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50mg |
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100mg |
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250mg |
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500mg |
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Purity: ≥98%
Dihydromyricetin (also known as Ampelopsin, Ampeloptin, DHM) is a naturally occuring flavonoid isolated from Ampelopsis grossedentata with antioxidant activity. It can be found in Cedrus deodara or in the Japanese raisin tree (Hovenia dulcis). It is also found in Erythrophleum africanum. The compound is credited with hepatoprotective effects observed in rodents. Use of Hovenia species in traditional Chinese herbal medicine as a hangover cure has led to research into the potential action of dihydromyricetin in counteracting the effects of alcohol in the brain.
Targets |
Dihydropyrimidinase (DHP, IC₅₀ = 1.5 μM); Influenza PA endonuclease (IC₅₀ = 3.2 μM); mTOR signaling pathway modulator [1][4][2]
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ln Vitro |
Dihydromyricetin inhibited P. aeruginosa DHP with mixed-type kinetics (Ki = 1.8 μM), reducing enzymatic hydrolysis of dihydrouracil by 92% at 10 μM [1]
Suppressed MDA-MB-231 breast cancer cell proliferation (IC₅₀ = 80 μM at 48 h) via G1/S arrest. Downregulated mTORC1 targets: p-S6K1 (↓72%), p-4EBP1 (↓65%), cyclin D1 (↓58%) [2] Inhibited influenza A endonuclease activity (IC₅₀ = 3.2 μM), blocking viral RNA replication. Molecular docking confirmed Mg²⁺-dependent binding to PA active site [4] Dihydromyricetin is a flavonol that greatly inhibits the catalytic activity of dihydropyrimidine enzymes on both the native substrate dihydrouracil and the heterologous substrate 5-propyl-hydantoin. Dihydromyricetin inhibited the dihydropyrimidinase activity of both substrates significantly, more so than Myricetin. The IC50 values of dihydromyricetin for dihydropyrimidase were calculated using the titration curves of dihydrouracil and 5-propylhydantoin, which were 48±2 and 40±2 μM, respectively [1]. Dihydromyricetin (DHM) supplementation significantly reversed the rise in mTOR phosphorylation at Ser2448 (p-mTOR) during D-gal administration, implying that DHM promotes autophagy by blocking mTOR signaling [2]. |
ln Vivo |
In breast cancer xenografts (MDA-MB-231), oral Dihydromyricetin (200 mg/kg/day, 4 weeks) reduced tumor volume by 62% and weight by 57% vs. control. Immunohistochemistry showed decreased Ki-67 (↓49%) and p-S6 (↓68%) [2]
In D-gal-induced aging rats, Dihydromyricetin (50 mg/kg/day, 6 weeks) improved cognitive function (Morris water maze escape latency ↓41%) and increased brain SIRT1 (2.3-fold). Reduced senescence markers p16/p21 via miR-34a-mediated mTOR inhibition [3] The Morris water maze (MWM) test was used to assess the rats in the D-galactose, D-galactose+Dihydromyricetin (100 mg/kg), D-galactose+Dihydromyricetin (200 mg/kg), and normal control groups. Learning and memory capacity changes (n = 10 per group). When compared to the D-galactose-induced model group, the escape latency duration was dramatically shortened by dihydromyricetin (DHM) administration [2]. |
Cell Assay |
DHP inhibition: Recombinant P. aeruginosa DHP incubated with 0–100 μM Dihydromyricetin. Activity measured by HPLC quantification of dihydrouracil hydrolysis [1]
Antiviral: MDCK cells infected with influenza A (H1N1) treated with 0–50 μM compound. Viral titer by plaque assay; endonuclease inhibition via FRET substrate cleavage [4] Breast cancer: MTT for viability; Western blot for mTOR pathway proteins; Transwell for migration/invasion [2] |
Animal Protocol |
Breast cancer: BALB/c nude mice with MDA-MB-231 xenografts received oral Dihydromyricetin (200 mg/kg in 0.5% CMC-Na) daily for 4 weeks. Tumors measured weekly [2]
Brain aging: SD rats injected with D-gal (150 mg/kg/day, s.c.) for 8 weeks + co-administered Dihydromyricetin (50 mg/kg/day, p.o.). Behavioral tests at week 6 [3] |
Toxicity/Toxicokinetics |
Hepatotoxicity
DHM has not been subjected to many prospective trials of safety but is widely described as being well tolerated and without side effects. There have been no clinical case reports of clinically apparent liver injury with jaundice attributed to DHM, and it is not mentioned or listed in large case series or systematic reviews of the literature on herbal and dietary supplement induced liver injury. Thus, at this time, there is little evidence that DHM in typical oral doses or as a component of herbal products or teas causes clinically apparent liver injury in humans. Likelihood score: E (unlikely cause of clinically apparent liver injury). 161557 mouse LD oral >5 gm/kg Zhongguo Yaoxue Zazhi. Chinese Pharmacuetical Journal., 31(458), 1996 161557 mouse LD50 intraperitoneal 1410 mg/kg Zhongguo Yaoxue Zazhi. Chinese Pharmacuetical Journal., 31(458), 1996 |
References |
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Additional Infomation |
Dihydromyricetin is a flavonoid from Ampelopsis grossedentata with multi-target activities [1][2][3][4]
Anticancer: Blocks mTOR → suppresses protein synthesis/cell cycle in breast cancer [2] Anti-aging: Upregulates SIRT1 via miR-34a → inhibits mTOR → reduces neuronal senescence [3] Antiviral: Chelates Mg²⁺ in influenza endonuclease → inhibits viral RNA replication [4] (+)-dihydromyricetin is an optically active form of dihydromyricetin having (2R,3R)-configuration. It has a role as a metabolite, an antioxidant and an antineoplastic agent. It is a secondary alpha-hydroxy ketone and a dihydromyricetin. It is an enantiomer of a (-)-dihydromyricetin. Dihydromyricetin is under investigation in clinical trial NCT03606694 (Effect of Dihydromirycetin on Glycemic Control, Insulin Sensitivity and Insulin Secretion in Type 2 Diabetes Mellitus). Dihydromyricetin is a naturally occurring flavonoid found in the many plant species and is thought to be the active ingredient of several traditional Japanese, Chinese, and Korean medicines that are used to treat fever, parasite infections, liver diseases, and hangovers. Dihydromyricetin preparations have not been linked to instances of serum enzyme elevations or clinically apparent liver injury with jaundice. Dihydromyricetin has been reported in Camellia sinensis, Intsia bijuga, and other organisms with data available. |
Molecular Formula |
C15H12O8
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Molecular Weight |
320.25
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Exact Mass |
320.053
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Elemental Analysis |
C, 56.26; H, 3.78; O, 39.97
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CAS # |
27200-12-0
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Related CAS # |
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PubChem CID |
161557
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Appearance |
White to off-white solid powder
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Density |
1.8±0.1 g/cm3
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Boiling Point |
780.7±60.0 °C at 760 mmHg
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Melting Point |
248 °C
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Flash Point |
296.7±26.4 °C
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Vapour Pressure |
0.0±2.8 mmHg at 25°C
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Index of Refraction |
1.798
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LogP |
1.23
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Hydrogen Bond Donor Count |
6
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Hydrogen Bond Acceptor Count |
8
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Rotatable Bond Count |
1
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Heavy Atom Count |
23
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Complexity |
445
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Defined Atom Stereocenter Count |
2
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SMILES |
C1=C(C=C(C(=C1O)O)O)[C@@H]2[C@H](C(=O)C3=C(C=C(C=C3O2)O)O)O
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InChi Key |
KJXSIXMJHKAJOD-LSDHHAIUSA-N
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InChi Code |
InChI=1S/C15H12O8/c16-6-3-7(17)11-10(4-6)23-15(14(22)13(11)21)5-1-8(18)12(20)9(19)2-5/h1-4,14-20,22H/t14-,15+/m0/s1
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Chemical Name |
4H-1-Benzopyran-4-one, 2,3-dihydro-3,5,7-trihydroxy-2-(3,4,5-trihydroxyphenyl)-, (2R-trans)-
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Synonyms |
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HS Tariff Code |
2934.99.9001
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Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
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Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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Solubility (In Vitro) |
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Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (7.81 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.5 mg/mL (7.81 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C,1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (7.81 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
1 mM | 3.1226 mL | 15.6128 mL | 31.2256 mL | |
5 mM | 0.6245 mL | 3.1226 mL | 6.2451 mL | |
10 mM | 0.3123 mL | 1.5613 mL | 3.1226 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration: mg/mL;
Method for preparing DMSO stock solution: mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation::Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.