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  • Brand : BIOFRON

  • Catalogue Number : BF-F2002

  • Specification : 98%

  • CAS number : 574-84-5

  • Formula : C10H8O5

  • Molecular Weight : 208.17

  • PUBCHEM ID : 5273569

  • Volume : 20mg

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Catalogue Number


Analysis Method






Molecular Weight



Light Yellow crystalline powder

Botanical Source

Datura metel,Xanthoceras sorbifolium,Sarcandra glabra,Fraxinus chinensis,Actinidia chinensis

Structure Type



Standards;Natural Pytochemical;API




Coumarin, 7,8-dihydroxy-6-methoxy-/6-methoxy-7,8-dihydroxycoumarin/7,8-Dihydroxy-6-methoxy-2H-chromen-2-one/2H-1-Benzopyran-2-one,7,8-dihydroxy-6-methoxy/7,8-Dihydroxy-6-methoxycoumarin/2H-1-Benzopyran-2-one, 7,8-dihydroxy-6-methoxy-/7,8-dihydroxy-6-methoxy-benzopyran-2-one/7,8-Dihydroxy-6-methoxy-2H-1-benzopyran-2-one/Fraxetin




1.5±0.1 g/cm3


Methanol; Ethanol

Flash Point

196.0±22.2 °C

Boiling Point

472.0±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#:574-84-5) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Lung cancer represents the leading cause of cancer-associated mortality, and non-small-cell lung cancer (NSCLC) is the most frequent histologic sub-type. It is therefore urgent to develop novel agents for the treatment of NSCLC. Fraxetin (FXT) is a potent plant-derived product and has been recognized as a promising anticancer agent for breast cancer and osteosarcoma. However, the anti-cancer potential of FXT for NSCLC remains to be elucidated. Accordingly, in the present study, we evaluated the inhibitory effect of FXT on the proliferation and growth of NSCLC cells using six human NSCLC cell lines: A549, H460, HCC827, H1650, PC-9 and H1975. FXT exhibited significant inhibitory effects on the proliferation of these cancer cell lines. By contrast, no inhibitory effect was observed on the viability of non-cancer lung cell lines even at the highest concentration of FXT (100 μM). Among the NSCLC cell lines, HCC827 and H1650 cells showed the most sensitive to FXT. Accordingly, HCC827 and H1650 cells were used for the subsequent experiments. Flow cytometric analysis revealed that FXT caused a significant cell cycle arrest and pro-apoptotic effects. Mechanistically, FXT suppressed the IL-6-induced phosphorylation of tyrosine residue (Tyr705) of signal transducer and activator of transcription 3 (STAT3) probably by binding to STAT3. Molecular docking and molecular dynamic simulations studies indicated that FXT interacts with STAT3 through hydrogen bond and hydrophobic interaction. In conclusion, these findings suggest that FXT could be a promising lead compound to be used as a novel STAT3 inhibitor and potential antitumor agent for the treatment of NSCLC.


coumarin; fraxetin; hydrogen bond and hydrophobic interaction; non-small-cell lung cancer; signal transducer and activator of transcription 3


Fraxetin Suppresses Proliferation of Non-Small-Cell Lung Cancer Cells via Preventing Activation of Signal Transducer and Activator of Transcription 3.


Zhang Y1, Wang L2, Deng Y1, Zhao P1, Deng W1, Zhang J1, Luo J1, Li R1.

Publish date

2019 May




Liver fibrosis is a chronic lesion which ultimately results in cirrhosis and possible death. Although the high incidence and lethality, few therapies are effective for liver fibrosis. Fraxetin (7,8-dihydroxy-6-methoxy coumarin), a natural product extracted from cortex fraxini, has exhibited a significant hepatoprotective and anti-fibrotic properties. However, the underlying mechanism of the anti-hepatic fibrotic property remains unknown.

48 Male Sprague Dawley rats were divided into four groups at random which were named as normal group, model group, fraxetin 25 mg/kg and 50 mg/kg group. The experimental model of liver fibrosis was founded by carbon tetrachloride (CCl4) rats which were simultaneously treated with fraxetin (25 mg/kg or 50 mg/kg). Normal groups received equal volumes of saline and peanut oil.

Results showed that fraxetin ameliorated CCl4 induced liver damage and fibrosis. Furthermore, histopathology examinations revealed that fraxetin improved the morphology and alleviated collagen deposition in fibrotic liver. Fraxetin inhibited inflammation and hepatocytes apoptosis by modulating the NF-κB/IκBα, MAPKs and Bcl-2/Bax signaling pathways.

Our findings indicate that fraxetin is effective in preventing liver fibrosis through inhibiting inflammation and hepatocytes apoptosis which is associated with regulating NF-κB/IκBα, MAPKs and Bcl-2/Bax signaling pathways in rats.

Copyright © 2019 Institute of Pharmacology, Polish Academy of Sciences. Published by Elsevier B.V. All rights reserved.


Fraxetin; Inflammation; Liver fibrosis; MAPKs; NF-κB


Antifibrotic effects of Fraxetin on carbon tetrachloride-induced liver fibrosis by targeting NF-κB/IκBα, MAPKs and Bcl-2/Bax pathways.


Wu B1, Wang R1, Li S1, Wang Y1, Song F1, Gu Y1, Yuan Y2.

Publish date

2019 Jun




This paper reports the successive isolation and purification of bioactive compounds from the stem bark of Jatropha podagrica, a widely known medicinal plant. The ethyl acetate extract of the stem bark exhibited the strongest antioxidant activity assessed by 2,2-diphenyl-1-picrylhydrazyl (DPPH), 2,2′-azinobis-(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) radical scavenging, and ferric reducing antioxidant power (FRAP) assays (IC50 = 46.7, 66.0, and 492.6, respectively). By column chromatography (CC) with elution of hexane and ethyl acetate at 8:2, 7:3, and 6:4 ratios, the isolation of this active extract yielded five fractions (C1⁻C5). Chemical structures of the constituents included in C1⁻C5 were elucidated by gas chromatography-mass spectrometry (GC-MS), electrospray ionization-mass spectrometry (ESI-MS), and nuclear magnetic resonance (NMR) and resolved as methyl gallate (C1, C2, C3, C4), gallic acid (C1, C2), fraxetin (C2, C3, C4, C5), and tomentin (C3). Mixture C2 (IC50 DPPH and ABTS = 2.5 µg/mL) and C3 (IC50 FRAP = 381 µg/mL) showed the highest antioxidant properties. Among the isolated fractions, C4 was the most potential agent in growth inhibition of six bacterial strains including Staphylococcus aureus, Escherichia coli, Klebsiella pneumoniae, Listeria monocytogenes, Bacillus subtilis, and Proteus mirabilis (MIC = 5, 20, 30, 20, 25, and 20 mg/mL, respectively). All identified constituents exerted an inhibitory activity on the growth of Lactuca sativa, of which the mixture C3 performed the maximal inhibition on shoot (IC50 = 49.4 µg/mL) and root (IC50 = 47.1 µg/mL) growth. Findings of this study suggest that gallic acid, methyl gallate, fraxetin, and tomentin isolated from J. podagrica possessed antioxidant, antibacterial, and growth inhibitory potentials.


Jatropha podagrica; allelopathic activity; antibacterial; antioxidant; fraxetin; gallic acid; methyl gallate; stem bark; tomentin


Isolation and Purification of Bioactive Compounds from the Stem Bark of Jatropha podagrica.


Minh TN1, Xuan TD2, Tran HD3, Van TM4, Andriana Y5, Khanh TD6,7, Quan NV8, Ahmad A9.

Publish date

2019 Mar 3

Description :

Antibacterial mechanism of fraxetin against Staphylococcus aureus. PUMID/DOI:25189268 Mol Med Rep. 2014 Nov;10(5):2341-5. Fraxetin is one of the main constituents of the traditional medicinal plant Fraxinus rhynchophylla. The inhibitory effect of fraxetin on various bacterial strains has been extensively reported, however, its mechanism of action on bacterial cells remains to be elucidated. In the present study, the antibacterial mechanism of fraxetin on Staphylococcus aureus was systematically investigated by examining its effect on cell membranes, protein synthesis, nucleic acid content and topoisomerase activity. The results indicated that fraxetin increased the permeability of the cell membrane but did not render it permeable to macromolecules, such as DNA and RNA. Additionally, the quantity of protein, DNA and RNA decreased to 55.74, 33.86 and 48.96%, respectively following treatment with fraxetin for 16 h. The activity of topoisomerase I and topoisomerase II were also markedly inhibited as fraxetin concentration increased. The result of the ultraviolet?visible spectrophotometry demonstrated that the DNA characteristics exhibited a blue shift and hypochromic effect following treatment with fraxetin. These results indicated that fraxetin had a marked inhibitory effect on S.aureus proliferation. Further mechanistic studies showed that fraxetin could disrupt nucleic acid and protein synthesis by preventing topoisomerase from binding to DNA. Antioxidant and intestinal anti-inflammatory effects of plant-derived coumarin derivatives. PUMID/DOI:24176844 Phytomedicine. 2014 Feb 15;21(3):240-6. All coumarin derivatives showed antioxidant activity in the DPPH assay, while daphnetin and Fraxetin also showed antioxidant activity by inhibiting lipid peroxidation. Coumarins, except 4-methyl-umbeliferone, also showed antioxidant activity through the counteraction of glutathione levels or through the inhibition of myeloperoxidase activity. Dual anti-oxidative effects of fraxetin isolated from Fraxinus rhinchophylla. PUMID/DOI:19721227 Biol Pharm Bull. 2009 Sep;32(9):1527-32. During the course of characterizing potential drug candidates from natural products, we isolated two major coumarins, esculetin and Fraxetin and found that Fraxetin has dual-antioxidative functions. Low concentrations (1-5 microM) of Fraxetin potently inhibited LDL oxidation induced by metal and free radicals. Moreover, treatment of vascular smooth muscle cells (VSMCs) with higher concentrations (above 30 microM) of Fraxetin significantly increased the protein level of heme oxygenase-1 (HO-1), a key enzyme that inhibits vascular proliferation and atherosclerosis. Subcellular fractionation and reporter gene analysis using an antioxidant response element (ARE) construct revealed that Fraxetin increased the level of nuclear factor (NF)-E2-related factor 2 (Nrf2) and reporter activity, and these were associated with the induction of antioxidant enzymes, such as HO-1 and glutathione S-transferase-alpha. In conclusion, Fraxetin has direct protective properties against LDL oxidation at lower concentrations, and higher concentrations of Fraxetin induce antioxidant enzymes via Nrf2/ARE activation. These effects suggest potential anti-atherosclerosis effects of Fraxinus rhynchophylla D. The hepatoprotective effect of fraxetin on carbon tetrachloride induced hepatic fibrosis by antioxidative activities in rats. PUMID/DOI:23994349 Int Immunopharmacol. 2013 Nov;17(3):543-7. The aim of the study was to investigate the potentially protective effects of Fraxetin on carbon tetrachloride (CCl4) induced oxidative stress and hepatic fibrosis in Sprague-Dawley rats. In this study, rats were divided into five groups, including normal controls, model, silymarin as the positive control, Fraxetin 20 mg/kg and Fraxetin 50 mg/kg. After 8 weeks, activities of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and total bilirubin (TBIL) were checked. The levels of protein carbonyls, thiobarbituric acid-reactive substances (TBARS) and antioxidant enzymes such as catalase, SOD and glutathione peroxidase (GSH-Px) were determined after Fraxetin administration. The hydroxyproline levels and histopathologic examinations of hepatocyte fibrosis were also determined. We found that Fraxetin at doses of 20 and 50 mg/kg for 8 weeks significantly reduced the levels of TBARS and protein carbonyls compared with CCl4 group. Fraxetin significantly increased the activities of catalase, SOD and GSH-Px in the liver. We also found that Fraxetin prevented CCl4 induced hepatic fibrosis by histological observations. These results indicate that Fraxetin exhibits potent protective effects against CCl4 induced oxidative stress and hepatic fibrosis. Fraxetin prevents rotenone-induced apoptosis by induction of endogenous glutathione in human neuroblastoma cells. PUMID/DOI:15996779 Neurosci Res. 2005 Sep;53(1):48-56. Fraxetin belongs to an extensive group of natural phenolic anti-oxidants. In the present study, using a human neuroblastoma SH-SY5Y cells, we have investigated the protective effects of this compound on modifications in endogenous reduced glutathione (GSH), intracellular oxygen species (ROS) and apoptotic death on rotenone-mediated cytoxicity. Incubation of cells with the Fraxetin led to a significant elevation dose-dependent of cellular GSH and this was accompanied by a marked protection against rotenone-mediated toxicity, which was also significantly reversed in the cells with buthionine sulfoximine (BSO) co-treatment. Taken together, this study suggested that intracellular GSH appeared to be an important factor in Fraxetin-mediated cytoprotection against rotenone-toxicity in SH-SY5Y cells. Fraxetin at 10-100 muM inhibited the formation of ROS, cytochrome c release, activation of caspase-3 and 9, and suppressed the up-regulation of Bax, whereas no significant change occurred in Bcl-2 levels. Our results indicated that the anti-oxidative and anti-apoptotic properties render this natural compound potentially protective against rotenone-induced cytotoxicity.