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Isofraxidin

$78

  • Brand : BIOFRON

  • Catalogue Number : BF-I3008

  • Specification : 98%

  • CAS number : 486-21-5

  • Formula : C11H10O5

  • Molecular Weight : 222.19

  • PUBCHEM ID : 5318565

  • Volume : 25mg

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Catalogue Number

BF-I3008

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

222.19

Appearance

White crystalline powder

Botanical Source

Morinda officinalis,Sarcandra glabra,Eleutherococcus senticosus,Impatiens balsamina,Eleutherococcus sessiliflorus

Structure Type

Phenylpropanoids

Category

Standards;Natural Pytochemical;API

SMILES

COC1=C(C(=C2C(=C1)C=CC(=O)O2)OC)O

Synonyms

isoferaxidin/7-Hydroxy-6,8-dimethoxy-2H-chromen-2-one/iso-Fraxidin/Phytodolor/6,8-dimethoxy-7-hydroxycoumarin/7-Hydroxy-6,8-dimethoxy-2H-1-benzopyran-2-one/7-Hydroxy-6,8-dimethoxy coumarin/2H-1- Benzopyran-2-one, 7-hydroxy-6,8-dimethoxy-/Coumarin,7-hydroxy-6,8-dimethoxy/Isofraxidin/7-hydroxy-6,8-dimethoxy-chromen-2-one/2H-1-Benzopyran-2-one, 7-hydroxy-6,8-dimethoxy-/6,8-Dimethoxyumbelliferone,7-Hydroxy-6,8-dimethoxychromen-2-one,7-Hydroxy-6,8-dimethoxycoumarin/Umbelliferone,6,8-dimethoxy/7-Hydroxy-6,8-dimethoxy-cumarin

IUPAC Name

7-hydroxy-6,8-dimethoxychromen-2-one

Density

1.4±0.1 g/cm3

Solubility

Methanol; Ethyl Acetate; Acetontrile; Water

Flash Point

183.2±22.2 °C

Boiling Point

452.1±45.0 °C at 760 mmHg

Melting Point

>300 °C(lit.)

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#:486-21-5) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

30299441

Abstract

Osteoarthritis (OA) is a major cause of joint pain and disability, resulting in large socioeconomic costs worldwide. Isofraxidin (ISO), a bioactive coumarin compound isolated from the functional foods Siberian ginseng and Apium graveolens, exerts anti-inflammatory effects in a variety of diseases. However, no studies have reported the protective effects of ISO against OA development. Accordingly, this study aimed to assess the therapeutic effect of ISO in human OA chondrocytes, and in a mouse model of OA induced by destabilisation of the medial meniscus (DMM). In vitro, lipopolysaccharide (LPS)-induced overproduction of nitric oxide (NO), prostaglandin E2 (PGE2), tumour necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) was decreased by ISO pre-treatment. Furthermore, ISO attenuated the increased expression of inflammatory enzymes, including inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), in response to LPS stimulation. Meanwhile, LPS-induced extracellular matrix (ECM) degradation was also reversed by ISO treatment. Mechanistically, ISO competitively inhibited Toll-like receptor 4 (TLR4)/myeloid differentiation protein-2 (MD-2) complex formation, and thus TLR4/nuclear factor kappa B (NF-κB) signalling cascades. In vivo, ISO treatment not only prevented the calcification and erosion of cartilage, as well as the thickening of subchondral bone, but also reduced the serum levels of inflammatory cytokines in the mouse OA model. Taken together, these data suggest that ISO has potential in the treatment of OA.

Title

Isofraxidin targets the TLR4/MD-2 axis to prevent osteoarthritis development.

Author

Jin J 1, Yu X , Hu Z , Tang S , Zhong X , Xu J , Shang P , Huang Y , Liu H .

Publish date

2018 Nov 14

PMID

30891836

Abstract

Inflammation has been demonstrated to be the key factor for intervertebral disc degeneration (IVD), which remains a major public health problem. Isofraxidin is a coumarin compound that possesses strong anti-inflammatory activity. However, the role of isofraxidin in IVD remains unclear. The aim of this study was to evaluate the effects of isofraxidin on inflammatory response in human nucleus pulposus cells (NPCs) exposed to interleukin-1β (IL-1β). The results proved that isofraxidin attenuated the IL-1β-induced significant increases in inflammatory mediators and cytokines including nitric oxide (NO), inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), tumor necrosis factor alpha (TNF-α), and IL-6. Besides, isofraxidin also inhibited the induction effect of IL-1β on matrix metalloproteinases (MMP)-3 and MMP-13. Moreover, the NF-κB activation caused by IL-1β was significantly inhibited by isofraxidin treatment. These findings suggested that isofraxidin alleviates IL-1β-induced inflammation in NPCs. Our work provided an idea that isofraxidin might act as a novel preventive role in IVD.

KEYWORDS

NF-κB pathway; interleukin-1β (IL-1β); intervertebral disc degeneration (IVD); isofraxidin

Title

Isofraxidin attenuates IL-1β-induced inflammatory response in human nucleus pulposus cells.

Author

Su X1, Liu B1, Gong F1, Yin J1, Sun Q1, Gao Y1, Lv Z2, Wang X1.

Publish date

2019 Aug

PMID

31916051

Abstract

Isofraxidin is a well-known coumarin compound refined from traditional Chinese medicines. It has been previously demonstrated to play an anti-inflammatory role in various inflammatory conditions. However, the effect of isofraxidin on myocardial infarction (MI) remains uncovered. In this study, we aimed to investigate the effect of isofraxidin on MI. MI mice was created and triphenyltetrazolium chloride (TTC) staining as well as echocardiographic evaluation were conducted to analyze the severity of MI. Oxygen-glucose deprivation (OGD) was used for the mimics of ischemic stress in murine cardiomyocytes, and Cell Counting Kit-8 (CCK-8), Annexin V, and lactate dehydrogenase (LDH) release assays were conducted for cell viability. Western blot was used for the detection of NOD-like receptor family, pyrin domain containing 3 (NLRP3), and adapter protein apoptosis-associated speck-like protein (ASC) in heart tissues and cardiomyocytes. Real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA) were applied for the detection of proinflammatory cytokines. We found that isofraxidin alleviated the severity of MI and produced a cardio-protective effect against OGD damage. Isofraxidin also decreased the overall and local inflammatory reaction in MI. Those effects were through the inhibition of the NLRP3 inflammasome. Taken together, we initially reported the cardio-protective and alleviative effect of isofraxidin on MI and uncovered its underlying mechanism related to the NLRP3 inflammasome inhibition.

KEYWORDS

NLRP3 inflammasome; cardiomyocyte; inflammation; isofraxidin; myocardial infarction

Title

Isofraxidin Alleviates Myocardial Infarction Through NLRP3 Inflammasome Inhibition.

Author

Chen G1, Song X2, Lin D3, Xu P4.

Publish date

2020 Jan 8


Description :

Isofraxidin protects mice from LPS challenge by inhibiting pro-inflammatory cytokines and alleviating histopathological changes. PUMID/DOI:25454811 Immunobiology. 2015 Mar;220(3):406-13. Isofraxidin (IF), the major bioactive component of Sarcandra glabra, has been reported to be an effective anti-inflammatory compound. In a previous study, we showed that Isofraxidin acts via the MAPK pathway to produce anti-inflammatory effects, both in vivo and in vitro. However, the effect and mechanism of action of Isofraxidin on inflammatory cytokines and NF-κB activation in vivo has not been investigated. We therefore aimed to evaluate how Isofraxidin regulates the production of inflammatory cytokines in vivo by intraperitoneal injection of Isofraxidin (1, 5 or 15mg/kg) prior to treatment with LPS (1mg/kg, i.p.). Macroscopic, biochemical and histopathological parameters were measured. Treatment with Isofraxidin prior to LPS challenge decreased mortality rate, body weight loss, organ coefficient and histopathological changes. Isofraxidin also suppressed the protein expression of NF-κB, levels of NO and IL-6 in serum and production of TNF-α in liver. Our results show that pretreatment with IF increases the survival rate following LPS stimulation in mice. The effect involves regulation of NF-κB signal which, in turn, regulates production of inflammatory cytokine TNF-α, suggesting that Isofraxidin may have a therapeutic effect against LPS-induced inflammatory disease. Protective effects of Isofraxidin against lipopolysaccharide-induced acute lung injury in mice. PUMID/DOI:25596039 Int Immunopharmacol. 2015 Feb;24(2):432-9. Acute lung injury (ALI) is a life-threatening disease characterized by serious lung inflammation and increased capillary permeability, which presents a high mortality worldwide. Isofraxidin (IF), a Coumarin compound isolated from the natural medicinal plants such as Sarcandra glabra and Acanthopanax senticosus, has been reported to have definite anti-bacterial, anti-oxidant, and anti-inflammatory activities. However, the effects of Isofraxidin against lipopolysaccharide-induced ALI have not been clarified. The aim of the present study is to explore the protective effects and potential mechanism of Isofraxidin against LPS-induced ALI in mice. In this study, We found that pretreatment with Isofraxidin significantly lowered LPS-induced mortality and lung wet-to-dry weight (W/D) ratio and reduced the levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and prostaglandin E2 (PGE2) in serum and bronchoalveolar lavage fluid (BALF). We also found that total cells, neutrophils and macrophages in BALF, MPO activity in lung tissues were markedly decreased. Besides, Isofraxidin obviously inhibited lung histopathological changes and cyclooxygenase-2 (COX-2) protein expression. These results suggest that Isofraxidin has a protective effect against LPS-induced ALI, and the protective effect of Isofraxidin seems to result from the inhibition of COX-2 protein expression in the lung, which regulates the production of PGE2. Isofraxidin, a potent reactive oxygen species (ROS) scavenger, protects human leukemia cells from radiation-induced apoptosis via ROS/mitochondria pathway in p53-independent manner. PUMID/DOI:24692054 Apoptosis. 2014 Jun;19(6):1043-53. Ionizing radiation (IR) leads to oxidizing events such as excessive reactive oxygen species (ROS) in the exposed cells, resulting in further oxidative damage to lipids, proteins and DNA. To screen the potential radio-protective drug, the intracellular ROS was measured in irradiated U937 cells pretreated with 80 candidate traditional herbal medicine, respectively. Isofraxidin (IF) was one possible radio-protector in these 80 drugs. This study investigated the radio-protective role of IF, a Coumarin compound, in human leukemia cell lines, for the first time. Results indicate that IF protects against IR-induced apoptosis in U937 cells in the time- and concentration- dependent manner. IF decreases IR-induced intracellular ROS generation, especially hydroxyl radicals formation, inhibits IR-induced mitochondrial membrane potential loss and reduces IR-induced high intracellular Ca(2+) levels regardless of ER stress. IF down-regulates the expression of caspase-3, phospho-JNK, phospho-p38 and activates Bax in mitochondria. IF inhibits cytochrome c release from mitochondria to cytosol. IF also moderates IR-induced Fas externalization and caspase-8 activation. IF also exhibits significant protection against IR-induced cell death in other leukemia cell lines such as Molt-4 cells and HL60 cells regardless of p53. Taken together, the data demonstrate that IF protects leukemia cells from radiation-induced apoptosis via ROS/mitochondria pathway in a p53-independent manner. Isofraxidin, a coumarin component from Acanthopanax senticosus, inhibits matrix metalloproteinase-7 expression and cell invasion of human hepatoma cells. PUMID/DOI:20930381 Biol Pharm Bull. 2010;33(10):1716-22. 7-Hydroxy-6,8-dimethoxy-2H-1-benzopyran-2-one (Isofraxidin) is a major coumarin component isolated from the stem bark of Acanthopanax senticosus, a widely used Chinese medicinal herb. We investigated Isofraxidin in its anti-tumor effects on human hepatoma cell lines HuH-7 and HepG2. Isofraxidin significantly inhibited hepatoma cell invasion, without affecting cell attachment or growth. Expression of 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced matrix metalloproteinase-7 (MMP-7) in hepatoma cells was inhibited by Isofraxidin at the both mRNA and protein levels. This inhibition tended to be greater in cells inoculated at low density than in those at high density. Isofraxidin showed an inhibitory effect on the phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) in hepatoma cells, whereas activator protein-1 (AP-1) DNA binding activity, nuclear factor-kappa B (NF-κB) nuclear translocation, and inhibitory kappa B (IκB) degradation were affected very little. These results indicate that Isofraxidin inhibits expression of MMP-7 and in vitro cell invasion at a non-toxic level through inhibiting ERK1/2 phosphorylation in hepatoma cell lines, which suggest Isofraxidin might become an effective agent for suppressing hepatoma cell invasion.