2150-11-0

3′,4′,7-Trihydroxyflavone Chemical Structure
2150-11-0

Chemical Structure

3′,4′,7-Trihydroxyflavone

  • CAS No.: 2150-11-0
  • Formula:C15H10O5
  • Molecular Weight:270.24

IUPAC Name: 2-(3,4-dihydroxyphenyl)-7-hydroxy-4H-chromen-4-one

InChIKey: PVFGJHYLIHMCQD-UHFFFAOYSA-N

SMILES: O=C1C2=CC=C(O)C=C2OC(C3=CC(O)=C(O)C=C3)=C1

Biological Activity: 3′,4′,7-Trihydroxyflavone is an orally active inhibitor of OXA-48 (IC50 = 1.89 μM) and COX-1 (IC50 = 36.37 μM). 3′,4′,7-Trihydroxyflavone exhibits antioxidant and anti-inflammatory properties, inhibiting the release of inflammatory cytokines such as IL-6, IL-8, and TNF-α. 3′,4′,7-Trihydroxyflavone inhibits H2O2-induced neuronal apoptosis and ROS accumulation, and exerts anti-neuroinflammatory effects by suppressing the JNK-STAT1 pathway. 3′,4′,7-Trihydroxyflavone exhibits antimicrobial and antibiotic-modifying activities against multidrug-resistant Gram-negative enteric bacteria. 3′,4′,7-Trihydroxyflavone inhibits RANKL-induced osteoclast formation via NFATc1. 3′,4′,7-Trihydroxyflavone activates the CREB-BDNF axis and restores scopolamine (HY-N0296)-induced memory deficits in mice[1][2][3][4][5][6][7][8][9].

Cat. No. Product Name Purity Description Pricing
HY-N2736
3′,4′,7-Trihydroxyflavone 99.04% 3′,4′,7-Trihydroxyflavone is an orally active inhibitor of OXA-48 (IC50 = 1.89 μM) and COX-1 (IC50 = 36.37 μM). 3′,4′,7-Trihydroxyflavone exhibits antioxidant and anti-inflammatory properties, inhibiting the release of inflammatory cytokines such as IL-6, IL-8, and TNF-α. 3′,4′,7-Trihydroxyflavone inhibits H2O2-induced neuronal apoptosis and ROS accumulation, and exerts anti-neuroinflammatory effects by suppressing the JNK-STAT1 pathway. 3′,4′,7-Trihydroxyflavone exhibits antimicrobial and antibiotic-modifying activities against multidrug-resistant Gram-negative enteric bacteria. 3′,4′,7-Trihydroxyflavone inhibits RANKL-induced osteoclast formation via NFATc1. 3′,4′,7-Trihydroxyflavone activates the CREB-BDNF axis and restores scopolamine (HY-N0296)-induced memory deficits in mice.
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