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Dihydromyricetin (Ampelopsin)

Alias: Ampelopsin; Dihydromyricetin; 27200-12-0; (+)-Dihydromyricetin; (+)-Ampelopsin; Telocapil; Ampelopsin (flavanol); Ampeloptin
Cat No.:V1290 Purity: ≥98%
Dihydromyricetin (also known as Ampelopsin, Ampeloptin, DHM) is a naturally occuring flavonoid isolated from Ampelopsis grossedentata with antioxidant activity.
Dihydromyricetin (Ampelopsin)
Dihydromyricetin (Ampelopsin) Chemical Structure CAS No.: 27200-12-0
Product category: GABA Receptor
This product is for research use only, not for human use. We do not sell to patients.
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Purity & Quality Control Documentation

Purity: ≥98%

Product Description

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.

Biological Activity I Assay Protocols (From Reference)
Targets
Dihydropyrimidinase (DHP, IC₅₀ = 1.5 μM); Influenza PA endonuclease (IC₅₀ = 3.2 μM); mTOR signaling pathway modulator [1][4][2]
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
Dihydrojasmonic acid (DHM) has not undergone extensive prospective safety trials, but it is generally considered to be well-tolerated and without side effects. Currently, there are no clinical case reports showing that DHM causes clinically significant liver injury (with jaundice), and DHM is not mentioned or listed in large case series studies or systematic reviews of liver injury caused by herbal and dietary supplements. Therefore, there is currently little evidence that typical oral doses of DHM, or DHM as an ingredient in herbal products or teas, cause clinically significant liver injury in humans. Probability Score: E (Unlikely to cause clinically significant liver injury). Oral LD50 of 161557 in mice: >5 gm/kg, Chinese Pharmaceutical Journal, 31(458), 1996. Intraperitoneal LD50 of 161557 in mice: 1410 mg/kg, Chinese Pharmaceutical Journal, 31(458), 1996.
References

[1]. Huang CY. Inhibition of a Putative Dihydropyrimidinase from Pseudomonas aeruginosa PAO1 by Flavonoids and Substrates of Cyclic Amidohydrolases. PLoS One. 2015 May 19;10(5):e0127634.

[2]. Ampelopsin suppresses breast carcinogenesis by inhibiting the mTOR signalling pathway. Carcinogenesis. 2014 Aug;35(8):1847-54.

[3]. Ampelopsin attenuates brain aging of D-gal-induced rats through miR-34a-mediated SIRT1/mTORsignal pathway. Oncotarget. 2016 Nov 15;7(46):74484-74495.

[4]. Unraveling the Anti-Influenza Effect of Flavonoids: Experimental Validation of Luteolin and its Congeners as Potent Influenza Endonuclease Inhibitors. Eur J Med Chem. 22 August 2020, 112754.

Additional Infomation
Dihydromyricetin is a flavonoid compound extracted from Ampelopsis grossedentata, which has a variety of activities [1][2][3][4]
Anticancer: Blocking mTOR → Inhibiting protein synthesis/cell cycle of breast cancer cells [2]
Antiaging: Upregulating SIRT1 through miR-34a → Inhibiting mTOR → Reducing neuronal senescence [3]
Antiviral: Chelating Mg²⁺ in influenza virus endonuclease → Inhibiting viral RNA replication [4]
(+)-dihydromyricetin is the optically active form of dihydromyricetin with (2R,3R) configuration. It is a metabolite, antioxidant and antitumor agent. It is a secondary α-hydroxy ketone and also a dihydromyricetin. It is the enantiomer of (-)-dihydromyricetin.
Dihydromyricetin is currently being studied in the clinical trial NCT03606694 (Effects of dihydromyricetin on glycemic control, insulin sensitivity, and insulin secretion in patients with type 2 diabetes).
Dihydromyricetin is a naturally occurring flavonoid compound found in various plants and is considered an active ingredient in many traditional Japanese, Chinese, and Korean medicines used to treat fever, parasitic infections, liver disease, and hangovers. No clinical liver injury cases with elevated serum enzymes or jaundice have been found associated with dihydromyricetin preparations.
Dihydromyricetin has been reported in tea (Camellia sinensis), custard apple (Intsia bijuga), and several other organisms with relevant data.
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C15H12O8
Molecular Weight
320.25
Exact Mass
320.053
Elemental Analysis
C, 56.26; H, 3.78; O, 39.97
CAS #
27200-12-0
Related CAS #
27200-12-0
PubChem CID
161557
Appearance
White to off-white solid powder
Density
1.8±0.1 g/cm3
Boiling Point
780.7±60.0 °C at 760 mmHg
Melting Point
248 °C
Flash Point
296.7±26.4 °C
Vapour Pressure
0.0±2.8 mmHg at 25°C
Index of Refraction
1.798
LogP
1.23
Hydrogen Bond Donor Count
6
Hydrogen Bond Acceptor Count
8
Rotatable Bond Count
1
Heavy Atom Count
23
Complexity
445
Defined Atom Stereocenter Count
2
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
InChi Key
KJXSIXMJHKAJOD-LSDHHAIUSA-N
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
Chemical Name
4H-1-Benzopyran-4-one, 2,3-dihydro-3,5,7-trihydroxy-2-(3,4,5-trihydroxyphenyl)-, (2R-trans)-
Synonyms
Ampelopsin; Dihydromyricetin; 27200-12-0; (+)-Dihydromyricetin; (+)-Ampelopsin; Telocapil; Ampelopsin (flavanol); Ampeloptin
HS Tariff Code
2934.99.9001
Storage

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
DMSO: 64 mg/mL (199.8 mM)
Water: 5 mg/mL (20.3 mM)
Ethanol:64 mg/mL (199.8 mM)
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.

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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.
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 corn oil and mix evenly.


 (Please use freshly prepared in vivo formulations for optimal results.)
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.

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Note: Chemical formula is case sensitive: C12H18N3O4  c12h18n3o4
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In vivo Formulation Calculator (Clear solution)
Step 1: Enter information below (Recommended: An additional animal to make allowance for loss during the experiment)
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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.

Clinical Trial Information
Phase I, Dose-Escalation Study of Dihydromyricetin (DHM) to Treat Alcohol-Associated Liver Disease
CTID: NCT05623501
Phase: Phase 1
Status: Not yet recruiting
Date: 2024-09-03
Effect of Dihydromirycetin on Glycemic Control, Insulin Sensitivity and Insulin Secretion in Type 2 Diabetes Mellitus
CTID: NCT03606694
Phase: Phase 2
Status: Unknown status
Date: 2023-05-23
Biological Data
  • Dihydromyricetin

    DHM ameliorates EtOH withdrawal symptoms in rats.J Neurosci.2012 Jan 4;32(1):390-401.
  • Dihydromyricetin

    DHM prevents the escalation of EtOH consumption in the voluntary intermittent two-bottle choice paradigm in rats.J Neurosci.2012 Jan 4;32(1):390-401.
  • Dihydromyricetin

    DHM potentiates GABAAR-mediated inhibition in a concentration-dependent manner in primary cultured hippocampal neurons (DIV14).J Neurosci.2012 Jan 4;32(1):390-401.
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