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    6,7-Dihydroxycoumarin
    Information
    CAS No. 305-01-1 Price $50 / 20mg
    Catalog No.CFN99115Purity>=98%
    Molecular Weight178.14Type of CompoundCoumarins
    FormulaC9H6O4Physical DescriptionPowder
    Download Manual    COA    MSDS    SDFSimilar structuralComparison (Web)
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    6,7-Dihydroxycoumarin Description
    Source: The peel of Aesculus hippocastanum L.
    Biological Activity or Inhibitors: 1. Esculetin(6,7-Dihydroxycoumarin) is known to inhibit proliferation and induce apoptosis in several types of human cancer cells and is regarded as a promising chemotherapeutic agent; it inhibits cell growth and induces apoptosis by suppressing Sp1 in HN22 and HSC4 cells, suggesting it to be a potent anticancer drug candidate for oral cancer.
    2. Esculetin blocks cell proliferation via the inhibition of an upstream effector of Ras and downstream events including p42/44 MAPK activation, PI 3-kinase activation, immediate early gene expression, as well as NF-kappaB and AP-1 activation; it also inhibits intimal hyperplasia after balloon vascular injury in the rat, indicating the therapeutic potential for treating restenosis after arterial injury.
    3. Esculetin induces apoptosis during the late stage of differentiation, it can alter fat cell number by direct effects on cell viability, adipogenesis, and apoptosis in 3T3-L1 cells.
    4. Esculetin exhibits competitive inhibition against the oxidation of 3-(3,4-dihydroxyphenyl)- alanine by mushroom, the IC50 value of esculetin is 43 microM.
    5. Esculetin reduces the incidence of liver lesions induced by t-BHP, including hepatocyte swelling, leukocyte infiltration, and necrosis, speculates that esculetin may play a chemopreventive role via reducing oxidative stress in living systems.
    6. Esculetin suppresses proteoglycan metabolism by inhibiting the production of matrix metalloproteinases in rabbit chondrocytes, suggests that it is a therapeutically effective candidate for inhibition of cartilage destruction in osteoarthritis and rheumatoid arthritis.
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
    Storage: 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

    After receiving: 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.
    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 5.6136 mL 28.0678 mL 56.1356 mL 112.2712 mL 140.3391 mL
    5 mM 1.1227 mL 5.6136 mL 11.2271 mL 22.4542 mL 28.0678 mL
    10 mM 0.5614 mL 2.8068 mL 5.6136 mL 11.2271 mL 14.0339 mL
    50 mM 0.1123 mL 0.5614 mL 1.1227 mL 2.2454 mL 2.8068 mL
    100 mM 0.0561 mL 0.2807 mL 0.5614 mL 1.1227 mL 1.4034 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    6,7-Dihydroxycoumarin References Information
    Citation [1]

    Int J Oncol. 2015 Jan;46(1):265-71.

    Esculetin (6,7-dihydroxycoumarin): a potential cancer chemopreventive agent through suppression of Sp1 in oral squamous cancer cells.[Pubmed: 25310400]
    Esculetin (6,7-Dihydroxycoumarin), a coumarin compound, is known to inhibit proliferation and induce apoptosis in several types of human cancer cells and is regarded as a promising chemotherapeutic agent.
    The results of the present study indicate that Esculetin (6,7-Dihydroxycoumarin) had anti-proliferative effect on the growth of OSCC cells (HN22 and HSC4) in a dose- and time-dependent manner. The treatment of HN22 and HSC4 cells with Esculetin (6,7-Dihydroxycoumarin) led to a significant reduction in growth and induced apoptosis, followed by the regulation of Sp1 and Sp1 regulatory protein. This indicates that Esculetin (6,7-Dihydroxycoumarin) inhibited cell growth and induced apoptosis by suppressing Sp1 in HN22 and HSC4 cells, suggesting it to be a potent anticancer drug candidate for oral cancer.
    Citation [2]

    Food Funct. 2014 Sep;5(9):2371-7.

    Esculetin inhibits the inflammatory response by inducing heme oxygenase-1 in cocultured macrophages and adipocytes.[Pubmed: 25088305]
    Obesity is associated with chronic low-grade inflammation of adipose tissue. In this study, we investigated the anti-inflammatory effects of Esculetin (6,7-Dihydroxycoumarin) through up-regulation of heme oxygenase-1 (HO-1) in cocultured macrophages and adipocytes. RAW264.7 macrophages and differentiated 3T3-L1 adipocytes were cocultured in serum-free Dulbecco's modified Eagle's medium with or without Esculetin (6,7-Dihydroxycoumarin) for 24 h. Nitric oxide (NO), tumor necrosis factor-α (TNF-α), and monocyte chemoattractant protein-1 (MCP-1) production was measured in the coculture supernatant. Esculetin (6,7-Dihydroxycoumarin) decreased the secretion of NO, TNF-α, and MCP-1. The expression of adipogenic proteins, including peroxisome proliferator-activated receptors γ (PPARγ) and CCAAT/enhancer binding protein α (C/EBPα) in cocultured adipocytes and inducible nitric oxide synthase (iNOS) in cocultured macrophages, was inhibited by Esculetin (6,7-Dihydroxycoumarin). Additionally, HO-1 expression was induced in cocultured macrophages and adipocytes. Silencing of HO-1 expression increased the production of NO, TNF-α, and MCP-1 in cocultured cells, in spite of the presence of Esculetin (6,7-Dihydroxycoumarin). This study demonstrated that Esculetin (6,7-Dihydroxycoumarin) exhibited anti-inflammatory properties by inhibiting the production of proinflammatory cytokines in the interaction between adipocytes and macrophages through HO-1 expression. Esculetin (6,7-Dihydroxycoumarin) may have the potential to improve chronic inflammation in obesity.
    Citation [3]

    Biochem Pharmacol. 2003 Jun 1;65(11):1897-905.

    Esculetin inhibits Ras-mediated cell proliferation and attenuates vascular restenosis following angioplasty in rats.[Pubmed: 12781342]
    Three predominant signaling pathways were identified to be inhibited by esculetin (6,7-Dihydroxycoumarin): (a) the activation of p42/44 mitogen-activated protein kinase (MAPK) and the downstream effectors of c-fos and c-jun immediate early genes by means of western and reverse transcription-polymerase chain reaction (RT-PCR) analyses; (b) the activation of nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1), using the electrophoretic mobility shift assay; and (c) the activation of phosphoinositide 3-kinase (PI 3-kinase) and cell cycle progression, by western blot analysis and flow cytometric detection. Furthermore, esculetin (6,7-Dihydroxycoumarin) also profoundly inhibited Ras activation, a shared upstream event of the above signaling cascades. In vascular injury studies, intraperitoneal administration of esculetin significantly suppressed intimal hyperplasia induced by balloon angioplasty. We conclude that esculetin (6,7-Dihydroxycoumarin) blocks cell proliferation via the inhibition of an upstream effector of Ras and downstream events including p42/44 MAPK activation, PI 3-kinase activation, immediate early gene expression, as well as NF-kappaB and AP-1 activation. It also inhibits intimal hyperplasia after balloon vascular injury in the rat, indicating the therapeutic potential for treating restenosis after arterial injury.
    Citation [4]

    Obesity (Silver Spring). 2006 Oct;14(10):1691-9.

    Esculetin induces apoptosis and inhibits adipogenesis in 3T3-L1 cells.[Pubmed: 17062797 ]
    In mature adipocytes, esculetin(6,7-Dihydroxycoumarin) caused a time- and dose-related increase in adipocyte apoptosis and a decrease in viability. Apoptosis was increased after only 6 hours by 400 and 800 microM esculetin (p < 0.05), and after 48 hours, as little as 50 microM esculetin(6,7-Dihydroxycoumarin) increased apoptosis (p < 0.05). In preadipocytes, apoptosis was detectable only after 48 hours (p < 0.05) with 200 microM esculetin and higher concentrations. However, results of the cell viability assay indicated a reduction in preadipocyte number in a time- and dose-related manner, beginning as early as 6 hours with 400 and 800 microM esculetin (p < 0.05). Esculetin(6,7-Dihydroxycoumarin) also inhibited adipogenesis of 3T3-L1 preadipocytes. Esculetin(6,7-Dihydroxycoumarin)-mediated inhibition of adipocyte differentiation occurred during the early, intermediate, and late stages of the differentiation process. In addition, esculetin(6,7-Dihydroxycoumarin) induced apoptosis during the late stage of differentiation. DISCUSSION: These findings suggest that esculetin(6,7-Dihydroxycoumarin) can alter fat cell number by direct effects on cell viability, adipogenesis, and apoptosis in 3T3-L1 cells.
    Citation [5]

    Biosci Biotechnol Biochem. 2003 Mar;67(3):631-4.

    Mushroom tyrosinase inhibitory activity of esculetin isolated from seeds of Euphorbia lathyris L.[Pubmed: 12723615 ]
    A tyrosinase inhibitor was isolated from the seeds of Euphorbia lathyris L. by bioassay-guided fractionation and purification, using silica gel column chromatography. It was identified as esculetin (6,7-Dihydroxycoumarin)by comparing its physical properties and spectral data with those of an authentic sample. The IC50 value of esculetin(6,7-Dihydroxycoumarin) in the mushroom tyrosinase activity test was 43 microM. The kinetic study indicates that esculetin(6,7-Dihydroxycoumarin) exhibited competitive inhibition against the oxidation of 3-(3,4-dihydroxyphenyl)-alanine by mushroom tyrosinase. The structure-activity relationships among five esculetin(6,7-Dihydroxycoumarin) analogs suggest that hydroxyl groups at the C6 and C7 positions of the coumarin skeleton played an important role in the expression of tyrosinase inhibitory activity.
    Citation [6]

    Arch Toxicol. 2000 Oct;74(8):467-72.

    Inhibitory effect of esculetin on oxidative damage induced by t-butyl hydroperoxide in rat liver.[Pubmed: 11097384]
    An in vivo study in rats showed that pretreatment with esculetin (6,7-Dihydroxycoumarin,i.p.) at concentrations of 0.5 and 5 mg/kg for 5 days before a single i.p. dose of t-BHP (0.1 mmol/kg) significantly lowered the serum levels of the hepatic enzyme markers (ALT and AST) and reduced oxidative stress in the liver. Histopathological evaluation of the rat livers revealed that esculetin(6,7-Dihydroxycoumarin) reduced the incidence of liver lesions induced by t-BHP, including hepatocyte swelling, leukocyte infiltration, and necrosis. Based on the results described above, we speculate that esculetin(6,7-Dihydroxycoumarin) may play a chemopreventive role via reducing oxidative stress in living systems.
    Citation [7]

    Eur. J. Pharmacol., 1999, 370(3):297-305

    Esculetin suppresses proteoglycan metabolism by inhibiting the production of matrix metalloproteinases in rabbit chondrocytes.[Pubmed: 10334506]
    The possible mechanism of the chondroprotective effect of 6,7-Dihydroxycoumarin (esculetin) was investigated using primary cultures of rabbit articular chondrocytes. Esculetin (EST) significantly suppressed the proteoglycan depletion and the release of pulse-labeled [35S]proteoglycan from the matrix layer of rabbit chondrocytes treated with recombinant human interleukin-1alpha. The matrix metalloproteinase inhibitor, 1,10-phenanthroline, also blocked the proteoglycan depletion and [35S]proteoglycan release. From these results, it is likely that recombinant human interleukin-1alpha-induced proteoglycan depletion is mediated by matrix metalloproteinases. Although esculetin did not directly inhibit collagenolytic activity in the culture media, it significantly suppressed the production of pro-matrix metalloproteinase-1/interstitial procollagenase and pro-matrix metalloproteinase-3/prostromelysin 1, accompanied by a decrease in the steady-state levels of their mRNAs. These results suggest that esculetin is a therapeutically effective candidate for inhibition of cartilage destruction in osteoarthritis and rheumatoid arthritis.