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    Licochalcone A
    CAS No. 58749-22-7 Price $88 / 20mg
    Catalog No.CFN99575Purity>=98%
    Molecular Weight338.40Type of CompoundChalcones
    FormulaC21H22O4Physical DescriptionYellow powder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Biological Activity
    Description: Licochalcone A is an estrogenic flavanoid extracted from licorice root, showing antimalarial, antileishmanial, anticancer, anti-inflammatory, antibacterial and antiviral activities. It could be a promising strategy in treating osteoporotic weight-bearing bones fractures with defects, and be a useful compound for the development of antibacterial agents for the preservation of foods containing high concentrations of salts and proteases, in which cationic peptides might be less effective.
    Targets: NF-kB | IL Receptor | IkB | P-gp | PARP | P450 (e.g. CYP17) | MMP(e.g.TIMP) | p65 | Caspase | TNF-α | NO | Antifection | IKK
    In vitro:
    Antimicrob Agents Chemother. 1994 Jul;38(7):1470-5.
    Licochalcone A, a new antimalarial agent, inhibits in vitro growth of the human malaria parasite Plasmodium falciparum and protects mice from P. yoelii infection.[Pubmed: 7979274]
    Licochalcone A, isolated from Chinese licorice roots, inhibited the in vitro growth of both chloroquine-susceptible (3D7) and chloroquine-resistant (Dd2) Plasmodium falciparum strains in a [3H]hypoxanthine uptake assay. The growth inhibition of the chloroquine-resistant strain by Licochalcone A was similar to that of the chloroquine-susceptible strain.
    To examine the activity of Licochalcone A on the different asexual blood stages of the parasite, Licochalcone A was added to highly synchronized cultures containing rings, trophozoites, and schizonts. The growth of the parasites at all stages was inhibited by Licochalcone A. The in vivo activity of Licochalcone A was tested in a mouse model of infection with P. yoelii. Licochalcone A administered either intraperitoneally or orally for 3 to 6 days protected the mice from the otherwise lethal P. yoelii infection.
    These results demonstrate that Licochalcone A exhibits potent antimalarial activity and might be developed into a new antimalarial drug.
    Antimicrob Agents Chemother. 2002 May;46(5):1226-30.
    Antibacterial activity of licochalcone A against spore-forming bacteria.[Pubmed: 11959549 ]
    Licochalcone A was isolated from the roots of licorice, Glycyrrhiza inflata, which has various uses in the food and pharmaceutical industries; isolation was followed by extraction with ethanol and column chromatography with silica gel.
    In this study, the activities of Licochalcone A against some food contaminant microorganisms were evaluated in vitro. The vegetative cell growth of Bacillus subtilis was inhibited in a Licochalcone A concentration-dependent manner and was completely prevented by 3 micrograms of Licochalcone A/ml. Licochalcone A showed a high level of resistance to heating at 80 to 121 degrees C for 15 min. Licochalcone A did not inhibit the germination of heat-treated spores of B. subtilis induced by L-alanine. Licochalcone A showed effects against all gram-positive bacteria tested and especially was effective against all Bacillus spp. tested, with MICs of 2 to 3 micrograms/ml, but was not effective against gram-negative bacteria or eukaryotes at 50 micrograms/ml. Although the cationic antimicrobial peptides protamine and epsilon-poly-L-lysine resulted in the loss of antimicrobial activity in the presence of either 3% (wt/vol) NaCl or protease at 20 micrograms/ml, the antibacterial activity of Licochalcone A was resistant to these conditions.
    Thus, Licochalcone A could be a useful compound for the development of antibacterial agents for the preservation of foods containing high concentrations of salts and proteases, in which cationic peptides might be less effective.
    In vivo:
    Exp Biol Med (Maywood). 2015 Jan;240(1):26-33.
    Role of licochalcone A on thymic stromal lymphopoietin expression: implications for asthma.[Pubmed: 25055998]
    Asthma is a common chronic inflammatory disease characterized by the infiltration and accumulation of memory-like Th2 cells and eosinophils. Viral infection has emerged as the most common cause of severe episodes of asthma. For the treatment of bronchial asthma, the root of liquorice (Glycyrrhiza glabra) has been used as a traditional medicine in the East and West. Licochalcone A is the predominant, characteristic chalcone in liquorice root.
    To determine whether Licochalcone A possesses an anti-inflammatory effect, we tested its effect on the expression and production of thymic stromal lymphopoietin (TSLP) in BEAS 2B cells and primary bronchial epithelial cells. We found that polyinosinic-polycytidylic acid (poly-IC)-induced TSLP expression was suppressed by treatment with Licochalcone A in a dose- and time-dependent manner. We also found that poly-IC-induced mRNA expression of other proinflammatory mediators such as MCP-1, RANTES, and IL-8 was suppressed by Licochalcone A. Furthermore, Licochalcone A suppressed poly-IC-induced nuclear factor kappa B (NF-κB) nuclear translocation and DNA-binding activity by suppressing the Iκβ kinase (IKK) activity but not by direct phosphorylation of p65 at serine 276.
    Collectively, our findings suggest that Licochalcone A suppresses poly-IC-induced TSLP expression and production by inhibiting the IKK/NF-κB signaling pathway, which might be involved in the pathogenesis of virus-exacerbated asthma. Further elucidation of the mechanisms underlying these observations can help develop therapeutic strategies for virally induced asthma.
    Biomaterials. 2014 Mar;35(9):2789-97.
    The effect of licochalcone A on cell-aggregates ECM secretion and osteogenic differentiation during bone formation in metaphyseal defects in ovariectomized rats.[Pubmed: 24439395 ]
    Treatment of weight-bearing bones fractures with defects is critical for patients with osteoporosis's rehabilitation. Although various tissue engineering methods were reported, the best treating strategy for tissue engineering remains to be identified as the limitation of enhancing the ability of the osteogenetic differentiation potential of seed cell is one of the cardinal issues to be solved. The objective of this study is to investigate the feasibility of applying licochalcone-A (L-A) and bone marrow mesenchymal stem cells (BMSC)-aggregate in bone repairing tissue engineering and further study the biological effects of L-A on the cell aggregate formation and osteogenic properties.
    80 female Sprague Dawley rats underwent bilateral ovariectomy were made with a 3.5 mm femurs bone defects without any fixation. These rats were then randomly assigned to five different treatment groups: (1) empty defect (n = 16), (2) CA-LA (n = 16), (3) CA-N (n = 16), (4) CA-L (n = 16), (5) CA-S (n = 16) and 16 female SD rats were treated as a control. Data showed that L-A administrated cell aggregate had a stronger osteogenic differentiation and mineralized formation potential than non-administrated group both in vitro and in vivo. For in vitro study, L-A administrated group had a more significant expression of ECM, osteogenic associated maker in addition with more mineralized area and higher ALP activity compared with the control group. For in vivo study, 3D reconstruction of micro-CT, HE staining and bone strength results showed that newly formed bone in groups administrated by L-A was significant higher than that in Sham group at 2, 4, 8 and 12 weeks after transplantation, especially for groups which was systematically injected with L-A at 8 weeks.
    Results of our study demonstrated that LA could positively affect cell behavior in cell-aggregate engineering and could be a promising strategy in treating osteoporotic weight-bearing bones fractures with defects.
    Licochalcone A Description
    Source: The roots of Glycyrrhiza 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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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 2.9551 mL 14.7754 mL 29.5508 mL 59.1017 mL 73.8771 mL
    5 mM 0.591 mL 2.9551 mL 5.9102 mL 11.8203 mL 14.7754 mL
    10 mM 0.2955 mL 1.4775 mL 2.9551 mL 5.9102 mL 7.3877 mL
    50 mM 0.0591 mL 0.2955 mL 0.591 mL 1.182 mL 1.4775 mL
    100 mM 0.0296 mL 0.1478 mL 0.2955 mL 0.591 mL 0.7388 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:
    Biopharm Drug Dispos. 2014 Oct;35(7):382-90.
    Effects of licochalcone A on the bioavailability and pharmacokinetics of nifedipine in rats: possible role of intestinal CYP3A4 and P-gp inhibition by licochalcone A.[Pubmed: 24903704]
    The purpose of this study was to investigate the possible effects of Licochalcone A (a herbal medicine) on the pharmacokinetics of nifedipine and its main metabolite, dehydronifedipine, in rats.
    The pharmacokinetic parameters of nifedipine and/or dehydronifedipine were determined after oral and intravenous administration of nifedipine to rats in the absence (control) and presence of Licochalcone A (0.4, 2.0 and 10 mg/kg). The effect of Licochalcone A on P-glycoprotein (P-gp) and cytochrome P450 (CYP) 3A4 activity was also evaluated. Nifedipine was mainly metabolized by CYP3A4. Licochalcone A inhibited CYP3A4 enzyme activity in a concentration-dependent manner with a 50% inhibition concentration (IC50 ) of 5.9 μm. In addition, Licochalcone A significantly enhanced the cellular accumulation of rhodamine-123 in MCF-7/ADR cells overexpressing P-gp. The area under the plasma concentration-time curve from time 0 to infinity (AUC) and the peak plasma concentration (Cmax ) of oral nifedipine were significantly greater and higher, respectively, with Licochalcone A. The metabolite (dehydronifedipine)-parent AUC ratio (MR) in the presence of Licochalcone A was significantly smaller compared with the control group.
    The above data could be due to an inhibition of intestinal CYP3A4 and P-gp by Licochalcone A. The AUCs of intravenous nifedipine were comparable without and with Licochalcone A, suggesting that inhibition of hepatic CYP3A4 and P-gp was almost negligible.
    Cell Research:
    Tumour Biol. 2014 Aug;35(8):7467-74.
    Antimetastatic effects of licochalcone A on oral cancer via regulating metastasis-associated proteases.[Pubmed: 24789273]
    Licochalcone A, a major phenolic constituent of the licorice species Glycyrrhiza inflata, has been proven to possess various biological benefits including anti-cancer activity. However, the detailed effects and molecular mechanisms of Licochalcone A on the invasiveness and metastasis of oral cancer cells have not been fully understood.
    Thus, SCC-25 oral cancer cells were subjected to a treatment with Licochalcone A at indicated concentrations (25, 50, and 100 μg/mL) for 36 h and then analyzed for the effect of Licochalcone A on the cell migration and invasion. In vitro assays, including wound healing, cell adhesion, and cell invasion/migration assays, revealed that Licochalcone A treatment significantly inhibited the cell migration/invasion capacities of SCC-25 cells. Also, results of zymography and Western blotting showed that activity and protein level of matrix metalloproteinase-2 (MMP-2) was suppressed, but TIMP-2 level was increased, indicating the important role of MMP-2 and TIPM-2 in anti-metastatic regulation of SCC-25 cells. Furthermore, Licochalcone A was shown to suppress the nuclear factor-kappa B (NF-κB) signal, as evidenced by the decreased expression of phosphorylated p65 (p-65) protein in Licochalcone A-treated SCC-25 cells. Notably, we also found that Licochalcone A treatment increased the expression of the epithelial marker E-cadherin and decreased the expression of mesenchymal markers N-cadherin in SCC-25 cells. This is the first report describing the effects and possible mechanisms of Licochalcone A on tumor invasion and metastasis of SCC-25 cells.
    Taken together, our findings support that Licochalcone A can be developed to a potent anti-metastatic candidate for oral cancer therapy.
    Animal Research:
    Antimicrob Agents Chemother. 1994 Jun; 38(6): 1339–44.
    Antileishmanial activity of licochalcone A in mice infected with Leishmania major and in hamsters infected with Leishmania donovani.[Pubmed: 8092835 ]
    This study was designed to examine the antileishmanial activity of the oxygenated chalcone Licochalcone A in mice and hamsters infected with Leishmania parasites.
    Intraperitoneal administration of Licochalcone A at doses of 2.5 and 5 mg/kg of body weight per day completely prevented lesion development in BALB/c mice infected with Leishmania major. Treatment of hamsters infected with L. donovani with intraperitoneal administration of Licochalcone A at a dose of 20 mg/kg of body weight per day for 6 consecutive days resulted in a > 96% reduction of parasite load in the liver and the spleen compared with values for untreated control animals. The [3H]thymidine uptake by the parasites isolated from the treated hamsters was only about 1% of that observed in parasites isolated from the controls. Oral administration of Licochalcone A at concentrations of 5 to 150 mg/kg of body weight per day for 6 consecutive days resulted in > 65 and 85% reductions of L. donovani parasite loads in the liver and the spleen, respectively, compared with those of untreated control hamsters.
    These data clearly demonstrate that Licochalcone A is a promising lead for the development of a new drug against leishmaniases.