Common name: Dihydroquercetin
Synonyms: TAXIFOLIN, (+)-Taxifolin, Taxifoliol, (2R,3R)-Dihydroquercetin Distylin
Active ingredients: Dihydroquercetin
CAS NO.: 480-18-2
Molecular Formula: C15H12O7
Molecular Weight: 304.25
Structure:

Main Specifications: 90%, 95%, 99%
Test method: HPLC
Appearance: off white to white powder
Heavy Metals: NMT10ppm
Residual solvent: Conform to USP39, EP8.0
Packing: 1kg, 5kg, 10kg cardboard drum
Storage: Store in cool and dry place and keep away from strong direct light and heat
Shelf Life: Two years when properly stored

Applications:

What’s Dihydroquercetin?

Taxifolin (5,7,3',4'-flavan-on-ol), also known as dihydroquercetin, belongs to the subclass flavanonols in the flavonoids, which in turn is a class of polyphenols.

Health Benefits of Dihydroquercetin

1. Taxifolin and COVID Pneumonia

Russian researchers are investigating the effects of the dietary supplement, Taxifolin, on people recovering from COVID-related pneumonia. Launched in 2021, this clinical trial involves the use of 30 milligrams (mg) daily of Taxifolin for 100 patients. The researchers hope to elucidate how the dietary supplement could impact respiratory function, the condition of the arterial wall, and overall quality of life.

2. Taxifolin and Antibiotics

The flavonoid taxifolin may increase the efficacy of certain antibiotics, including levofloxacin and ceftazidime. This enhanced potency could benefit people suffering from antibiotic-resistant conditions, such as MRSA.

3. Antioxidant activity

Taxifolin is associated with antioxidant activity and capillary protecting action. Additionally, it has also been found that the effectiveness of taxifolin is 3.4 times greater than quercetin at the dose of 100 mg/kg and 4.9 times for the dose of 300 mg/kg. It is also shown that taxifolin has antioxidant activity in vivo, which was evaluated in Wistar rats, suffering from tetrachloromethane induced hepatitis. In another study, the rats treated with taxifolin show a decrease in the lipid peroxidation in liver and serum by reacting with the thiobarbituric acid, which reveals the antioxidant property of taxifolin. The antioxidant activity of taxifolin is also exhibited through its neuroprotective effects via the inhibition of oxidative neuronal injuries in rat cortical cells, which was supported by the DPPH radical scavenging activity and the inhibition of lipid peroxidation. The antioxidant potential of taxifolin was also evaluated by the deoxyribose degradation assay for its electrochemical redox potentials. Taxifolin inhibits the H2O2-mediated poly (ADP-ribose) polymerase cleavage through the Nrf2 translocation to the nucleus and the activation of mRNA and protein expression. This showed the protective effect of taxifolin on RPE cells against apoptosis, induced by oxidative stress, through the activation of NRF2 and the phase II antioxidant enzyme system.

4. Cardiovascular activity

Hyperlipidemia is the most crucial factor for the development of atherosclerosis and coronary heart disease due to increase in the cholesterol or LDL cholesterol level. Several studies have showed that taxifolin possesses anti-hyperlipidemic activity which has been evaluated by the assessment of the hyperlipidemic rats treated with taxifolin. Results showed that taxifolin maintains the normal lipid profile in the serum and liver, and lipid excretion in fecal of rats, which has been supplemented with cholesterol rich diet. The result from the in vivo study also reveals that taxifolin treated animals showed lower levels of total liver cholesterol along with the reduction in thiobarbituric acid reactive substance levels in both serum and liver. In a study it has been shown that the pretreatment of HepG2 cells with taxifolin causes the inhibition of the cholesterol synthesis along with the reduction of the HMG-CoA reductase activity. Taxifolin also causes the suppression of esterification of cellular cholesterol, triacylglycerol and phospholipid syntheses. In addition, taxifolin reduced the hepatic lipid synthesis via altering the secretion of apoB and apoA-I. Currently taxifolin has been reported to inhibit the stress induced apoptosis, mainly oxidative stress and endoplasmic reticulum stress, via the PI3K/Akt pathway, which provides the cardioprotective activity against ischemia-reperfusion injury. Furthermore, taxifolin also delays the onset of endoplasmic reticulum stress by regulating certain protein expression. In another study, taxifolin has been evaluated to identify the effect and mechanism on myocardial ischemia/reperfusion (I/R) injury. Taxifolin improved the ventricular functional recovery and the levels of SOD, GSH-PX. The upregulation of antiapoptotic proteins such as Bcl2 and downregulation of proapoptoic proteins (Bax, Cyt-c, caspase 3 and 9) was shown, that leads to the inhibition of the myocardial apoptosis by the action of taxifolin. As a result it was proved that taxifolin significantly improved the cardiac function and regulated oxidative stress and attenuated apoptosis. Besides the regulation of lipid profile taxifolin has also been found to act on the several pathways to regulate the blood pressure and showed antihypertensive activity. Taxifolin has been found to have the capacity to lower blood pressure and to improve endothelial function. Bernatova and Liskova documented all the possible mechanisms from preclinical studies through which taxifolin showed its antihypertensive activity in the cardiovascular system mainly via endothelial NO production, and the reduction of ACE activity and iNOS expression. Additionally, it also protects the endothelial function and thus participated in the blood pressure regulating mechanisms in various experimental hypertension models.

5. Anti-Alzheimer activity

Taxifolin is also effective in the treatment of Alzheimer. According to studies, taxifolin, either used alone or in conjunction with cilostazol, significantly reduces elevated αβ and C99 levels in N2a Swe cells. Additionally, it is also associated with the synergistic inhibition of the amyloidogenesis via the downregulation of P-JAK2/P-STAT3-coupled NF-κB linked BACE1 expression through the SIRT1 upregulation. Taxifolin blocks the formation of amyloid-β oligomer, restoring the vascular integrity and memory in cerebral amyloid angiopathy (CAA). In a recent study by Inoue et al., it is showed that taxifolin increases cerebral blood flow and removes amyloid-β from the brain and inhibits the cognitive dysfunction through the suppression of ApoE–ERK1/2–amyloid-β precursor protein axis. The novel derivatives of taxifolin namely 7-O-cinnamoyltaxifolin and 7-O-feruloyltaxifolin showed significant neuroprotective effects against oxytosis, ferroptosis and ATP depletion in HT22 cell model. The compounds cause the reduction of the LPS-induced neuroinflammation in BV-2 microglia cells. They also showed improved efficacy for short term memory in an AD mouse model, which highlights the neuroprotective activity of taxifolin derivatives. The inhibitory effect of taxifolin on the Amyloid-β-associated neurodegenerative diseases and related disorders has been briefly explained by Tanaka and his fellow researchers. The findings showed the recent advances in taxifolin research based on in vitro, in vivo and in silico approaches with future research directions for novel therapeutic strategies for CAA, AD, and metabolic diseases with an increased risk for dementia. Furthermore, for the treatment of CAA the implementation of the novel taxifolin has also been well documented by Saito et al. and his co-researchers. In accordance to their study taxifolin facilitated disassembly, prevent oligomer formation and increase clearance of Aβ in a mouse model of CAA with excellent preventive measures for disturbed cerebrovascular reactivity and spatial reference memory impairment in CAA.