Taxifolin

Pharmacology & Research

Taxifolin (dihydroquercetin) is a flavanonol — structurally it is quercetin with its C-ring double bond saturated (the 2,3-dihydro form), and in plants it is the biosynthetic precursor that is oxidised to quercetin ^{3Reference 32025Modern developing directions in the dihydroquercetin studyView study →}. That one structural difference is the selling point and the caveat. The selling point: the saturated ring makes taxifolin more chemically and oxidatively stable than quercetin in solution and storage ^{2Reference 2Das A et al. · 2021ReviewPharmacological basis and new insights of taxifolin: a comprehensive reviewView study →}. The caveat: it shares quercetin’s poor oral bioavailability, and losing the ring conjugation arguably makes it a somewhat weaker direct radical scavenger ^{5Reference 52019Redox properties of individual quercetin moietiesView study →} — so “more stable” does not mean “more potent.” Its evidence base is overwhelmingly preclinical (antioxidant, Nrf2 induction, amyloid anti-aggregation), with only a small human surrogate-endpoint trial ^{9Reference 92023RCTIngestion of taxifolin-rich foods affects brain activity, mental fatigue and the whole-blood transcriptome in healthy young adults: a randomised crossover trialView study →}; the larch-derived extract does, however, hold EU novel-food authorisation ^{16Reference 16EFSA · 2017Scientific opinion on taxifolin-rich extract from Dahurian larch (Larix gmelinii)View study →}.

1. Antioxidant / cytoprotective

The marquee property. Taxifolin’s catechol B-ring makes it a direct radical scavenger and metal chelator, and it induces the Nrf2/HO-1 antioxidant and phase-II program — for example protecting mice against cyclophosphamide-induced oxidative liver stress ^{6Reference 62023Hepatoprotective effect of taxifolin on cyclophosphamide-induced oxidative stress via Nrf2/HO-1 signallingView study →}. Its saturated C-ring makes it more stable and less pro-oxidant than quercetin under some conditions, though that same feature costs it some scavenging power ^{5Reference 52019Redox properties of individual quercetin moietiesView study →}.

Gap: essentially all outcome data are preclinical — “antioxidant” here is a mechanism and biomarker, not a demonstrated human clinical benefit ^{5,2Reference 52019Redox properties of individual quercetin moietiesView study →Reference 2Das A et al. · 2021ReviewPharmacological basis and new insights of taxifolin: a comprehensive reviewView study →}.

2. Neuroprotective (amyloid)

Taxifolin’s single most-cited finding: it inhibited amyloid-β oligomer formation and fully restored cerebrovascular integrity and memory in a mouse model of cerebral amyloid angiopathy (CAA) ^{7Reference 7Saito S et al. · 2017Taxifolin inhibits amyloid-β oligomer formation and fully restores vascular integrity and memory in cerebral amyloid angiopathyView study →}, and has been reviewed as a candidate CAA therapeutic ^{8Reference 82021Taxifolin: a potential therapeutic agent for cerebral amyloid angiopathyView study →}. A randomised, double-blind, placebo-controlled crossover trial in healthy young adults found taxifolin-rich foods altered brain activity, mental fatigue and the blood transcriptome ^{9Reference 92023RCTIngestion of taxifolin-rich foods affects brain activity, mental fatigue and the whole-blood transcriptome in healthy young adults: a randomised crossover trialView study →}.

Gap: the amyloid data are mouse-only, and the human trial is a small crossover on surrogate/subjective endpoints in healthy people — not a dementia or CAA outcome trial, with delivery the recognised bottleneck ^{7,9Reference 7Saito S et al. · 2017Taxifolin inhibits amyloid-β oligomer formation and fully restores vascular integrity and memory in cerebral amyloid angiopathyView study →Reference 92023RCTIngestion of taxifolin-rich foods affects brain activity, mental fatigue and the whole-blood transcriptome in healthy young adults: a randomised crossover trialView study →}.

3. Anti-inflammatory

Taxifolin suppresses NF-κB signalling and pro-inflammatory cytokines while boosting Nrf2/HO-1 across tissue-injury models ^{6,1Reference 62023Hepatoprotective effect of taxifolin on cyclophosphamide-induced oxidative stress via Nrf2/HO-1 signallingView study →Reference 12026ReviewExploring the therapeutic potential of naturally occurring taxifolin, a dietary flavonoid: an updated comprehensive reviewView study →}.

Gap: preclinical, with no standalone human anti-inflammatory endpoint trial ^{1Reference 12026ReviewExploring the therapeutic potential of naturally occurring taxifolin, a dietary flavonoid: an updated comprehensive reviewView study →}.

4. Metabolic / antidiabetic

Taxifolin improved glycemic control in mice when its bioavailability was engineered (selenized liposomes) ^{12Reference 122025Nanometerising taxifolin into selenized liposomes to ameliorate its hypoglycemic effect by improving bioavailabilityView study →}, and it (and its derivatives) inhibit α-amylase and α-glucosidase in silico and in vitro ^{14Reference 142025In-silico and in-vitro evaluation of flavonoid derivatives for diabetes management (α-amylase/α-glucosidase)View study →}.

Gap: the free molecule’s own effect is limited by poor absorption — the animal benefit largely depends on formulation, and there is no human glycemic trial ^{12,14Reference 122025Nanometerising taxifolin into selenized liposomes to ameliorate its hypoglycemic effect by improving bioavailabilityView study →Reference 142025In-silico and in-vitro evaluation of flavonoid derivatives for diabetes management (α-amylase/α-glucosidase)View study →}.

5. Anticancer

Taxifolin is pro-apoptotic, anti-proliferative and anti-metastatic across cell lines and xenografts, as summarised in a dedicated 2026 review ^{4Reference 42026Taxifolin as a promising anticancer agent: molecular mechanisms and therapeutic potentialsView study →}.

Gap: entirely preclinical, with no human oncology data — the standard “promising in a dish” caveat ^{4Reference 42026Taxifolin as a promising anticancer agent: molecular mechanisms and therapeutic potentialsView study →}.

Mechanisms

Target / pathway	Effect	Relevant to
Direct radical scavenging (catechol B-ring); metal chelation	neutralises ROS; more stable but weaker conjugation than quercetin	antioxidant
Nrf2 / HO-1 induction	↑ endogenous antioxidant + phase-II enzymes	cyto/hepatoprotection, anti-inflammatory
NF-κB suppression	↓ pro-inflammatory cytokine transcription	anti-inflammatory
Amyloid-β oligomer anti-aggregation	blocks Aβ oligomer formation; restores cerebrovascular integrity (mouse)	neuroprotection / CAA
α-amylase / α-glucosidase inhibition (in silico/in vitro)	slows carbohydrate hydrolysis	metabolic
Dihydroflavonol → flavonol (flavonol synthase)	taxifolin is oxidised to quercetin in planta	chemistry / precursor to quercetin

Pharmacokinetics

Load-bearing. Taxifolin shares quercetin’s core problem — low, variable oral bioavailability from poor aqueous solubility and extensive phase-II glucuronidation/sulfation — but its saturated C-ring makes the molecule more chemically and oxidatively stable in solution and storage, which is its main practical advantage ^{2,1Reference 2Das A et al. · 2021ReviewPharmacological basis and new insights of taxifolin: a comprehensive reviewView study →Reference 12026ReviewExploring the therapeutic potential of naturally occurring taxifolin, a dietary flavonoid: an updated comprehensive reviewView study →}. It is a biosynthetic precursor to quercetin (dihydroflavonol → flavonol) in plants ^{3Reference 32025Modern developing directions in the dihydroquercetin studyView study →}. Tellingly, the bulk of recent pharmacokinetic literature is formulation work aimed at fixing absorption — microencapsulation to improve stability and bioaccessibility ^{11Reference 112025Preparation of dihydroquercetin microcapsules to improve stability, solubility and bioaccessibilityView study →}, selenized liposomes to raise bioavailability ^{12Reference 122025Nanometerising taxifolin into selenized liposomes to ameliorate its hypoglycemic effect by improving bioavailabilityView study →}, and nanoparticle, nasal-gel and self-propelled-nanomotor systems ^{10,13Reference 102024Dihydroquercetin nanoparticle nasal gel for the amelioration of Alzheimer’s diseaseView study →Reference 132026Rice-bran-protein self-propelled nanomotors for targeted delivery of dihydroquercetin: anti-atherosclerosisView study →}. The interpretation: free-form oral taxifolin reaches only modest plasma levels, and most efficacy data assume a delivery enhancement not present in a plain capsule.

Clinical trials

The human evidence is thin. The one retrievable quality trial is a randomised, double-blind, placebo-controlled crossover of taxifolin-rich foods in healthy young adults, reporting effects on brain activity, mental fatigue and the blood transcriptome — small, on surrogate/subjective endpoints in a healthy population ^{9Reference 92023RCTIngestion of taxifolin-rich foods affects brain activity, mental fatigue and the whole-blood transcriptome in healthy young adults: a randomised crossover trialView study →}. Regulatory-grade human-relevant documentation exists via EFSA’s novel-food assessment of the larch extract ^{16,17Reference 16EFSA · 2017Scientific opinion on taxifolin-rich extract from Dahurian larch (Larix gmelinii)View study →Reference 17EFSA · 2017Statement on the safety of taxifolin-rich extract from Dahurian larch (Larix gmelinii)View study →}. The historical Russian “Diquertin”/dihydroquercetin clinical usage (cardiovascular, pulmonary) is real in the Russian-language literature but is not represented by retrievable, peer-reviewed, English-indexed trials of adequate quality — treat those claims as unverified. No disease-outcome trial has been verified.

Last checked: July 2026.

Toxicity & Safety

Taxifolin has low toxicity and is well characterised for the larch-derived material: a GLP toxicology and genotoxicity battery on a dihydroquercetin-rich Larix gmelinii extract (Lavitol) found low toxicity and no genotoxicity ^{15Reference 152015Toxicological and genotoxicity assessment of a dihydroquercetin-rich Dahurian larch (Larix gmelinii) extract (Lavitol)View study →}, and EFSA issued a favourable opinion authorising the taxifolin-rich Dahurian-larch extract as a novel food — the closest thing to a “GRAS-adjacent” regulatory standing ^{16,17Reference 16EFSA · 2017Scientific opinion on taxifolin-rich extract from Dahurian larch (Larix gmelinii)View study →Reference 17EFSA · 2017Statement on the safety of taxifolin-rich extract from Dahurian larch (Larix gmelinii)View study →}. Interactions are not well studied: no dedicated human interaction or CYP study is available, so the theoretical additive effects with anticoagulants/antiplatelets or antihyperglycemics, and the generic flavonoid CYP/UGT-competition caution, are extrapolation rather than evidence and should be labelled as such.

Pregnancy & lactation

Not established — avoid concentrated supplements. No reproductive-toxicity or human pregnancy/lactation data have been verified, and the EFSA authorisation does not extend to a demonstrated pregnancy safety margin — so concentrated supplemental taxifolin is best avoided in pregnancy and lactation.

Dosage

There is no established therapeutic dose, and nothing here is a recommendation. Larch dihydroquercetin supplements (e.g. Lavitol / Siberian-larch DHQ) are commonly sold at roughly 25–100 mg/day, with some products and studies using up to a few hundred mg/day; the one human trial delivered taxifolin via taxifolin-rich foods rather than a standardised isolated dose ^{9Reference 92023RCTIngestion of taxifolin-rich foods affects brain activity, mental fatigue and the whole-blood transcriptome in healthy young adults: a randomised crossover trialView study →}. Poor bioavailability means the effective free-form dose is undefined and formulation-dependent.

References