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    alpha-Asarone
    Information
    CAS No. 2883-98-9 Price $40 / 20mg
    Catalog No.CFN93217Purity>=98%
    Molecular Weight208.25Type of CompoundPhenylpropanoids
    FormulaC12H16O3Physical DescriptionPowder
    Download Manual    COA    MSDS    SDFSimilar structuralComparison (Web)  (SDF)
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    alpha-Asarone

    alpha-Asarone
    Product Name alpha-Asarone
    CAS No.: 2883-98-9
    Catalog No.: CFN93217
    Molecular Formula: C12H16O3
    Molecular Weight: 208.25 g/mol
    Purity: >=98%
    Type of Compound: Phenylpropanoids
    Physical Desc.: Powder
    Targets: P-gp | ROS | NO | eNOS | LDL | SOD | GPx | pCREB | BDNF
    Source: The seeds of Daucus carota
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
    Price: $40 / 20mg
    Inquire / Order: manager@chemfaces.com
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  • Related Screening Libraries
    Size /Price /Stock 10 mM * 100 uL in DMSO / Inquiry / In-stock
    10 mM * 1 mL in DMSO / Inquiry / In-stock
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  • Biological Activity
    Description: alpha-Asarone has antioxidant activity, it effectively reversed MDR by inhibiting P-gp function and expression. alpha-Asarone protects against Ang II-mediated damage of endothelial cells and may be developed to prevent injury to cardiovascular tissues. Alpha-asarone congeners as hypolipidemic agents, they appeared to be promising for the treatment of human hyperlipidaemia and thrombotic diseases.Alpha-asarone also attenuates depression-like behavior in nicotine-withdrawn mice.
    Targets: P-gp | ROS | NO | eNOS | LDL | SOD | GPx | pCREB | BDNF
    In vitro:
    BIOTECHNOLOGY LETTERS, 2014, 36(4):685.
    Reversing P-glycoprotein-mediated multidrug resistance in vitro by α-asarone and β-asarone, bioactive cis–trans isomers from Acorus tatarinowii.[Reference: WebLink]
    P-Glycoprotein (P-gp), an ATP-binding cassette transporter, plays an important role in multidrug resistance (MDR).
    METHODS AND RESULTS:
    alpha-Asarone and β-asarone, bioactive cis–trans isomers found in Acorus tatarinowii Schott, were tested for their potential ability to modulate the expression and function of P-gp in Caco-2 cells. MTT assays revealed that both alpha-Asarone and β-asarone significantly enhanced the vincristine-induced cytotoxicity to cells. β-Asarone was the most potent. Flow cytometry showed that alpha-Asarone and β-asarone increased Rhodamine 123 (Rh123) uptake and inhibited Rh123 efflux in Caco-2 cells in a concentration-dependent manner. Furthermore, P-gp expression and P-gp mRNA in cells were decreased by exposure to alpha-Asarone and β-asarone. In addition, β-asarone increased the inhibition of P-gp activity in cells more than α-asarone.
    CONCLUSIONS:
    Thus, alpha-Asarone and β-asarone effectively reversed MDR by inhibiting P-gp function and expression.
    Evidence-Based Complementary and Alternative Medicine, 2014, 2014:1-7.
    Alpha-Asarone Protects Endothelial Cells from Injury by Angiotensin II.[Pubmed: 24757494 ]
    alpha-Asarone is the major therapeutical constituent of Acorus tatarinowii Schott.
    METHODS AND RESULTS:
    In this study, the potential protective effects of alpha-Asarone against endothelial cell injury induced by angiotensin II were investigated in vitro. The EA.hy926 cell line derived from human umbilical vein endothelial cells was pretreated with alpha-Asarone (10, 50, 100 µmol/L) for 1 h, followed by coincubation with Ang II (0.1 µmol/L) for 24 h. Intracellular nitric oxide (NO) and reactive oxygen species (ROS) were detected by fluorescent dyes, and phosphorylation of endothelial nitric oxide synthase (eNOS) at Ser1177 was determined by Western blotting. alpha-Asarone dose-dependently mitigated the Ang II-induced intracellular NO reduction (P < 0.01 versus model) and ROS production (P < 0.01 versus model). Furthermore, eNOS phosphorylation (Ser1177) by acetylcholine was significantly inhibited by Ang II, while pretreatment for 1 h with alpha-Asarone partially prevented this effect (P < 0.05 versus model). Additionally, cell viability determined by the MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay (105~114.5% versus control, P > 0.05) was not affected after 24 h of incubation with α-asarone at 1–100 µmol/L.
    CONCLUSIONS:
    Therefore, alpha-Asarone protects against Ang II-mediated damage of endothelial cells and may be developed to prevent injury to cardiovascular tissues.
    In vivo:
    Journal of Pharmacy & Pharmacology, 2010, 58(10):1343-1349.
    Hypolipidaemic and antiplatelet activity of phenoxyacetic acid derivatives related to α-asarone.[Reference: WebLink]
    The phenoxyacetic acid derivatives 1-6 [2-methoxy-4-(2-propenyl)phenoxyacetic acid (1); 2-methoxy-5-nitro-4-(2-propenyl)phenoxyacetic acid (2); methyl 2-methoxy-4-(2-propenyl)phenoxyacetate (3); ethyl 2-methoxy-4-(2-propenyl)phenoxyacetate (4); methyl 2-methoxy-5-nitro-4-(2-propenyl)phenoxyacetate (5); ethyl 2-methoxy-5-nitro-4-(2-propenyl)phenoxyacetate (6)] related to alpha-Asarone have been reported previously as hypolipidaemic agents in diet-induced hyperlipidaemic mice. We have aimed to expand the pharmacological profile of these derivatives by investigating their hypolipidaemic activity in rats and mice under different experimental conditions. The antiplatelet activity was tested also in-vitro from blood derived from consenting healthy volunteers.
    METHODS AND RESULTS:
    In normolipidaemic rats, compounds 2, 3 and 5 at oral doses of 40 and 80 mg kg(-1) significantly decreased total cholesterol and LDL-cholesterol levels. Moreover, analogues 3 and 5 administered to hypercholesterolaemic rats at the same doses for seven days also produced a reduction in the content of these same lipoproteins. In neither case were the high-density lipoprotein cholesterol and triglyceride concentrations affected. However, practically all tested compounds were found to be hypocholesterolaemic agents, and were shown to effectively lower low-density lipoprotein cholesterol and triglyceride levels in Triton-induced hyperlipidaemic mice at oral doses of 50 and 100 mg kg(-1).
    CONCLUSIONS:
    In all tests, all animals appeared to be healthy throughout the experimental period in their therapeutic ranges. Triton-induced hypercholesterolaemic mice appeared to be a desirable model for this class of hypolipidaemic drugs. On the other hand, compounds 1, 2, 4 and 5 significantly inhibited ADP-induced aggregation in-vitro. These findings indicated that all of these compounds appeared to be promising for the treatment of human hyperlipidaemia and thrombotic diseases.
    alpha-Asarone Description
    Source: The seeds of Daucus carota
    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.
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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 4.8019 mL 24.0096 mL 48.0192 mL 96.0384 mL 120.048 mL
    5 mM 0.9604 mL 4.8019 mL 9.6038 mL 19.2077 mL 24.0096 mL
    10 mM 0.4802 mL 2.401 mL 4.8019 mL 9.6038 mL 12.0048 mL
    50 mM 0.096 mL 0.4802 mL 0.9604 mL 1.9208 mL 2.401 mL
    100 mM 0.048 mL 0.2401 mL 0.4802 mL 0.9604 mL 1.2005 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.
    Protocol
    Animal Research:
    Pharmacological Research, 2005, 52(6):467-474.
    Antioxidant property of alpha-asarone against noise-stress-induced changes in different regions of rat brain.[Reference: WebLink]
    Free radicals and other reactive species are considered to be an important causative factor in the development of neurodegenerative diseases. Recent reports have indicated that exposure to loud noise generates excess oxygen free radicals (OFR) in the brain. Antioxidant properties of medicinal plants are attracting more and more research in medicine, to counteract OFR and to minimize the neurodegenerative processes.
    METHODS AND RESULTS:
    The drug alpha-Asarone (3, 6 and 9 mg kg(-1) body weight, i.p., for 30 days), one of the active principle components of Acorus calamus Linn., was administered intraperitoneally 1/2 h before the animals were exposed to noise-stress (100 dB for 4 h d(-1), for 30 days). We investigated whether 30 days exposure of noise can produce an oxidative stress. Further, if yes then, could alpha-Asarone counteract the stress. This was verified by measuring the activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), levels of reduced glutathione (GSH), Vitamin C, Vitamin E, protein thiols and lipid peroxidation (LPO) in different regions of the rat brain. All the three doses of alpha-Asarone had an effectively protective role by normalizing the increased SOD and LPO, decreased CAT, GPx, GSH, Vitamins C and E and protein thiols due to noise exposure. Thus, action of alpha-Asarone against noise-stress may be due its antioxidant property.
    CONCLUSIONS:
    Our data proved that antioxidant property of alpha-Asarone against noise-stress induced changes in the rat brain. Further, more clinical studies are required to investigate effectiveness of the alpha-Asarone in noisy environment in human subjects.
    European Journal of Pharmacology, 2017:S001429991730674X.
    Alpha-asarone attenuates depression-like behavior in nicotine-withdrawn mice: Evidence for the modulation of hippocampal pCREB levels during nicotine-withdrawal.[Pubmed: 29042206]
    In the present study, the effect alpha-Asarone on nicotine withdrawal-induced depression-like behavior in mice was investigated.
    METHODS AND RESULTS:
    In this study, mice were exposed to drinking water or nicotine solution (10–200 µg/ml) as a source of drinking for forty days. During this period, daily fluid consumption, food intake and body weight were recorded. The serum cotinine level was estimated before nicotine withdrawal. Naïve mice or nicotine-withdrawn mice were treated with alpha-Asarone (5, 10 and 20 mg/kg, i.p.) or bupropion (10 mg/kg, i.p.) for eight consecutive days and the forced swim test (FST) or locomotor activity test was conducted. In addition, the effect of alpha-Asarone or bupropion on the hippocampal pCREB, CREB and BDNF levels during nicotine-withdrawal were measured. Results indicated that alpha-Asarone (5, 10 and 20 mg/kg, i.p.) or bupropion (10 mg/kg, i.p.) pretreatment did not significantly alter the immobility time in the FST or spontaneous locomotor activity in naïve mice. However, the immobility time of nicotine-withdrawn mice was significantly attenuated with alpha-Asarone (5, 10 and 20 mg/kg, i.p.) or bupropion (10 mg/kg, i.p.) pretreatment in the FST. Besides, alpha-Asarone (5, 10 and 20 mg/kg, i.p.) or bupropion (10 mg/kg, i.p.) pretreatment significantly attenuated the hippocampal pCREB levels in nicotine-withdrawn mice.
    CONCLUSIONS:
    Overall, the present results indicate that alpha-Asarone treatment attenuated the depression-like behavior through the modulation of hippocampal pCREB levels during nicotine-withdrawal in mice.
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