Hesperidin methylchalcone

Hesperidin methylchalcone
Product Name Hesperidin methylchalcone
CAS No.: 24292-52-2
Catalog No.: CFN80405
Molecular Formula: C29H36O15
Molecular Weight: 624.59 g/mol
Purity: >=98%
Type of Compound: Flavonoids
Physical Desc.: Powder
Targets: TNF-α | IL Receptor | TGF-β/Smad | NF-kB | Caspase | Nrf2 | HO-1 | NADPH-oxidase | TRPV | Akt | PKC
Source: The fruits of Myrtus communis
Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
Price: $30/20mg
Hesperidin methylchalcone has anti-inflammatory effects, it can suppresse experimental gout arthritis in mice by inhibiting NF-κB activation. Hesperidin methylchalcone can regulate the expression of adhesion molecules in tumor necrosis factor-alpha-stimulated human umbilical vein endothelial cells. Hesperidin methylchalcone has a protective effect against leakage of FITC-dextran in the cheek pouch after administration of various permeability-increasing substances. It is a promising new therapeutic approach to protecting the skin from the deleterious effects of UVB irradiation.
Inquire / Order: manager@chemfaces.com
Technical Inquiries: service@chemfaces.com
Tel: +86-27-84237783
Fax: +86-27-84254680

Address:
1 Building, No. 83, CheCheng Rd., Wuhan Economic and Technological Development Zone, Wuhan, Hubei 430056, PRC
Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
  • Med Sci Monit.2019, 25:9499-9508
  • Free Radic Biol Med.2017, 112:191-199
  • Antioxidants (Basel).2022, 11(12):2411.
  • Mol Neurobiol.2022, 02873-9.
  • Medicina (Kaunas).2020, 56(12):685.
  • J Insect Sci.2020, 20(5):18.
  • APMIS.2019, 127(10):688-695
  • Sci Rep.2019, 9:19059
  • Food Funct.2022, 13(13):6923-6933.
  • Int J Med Sci.2021, 18(10):2155-2161.
  • Trilobatin 2''-acetate

    Catalog No: CFN97111
    CAS No: 647853-82-5
    Price: Inquiry(manager@chemfaces.com)
    Nothofagin

    Catalog No: CFN92888
    CAS No: 11023-94-2
    Price: Inquiry(manager@chemfaces.com)
    Phloretin 3',5'-Di-C-glucoside

    Catalog No: CFN95306
    CAS No: 357401-40-2
    Price: $318/10mg
    Naringin dihydrochalcone

    Catalog No: CFN90437
    CAS No: 18916-17-1
    Price: $40/20mg
    Sieboldin

    Catalog No: CFN70294
    CAS No: 18777-73-6
    Price: Inquiry(manager@chemfaces.com)
    Neosperidin dihydrochalcone

    Catalog No: CFN98168
    CAS No: 20702-77-6
    Price: $40/20mg
    Hesperidin methylchalcone

    Catalog No: CFN80405
    CAS No: 24292-52-2
    Price: $30/20mg
    Diosmin Impurity 5

    Catalog No: CFN95311
    CAS No: 122087-66-5
    Price: $318/10mg
    Dihydromarein

    Catalog No: CFN90853
    CAS No: N/A
    Price: $418/5mg
    Marein

    Catalog No: CFN90851
    CAS No: 535-96-6
    Price: $238/10mg
    Photochem Photobiol Sci. 2016 Apr;15(4):554-63.
    Topical formulation containing hesperidin methyl chalcone inhibits skin oxidative stress and inflammation induced by ultraviolet B irradiation.[Pubmed: 27021784]
    Skin exposure to ultraviolet B (UVB) irradiation has increased significantly in recent years due to ozone depletion, and it represents the main cause of many skin diseases. Hesperidin methylchalcone (HMC) is a compound used to treat vascular diseases that has demonstrated anti-inflammatory activities in pre-clinical studies.
    METHODS AND RESULTS:
    Herein, we tested the antioxidant activity of HMC in cell free systems and the in vivo effects of a stable topical formulation containing HMC in a mouse model of skin oxidative stress and inflammation induced by UVB irradiation. HMC presented ferric reducing power, neutralized 2,2'-azino-bis (3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) and hydroxyl free radicals, and inhibited lipid peroxidation. In hairless mice, a topical formulation containing HMC inhibited UVB irradiation-induced skin edema, depletion of antioxidant capacity (ferric and ABTS reducing abilities and catalase activity), lipid peroxidation, superoxide anion production and mRNA expression of gp91phox (nicotinamide adenine dinucleotide phosphate [NADPH] oxidase 2 sub-unity). In addition, HMC inhibited UVB irradiation-induced depletion of reduced glutathione levels by maintaining glutathione peroxidase-1 and glutathione reductase mRNA expression, prevented down-regulation of nuclear factor erythroid 2-related factor 2 (Nrf2) mRNA expression and increased heme oxygenase-1 mRNA expression. Finally, we demonstrated that topical application of the formulation containing HMC inhibited cytokine (TNF-α, IL-1β, IL-6, and IL-10) production induced by UVB irradiation.
    CONCLUSIONS:
    Therefore, this topical formulation containing HMC is a promising new therapeutic approach to protecting the skin from the deleterious effects of UVB irradiation.
    Chem Biol Interact. 2015 Feb 25;228:88-99.
    Protective effects of the flavonoid hesperidin methyl chalcone in inflammation and pain in mice: role of TRPV1, oxidative stress, cytokines and NF-κB.[Pubmed: 25617481 ]
    Cytokines and reactive oxygen species are inflammatory mediators that lead to increased sensitivity to painful stimuli, and their inhibition represents a therapeutic approach in controlling acute and chronic pain. The water-soluble flavonone Hesperidin methylchalcone (HMC) is used in the treatment of venous diseases, but its bioactivity as anti-inflammatory and analgesic is poorly understood. The present study evaluated the protective effects of HMC in widely used mouse models of acute and prolonged inflammation and pain.
    METHODS AND RESULTS:
    Male Swiss mice were treated with HMC (3-100 or 30 mg/kg, intraperitoneally) or vehicle (saline) 1h before inflammatory stimuli. In overt pain-like behavior tests, HMC inhibited acetic acid- and phenyl-p-benzoquinone-induced writhing, and capsaicin-, Complete Freund's Adjuvant (CFA)- and formalin-induced paw flinching and licking. HMC also inhibited carrageenan-, capsaicin- and CFA-induced mechanical and thermal hyperalgesia. Mechanistically, HMC inhibited carrageenan-induced cytokine (TNF-α, IL-1β, IL-6, and IL-10) production, oxidative stress and NF-κB activation. Furthermore, HMC did not cause gastric or hepatic injury in a 7 days treatment protocol.
    CONCLUSIONS:
    Thus, this is the first report that HMC reduces inflammation and inflammatory pain by targeting TRPV1 (transient receptor potential vanilloid type 1) receptor activity, oxidative stress, cytokine production, and NF-κB activity, which suggests its potential applicability in inflammatory diseases.
    J Cardiovasc Pharmacol. 1993 Aug;22(2):225-30.
    Inhibitory effect of the Ruscus extract and of the flavonoid hesperidine methylchalcone on increased microvascular permeability induced by various agents in the hamster cheek pouch.[Pubmed: 7692162]
    The Ruscus extract and the flavonoid Hesperidin methylchalcone (HMC) are used in treatment of venous insufficiency. In the present study, we used the hamster cheek pouch preparation and investigated the effects of these substances on increased microvascular permeability induced by bradykinin, histamine, and leukotriene B4 (LTB4) applied topically.
    METHODS AND RESULTS:
    Experiments were performed on male hamsters; 30 min after completion of the cheek pouch preparation, fluorescein-labeled dextran [molecular weight (mol wt) 150,000] was given intravenously (i.v.). Bradykinin, histamine, and LTB4 increased the number of fluorescent vascular leakage sites from postcapillary venules, evidence for an increase in macromolecular permeability, which was quantified in ultraviolet (UV)-light microscope as the number of leaky sites in the prepared area. Ruscus extract and HMC, given i.v., significantly inhibited the macromolecular permeability-increasing effect of bradykinin, LTB4, and histamine. Ruscus extract, applied topically, dose dependently inhibited the macromolecular permeability-increasing effect of histamine.
    CONCLUSIONS:
    Our results show that Ruscus extract and HMC have a protective effect against leakage of FITC-dextran in the cheek pouch after administration of various permeability-increasing substances, which further supports data previously reported on patients with venous insufficiency.
    Int Immunopharmacol. 2008 May;8(5):670-8.
    Hesperidin, hesperidin methyl chalone and phellopterin from Poncirus trifoliata (Rutaceae) differentially regulate the expression of adhesion molecules in tumor necrosis factor-alpha-stimulated human umbilical vein endothelial cells.[Pubmed: 18387509]
    The fruits of Poncirus trifoliata (L.) are widely used in Oriental medicine to treat allergic inflammation. Recently, several active compounds including hesperidin, Hesperidin methylchalcone and phellopterin from P. trifoliata (Rutaceae) were isolated and characterized. The goal of this study was to investigate the differential effect of hesperidin, hesperidin methylchalone and phellopterin derived from P. trifoliata (Rutaceae) on the induction of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) by TNF-alpha and the possible molecular mechanisms by which they differentially regulate ICAM-1 and VCAM-1 expressions.
    METHODS AND RESULTS:
    Stimulation of human umbilical vein endothelial cells (HUVECs) with TNF-alpha resulted in the increase of ICAM-1 and VCAM-1 expressions, while pretreatment with the three components completely inhibited VCAM-1 expression in a dose-dependent manner but had no effect on ICAM-1 expression. All three compounds failed to block TNF-alpha-induced phosphorylation of ERK1/2, which is involved in regulating ICAM-1 production by TNF-alpha. Furthermore, they efficiently inhibited the phosphorylation of Akt and PKC, suggesting that Akt or PKC pathways are an important target by which these compounds regulate TNF-alpha-induced VCAM-1 but not ICAM-1. Additionally, treatment with these chemicals also inhibited U937 monocyte adhesion to HUVECs stimulated with TNF-alpha. Interestingly, the inhibitory effect of hesperidin, Hesperidin methylchalcone and phellopterin on monocyte adhesion to HUVECs was recapitulated by transfecting cells with VCAM-1 siRNA.
    CONCLUSIONS:
    Taken together, hesperidin, Hesperidin methylchalcone and phellopterin reduce TNF-alpha-induced VCAM-1 expression through regulation of the Akt and PKC pathway, which contributes to inhibit the adhesion of monocytes to endothelium.
    J Agric Food Chem. 2018 Jun 27;66(25):6269-6280.
    Hesperidin Methylchalcone Suppresses Experimental Gout Arthritis in Mice by Inhibiting NF-κB Activation.[Pubmed: 29852732 ]
    Gout arthritis is a painful inflammatory disease induced by monosodium urate (MSU) crystals. We evaluate the therapeutic potential of the flavonoid Hesperidin methylchalcone (HMC) in a mouse model of gout arthritis induced by intra-articular injection of MSU (100 μg/10 μL).
    METHODS AND RESULTS:
    Orally given HMC (3-30 mg/kg, 100 μL) reduced in a dose-dependent manner the MSU-induced hyperalgesia (44%, p < 0.05), edema (54%, p < 0.05), and leukocyte infiltration (70%, p < 0.05). HMC (30 mg/kg) inhibited MSU-induced infiltration of LysM-eGFP+ cells (81%, p < 0.05), synovitis (76%, p < 0.05), and oxidative stress (increased GSH, FRAP, and ABTS by 62, 78, and 73%, respectively; reduced O2- and NO by 89 and 48%, p < 0.05) and modulated cytokine production (reduced IL-1β, TNF-α, IL-6, and IL-10 by 35, 72, 37, and 46%, respectively, and increased TGF-β by 90%, p < 0.05). HMC also inhibited MSU-induced NF-κB activation (41%, p < 0.05), gp91phox (66%, p < 0.05) and NLRP3 inflammasome components mRNA expression in vivo (72, 77, 71, and 73% for NLRP3, ASC, pro-caspase-1, and pro-IL-1 β, respectively, p < 0.05), and induced Nrf2/HO-1 mRNA expression (3.9- and 5.1-fold increase, respectively, p < 0.05). HMC (30, 100, and 300 μM) did not inhibit IL-1β secretion by macrophages primed by LPS and challenged with MSU (450 μg/mL), demonstrating that the anti-inflammatory effect of HMC in gout arthritis depends on inhibiting NF-κB but not on direct inhibition of inflammasome.
    CONCLUSIONS:
    The pharmacological effects of HMC indicate its therapeutic potential for the treatment of gout.
    J Photochem Photobiol B. 2015 Jul;148:145-153.
    Hesperidin methyl chalcone inhibits oxidative stress and inflammation in a mouse model of ultraviolet B irradiation-induced skin damage.[Pubmed: 25916506 ]
    Hesperidin methylchalcone (HMC) is a safe flavonoid used to treat chronic venous diseases, but its effects and mechanisms on UVB irradiation-induced inflammation and oxidative stress have never been described in vivo. Thus, the purpose of this study was to evaluate the effects of systemic administration of HMC in skin oxidative stress and inflammation induced by UVB irradiation.
    METHODS AND RESULTS:
    To induce skin damage, hairless mice were exposed to an acute UVB irradiation dose of 4.14 J/cm(2), and the dorsal skin samples were collected to evaluate oxidative stress and inflammatory response. The intraperitoneal treatment with HMC at the dose of 300 mg/kg inhibited UVB irradiation-induced skin edema, neutrophil recruitment, and matrix metalloproteinase-9 activity. HMC also protected the skin from UVB irradiation-induced oxidative stress by maintaining ferric reducing antioxidant power (FRAP), 2,2'-azino-bis (3-ethylbenzothiazoline-6-sulfonic acid) radical (ABTS) scavenging ability and antioxidant levels (reduced glutathione and catalase). Corroborating, HMC inhibited UVB irradiation-induced superoxide anion generation and gp91phox (NADPH oxidase subunit) mRNA expression. Furthermore, the antioxidant effect of HMC resulted in lower production of inflammatory mediators, including lipid hydroperoxides and a wide range of cytokines.
    CONCLUSIONS:
    Taken together, these results unveil a novel applicability of HMC in the treatment of UVB irradiation-induced skin inflammation and oxidative stress.
    6-Hydroxywogonin

    Catalog No: CFN95009
    CAS No: 76844-70-7
    Price: $368/5mg
    Betmidin

    Catalog No: CFN95047
    CAS No: 35589-22-1
    Price: $413/5mg
    5-Hydroxy-7-(4'-hydroxy-3'-methoxyphenyl)-1-phenyl-3-heptanone (DHPA)

    Catalog No: CFN95135
    CAS No: 79559-61-8
    Price: $268/20mg
    Yuanhunine

    Catalog No: CFN95179
    CAS No: 104387-15-7
    Price: $368/5mg
    Neoarctin B

    Catalog No: CFN95243
    CAS No: 155969-67-8
    Price: $318/10mg
    Quercetin 3-O-beta-D-glucosyl-(1->2)-rhamnoside

    Catalog No: CFN95277
    CAS No: 143016-74-4
    Price: $238/20mg
    Rosmarinyl glucoside

    Catalog No: CFN95297
    CAS No: 910028-78-3
    Price: $413/5mg
    Isochlorogenic acid C 4'-O-glucoside

    Catalog No: CFN95405
    CAS No: N/A
    Price: $413/5mg
    Otobaphenol

    Catalog No: CFN95476
    CAS No: 10240-16-1
    Price: $318/10mg
    Kihadanin D

    Catalog No: CFN95482
    CAS No: 2770024-83-2
    Price: $413/5mg