sEH inhibitor-20
sEH inhibitor-20 is an orally active and metabolically stable sEH inhibitor (IC50: 0.2 nM). sEH inhibitor-20 has significant analgesic and anti-inflammatory activities and is expected to become a potential candidate compound for the study of neuropathic pain.
For research use only. We do not sell to patients.
- Formula: C19H15F3N4O3
- Molecular Weight:404.34
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
sEH inhibitor-20 (Compound FP9) (0.1 μM, 1 h) shows excellent metabolic stability (t₁/₂ > 184 min) in human and mouse liver microsomes, indicating that it is not easily metabolized by the liver in vivo[1].
sEH inhibitor-20 (10 μM, 16 h) shows moderate brain permeability in the PAMPA-BBB model (Pe : 3.83 × 10⁻⁶ cm/s)[1].
sEH inhibitor-20 (1-1000 nM, pre-treat for 0.5 h, then treat for 6 h) significantly reduces TNF-α and IL-6 levels in the LPS-induced PBMC inflammation model without cytotoxicity (10 μM still does not affect cell survival)[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Parmacokinetics
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6 mice (male, aged 6-8 weeks) intraperitoneally injected with Paclitaxel (5 mg/mL)[1]
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Dosage:10, 30 mg/kg
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Administration:acute : p.o. one dose; chronic : p.o. once a day for 14 consecutive days
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Result:Exhibited its maximum acute analgesic effect at 2 hours post-administration (30 mg/kg), with the effect persisting for 4 hours, demonstrating both longer duration and superior efficacy compared to gabapentin.
Maintained stable chronic analgesic effects at 30 mg/kg without inducing tolerance.
Chemical Information
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Molecular Weight 404.34
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Formula C19H15F3N4O3
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SMILES
O=C1NN=C(C2=CC=C(NC(NCC3=CC=CC=C3OC(F)(F)F)=O)C=C2)C=C1
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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)