1-Oxo Ibuprofen
1-Oxo Ibuprofen (Ibuprofen EP impurity J) is a potential impurity in the formulation of Ibuprofen (HY-78131). Ibuprofen is an anti-inflammatory inhibitor targeting COX-1 and COX-2, with IC50 values of 13 μM and 370 μM, respectively.
For research use only. We do not sell to patients.
- CAS No.: 65813-55-0
- Formula: C13H16O3
- Molecular Weight:220.26
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
1-Oxo Ibuprofen is a major transformation product of Ibuprofen generated during the ozonation water treatment process, formed by the further oxidation of the hydroxyl group in 1-OH-IBU into a ketone group. During the ozonation reaction, the concentration of 1-Oxo Ibuprofen peaks at 60 minutes, accounting for approximately 3% of the initial Ibuprofen concentration, and then gradually decreases, indicating that it can be further degraded and transformed by ozone. Research on 1-Oxo Ibuprofen falls within the fields of environmental chemistry and wastewater treatment[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 65813-55-0
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Molecular Weight 220.26
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Formula C13H16O3
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SMILES
O=C(O)C(C)C1=CC=C(C(C(C)C)=O)C=C1
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Synonyms
Ibuprofen EP impurity J
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)