We Offer Worldwide Shipping
Login Wishlist

Farrerol

$250

  • Brand : BIOFRON

  • Catalogue Number : BF-F3004

  • Specification : 98%

  • CAS number : 24211-30-1

  • Formula : C17H16O5

  • Molecular Weight : 300.31

  • PUBCHEM ID : 91144

  • Volume : 100mg

In stock

Quantity
Checkout Bulk Order?

Catalogue Number

BF-F3004

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

300.31

Appearance

White flake crystal

Botanical Source

Rhododendron dauricum,Hypericum pseudohenryi,Pentarhizidium orientale,Rhododendron primuliflorum,Valeriana hardwickii

Structure Type

Flavonoids

Category

Standards;Natural Pytochemical;API

SMILES

CC1=C(C(=C2C(=C1O)C(=O)CC(O2)C3=CC=C(C=C3)O)C)O

Synonyms

4',5,7-Trihydroxy-6,8-dimethylflavanone/4H-1-Benzopyran-4-one, 2,3-dihydro-5,7-dihydroxy-2-(4-hydroxyphenyl)-6,8-dimethyl-/Farrerol/5,7-Dihydroxy-2-(4-hydroxyphenyl)-6,8-dimethylchroman-4-one/5,7-Dihydroxy-2-(4-hydroxyphenyl)-6,8-dimethyl-2,3-dihydro-4H-chromen-4-one/Farresol/Cyrtopterinetin/6,8-dimethyl-5,7,4'-trihydroxyflavanone/matteucinol

IUPAC Name

5,7-dihydroxy-2-(4-hydroxyphenyl)-6,8-dimethyl-2,3-dihydrochromen-4-one

Density

1.4±0.1 g/cm3

Solubility

Methanol; Ethanol; Acetontrile; DMSO

Flash Point

219.7±23.6 °C

Boiling Point

583.0±50.0 °C at 760 mmHg

Melting Point

InChl

InChl Key

WGK Germany

RID/ADR

HS Code Reference

2938900000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:24211-30-1) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

30906210

Abstract

Farrerol has been shown to have antioxidative potential via Nrf2 activation, which in turn is involved in the prevention of hepatotoxicity. The purpose of the current study was to explore the protective effect of farrerol against acetaminophen-induced hepatotoxicity and its underlying mechanisms. Mice were used to evaluate the hepatoprotective effect of farrerol on liver injury induced by acetaminophen in vivo. HepG2 cells were utilized to further determine the functional role and mechanisms by which Nrf2 and autophagy are involved in the hepatoprotective effect of farrerol in vitro. We found that treatment with farrerol leads to a significant reduction in acetaminophen-induced hepatotoxicity by decreasing mortality, histopathological liver changes, and ALT and AST levels. Furthermore, farrerol effectively suppressed mitochondrial dysfunction by reducing JNK phosphorylation, Bax mitochondrial translocation, AIF and cytochrome c release. Further investigations revealed that the activation of Nrf2 and the induction of autophagy via the AMPK/AKT pathway by farrerol contributed to its hepatoprotective activity in vitro. In addition, farrerol inhibited acetaminophen-induced the mortality and histopathological changes in WT mice were evidently alleviated but not abrogated in Nrf2 -/- mice, which attributed to the induction of autophagy. Together, farrerol has protective potential against acetaminophen-induced hepatotoxicity which may be associated with activation of Nrf2 and autophagy.

KEYWORDS

APAP; Autophagy; Farrerol; Hepatotoxicity; Nrf2.

Title

Farrerol Ameliorates APAP-induced Hepatotoxicity via Activation of Nrf2 and Autophagy

Author

Lidong Wang 1 , Wei Wei 1 , Qingfei Xiao 1 , Huahong Yang 1 , Xinxin Ci 1

Publish date

2019 Jan 29

PMID

29904013

Abstract

Farrerol has been proved to have an anti-inflammatory effect. However, the effects of farrerol on mastitis have not been investigated. This study was aimed to investigate the effect and mechanism of farrerol in lipopolysaccharide (LPS)-induced mouse mastitis and LPS-induced inflammatory response of mouse mammary epithelial cells (mMECs). In vivo, LPS were injected to the tetrad pair of nipples for establishing mouse mastitis, and then tested the effect of farrerol on histopathological changes, inflammatory response and activation degree of protein kinase B (AKT), nuclear factor-kappa B p65 (NF-κB p65), p38, extracellular regulated protein kinase (ERK1/2). In vitro, the mMECs were incubated by farrerol for 1 h following by stimulating with LPS, and then the inflammatory response and the related signaling pathways were detected. The in vivo results found that farrerol could improve pathological injury of mammary gland, attenuate the activity of myeloperoxidase (MPO), inhibit the production of pro-inflammatory mediators and the phosphorylation of AKT, NF-κB p65, p38 and ERK1/2. The in vitro results also found farrerol inhibited inflammatory response and the related signaling pathways. Collectively, this study revealed that farrerol inhibits the further development of LPS-induced mastitis by inhibiting inflammatory response via down regulating phosphorylation of AKT, NF-κB p65, p38, and ERK1/2. These findings suggest that farrerol may be used as an anti-inflammatory drug for mastitis.

KEYWORDS

APAP; Autophagy; Farrerol; Hepatotoxicity; Nrf2.

Title

Farrerol Relieve Lipopolysaccharide (LPS)-Induced Mastitis by Inhibiting AKT/NF-κB p65, ERK1/2 and P38 Signaling Pathway

Author

Yanwei Li 1 , Qian Gong 2 , Wenjin Guo 3 , Xingchi Kan 4 , Dianwen Xu 5 , He Ma 6 , Shoupeng Fu 7 , Juxiong Liu 8

Publish date

2018 Jun 14

PMID

30011811

Abstract

Farrerol, a type of 2, 3-dihydro-flavonoid, is obtained from Rhododendron. Previous studies have shown that Farrerol performs multiple biological activities, such as anti-inflammatory, antibacterial, and antioxidant activity. In this study, we aim to investigate the effect of Farrerol on colonic inflammation and explore its potential mechanisms. We found that the effect of Farrerol was evaluated via the 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis model in mice and found that Farrerol has a protective effect on TNBS-induced colitis. Farrerol administration significantly improved the weight change, clinical scores, colon length, and intestinal epithelium barrier damage and markedly decreased the inflammatory cytokines production in TNBS-induced mice. The protective effect of Farrerol was also observed in LPS-induced RAW264.7 cells. We found that Farrerol observably reduced the production of inflammatory mediators including IL-1β, IL-6, TNF-α, COX-2, and iNOS in LPS-induced RAW264.7 cells via suppressing AKT, ERK1/2, JNK1/2, and NF-κB p65 phosphorylation. In conclusion, the study found that Farrerol has a beneficial effect on TNBS-induced colitis and might be a natural therapeutic agent for IBD treatment.

KEYWORDS

Farrerol; IBD; MAPK; NF-κB; colitis

Title

Farrerol Ameliorates TNBS-Induced Colonic Inflammation by Inhibiting ERK1/2, JNK1/2, and NF-κB Signaling Pathway

Author

Xin Ran 1 , Yuhang Li 2 , Guangxin Chen 3 , Shoupeng Fu 4 , Dewei He 5 , Bingxu Huang 6 , Libin Wei 7 , Yuanqing Lin 8 , Yingcheng Guo 9 , Guiqiu Hu 10

Publish date

2018 Jul 13


Description :

Farrerol is a bioactive constituent of Rhododendron, with broad activities such as anti-oxidative, anti-inflammatory, anti-tumor, neuroprotective and hepatoprotective effects[1][2][3][4][5][6].