Israpafant
Israpafant (Y-24180) is a potent, selective and long-acting platelet activation factor (PAF) receptor antagonist with IC50s of 0.84 nM and 3.84 nM against PAF-induced human and rabbit platelet aggregation, respectively. Israpafant stimulates both extracellular Ca2+ influx and intracellular Ca2+ release in prostate cancer cells. Israpafant suppresses the allergic cutaneous reactions including eosinophilia, cytokine production, edema and erythema in mice.
For research use only. We do not sell to patients.
- CAS No.: 117279-73-9
- Formula: C28H29ClN4S
- Molecular Weight:489.07
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
IC50: 0.84 nM (PAF-induced human platelet aggregation), 3.84 nM (PAF-induced rabbit platelet aggregation)[1]
Chemical Information
-
CAS No. 117279-73-9
-
Molecular Weight 489.07
-
Formula C28H29ClN4S
-
SMILES
CC1=NN=C2N1C3=C(C(C4=C(Cl)C=CC=C4)=NC2C)C=C(S3)CCC5=CC=C(C=C5)CC(C)C
-
Synonyms
Y 24180
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
-
Ca2+ Staining Technique
Ca2+ staining is an experimental technique that utilizes specific fluorescent probes (such as Fluo-4 AM, Fura-2, etc.) to qualitatively or quantitatively detect dynamic changes in intracellular Ca2+ concentrations; this is achieved by monitoring the changes in fluorescent signals generated when these probes bind to free intracellular calcium ions. The underlying principle relies primarily on the presence of chelating groups within the probe's molecular structure that possess high affinity for calcium ions.
-
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)