BAY-386
BAY-386, a chemical probe, is a PAR-1 antagonist that inhibits the expression of pro-inflammatory factors MCP-1 and CXCL1 in HUVEC.
For research use only. We do not sell to patients.
- CAS No.: 1256941-06-6
- Formula: C22H25F3N4O5S
- Molecular Weight:514.52
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
PAR-1, CXCL1[1]
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| Platelet | IC50 |
>100 μM
Compound: EUB0000291
|
Inhibition of platelet aggregation (human plasma, ADP, Collagen)
Inhibition of platelet aggregation (human plasma, ADP, Collagen)
|
10.6019/CHEMBL4507269 |
| Platelet | IC50 |
0.14 μM
Compound: EUB0000291
|
Inhibition of platelet aggregation (human plasma, thrombin)
Inhibition of platelet aggregation (human plasma, thrombin)
|
10.6019/CHEMBL4507269 |
| Platelet | IC50 |
0.43 μM
Compound: EUB0000291
|
Inhibition of platelet aggregation (human plasma, TRAP-6) (IC50)
Inhibition of platelet aggregation (human plasma, TRAP-6) (IC50)
|
10.6019/CHEMBL4507269 |
Chemical Information
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CAS No. 1256941-06-6
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Molecular Weight 514.52
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Formula C22H25F3N4O5S
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SMILES
O=C(N1C[C@@H](C2=NC(C3CC3)=NO2)C[C@@H](C4=CC=C(OC(F)(F)F)C=C4)C1)N5CCS(CC5)(=O)=O
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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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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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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)