| Size | Price | Stock | Qty |
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| 5mg |
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| 25mg |
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| 50mg |
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Purity: =99.15%
Licochalcone A is a naturally occuring chalconoid/phenol and estrogenic chalcone compound extracted from licorice root (Glycyrrhiza glabra or Glycyrrhiza inflata) with antimalarial, anticancer, antibacterial and antiviral activities. Licochalcone A markedly inhibits the in vitro growth of L. major amastigotes in human MDMs and U937 cells. Licochalcone A shows antibacterial effects against all gram-positive bacteria tested and especially against all Bacillus spp. In CT-26 colon cancer cells, Licochalcone A reduces the cell viability and DNA synthesis.
| Targets |
Natural product; UGTs/UDP-glucuronosyltransferases
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| ln Vitro |
Licochalcone A (LCA) demonstrates substantial inhibitory effects against UGT1A1, 1A3, 1A4, 1A6, 1A7, 1A9, and 2B7 (both IC50 and Ki values lower than 5 μM) [2].
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| ln Vivo |
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| Enzyme Assay |
Determination of lipid peroxidation. [3]
The content of MDA, as an index of the extent of lipid peroxidation, was assayed in the form of thiobarbituric acid-reactive substances as previously described [31]. The reaction mixture (4 ml) consisted of 0.2 ml of 8.1% sodium dodecyl sulfate, 1.5 ml of 20% acetic acid (pH 3.5), 1.5 ml of 0.8% thiobarbituric acid, 0.2 ml of the homogenate, and distilled water. The mixture was incubated for 1 hr at 95°, cooled for 5 min with tap water, vigorously mixed with 5 ml of a n-butanol-pyridine (15-1, v/v) mixture, and centrifuged for 10 min at 1200 ×g. The absorbance of the organic layer (upper n-butanol phase) was determined at 532 nm. 1,1,3,3-Tetramethoxypropane was utilized to establish the standard curve, and the final MDA concentration was expressed as nmol MDA per mg protein.[3] Determination of GSH level. [3] To determine GSH content in accordance with the method described by Higach, 0.1 ml of the tissue homogenate was added to an equal volume of 10% trichloroacetic acid solution, then centrifuged for 20 min at 1200 ×g. 0.1 ml of the supernatant was added to 0.5 ml of a 0.2 N H2SO4 solution containing 1 mM NaNO2 and incubated for 5 min at room temperature, followed by the addition of 0.2 ml of a 0.5% sulfamic acid ammonium solution, 1 ml of a 0.4 N HCl solution containing 0.1% HgCl2 and 3% sulfanilamide, and 1 ml of a 0.4 N HCl solution containing 0.1% N-(1-naphthyl)ethylenediamine. Five minutes later, the absorbance was determined at 540 nm. The GSH content was expressed as nmol GSH per mg protein using GSH standard calibration curve. |
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| Cell Assay |
Licochalcone A (LCA), a flavonoid isolated from the famous Chinese medicinal herb Glycyrrhiza uralensis Fisch, presents obvious anti-cancer effects. In this study, the anti-cancer effects and potential mechanisms of LCA in non-small cell lung cancer (NSCLC) cells were studied. LCA decreased cell viability, increased lactate dehydrogenase release, and induced apoptosis in a concentration-dependent manner in NSCLC cells while not in human embryonic lung fibroblast cells. The expression of phosphatidylethanolamine-modified microtubule-associated protein light-chain 3 (LC3-II) and formation of GFP-LC3 punta, two autophagic markers, were increased after treatment with LCA. LCA-induced LC3-II expression was increased when combined with chloroquine (CQ), while knock-down of autophagy related protein (ATG) 7 or ATG5 reversed LCA-induced LC3-II expression and GFP-LC3 punta formation, suggesting that LCA induced autophagy in NSCLC cells. Inhibition of autophagy could not reverse the LCA-induced cell viability decrease and apoptosis. In addition, LCA increased the expression of endoplasmic reticulum stress related proteins, such as binding immunoglobulin protein and C/EBP homologous protein (CHOP). Knock-down of CHOP reversed LCA-induced cell viability decrease, apoptosis, and autophagy. Taken together, LCA-induced autophagic effect is an accompanied phenomenon in NSCLC cells, and CHOP is critical for LCA-induced cell viability decrease, apoptosis, and autophagy.[1]
Human erythrocytes drawn from healthy individuals were exposed for 24 hours to 1-10 µg/ml licochalcone A. Flow cytometry was subsequently employed to estimate phosphatidylserine exposure at the cell surface from annexin V binding, cell volume from forward scatter, [Ca2+]i from Fluo3-fluorescence, and ceramide utilizing specific antibodies. In addition, hemolysis was quantified from hemoglobin release.[2] |
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| Animal Protocol |
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| References |
[1]. Induction of C/EBP homologous protein-mediated apoptosis and autophagy by licochalcone A in non-small cell lung cancer cells. Sci Rep. 2016 May 17;6:26241.
[2]. Licochalcone A Induced Suicidal Death of Human Erythrocytes. Cell Physiol Biochem. 2015;37(5):2060-70. [3]. Licochalcone A inhibits the growth of colon carcinoma and attenuates cisplatin-induced toxicity without a loss of chemotherapeutic efficacy in mice. Basic Clin Pharmacol Toxicol . 2008 Jul;103(1):48-54. |
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| Additional Infomation |
Licochalcone A is a member of chalcones.
Licochalcone a has been reported in Glycyrrhiza uralensis, Euphorbia helioscopia, and other organisms with data available. Licochalcone A is a derivative of the phenol chalconoid, found in and extracted from the roots of Glycyrrhiza species G. glabra and inflata, with potential anti-inflammatory, antibacterial, and anticancer activities. Upon administration, licochalcone A inhibits the phosphatidylinositol-3-kinase/Akt/mammalian target of rapamycin (PI3K/Akt/mTOR) signaling pathway and inhibits the activity of c-Jun N-terminal kinase 1 (JNK-1), a member of the mitogen-activated protein kinase (MAPK) family that plays a role in the MAPK-mediated signaling pathway. Inhibition of the PI3K/Akt/mTOR- and MAPK-signaling pathways induces cell cycle arrest and apoptosis, decreases migration and invasion of cancer cells, and inhibits tumor cell proliferation. Licochalcone A also prevents the production of reactive oxygen species (ROS), and reduces oxidative stress through the nuclear factor-erythroid 2-related factor 2 (Nrf2) pathway. |
| Molecular Formula |
C21H22O4
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| Molecular Weight |
338.3970
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| Exact Mass |
338.151
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| Elemental Analysis |
C, 74.54; H, 6.55; O, 18.91
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| CAS # |
58749-22-7
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| Related CAS # |
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| PubChem CID |
5318998
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| Appearance |
Yellow to orange solid powder
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| Density |
1.2±0.1 g/cm3
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| Boiling Point |
532.6±50.0 °C at 760 mmHg
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| Melting Point |
100°
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| Flash Point |
186.9±23.6 °C
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| Vapour Pressure |
0.0±1.5 mmHg at 25°C
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| Index of Refraction |
1.611
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| LogP |
4.95
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| Hydrogen Bond Donor Count |
2
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| Hydrogen Bond Acceptor Count |
4
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| Rotatable Bond Count |
6
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| Heavy Atom Count |
25
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| Complexity |
488
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| Defined Atom Stereocenter Count |
0
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| SMILES |
O([H])C1C([H])=C(C(/C(/[H])=C(\[H])/C(C2C([H])=C([H])C(=C([H])C=2[H])O[H])=O)=C([H])C=1C(C([H])=C([H])[H])(C([H])([H])[H])C([H])([H])[H])OC([H])([H])[H]
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| InChi Key |
KAZSKMJFUPEHHW-DHZHZOJOSA-N
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| InChi Code |
InChI=1S/C21H22O4/c1-5-21(2,3)17-12-15(20(25-4)13-19(17)24)8-11-18(23)14-6-9-16(22)10-7-14/h5-13,22,24H,1H2,2-4H3/b11-8+
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| Chemical Name |
(E)-3-(4-hydroxy-2-methoxy-5-(2-methylbut-3-en-2-yl)phenyl)-1-(4-hydroxyphenyl)prop-2-en-1-one
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| Synonyms |
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
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| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (7.39 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly. Solubility in Formulation 2: 2.08 mg/mL (6.15 mM) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. View More
Solubility in Formulation 3: 2.08 mg/mL (6.15 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.9551 mL | 14.7754 mL | 29.5508 mL | |
| 5 mM | 0.5910 mL | 2.9551 mL | 5.9102 mL | |
| 10 mM | 0.2955 mL | 1.4775 mL | 2.9551 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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