CGS 24891
CGS 24891 is an orally active 5-lipoxygenase (5-LO) inhibitor, with an IC50 value of 0.051 μM in guinea pigs and 0.11 μM in dogs. CGS 24891 inhibits the production of 5-hydroxyeicosatetraenoic acid (5-HETE) and leukotriene B4 (LTB4) from arachidonic acid. CGS 24891 weakly inhibits 12-lipoxygenase (12-LO) with an IC50 of 0.41 μM. CGS 24891 is applicable to research on inflammation and allergic reactions.
For research use only. We do not sell to patients.
- CAS No.: 134823-10-2
- Formula: C18H17FN2O4
- Molecular Weight:344.34
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
5-LO 0.051 (gui μM (IC50) |
5-LO 0.11 (dogs μM (IC50) |
12-LOX 0.41 μM (IC50) |
In Vitro
CGS 24891 potently inhibits 5-lipoxygenase activity in guinea pig polymorphonuclear leukocytes (PMNs) with an IC50 value of 51 nM[1].
CGS 24891 inhibits the activity of 5-lipoxygenase in canine whole blood, with an IC50 of 0.11 μM[1].
CGS 24891 inhibits 12-lipoxygenase activity in platelets with an IC50 of 0.41 μM[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
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CAS No. 134823-10-2
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Molecular Weight 344.34
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Formula C18H17FN2O4
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SMILES
O=C(N(CC1=CC2=C(OC1)C=CC(OC3=CC=C(C=C3)F)=C2)O)NC
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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)