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  • Brand : BIOFRON

  • Catalogue Number : BF-Y2001

  • Specification : 98%

  • CAS number : 500-62-9

  • Formula : C15H14O4

  • Molecular Weight : 258.27

  • PUBCHEM ID : 5281575

  • Volume : 20mg

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Catalogue Number


Analysis Method






Molecular Weight



White crystalline powder

Botanical Source

Piper methysticum

Structure Type



Standards;Natural Pytochemical;API




4-Methoxy-6-[(E)-2-(4-methoxyphenyl)vinyl]-2H-pyran-2-one/5-Hydroxy-3-methoxy-7-(p-methoxyphenyl)-2,4,6-heptatrienoic Acid d-Lactone/4-Methoxy-6-[(E)-2-(4-methoxyphenyl)ethenyl]-2H-pyran-2-one/2H-Pyran-2-one, 4-methoxy-6-[2-(4-methoxyphenyl)ethenyl]-, (E)-/2H-Pyran-2-one, 4-methoxy-6-[(E)-2-(4-methoxyphenyl)ethenyl]-/4-methoxy-6-[(E)-2-(4-methoxyphenyl)ethenyl]-2H-pyran-2-one/4-Methoxy-6-((E)-4-methoxystyryl)pyran-2-one/4-Methoxy-6-[b-(p-anisyl)vinyl]-a-pyrone/6-(p-Methoxystyryl)-4-methoxy-a-pyrone/Yangonin/(E)-4-Methoxy-6-[2-(4-methoxyphenyl)ethenyl]-2H-pyran-2-one




1.2±0.1 g/cm3


Ethyl Acetate; Chloroform

Flash Point

219.7±28.8 °C

Boiling Point

487.6±45.0 °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#:500-62-9) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Estrogen-induced cholestasis is a common etiology of hepatic diseases in women with contraceptives administration, pregnancy or hormone replacement therapy. Farnesoid X receptor (FXR) is a member of nuclear receptor super family of ligand-activated transcription factors that is highly expressed in liver. FXR is acknowledged to contribute to the bile acid homeostasis, as well as the pathogenesis and progression of cholestasis. Specific targeting of FXR is an innovative approach for the treatment of cholestasis. The current study aimed to verify the anti-cholestasis effect of yangonin that is a natural product isolated from Kava via FXR signaling pathway in vivo and in vitro. The analyses of FXR gain- or loss-of-function were performed. Yangonin treatment ameliorates estrogen-induced cholestasis through increasing bile flow and biliary bile acid output. The mechanisms were an induction in the hepatic efflux transporters (Bsep and Mrp2) and an inhibition in hepatic uptake transporter (Ntcp) by yangonin. Likewise, yangonin through repressing Cyp7a1, Cyp8b1 and inducing Sult2a1 expression suppressed bile acid synthesis and promoted bile acid metabolism. Furthermore, yangonin improved estrogen-induced inflammatory cell infiltration and the inflammation gene expression. In vitro experiments further consolidated that yangonin alleviated estrogen-caused cholestasis via FXR activation. Noteworthily, the effects of yangonin were enhanced by FXR expression plasmids but abrogated by FXR siRNA. In conclusion, yangonin alleviates estrogen-induced cholestasis, due to FXR-mediated gene regulation.

Copyright © 2019 Elsevier B.V. All rights reserved.


Enzymes; Estrogen-induced cholestasis; FXR; Transporters; Yangonin


Yangonin protects against estrogen-induced cholestasis in a farnesoid X receptor-dependent manner.


Dong R1, Wang J1, Gao X2, Wang C3, Liu K3, Wu J3, Liu Z3, Sun H3, Ma X1, Meng Q4.

Publish date

2019 Aug 15




Cholestasis is a clinical syndrome with systemic and intrahepatic accumulation of excessive toxic bile acids that ultimately cause hepatobiliary injury. Recently obeticholic acid (OCA) which is a farnesoid X receptor (FXR) agonist was approved by FDA to treat cholestatic liver diseases, which provided us a newly therapeutic strategy against cholestasis. The purpose of the current study is to screen novel FXR agonists and verify the anti-cholestasis effect of yangonin in vivo and in vitro. The computational strategy of two-dimensional virtual screening was used to search for new FXR agonists, and dual-luciferase reporter gene assay was used to further demonstrate FXR activation by yangonin. Then, the hepatoprotective effect of yangonin via FXR activation against cholestasis and hepatotoxity was evaluated in mice and was investigated using FXR silence in cells. Yangonin was found to activate FXR to exert hepatoprotective effect against cholestatic liver injury. Dynamic change analysis of bile acids and gene analysis revealed that yangonin promoted bile acid efflux into bile and reduced hepatic uptake via the regulation of FXR-target genes Bsep, Mrp2 and Ntcp expression. Furthermore, yangonin modulated enzymes involved in bile acid synthesis and metabolism including Cyp7a1 Cyp8b1 and Sult2a1. In addition, yangonin promoted liver repair and suppressed liver inflammation. However, the changes in these genes and protein, as well as ameliorative liver histology induced by yangonin were abrogated by FXR antagonist guggulsterone in vivo and FXR siRNA in vitro. Yangonin produces protective effect against cholestasis via FXR activation. Yangonin may be an effective approach for the prevention and treatment for cholestatic liver diseases.

Copyright © 2018 Elsevier Inc. All rights reserved.


Cholestasis; Farnesoid X receptor (FXR); Liver inflammation; Liver repair; Transporters


Yangonin protects against cholestasis and hepatotoxity via activation of farnesoid X receptor in vivo and in vitro.


Gao X1, Fu T2, Wang C3, Ning C1, Liu K3, Liu Z3, Sun H3, Ma X3, Huo X1, Yang X3, Zou M2, Meng Q4.

Publish date

2018 Jun 1




Non-alcoholic fatty liver disease (NAFLD) is currently evolving as the most common liver disease worldwide. Dyslipidemia, pathoglycemia and insulin resistance are the major risk factors for the development of NAFLD. To date, no effective drug therapies for this condition have been approved.

The present study was to investigate the protective effects of yangonin, a kavalactone isolated from Kava, against NAFLD and further elucidate the mechanisms in vivo and in vitro.

A high-fat diet (HFD) induced mouse NAFLD model was used with or without yangonin treatment.

The body weight, relative liver weight and serum biochemical indicators were measured. H&E and Oil Red O staining were used to identify the amelioration of the liver histopathological changes. Serum and hepatic triglyceride, free fatty acids and total cholesterol were analyzed. siRNA, quantitative real-time PCR and Western blot assay were used to clarify the mechanisms underlying yangonin protection.

Yangonin had obvious protective effects against NAFLD via farnesoid X receptor (FXR) activation. Through FXR activation, yangonin attenuated lipid accumulation in the liver via inhibition of hepatic lipogenesis-related protein including sterol regulatory element-binding protein 1c (SREBP-1c), fatty acid synthetase (FAS), acetyl-CoA carboxylase 1 (ACC1) and stearoyl-CoA desaturase 1 (SCD1). Besides, yangonin promoted lipid metabolism through an induction in genes required for lipoprotein lipolysis and fatty acid β-oxidation. Furthermore, yangonin modulated blood glucose homeostasis through regulation of gluconeogenesis-related gene phosphoenol pyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase), and glycogen synthesis-related gene glycogen synthase kinase 3β (GSK3β) and pyruvate dehydrogenase (PDase). Also, yangonin increased insulin sensitivity through upregulating phosphorylation of insulin responsive substrate 1, 2 (IRS-1 and IRS-2). Then, in vivo and in vitro evidence further demonstrated the involvement of FXR activation in yangonin hepatoprotection.

Yangonin protects against NAFLD due to its activation of FXR signalling to inhibit hepatic lipogenesis and gluconeogenesis, and to promote lipid metabolism and glycogen synthesis, as well as insulin sensitivity.

Copyright © 2018 Elsevier GmbH. All rights reserved.


FXR; Glucose homeostasis; Lipid homeostasis; NAFLD; Yangonin


Yangonin protects against non-alcoholic fatty liver disease through farnesoid X receptor.


Dong R1, Yang X2, Wang C1, Liu K1, Liu Z1, Ma X2, Sun H1, Huo X1, Fu T3, Meng Q4.

Publish date

2019 Feb

Description :

Yangonin exhibits affinity for the human recombinant cannabinoid CB1 receptor with an IC50 and a Ki of 1.79 ± 0.53 μM and 0.72±0.21 μM, respectively.