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  • Brand : BIOFRON

  • Catalogue Number : BF-N3008

  • Specification : 98%

  • CAS number : 10236-47-2

  • Formula : C27H32O14

  • Molecular Weight : 580.53

  • PUBCHEM ID : 442428

  • Volume : 25mg

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Catalogue Number


Analysis Method






Molecular Weight



Off-white crystalline powder

Botanical Source

Citrus aurantium,Glycyrrhiza uralensis,Hedysarum polybotrys

Structure Type



Standards;Natural Pytochemical;API




2,6-Dimethylpyrimidin-4(1H)-one/2,6-Dimethylpyrimidin-4-ol/Naringenin 7-neohesperidoside/2,6-Dimethyl-4(1H)-pyrimidinone/T6N CNJ B1 DQ F1/T6VM DNJ C1 E1/2,6-Dimethyl-4(3H)-pyrimidinone/Naringenin 7-Rhamnoglucoside Hydrate/Naringenoside/Nobiletin/Naringin Hydrate/2,6-Dimethylpyrimidin-4(3H)-one/4(3H)-Pyrimidinone, 2,6-dimethyl-/4-pyrimidinol, 2,6-dimethyl-




1.2±0.1 g/cm3



Flash Point

308.5±27.8 °C

Boiling Point

928.1±65.0 °C at 760 mmHg

Melting Point

166 °C


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#:10236-47-2) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Naringin, a natural occurring flavonoid compound, enriches in citrus fruits. We aimed to evaluate the inhibitory effect of naringin on colitis and chronic inflammation-driven carcinogenesis. Male C57BL/6 mice were exposed to AOM/DSS to induce colorectal inflammation and carcinogenesis. Naringin by oral administration prevented AOM/DSS-induced ulcerative colitis and carcinogenesis without significant side effects. Naringin attenuated the severity of colitis and colorectal adenomas through inhibiting myeloid-derived suppressor cells (MDSCs), pro-inflammatory mediators GM-CSF/M-CSF, IL-6 and TNF-α and the NF-κB/IL-6/STAT3 cascades in colorectal tissues. Naringin-treated mice exhibited normalized structures of colorectal tissues. Electron microscopy analysis showed the suppression of robust endoplasmic reticulum (ER) stress-induced autophagy. Naringin inhibited the secretion of the ER-spanning transmembrane proteins, such as GRP78 ATF6, IRE1α and activated PERK phosphorylated eIF-2α and complex of autophagosomes ATG3, ATG5, ATG7, ATG12, ATG16 and ATG16L1 in the colorectal mucosal cells.
Conclusion: Naringin prevented colitis and colorectal carcinogenesis through suppressing robust ER stress-induced autophagy in colorectal mucosal cells. Naringin could develop a promising therapeutic agent for the prevention of ulcerative colitis and colorectal tumor.


Aspirin; Colitis; Endoplasmic reticulum (ER) stress; MDSCs; Naringin; autophagy; colorectal carcinogenesis.


Natural Dietary Compound Naringin Prevents Azoxymethane/Dextran Sodium Sulfate-Induced Chronic Colorectal Inflammation and Carcinogenesis in Mice


Yu-Sheng Zhang 1 , Feng Wang 2 , Shu-Xiang Cui 2 , Xian-Jun Qu 1

Publish date

2018 Aug 3




Background: The Nucleotide binding and oligomerization domain-like receptorfamily pyrin domain-containing 3 (NLRP3)-inflammasome plays an important role in various diseases, including a variety of kidney diseases. Naringin exhibits anti-inflammatory and anti-oxidation effects among others, but its specific mechanisms are not clear. We investigated the expression of the NLRP3-inflammasome under high-glucose conditions, assessed the effects of naringin on that process, and further elucidated the role of naringin in the pathogenesis of diabetic kidney disease(DKD).
Methods: To assess the therapeutic potential of naringin and the mechanisms involved, we cultured rat glomerular mesangial cells and grouped them according to different glucose concentrations, different action times, different concentrations of MCC950, and different concentrations of naringin.The cell proliferation was measured by MTT assay. The expression of Interleukin-1β(IL-1β) and Interleukin18 (IL-18) in the cell supernatant were detected by ELISA. The expression and activity of NLPR3, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) and Caspase-1 were detected by Western Blot.
Results: The expressions of NLRP3, ASC, caspase-1, IL-1β, and IL-18 in rat glomerular mesangial cells were significantly higher in the high glucose (HG) group than in the control normal glucose (NG) group and exhibited time-dependence activity. The expression levels of NLRP3, caspase-1, IL-1β, and IL-18 in different treatment groups were significantly lower compared with the HG group after 48 h of MCC950 pre-treatment (p < 0.05). Pre-treatment with naringin produced the same results. Naringin also inhibited the proliferation of cells.
Conclusions: The NLRP3-inflammasome potentially plays a role in the process of activation and inflammation of glomerular mesangial cells as induced by high-glucose conditions. Naringin inhibited the proliferation of cells that were induced by high glucose. Further, it reduced the expression of inflammatory factors that are mediated by NLRP3 through the NLRP3-caspase-1-IL-1β/IL-18 signaling pathway, which makes naringin a potentially novel treatment for DKD disease.


Diabetes mellitus; Diabetic kidney disease; NLRP3 inflammasome; NLRP3-caspase-1-IL-1β/IL-18 signaling pathway; Naringin.


Naringin Ameliorates the High Glucose-Induced Rat Mesangial Cell Inflammatory Reaction by Modulating the NLRP3 Inflammasome


Fenqin Chen 1 , Guozhu Wei 2 , Jiao Xu 1 , Xiaoyu Ma 1 , Qiuyue Wang 3

Publish date

2018 Jun 22




Excessive autophagy/mitophagy plays important roles during cerebral ischemia-reperfusion (I/R) injury. Peroxynitrite (ONOO-), a representative reactive nitrogen species, mediates excessive mitophagy activation and exacerbates cerebral I/R injury. In the present study, we tested the hypothesis that naringin, a natural antioxidant, could inhibit ONOO–mediated mitophagy activation and attenuate cerebral I/R injury. Firstly, we demonstrated that naringin possessed strong ONOO- scavenging capability and also inhibited the production of superoxide and nitric oxide in SH-SY5Y cells exposed to 10 h oxygen-glucose-deprivation plus 14 h of reoxygenation or ONOO- donor 3-morpholinosydnonimine conditions. Naringin also inhibited the expression of NADPH oxidase subunits and iNOS in rat brains subjected to 2 h ischemia plus 22 h reperfusion. Next, we found that naringin was able to cross the blood-brain barrier, and naringin decreased neurological deficit score, reduced infarct size, and attenuated apoptotic cell death in the ischemia-reperfused rat brains. Furthermore, naringin reduced 3-nitrotyrosine formation, decreased the ratio of LC3-II to LC3-I in mitochondrial fraction, and inhibited the translocation of Parkin to the mitochondria. Taken together, naringin could be a potential therapeutic agent to prevent the brain from I/R injury via attenuating ONOO–mediated excessive mitophagy.


Cerebral ischemia-reperfusion injury; Mitophagy; Naringin; Nitrative stress; Peroxynitrite.


Naringin Attenuates Cerebral Ischemia-Reperfusion Injury Through Inhibiting Peroxynitrite-Mediated Mitophagy Activation


Jinghan Feng 1 , Xingmiao Chen 1 , Shengwen Lu 2 , Wenting Li 1 , Dan Yang 3 , Weiwei Su 4 , Xijun Wang 5 , Jiangang Shen 6

Publish date

2018 Dec

Description :

Naringin is a major flavanone glycoside obtained from tomatoes, grapefruits, and many other citrus fruits. Naringin exhibits biological properties such as antioxidant, anti-inflammatory, and antiapoptotic activities.