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Formononetin

$43

  • Brand : BIOFRON

  • Catalogue Number : BF-F3003

  • Specification : 98%

  • CAS number : 485-72-3

  • Formula : C16H12O4

  • Molecular Weight : 268.27

  • PUBCHEM ID : 5280378

  • Volume : 25mg

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Catalogue Number

BF-F3003

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

268.27

Appearance

White crystalline powder

Botanical Source

Callerya speciosa,Periploca forrestii,Pueraria montana var. lobata,Solanum lyratum,Trifolium pratense

Structure Type

Flavonoids

Category

Standards;Natural Pytochemical;API

SMILES

COC1=CC=C(C=C1)C2=COC3=C(C2=O)C=CC(=C3)O

Synonyms

4H-1-Benzopyran-4-one, 7-hydroxy-3-(4-methoxyphenyl)-/7-hydroxy-4'-methoxy-Isoflavone (8CI)/7-Hydroxy-3-(4-methoxyphenyl)-4H-chromen-4-one/Formononetol/4'-O-methyl-daidzein/4H-1-Benzopyran-4-one, 7-hydroxy-3- (4-methoxyphenyl)-/BIOCHANIN B/ForMonentin/BIOCHANIN A/Flavosil/7-Hydroxy-4'-methoxyisoflavone/Neochanin/Myconate/BiocaninB/FORMONETIN/7-Hydroxy-3-(4-methoxyphenyl)-4H-1-benzopyran-4-one/Formononetin/7-Hydroxy-3-(4-methoxyphenyl)chromone/forMonoetin

IUPAC Name

7-hydroxy-3-(4-methoxyphenyl)chromen-4-one

Density

1.3±0.1 g/cm3

Solubility

DMSO

Flash Point

183.4±22.2 °C

Boiling Point

479.4±45.0 °C at 760 mmHg

Melting Point

256-260 °C

InChl

InChl Key

WGK Germany

RID/ADR

HS Code Reference

2932990000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:485-72-3) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

29913427

Abstract

Formononetin is a bioactive non-steroidal polyphenol found in a variety of plants. In this study we evaluated the effects of formononetin on neuroinflammation in LPS-stimulated BV2 microglia. Results showed that formononetin significantly reduced the production of TNF-α, IL-6 and IL-1β, nitrite and PGE2, as well as protein levels of iNOS and COX-2. Reporter gene assays showed that formononetin produced inhibition of NF-κB luciferase activity in HEK293 cells stimulated with TNF-α. Immunoblotting experiments revealed an inhibition of IKKα phosphorylation, with the resultant attenuation of phosphorylation and degradation of IκBα following LPS stimulation. Formononetin also produced an inhibition of nuclear translocation and DNA binding by NF-κB following LPS stimulation. RNAi experiments showed that transfection of BV2 microglia with ERβ siRNA resulted in the loss of anti-inflammatory action of formononetin. MTT assay and MAP2 immunoreactivity experiments showed that formononetin produced significant neuroprotective activity by preventing BV2 microglia conditioned media-induced toxicity to HT22 neurons. Investigations on the effect of formononetin on MCF7 breast cancer cells revealed that, while the compound significantly increased ER-luciferase activity, its effects on proliferation were modest. This study has established that formononetin inhibits neuroinflammation by targeting NF-κB signalling pathway in BV2 microglia, possibly through mechanisms involving ERβ. Formononetin appears to modulate ERβ in MCF7 breast cancer cells with limited proliferative effect. Formononetin could therefore serve as a chemical scaffold for the development of novel compounds which have selective neuroprotective actions in the brain.
Copyright © 2018 Elsevier B.V. All rights reserved.

KEYWORDS

ERβ; Formononetin; NF-κB; Neuroinflammation

Title

Formononetin inhibits neuroinflammation and increases estrogen receptor beta (ERβ) protein expression in BV2 microglia.

Author

El-Bakoush A1, Olajide OA2.

Publish date

2018 Aug

PMID

29507526 Formononetin is a kind of isoflavone compound and has been reported to possess anti-inflammatory properties. In this present study, we aimed to explore the protective effects of formononetin on dextran sulfate sodium- (DSS-) induced acute colitis. By intraperitoneal injection of formononetin in mice, the disease severity of colitis was attenuated in a dose-dependent manner, mainly manifesting as relieved clinical symptoms of colitis, mitigated colonic epithelial cell injury, and upregulations of colonic tight junction proteins levels (ZO-1, claudin-1, and occludin). Meanwhile, our study found that formononetin significantly prevented acute injury of colonic cells induced by TNF-α in vitro, specifically manifesting as the increased expressions of colonic tight junction proteins (ZO-1, claudin-1, and occludin). In addition, the result showed that formononetin could reduce the NLRP3 pathway protein levels (NLRP3, ASC, IL-1β) in vivo and vitro, and MCC950, the NLRP3 specific inhibitor, could alleviate the DSS-induced mice acute colitis. Furthermore, in the foundation of administrating MCC950 to inhibit activation of NLRP3 inflammasome, we failed to observe the protective effects of formononetin on acute colitis in mice. Collectively, our study for the first time confirmed the protective effects of formononetin on DSS-induced acute colitis via inhibiting the NLRP3 inflammasome pathway activation.

Title

Formononetin Administration Ameliorates Dextran Sulfate Sodium-Induced Acute Colitis by Inhibiting NLRP3 Inflammasome Signaling Pathway.

Author

Wu D1,2, Wu K1,2, Zhu Q2, Xiao W1,2, Shan Q2, Yan Z1,2, Wu J1,2, Deng B1,2, Xue Y1,2, Gong W1,2,3, Lu G1,2, Ding Y1,2.

Publish date

2018 Jan 8

PMID

30928103

Abstract

Cholestasis, which is characterized by bile acid (BA) overload within the hepatocytes, is a major contributor to liver injury. The dysregulation of bile acid homeostasis, such as excessive bile acid synthesis and defected secretion, leads to intracellular retention of hydrophobic bile acid which undermines the physiological function of hepatocytes. Cholestasis can further develop into hepatic fibrosis and cirrhosis, and eventually life-threating liver failure. In the liver, BA-activated FXR can reduce hepatic BA concentration by negative feedback regulation. Clinically, FXR and PPARα are the pharmacological targets of obeticholic acid and fenofibrate for the treatment of primary biliary cirrhosis, respectively. Formononetin, a natural isoflavone compound, exerts beneficial effects in various biological processes, such as anti-inflammation, anti-tumor. However, the role of formononetin in bile acid metabolism remains unclear. Herein, we show that formononetin improves hepatic/systemic bile acid metabolism and protects against ANIT-induced liver injury. Mechanistically, formononetin improves the genes profile orchestrating bile acid homeostasis through modulating SIRT1-FXR signaling pathway. Moreover, formononetin attenuated ANIT-induced inflammatory response by inactivating JNK inflammation pathway in PPARα dependent manner. Taken together, our study demonstrates that formononetin ameliorates hepatic cholestasis by upregulating expression of SIRT1 and activating PPARα, which is an important anti-cholestatic mechanism of formononetin.
Copyright © 2019 Elsevier Inc. All rights reserved.

KEYWORDS

Formononetin; Hepatic cholestasis; PPARα; SIRT1

Title

Formononetin ameliorates cholestasis by regulating hepatic SIRT1 and PPARα.

Author

Yang S1, Wei L2, Xia R3, Liu L4, Chen Y5, Zhang W6, Li Q4, Feng K4, Yu M7, Zhang W4, Qu J8, Xu S8, Mao J8, Fan G9, Ma C10.

Publish date

2019 May 14


Description :

Formononetin (Formononetol; Flavosil) is a bioactive component extracted from the red clover; inhibits the proliferation of DU-145/PC-3 cells in a dose-dependent manner.IC50 value:Target: anti-cancer in vitro: formononetin inhibited the proliferation of DU-145 cells in a dose-dependent manner. DU-145 cells treated with different concentrations of formononetin displayed obvious morphological changes of apoptosis under fluorescence microscopy. In addition, formononetin increased the proportion of early apoptotic DU-145 cells, down-regulated the protein levels of Bcl-2 and up-regulated those of RASD1 and Bax [1]. Formononetin significantly inhibited the cell growth of PC-3 in a dose-dependent manner, but no such effect was observed in RWPE1 cells. Formononetin treatment contributed to the reduced Bcl-2 protein level and the elevated Bax expression in PC-3 cells, thereby resulting in the increasing Bax/Bcl-2 ratios. Furthermore, the phosphorylated level of p38 in PC-3 cells was activated through the FN treatment, whereas the endogenous Akt phosphorylation was blocked [2]. Compared with the control, formononetin inhibited the proliferation of MCF-7 cells and effectively induced cell cycle arrest. The levels of p-IGF-1?R, p-Akt, cyclin D1 protein expression, and cyclin D1 mRNA expression were also downregulated [3].in vivo: formononetin also prevented the tumor growth of human breast cancer cells in nude mouse xenografts [3].