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    CAS No. 860-79-7 Price $60 / 20mg
    Catalog No.CFN99176Purity>=98%
    Molecular Weight402.66Type of CompoundAlkaloids
    FormulaC26H46N2OPhysical DescriptionWhite cryst.
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Biological Activity
    Description: Cyclovirobuxine D(CVB-D) has vasorelaxant effect, it has been widely used for treatment of cardiac insufficiency and arrhythmias in China, the antiarrhythmic and proarrhythmic potential of this drug might be concerned with prolongation of action potential duration and QT interval. CVB-D can induce autophagy in the MCF-7 human breast cancer cell line by attenuating the phosphorylation of Akt and mTOR , CVB-D-induced autophagy and decrease in cell viability could be blocked by 3-methyladenine, a well-established autophagy inhibitor.
    Targets: Nrf2 | Akt | mTOR
    In vitro:
    J Pharmacol Sci. 2014;125(1):74-82. Epub 2014 Apr 24.
    Cyclovirobuxine D induces autophagy-associated cell death via the Akt/mTOR pathway in MCF-7 human breast cancer cells.[Pubmed: 24758922]
    Autophagy is a highly regulated and multi-step biological process that serves to remove damaged cytoplasmic components and organelles. It has been suggested that the activation of autophagy may be a promising therapeutic strategy for cancer treatment by triggering cell death.
    In this study, we reported that Cyclovirobuxine D (CVB-D), an alkaloid component in a traditional Chinese herb, could induce autophagy in the MCF-7 human breast cancer cell line. CVB-D inhibited the viability of MCF-7 cells in a concentration- and time-dependent manner. Activation of autophagy was characterized by transmission electron microscopy, monodansylcadaverine staining, and expression of autophagy marker microtubule-associated protein 1 light chain 3 (LC3). After CVB-D treatment, a clear accumulation of autophagosomes was observed accompanied with elevated LC3 fluorescent puncta. Western blot analysis revealed that CVB-D significantly promoted the conversion from LC3-I to LC3-II and the expression of autophagy-related protein 5 (ATG5), which are both essential for autophagosome formation. On the other hand, CVB-D-induced autophagy and decrease in cell viability could be blocked by 3-methyladenine, a well-established autophagy inhibitor. Moreover, CVB-D attenuated the phosphorylation of Akt and mTOR, two pivotal suppressors in autophagy pathways.
    These findings shed new light on the pharmacological actions and mechanism of CVB-D and may support the potential utility of autophagy inducers in cancer treatment.
    Chinese Journal of New Drugs, 2012, 21(3):240-5.
    Comparison of the vasorelaxant effects of cyclovirobuxine D and its derivatives in rat aorta rings[Reference: WebLink]
    To compare the vasorelaxant effects of Cyclovirobuxine D (CVB-D) and its derivatives in isolated rat thoracic aorta rings.
    Effects of CVB-D and its derivatives at various concentrations (from 1×10 -5 to 6×10 -4 mol·L -1) on contraction of aorta rings induced by potassium chloride (KCl) or phenylephrine (PE) were evaluated. Effects of preincubation with CVB-D or CBV-D3 at 6×10 -4 mol·L -1 on KCl- or PE-induced contraction were assessed in the aorta rings. In KCl- or PE-precontracted aorta rings, CVB-D showed a concentration-dependent vasorelaxant effect, CVB-D1 showed a weak vessel relaxation effect, but CVB-D2 showed no effect at concentrations of 1×10 -5~6×10 -4 mol·L -1. CVB-D3 showed a stronger vesorelaxant effect than CVB-D in the rings precontracted by KCl or PE. Furthermore, both CVB-D and CVB-D3 exhibited stronger vasorelaxation effects in the aorta rings with intacted endothelium than in the aorta rings with denuded endothelium. Additionally, preincubation with both CVB-D and CVB-D3 inhibited KCl- or PE-induced contraction, and the inhibitive effect of CVB-D3 was stronger than CVB-D.
    CVB-D and CVB-D3 have similar vasorelaxant effect, but CVB-D3 owned a higher maximum effect than CVB-D.
    In vivo:
    Fitoterapia. 2011 Sep;82(6):868-77.
    Beneficial effect of Cyclovirobuxine D on heart failure rats following myocardial infarction.[Pubmed: 21575690]
    The effect of Cyclovirobuxine D, an active ingredient from Buxus microphylla, was investigated in the potential prevention of cardiac dysfunction in rats with congestive heart failure.
    Heart failure was induced by left coronary artery occlusion and verified using echocardiography. Cyclovirobuxine D was administered for 30 days (0.5, 1.0 and 2.0mg/kg, ig) and mortality, cardiac function, hemodynamics, microcirculation, histology and ultrastructure assessments were observed.
    Results from the present study suggest that Cyclovirobuxine D is beneficial for heart failure induced by myocardial infarction and supports the potential for Cyclovirobuxine D as a new therapy for heart failure.
    Cyclovirobuxine Description
    Source: The barks of Buxus sinica var. parvifolia M. Cheng.
    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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    Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals

    Cell. 2018 Jan 11;172(1-2):249-261.e12.
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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 2.4835 mL 12.4174 mL 24.8348 mL 49.6697 mL 62.0871 mL
    5 mM 0.4967 mL 2.4835 mL 4.967 mL 9.9339 mL 12.4174 mL
    10 mM 0.2483 mL 1.2417 mL 2.4835 mL 4.967 mL 6.2087 mL
    50 mM 0.0497 mL 0.2483 mL 0.4967 mL 0.9934 mL 1.2417 mL
    100 mM 0.0248 mL 0.1242 mL 0.2483 mL 0.4967 mL 0.6209 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.
    Kinase Assay:
    Spectrochim Acta A Mol Biomol Spectrosc. 2014 Jul 15;128:552-8.
    Experimental and theoretical investigation on the interaction between cyclovirobuxine D and human serum albumin.[Pubmed: 24691369]
    Cyclovirobuxine D is an active compound extracted from the plant Buxux microphylla, and widely available as medications; however, its abuse may casts potential detrimental effects on human health. By using multispectroscopic techniques and molecular modeling, the interaction of Cyclovirobuxine D with human serum albumin was investigated. The fluorescence results manifested that static type was the operative mechanism for the interaction with human serum albumin. The structural investigation of the complexed HSA through CD, three-dimensional, FT-IR and synchronous fluorescence shown the polypeptide chain of HSA partially destabilizing. Docking studies revealed the molecule to be bound in the subdomain IIA. Finally, we investigated the distance between the bound ligand and Trp-214 of human serum albumin.
    Cell Research:
    Oxid Med Cell Longev. 2015;2015:151972.
    Cyclovirobuxine D Attenuates Doxorubicin-Induced Cardiomyopathy by Suppression of Oxidative Damage and Mitochondrial Biogenesis Impairment.[Pubmed: 26075032]
    The clinical application of doxorubicin (DOX) is compromised by its cardiac toxic effect. Cyclovirobuxine D (CVB-D) is a steroid alkaloid extracted from a traditional Chinese medicine, Buxus microphylla.
    Our results showed that CVB-D pretreatment markedly attenuated DOX-induced cardiac contractile dysfunction and histological alterations. By using TUNEL assay and western blot analysis, we found that CVB-D pretreatment reduced DOX-induced apoptosis of myocardial cells and mitochondrial cytochrome c release to cytosol. CVB-D pretreatment ameliorated DOX-induced cardiac oxidative damage including lipid peroxidation and protein carbonylation and a decrease in the ratio of reduced glutathione (GSH) to oxidized glutathione (GSSG). Moreover, CVB-D was found to prevent DOX-induced mitochondrial biogenesis impairment as evidenced by preservation of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) and nuclear respiratory factor 1 (NRF1), as well as mitochondrial DNA copy number.
    These findings demonstrate that CVB-D protects against DOX-induced cardiomyopathy, at least in part, by suppression of oxidative damage and mitochondrial biogenesis impairment.
    Animal Research:
    Zhong Yao Cai. 2014 Jul;37(7):1213-7.
    Ameliorated effects of cyclovirobuxine D on oxidative stress and energy metabolism in experimental cardiac injured rats induced by sympathetic overactivity in vivo[Pubmed: 25566659]
    To investigate the ameliorated effect of CVB-D on oxidative stress and energy metabolism in experimental cardiac injuried rats induced by sympathetic overactivity in vivo.
    SD rats were randomly divided into five groups as following: control group, model group, Vitamin E 150 mg/kg group, CVB-D low dose and high dose groups, respectively. The rat experimental cardiac injury model was established by exposed to norepinephrine (NE) 3 mg/kg by ip for 16 d. The drugs were administrated to rat for 16 d by ig. The body weight of rats were monitored during all of the experimental period. At the designing ending-time point the indexes were assayed as following: cardiac index, hydroxyproline, histopathologically examination, oxidative stress ( MDA, SOD, CAT, GSH-Px and T-AOC) and energy metabolism indicatricle ( Na+, K(+) -ATPase, and Ca2+, Mg(2+) -ATPase). After exposed with NE for 16 d, the rats of model group was appeared dysfunction of oxidative stress and energy metabolism such as decreasing body weight, increasing cardiac index and hydroxyproline in cardiac tissue, decreasing Na+, K(+) -ATPase and Ca(2+), Mg(2+) -ATPase activities, and deteriorating the oxidative stress. Treated with CVB-D could ameliorate all of the exacerbated indexes.
    CVB-D has protective effect against oxidative stress and energy metabolism in rats of experimental myocardial injury induced by sympathetic overactivity.