dihidromiricetina

Dihydromyricetin (DHM / DMY): A Comprehensive Reference

1. Identity, Chemical Profile, and Natural Sources

Names and Classification

Dihydromyricetin (DHM or DMY) is a flavonoid derived from natural sources with a range of confirmed biological benefits. It is also widely known by the synonym ampelopsin. Its systematic IUPAC name is (2R,3R)-3,5,7-trihydroxy-2-(3,4,5-trihydroxyphenyl)-2,3-dihydrochromen-4-one, and it belongs to the flavanonol subgroup of flavonoids (PubChem CID: 161557 and ChEBI: 28429). It is a polyphenolic hydroxy dihydroflavanol with a molecular weight of 320.25 g/mol and a molecular formula of C₁₅H₁₂O₈. Its CAS number is 27200-12-0.

Botanical Sources

DHM is a flavonoid extracted from the young stems and leaves of Ampelopsis grossedentata. DHM is also widely distributed in plants such as grapes, mulberries, and ginkgo biloba. Particularly high concentrations are found in vine tea, reaching up to 30–40%. Dihydromyricetin can also be found in Cedrus deodara (Deodar cedar), the Japanese raisin tree (Hovenia dulcis), Erythrophleum africanum, and vine tea extract. Other natural sources include Myrica rubra (Chinese bayberry, also called Japanese bayberry, red bayberry, yumberry, or waxberry). Hovenia dulcis is a natural source for dihydromyricetin, which is primarily found in the tree's leaves, stems, and bark.

Physical and Chemical Properties

The compound appears as a pale yellow to white powder or crystal; its solubility in water at 25°C is approximately 4%; it is fully soluble in boiling water; easily soluble in acidic solution, ethanol, and acetone; and only slightly soluble in acetic ether. It is stable in heat up to a point, but when heated above 100°C it is irreversibly oxidized; it is stable in acidic and neutral conditions. The compound exists in two principal stereoisomeric forms; the active compound was identified as 2R,3R-dihydromyricetin from pine needles of Cedrus deodara based on mass spectrometry and NMR data.

Commercial Forms and Preparations

DHM is an important plant flavonoid that has received great attention due to its health-benefiting activities, including antioxidant, antimicrobial, anti-inflammatory, anticancer, antidiabetic, and neuroprotective activities. DHM capsules have been sold in the US as a nutraceutical supplement to prevent alcoholic hangovers. DHM is marketed as a dietary supplement in the United States and is not regulated by the Food and Drug Administration (FDA) as a drug. Commercially, it is available in standardized extract capsules (typically 98% purity by HPLC), as a component in functional beverages, and as powdered vine tea extract at lower standardizations. A major disadvantage associated with DHM is its chemical instability and poor bioavailability caused by combined effects of its low solubility. Researchers have explored nanoparticle delivery systems, phospholipid complexes, and sustained-release tablets as strategies to improve oral absorption.

2. Traditional and Historical Use

Traditional Chinese Medicine

Hovenia dulcis has been used for centuries in Traditional Chinese Medicine as a remedy for alcohol poisoning and hangover, and it is listed among the premier liver herbs and anti-hangover remedies in the Chinese pharmacopoeia, including the Tang Materia Medica. In the Materia Medica Compendium (A.D. 1578), Hovenia dulcis is listed as a TCM with anti-alcoholic properties. Chinese herbal texts from the Tang dynasty mention it under the name "zao jiao guo," praising its warming sweet-energy and "liver-clearing" prowess to relieve summer heat and alcohol overindulgence.

In ancient Chinese medicine, the fruits and pedicels were also used as a febrifuge and administered for parasitic infections, as an antispasmodic, laxative, and diuretic. The seeds were used as a diuretic and were also effective in alcoholism.

Korean and Japanese Traditional Medicine

Hovenia dulcis has been used in traditional Chinese, Korean, and Japanese medicines to treat fever, parasitic infection, as a laxative, and as a treatment of liver diseases and as a hangover treatment. Hovenia dulcis has a storied background tracing back over a thousand years across China, Korea, and Japan.

Vine Tea Use in Southern China

Ampelopsis grossedentata W.T. Wang is a medicinal and edible plant widely distributed in southern China, and its tender stems and leaves have been used as medicinal tea for the prevention and treatment of common cold, sore throat, and icteric viral hepatitis for hundreds of years. Vine tea is called "dragon-boat tea" or "dragon-whisker tea," made from the young stems and leaves of Ampelopsis grossedentata, a plant growing at 1,300–1,950 m in hillside shrubs or valley woodland, and has long been considered a legendary healthy tea.

3. Key Constituents and Phytochemistry of Source Plants

The chemical components of Hovenia dulcis include DHM, quercetin, naringenin, and others. Research on the chemical composition of Hovenia dulcis has documented a total of 44 species, including flavonoids, triterpenoid saponins, and alkaloids; flavonoids constitute up to 27.61% as the main bioactive components. Key identified bioactive constituents of Hovenia dulcis include DHM (a flavanonol known for hepatoprotective and hangover-relief effects), myricetin (a flavonol with antioxidant, anti-inflammatory, and potential cardioprotective action), quercetin derivatives (contributing to free-radical scavenging), hovenodulin (a novel phenolic glycoside from the bark with preliminary in vitro anti-inflammatory activity), and polysaccharides found in the fruit stalk mucilage with potential mild immunomodulatory activity.

Within Ampelopsis grossedentata, DHM is the dominant bioactive compound. Particularly high concentrations are found in vine tea, reaching up to 30–40%.

4. Mechanisms of Action

GABA_A Receptor Modulation

Dihydromyricetin is a natural bioactive flavonoid with unique GABA_A receptor activity with a putative mechanism of action to reduce the intoxication effects of ethanol. DHM counteracts acute ethanol intoxication in a dose-dependent manner and effectively ameliorates ethanol withdrawal symptoms such as anxiety and hyperexcitability; the molecular mechanism is attributed to antagonizing GABA_A receptor potentiation and positively modulating GABA_A receptors at benzodiazepine sites in the hippocampus. DHM's protection against alcohol toxicity in cell models appears to be mediated primarily via the benzodiazepine receptor site of the GABA_A receptor.

Enhanced Ethanol Metabolism

DHM alleviated ethanol intoxication as evidenced by findings that DHM increased the expression of ethanol-metabolizing enzymes, reduced the levels of circulating ethanol and acetaldehyde, and reversed ethanol-mediated depletion of nicotinamide adenine dinucleotide (NAD+). The enhancement of ethanol metabolic activity is likely contributed to by the hepatic increase of nicotinamide adenine dinucleotide (NAD), a cofactor required for ethanol metabolism; additionally, the collective effects of DHM increase antioxidant enzymes and induce AMP-activated protein kinase (AMPK) metabolic signaling, thereby resulting in reduced steatosis and inflammation.

AMPK Pathway Activation

DHM displays hypoglycemic effects via improving glucose and lipid metabolism, attenuating inflammatory responses, and reducing oxidative stress, with signal transduction pathways underlying the regulation of AMPK or mTOR/autophagy, and relevant downstream cascades, including PGC-1α/SIRT3, MEK/ERK, and PI3K/Akt signaling pathways.

Anti-Inflammatory Mechanisms

DHM exhibits anti-inflammatory, antioxidant, anti-tumor, and anti-viral activities. Mechanistically, DHM can effectively regulate mammalian target of rapamycin (mTOR), noncoding RNA-mediated signaling, phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway, nuclear factor-κB (NF-κB), p53, and endoplasmic reticulum stress-driven signaling in different types of cancers.

Antioxidant Activity

The compound exhibits antioxidant activity attributed to its hexahydroxylated polyphenolic structure. In addition to its impact on numerous signaling pathways associated with inflammation and oxidative stress, DHM regulates various cell death modes, including apoptosis, autophagy, pyroptosis, and ferroptosis.

Neuroprotective Mechanisms

In vitro and in vivo studies have revealed DHM's substantial antioxidant, anti-inflammatory, and neuroprotective properties, making it a promising candidate for the treatment of central nervous system disorders. DHM exhibits antioxidant, anti-inflammatory, and neuroprotective properties and has shown therapeutic promise in Alzheimer's disease research. DHM has been identified as a positive allosteric modulator of GABA_A receptors, which may help to restore the excitatory-inhibitory balance in the Alzheimer's disease brain.

5. Scientific Evidence by Area of Use

5.1 Alcohol Intoxication and Alcohol Use Disorder

Preclinical Evidence

In rats given intraperitoneal injections of DHM, animals had decreased voluntary intake of alcohol, less evidence of alcohol central nervous system effects, and fewer signs of subsequent alcohol withdrawal; the effects were attributed to DHM's effects on GABA signaling. Dihydromyricetin at 50 mg/kg intraperitoneally administered 0 or 15 minutes prior to ethanol significantly reduced ethanol-induced loss of righting reflex in mice.

Shen and colleagues found that DHM potentiates GABA_A receptors and reduces the effects of ethanol on those same receptors; this activity resulted in a DHM reduction of ethanol intoxication as well as a reduction of alcohol withdrawal syndrome in rats.

Human/Clinical Evidence

While DHM has been used for herbal tea in traditional Chinese medicine for hundreds of years, and there has been a small clinical trial using DHM in China among individuals with non-alcoholic fatty liver disease, there have been no controlled human studies published that have assessed the safety, pharmacokinetics, or optimal dosing of DHM in humans specifically for alcohol use disorder. A first-in-human Phase 1 open-label, dose-escalation study has been designed to assess the safety, pharmacokinetics, and the maximum tolerated dose of DHM among healthy volunteers using a purified form of DHM from a cGMP compliant source (NCT05623501). The clinical evidence base for DHM in human alcohol intoxication and alcohol use disorder therefore remains very limited, with robust trials yet to be reported.

5.2 Liver Disease: Non-Alcoholic Fatty Liver Disease (NAFLD / MASLD)

Clinical Evidence — NAFLD (2015 RCT)

Investigators examined the effects of dihydromyricetin on glucose and lipid metabolism, inflammatory mediators, and several biomarkers in non-alcoholic fatty liver disease. In a double-blind clinical trial, sixty adult NAFLD patients were randomly assigned to receive either two dihydromyricetin or two placebo capsules (150 mg) twice daily for three months. The serum levels of alanine aminotransferase, aspartate aminotransferase, γ-glutamyl transpeptidase, glucose, LDL-cholesterol, apolipoprotein B, and the homeostasis model assessment of insulin resistance (HOMA-IR) index were significantly decreased in the dihydromyricetin group compared with the placebo group. The investigators concluded that DHM supplementation improves glucose and lipid metabolism as well as various biochemical parameters in patients with NAFLD, and the therapeutic effects are likely attributable to improved insulin resistance and decreases in serum levels of tumor necrosis factor-alpha, cytokeratin-18, and fibroblast growth factor 21. To the best of the authors' knowledge, this constituted the first randomized, double-blind clinical pilot study that investigated the effects of DHM supplementation on NAFLD.

Clinical Evidence — MASLD (2025 RCT)

In a more recent double-blind, placebo-controlled, randomized clinical trial, adult MASLD patients were randomized to receive a dietary supplement containing DHM at 300 mg/day combined with vitamins C/E and choline (group A), or an identical placebo (group B), for 12 months. Median liver enzymes decreased at 6 or 12 months only in group A; group A compared to group B patients achieved higher 12-month rates of combined alanine aminotransferase/γ-glutamyl transpeptidase normalization. A limitation of this trial is that DHM was administered as part of a multi-ingredient combination, making it impossible to attribute effects to DHM alone.

Preclinical Evidence

Investigations utilizing DHM have demonstrated its ability to alleviate ethanol-induced disruptions in mitochondrial and lipid metabolism, while demonstrating hepatoprotective activity. DHM supplementation could effectively ameliorate the development of NAFLD by inhibiting hepatic lipid accumulation both in HFD-fed wild-type mice and in palmitic acid-induced hepatocytes; mitochondrial dysfunction characterized by ATP depletion and augmented oxidative stress could be reversed by DHM treatment.

Evidence strength: One small double-blind RCT in NAFLD (n=60, 3 months) showed favorable metabolic effects. A second RCT used DHM in combination with other nutrients. The overall clinical evidence is preliminary. The bulk of the mechanistic data comes from animal and cell models.

5.3 Diabetes and Metabolic Syndrome

Clinical Evidence

A study involving supplementation with Ampelopsis grossedentata leaf extract containing 970 mg of dihydromyricetin showed improved glycaemic control in patients with type 2 diabetes mellitus. According to ClinicalTrials.gov (as of 2020), there was one ongoing Phase 2 clinical trial (NCT03606694) testing DHM against metformin for its effects on glycemic control, insulin sensitivity, and insulin secretion in type 2 diabetes mellitus.

Preclinical Evidence

Increasing evidence implicates DHM in hypoglycemic effects in diabetes mellitus via improving glucose and lipid metabolism, attenuating inflammatory responses, and reducing oxidative stress, through AMPK- or mTOR/autophagy-dependent pathways and their downstream cascades including PGC-1α/SIRT3, MEK/ERK, and PI3K/Akt signaling pathways.

Evidence strength: Preclinical evidence is substantial and mechanistically coherent. Human clinical trial data are very limited; according to ClinicalTrials.gov, only four clinical studies have been published on DHM against human diseases to date, and clinical studies of DHM are very limited, as the low bioavailability of DMY is a challenge.

5.4 Neurology: Alzheimer's Disease, Parkinson's Disease, and Other CNS Conditions

Alzheimer's Disease

The neurological phenotype of Alzheimer's disease, involving a loss of cognition often in combination with neuropsychiatric features such as seizures and anxiety, suggests there may be an underlying dysfunction in inhibitory GABAergic neurotransmission. DHM has been identified as a positive allosteric modulator of GABA_A receptors, which may help to restore the excitatory-inhibitory balance in the AD brain. DHM exerts a protective role in AD via upregulation of the AMPK/SIRT1 pathway to inhibit inflammatory responses and hippocampal cell apoptosis and ameliorate cognitive function in animal models. Neurological disorders including Alzheimer's disease, Parkinson's disease, and stroke significantly affect the quality of life of patients, and available treatments have poor or limited efficacy.

General Neuroprotection

Analyses of DHM's most important effects include its antioxidant, anti-inflammatory, and neuroprotective effects, as well as its ability to restore GABA neurotransmission and improve motor and cognitive behavior in animal models. Reviews suggest that DHM possesses significant potential for the management of neurological disorders.

Evidence strength: All neuroprotection evidence is preclinical (animal and cell models). No human clinical trials on DHM for cognitive disorders have been published as of the sources reviewed. Current research on DHM remains primarily at the cellular and animal levels, with very few reported clinical studies.

5.5 Cardiovascular Disease

DHM has the effects of cardioprotection, anti-diabetes, hepatoprotection, neuroprotection, anti-tumor, and dermatoprotection. Research found that DHM inhibited p53 activation, regulated Bcl-2 and Bax, reduced cytochrome c release, and suppressed caspase-9/3 expression and PARP cleavage in human umbilical vein endothelial cells, suggesting that DMY is a promising agent for prevention or treatment of cardiovascular diseases.

Evidence strength: Preclinical only. No published human clinical trials specifically for cardiovascular endpoints have been identified in the peer-reviewed sources reviewed.

5.6 Cancer

Dihydromyricetin, a natural flavonoid with various beneficial biological activities, has significantly progressed in its role and mechanism in cancer prevention research. Mechanistically, DHM can effectively regulate mTOR, noncoding RNA-mediated signaling, the PI3K/Akt pathway, NF-κB, p53, and endoplasmic reticulum stress-driven signaling in different types of cancers. DHM has synergistic anti-tumor activity when used with irinotecan in mouse models of colon cancer, but did not potentiate the anti-tumor activity of the chemotherapeutic gemcitabine.

Evidence strength: All available cancer evidence is in vitro or from animal models. No human clinical trials for oncological indications have been reported in the reviewed peer-reviewed literature.

5.7 Alcoholic Liver Disease

DHM administration has been found to reduce ethanol-dependent lipid accumulation in the liver via mechanisms of increased autophagy and reducing inflammatory responses. The collective effects of DHM increase antioxidant enzymes and induce AMPK metabolic signaling, resulting in reduced steatosis and inflammation. Collectively, DHM shows significant preclinical effects in reducing alcohol-related liver injury and damage.

Evidence strength: Preclinical animal and cell model data are robust. No published human-controlled trials specifically for alcohol-associated liver disease (ALD) have been completed, though a Phase 1 dose-escalation trial (NCT05623501) is registered for this indication.

6. Body Systems and Health Areas of Association

• Hepatic/Digestive system: DHM has been studied for pharmacological properties and mechanisms in the digestive system. Hepatoprotection, modulation of lipid and glucose metabolism in the liver, antifibrotic potential, and modification of gut microbiota composition have all been investigated.
• Nervous system: DHM's pharmacological properties and mechanisms in the nervous system have been reviewed. GABA_A receptor modulation, neuroprotection, anti-neuroinflammation, and behavioral effects in models of addiction, neurodegeneration, and anxiety have been studied.
• Cardiovascular system: DMY has effects of cardioprotection studied in cell and animal models, including protection of vascular endothelium from oxidative injury.
• Urinary system: DHM's pharmacological properties in the urinary system have been examined, including nephroprotective effects in models of cisplatin-induced acute kidney injury.
• Metabolic/Endocrine system: Anti-diabetic effects and insulin sensitization via AMPK and related pathways have been documented preclinically and in limited human trials.
• Respiratory system: DMY was also applied for conditions such as bacterial infection, osteoporosis, asthma, and kidney injury.
• Oncology: Anti-tumor activity has been investigated in multiple cancer cell lines via several molecular pathways.

7. Dosage Forms and Reported Dosages

DHM is available commercially in the following forms: standardized extract capsules (typically 90–98% DHM by HPLC), vine tea extract powder (lower DHM content), and as an ingredient in multi-component dietary supplements and functional beverages.

The following dosages are drawn directly from published studies and registered trials:

• In a double-blind clinical trial in NAFLD patients, the dose was two 150 mg capsules twice daily (600 mg/day) for three months.
• In a 12-month MASLD trial, the intervention arm received a dietary supplement containing DHM at 300 mg/day alongside vitamins C/E and choline.
• A study supplementing with Ampelopsis grossedentata leaf extract containing 970 mg of dihydromyricetin was used in patients with type 2 diabetes mellitus.
• In mouse studies, DHM at 50 mg/kg intraperitoneally administered prior to ethanol significantly reduced ethanol-induced loss of righting reflex.

Clinical studies of DMY are very limited; the low bioavailability of DMY presents a challenge, and the "dose-time-toxic-function" relationship of DMY remains unclear. No widely accepted or regulatory-approved human dosage recommendation exists.

8. Pharmacokinetics and Bioavailability

The pharmacokinetic parameters of DHM have so far been identified in rats after oral administration, indicating that DHM is poorly absorbed into the bloodstream, with a bioavailability of only 4.02%. The time required to reach peak plasma concentration is 2.67 hours after oral administration at a dose of 20 mg/kg. The mean residence time (MRT) for the intravenous group and the oral group were 2.62 ± 0.36 h and 5.98 ± 0.58 h, respectively; the AUC(0-t) values were 410.73 ± 78.12 and 164.97 ± 41.76 ng·L/mL respectively, yielding an absolute bioavailability of 4.02%, which was poor.

A major obstacle to DHM's clinical efficacy is its suboptimal pharmacokinetic properties, especially when targeting CNS effects. As with most flavonoids, DHM is poorly absorbed into the bloodstream when taken orally, with a short, variable half-life that is not consistent with reliable clinical efficacy. The poor bioavailability of DHM is linked to its multiple hydroxyl substituents, resulting in a high polar surface area (PSA = 147), well outside the ideal for drug candidates.

Dihydromyricetin was detected in brain tissue following both oral and intraperitoneal administration at 15 minutes post-administration. DHM was not detected in brain samples 45 minutes or longer post oral or intraperitoneal administration, indicating a very short window of CNS exposure.

Since low bioavailability limits the pharmacologic value, several research groups have made diverse preparations with better solubility or permeability, mainly tested in in vitro studies. Approaches under investigation include nanoparticle encapsulation, phospholipid complexation, and gastric floating sustained-release tablets.

9. Safety Considerations and Drug Interactions

General Toxicity Profile

DHM is nearly non-toxic and demonstrates an excellent safety profile. At concentrations ranging from 150 mg/kg to 1.5 g/kg, DHM did not cause any acute toxicity or significant side effects in mice; this suggests that DHM has very low toxicity; however, more in vitro and in vivo tests are needed to establish reliable safety limits. DHM has not been reported to be toxic in the conventional dose range; there is no significant change in physiological indexes such as body weight and temperature after oral administration of 150–1500 mg/kg DHM in rats. No obvious cytotoxicity of DHM has been found in normal cells, which indicates its high biosafety.

Clinical Safety Record

DHM has a good safety record in short-term RCTs and animal studies, which may be due to low bioavailability. A systematic compilation of all publications on the hepatotoxicity of specific herbal products identified 185 publications on 60 different herbs, herbal drugs, and supplements but does not list or mention DHM, indicating an absence of documented hepatotoxicity cases in the literature reviewed up to that date.

CYP450 Enzyme Inhibition and Drug Interaction Potential

The inhibitory effects of DHM were investigated on eight human liver CYP isoforms in vitro using human liver microsomes. The results showed that DHM could inhibit the activity of CYP3A4, CYP2E1, and CYP2D6, with IC₅₀ values of 14.75, 25.74, and 22.69 μM, respectively, while other CYP isoforms were not affected. Enzyme kinetic studies showed that DHM was a non-competitive inhibitor of CYP3A4 and a competitive inhibitor of CYP2E1 and CYP2D6, with Ki values of 6.06, 9.24, and 10.52 μM, respectively. DHM is also a time-dependent inhibitor of CYP3A4. In vitro studies indicate that DHM has the potential to cause pharmacokinetic drug interactions with other co-administered drugs metabolized by CYP3A4, CYP2E1, and CYP2D6; further clinical studies are needed to evaluate the significance of this interaction.

Pharmacokinetic properties may differ across patient populations, and DHM may have drug interactions due to projected CYP inhibition activity. In vitro inhibition at the concentrations tested may not translate directly to clinically relevant interactions at doses achievable through oral supplementation, given DHM's poor oral bioavailability; however, this has not been formally confirmed in vivo.

Stability Limitations

The main factors affecting the development and utilization of dihydromyricetin include its stability and relatively low bioavailability. Chemical oxidation above 100°C and instability under certain conditions may reduce effective compound delivery.

Overall Limitations of the Evidence Base

Current research on DHM remains primarily at the cellular and animal levels, with very few reported clinical studies. This limitation may arise from the instability and relatively low bioavailability of DHM. Further comprehensive mechanistic and toxicological studies are essential to advance our understanding of DMY's effects. For all areas of use discussed in this article outside of the NAFLD and diabetes clinical trials, the available evidence is preclinical and should not be extrapolated to established human efficacy.

References

• He C, et al. "Dihydromyricetin: an emerging compound with comprehensive effects on multiple systems." Frontiers in Pharmacology, 2025. PMC11739078
• Xian T, et al. "Dihydromyricetin: A review on identification and quantification methods, biological activities, chemical stability, metabolism and approaches to enhance its bioavailability." PMC7127391
• Jiang S, et al. "Recent Update on the Pharmacological Effects and Mechanisms of Dihydromyricetin." PMC6209623
• Moradian R, et al. "Identification of Dihydromyricetin and Metabolites in Serum and Brain Associated with Acute Anti-Ethanol Intoxicating Effects in Mice." PMC8307506
• Silva J, et al. "Dihydromyricetin Protects the Liver via Changes in Lipid Metabolism and Enhanced Ethanol Metabolism." Alcoholism: Clinical and Experimental Research, 2020. PMC7211127
• National Institute of Diabetes and Digestive and Kidney Diseases. "Dihydromyricetin." LiverTox®, 2023. NBK594407
• Chen S, et al. "Dihydromyricetin improves glucose and lipid metabolism and exerts anti-inflammatory effects in nonalcoholic fatty liver disease: A randomized controlled trial." Pharmacological Research, 2015. PMID: 26032587
• Dietary supplement based on dihydromyricetin in metabolic dysfunction-associated steatotic liver disease: a double-blind, placebo-controlled, randomized clinical trial. PMC12850692
• Liang J, et al. "Preclinical Research of Dihydromyricetin for Brain Aging and Neurodegenerative Diseases." PMC6859532
• Protective role of Dihydromyricetin in Alzheimer's disease rat model associated with activating AMPK/SIRT1 signaling pathway. PMC6328867
• Zhang Y, et al. "Pharmacological mechanisms and potential clinical applications of Dihydromyricetin in neurological disorders." Frontiers in Pharmacology, 2025. PMC12308142
• "Present Status, Challenges, and Prospects of Dihydromyricetin in the Battle against Cancer." PMC9317349
• "Research progress of dihydromyricetin in the treatment of diabetes mellitus." PMC10507363
• Liu L, et al. "In vitro inhibitory effects of dihydromyricetin on human liver cytochrome P450 enzymes." PMC7012011
• "Strategic developments in the drug delivery of natural product dihydromyricetin: applications, prospects, and challenges." PMC9518266
• "Determination of dihydromyricetin in rat plasma by LC-MS/MS and its application to a pharmacokinetic study." PMC6130699
• "Hovenia dulcis: a Chinese medicine that plays an essential role in alcohol-associated liver disease." Frontiers in Pharmacology, 2024
• Dihydromyricetin supplementation improves ethanol-induced lipid accumulation and inflammation. PMC10481966
• Alzheimer's Drug Discovery Foundation. "Dihydromyricetin: Cognitive Vitality Report." 2020
• ClinicalTrials.gov. "Phase I, Dose-Escalation Study of Dihydromyricetin (DHM) to Treat Alcohol-Associated Liver Disease." NCT05623501
• Wikipedia. "Hovenia dulcis."
• Dihydromyricetin Protects Against Ethanol-Induced Toxicity in SH-SY5Y Cell Line: Role of GABAA Receptor. PubMed PMID: 35386023
• Dihydromyricetin Ameliorates Nonalcoholic Fatty Liver Disease by Improving Mitochondrial Respiratory Capacity and Redox Homeostasis Through Modulation of SIRT3 Signaling. PubMed PMID: 29310441
• Interaction of myricetin, ampelopsin (dihydromyricetin), and their sulfate metabolites with serum albumin, CYP enzymes, and OATPs. PMC11440035