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  • Brand : BIOFRON

  • Catalogue Number : BD-P0592

  • Specification : 98.0%(HPLC)

  • CAS number : 2957-21-3

  • Formula : C16H14O5

  • Molecular Weight : 286.3

  • PUBCHEM ID : 73571

  • Volume : 20mg

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Catalogue Number


Analysis Method





Molecular Weight




Botanical Source

This product is isolated and purified from the leaves of Oryza sativa L.

Structure Type





5-hydroxy-2-(4-hydroxyphenyl)-7-methoxy-2,3-dihydrochromen-4-one/4',5-Dihydroxy-7-methoxyflavanone/(S)-(-)-4',5-dihydroxy-7-methoxyflavanone/4',5-DIHYDROXY-7-METHOXYFLAVONE/4H-1-Benzopyran-4-one, 2,3-dihydro-5-hydroxy-2-(4-hydroxyphenyl)-7-methoxy-, (2S)-/Naringenin 7-O-methyl ether/5,4'-dihydroxy-7-methoxyflavanone/(2S)-sakuranetin/7-O-Methylnaringenin/naringenin 7-methylether/(S)-(-)-4',5-Dihydroxy-7-methoxy-flavanone/(2S)-5-Hydroxy-2-(4-hydroxyphenyl)-7-methoxy-2,3-dihydro-4H-chromen-4-one/Sakuranetin/Naringenin 7-methyl ether



1.4±0.1 g/cm3


Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.

Flash Point

212.4±23.6 °C

Boiling Point

555.9±50.0 °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#:2957-21-3) 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.




Alzheimer’s disease (AD) is a high-incidence neurodegenerative disease with complex and diverse pathogenesis. With aging of the population and continuous improvement of living standards, the incidence of AD is on the increase. Therefore, there is need to develop more effective AD drugs in order to improve the quality of life of the elderly. Sakuranetin (SAK) is a dihydroflavonoid compound extracted from plants. It has many physiological properties. In this study, the effect of SAK on spatial discrimination in a rat model of cognitive dysfunction exposed to D-galactose was investigated with respect to its effect on malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GPx) levels, and on the expressions of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and nuclear factor-κB inhibitory factor-α (IκBα) in hippocampus of rats. The results obtained suggest that SAK may exert protective effects on brain cells through anti-oxidation mechanism. Moreover, the improvement in learning and memory impairment by SAK may also be related to the inhibition of inflammatory mediators in brain tissue. These findings provide scientific evidence that can be exploited for more effective treatment of Alzheimer’s disease.


Brain cells; D-galactose.; Dementia model; Sakuranetin


Protective effect of sakuranetin in brain cells of dementia model rats.


Li C1, Hu C1, Wang R1, Wang H1, Ma Q1, Chen S1, He Y1.

Publish date

2019 Jun 30




Pruni Cortex is a herbal drug from the bark of the Japanese flowering cherries, Prunus jamasakura or Prunus verecunda, and is included in the traditional Japanese herbal (Kampo) formula Jumihaidokuto, which is administered orally to patients suffering from inflammatory skin diseases. The flavanones contained in Pruni Cortex (e.g., sakuranetin and naringenin) have potent anti-inflammatory, anti-allergic, and anti-microbial activities. Although the effects of Pruni Cortex on skin disease have been well studied, reports regarding its pharmacological effects on the liver are limited. In this study, we extracted the bark of Prunus jamasakura and purified it to isolate the pharmacologically active constituents by monitoring nitric oxide (NO) production in rat hepatocytes that were treated with the pro-inflammatory cytokine, interleukin (IL)-1β. Sakuranetin and (-)-naringenin, which were present in an ethyl acetate-soluble fraction of the bark extract, significantly inhibited NO induction and inducible nitric oxide synthase (iNOS) expression. These two flavanones decreased the expression of type 1 IL-1 receptor gene and phosphorylation of Akt, also known as protein kinase B, which is regulated by phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K). Furthermore, sakuranetin decreased the phosphorylation of the activator isoforms of CCAAT/enhancer-binding protein β (C/EBPβ), which synergistically activates the transcription of the iNOS gene with nuclear factor κB (NF-κB). Therefore, sakuranetin inhibited the co-activating activity of C/EBPβ with NF-κB, leading to the suppression of iNOS gene expression in hepatocytes. Taken together, sakuranetin in Pruni Cortex downregulated the iNOS gene by inhibiting PI3K/Akt signal transduction and the phosphorylation of C/EBPβ. These results imply that sakuranetin may be primarily responsible for the anti-inflammatory effects of Pruni Cortex in the liver.


CCAAT/enhancer-binding protein β; Cherry bark; Interleukin 1 receptor; Kampo medicine; Nitric oxide; Nuclear factor κB


Sakuranetin downregulates inducible nitric oxide synthase expression by affecting interleukin-1 receptor and CCAAT/enhancer-binding protein β.


Yamauchi Y1, Okuyama T1, Ishii T1, Okumura T2,3, Ikeya Y4, Nishizawa M1.

Publish date

2019 Mar;




This study aimed to investigate in vitro the anti-influenza B/Lee/40 virus effect of sakuranetin and mode of its action. The sakuranetin exhibited potent antiviral activity against influenza B/Lee/40 virus, reducing the formation of a visible cytopathic effect, with a 50% inhibitory concentration (IC50 ) of 7.21 μg/ml and no cytotoxicity at a concentration of 100 μg/ml, and the derived therapeutic index (TI) was >13.87. Oseltamivir showed weak anti-influenza B/Lee/40 virus activity with IC50 of 80.74 μg/ml, 50% cytotoxicity concentration of >100 μg/ml, and TI of >1.24. Sakuranetin also showed effective inhibitory effects when added at the viral attachment, entry, and postentry steps. Moreover, sakuranetin effectively inactivated influenza B/Lee/40 virus infection in dose- and temperature-dependent manners. Sakuranetin indicated an inhibitory effect in viral RNA synthesis in the presence of 100 μg/ml of sakuranetin. Overall, this research revealed that sakuranetin could inhibit influenza B/Lee/40 virus replication and that sakuranetin may be involved in the virus attachment, entry, and postentry. Therefore, sakuranetin is a good candidate for a chemopreventive agent for influenza virus-related diseases.

© 2018 John Wiley & Sons, Ltd.


antiviral; influenza; mode; sakuranetin


Suppression of influenza B virus replication by sakuranetin and mode of its action.


Kwon DH1, Ji JH2, Yim SH3, Kim BS4, Choi HJ5.

Publish date

2018 Dec;3

Description :

Sakuranetin Induces Melanogenesis in B16BL6 Melanoma Cells through Inhibition of ERK and PI3K/AKT Signaling Pathways.[Pubmed: 27000529]Phytother Res. 2016 Jun;30(6):997-1002. Asthma is a disease of high prevalence and morbidity that generates high costs in hospitalization and treatment. Although the airway is involved in the physiopathology of asthma, there is also evidence of the importance of vascular and lung parenchyma inflammation and remodeling, which can contribute to the functional pulmonary alterations observed in asthmatic patients. Our aim was to evaluate treatment using Sakuranetin, a flavone isolated from the twigs of Baccharis retusa (Asteraceae), on vascular and lung parenchyma alterations in an experimental murine model of asthma. METHODS AND RESULTS: Male BALB/c mice were subjected to a sensitization protocol with ovalbumin for 30days and were treated with or without Sakuranetin (20mg/kg/mice) or dexamethasone (5mg/kg/mice); then, the lungs were collected for histopathological analysis. We evaluated extracellular matrix remodeling (collagen and elastic fibers), inflammation (eosinophils and NF-kB) and oxidative stress (8-isoprostane) in the pulmonary vessels and lung parenchyma. The thickness of the vascular wall was quantified, as well as the vascular endothelial growth factor (VEGF) levels. We demonstrated that Sakuranetin reduced the number of eosinophils and elastic fibers in both the pulmonary vessels and the lung parenchyma, probably due to a reduction of oxidative stress and of the transcription factor NF-kB and VEGF levels in the lung. In addition, it reduced the thickness of the pulmonary vascular wall. The treatment had no effect on the collagen fibers. In most of the parameters, the effect of Sakuranetin was similar to the dexamethasone effect. CONCLUSIONS: Sakuranetin had anti-inflammatory and antioxidant effects, preventing vascular and distal parenchyma changes in this experimental model of asthma.