|Molecular weight||304.254 g/mol|
|Names and Identifiers|
|Traditional Name||Dihydroquercetin, Taxifoliol, Distylin, Catechin hydrate|
|CAS Registry Number||480-18-2|
Dihydroquercetin (Taxifolin) is not mutagenic and less toxic than the related compound quercetin. It acts as a potential chemopreventive agent by regulating genes via an ARE-dependent mechanism. Taxifolin has shown to inhibit the ovarian cancer cell growth in a dose-dependent manner. However, in this same study, taxifolin was the least effective flavonoid in the inhibition of VEGF expression. There is also a strong correlation (with a correlation coefficient of 0.93) between the antiproliferative effects of dihydroquercetin (DHQ, Taxifolin) derivatives on murine skin fibroblasts and human breast cancer cells.
Taxifolin has shown to have anti-proliferative effects on many types of cancer cells by inhibiting cancer cell lipogenesis. By inhibiting the fatty acid synthase in cancer cells, taxifolin is able to prevent the growth and spread of cancer cells.
The capacity of taxifolin to stimulate fibril formation and promote stabilization of fibrillar forms of collagen can be used in medicine. Also taxifolin inhibited the cellular melanogenesis as effectively as arbutin, one of the most widely used hypopigmenting agents in cosmetics. However, arbutin acts as quercetin extremely mutagenic, carcinogenic and toxic.
Taxifolin enhanced also the efficacy of conventional antibiotics like levofloxacin and ceftazidime in vitro, which have potential for combinatory therapy of patients infected with methicillin-resistant Staphylococcus aureus (MRSA).
Taxifolin, as well as many other flavonoids, has been found to act as a non-selective antagonist of the opioid receptors, albeit with somewhat weak affinity.
Taxifolin has been found to act as an agonist of the adiponectin receptor 2 (AdipoR2).