c6e043c527d2a59f8fee8cfe5ffcf29daf7", "start_char": 0, "end_char": 957, "text_sha256": "efb8422d9d57d38da8a5cea4e37f5c6e043c527d2a59f8fee8cfe5ffcf29daf7"} [ibu-p6420135] Reversible renal failure associated with ibuprofen: case report and review of the literature. (1984). https://pubmed.ncbi.nlm.nih.gov/6420135/ DOI: 10.1177/106002808401800103

evidence_span

{"source_cache": "artifacts/ibuprofen-research/8831731.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d3161aac692f44c874cafb498e9606f0382b380662ccb58cd1683139f1c1df99", "start_char": 0, "end_char": 1993, "text_sha256": "d3161aac692f44c874cafb498e9606f0382b380662ccb58cd1683139f1c1df99"}

experimental_model

Chinese hamster ovary cell lines stably expressing each human cyclooxygenase isoform, with cell-free comparison

exposure

Ibuprofen, indomethacin, NS-398 and DuP-697 across intact cells and microsomal preparations

limitations

Shows that the selectivity numbers depend on the assay, which bears on every potency ratio quoted for this drug class. A heterologous expression system.

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 enzyme in hamster cells

plain_language

Against both enzymes it is a reversible blocker, and the numbers you get depend on which assay you use.

primary_references

[ibu-p8831731] Mechanism of selective inhibition of human prostaglandin G/H synthase-1 and -2 in intact cells. (1996). https://pubmed.ncbi.nlm.nih.gov/8831731/ DOI: 10.1016/0006-2952(96)00462-5

tissue_or_cell_type

Intact cells and cell-free preparations

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 292–303

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Chinese hamster ovary cell lines stably expressing each human cyclooxygenase isoform, with cell-free comparison · source_derived_draft · unverified_draft

### ibu-reversible-against-both-isoforms Reversible inhibition of both cellular cyclooxygenase-1 and cyclooxygenase-2 was observed with the nonselective drugs ibuprofen and indomethacin, whereas the selective inhibitor DuP-697 was reversible against cyclooxygenase-1 but irreversible against cyclooxygenase-2, and indomethacin displayed time-dependent inhibition of both cellular isoforms; the selectivities and potencies of inhibitors determined using intact cells are affected by substrate concentration and differ from those determined in cell-free microsomal or purified enzyme preparations. 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: Against both enzymes it is a reversible blocker, and the numbers you get depend on which assay you use. organism: Human enzyme in hamster cells tissue_or_cell_type: Intact cells and cell-free preparations experimental_model: Chinese hamster ovary cell lines stably expressing each human cyclooxygenase isoform, with cell-free comparison limitations: Shows that the selectivity numbers depend on the assay, which bears on every potency ratio quoted for this drug class. A heterologous expression system. exposure: Ibuprofen, indomethacin, NS-398 and DuP-697 across intact cells and microsomal preparations evidence_span: {"source_cache": "artifacts/ibuprofen-research/8831731.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d3161aac692f44c874cafb498e9606f0382b380662ccb58cd1683139f1c1df99", "start_char": 0, "end_char": 1993, "text_sha256": "d3161aac692f44c874cafb498e9606f0382b380662ccb58cd1683139f1c1df99"} [ibu-p8831731] Mechanism of selective inhibition of human prostaglandin G/H synthase-1 and -2 in intact cells. (1996). https://pubmed.ncbi.nlm.nih.gov/8831731/ DOI: 10.1016/0006-2952(96)00462-5

availability_state

biomarker_context Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/aspirin-research/6411052.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a685344a88574182dbad6f8d70308dce88384a63ed0c561ccaec4d522000b132", "start_char": 0, "end_char": 1551, "text_sha256": "a685344a88574182dbad6f8d70308dce88384a63ed0c561ccaec4d522000b132"}

experimental_model

Platelet aggregation and cyclooxygenase activity in subjects given ibuprofen before aspirin, in vitro and in vivo

exposure

Ibuprofen ingestion followed by 650 milligrams of aspirin, with recovery followed to 26 hours

limitations

The observation is clean and has been confirmed since. The authors’ inference from it, that aspirin must act on the heme group rather than by acetylating the protein, is contradicted by the mutant and crystallographic records in this collection and is not adopted here.

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

Take ibuprofen first and aspirin never gets its chance; the protection wears off in a day like ibuprofen, not like aspirin.

primary_references

[asa-p6411052] Ibuprofen protects platelet cyclooxygenase from irreversible inhibition by aspirin. (1983). https://pubmed.ncbi.nlm.nih.gov/6411052/ DOI: 10.1161/01.atv.3.4.383

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 442–453

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Platelet aggregation and cyclooxygenase activity in subjects given ibuprofen before aspirin, in vitro and in vivo · source_derived_draft · unverified_draft

### asa-ibuprofen-blocks-aspirin Platelet function and prostaglandin synthesis recovered completely 26 hours after ingestion of ibuprofen but remained compromised 26 hours after taking aspirin, and when 650 milligrams of aspirin was administered after ibuprofen, platelet function and cyclooxygenase activity recovered as completely at 26 hours as in platelets exposed to ibuprofen alone, so prior exposure to ibuprofen in vivo completely protected cyclooxygenase from the irreversible effects of 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: Take ibuprofen first and aspirin never gets its chance; the protection wears off in a day like ibuprofen, not like aspirin. organism: Human tissue_or_cell_type: Platelets experimental_model: Platelet aggregation and cyclooxygenase activity in subjects given ibuprofen before aspirin, in vitro and in vivo limitations: The observation is clean and has been confirmed since. The authors’ inference from it, that aspirin must act on the heme group rather than by acetylating the protein, is contradicted by the mutant and crystallographic records in this collection and is not adopted here. exposure: Ibuprofen ingestion followed by 650 milligrams of aspirin, with recovery followed to 26 hours evidence_span: {"source_cache": "artifacts/aspirin-research/6411052.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a685344a88574182dbad6f8d70308dce88384a63ed0c561ccaec4d522000b132", "start_char": 0, "end_char": 1551, "text_sha256": "a685344a88574182dbad6f8d70308dce88384a63ed0c561ccaec4d522000b132"} [asa-p6411052] Ibuprofen protects platelet cyclooxygenase from irreversible inhibition by aspirin. (1983). https://pubmed.ncbi.nlm.nih.gov/6411052/ DOI: 10.1161/01.atv.3.4.383

evidence_span

{"source_cache": "artifacts/ibuprofen-research/8907587.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "99f3a26e6399b5f81c18859b9f62eafcd7aa6fc4e483d97a39e8c35c060a9d75", "start_char": 0, "end_char": 1101, "text_sha256": "99f3a26e6399b5f81c18859b9f62eafcd7aa6fc4e483d97a39e8c35c060a9d75"}

experimental_model

Lipopolysaccharide-challenged human whole blood with prostaglandin E2 and thromboxane B2 as isoform indices

exposure

Lipopolysaccharide induction of cyclooxygenase-2 with a single oral indomethacin dose ex vivo

limitations

Establishes the assay the other records rely on. Indomethacin rather than ibuprofen is the drug dosed here.

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 first enzyme is always there and the second one appears when tissue is provoked; most of these drugs hit the first harder.

primary_references

[ibu-p8907587] A human whole blood assay for clinical evaluation of biochemical efficacy of cyclooxygenase inhibitors. (1996). https://pubmed.ncbi.nlm.nih.gov/8907587/ DOI: 10.1007/bf02265118

tissue_or_cell_type

Whole blood and mononuclear cells

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 357–368

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Lipopolysaccharide-challenged human whole blood with prostaglandin E2 and thromboxane B2 as isoform indices · source_derived_draft · unverified_draft

### ibu-most-nsaids-favour-cox1 Incubation of human mononuclear cells with lipopolysaccharide induced a time-dependent increase in cyclooxygenase-2 protein of more than a hundredfold at 24 hours with increased prostaglandin E2 production, while cyclooxygenase-1 protein was present at time zero and not induced, and most non-steroidal anti-inflammatory drugs are more potent at inhibiting cyclooxygenase-1 than cyclooxygenase-2, with five experimental compounds showing greater selectivity for cyclooxygenase-2. 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 first enzyme is always there and the second one appears when tissue is provoked; most of these drugs hit the first harder. organism: Human tissue_or_cell_type: Whole blood and mononuclear cells experimental_model: Lipopolysaccharide-challenged human whole blood with prostaglandin E2 and thromboxane B2 as isoform indices limitations: Establishes the assay the other records rely on. Indomethacin rather than ibuprofen is the drug dosed here. exposure: Lipopolysaccharide induction of cyclooxygenase-2 with a single oral indomethacin dose ex vivo evidence_span: {"source_cache": "artifacts/ibuprofen-research/8907587.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "99f3a26e6399b5f81c18859b9f62eafcd7aa6fc4e483d97a39e8c35c060a9d75", "start_char": 0, "end_char": 1101, "text_sha256": "99f3a26e6399b5f81c18859b9f62eafcd7aa6fc4e483d97a39e8c35c060a9d75"} [ibu-p8907587] A human whole blood assay for clinical evaluation of biochemical efficacy of cyclooxygenase inhibitors. (1996). https://pubmed.ncbi.nlm.nih.gov/8907587/ DOI: 10.1007/bf02265118

evidence_access

Primary abstract

experimental_model

Human transporter voltage-clamp experiments.

limitations

High bath concentrations do not prove clinically meaningful butyrate depletion or justify changing a medicine.

nutrient_topic

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

plain_language

Drugs can block this transporter under experimental conditions.

primary_references

The human tumour suppressor gene SLC5A8 expresses a Na+-monocarboxylate cotransporter. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15090606/ · DOI 10.1113/jphysiol.2004.063859

Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 118–124

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human transporter voltage-clamp experiments. · source_derived_draft · unverified_draft

## butyrate-smct1-drug-block Drugs can block this transporter under experimental conditions. Probenecid or ibuprofen at 1 mM strongly inhibited human SLC5A8 activity in the oocyte assay. Model: Human transporter voltage-clamp experiments. Limitations: High bath concentrations do not prove clinically meaningful butyrate depletion or justify changing a medicine. Evidence access: Primary abstract The human tumour suppressor gene SLC5A8 expresses a Na+-monocarboxylate cotransporter. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15090606/ · DOI 10.1113/jphysiol.2004.063859

evidence_span

{"source_cache": "artifacts/ibuprofen-research/12637581.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e0da78f88f2dfa34808abab5f1d223bdbc0372f5ea26a626b9697e0ad2255a7c", "start_char": 0, "end_char": 1209, "text_sha256": "e0da78f88f2dfa34808abab5f1d223bdbc0372f5ea26a626b9697e0ad2255a7c"}

experimental_model

In vitro gamma-secretase assay on solubilised HeLa membrane fractions with recombinant amyloid precursor protein C100

exposure

Sulindac sulfide applied to isolated gamma-secretase activity

limitations

A cell-free assay that can distinguish direct action on the enzyme from an effect on the cell. It tests sulindac sulfide rather than ibuprofen, which is recorded on the claim.

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 cells

plain_language

Taken out of the cell entirely, the drug still acts on the enzyme itself, and prefers the reaction that makes the harmful fragment.

primary_references

[ibu-p12637581] Sulindac sulfide is a noncompetitive gamma-secretase inhibitor that preferentially reduces Abeta 42 generation. (2003). https://pubmed.ncbi.nlm.nih.gov/12637581/ DOI: 10.1074/jbc.m301619200

tissue_or_cell_type

Solubilised membrane fractions

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 409–420

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · In vitro gamma-secretase assay on solubilised HeLa membrane fractions with recombinant amyloid precursor protein C100 · source_derived_draft · unverified_draft

### ibu-direct-on-gamma-secretase Sulindac sulfide directly acts on gamma-secretase and preferentially inhibits the activity generating amyloid-beta 42 from solubilised membrane fractions in an in vitro assay using recombinant amyloid precursor protein C100 as substrate, also inhibiting generation of amyloid-beta 40 and of the Notch intracellular domain at higher concentrations, and displaying linear noncompetitive inhibition profiles for the amyloid-beta 42 generating activity. 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: Taken out of the cell entirely, the drug still acts on the enzyme itself, and prefers the reaction that makes the harmful fragment. organism: Human cells tissue_or_cell_type: Solubilised membrane fractions experimental_model: In vitro gamma-secretase assay on solubilised HeLa membrane fractions with recombinant amyloid precursor protein C100 limitations: A cell-free assay that can distinguish direct action on the enzyme from an effect on the cell. It tests sulindac sulfide rather than ibuprofen, which is recorded on the claim. exposure: Sulindac sulfide applied to isolated gamma-secretase activity evidence_span: {"source_cache": "artifacts/ibuprofen-research/12637581.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e0da78f88f2dfa34808abab5f1d223bdbc0372f5ea26a626b9697e0ad2255a7c", "start_char": 0, "end_char": 1209, "text_sha256": "e0da78f88f2dfa34808abab5f1d223bdbc0372f5ea26a626b9697e0ad2255a7c"} [ibu-p12637581] Sulindac sulfide is a noncompetitive gamma-secretase inhibitor that preferentially reduces Abeta 42 generation. (2003). https://pubmed.ncbi.nlm.nih.gov/12637581/ DOI: 10.1074/jbc.m301619200

evidence_span

{"source_cache": "artifacts/ibuprofen-research/20089905.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "77e2dbb010dcee44bd66645ec26cb844d7041ea4930f6373ae5dd6b10da37df3", "start_char": 0, "end_char": 1812, "text_sha256": "77e2dbb010dcee44bd66645ec26cb844d7041ea4930f6373ae5dd6b10da37df3"}

experimental_model

Neuron-like PC12 and B104 cells and primary cultured neurons with small interfering RNA knockdown

exposure

Ibuprofen with peroxisome proliferator-activated receptor gamma agonists, antagonists and knockdown

limitations

The knockdown and the selective antagonist together make the receptor requirement a test rather than a correlation. Cell lines and primary culture rather than an animal.

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

Rat

plain_language

The drug reaches a growth-blocking switch in neurons through a fat-sensing receptor, not through prostaglandins.

primary_references

[ibu-p20089905] A molecular mechanism for ibuprofen-mediated RhoA inhibition in neurons. (2010). https://pubmed.ncbi.nlm.nih.gov/20089905/ DOI: 10.1523/jneurosci.5045-09.2010

tissue_or_cell_type

Neurons

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 422–433

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Neuron-like PC12 and B104 cells and primary cultured neurons with small interfering RNA knockdown · source_derived_draft · unverified_draft

### ibu-pparg-couples-to-rhoa Ibuprofen activates peroxisome proliferator-activated receptor gamma in neuron-like PC12 and B104 cells, activation with traditional agonists mimics the RhoA-inhibiting properties of ibuprofen and promotes neurite elongation in primary neurons exposed to axonal growth inhibitors, small interfering RNA against the receptor blocks RhoA suppression by those agonists, and selective receptor inhibition prevents the effect of ibuprofen on RhoA activity and neurite growth, supporting an essential role for the receptor in coupling ibuprofen to RhoA inhibition. 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 drug reaches a growth-blocking switch in neurons through a fat-sensing receptor, not through prostaglandins. organism: Rat tissue_or_cell_type: Neurons experimental_model: Neuron-like PC12 and B104 cells and primary cultured neurons with small interfering RNA knockdown limitations: The knockdown and the selective antagonist together make the receptor requirement a test rather than a correlation. Cell lines and primary culture rather than an animal. exposure: Ibuprofen with peroxisome proliferator-activated receptor gamma agonists, antagonists and knockdown evidence_span: {"source_cache": "artifacts/ibuprofen-research/20089905.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "77e2dbb010dcee44bd66645ec26cb844d7041ea4930f6373ae5dd6b10da37df3", "start_char": 0, "end_char": 1812, "text_sha256": "77e2dbb010dcee44bd66645ec26cb844d7041ea4930f6373ae5dd6b10da37df3"} [ibu-p20089905] A molecular mechanism for ibuprofen-mediated RhoA inhibition in neurons. (2010). https://pubmed.ncbi.nlm.nih.gov/20089905/ DOI: 10.1523/jneurosci.5045-09.2010

availability_state

biomarker_context Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/ibuprofen-research/4005104.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "81a2d4fb66dca9706eb1bd4119a918b24385de69633f4c4d01692e7c5bd805d1", "start_char": 0, "end_char": 945, "text_sha256": "81a2d4fb66dca9706eb1bd4119a918b24385de69633f4c4d01692e7c5bd805d1"}

experimental_model

Four healthy male subjects given racemic ibuprofen and each enantiomer separately

exposure

800 milligrams racemic ibuprofen and 400 milligrams of each enantiomer, on separate occasions

limitations

The design that matters: giving each enantiomer alone as well as the racemate is the only way to see the inversion and the interaction between them. Four subjects.

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

Roughly two thirds of the R half turns into the S half, and none of it comes back.

primary_references

[ibu-p4005104] Stereoselective disposition of ibuprofen enantiomers in man. (1985). https://pubmed.ncbi.nlm.nih.gov/4005104/ DOI: 10.1111/j.1365-2125.1985.tb02694.x

tissue_or_cell_type

Whole body

trigger_kind

biomarker_context Imported condition classification; unverified.

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 71–82

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four healthy male subjects given racemic ibuprofen and each enantiomer separately · source_derived_draft · unverified_draft

### ibu-sixty-three-percent-inverts A mean of 63 plus or minus 6% of an administered dose of R(-)-ibuprofen was stereospecifically inverted to the S(+) enantiomer in four healthy male subjects, with no measurable inversion of S(+) to R(-), while the kinetics of the individual enantiomers were altered by concurrent administration of the respective optical antipode, likely reflecting an interaction at plasma protein binding sites, and formation of ester glucuronide conjugates stereoselectively favoured the S enantiomer. Condition category: biomarker_context 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: Roughly two thirds of the R half turns into the S half, and none of it comes back. organism: Human tissue_or_cell_type: Whole body experimental_model: Four healthy male subjects given racemic ibuprofen and each enantiomer separately limitations: The design that matters: giving each enantiomer alone as well as the racemate is the only way to see the inversion and the interaction between them. Four subjects. exposure: 800 milligrams racemic ibuprofen and 400 milligrams of each enantiomer, on separate occasions evidence_span: {"source_cache": "artifacts/ibuprofen-research/4005104.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "81a2d4fb66dca9706eb1bd4119a918b24385de69633f4c4d01692e7c5bd805d1", "start_char": 0, "end_char": 945, "text_sha256": "81a2d4fb66dca9706eb1bd4119a918b24385de69633f4c4d01692e7c5bd805d1"} [ibu-p4005104] Stereoselective disposition of ibuprofen enantiomers in man. (1985). https://pubmed.ncbi.nlm.nih.gov/4005104/ DOI: 10.1111/j.1365-2125.1985.tb02694.x

evidence_span

{"source_cache": "artifacts/ibuprofen-research/14741265.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "244b7634bca0e2a090e86f49257289d02d19637b2c540260e94662dcdaa4111a", "start_char": 0, "end_char": 405, "text_sha256": "244b7634bca0e2a090e86f49257289d02d19637b2c540260e94662dcdaa4111a"}

experimental_model

Chemical modification of flurbiprofen and ibuprofen to alter cyclooxygenase-1 binding kinetics

exposure

Halogenated and carboxylate-modified analogues tested for slow tight-binding behaviour

limitations

A structure-activity result on the kinetic class of inhibition rather than on potency. It does not report the potencies themselves.

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

Enzyme

plain_language

Cap the acid group and the drug can no longer settle into the slow, tenacious kind of binding.

primary_references

[ibu-p14741265] Manipulation of kinetic profiles in 2-aryl propionic acid cyclooxygenase inhibitors. (2004). https://pubmed.ncbi.nlm.nih.gov/14741265/ DOI: 10.1016/j.bmcl.2003.11.034

tissue_or_cell_type

Cyclooxygenase-1

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 266–277

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Chemical modification of flurbiprofen and ibuprofen to alter cyclooxygenase-1 binding kinetics · source_derived_draft · unverified_draft

### ibu-the-free-acid-is-required Conversion of the carboxylate moiety of flurbiprofen to an ester or amide abolishes slow tight-binding behaviour regardless of halogenation state, and contrary to prior predictions a halogen substituent is not sufficient to confer slow tight-binding behaviour. 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: Cap the acid group and the drug can no longer settle into the slow, tenacious kind of binding. organism: Enzyme tissue_or_cell_type: Cyclooxygenase-1 experimental_model: Chemical modification of flurbiprofen and ibuprofen to alter cyclooxygenase-1 binding kinetics limitations: A structure-activity result on the kinetic class of inhibition rather than on potency. It does not report the potencies themselves. exposure: Halogenated and carboxylate-modified analogues tested for slow tight-binding behaviour evidence_span: {"source_cache": "artifacts/ibuprofen-research/14741265.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "244b7634bca0e2a090e86f49257289d02d19637b2c540260e94662dcdaa4111a", "start_char": 0, "end_char": 405, "text_sha256": "244b7634bca0e2a090e86f49257289d02d19637b2c540260e94662dcdaa4111a"} [ibu-p14741265] Manipulation of kinetic profiles in 2-aryl propionic acid cyclooxygenase inhibitors. (2004). https://pubmed.ncbi.nlm.nih.gov/14741265/ DOI: 10.1016/j.bmcl.2003.11.034

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