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    Natural Products
    CAS No. 479-91-4 Price $158 / 20mg
    Catalog No.CFN98172Purity>=98%
    Molecular Weight374.34Type of CompoundFlavonoids
    FormulaC19H18O8Physical DescriptionYellow powder
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    Product Name Vitexicarpin
    CAS No.: 479-91-4
    Catalog No.: CFN98172
    Molecular Formula: C19H18O8
    Molecular Weight: 374.34 g/mol
    Purity: >=98%
    Type of Compound: Flavonoids
    Physical Desc.: Yellow powder
    Targets: TNF-伪 | ROS | NF-kB | Bcl-2/Bax | VEGFR | Histamine Receptor
    Source: The fruits of Vitex trifolia L. var. simplicifolia Cham.
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
    Price: $158 / 20mg
    Inquire / Order:
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    1 Building, No. 83, CheCheng Rd., Wuhan Economic and Technological Development Zone, Wuhan, Hubei 430056, PRC
  • Plants (Basel).2021, 10(4):702.
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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: Vitexicarpin has shown antitumor, cytotoxicity, anti-inflammatory, analgesic and immunoregulatory properties.Vitexicarpin can act as a novel angiogenesis inhibitor, it exerts good antiangiogenic effects by inhibiting vascular-endothelial-growth-factor-(VEGF-) induced endothelial cell proliferation, migration, and capillary-like tube formation on matrigel in a dose-dependent manner. It can significantly reduce vascular inflammation, through inhibition of ROS-NF-κB pathway in vascular endothelial cells.
    Targets: TNF-α | ROS | NF-kB | Bcl-2/Bax | VEGFR | Histamine Receptor
    In vitro:
    Asian Pac J Cancer Prev. 2012;13(12):6369-74.
    Vitexicarpin induces apoptosis in human prostate carcinoma PC-3 cells through G2/M phase arrest.[Pubmed: 23464460]
    Vitexicarpin (3', 5-dihydroxy-3, 4', 6, 7-tetramethoxyflavone), a polymethoxyflavone isolated from Viticis Fructus (Vitex rotundifolia Linne fil.), has long been used as an anti-inflammatory herb in traditional Chinese medicine. It has also been reported that Vitexicarpin can inhibit the growth of various cancer cells. However, there is no report elucidating its effect on human prostate carcinoma cells.
    The aim of the present study was to examine the apoptotic induction activity of Vitexicarpin on PC-3 cells and molecular mechanisms involved. MTT studies showed that Vitexicarpin dose-dependently inhibited growth of PC-3 cells with an IC50~28.8 μM. Hoechst 33258 staining further revealed that Vitexicarpin induced apoptotic cell death. The effect of Vitexicarpin on PC-3 cells apoptosis was tested using prodium iodide (PI)/Annexin V-FITC double staining and flow cytometry. The results indicated that Vitexicarpin induction of apoptotic cell death in PC-3 cells was accompanied by cell cycle arrest in the G2/M phase. Furthermore, our study demonstrated that Vitexicarpin induction of PC-3 cell apoptosis was associated with upregulation of the proapoptotic protein Bax, and downregulation of antiapoptotic protein Bcl-2, release of Cytochrome c from mitochondria and decrease in mitochondrial membrane potential.
    Our findings suggested that Vitexicarpin may become a potential leading drug in the therapy of prostate carcinoma.
    Planta Med. 2002 Nov;68(11):1047-9.
    Tracheospasmolytic activity of viteosin-A and vitexicarpin isolated from vitex trifolia.[Pubmed: 12451502]

    The n-hexane extract that has shown activity in the tracheospasmolytic bioassay was fractionated by solvent extraction and from the major active fraction two compounds were isolated and identified as viteosin-A and Vitexicarpin. These compounds blocked spontaneous contraction of isolated male guinea pig trachea induced by histamine; however only Vitexicarpin was active in a model using sensitized guinea pig trachea stimulated by ovalbumin up to minimum dose of 1.3 x 10(-5) M.
    The result suggests that Vitexicarpin is able to block effects of histamine released from sensitized mast cells possibly by stabilizing the mast cells membrane function.
    Oncotarget . 2017 Apr 27;8(34):56267-56280.
    Casticin attenuates liver fibrosis and hepatic stellate cell activation by blocking TGF-β/Smad signaling pathway[Pubmed: 28915589]
    Abstract Although many advances have been made in understanding the pathogenesis of liver fibrosis, few options are available for treatment. Casticin, one of the major flavonoids in Fructus Viticis extracts, has shown hepatoprotective potential, but its effects on liver fibrosis are not clear. In this study, we investigated the antifibrotic activity of casticin and its underlying mechanism in vivo and in vitro. Male mice were injected intraperitoneally with carbon tetrachloride (CCl4) or underwent bile duct ligation (BDL) to induce liver fibrosis, followed by treatment with casticin or vehicle. In addition, transforming growth factor-β1(TGF-β1)-activated LX-2 cells were used. In vivo experiments showed that treatment with casticin alone had no toxic effect while significantly attenuating CCl4-or BDL-induced liver fibrosis, as indicated by reductions in the density of fibrosis, hydroxyproline content, expression of α-SMA and collagen α1(I) mRNA. Moreover, casticin inhibited LX2 proliferation, induced apoptosis in a time- and dose-dependent manner in vitro. The underlying molecular mechanisms for the effect of casticin involved inhibition of hepatic stellate cell (HSC) activation and reduced the expression of matrix metalloproteinase (MMP)-2, MMP-9, tissue inhibitor of metalloproteinases (TIMP)-1 and TIMP-2 resulting from blocking TGF-β1/Smad signaling, as well as increased the apoptosis of HSCs. The results suggest that casticin has potential benefits in the attenuation and treatment of liver fibrosis. Keywords: CCl4; TGF-β/Smad; casticin; hepatic stellate cell; liver fibrosis.
    J Cell Biochem . 2019 Jun;120(6):9787-9798.
    Casticin inhibits growth and enhances ionizing radiation-induced apoptosis through the suppression of STAT3 signaling cascade[Pubmed: 30520154]
    Abstract Casticin (CTC), one of the major components of Vitex rotundifolia L., has been reported to exert significant beneficial pharmacological activities and can function as an antiprolactin, anticancer, anti-inflammatory, neuroprotective, analgesic, and immunomodulatory agent. This study aimed at investigating whether the proapoptotic effects of CTC may be mediated through the abrogation of signal transducers and activators of transcription-3 (STAT3) signaling pathway in a variety of human tumor cells. We found that CTC significantly decreased cell viability in a concentration-dependent manner and suppressed cell proliferation in 786-O, YD-8, and HN-9 cells. CTC also induced programmed cell death that was found to be mediated via caspase-3 activation and induction of poly(ADP-ribose) polymerase cleavage. Interestingly, CTC repressed both constitutive and interleukin-6-induced STAT3 activation in 786-O and YD-8 cells but only affected constitutive STAT3 phosphorylation in HN-9 cells. Moreover, CTC could potentiate ionizing radiation-induced apoptotic effects leading to the downregulation of STAT3 activation and thus may be used in combination with radiation against diverse malignancies. Keywords: apoptosis; cancer; casticin; radiation; signal transducers and activators of transcription-3.
    Vitexicarpin Description
    Source: The fruits of Vitex trifolia L. var. simplicifolia Cham.
    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:

    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 2.6714 mL 13.3568 mL 26.7137 mL 53.4274 mL 66.7842 mL
    5 mM 0.5343 mL 2.6714 mL 5.3427 mL 10.6855 mL 13.3568 mL
    10 mM 0.2671 mL 1.3357 mL 2.6714 mL 5.3427 mL 6.6784 mL
    50 mM 0.0534 mL 0.2671 mL 0.5343 mL 1.0685 mL 1.3357 mL
    100 mM 0.0267 mL 0.1336 mL 0.2671 mL 0.5343 mL 0.6678 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:
    Inflammation. 2012 Apr;35(2):584-93.
    Vascular protective role of vitexicarpin isolated from Vitex rotundifolia in human umbilical vein endothelial cells.[Pubmed: 21614554]
    Pro-inflammatory cytokines induce injury of endothelial cells caused by increases of adhesion molecules, leading to vascular inflammation and the development of atherosclerosis. Recent pharmacological studies have demonstrated that Vitexicarpin, a flavonoid isolated from Vitex rotundifolia, has anti-inflammatory, antitumor, and analgesic properties.
    In this study, we investigated whether Vitexicarpin (5-100 nM) prevented the TNF-α-induced vascular inflammation process in human umbilical vein endothelial cells (HUVEC). We found that pretreatment with Vitexicarpin decreased TNF-α (10 ng/ml)-induced expression of cell adhesion molecules such as vascular cell adhesion molecule-1, intracellular adhesion molecule-1, and E-selectin as well as matrix metalloproteinase-2 and -9 expression. Preincubation with Vitexicarpin also dose-dependently inhibited TNF-α-induced adhesion of HL-60 monocytic cells. Vitexicarpin significantly decreased TNF-α-induced intracellular reactive oxygen species (ROS) production. Furthermore, Vitexicarpin suppressed NF-κB nuclear translocation and transcriptional activity in TNF-α-treated HUVEC.
    In conclusion, Vitexicarpin significantly reduced vascular inflammation, through inhibition of ROS-NF-κB pathway in vascular endothelial cells.
    Evid Based Complement Alternat Med. 2013;2013:278405.
    Vitexicarpin acts as a novel angiogenesis inhibitor and its target network.[Pubmed: 23476684]
    Vitexicarpin (VIT) isolated from the fruits of Vitex rotundifolia has shown antitumor, anti-inflammatory, and immunoregulatory properties.
    This work is designed to evaluate the antiangiogenic effects of VIT and address the underlying action mechanism of VIT by a network pharmacology approach. The results validated that VIT can act as a novel angiogenesis inhibitor. Firstly, VIT can exert good antiangiogenic effects by inhibiting vascular-endothelial-growth-factor- (VEGF-) induced endothelial cell proliferation, migration, and capillary-like tube formation on matrigel in a dose-dependent manner. Secondly, VIT was also shown to have an antiangiogenic mechanism through inhibition of cell cycle progression and induction of apoptosis. Thirdly, VIT inhibited chorioallantoic membrane angiogenesis as well as tumor angiogenesis in an allograft mouse tumor model. We further addressed VIT's molecular mechanism of antiangiogenic actions using one of our network pharmacology methods named drugCIPHER. Then, we tested some key molecules in the VEGF pathway targeted by VIT and verified the inhibition effects of VIT on AKT and SRC phosphorylation.
    Taken together, this work not only identifies VIT as a novel potent angiogenesis inhibitor, but also demonstrates that network pharmacology methods can be an effective and promising approach to make discovery and understand the action mechanism of herbal ingredients.
    Structure Identification:
    J Nat Prod. 2003 Jun;66(6):865-7.
    Cytotoxic flavone analogues of vitexicarpin, a constituent of the leaves of Vitex negundo.[Pubmed: 12828478 ]

    Bioassay-guided fractionation of the chloroform-soluble extract of the leaves of Vitex negundo led to the isolation of the known flavone Vitexicarpin (1), which exhibited broad cytotoxicity in a human cancer cell line panel. In an attempt to increase the cytotoxic potency of 1, a series of acylation reactions was performed on this compound to obtain its methylated (2), acetylated (3), and six new acylated (4-9) derivatives. Compound 9, the previously unreported 5,3'-dihexanoyloxy-3,6,7,4'-tetramethoxyflavone, showed comparative cytotoxic potency to compound 1 and was selected for further evaluation. However, this compound was found to be inactive when evaluated in the in vivo hollow fiber assay with Lu1, KB, and LNCaP cells at the highest dose (40 mg/kg/body weight) tested, and in the in vivo P-388 leukemia model (135 mg/kg), using the ip administration route.
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