Fig. 1 · Structure

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Dihydromyricetin (Ampeloptin)

Cat. No. A10252 CAS 27200-12-0

Dihydropyrimidinase Inhibitor

Dihydromyricetin (Ampelopsin (flavanol); Ampeloptin) is a natural antioxidant with good prospects.

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Biological Activity

Bioactivity / Mechanism

Dihydromyricetin displaced benzodiazepine-site [3H]flunitrazepam binding in rat cortical membranes (IC50 4.36 μM). In hippocampal slices, it attenuated ethanol-potentiated GABA_A currents, with reversal by flumazenil. These experiments support GABA_A receptor involvement. [1]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Target & Activity

Target Activity Value
GABAA receptor
GABAA receptor

Cellular Effect

Cell Line Activity Value Description Reference
A549 IC50 > 10 μM Cytotoxicity against human A549 cells after 48 hrs by SRB assay [PMID: 28165740]
BT-549 IC50 > 10 μM Cytotoxicity against human BT549 cells after 48 hrs by SRB assay [PMID: 28165740]
BV-2 IC50 32.66 μM Antiinflammatory activity in mouse BV2 cells assessed as inhibition of LPS-induced nitrite production after 24 hrs by Griess assay [PMID: 28165740]
SK-MEL-2 IC50 > 10 μM Cytotoxicity against human SK-MEL-2 cells after 48 hrs by SRB assay [PMID: 28165740]
SK-OV-3 IC50 > 10 μM Cytotoxicity against human SKOV3 cells after 48 hrs by SRB assay [PMID: 28165740]

In Vitro Studies

In rat hippocampal slices, DHM at 0.3–1 μM attenuated current potentiation by 60 mM ethanol. Quercetin at the same tested concentrations lacked this effect. This is an acute neuronal assay. [1]

Benzodiazepine-site radioligand displacement

Biochemical assay · Naive adult rat cortical membrane homogenates [1]

DHM displaced benzodiazepine-site radioligand binding. This supports site interaction but does not establish receptor-subtype selectivity or a clinical dose.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Inhibition of [3H]flunitrazepam bindingIC50 4.36 μM[1]

Literature-Reported Treatment Conditions

Treatment concentration
0.03–100 μM
Exposure duration
30 min on ice
Method
[3H]flunitrazepam competition assay
Vehicle
DMSO stock; assay-specific final DMSO fraction not separately specified
Co-treatment
[3H]flunitrazepam 1 nM; nonspecific binding defined with flurazepam 10 μM
Reported limits
Two experiments, each point in triplicate; technical replicates are not independent animals.
Methods and source locations

Compound reported in the paper: Dihydromyricetin; Compound label in the paper: DHM

Compound-level evidence; no Adooq lot validation.

Materials and Methods: Chemicals; Tissue preparation and [3H]flunitrazepam binding assays; Results: DHM is a positive modulator of GABAARs at the BZ sites; Figure 5G and caption

Inhibition of [3H]flunitrazepam binding: One-site competition fit; n = 2 experiments, each point in triplicate — Figure 5G; corresponding Results and binding Methods

Attenuation of ethanol-potentiated GABA_A currents

Cell-based study · Dentate gyrus granule cells in hippocampal slices from adult male Sprague Dawley rats [1]

DHM attenuated ethanol-potentiated tonic and miniature inhibitory postsynaptic currents. Flumazenil reversed this effect; quercetin lacked a comparable effect at the tested concentrations.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Ethanol-potentiated tonic current and mIPSC areaQualitative response Attenuated by DHM 0.3 and 1 μM (n = 8 neurons/3 rats); flumazenil reversed the DHM 3 μM effect (n = 5 neurons); quercetin did not attenuate potentiation (n = 5 neurons).[1]

Literature-Reported Treatment Conditions

Treatment concentration
DHM 0.3 and 1.0 μM; separate antagonist sequence used DHM 3 μM
Exposure duration
Acute sequential bath application; fixed exposure duration not specified for each step
Method
Whole-cell patch clamp at −70 mV
Vehicle
DMSO stock; final chamber DMSO did not exceed 0.01%
Co-treatment
Ethanol 60 mM; flumazenil 10 μM; quercetin comparison 0.3 and 1 μM; picrotoxin 100 μM defined blocked-current baseline
Reported limits
Rat counts for antagonist/quercetin sequences differ between text and caption; no unique rat count assigned to those sequences. Exact per-step times not reported.
Methods and source locations

Compound reported in the paper: Dihydromyricetin; Compound label in the paper: DHM

Acute ex vivo neuronal evidence; not a measurement of human intoxication.

Figure 4A–I and caption; Results: DHM antagonizes EtOH-induced GABAAR potentiation; Materials and Methods: Animals, Chemicals, patch clamp and current analysis

Ethanol-potentiated tonic current and mIPSC area: Paired sequential recording conditions; reported one-way repeated-measures ANOVA and post hoc comparisons; no curve-derived decimals extracted. — Figure 4A–I; corresponding Results

In Vivo Studies

Mouse serum exposure to DHM depended on administration route and sex. At 50 mg/kg, intraperitoneal dosing produced higher serum AUC than oral gavage; these exposure measurements do not establish human efficacy. [2]

In a small male Wistar rat experiment, oral DHM 10 mg/kg did not significantly lower blood ethanol or acetaldehyde after the first ethanol challenge. Blood concentrations were higher at 60 minutes after next-day ethanol-only rechallenge in animals previously given DHM. [3]

Route and sex dependence of serum DHM exposure

Animal study · Eight-week-old male and female C57BL/6J mice [2]

At the same nominal dose, serum exposure was higher after intraperitoneal administration than oral gavage. Values below follow Table 1 and Results §2.2; abstract fold-change sex labels are inconsistent.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Serum DHM exposure, AUC0→24AUC Female PO: 728 ± 461; male PO: 2508 ± 988; female IP: 17,360 ± 2734; male IP: 18,079 ± 3840 nM × h (mean ± SEM)[2]

Conditions shared by the study groups

Frequency
Single administration
Treatment course
Serum sampling through 24 h
Vehicle
0.9% saline with 10% DMSO
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Female Oral gavage
50 mg/kg DHM
Equal nominal dose compared across sex and route; DHM reference standard and internal standard for bioanalysisSerum AUC0→24: 728 ± 461 nM × h (mean ± SEM)[2]
Male Oral gavage
50 mg/kg DHM
Equal nominal dose compared across sex and route; DHM reference standard and internal standard for bioanalysisSerum AUC0→24: 2508 ± 988 nM × h (mean ± SEM)[2]
Female Intraperitoneal injection
50 mg/kg DHM
Equal nominal dose compared across sex and route; DHM reference standard and internal standard for bioanalysisSerum AUC0→24: 17,360 ± 2734 nM × h (mean ± SEM)[2]
Male Intraperitoneal injection
50 mg/kg DHM
Equal nominal dose compared across sex and route; DHM reference standard and internal standard for bioanalysisSerum AUC0→24: 18,079 ± 3840 nM × h (mean ± SEM)[2]
Female Oral gavage
Model: Female C57BL/6J mice
Route: Oral gavage
Reported limits: No IV comparator; absolute bioavailability not determined.
Male Oral gavage
Model: Male C57BL/6J mice
Route: Oral gavage
Reported limits: No IV comparator; absolute bioavailability not determined.
Female Intraperitoneal injection
Model: Female C57BL/6J mice
Route: Intraperitoneal injection
Reported limits: No IV comparator; absolute bioavailability not determined.
Male Intraperitoneal injection
Model: Male C57BL/6J mice
Route: Intraperitoneal injection
Reported limits: No IV comparator; absolute bioavailability not determined.
Methods and source locations

Compound reported in the paper: Dihydromyricetin; Compound label in the paper: DHM

Serum exposure in mice; no human dose or free brain concentration inference.

Table 1 serum rows and Figure 2; Results §2.2; Methods §§4.1–4.5 and 4.9

Serum DHM exposure, AUC0→24: UPLC-QqQ/MS; DHM standard retention time/MRM and calibration curve; isoquercetin internal standard; n = 3–4 per sex/time point; AUC by noncompartmental trapezoidal integration (§4.9) — Table 1 serum AUC row; Results §2.2; Methods §§4.2–4.5 and 4.9

Female Oral gavage · Table 1 serum AUC row; Methods §§4.1–4.5

Male Oral gavage · Table 1 serum AUC row; Methods §§4.1–4.5

Female Intraperitoneal injection · Table 1 serum AUC row; Methods §§4.1–4.5

Male Intraperitoneal injection · Table 1 serum AUC row; Methods §§4.1–4.5

Oral DHM did not accelerate ethanol disappearance in a rat experiment

Animal study · Male Wistar rats, 300–400 g [3]

The first challenge showed no significant decrease in blood ethanol or acetaldehyde with DHM. On next-day ethanol rechallenge, blood ethanol was higher at 60 min in rats previously given DHM. Small animal groups limit precision.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Blood ethanol and acetaldehyde after first exposure and next-day rechallengeQualitative comparison No significant first-day decrease; higher blood ethanol and acetaldehyde at 60 min after next-day ethanol-only rechallenge in the prior-DHM group (Figure 4B,D).[3]

Conditions shared by the study groups

Route
Gastric gavage
Frequency
One DHM coadministration on day 1
Treatment course
Blood sampling 5–60 min on day 1 and after ethanol-only rechallenge 24 h later
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
DHM plus ethanol versus ethanol alone, with rechallenge
DHM 10 mg/kg on day 1
40% ethanol alone; both groups received ethanol only on rechallengeNo significant reduction on first day; higher ethanol and acetaldehyde at the 60-min rechallenge point in prior-DHM animals.[3]
DHM plus ethanol versus ethanol alone, with rechallenge
Model: Male Wistar rats
Reported limits: Ethanol administered volume/g/kg dose and separate DHM solvent not specified; n falls from 4 to 2 per group on rechallenge.
Methods and source locations

Compound reported in the paper: Dihydromyricetin; Compound label in the paper: DHM

Results apply to the reported DHM preparation; exact stereochemical/lot equivalence to this SKU is unverified.

Methods: reagents, Animals, Alcohol metabolism in vivo, Statistics; Results: Effect of DHM on metabolism of ethanol in vivo; Figure 4A–D and caption

Blood ethanol and acetaldehyde after first exposure and next-day rechallenge: Headspace GC in triplicate; n = 4 rats/group first day and n = 2/group rechallenge; technical triplicates do not increase animal n; caption reports mean ± SD. — Figure 4A–D; Alcohol metabolism in vivo; corresponding Results

DHM plus ethanol versus ethanol alone, with rechallenge · Alcohol metabolism in vivo; Figure 4A–D and caption; corresponding Results

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 27200-12-0
Applications Dihydropyrimidinase Inhibitor
Formula C15H12O8
Molecular Weight 320.3
Synonyms Ampeloptin
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

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 63 mg/mL (196.72 mM)
Water Insoluble
Ethanol 63 mg/mL (196.72 mM)

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Yi Shen, A. Kerstin Lindemeyer, Claudia Gonzalez, et al. Dihydromyricetin as a novel anti-alcohol intoxication medication Journal of Neuroscience (2012). PMID: 22219299 DOI: 10.1523/JNEUROSCI.4639-11.2012 Source material
  2. [2] Eileen Carry, Dushyant Kshatriya, Joshua Silva, et al. Identification of Dihydromyricetin and Metabolites in Serum and Brain Associated with Acute Anti-Ethanol Intoxicating Effects in Mice International Journal of Molecular Sciences (2021). PMID: 34299083 DOI: 10.3390/ijms22147460 Source material
  3. [3] Aneta Skotnicová, Gabriela Boubínová, Zdislava Boštíková, et al. Does dihydromyricetin impact on alcohol metabolism Physiological Research (2020). PMID: 33656905 DOI: 10.33549/physiolres.934606 Source material

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