Myricetin

SKU: orb1310476

Description

Myricetin (Cannabiscetin) is a naturally occurring flavonoid and MEK1 inhibitor. It exhibits a range of biological activities, including hypoglycemic, antioxidant, hepatoprotective, anti-tumor, and anti-inflammatory effects, making it a valuable tool for research in diabetes, oncology, and inflammation studies using both in vitro and in vivo models.

Research Area

Cell Biology, Metabolism Research, Signal Transduction

Key Properties

• CAS Number: 529-44-2
• MW: 318.24
• Purity: 99.85% (May vary between batches)
• Formula: C₁₅H₁₀O₈
• SMILES: O=C1C=2C(OC(=C1O)C3=CC(O)=C(O)C(O)=C3)=CC(O)=CC2O
• Target: Apoptosis,Autophagy,Endogenous Metabolite,PI3K
• Solubility: DMSO:55 mg/mL (172.83 mM);H2O:< 1 mg/mL (insoluble or slightly soluble);10% DMSO+40% PEG300+5% Tween 80+45% Saline:6.3 mg/mL (19.8 mM);Ethanol:20 mg/mL (62.85 mM)

Bioactivity

• Target IC50:
  A549 cells:14.8 mg/mL|BV-2 cells:> 100 μM|HepG2 cells:> 20 μM|HCT116 cells:23 μM|HEK293 cells:> 10 μM|CWR22R:13.1 μM|SKBR3 cells:13.5 μM|PI3Kγ:0.17 μM (Kd)|H9 cells:69 μM|Jurkat cells:10 μM|MCF-7 cells:4.7 mg/mL
• In Vivo:
  METHODS: To detect anti-tumor activity in vivo, Myricetin (30 mg/kg once a day) and cisplatin (5 mg/kg every three days) were intraperitoneally injected into BALB/c nude mice bearing Huh-7 xenografts for two weeks. RESULTS: Treatment with Myricetin or cisplatin alone moderately inhibited tumor growth, but the combination treatment inhibited tumor growth more significantly than Myricetin or cisplatin alone.
• In Vitro:
  METHODS: Human hepatocellular carcinoma cells HepG2 and Huh-7 were treated with Myricetin (100-200 µM) for 72 h. Cell viability was measured by CCK-8 assay. RESULTS: Myricetin significantly inhibited cell growth in a dose-dependent manner. METHODS: Ovarian cancer cells A2780 and OVCAR3 were treated with Myricetin (25 µM) for 48 h. Apoptosis was detected by single stranded-DNA Apoptosis ELISA kit. RESULTS: In A2780 cells treated with Myricetin, an approximately 2.5-fold increase in apoptotic signaling was observed compared to untreated cells, whereas under similar treatment conditions, apoptotic signaling in OVCAR3 cells increased approximately 4-fold compared to untreated cells.
• Cell Research:
  Pancreatic cancer cells (MIA PaCa-2, Panc-1 or S2-013) or normal pancreatic ductal cells (PDCs) are treated with myricetin (12.5–200 μM). Cell viability is determined using the Dojindo Cell Counting Kit-8. Cells are seeded onto a 96-well plate at 1×104 cells per well and allowed to adhere overnight. After treatment with myricetin at various concentrations for 24 hours, 10 μL of the tetrazolium substrate is added to each well of the plate. Plates are incubated at 37°C for 1 hour, after which the absorbance at 450 nm is measured.

Storage & Handling

• Storage: keep away from direct sunlight,keep away from moisture | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice/Shipping at ambient temperature.
• Expiration Date: 12 months from date of receipt.
• Disclaimer: For research use only

Alternative Names

Apoptosis, Autophagy, Cannabiscetin, Myricetin, inhibit, Inhibitor, EndogenousMetabolite, Endogenous Metabolite, PI3Kγ

Compound Identifiers

PubChem CID

5281672