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Licochalcone B


  • Brand : BIOFRON

  • Catalogue Number : BD-P0909

  • Specification : 98.0%(HPLC)

  • CAS number : 58749-23-8

  • Formula : C16H14O5

  • Molecular Weight : 286.28

  • PUBCHEM ID : 5318999

  • Volume : 25mg

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Catalogue Number


Analysis Method





Molecular Weight



White powder

Botanical Source

This product is isolated and purified from the roots of Glycyrrhiza glabra L.

Structure Type





2-methoxy-3,4,4'-trihydroxychalcone/Licochalcone B/Licochalcon B/(2E)-3-(3,4-Dihydroxy-2-methoxyphenyl)-1-(4-hydroxyphenyl)-2-propen-1-one/2-Propen-1-one, 3-(3,4-dihydroxy-2-methoxyphenyl)-1-(4-hydroxyphenyl)-, (2E)-/licochalcone



Hepatoprotective effects of licochalcone B on carbon tetrachloride-induced liver toxicity in mice.[Pubmed: 27746874 ]Iran J Basic Med Sci. 2016 Aug;19(8):910-5. The objective of this study was to investigate the hepatoprotective effect of Licochalcone B (LCB) in a mice model of carbon tetrachloride (CCl4)-induced liver toxicity. METHODS AND RESULTS:CCl4-induced hepatotoxicity was manifested by an increase in the levels of ALT, AST, MDA, IL-6, CRP, and TNF-ɑ, and a decrease in the SOD level and GSH/GSSG ratio in the serum. The histopathological examination of the liver sections revealed necrosis and inflammatory reactions. Pretreatment with LCB decreased the levels of ALT, AST, MDA, GSSG, IL-6, CRP, TNF-ɑ, and the protein expression of p38 and NF-κB, increased the level of SOD and GSH, and normalized the hepatic histo-architecture. CONCLUSIONS: LCB protected the liver from CCl4-induced injury. Protection may be due to inhibition of p38 and NFκB signaling, which subsequently reduced inflammation in the liver.


1.4±0.1 g/cm3


Methanol; Ethanol; DMF

Flash Point

208.5±23.6 °C

Boiling Point

550.5±50.0 °C at 760 mmHg

Melting Point



InChl Key


WGK Germany


HS Code Reference

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:58749-23-8) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.




The present study explored the molecular mechanism by which licochalcone B induces the cell cycle arrest and apoptosis in human hepatoma cell HepG2. Initial extraction and identification were performed by HPLC, UPLC-TOF-MS/MS, and NMR analysis, respectively. Licochalcone B inhibited the HepG2 growth with IC50 (110.15 μM) after 24 h, caused morphological distortion, and seized the cell cycle in the G2/M phase (cell arrest in G2/M:43.1 ± 2.2% for 120 μM versus 23.7 ± 1.2% for control), as well as induced apoptosis and intracellular ROS generation. Furthermore, exposure to licochalcone B markedly affected the cell cycle (up/down regulation) at mRNA and protein levels. Apoptosis was induced through the activation of receptor-mediated and mitochondrial pathways. The inhibition of Caspase 8 and Caspase 9 proteins abolished the licochalcone B induced apoptosis. The present work suggested that licochalcone B may further be identified as a potent functional food component with specific health benefits.


Glycyrrhiza uralensis Fisch; HepG2 cells; apoptosis; licochalcone B; mechanisms


Licochalcone B Extracted from Glycyrrhiza uralensis Fisch Induces Apoptotic Effects in Human Hepatoma Cell HepG2.


Wang J1, Liao AM2, Thakur K1, Zhang JG1, Huang JH2,3, Wei ZJ1,4.

Publish date

2019 Mar 27




Oxidative stress has been established as a key cause of alcohol-induced hepatotoxicity. Licochalcone B, an extract of licorice root, has shown antioxidative properties. This study was to investigate the effects and mechanisms of licochalcone B in ethanol-induced hepatic injury in an in vitro study.

An in vitro model of Ethanol-induced cytotoxicity in BRL cells was used in this study. Cell injury was assessed using WST-1 assay and lactate dehydrogenase, alanine transaminase, and aspartate aminotransferase release assay. Cell apoptosis were quantified by flow cytometric analysis. The intracellular oxidative level was evaluated by reactive oxidative species, malondialdehyde and glutathione detection. Furthermore, the expression level of Erk, p-Erk, Nrf-2 were assessed using Western blot.

Treatment with ethanol induced marked cell injury and cell apoptosis in BRL cells. Licochalcone B significantly attenuated ethanol-induced cell injury, and inhibited cell apoptosis. Furthermore, licochalcone B significantly inhibited ethanol-induced intracellular oxidative level, upregulated the expression of p-Erk, and promoted nuclear localization of Nrf2. Additionally, this hepatoprotective role was significantly abolished by inhibition of Erk signaling. However, no apparent effects of Erk inhibition were observed on ethanol-induced hepatotoxicity.

This study demonstrates that licochalcone B protects hepatocyte from alcohol-induced cell injury, and this hepatoprotective role might be attributable to apoptosis reduction, inhibition of oxidative stress, and upregulation of Erk-Nrf2. Therefore, licochalcone B might possess potential as a novel therapeutic drug candidate for alcohol-related liver disorders.


Alcohol; BRL cells; Erk; Hepatotoxicity; Nrf; Oxidative stress


Protective role of licochalcone B against ethanol-induced hepatotoxicity through regulation of Erk signaling.


Gao XP1, Qian DW2, Xie Z3, Hui H3.

Publish date

2017 Feb




Epidermal growth factor receptor (EGFR) gene alterations are associated with sensitization to tyrosine kinase inhibitors such as gefitinib in lung cancer. Some patients suffering from non-small cell lung cancer (NSCLC) have difficulty in treating the cancer due to resistance acquired to gefitinib with MET amplification. Therefore EGFR and MET may be attractive targets for lung cancer therapy.

This study aimed to investigate the anti-cancer activity of Licochalcone (LC)B extracted from Glycyrrhiza inflata, in gefitinib-sensitive or gefitinib-resistant NSCLC cells, and to define its mechanisms.

We investigated the mechanism of action of LCB by targeting EGFR and MET in human NSCLC cells.

We used the HCC827 and HCC827GR lines as gefitinib-sensitive and -resistant cells respectively, and determined the effects of LCB on both, by performing cell proliferation assay, flow cytometry analysis and Western blotting. Targets of LCB were identified by pull-down/kinase assay and molecular docking simulation.

LCB inhibited both EGFR and MET kinase activity by directly binding to their ATP-binding pockets. The ability of this interaction was verified by computational docking and molecular dynamics simulations. LCB suppressed viability and colony formation of both HCC827 and HCC827GR cells while exhibiting no cytotoxicity to normal cells. The induction of G2/M cell-cycle arrest and apoptosis by LCB was confirmed by Annexin V/7-AAD double staining, ER stress and reactive oxygen species induction, mitochondrial membrane potential loss and caspase activation as well as related-proteins regulation. Inhibition of EGFR and MET by LCB decreased ERBB3 and AKT axis activation.

We provide insights into the LCB-mediated mechanisms involved in reducing cell proliferation and inducing apoptosis in NSCLC cells. This occurs through dual inhibition of EGFR and MET in NSCLC cells regardless of their sensitivity or resistance to gefitinib. LCB may be a promising novel therapeutic medicine for gefitinib-sensitive or resistant NSCLC treatment.

Copyright © 2019 Elsevier GmbH. All rights reserved.


Apoptosis; EGFR; Licochalcone B; MET; Non-small cell lung cancer


Licochalcone B inhibits growth and induces apoptosis of human non-small-cell lung cancer cells by dual targeting of EGFR and MET.


Oh HN1, Lee MH2, Kim E3, Yoon G1, Chae JI4, Shim JH5.

Publish date

2019 Oct