Aequinetin
Aequinetin is a tyrosinase inhibitor, and docking results show that it forms hydrogen bonds and hydrophobic interactions with key protein residues of NF-κB p65, MAPK10 and ERK1.
For research use only. We do not sell to patients.
- CAS No.: 31025-53-3
- Formula: C21H20O9
- Molecular Weight:416.38
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
Aequinetin (chrysin 7-β-D-glucoside) is synthesized via in vitro enzymatic catalysis by glucosyltransferase from Phytolacca americana to perform site-specific glycosylation modification of Chrysin (HY-14589)[1].
Aequinetin exhibits stronger inhibitory activity against white mushroom tyrosinase than Chrysin[1].
Aequinetin docking results showed strong binding affinity to human NF-κB p65, MAPK10, and ERK1[2].
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. 31025-53-3
-
Molecular Weight 416.38
-
Formula C21H20O9
-
SMILES
O=C1C2=C(O)C=C(O[C@@H]3O[C@@H]([C@H]([C@@H]([C@H]3O)O)O)CO)C=C2OC(C4=CC=CC=C4)=C1
-
Synonyms
Chrysin 7-β--D-glucoside
-
Structure Classification
-
Initial Source
-
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)