STAT6-IN-12
STAT6-IN-12 is a potent STAT6 inhibitor with an IC50 of 50 nM. STAT6-IN-12 also inhibits Smad2/3 with an IC50 of 68 nM. STAT6-IN-12 inhibits TGFβ-dependent Smad2/3 signaling pathway, IL-4-dependent STAT6 signaling pathway, and cellular inflammatory responses. STAT6-IN-12 can be used for the research of inflammation.
For research use only. We do not sell to patients.
- CAS No.: 2949393-27-3
- Formula: C18H21ClO6
- Molecular Weight:368.81
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
|
Smad2/3 68 nM (IC50) |
IL-4 |
STAT6 50 nM (IC50) |
In Vitro
STAT6-IN-12 (compound 27) (24 h) potently inhibits both IL-4-induced STAT6 and TGF-β-induced Smad2/3 signaling pathways in HepG2 cells, with IC50 values of 50 nM and 68 nM, respectively[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
-
CAS No. 2949393-27-3
-
Molecular Weight 368.81
-
Formula C18H21ClO6
-
SMILES
OC1=C(C(/C(C)=C/C[C@H](O)[C@H](C)[C@@H](C)OC2=O)=O)C(C2)=C(Cl)C(O)=C1
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
-
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)