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    Glycyrrhetinic acid
    CAS No. 471-53-4 Price $30 / 20mg
    Catalog No.CFN99152Purity>=98%
    Molecular Weight470.64Type of CompoundTriterpenoids
    FormulaC30H46O4Physical DescriptionPowder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Biological Activity
    Description: Glycyrrhetinic acid, an AChE activator, has anti-inflammatory,and antileukaemic activities. It is a potent inducer of mitochondrial permeability transition and can trigger the pro-apoptotic pathway, it has a low but definite affinity for mineralocorticoid receptors and thus appears to have a direct mineralocorticoid action.
    Targets: PERK | CDK | E2F‑1 | AChR
    In vitro:
    Int J Oncol. 2015 Mar;46(3):981-8.
    Glycyrrhetinic acid induces G1‑phase cell cycle arrest in human non‑small cell lung cancer cells through endoplasmic reticulum stress pathway.[Pubmed: 25573651]
    Glycyrrhetinic acid (GA) is a natural compound extracted from liquorice, which is often used in traditional Chinese medicine.
    The purpose of the present study was to investigate the antitumor effect of GA in human non‑small cell lung cancer (NSCLC), and its underlying mechanisms in vitro. We have shown that GA suppressed the proliferation of A549 and NCI‑H460 cells. Flow cytometric analysis showed that GA arrested cell cycle in G0/G1 phase without inducing apoptosis. Western blot analysis indicated that GA mediated G1‑phase cell cycle arrest by upregulation of cyclin‑dependent kinase inhibitors (CKIs) (p18, p16, p27 and p21) and inhibition of cyclins (cyclin‑D1, ‑D3 and ‑E) and cyclin‑dependent kinases (CDKs) (CDK4, 6 and 2). GA also maintained pRb phosphorylation status, and inhibited E2F transcription factor 1 (E2F‑1) in both cell lines. GA upregulated the unfolded proteins, Bip, PERK and ERP72. Accumulation of unfolded proteins in the endoplasmic reticulum (ER) triggered the unfolded protein response (UPR), which could be the mechanism by which GA inhibited cell proliferation in NSCLC cells. GA then coordinated the induction of ER chaperones, which decreased protein synthesis and induced cell cycle arrest in the G1 phase.
    This study provides experimental evidence to support the development of GA as a chemotherapeutic agent for NSCLC.
    Biochem Pharmacol. 2003 Dec 15;66(12):2375-9.
    Glycyrrhetinic acid-induced permeability transition in rat liver mitochondria.[Pubmed: 14637195]
    Glycyrrhetinic acid, a hydrolysis product of one of the main constituents of licorice, the triterpene glycoside of glycyrrhizic acid, when added to rat liver mitochondria at micromolar concentrations induces swelling, loss of membrane potential, pyridine nucleotide oxidation, and release of cytochrome c and apoptosis inducing factor. These changes are Ca(2+) dependent and are prevented by cyclosporin A, bongkrekic acid, and N-ethylmaleimide. All these observations indicate that Glycyrrhetinic acid is a potent inducer of mitochondrial permeability transition and can trigger the pro-apoptotic pathway.
    In vivo:
    J. Pharm. Pharmacol., 2011, 10(1):613-20.
    The antiinflammatory activity of glycyrrhetinic acid and derivatives.[Reference: WebLink]
    The anti-inflammatory activities of different fractions of Glycyrrhetinic acid or glycyrrhetic acid and some of its derivatives have been assessed in laboratory animals. Some, but not all, preparations have been found to be active using four established methods for testing anti-inflammatory drugs. The findings provide a scientific basis for the clinical use of these compounds in inflammatory diseases, and may explain the discrepancies in the early clinical trials with this drug.
    Glycyrrhetinic acid Description
    Source: The roots of Glycyrrhize glabra L.
    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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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 2.1248 mL 10.6238 mL 21.2477 mL 42.4953 mL 53.1192 mL
    5 mM 0.425 mL 2.1248 mL 4.2495 mL 8.4991 mL 10.6238 mL
    10 mM 0.2125 mL 1.0624 mL 2.1248 mL 4.2495 mL 5.3119 mL
    50 mM 0.0425 mL 0.2125 mL 0.425 mL 0.8499 mL 1.0624 mL
    100 mM 0.0212 mL 0.1062 mL 0.2125 mL 0.425 mL 0.5312 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:
    Bioorg Med Chem. 2014 Jul 1;22(13):3370-8.
    Amino derivatives of glycyrrhetinic acid as potential inhibitors of cholinesterases.[Pubmed: 24853320]
    The development of remedies against the Alzheimer's disease (AD) is one of the biggest challenges in medicinal chemistry nowadays. Although not completely understood, there are several strategies fighting this disease or at least bringing some relief. During the progress of AD, the level of acetylcholine (ACh) decreases; hence, a therapy using inhibitors should be of some benefit to the patients. Drugs presently used for the treatment of AD inhibit the two ACh controlling enzymes, acetylcholinesterase as well as butyrylcholinesterase; hence, the design of selective inhibitors is called for.
    Glycyrrhetinic acid seems to be an interesting starting point for the development of selective inhibitors. Although its glycon, Glycyrrhetinic acid is known for being an AChE activator, several derivatives, altered in position C-3 and C-30, exhibited remarkable inhibition constants in micro-molar range. Furthermore, five representative compounds were subjected to three more enzyme assays (on carbonic anhydrase II, papain and the lipase from Candida antarctica) to gain information about the selectivity of the compounds in comparison to other enzymes. In addition, photometric sulforhodamine B assays using murine embryonic fibroblasts (NiH 3T3) were performed to study the cytotoxicity of these compounds. Two derivatives, bearing either a 1,3-diaminopropyl or a 1H-benzotriazolyl residue, showed a BChE selective inhibition in the single-digit micro-molar range without being cytotoxic up to 30μM.
    In silico molecular docking studies on the active sites of AChE and BChE were performed to gain a molecular insight into the mode of action of these compounds and to explain the pronounced selectivity for BChE.
    Cell Research:
    Int J Mol Cell Med. 2014 Fall;3(4):272-8.
    Glycyrrhetinic Acid Induces Apoptosis in Leukemic HL60 Cells Through Upregulating of CD95/ CD178.[Pubmed: 25635254]
    Acute leukemia is characterized by the accumulation of neoplastic cells in the bone marrow and peripheral blood. Currently, chemotherapy and differentiating agents have been used for the treatment of leukemia. Recently, plant extracts, either alone or in combination with chemo agents, have been proposed to be used for the treatment of cancers.
    The aim of the present research was to study the cytotoxicity and apoptosis effects of an active licorice-derived compound, Glycyrrhetinic acid (GA), on human leukemic HL60 cells. HL60 cells were cultured in RPMI1640 containing 10% fetal bovine serum. Cells were treated with different doses of GA and their viability and proliferation were detected by dye exclusion and 3-bis-(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide (XTT) assays. Apoptosis induction and expression of CD95 and CD178 were analyzed by flow cytometry. We observed that GA decreases cell viability and suppresses cells proliferation in a dose- dependent manner. In addition, our flow cytometry data show that GA not only induces apoptosis in HL60 cells, but also upregulates both CD95 and CD178 expression on the cell surface of these cells in a dose-dependent manner.
    The combination of GA with cytotoxic drugs and differentiation agents requires further investigation.