Activation of nuclear factor kappa B in response to T-cell stimulation: molecular mechanisms & dependencies

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What it does

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Recorded relationships

What acts on it

R(-)-ibuprofen with a half-maximal inhibitory concentration of 121.8 micromolar and S(+)-ibuprofen at 61.7 micromolar both inhibited activation of nuclear factor kappa B in response to T-cell stimulation, the effect was specific in that ibuprofen up to 10 millimolar did not affect heat shock transcription factor or activation by prostaglandin E2, concentrations of 20 millimolar did not prevent binding to DNA in vitro, and immunofluorescence and nuclear import experiments indicate the site of action is upstream of dissociation of the nuclear factor kappa B-I-kappa-B complex; only the S(+) enantiomer is an effective cyclooxygenase inhibitor, so the mechanism by which R(-) exerts anti-inflammatory and antinociceptive effects remains unknown.
R(-)-ibuprofen → Activation of nuclear factor kappa B in response to T-cell stimulation source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/ibuprofen-research/9517383.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7a3938a95448a472769fdce1c05ac55d853bfdbdbcda7554ec5b79dcb423db35", "start_char": 0, "end_char": 1478, "text_sha256": "7a3938a95448a472769fdce1c05ac55d853bfdbdbcda7554ec5b79dcb423db35"}
experimental_model
Electrophoretic mobility-shift assays, transient transfection, confocal immunofluorescence and nuclear import experiments
exposure
R(-)- and S(+)-ibuprofen compared as inhibitors of nuclear factor kappa B activation
limitations
Compares the enantiomers on a target where the cyclooxygenase argument does not apply. The concentrations are high, in the tens to hundreds of micromolar.
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
On this target the two hands are only twofold apart, not thirty, which is a route by which the so-called inactive one could work.
primary_references
[ibu-p9517383] Modulation of transcription factor NF-kappaB by enantiomers of the nonsteroidal drug ibuprofen. (1998). https://pubmed.ncbi.nlm.nih.gov/9517383/ DOI: 10.1038/sj.bjp.0701652
tissue_or_cell_type
T lymphocytes
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 370–381
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Electrophoretic mobility-shift assays, transient transfection, confocal immunofluorescence and nuclear import experiments · source_derived_draft · unverified_draft
### ibu-both-hands-block-nfkb R(-)-ibuprofen with a half-maximal inhibitory concentration of 121.8 micromolar and S(+)-ibuprofen at 61.7 micromolar both inhibited activation of nuclear factor kappa B in response to T-cell stimulation, the effect was specific in that ibuprofen up to 10 millimolar did not affect heat shock transcription factor or activation by prostaglandin E2, concentrations of 20 millimolar did not prevent binding to DNA in vitro, and immunofluorescence and nuclear import experiments indicate the site of action is upstream of dissociation of the nuclear factor kappa B-I-kappa-B complex; only the S(+) enantiomer is an effective cyclooxygenase inhibitor, so the mechanism by which R(-) exerts anti-inflammatory and antinociceptive effects remains unknown. 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: On this target the two hands are only twofold apart, not thirty, which is a route by which the so-called inactive one could work. organism: Human cells tissue_or_cell_type: T lymphocytes experimental_model: Electrophoretic mobility-shift assays, transient transfection, confocal immunofluorescence and nuclear import experiments limitations: Compares the enantiomers on a target where the cyclooxygenase argument does not apply. The concentrations are high, in the tens to hundreds of micromolar. exposure: R(-)- and S(+)-ibuprofen compared as inhibitors of nuclear factor kappa B activation evidence_span: {"source_cache": "artifacts/ibuprofen-research/9517383.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7a3938a95448a472769fdce1c05ac55d853bfdbdbcda7554ec5b79dcb423db35", "start_char": 0, "end_char": 1478, "text_sha256": "7a3938a95448a472769fdce1c05ac55d853bfdbdbcda7554ec5b79dcb423db35"} [ibu-p9517383] Modulation of transcription factor NF-kappaB by enantiomers of the nonsteroidal drug ibuprofen. (1998). https://pubmed.ncbi.nlm.nih.gov/9517383/ DOI: 10.1038/sj.bjp.0701652
Complete structured claim and evidence

Where it participates (unsigned role)

R-ibuprofen and R-flurbiprofen, with poor cyclooxygenase-inhibiting activity, reduce amyloid-beta 42 production by human cells, and although these R enantiomers inhibit nuclear factor kappa B activation and that factor can selectively regulate amyloid-beta 42, the reduction is not mediated by inhibition of nuclear factor kappa B activation; clinical use of these drugs for Alzheimer’s disease has been hampered by dose-limiting toxicity believed to be due to cyclooxygenase inhibition, which is reportedly not essential for selective amyloid-beta 42 reduction.
R(-)-ibuprofen → Amyloid-beta 42, the 42-residue isoform source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/ibuprofen-research/12421374.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bb022923aad1deb90ae4c540e3e8aab4080a3b78aa9c4a9356447385c31e9c8b", "start_char": 0, "end_char": 1003, "text_sha256": "bb022923aad1deb90ae4c540e3e8aab4080a3b78aa9c4a9356447385c31e9c8b"}
experimental_model
Human cells treated with single enantiomers of ibuprofen and flurbiprofen
exposure
R-ibuprofen and R-flurbiprofen, chosen for their poor cyclooxygenase-inhibiting activity
limitations
Uses the enantiomer as the control for cyclooxygenase involvement, which is cleaner than comparing different drugs. It also rules out the nuclear factor kappa B route explicitly.
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
The half of the molecule that cannot block cyclooxygenase is the half that lowers the Alzheimer peptide.
primary_references
[ibu-p12421374] Selective inhibition of Abeta42 production by NSAID R-enantiomers. (2002). https://pubmed.ncbi.nlm.nih.gov/12421374/ DOI: 10.1046/j.1471-4159.2002.01195.x
tissue_or_cell_type
Cultured cells
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 396–407
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human cells treated with single enantiomers of ibuprofen and flurbiprofen · source_derived_draft · unverified_draft
### ibu-r-enantiomer-lowers-abeta42 R-ibuprofen and R-flurbiprofen, with poor cyclooxygenase-inhibiting activity, reduce amyloid-beta 42 production by human cells, and although these R enantiomers inhibit nuclear factor kappa B activation and that factor can selectively regulate amyloid-beta 42, the reduction is not mediated by inhibition of nuclear factor kappa B activation; clinical use of these drugs for Alzheimer’s disease has been hampered by dose-limiting toxicity believed to be due to cyclooxygenase inhibition, which is reportedly not essential for selective amyloid-beta 42 reduction. 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 half of the molecule that cannot block cyclooxygenase is the half that lowers the Alzheimer peptide. organism: Human cells tissue_or_cell_type: Cultured cells experimental_model: Human cells treated with single enantiomers of ibuprofen and flurbiprofen limitations: Uses the enantiomer as the control for cyclooxygenase involvement, which is cleaner than comparing different drugs. It also rules out the nuclear factor kappa B route explicitly. exposure: R-ibuprofen and R-flurbiprofen, chosen for their poor cyclooxygenase-inhibiting activity evidence_span: {"source_cache": "artifacts/ibuprofen-research/12421374.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bb022923aad1deb90ae4c540e3e8aab4080a3b78aa9c4a9356447385c31e9c8b", "start_char": 0, "end_char": 1003, "text_sha256": "bb022923aad1deb90ae4c540e3e8aab4080a3b78aa9c4a9356447385c31e9c8b"} [ibu-p12421374] Selective inhibition of Abeta42 production by NSAID R-enantiomers. (2002). https://pubmed.ncbi.nlm.nih.gov/12421374/ DOI: 10.1046/j.1471-4159.2002.01195.x
Complete structured claim and evidence

The events it takes part in

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Situations it appears in

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In the sources

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Open hypotheses

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

Activation of nuclear factor kappa B in response to T-cell stimulation