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  • Brand : BIOFRON

  • Catalogue Number : BD-P0772

  • Specification : 97%

  • CAS number : 520-26-3

  • Formula : C28H34O15

  • Molecular Weight : 610.6

  • PUBCHEM ID : 10621

  • Volume : 25mg

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Catalogue Number


Analysis Method





Molecular Weight




Botanical Source

This product is isolated and purified from the peel of Citrus sinensis

Structure Type





usafcf-3/Hesperetin 7-rhamnoglucoside,Hesperitin-7-rutinoside/VITAMIN P/HespeidinHespiridin/Hesperiden/Neobiletin/cirantin/Hesperetin7-rutinoside/Cirontin/Hesperidoside/Hesperetin7-rhamnoglucoside/Hesperidin



Hesperidin, a citrus flavonoid, inhibits bone loss and decreases serum and hepatic lipids in ovariectomized mice.[Pubmed: 12771335]Protective effect of hesperidin against lung injury induced by intestinal ischemia/reperfusion in adult albino rats: histological, immunohistochemical and biochemical study.[Pubmed: 25063207 ]Tissue Cell. 2014 Oct;46(5):304-10. Hesperidin is a naturally common flavonoid. It is an abundant and cheap by-product of citrus cultivation. It is reported to have antioxidative, anti-inflammatory and anticarcinogenic effects. This work was performed to investigate the possible protective role of Hesperidin in ameliorating the effect of experimentally induced intestinal ischemia/reperfusion injury (I/R) on lung tissue, histologically, immunohistochemically and biochemically. METHODS AND RESULTS:Thirty male Wistar adult albino rats were randomized into three groups named: group I (control group); group II (I/R); and group III (I/R with Hesperidin). Intestinal I/R was induced by occluding the superior mesenteric artery for 60 min, followed by 120 min of reperfusion period. Animals were given Hesperidin orally 1h before the onset of ischemia. At the end of the reperfusion period the lung tissues were extracted for histopathological examination and immunohistochemical detection of the distribution of inducible nitric oxide synthase (iNOS). Pulmonary edema was evaluated by lung tissue wet/dry weight ratios. The levels of malondialdehyde (MDA, a biomarker of oxidative damage), myeloperoxidase (MPO, an index of the degree of neutrophil accumulation) and glutathione (GSH, a biomarker of protective oxidative injury) were also determined in all dissected tissues. Pretreatment with Hesperidin (in group III) alleviated lung morphological changes noticed in I/R group and the levels of MDA and MPO were significantly decreased whereas those of GSH were significantly increased. Immunohistochemical study revealed a significant decrease in the iNOS. Hesperidin also significantly alleviated the formation of pulmonary edema as evidenced by the decreased organ wet/dry weight ratios. CONCLUSIONS:Hesperidin exerts a protective effect against lung damage induced by intestinal I/R injury in rats by reducing oxidative stress.J Nutr. 2003 Jun;133(6):1892-7. The purpose of this study was to examine whether Hesperidin inhibits bone loss in ovariectomized mice (OVX), an animal model of postmenopausal osteoporosis. METHODS AND RESULTS:Forty 8-wk-old female ddY mice were assigned to five groups: a sham-operated group fed the control diet (AIN-93G), an OVX group fed the control diet, an OVX+HesA group fed the control diet containing 0.5 g/100 g Hesperidin, and an OVX+HesB group fed the control diet containing 0.7 g/100 g alpha-glucosylHesperidin and an OVX+17beta-estradiol (E(2)) group fed the control diet and administered 0.03 micro g E(2)/d with a mini-osmotic pump. After 4 wk, the mice were killed and blood, femoral, uterine and liver were sampled immediately. Hesperidin administration did not affect the uterine weight. In OVX mice, the bone mineral density of the femur was lower than in the sham group (P < 0.05) and this bone loss was significantly prevented by dietary Hesperidin or alpha-glucosylHesperidin. The Ca, P and Zn concentrations in the femur were significantly higher in the Hesperidin-fed and E(2) groups than in the OVX group. Histomorphometric analyses showed that the trabecular bone volume and trabecular thickness in the femoral distal metaphysis were markedly decreased (P < 0.05) by OVX, and alpha-glucosylHesperidin significantly prevented this bone loss. Furthermore, Hesperidin decreased the osteoclast number of the femoral metaphysis in OVX mice, as did E(2). Serum and hepatic lipids were lower in mice that consumed the Hesperidin-containing diets (P < 0.05) than in the OVX group fed the control diet. CONCLUSIONS:These results suggest a possible role for citrus flavonoids in the prevention of lifestyle-related diseases because of their beneficial effects on bone and lipids.


1.7±0.1 g/cm3


Methanol; DMF; DMSO

Flash Point

305.5±27.8 °C

Boiling Point

930.1±65.0 °C at 760 mmHg

Melting Point

250-255 °C (dec.)(lit.)


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#:520-26-3) 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.




A marked decrease in human cancers, including breast cancer, bone cancer, and cervical cancer, has been linked to the consumption of vegetable and fruit, and the corresponding chemoprotective effect has been associated with the presence of several active molecules, such as kaempferol. Kaempferol is a major flavonoid aglycone found in many natural products, such as beans, bee pollen, broccoli, cabbage, capers, cauliflower, chia seeds, chives, cumin, moringa leaves, endive, fennel, and garlic. Kaempferol displays several pharmacological properties, among them antimicrobial, anti-inflammatory, antioxidant, antitumor, cardioprotective, neuroprotective, and antidiabetic activities, and is being applied in cancer chemotherapy. Specifically, kaempferol-rich food has been linked to a decrease in the risk of developing some types of cancers, including skin, liver, and colon. The mechanisms of action include apoptosis, cell cycle arrest at the G2/M phase, downregulation of epithelial-mesenchymal transition (EMT)-related markers, and phosphoinositide 3-kinase/protein kinase B signaling pathways. In this sense, this article reviews data from experimental studies that investigated the links between kaempferol and kaempferol-rich food intake and cancer prevention. Even though growing evidence supports the use of kaempferol for cancer prevention, further preclinical and clinical investigations using kaempferol or kaempferol-rich foods are of pivotal importance before any public health recommendation or formulation using kaempferol.


anticancer; antioxidant; apoptosis; cell cycle arrest; chemoprevention; kaempferol; metastasis; pharmacodynamics; pharmacokinetics; reactive oxygen species


Kaempferol: A Key Emphasis to Its Anticancer Potential.


Imran M1, Salehi B2, Sharifi-Rad J3, Aslam Gondal T4, Saeed F5, Imran A6, Shahbaz M7, Tsouh Fokou PV8, Umair Arshad M9, Khan H10, Guerreiro SG11,12,13, Martins N14,15, Estevinho LM16,17.

Publish date

2019 Jun 19




Anticancer drug like Cisplatin are associated with serious problem like nephrotoxicity. The effect of Kaempferol is a plant-derived flavonoid compound. The present work evaluated the effect of Kaempferol in mouse model of Cisplatin mediated nephrotoxicity also the involved mechanism. Oxidative stress, kidney function, histology, inflammation, apoptosis, level of proteins, Nrf2 translocation and its effect on cascades such as NF-κB and ERK were studied. It was observed that the pre-treatment of KPF reduced the Cisplatin mediated oxidative stress, inflammation, apoptosis and ameliorated renal injury and its functioning. Kaempferol suppressed the Cisplatin induced infiltration of mononuclear cells, levels of TNF-α, iNOS, IL-12, activation of NF-κB, phosphorylation of IκBα and nuclear translocation of p65 in renal tissues. Also KPF attenuated Cisplatin mediated phosphorylation of p38, ERK1/2 and JNK in renal tissues. KPF also corrected the levels of renal antioxidants and elevated the nuclear levels of HO-1 and Nrf2 in renal tissues. KPF attenuated the Cisplatin mediated apoptosis via down-regulating the levels of TP53, Bax/Bcl2 imbalance, activating caspase-3/9 and PARP. The outcomes conclude that KPF ameliorates Cisplatin-mediated nephrotoxicity by modulating oxidative stress, inflammation and apoptosis via ERK and NF-κB pathway.


Kaempferol ameliorates Cisplatin induced nephrotoxicity by modulating oxidative stress, inflammation and apoptosis via ERK and NF-κB pathways.


Wang Z1, Sun W1, Sun X2, Wang Y1, Zhou M3.

Publish date

2020 Mar 26




Kaempferol, a plant-derived flavonoid, has been reported to have activity against Japanese encephalitis virus (JEV) in BHK-21 cells. To determine the broader utility of this compound, we initially evaluated the activity of kaempferol against JEV and dengue virus (DENV) in HEK293T/17 cells. Results showed no significant antiviral activity against either virus. We subsequently investigated the activity of kaempferol against both JEV and DENV in BHK-21 cells. Results showed a significant inhibition of JEV infection but, surprisingly, a significant enhancement of DENV infection. The effect of kaempferol on both host protein expression and transcription was investigated and both transcriptional and translational inhibitory effects were observed, although a more marked effect was observed on host cell protein expression. Markedly, while GRP78 was increased in DENV infected cells treated with kaempferol, it was not increased in JEV infected cells treated with kaempferol. These results show that cellular alteration induced by one compound can have opposite effects on viruses from the same family, suggesting the presence of distinct replication strategies for these two viruses.


Discordant Activity of Kaempferol Towards Dengue Virus and Japanese Encephalitis Virus.


Care C1, Sornjai W1, Jaratsittisin J1, Hitakarun A1, Wikan N1, Triwitayakorn K1, Smith DR1.

Publish date

2020 Mar 10