BCX-3607
BCX-3607 is an orally active tissue factor/factor VIIa (TF-FVIIa) inhibitor (IC50: 4 nM). BCX-3607 blocks the extrinsic coagulation pathway by inhibiting the TF-FVIIa complex and significantly prolongs the prothrombin time (PT). BCX-3607 has a higher selectivity for TF-FVIIa than other serine proteases (such as thrombin, FXa, etc.). BCX-3607 can reduce thrombus weight and inflammatory response, and has both anti-thrombotic and anti-inflammatory effects. BCX-3607 can be used in the study of thrombosis-related diseases.
For research use only. We do not sell to patients.
- CAS No.: 885684-79-7
- Formula: C27H29N5O3
- Molecular Weight:471.55
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
TF-FVIIa
Chemical Information
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CAS No. 885684-79-7
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Molecular Weight 471.55
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Formula C27H29N5O3
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SMILES
O=C(C1=CC(C(NCC(C)C)=O)=CC=C1C2=CC=C(C=C)C=C2CNC3=NC=C(C(N)=N)C=C3)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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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)