a-FABP-IN-1
Based on 1 publication(s) in Google Scholar
a-FABP-IN-1 (Compound 5g) is a potent and selective human adipocyte fatty acid-binding protein (a-FABP) inhibitor with a Ki below 1.0 nM. a-FABP-IN-1 inhibits the pro-inflammatory cytokine production.
For research use only. We do not sell to patients.
- CAS No.: 1310361-52-4
- Formula: C29H23ClN2O3S
- Molecular Weight:515.02
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications Citing Use of MedChemExpress (MCE) a-FABP-IN-1
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Biological Activity
Description
IC50 & Target
Ki: <1.0 nM (a-FABP)[1]
Chemical Information
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CAS No. 1310361-52-4
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Molecular Weight 515.02
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Formula C29H23ClN2O3S
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SMILES
CC(OC1=CC(C2=CC=CC=C2C3=NN(C(C4=CC=CS4)=C3)C5=CC=C(C=C5)Cl)=CC=C1)(C(O)=O)C
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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.
Publications (1)
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Journal Impact Factor
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Most Recent
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Free Radic Biol Med
Redox-driven FABP1/PPARγ signaling fuels peroxisomal fatty acid oxidation and confers cetuximab resistance in drug-tolerant head and neck cancer cells. [Abstract]2026 Mar 16:246:209-222. PMID: 41534570
Protocols
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Large-size fat particle sorting
Large-size fat particle sorting is widely used to isolate cells up to 200 μm in diameter. Single-cell flow sorting will allow greater insight into adipocyte heterogeneity by identifying gene expression, protein composition, and metabolic signatures at the single-cell level.
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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)