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  • Brand : BIOFRON

  • Catalogue Number : AV-H17102

  • Specification : 98%

  • CAS number : 4443-09-8

  • Formula : C15H10O5

  • Molecular Weight : 270.24

  • PUBCHEM ID : 5281674

  • Volume : 20mg

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Catalogue Number


Analysis Method






Molecular Weight



Yellow crystalline powder

Botanical Source

Scutellaria baicalensis Georgi

Structure Type



Standards;Natural Pytochemical;API











Flash Point


Boiling Point

528.4ºC at 760 mmHg

Melting Point

258 ºC (ethanol )



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#:4443-09-8) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.



BACKGROUND: Nor-wogonin, a polyhydroxy flavone, has been shown to possess antitumor activity. However, the mechanisms responsible for its antitumor activity are poorly studied. Herein, we investigated the mechanisms of nor-wogonin actions in triple-negative breast cancer (TNBC) cells. METHODS: Effects of nor-wogonin on cell proliferation and viability of four TNBC cell lines (MDA-MB-231, BT-549, HCC70, and HCC1806) and two non-tumorigenic breast cell lines (MCF-10A and AG11132) were assessed by BrdU incorporation assays and trypan blue dye exclusion tests. Cell cycle and apoptosis analyses were carried out by flow cytometry. Protein expression was analyzed by immunoblotting. RESULTS: Nor-wogonin significantly inhibited the growth and decreased the viability of TNBC cells; however, it exhibited no or minimal effects in non-tumorigenic breast cells. Nor-wogonin (40 μM) was a more potent anti-proliferative and cytotoxic agent than wogonin (100 μM) and wogonoside (100 μM), which are structurally related to nor-wogonin. The antitumor effects of nor-wogonin can be attributed to cell cycle arrest via reduction of the expression of cyclin D1, cyclin B1, and CDK1. Furthermore, nor-wogonin induced mitochondrial apoptosis, (as evidenced by the increase in % of cells that are apoptotic), decreases in the mitochondrial membrane potential (ΔΨm), increases in Bax/Bcl-2 ratio, and caspase-3 cleavage. Moreover, nor-wogonin attenuated the expression of the nuclear factor kappa-B and activation of signal transducer and activator of transcription 3 pathways, which can be correlated with suppression of transforming growth factor-β-activated kinase 1 in TNBC cells. CONCLUSION: These results showed that nor-wogonin might be a potential multi-target agent for TNBC treatment. Copyright ? 2019 Institute of Pharmacology, Polish Academy of Sciences. Published by Elsevier B.V. All rights reserved.

Apoptosis; Breast cancer; Cell cycle arrest; Multi-target flavone; Nor-wogonin


Anticancer effect of nor-wogonin (5, 7, 8-trihydroxyflavone) on human triple-negative breast cancer cells via downregulation of TAK1, NF-κB, and STAT3.


Abd El-Hafeez AA1, Khalifa HO2, Mahdy EAM3, Sharma V4, Hosoi T5, Ghosh P6, Ozawa K5, Montano MM4, Fujimura T7, Ibrahim ARN8, Abdelhamid MAA9, Pack SP10, Shouman SA11, Kawamoto S7.

Publish date

2019 Apr;



Tyrosinase is a ubiquitous enzyme that plays an essential role in the production of melanin. Effective inhibitors of tyrosinase have extensive applications in the medical, cosmetic and food industries. In this study, a combination of enzyme kinetics, ultraviolet (UV)-visible absorption, fluorescence spectroscopic techniques and a computational simulation method was used to characterize the inhibitory mechanism of 7,8,4´-trihydroxyflavone on tyrosinase. 7,8,4´-Trihydroxyflavone was found to strongly inhibit the oxidation of l-DOPA by tyrosinase with an IC50 value of 10.31 ± 0.41 μM. The inhibitory mechanism was determined to be reversible and non-competitive with a Ki of 9.50 ± 0.40 μM. The UV absorption spectra showed that 7,8,4´-trihydroxyflavone could chelate with copper ions and form a complex with tyrosinase. The intrinsic fluorescence of tyrosinase was quenched by 7,8,4´-trihydroxyflavone through a static quenching mechanism. 7,8,4´-Trihydroxyflavone was found to occupy a single binding site with a binding constant of 7.50 ± 1.20 × 104 M-1 at 298 K. The conformation of tyrosinase changed, and the microenvironment became more hydrophilic after 7,8,4´-trihydroxyflavone binding. Thermodynamics parameters indicated that the binding was a spontaneous process and involved hydrogen bonds and van der Waals forces. The binding distance was evaluated to be 4.54 ± 0.05 nm. Docking simulation analysis further authenticated that 7,8,4´-trihydroxyflavone could form hydrogen bonds with the residues His244 and Met280 within the tyrosinase active site. Our results will contribute to further understanding of the inhibitory mechanisms of 7,8,4´-trihydroxyflavone against tyrosinase and will facilitate future screening for tyrosinase inhibitors. Copyright ? 2018 John Wiley & Sons, Ltd.

7,8,4´-trihydroxyflavone; UV-visible spectra; conformation; fluorescence spectra; tyrosinase


The effect of 7,8,4´-trihydroxyflavone on tyrosinase activity and conformation: Spectroscopy and docking studies.


Shang C1, Zhang Y1, You X1, Guo N1, Wang Y1, Fan Y1, Liu W1.

Publish date

2018 Jun;



The flavonoids mosloflavone, oroxylin A, and norwogonin, which were purified from Scutellaria baicalensis Georgi, significantly protected Vero cells against Coxsackievirus B3 (CVB3)-induced cell death. To investigate the in vivo antiviral activity of oroxylin A, we intraperitoneally inoculated CVB3 into 4-week-old BALB/c mice. Body weights and blood glucose levels of the mice were decreased after CVB3 infection, and these changes were attenuated by the administration of oroxylin A. Importantly, treatment of mice with oroxylin A reduced viral titers in the pancreas and decreased the serum levels of the inflammatory cytokines including interleukin-6 (IL-6) and tumor necrosis factor (TNF)-α. Additionally, the administration of oroxylin A mitigated the histological pancreatic lesions and apoptotic cell death induced by CVB3 infection and increased the levels of phospho-eIF2α in infected pancreata. The results suggest that oroxylin A may represent a potent antiviral agent against CVB3 infection.

Antiviral Activity of Oroxylin A against Coxsackievirus B3 Alleviates Virus-Induced Acute Pancreatic Damage in Mice.


Kwon BE1, Song JH1, Song HH2, Kang JW3, Hwang SN3, Rhee KJ3, Shim A1, Hong EH1, Kim YJ4, Jeon SM5, Chang SY5, Kim DE6, Cho S6, Ko HJ1.

Publish date

2016 May 19

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