578-86-9

Basic information

• Product Name: LIQUIRITIGENIN
• Synonyms: 4',7-DIHYDROXYFLAVANONE;7,4'-DIHYDROXYFLAVANONE;LIQUIRITIGENIN;LIQUIRITIGENIN(P);LIQUIRITIGENIN WITH HPLC;7,4''-DIHYDROXYFLAVANONE hplc;(2S)-2α-(4-Hydroxyphenyl)-7-hydroxy-2,3-dihydro-4H-1-benzopyran-4-one;(2S)-2α-(4-Hydroxyphenyl)-7-hydroxy-3,4-dihydro-2H-1-benzopyran-4-one
• CAS NO: 578-86-9
• Molecular Formula: C₁₅H₁₂O₄
• Molecular Weight: 256.25
• Product Categories: Flavanones;sy;chemical reagent;pharmaceutical intermediate;phytochemical;reference standards from Chinese medicinal herbs (TCM).;standardized herbal extract
• Mol File: 578-86-9.mol
• Article Data: 10

Chemical Properties

• Melting Point: 206-208°C
• Boiling Point: 529.5 °C at 760 mmHg
• Flash Point: 207℃
• Appearance: /
• Density: 1.386 g/cm³
• Vapor Pressure: 7.94E-12mmHg at 25°C
• Refractive Index: 1.661
• Storage Temp.: under inert gas (nitrogen or Argon) at 2-8°C
• PKA: 7.71±0.40(Predicted)
• BRN: 359378
• CAS DataBase Reference: LIQUIRITIGENIN(CAS DataBase Reference)
• NIST Chemistry Reference: LIQUIRITIGENIN(578-86-9)
• EPA Substance Registry System: LIQUIRITIGENIN(578-86-9)

Safety Data

• WGK Germany: 3
• Hazardous Substances Data: 578-86-9(Hazardous Substances Data)

Usage

Description

Liquiritigenin is an active estrogenic component in extracts of Glycyrrhizae radix. Glycyrrhizae radix (G. radix, licorice, liquorice) is frequently used for life-enhancing properties, for the treatment of injury or swelling, for detoxification in traditional Oriental medicine, as well as a food supplement in many of the countries in the world.? Liquiritigenin is a selective estrogen receptor-β (ERβ) agonist.? Liquiritigenin activates multiple ER regulatory elements and native target genes with ERβ but not ERα. The ERβ-selectivity of liquiritigenin is due to the selective recruitment of the coactivator steroid receptor coactivator-2 to target genes. As the targeting ERβ is associated with anti-inflammatory effects, liquiritigenin exerts anti-inflammatory effects. Liquiritigenin is also reported to antihyperlipidemic, antiallergic and antihepatocellular carcinoma effects.

References

[1] J. E. Mersereau, N. Levy, R. E. Staub, S. Baggett, T. Zogric, S. Chow, W. A. Ricke, M. Tagliaferri, I. Cohen, L. F. Bjeldanes (2008) Liquiritigenin is a plant-derived highly selective estrogen receptor β agonist, Molecular and Cellular Endocrinology, 283, 49-57 [2] Di Wang, Jiahui Lu, Yan Liu, Qingfan Meng, Jing Xie, Zhenzuo Wang,Lesheng Teng (2014) Liquiritigenin Induces Tumor Cell Death through Mitogen-Activated Protein Kinase- (MPAKs-) Mediated Pathway in Hepatocellular Carcinoma Cells, BioMed Research International, 2014, Article ID 965316

Uses

Liquiritigenin has been used:to study its inhibitory effect on tumor metastasis in the treatment of colorectal canceras a reference standard for ultra-performance liquid chromatography (UPLC) of Chaihu-Shugan-San (CSS) extractas a potential antiviral drug against hepatitis C virus (HCV) infection

Definition

ChEBI: A dihydroxyflavanone compound having the two hydroxy substituents at the 4'- and 7-positions. Isolated from the root of Glycyrrhizae uralensis, it is a selective agonist for oestrogen receptor beta.

General Description

Liquiritigenin is a flavonoid and an estrogenic compound found in licorice (Glycyrrhizae radix) root extract and several other plants.

Biochem/physiol Actions

Liquiritigenin displays anti-diabetic and choleretic properties. It exerts anti-inflammatory activity on Raw246.7 cells by inhibiting nuclear factor kappa light chain enhancer of activated B cells (NF-κB)-dependent-induction of inducible NOS (iNOS). Liquiritigenin inhibits liver fibrogenesis by blocking Hippo/Yes-associated protein (YAP) and transforming growth factor-β1 (TGF-β1)/small mothers against decapentaplegic (Smad) components. It is a selective estrogen receptor β agonist cells. Liquiritigenin induces apoptosis in SMM-721 cells by disruption of the mitochondrial membrane potential and increased production of reactive oxygen species.

Purification Methods

It crystallises from aqueous 50% EtOH. [Beilstein 18 III/IV 1780, 18/4 V 82.]

InChI:InChI=1/C15H12O4/c16-10-3-1-9(2-4-10)14-8-13(18)12-6-5-11(17)7-15(12)19-14/h1-7,14,16-17H,8H2/t14-/m0/s1

Upstream product

• 961-29-5 isoliquirtigenin 
• 551-15-5 liquiritin 
• 151-10-0 1,3-Dimethoxybenzene 
• 943-89-5 (E)-3-(4-methoxyphenyl)acrylic acid 
• 69097-97-8 7,4'-dihydroxy-dihydroflavone 
• 60-18-4 L-tyrosine 

Downstream Products

• 2196-14-7 7,4'-Dihydroxyflavon 
• 2034-65-3 resokaempferol 
• 528-48-3 3,7,3',4'-tetrahydroxyflavone 
• 486-66-8 daidzein 
• 7400-08-0 para-coumaric acid 
• 108-46-3 recorcinol 
• 131887-80-4 (2R,3S)-2,7,4'-trihydroxyisoflavanone 
• 92549-54-7 (2S)-7,4'-dihydroxyflavan-4-ol 
• 54301-00-7 liquiritigenin-7,4'-diacetate 
• 961-29-5 isoliquirtigenin 
• 31524-62-6 ((2S)-2,3-dihydro-7-hydroxy-2-hydroxyphenyl)-8-(3-methyl-2-buten-1-yl)-4H-1-benzopyran-4-one 

Relevant articles and documents

Liquiritigenin inhibits hepatic fibrogenesis and TGF-β1/Smad with Hippo/YAP signal

Background: Recent reports highlighted the possibility that Yes-associated protein (YAP) and transforming growth factor-β1 (TGF-β1) can act as critical regulators of hepatic stellate cells (HSCs) activation; therefore, it is natural for compounds targeting Hippo/YAP and TGF-β1/Smad signaling pathways to be identified as potential anti-fibrotic candidates. Purpose: Liquiritigenin (LQ) is an aglycone of liquiritin and has been reported to protect the liver from injury. However, its effects on the Hippo/YAP and TGF-β1/Smad pathways have not been identified to date. Methods: We conducted a series of experiments using CCl4-induced fibrotic mice and cultured LX-2 cells. Result: LQ significantly inhibited liver fibrosis, as indicated by decreases in regions of hepatic degeneration, inflammatory cell infiltration, and the intensity of α-smooth muscle actin (α-SMA) staining in mice. Moreover, LQ blocked the TGF-β1-induced phosphorylation of Smad 3, and the transcript levels of plasminogen activator inhibitor-1 (PAI-1) and matrix metalloproteinase-2 (MMP-2) in LX-2 cells, which is similar with resveratrol and oxyresveratrol (positive controls). Furthermore, LQ increased activation of large tumor suppressor kinase 1 (LATS1) with the induction of YAP phosphorylation, thereby preventing YAP transcriptional activity and suppressing the expression of exacerbated TGF-β1/Smad signaling molecules. Conclusion: These results clearly show that LQ ameliorated experimental liver fibrosis by acting on the TGF-β1/Smad and Hippo/YAP pathways, indicating that LQ has the potential for effective treatment of liver fibrosis.

METHOD FOR PRODUCING LIQUIRITIGENIN PRECURSOR

An objective of this invention is to provide a mass manufacturing method for providing liquiritigenin by a proper method. The present invention provides a method for producing isoliquiritigenin by bringing a 4-alkoxy cinnamic acid represented by formula (I) and a 1,3-alkoxybenzene represented by formula (II) into Friedel-Crafts reaction (A) for coupling to a trialkoxy isoliquiritigenin represented by a synthesis formula (III) and allowing it to be crystal, and removing protection group to obtain an isoliquiritigenin represented by formula (IV), wherein, an in situ liquiritigenin (-) pharmacological effect is obtained by administrating the isoliquiritigenin represented by formula (IV)as a precursor of liquiritigenin into body.

Highly efficient and green synthesis of flavanones and tetrahydroquinolones

Highly efficient and green catalytic conversion of 2′-hydroxy and 2′-amino chalcones to flavanones and tetrahydroquinolones is reported herein. 2′-Hydroxy and 2′-amino chalcones can be almost completely converted to flavanones and tetrahydroquinolones in just 2 min in the presence of piperidine and KOH under room temperature. Liquiritigenin is also efficiently synthesized under similar conditions.