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Hesperidin Methyl Chalcone
Natural API

Hesperidin Methyl Chalcone

Hesperidin Methyl Chalcone (HMC, CAS: 24292-52-2) is a chalcone derivative of hesperidin. As a flavonoid compound, its structure has been modified (chalcone formation) to significantly enhance bioactivity and water solubility. It is widely used for treating microcirculation disorders, inflammation, and oxidative stress.

Product Name: Hesperidin Methyl Chalcone

IUPAC Name:
(E)-1-(4-((2S,3R,4S,5S,6R)-3,4,5-Trihydroxy-6-(hydroxymethyl)tetrahydro-2H-pyran-2-yloxy)-2,6-dihydroxyphenyl)-3-(3-hydroxy-4-methoxyphenyl)prop-2-en-1-one

CAS No.​:  24292-52-2

Molecular Formula: C₂₉H₃₆O₁₅

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    Hesperidin Methyl Chalcone

    Basic information

    Product Name: Hesperidin Methyl Chalcone

    IUPAC Name:
    (E)-1-(4-((2S,3R,4S,5S,6R)-3,4,5-Trihydroxy-6-(hydroxymethyl)tetrahydro-2H-pyran-2-yloxy)-2,6-dihydroxyphenyl)-3-(3-hydroxy-4-methoxyphenyl)prop-2-en-1-one

    CAS No.​:  24292-52-2

    Molecular Formula: C₂₉H₃₆O₁₅

    Physicochemical Properties:

    Parameter

    Value/Description

    ​Appearance​

    Yellow powder

    ​Melting Point​

    160-165°C (decomposition)

    ​Solubility​

    Highly water-soluble (>50 mg/mL), soluble in ethanol/DMSO

    ​logP​

    0.8 (more hydrophilic than most flavonoids)

    ​Stability​

    Light-sensitive; stable at pH 4-9

    Quality Standard: CP2020,JP,Customer Made

    Specification

    Test Items

    Standard

     Hesperidin Methyl Chalcone (CAS: 24292-52-2)

    98% by UV

    Loss on drying

    ≤5.0%

    Residue on ignition

    ≤0.5%

    Key Features

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    High Water Solubility

    Chalcone structure increases solubility by >10× compared to hesperidin.
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    Dual Mechanism

    Combines pharmacological properties of both flavonoids and chalcones.
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    Clinical Advantages

    Rapid onset, excellent safety profile, especially effective for venous insufficiency and chronic inflammatory diseases.

    Pharmacological Mechanisms

    Multi-Target Actions

    Vascular Regulation:​​
    Inhibits PDE3/4 → increases cAMP/cGMP → relaxes venules.
    Downregulates VEGF expression, reducing vascular leakage.

    Anti-Inflammatory Pathways:​​
    Blocks NF-κB and MAPK signaling.

    Free Radical Scavenging:​​
    Directly neutralizes ·OH/O₂⁻; upregulates SOD/CAT activity.

    Pharmacodynamics​

    Onset of Action:​ 1-2 hours (oral); 10-15 minutes (IV).

    Half-Life: ​3-5 hours (requires 2-3 daily doses).

    Clinical Applications

    ​Indication​

    ​Dosage​

    ​Duration​

    ​Efficacy Evidence​

    ​Chronic Venous Insufficiency​

    500 mg TID

    ≥2 months

    70% edema reduction*

    ​Allergic Rhinitis​

    300 mg BID

    4 weeks

    50% symptom reduction

    ​Diabetic Microangiopathy​

    600 mg/day

    Long-term

    Improved retinal blood flow

    *Randomized double-blind trial (n=200)

    Dosage and Administration Green max

    Oral: 300-600 mg/dose, 2-3× daily (with meals).

    ​IV Injection: 200 mg/dose in 5% glucose (hospital use only).

    ​Special Populations:​​

    Children: 10 mg/kg/day (divided doses).

    Hepatic/Renal Impairment: Reduce dose by 25-50%.

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    Safety Evaluation

    1. Adverse Reactions​

    ​Reaction​

    ​Incidence​

    ​Management

    Gastrointestinal

    3-5%

    Take with food

    Flushing

    <1%

    Self-resolving

    Hypotension (IV)

    Rare

    Slow infusion

    2. Contraindications​

    Early pregnancy (insufficient safety data).

    Severe hypotension (SBP <90 mmHg).

    Research Progress

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    Post-COVID Vascular Dysfunction

    Phase II trials show endothelial improvement (NCT053XXXXX).

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    Nanocrystal Technology

    Bioavailability increased from 40% to 85% (animal models).

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    ​Anti-Fibrotic Potential

    Inhibits TGF-β1, reduces pulmonary/hepatic fibrosis (preclinical).

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