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    Natural Products
    beta-Asarone
    Information
    CAS No. 5273-86-9 Price
    Catalog No.CFN98870Purity>=98%
    Molecular Weight208.3 Type of CompoundPhenylpropanoids
    FormulaC12H16O3Physical DescriptionOil
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    beta-Asarone

    beta-Asarone
    Product Name beta-Asarone
    CAS No.: 5273-86-9
    Catalog No.: CFN98870
    Molecular Formula: C12H16O3
    Molecular Weight: 208.3 g/mol
    Purity: >=98%
    Type of Compound: Phenylpropanoids
    Physical Desc.: Oil
    Targets: NF-kB | NO | NOS | COX | JNK | Beta Amyloid | mTOR | Akt | p53 | p21 | ROCK
    Source: The herbs of Asarum sieboldii Miq.
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
    Price:
    Inquire / Order: manager@chemfaces.com
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  • Processes2021, 9(11),2065.
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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: beta-Asarone has neuroprotection, anti-tumor, anthelmintic, anti-inflammary, and anticoagulant effects, it can afford a beneficial inhibition on both mRNA and protein expression of Bad, Bax, and cleavage of caspases 9 in rat hippocampus following intrahippocampal injections of Abeta (1-42).beta-Asarone prevents autophagy and synaptic loss by reducing ROCK expression in SAMP8 mice. beta Asarone can cause liver and cardiac damages, it also has reproductive toxicity.
    Targets: NF-kB | NO | NOS | COX | JNK | Beta Amyloid | mTOR | Akt | p53 | p21 | ROCK
    In vitro:
    Nat Prod Commun. 2009 Feb;4(2):275-8.
    Compositional variations and anthelmentic activity of essential oils from rhizomes of different wild populations of Acorus calamus L. and its major component, beta-Asarone.[Pubmed: 19370938]
    Hydro-distilled essential oils from Acorus calamus rhizomes collected from six different geographical zones in the northwest Himalayan region of Uttarakhand have been analyzed by GC and GC/MS.
    METHODS AND RESULTS:
    All the oils differed in their qualitative and quantitative make up, although beta-Asarone was the major constituent of all of them. The essential oils and the isolated beta-Asarone were screened for anthelmintic activity using contractility of Ascaridia galli. beta-Asarone, in particular, showed potent activity with IC50 values of 75.4 +/- 61.8 ng/mL.
    Food Chem Toxicol. 2014 Oct;72:265-72.
    β-Asarone (cis-2,4,5-trimethoxy-1-allyl phenyl), attenuates pro-inflammatory mediators by inhibiting NF-κB signaling and the JNK pathway in LPS activated BV-2 microglia cells.[Pubmed: 25066769]
    Acorus species contains diverse pharmacologically active phytochemicals including α-asarone, beta-Asarone, and eugenol.
    METHODS AND RESULTS:
    We determined if beta-Asarone isolated from Acorus gramineus (AG) Solander would be efficacious in protecting BV-2 microglia cells from lipopolysaccharide (LPS)-induced stress signaling. BV-2 microglial cells were pretreated with an AG ethanol extract (1, 10, and 100 μg/mL) or beta-Asarone (10, 50, and 100 μM) prior to exposure to LPS (100 ng/mL). AG and beta-Asarone inhibited LPS-induced production of nitric oxide in a dose-dependent manner. The mRNA and protein levels of inducible nitric oxide synthase and cyclooxygenase-2 also decreased dose dependently following AG and beta-Asarone treatments. Immunostaining and immunoblot studies revealed that beta-Asarone also suppressed nuclear factor (NF)-κB activation by blocking IkB degradation. Further mechanistic studies revealed that beta-Asarone acted through the JNK/MAPK pathway.
    CONCLUSIONS:
    Taken together, our findings demonstrate that beta-Asarone exhibits anti-inflammatory effects by suppressing the production of pro-inflammatory mediators through NF-κB signaling and the JNK pathways in activated microglial cells and might be developed as a promising candidate to treat various neuroinflammatory diseases.
    In vivo:
    Phytomedicine. 2013 Apr 15;20(6):512-20.
    β-Asarone induces senescence in colorectal cancer cells by inducing lamin B1 expression.[Pubmed: 23357361 ]
    Colorectal cancer is a leading cause of cancer mortality with a complex carcinogenesis that includes reduced cellular senescence. Lamin proteins are decreased in senescing cells, and frequently decreased in malignancies.
    METHODS AND RESULTS:
    This study identified a new drug candidate for colorectal cancer that appears to target cell senescence via a lamin protein. beta-Asarone (1-propenyl-2,4,5-methoxybenzol) is a compound from the traditional medical herb Acorus calamus Linn. This study tested the in vitro and in vivo effects of beta-Asarone on colorectal cancer cells by testing cell viability using human colorectal cell lines HT29 and SW480 in MTT assays; tumorigenesis using xenografts in nude mice and a mouse model of colorectal cancer; cell senescence using senescence-associated β-galactosidase activity; and expression of cancer and senescence-related proteins, specifically lamins, Oct-1, p53, p21, and p15, by Western blot. beta-Asarone appeared to increase expression of lamin B1, p53, p21, but not lamin A/C. beta-Asarone regulates p15 expression by regulation of Oct-1 binding.
    CONCLUSIONS:
    Collectively, the results suggested that beta-Asarone inhibits colon cancer formation in vivo and in vitro by inducing senescence. Since beta-Asarone induced lamin B1 expression, a model is proposed in which beta-Asarone inhibits colorectal cancer by inducing senescence through lamin B1.
    Biomed Pharmacother . 2016 Oct;83:153-159.
    Beta-asarone protects against MPTP-induced Parkinson's disease via regulating long non-coding RNA MALAT1 and inhibiting α-synuclein protein expression[Pubmed: 27470562]
    Abstract Objective: Numerous long non-coding RNAs (lncRNA) have been identified in neurodegenerative disorders including Parkinson's disease (PD). Emerging evidence demonstrates that β-asarone functions as neuroprotective effects in both in vitro and in vivo models. However, the role of β-asarone and its potential mechanism in PD remain not completely clear. Methods: MPTP-induced PD mouse model and SH-SY5Y cells subjected to MPP+ as its in vitro model were used to evaluate the effects of β-asarone on PD. LncRNA MALAT1 and α-synuclein expression were determined by real-time PCR and western blot methods. Results: β-Asarone significantly increased the TH+ cells number and decreased the expression levels of MALAT1 and α-synuclein in midbrain tissue of PD mice. RNA pull-down and immunoprecipitation assays confirmed that MALAT1 associated with α-synuclein, leading to the increased stability of α-synuclein and its expression in SH-SY5Y cells. β-asarone elevated the viability of cells exposed to MPP+. Either overexpressed MALAT1 or α-synuclein could canceled the protective effect of β-asarone on cell viability. In PD mice, pcDNA-MALAT1 also decreased the TH+ cells number and increased the α-synuclein expression in PD mice with treatment of β-asarone. Conclusion: β-Asarone functions as a neuroprotective effect in both in vivo and in vitro models of PD via regulating MALAT1 and α-synuclein expression. Keywords: Long non-coding RNA; Parkinson’s disease; α-Synuclein; β-Asarone.
    beta-Asarone Description
    Source: The herbs of Asarum sieboldii Miq.
    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 4.8008 mL 24.0038 mL 48.0077 mL 96.0154 mL 120.0192 mL
    5 mM 0.9602 mL 4.8008 mL 9.6015 mL 19.2031 mL 24.0038 mL
    10 mM 0.4801 mL 2.4004 mL 4.8008 mL 9.6015 mL 12.0019 mL
    50 mM 0.096 mL 0.4801 mL 0.9602 mL 1.9203 mL 2.4004 mL
    100 mM 0.048 mL 0.24 mL 0.4801 mL 0.9602 mL 1.2002 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
    Kinase Assay:
    Eur J Pharmacol. 2014 Oct 15;741:195-204.
    Beta-asarone attenuates amyloid beta-induced autophagy via Akt/mTOR pathway in PC12 cells.[Pubmed: 25160744]
    Alzheimer's disease (AD) is an age related and progressive neurodegenerative disease. Autophagy is a self-degradative process and plays a critical role in removing long-lived proteins and damaged organelles. Recent evidence suggests that autophagy might be involved in the pathogenesis of AD. beta-Asarone have various neuroprotective effects. However, the effect of β-asarone on autophagy in amyloid β-peptide (Aβ) induced cell injury is unclear, and little is known about the signaling pathway of β-asarone in autophagy regulation. The aim of the present study was to determine whether beta-Asarone protects cells from Aβ1-42 induced cytotoxicity via regulation of Beclin-1 dependent autophagy and its regulating signaling pathway.
    METHODS AND RESULTS:
    We examined effects of beta-Asarone on cell morphology, cell viability, neuron specific enolase (NSE) levels, autophagosomes and regulating Beclin-1, p-Akt and p-mTOR expressions in Aβ1-42 treated PC12 cells. We found that beta-Asarone could maintain the original morphology of cells and increase cell viability and decrease NSE levels significantly. Meanwhile, beta-Asarone decreased Beclin-1 expression significantly. In addition, beta-Asarone can increase levels of p-Akt and p-mTOR. These results showed that beta-Asarone protected cells from Aβ1-42 induced cytotoxicity and attenuated autophagy via activation of Akt-mTOR signaling pathway, which could be involved in neuroprotection of beta-Asarone against Aβ toxicity.
    CONCLUSIONS:
    Our findings suggest that beta-Asarone might be a potential preventive drug for AD.
    Animal Research:
    Proc West Pharmacol Soc. 1991;34:107-12.
    The anticoagulant effect of beta-asarone in the mouse and the rat.[Pubmed: 1788271]
    The anticoagulant effect of beta-Asarone in the mouse and the rat.
    Life Sci. 2017 Mar 15;173:150-160.
    Assessing reproductive toxicity and antioxidant enzymes on beta asarone induced male Wistar albino rats: In vivo and computational analysis.[Pubmed: 27569590 ]
    beta-Asarone is the major constituent of oil obtained from Acorus calamus, the Indian traditional medicine plant. Several studies have shown that beta-Asarone causes liver and cardiac damages but the reproductive toxicity is not well understood. The present study was initiated to investigate whether beta-Asarone has the potential to cause reproductive toxicity by inducing oxidative stress in the testis of male Wistar albino rats.
    METHODS AND RESULTS:
    For this study, the animals were divided into six groups: Group I was treated with saline (normal saline), Group II with DMSO (vehicle control) and Group III with cisplatin (10mg/kgb.wt.). Group IV, V and VI animals were administrated at three dose levels of beta-Asarone 12.5, 25 and 50mg/kgb.wt. The treatment was carried out for 14days and animals were sacrificed on 29th day and processed for sperm analysis, hormone assay, histopathological, and antioxidant enzymatic assays. We also used molecular docking studies to predict the binding nature of beta-Asarone with luteinizing hormone receptor (LHR) and follicle-stimulating hormone receptor (FSHR). beta-Asarone administered at a dose of 50mg/kgb.wt. was responsible for inducing certain noticeable degenerative changes in histopathological analysis of the tissue. This was supported by altered sperm morphology and hormonal variations when compared to the control groups. Antioxidant enzyme levels were also found to be decreased. This was further validated by molecular docking studies.
    CONCLUSIONS:
    The present study provides evidence that beta-Asarone administered at a dose of 50mg/kg b.wt. is capable enough in bringing about moderate amount of degenerative changes in rat testis and altered antioxidant status. Therefore provides a suitable evidence to prove that beta-Asarone causes reproductive toxicity.
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