Myricetin

Myricetin is produced from the parent compound taxifolin through the (+) -dihydromyricetin intermediate and can be further processed to form laricitrin and then syringetin, both members of the flavonol class of flavonoids. Dihydromyricetin is frequently sold as a supplement and has controversial function as a partial GABAA receptor potentiator and treatment in Alcohol Use Disorder (AUD) . (In Vitro) :Myricetin exhibits the scavenging activity towards a number of radicals and ions. It displays poor activity (IC50 value=1.4 mg/mL) in a superoxide dismutase (SOD) -like activity assay. It prevents cancer cell death via apoptosis via regulation of PI3K/Akt and MAPK signalling pathways. Myricetin exhibits antiphotoaging effects by quenching causative free radicals in the skin. Myricetin is able to suppress UVB-induced COX-2 expression in mouse skin epidermal JB6 P+ cells. It inhibits UVB-induced initiation of activator protein-1 and NF-κβ, as well as Fyn kinase activity. Myricetin inhibits viability of SKOV3 ovarian cancer cells in a dose-dependent manner. It induces DNA DSBs and ER stress, which leads to apoptosis in SKOV3 cells. Myricetin inhibits human Hsp70 by more than 80% with IC50 values of 83, 11 and 12 μM, respectively. (In Vivo) :Treatment of orthotopic pancreatic tumors with myricetin results in tumor regression and decreases metastatic spread. Exposure to 150 μM myricetin causes 14%, 26%, 5% and 49% inhibition of rabbit platelet aggregation, induced by ADP, arachidonic acid, collagen and PAF, respectively.

529-44-2

Cannabiscetin | NSC 407290

>98% (HPLC)

Ethanol: 20 mg/mL warmed (62.84 mM) ; DMSO: 63 mg/mL (197.96 mM)

O=C1C (O) =C (C2=CC (O) =C (O) C (O) =C2) OC3=C1C (O) =CC (O) =C3

C15H10O8

318.24

Storage temperature: -20°C. Stability: ≥ 2 years

For research use only.