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Licochalcone A


  • Brand : BIOFRON

  • Catalogue Number : BF-L1001

  • Specification : 98%

  • CAS number : 58749-22-7

  • Formula : C21H22O4

  • Molecular Weight : 338.4

  • PUBCHEM ID : 5318998

  • Volume : 20mg

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Catalogue Number


Analysis Method






Molecular Weight



Yellow crystalline powder

Botanical Source

Glycyrrhiza uralensis

Structure Type



Standards;Natural Pytochemical;API




(E)-3-[5-(1,1-Dimethyl-2-propenyl)-4-hydroxy-2-methoxyphenyl]-1-(4-hydroxyphenyl)-2-propen-1-one/Licochalcone A/(2E)-3-[5-(1,1-dimethyl-2-propenyl)-4-hydroxy-2-methoxyphenyl]-1-(4-hdyroxyphenyl)-2-propen-1-one/LicochalconeA/LICOAGROCHACONE A/(2E)-3-[4-Hydroxy-2-methoxy-5-(2-methyl-3-buten-2-yl)phenyl]-1-(4-hydroxyphenyl)-2-propen-1-one/2-Propen-1-one,3-(5-(1,1-dimethyl-2-propenyl)-4-hydroxy-2-methoxyphenyl)-1-(4-hydroxyphenyl)-,(E)/(2E)-3-[4-Hydroxy-2-methoxy-5-(2-methylbut-3-en-2-yl)phenyl]-1-(4-hydroxyphenyl)prop-2-en-1-one/Licochalcone-A,Synthetic/5-(1,1-dimethylallyl)-4,4'-dihydroxy-2-methoxychalcone/(2E)-3-[5-(1,1-dimethylprop-2-en-1-yl)-4-hydroxy-2-methoxyphenyl]-1-(4-hydroxyphenyl)prop-2-en-1-one/3-Dimethylallyl-4,4'-dihydroxy-6-methoxychalcone/2-Propen-1-one, 3-[5-(1,1-dimethyl-2-propen-1-yl)-4-hydroxy-2-methoxyphenyl]-1-(4-hydroxyphenyl)-, (2E)-




1.2±0.1 g/cm3


Methanol; Ethanol; Acetone; Acetontrile; Ethyl Acetate

Flash Point

186.9±23.6 °C

Boiling Point

532.6±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#:58749-22-7) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Activation of the NACHT, LRR and PYD domains-containing protein 3 (NLRP3) inflammasome by Propionibacterium acnes (P. acnes) is critical for inducing inflammation and aggravating the development of acne lesions. We searched for available small-molecule inhibitors of the NLRP3 inflammasome that could be topically administered for the treatment of acne. We found that licochalcone A, a chalconoid isolated from the root of Glycyrrhiza inflate, was an effective inhibitor for P. acnes-induced NLRP3 inflammasome activation. Licochalcone A blocked P. acnes-induced production of caspase-1(p10) and IL-1β in primary mouse macrophages and human SZ95 sebocytes, indicating the suppression of NLRP3 inflammasome. Licochalcone A suppressed P. acnes-induced ASC speck formation and mitochondrial reactive oxygen species. Topical application of licochalcone A to mouse ear skin attenuated P. acnes-induced skin inflammation as shown by histological assessment, ear thickness measurement, and inflammatory gene expression. Licochalcone A reduced caspase-1 activity and IL-1β production in mouse ear injected with P. acnes. This study demonstrated that licochalcone A is effective in the control of P. acnes-induced skin inflammation as an efficient inhibitor for NLRP3 inflammasome. Our study provides a new paradigm for the development of anti-acne therapy via targeting NLRP3 inflammasome.

© 2018 John Wiley & Sons, Ltd.


acne; inflammation; innate immunity; phytochemical; skin


Licochalcone A attenuates acne symptoms mediated by suppression of NLRP3 inflammasome.


Yang G1, Lee HE1, Yeon SH1, Kang HC1, Cho YY1, Lee HS1, Zouboulis CC2, Han SH3, Lee JH3, Lee JY1.

Publish date

2018 Dec




Licochalcone A, a flavonoid extracted from licorice root, has been shown to exhibit broad anti-inflammatory, anti-bacterial, anticancer, and antioxidative bioactivity. In this study, we investigated the antitumor activity of Licochalcone A against human osteosarcoma cell lines. The data showed that Licochalcone A significantly suppressed cell viability in MTT assay and colony formation assay in osteosarcoma cell lines. Exposure to Licochalcone A blocked cell cycle progression at the G2/M transition and induced extrinsic apoptotic pathway in osteosarcoma cell lines. Furthermore, we found the Licochalcone A exposure resulted in rapid ATM and Chk2 activation, and high levels of nuclear foci of phosphorylated Chk2 at Thr 68 site in osteosarcoma cell lines. In addition, Licochalcone A exposure significantly induced autophagy in osteosarcoma cell lines. When Licochalcone A-induced autophagy was blocked by the autophagy inhibitor chloroquine, the expression of activated caspase-3 and Annexin V positive cells were reduced, and cell viability was rescued in Licochalcone A-treated osteosarcoma cell lines. These data indicate that the activation of ATM-Chk2 checkpoint pathway and autophagy may contribute to Licochalcone A-induced anti-proliferating effect in osteosarcoma cell lines. Our findings display the possibility that Licochalcone A may serve as a potential therapeutic agent against osteosarcoma.


ATM-Chk2; Licochalcone A; autophagy; osteosarcoma


Licochalcone A Suppresses the Proliferation of Osteosarcoma Cells through Autophagy and ATM-Chk2 Activation.


Shen TS1, Hsu YK1, Huang YF2, Chen HY2, Hsieh CP1,2, Chen CL3,4.

Publish date

2019 Jul 2




Hypoxic cellular proliferation is a common feature of tumor cells and is associated with tumor progression. Therefore, the inhibition of hypoxic cellular proliferation is expected to regulate malignancy processes. Licochalcone A (LicA) is known to show inhibitory effects on cell growth in normoxia, but it is unclear whether LicA exerts similar effects in hypoxia. Here, we studied the inhibitory activity of LicA in the hypoxic cellular proliferation of tumor cells and its molecular mechanism using human cell lines derived from various tumors including neuroblastoma and colorectal cancer. LicA inhibited cell growth at a 50% inhibitory concentration between 7.0 and 31.1 µM in hypoxia. LicA significantly suppressed hypoxic induction of tropomyosin receptor kinase B (TrkB) gene expression at the transcription level. LicA also downregulated mRNA levels of the TrkB high-affinity ligand brain-derived neurotrophic factor, but not neurotrophin-4, another TrkB ligand, or glyceraldehyde-3-phosphate dehydrogenase, indicating that the inhibitory activity of LicA is selective. Since both LicA-treatment and TrkB-knockdown decreased activation of protein kinase B in hypoxia, LicA exerts its inhibitory effect against hypoxic cell growth through inhibition of the TrkB-AKT axis. These results suggest that LicA has therapeutic potential for malignant tumors including neuroblastoma and colorectal cancer.


BDNF/TrkB; human established cell lines; hypoxia; licochalcone A; transcriptional inhibitor


Licochalcone A Inhibits BDNF and TrkB Gene Expression and Hypoxic Growth of Human Tumor Cell Lines.


Arita M1, Koike J2, Yoshikawa N3, Kondo M1, Hemmi H1.

Publish date

2020 Jan 13

Description :

Licochalcone A, a flavonoid isolated from the famous Chinese medicinal herb Glycyrrhiza uralensis Fisch, presents obvious anti-cancer effects. The IC50 value is 0.97 μM for UGT1A1.