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    CAS No. 6681-13-6 Price
    Catalog No.CFN89519Purity>=98%
    Molecular Weight652.77Type of CompoundAlkaloids
    FormulaC39H44N2O7Physical DescriptionPowder
    Download     COA    MSDSSimilar structuralComparison (Web)
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    According to end customer requirements, ChemFaces provide solvent format. This solvent format of product intended use: Signaling Inhibitors, Biological activities or Pharmacological activities.
    Size /Price /Stock 10 mM * 1 mL in DMSO / Inquiry
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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
    Related Libraries
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  • Biological Activity
    Description: Hernandezine, a novel AMPK activator, can inhibit LPS-induced TNFα expression/production in human macrophage cells (THP-1 and U937 lines). Hernandezine is a potent and selective reversing agent for ABCB1-mediated MDR in cancer cells, it induces autophagic cell death in drug-resistant cancers. Hernandezine inhibits calcium-depletion stimulated calcium entry in human and bovine endothelial cells.
    Targets: AMPK | TNF-α | ROS | NF-kB | Autophagy | Calcium Channel
    In vitro:
    J Nat Prod. 2016 Aug 26;79(8):2135-42.
    Hernandezine, a Bisbenzylisoquinoline Alkaloid with Selective Inhibitory Activity against Multidrug-Resistance-Linked ATP-Binding Cassette Drug Transporter ABCB1.[Pubmed: 27504669 ]
    Considering the wide range of diversity and relatively nontoxic nature of natural products, developing a potential modulator of ABCB1 from natural sources is particularly valuable.
    Through screening of a large collection of purified bioactive natural products, Hernandezine was identified as a potent and selective reversing agent for ABCB1-mediated MDR in cancer cells. Experimental data demonstrated that the bisbenzylisoquinoline alkaloid Hernandezine is selective for ABCB1, effectively inhibits the transport function of ABCB1, and enhances drug-induced apoptosis in cancer cells. More importantly, Hernandezine significantly resensitizes ABCB1-overexpressing cancer cells to multiple chemotherapeutic drugs at nontoxic, nanomolar concentrations.
    Collectively, these findings reveal that Hernandezine has great potential to be further developed into a novel reversal agent for combination therapy in MDR cancer patients.
    Oncotarget. 2016 Feb 16;7(7):8090-104.
    Hernandezine, a novel AMPK activator induces autophagic cell death in drug-resistant cancers.[Pubmed: 26811496]
    Drug resistance hinder most cancer chemotherapies and leads to disease recurrence and poor survival of patients. Resistance of cancer cells towards apoptosis is the major cause of these symptomatic behaviours.
    Here, we showed that isoquinoline alkaloids, including liensinine, isoliensinine, dauricine, cepharanthine and Hernandezine, putatively induce cytotoxicity against a repertoire of cancer cell lines (HeLa, A549, MCF-7, PC3, HepG2, Hep3B and H1299). Proven by the use of apoptosis-resistant cellular models and autophagic assays, such isoquinoline alkaloid-induced cytotoxic effect involves energy- and autophagy-related gene 7 (Atg7)-dependent autophagy that resulted from direct activation of AMP activated protein kinase (AMPK). Hernandezine possess the highest efficacy in provoking such cell death when compared with other examined compounds. We confirmed that isoquinoline alkaloid is structurally varied from the existing direct AMPK activators.
    In conclusion, isoquinoline alkaloid is a new class of compound that induce autophagic cell death in drug-resistant fibroblasts or cancers by exhibiting its direct activation on AMPK.
    Hernandezine Description
    Source: The roots of Thalictrum podocarpum.
    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

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    PMID: 29328914

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    doi: 10.1016/j.cmet.2020.01.002.

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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 1.5319 mL 7.6597 mL 15.3193 mL 30.6387 mL 38.2983 mL
    5 mM 0.3064 mL 1.5319 mL 3.0639 mL 6.1277 mL 7.6597 mL
    10 mM 0.1532 mL 0.766 mL 1.5319 mL 3.0639 mL 3.8298 mL
    50 mM 0.0306 mL 0.1532 mL 0.3064 mL 0.6128 mL 0.766 mL
    100 mM 0.0153 mL 0.0766 mL 0.1532 mL 0.3064 mL 0.383 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:
    Oncotarget. 2017 Jun 5;8(40):67218-67226.
    A novel AMPK activator hernandezine inhibits LPS-induced TNFα production.[Pubmed: 28978028 ]

    Here, we found that Hernandezine, a novel AMPK activator, inhibited LPS-induced TNFα expression/production in human macrophage cells (THP-1 and U937 lines). Activation of AMPK is required for Hernandezine-induced anti-LPS response. AMPKα shRNA or dominant negative mutation (T172A) blocked Hernandezine-induced AMPK activation, which almost completely reversed anti-LPS activity by Hernandezine. Exogenous expression of the constitutively activate AMPKα (T172D, caAMPKα) also suppressed TNFα production by LPS. Remarkably, Hernandezine was unable to further inhibit LPS-mediated TNFα production in caAMPKα-expressing cells. Hernandezine inhibited LPS-induced reactive oxygen species (ROS) production and nuclear factor kappa B (NFκB) activation. Treatment of Hernandezine in ex-vivo cultured primary human peripheral blood mononuclear cells (PBMCs) also largely attenuated LPS-induced TNFα production.
    Together, we conclude that AMPK activation by Hernandezine inhibits LPS-induced TNFα production in macrophages/monocytes.
    Life Sci. 1996;58(25):2327-35.
    Plant alkaloids, tetrandrine and hernandezine, inhibit calcium-depletion stimulated calcium entry in human and bovine endothelial cells.[Pubmed: 8649222]
    Depletion of internal Ca2+ stores causes capacitative Ca2+ entry which occurs through non-selective cation channels sensitive to blockade by SK&F 96365. Recently, alkaloids of Chinese herbal medicinal origin, tetrandrine and Hernandezine, have been shown to possess actions including inhibition of Ca2+ channels in non-excitable cell types.
    In this study, we compared the actions of these novel inhibitors to those of SK&F 96365 in fura-2-loaded endothelial cells from human umbilical vein and bovine pulmonary artery. Depletion of Ca2+ from the internal stores was accomplished in Ca(2+)-free medium using an endoplasmic reticulum Ca2+ pump inhibitor, cyclopiazonic acid (CPA) or receptor agonists, histamine and bradykinin. Stimulation with histamine or bradykinin caused a marked and rapid transient increase in Ca2+ signal whereas CPA caused a smaller amplitude increase of longer duration. Restoring Ca2+ to the medium caused marked and sustained increases in the fluorescence indicating movement of Ca2+ into the cytosol presumably stimulated by the emptied Ca2+ stores. SK&F 96365 as well as tetrandrine and Hernandezine antagonized depletion-induced Ca2+ entry.
    The results suggest that these putative inhibitors interact with Ca2+ entry triggered by depletion of the internal Ca2+ stores and their action is presumed to be on the non-selective cation channels. Their effectiveness may be enhanced by the mechanisms which lead to the opening of the Ca2+ influx channel.