Dihydroquercetin

• Potent antioxidant activity
• Anti-inflammatory effects
• Cardiovascular protection
• Hepatoprotection

• Neuroprotection
• Anti-cancer properties
• Blood glucose regulation
• Immune system modulation
• Skin health and protection
• Anti-viral activity
• Capillary strengthening
• Anti-allergic effects

Dihydroquercetin (taxifolin) exerts its diverse biological effects through multiple molecular mechanisms and signaling pathways. As a potent antioxidant, dihydroquercetin directly scavenges reactive oxygen species (ROS) including superoxide anions, hydroxyl radicals, and peroxynitrite due to its hydroxyl groups at positions 3, 5, 7, 3′, and 4′. This structure allows for efficient electron donation and stabilization of resulting radicals through resonance. Beyond direct scavenging, dihydroquercetin activates the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway by modifying Keap1 cysteine residues, leading to nuclear translocation of Nrf2 and subsequent upregulation of antioxidant enzymes including heme oxygenase-1 (HO-1), NAD(P)H:quinone oxidoreductase 1 (NQO1), glutathione S-transferase (GST), and superoxide dismutase (SOD).

Dihydroquercetin exhibits potent anti-inflammatory properties primarily through inhibition of the nuclear factor-kappa B (NF-κB) signaling pathway. It blocks IκB kinase (IKK) activation, preventing IκB phosphorylation and subsequent NF-κB nuclear translocation, thereby reducing the expression of pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6). Additionally, dihydroquercetin inhibits the NLRP3 inflammasome assembly and activation, reducing IL-1β and IL-18 production. It also suppresses cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) expression, decreasing prostaglandin E2 (PGE2) and nitric oxide (NO) production.

In the cardiovascular system, dihydroquercetin enhances endothelial function by increasing nitric oxide (NO) bioavailability through multiple mechanisms: it upregulates endothelial nitric oxide synthase (eNOS) expression and activity, reduces NO degradation by scavenging superoxide, and prevents eNOS uncoupling by maintaining tetrahydrobiopterin (BH4) levels. Dihydroquercetin inhibits platelet aggregation by antagonizing thromboxane A2 receptors and inhibiting phospholipase C activation. It also improves lipid metabolism by inhibiting HMG-CoA reductase and increasing LDL receptor expression, leading to reduced cholesterol levels. Furthermore, dihydroquercetin strengthens capillaries by inhibiting hyaluronidase and elastase, enzymes that degrade components of the vascular wall.

For hepatoprotection, dihydroquercetin reduces oxidative stress in hepatocytes, inhibits hepatic stellate cell activation (key cells in liver fibrosis), and enhances phase II detoxification enzymes. It also stimulates bile production and flow, facilitating the elimination of toxins and waste products. In the central nervous system, dihydroquercetin provides neuroprotection through multiple mechanisms. It reduces neuroinflammation by inhibiting microglial activation and decreasing pro-inflammatory cytokine production.

Dihydroquercetin attenuates glutamate-induced excitotoxicity by modulating NMDA receptors and maintaining calcium homeostasis. It also inhibits acetylcholinesterase, potentially enhancing cholinergic neurotransmission. Additionally, dihydroquercetin promotes neurogenesis and synaptic plasticity by enhancing brain-derived neurotrophic factor (BDNF) expression. For metabolic regulation, dihydroquercetin improves insulin sensitivity by activating the AMP-activated protein kinase (AMPK) pathway and enhancing glucose transporter type 4 (GLUT4) translocation to the cell membrane.

It inhibits α-glucosidase and α-amylase, reducing carbohydrate digestion and postprandial glucose spikes. Dihydroquercetin also modulates adipocyte differentiation and function through peroxisome proliferator-activated receptor gamma (PPARγ) regulation. Dihydroquercetin’s anticancer properties involve multiple mechanisms: induction of apoptosis through both intrinsic (mitochondrial) and extrinsic (death receptor) pathways, cell cycle arrest primarily at G1/S and G2/M checkpoints, inhibition of angiogenesis by reducing vascular endothelial growth factor (VEGF) expression, and suppression of matrix metalloproteinases (MMPs) to reduce tumor invasion and metastasis. It also inhibits multiple oncogenic signaling pathways including PI3K/Akt/mTOR and MAPK/ERK.

The molecular structure of dihydroquercetin, with its flavanonol backbone and hydroxyl groups, allows it to interact with various cellular receptors, enzymes, and signaling molecules, contributing to its pleiotropic effects. However, its limited water solubility and extensive phase II metabolism (primarily glucuronidation and sulfation) affect its bioavailability and in vivo efficacy.

The optimal dosage of dihydroquercetin (taxifolin) varies based on the specific health condition being addressed and individual factors. Based on available clinical studies and traditional usage, typical dosages range from 50-500 mg daily for adults. For general antioxidant support and health maintenance, lower doses of 50-100 mg daily are often recommended. For specific therapeutic purposes, higher doses of 200-500 mg daily, sometimes divided into 2-3 administrations, may be more appropriate.

Clinical safety studies have tested single doses up to 2800 mg without significant adverse effects, though such high doses are not typically recommended for regular use.

Dihydroquercetin (taxifolin) exhibits relatively poor oral bioavailability, typically ranging from 15-30% in animal studies, with human data suggesting similar limitations. This limited bioavailability is attributed to several factors, including poor water solubility (approximately 0.06 mg/mL), extensive first-pass metabolism in the intestine and liver, and active efflux by P-glycoprotein transporters in the intestinal epithelium. Upon oral administration, dihydroquercetin undergoes extensive phase II metabolism, primarily glucuronidation and sulfation by UDP-glucuronosyltransferases (UGTs) and sulfotransferases (SULTs) in the intestinal epithelium and liver, forming various conjugated metabolites. This pre-systemic metabolism significantly reduces the amount of free dihydroquercetin reaching the systemic circulation.

Pharmacokinetic studies in humans show that dihydroquercetin reaches peak plasma concentrations (Cmax) within 0.5-2 hours after oral administration, with a relatively short plasma half-life of 2-4 hours for the parent compound. The glucuronide and sulfate metabolites often achieve higher plasma concentrations and longer half-lives (6-12 hours) than the parent compound. These metabolites may contribute to the biological effects of dihydroquercetin, as they can be deconjugated back to dihydroquercetin in target tissues by β-glucuronidases and sulfatases, particularly at sites of inflammation where these enzymes are often upregulated. Dihydroquercetin demonstrates moderate tissue distribution, with higher concentrations observed in the liver, kidneys, and lungs.

Limited penetration across the blood-brain barrier has been reported, with brain concentrations typically less than 5% of plasma concentrations, which may affect its efficacy for neurological conditions.

Liposomal encapsulation: Incorporating dihydroquercetin into liposomes has been shown to increase bioavailability by 2-3 fold in animal studies by enhancing solubility, protecting from pre-systemic metabolism, and potentially bypassing efflux transporters, Nanoparticle formulations: Polymeric nanoparticles, solid lipid nanoparticles, and nanoemulsions can improve dihydroquercetin solubility and protect it from metabolism, potentially increasing bioavailability by 3-5 fold, Phospholipid complexes: Forming complexes with phospholipids (phytosomes) increases the lipophilicity of dihydroquercetin, enhancing its ability to cross cell membranes and improving bioavailability by 2-4 fold, Self-microemulsifying drug delivery systems (SMEDDS): These formulations can increase dihydroquercetin solubility and provide a large surface area for absorption, potentially improving bioavailability by 3-6 fold, Spray drying: Spray-dried formulations of dihydroquercetin have shown improved dissolution rates and bioavailability, with studies reporting up to 2.2-fold higher water solubility compared to crystalline forms, Co-administration with P-glycoprotein inhibitors: Natural compounds like quercetin or piperine may reduce efflux and enhance dihydroquercetin absorption, Cyclodextrin inclusion complexes: These can improve dihydroquercetin solubility and stability in the gastrointestinal environment, with β-cyclodextrin showing particular promise, Micronization: Reducing particle size increases the surface area available for dissolution and absorption, Co-administration with fat-soluble vitamins or oils: Taking dihydroquercetin with a small amount of fat may enhance absorption through increased bile secretion and potential lymphatic transport, Amorphous solid dispersions: Converting crystalline dihydroquercetin to amorphous forms using suitable carriers can significantly improve dissolution rates and bioavailability

Due to its relatively poor bioavailability and interaction with food components, the timing of dihydroquercetin administration can significantly impact its absorption and efficacy. Taking dihydroquercetin on an empty stomach (at least 30 minutes before meals or 2 hours after meals) may enhance absorption by minimizing interference from food components and digestive processes. However, some individuals may experience mild gastrointestinal discomfort when taking dihydroquercetin on an empty stomach, in which case taking it with a small amount of fat (such as a teaspoon of olive oil or coconut oil) may improve tolerability while potentially enhancing absorption through increased bile secretion and lymphatic transport. For cardiovascular and antioxidant effects, consistent daily dosing is recommended, with some evidence suggesting that dividing the daily dose into two administrations (morning and evening) may provide more stable plasma levels.

When using dihydroquercetin for liver support, taking it 30 minutes before meals may enhance its hepatoprotective effects by ensuring higher concentrations during nutrient metabolism. Co-administration with vitamin C may enhance the antioxidant effects of dihydroquercetin through synergistic mechanisms, though direct evidence for improved bioavailability is limited. Avoiding simultaneous intake with mineral supplements (particularly iron, calcium, and zinc) is advisable, as these may form complexes with dihydroquercetin and reduce absorption. For individuals taking medications, separating dihydroquercetin administration by at least 2 hours from medication intake may reduce the risk of potential interactions, particularly with drugs that are substrates for P-glycoprotein transporters or those with narrow therapeutic windows.

• Mild gastrointestinal discomfort (nausea, bloating, occasional diarrhea)
• Headache (uncommon)
• Dizziness (rare)
• Dry mouth (uncommon)
• Skin rash or itching (rare, may indicate allergic reaction)
• Fatigue (uncommon)
• Potential mild hypoglycemic effects (more common with higher doses)
• Increased urination (due to mild diuretic effect)

• Known allergy or hypersensitivity to dihydroquercetin, other flavonoids, or source plants (larch, milk thistle, etc.)
• Pregnancy and breastfeeding (due to insufficient safety data)
• Scheduled surgery (discontinue at least 2 weeks before due to potential effects on blood clotting)
• Bleeding disorders (due to potential anticoagulant and antiplatelet effects)
• Severe liver or kidney disease (due to limited data on metabolism and elimination in these conditions)
• Hypoglycemia or poorly controlled diabetes (due to potential glucose-lowering effects)
• Children under 18 years (due to insufficient safety data)

• Anticoagulant and antiplatelet medications (may have additive effects on blood clotting, increasing bleeding risk)
• Hypoglycemic medications (may enhance blood glucose-lowering effects, potentially causing hypoglycemia)
• Medications metabolized by cytochrome P450 enzymes, particularly CYP1A2 and CYP3A4 (dihydroquercetin may inhibit these enzymes, potentially increasing blood levels of affected drugs)
• Medications transported by P-glycoprotein (dihydroquercetin may compete for the same transport mechanisms, affecting drug absorption and elimination)
• Diuretic medications (may have additive effects on urine output)
• Medications with narrow therapeutic windows (warfarin, digoxin, lithium, etc.) should be used with caution due to potential interactions
• Immunosuppressant medications (theoretical concern for interference with therapeutic effects due to immunomodulatory properties)
• Hormone replacement therapy or hormonal contraceptives (theoretical interaction due to potential effects on hormone metabolism)

No established upper limit has been determined for dihydroquercetin in humans. Clinical studies have tested single doses up to 2800 mg and multiple doses up to 600 mg daily for several weeks without serious adverse effects. However, these studies were conducted in healthy volunteers under controlled conditions and for relatively short durations. Based on available research and the traditional use of dihydroquercetin-containing extracts, a conservative upper limit for regular daily use would be approximately 500-700 mg of purified dihydroquercetin for adults.

For larch extracts standardized to contain 80-95% dihydroquercetin, an upper limit of 600-800 mg of extract daily would be reasonable. However, these are theoretical limits based on limited data, and individual sensitivity may vary. As with any supplement, it is advisable to start with lower doses and gradually increase as tolerated, particularly for individuals with sensitive systems or pre-existing health conditions. Long-term safety studies (>1 year) are lacking, suggesting caution with extended use at high doses.

In the United States, dihydroquercetin (taxifolin) is not approved as a drug by the FDA for any specific indication. It may be sold as a dietary supplement ingredient under the Dietary Supplement Health and Education Act (DSHEA) of 1994, provided it meets the definition of a dietary ingredient and was not first marketed as a drug. As a supplement ingredient, dihydroquercetin or extracts standardized for dihydroquercetin content cannot make claims to diagnose, treat, cure, or prevent any disease. Structure/function claims (e.g., ‘supports antioxidant defenses’) are permitted with appropriate disclaimer statements.

The FDA has not established a specific regulatory framework or monograph for dihydroquercetin. Larch tree extracts and milk thistle extracts, which contain dihydroquercetin, are generally recognized as safe (GRAS) for use in dietary supplements and have a long history of use in traditional medicine.

Eu: In the European Union, dihydroquercetin from Dahurian Larch (Larix gmelinii) was approved as a Novel Food ingredient in 2012 by the European Food Safety Authority (EFSA). It is authorized for use in food supplements at a maximum dose of 100 mg per day and in non-alcoholic beverages, yogurt, and chocolate confectionery at specified levels. This approval followed extensive safety assessments and toxicological studies. For medicinal purposes, dihydroquercetin is not approved as a medicinal product by the European Medicines Agency (EMA), though it may be present in traditional herbal medicinal products, particularly those containing milk thistle, subject to national regulations in individual member states.

Russia: In Russia, dihydroquercetin has the most advanced regulatory status. It is approved as both a pharmaceutical ingredient and a food additive. As a pharmaceutical, it is included in several registered medications for cardiovascular conditions, liver protection, and as an antioxidant therapy. As a food additive, it is approved for use as a preservative (E161q) and functional ingredient in various food products. Russia has established specific quality standards for dihydroquercetin in its pharmacopeia, with requirements for purity, identification, and standardization. The extensive research and development of dihydroquercetin in Russia has led to its widespread use in both medical and food applications.

Canada: Health Canada has not approved dihydroquercetin as a prescription drug. Larch extracts and milk thistle extracts containing dihydroquercetin may be sold as Natural Health Products (NHPs) with appropriate licenses, though specific claims are limited and must be supported by evidence. Health Canada has not established specific monographs or regulatory frameworks specifically for purified dihydroquercetin, though it is included as a component in the milk thistle monograph.

Australia: The Therapeutic Goods Administration (TGA) has not approved dihydroquercetin as a prescription medicine in Australia. Larch extracts and milk thistle extracts are recognized in the TGA’s list of permitted ingredients for listed medicines. Products containing these extracts standardized for dihydroquercetin content may be sold as listed complementary medicines, subject to quality and safety requirements. Specific therapeutic claims require higher levels of evidence and appropriate registration.

Japan: In Japan, dihydroquercetin is not approved as a pharmaceutical drug. It may be present in Foods with Health Claims under appropriate categories if they meet the established requirements, though specific approved claims for dihydroquercetin have not been established. Milk thistle extracts containing dihydroquercetin are used in various health food products.

Purified dihydroquercetin (≥95% purity) has a moderate to high relative cost compared to many common dietary supplements, though it is generally less expensive than some other specialized flavonoids. The cost is primarily influenced by the extraction and purification processes required, as well as the limited number of commercial producers, most of which are based in Russia and China. Standardized larch extracts with specified dihydroquercetin content (typically 80-95%) have a medium relative cost, more accessible than purified dihydroquercetin but higher than many common herbal supplements. Milk thistle extracts, which contain dihydroquercetin as part of the silymarin complex, have a low to medium relative cost and represent the most economical way to obtain some dihydroquercetin, albeit in lower and less standardized amounts.

Novel delivery systems designed to enhance bioavailability, such as liposomal or nanoparticle formulations, typically command premium prices, though they may potentially deliver more bioavailable dihydroquercetin.

For purified dihydroquercetin (≥95% purity), the cost per effective daily dose (100-300 mg) typically ranges from $1-3, making

it moderately expensive for long-term use but still accessible compared to many pharmaceutical options. For standardized larch extracts (80-95% dihydroquercetin), the cost per effective daily dose (providing approximately 100-300 mg of dihydroquercetin) ranges from $0.70-2.00, representing a more economical option with similar benefits. For milk thistle extracts standardized for silymarin content (which includes dihydroquercetin), the cost per daily dose (providing approximately 20-50 mg of dihydroquercetin as part of the silymarin complex) ranges from $0.30-1.00, though the dihydroquercetin content is lower and less standardized. Enhanced delivery systems such as liposomal formulations typically cost $2-5 per daily dose, though

they may potentially deliver more bioavailable dihydroquercetin, potentially improving the cost-to-benefit ratio

despite the higher price point.

The value proposition of dihydroquercetin varies significantly depending on the form, intended use, and individual health considerations. For general antioxidant support and preventive health maintenance, standardized larch extracts offer the best balance of cost and efficacy, providing reliable amounts of dihydroquercetin at a reasonable price point. For specific therapeutic purposes, particularly cardiovascular and liver support, purified dihydroquercetin may offer superior value despite its higher cost, as the precise dosing and higher purity may be important for achieving desired outcomes. Milk thistle extracts provide good value for liver-specific applications, as the combination of dihydroquercetin with other silymarin components offers synergistic benefits specifically for hepatic health.

For individuals with absorption challenges or those seeking maximum efficacy, enhanced delivery systems may justify their premium pricing through improved bioavailability, though more clinical research is needed to definitively establish their superior value. When comparing dihydroquercetin to other antioxidant supplements, it offers competitive value due to its multiple mechanisms of action and diverse health benefits beyond simple antioxidant activity. Its strong safety profile also enhances its value proposition, as the risk-to-benefit ratio is favorable even with long-term use. For specific conditions with stronger research support, such as cardiovascular protection and liver support, the value proposition improves further, as the potential health benefits may offset the moderate cost.

Future developments in production technology and increased competition may improve the cost-efficiency of dihydroquercetin supplements, making them more accessible to a broader population.

Purified dihydroquercetin in crystalline powder form, when properly stored, typically has a shelf life of 2-3 years. Amorphous or spray-dried forms may have shorter shelf lives of 1-2 years due to their higher reactivity, though this can be extended with appropriate stabilizers and packaging. In standardized extracts, the shelf life is generally 1-2 years, depending on the specific formulation and storage conditions. Liquid formulations containing dihydroquercetin tend to have shorter shelf lives of approximately 1 year due to increased potential for oxidation and degradation.

Novel formulations such as liposomal or nanoparticle preparations may have different stability profiles and should be evaluated on a case-by-case basis. The shelf life can be significantly reduced by improper storage conditions, particularly exposure to heat, light, moisture, or oxygen.

Purified dihydroquercetin powder should be stored in airtight, opaque containers protected from light, heat, moisture, and oxygen. Optimal storage temperature is between 2-8°C (refrigerated), though room temperature storage (15-25°C) is acceptable for short periods if humidity is controlled. Desiccants should be used in the container to minimize moisture exposure. For standardized extracts containing dihydroquercetin, storage in tightly sealed, opaque containers at room temperature (15-25°C) away from direct sunlight is generally sufficient.

Liquid formulations may require refrigeration after opening to prevent oxidation and microbial growth. Freeze-thaw cycles should be avoided for all formulations as they can accelerate degradation. For long-term storage of research-grade material, storage at -20°C under inert gas (nitrogen or argon) is recommended. Once a container is opened, it’s advisable to use the product within 6 months, even if the overall shelf life is longer, as exposure to air accelerates oxidation.

Amorphous or spray-dried forms require particularly careful storage to maintain their physical state and enhanced dissolution properties, with controlled humidity being especially important.

Oxidation: Dihydroquercetin is susceptible to oxidation due to its multiple hydroxyl groups, particularly in the presence of oxygen, light, or catalytic metal ions, Light exposure: UV and visible light can accelerate the degradation of dihydroquercetin through photo-oxidation processes, Heat: Temperatures above 40°C significantly accelerate degradation through multiple mechanisms, Moisture: High humidity environments can promote hydrolysis and may facilitate microbial growth in formulations, Alkaline pH: Dihydroquercetin is more stable in slightly acidic to neutral conditions (pH 5-7) and may degrade more rapidly in alkaline environments, Metal ions: Certain metal ions, particularly iron and copper, can catalyze oxidative degradation, Microbial contamination: Certain microorganisms can enzymatically degrade dihydroquercetin, Enzymatic degradation: Exposure to specific enzymes, particularly oxidases, can accelerate degradation, Physical state changes: Amorphous forms can recrystallize under certain conditions, potentially affecting dissolution properties and bioavailability, Incompatible excipients: Some pharmaceutical excipients may interact with dihydroquercetin and reduce stability, Freeze-thaw cycles: Repeated freezing and thawing can disrupt the physical structure of formulations and accelerate chemical degradation

Synthesis Methods

Natural Sources

Quality Considerations

While dihydroquercetin (taxifolin) itself was not specifically identified or isolated until modern times, its primary natural sources have rich histories of traditional use across various cultures. Larch trees (Larix species), the primary commercial source of dihydroquercetin today, have been used medicinally by indigenous peoples of Siberia, the Russian Far East, and Northern Europe for centuries. The Siberian and Dahurian larch trees were particularly valued by native Siberian tribes, who prepared decoctions from the bark and resin to treat respiratory conditions, infections, and wounds. These preparations were also used to enhance overall vitality and resistance to harsh environmental conditions.

The resin, known as ‘Siberian Venice turpentine,’ was applied topically for skin conditions and wounds, while tea made from the needles and young shoots was consumed for respiratory ailments and as a general tonic. In traditional Russian folk medicine, larch preparations were used to strengthen blood vessels, improve circulation, and treat inflammatory conditions. The bark was also used to make a reddish-brown dye, which incidentally contained significant amounts of dihydroquercetin. Milk thistle (Silybum marianum), another source of dihydroquercetin as part of its silymarin complex, has an even longer documented history of medicinal use dating back over 2,000 years.

Ancient Greek and Roman physicians, including Dioscorides and Pliny the Elder, documented its use for liver and biliary disorders. In medieval Europe, milk thistle was widely used for liver ailments, jaundice, and gallbladder problems. The seeds were also used to stimulate milk production in nursing mothers, which gave the plant its common name. In traditional Chinese medicine, milk thistle was classified as a liver-protective herb and used to clear ‘heat’ and resolve ‘toxicity.’ In Native American traditions, certain tribes used milk thistle for similar purposes, particularly for liver conditions and as a spring tonic.

Douglas fir (Pseudotsuga menziesii), another source of dihydroquercetin, was used extensively by indigenous peoples of the Pacific Northwest. The Coast Salish, Haida, and other tribes prepared medicinal teas from the needles and bark for respiratory conditions, rheumatism, and as a general tonic. The pitch was applied topically for wounds and skin conditions. The scientific identification and isolation of dihydroquercetin began in the mid-20th century, with significant research emerging in the 1970s and 1980s, particularly in Russia and Eastern Europe.

Russian scientists pioneered much of the early research on dihydroquercetin extracted from Siberian larch, documenting its antioxidant, capillary-strengthening, and hepatoprotective properties. In the 1990s and early 2000s, commercial production of purified dihydroquercetin from larch trees began in Russia, with products like Lavitol gaining popularity as dietary supplements. In recent decades, scientific interest in dihydroquercetin has expanded globally, with research exploring its potential applications in pharmaceuticals, nutraceuticals, cosmetics, and food preservation. Today, while purified dihydroquercetin represents a bridge between traditional herbal medicine and modern pharmacological approaches, many people still consume it in its traditional forms through larch and milk thistle preparations, embodying the ongoing evolution of traditional knowledge through scientific investigation.

No comprehensive meta-analyses specifically focused on dihydroquercetin (taxifolin) in human clinical trials have been published to date. Most systematic reviews have examined flavonoids as a class or focused on quercetin rather than its dihydro form., A systematic review by Das et al. (2021) in Biomedicine & Pharmacotherapy examined the pharmacological basis and therapeutic potential of taxifolin across multiple health conditions, concluding that it shows promising effects for cardiovascular, hepatic, and neurological conditions, though noting the need for more rigorous clinical trials., Liu et al. (2023) published a comprehensive review in Frontiers in Pharmacology analyzing novel therapeutic potentials of taxifolin, with particular emphasis on recent (2019-2022) breakthroughs in various body systems. The review highlighted strong preclinical evidence but identified gaps in clinical research that need to be addressed.

Several clinical trials investigating dihydroquercetin (taxifolin) are ongoing, primarily in Russia, China, and Eastern European countries, for conditions including cardiovascular disease, metabolic syndrome, and liver disorders., Research is actively exploring novel delivery systems to improve the bioavailability of dihydroquercetin, including nanoparticle formulations, liposomal encapsulation, and spray-dried amorphous forms., Preclinical research continues to investigate dihydroquercetin’s potential in neurodegenerative diseases, cancer prevention, and as an adjunct to conventional therapies for various conditions., Studies examining the synergistic effects of dihydroquercetin with other natural compounds and conventional medications are underway, aiming to develop more effective therapeutic combinations., Investigations into the potential role of dihydroquercetin in viral infections, including respiratory viruses, have gained momentum following preliminary evidence of its antiviral and immunomodulatory properties.