Product Name Poncirin
CAS No.: 14941-08-3
Catalog No.: CFN90448
Molecular Formula: C28H34O14
Molecular Weight: 594.56 g/mol
Purity: >=98%
Type of Compound: Flavonoids
Physical Desc.: Powder
Targets: PGE | IL Receptor | NOS | COX | TNF-α | NF-kB | p65 | PPAR
Source: The fruits of Poncirus trifoliata (L.) Raf.
Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
Price: $218/20mg
Poncirin has anticancer, anti-bacterial and anti-inflammatory activities; it prevents adipogenesis, enhances osteoblast differentiation in mesenchymal stem cellsincreased bone mineral density, and improves trabecular microarchitecture likely reflect increases bone formation and decreases bone resorption in GIO mice. Poncirin inhibits iNOS, COX-2, TNF-alpha and IL-6 expression via the down-regulation of NF-kappaB binding activity.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Int J Mol Sci. 2013 Apr 24;14(5):8684-97.
    Characterization, Purification of Poncirin from Edible Citrus Ougan (Citrus reticulate cv. Suavissima) and Its Growth Inhibitory Effect on Human Gastric Cancer Cells SGC-7901.[Pubmed: 23615464]
    Poncirin is a bitter flavanone glycoside with various biological activities. Poncirin was isolated from four different tissues (flavedo, albedo, segment membrane, and juice sac) of Ougan fruit (Citrus reticulate cv. Suavissima).
    The highest content of Poncirin was found in the albedo of Ougan fruit (1.37 mg/g DW). High speed counter-current chromatography (HSCCC) combined with D101 resin chromatography was utilized for the separation and purification of Poncirin from the albedo of Ougan fruit. After this two-step purification, Poncirin purity increased from 0.14% to 96.56%. The chemical structure of the purified Poncirin was identified by both HPLC-PDA and LC-MS. Poncirin showed a significant in vitro inhibitory effect on the growth of the human gastric cancer cells, SGC-7901, in a dose-dependent manner.
    Thus, Poncirin from Ougan fruit, may be beneficial for gastric cancer prevention. The purification method demonstrated here will be useful for further studies on the pharmacological mechanism of Poncirin activity, as well as for guiding the consumption of Ougan fruit.
    J Microbiol Biotechnol. 2015 Jan 28;25(1):18-25.
    Metabolism of rutin and poncirin by human intestinal microbiota and cloning of their metabolizing α-L-rhamnosidase from Bifidobacterium dentium.[Pubmed: 25179902]

    To understand the metabolism of flavonoid rhamnoglycosides by human intestinal microbiota, we measured the metabolic activity of rutin and Poncirin (distributed in many functional foods and herbal medicine) by 100 human stool specimens. The average α-Lrhamnosidase activities on the p-nitrophenyl-α-L-rhamnopyranoside, rutin, and Poncirin subtrates were 0.10 ± 0.07, 0.25 ± 0.08, and 0.15 ± 0.09 pmol/min/mg, respectively. To investigate the enzymatic properties, α-L-rhamnosidase-producing bacteria were isolated from the specimens, and the α-L-rhamnosidase gene was cloned from a selected organism, Bifidobacterium dentium, and expressed in E. coli. The cloned α-L-rhamnosidase gene contained a 2,673 bp sequcence encoding 890 amino acid residues. The cloned gene was expressed using the pET 26b(+) vector in E. coli BL21, and the expressed enzyme was purified using Ni(2+)-NTA and Q-HP column chromatography. The specific activity of the purified α-L-rhamnosidase was 23.3 μmol/min/mg. Of the tested natural product constituents, the cloned α-L-rhamnosidase hydrolyzed rutin most potently, followed by Poncirin, naringin, and ginsenoside Re. However, it was unable to hydrolyze quercitrin.
    This is the first report describing the cloning, expression, and characterization of α-L-rhamnosidase, a flavonoid rhamnoglycosidemetabolizing enzyme, from bifidobacteria. Based on these findings, the α-L-rhamnosidase of intestinal bacteria such as B. dentium seem to be more effective in hydrolyzing (1-->6) bonds than (1-->2) bonds of rhamnoglycosides, and may play an important role in the metabolism and pharmacological effect of rhamnoglycosides.
    Biol Pharm Bull. 1999 Apr;22(4):422-4.
    Anti-Helicobacter pylori activity of the metabolites of poncirin from Poncirus trifoliata by human intestinal bacteria.[Pubmed: 10328566]
    Poncirin was isolated from water extract of the fruits of Poncirus trifoliata and metabolized by human intestinal bacteria.
    The inhibitory effect of Poncirin and its metabolites by these bacteria on the growth of Helicobacter pylori (HP) was investigated. Among them, ponciretin (5,7-dihydroxy-4'-methoxyflavanone), the main metabolite most potently inhibited the growth of HP, with a minimum inhibitory concentration (MIC) of 10-20 microg/ml.
    However, Poncirin and its metabolites except ponciretin did not inhibit the growth of HP, nor did they inhibit HP urease.
    J Bone Miner Metab. 2012 Sep;30(5):509-16.
    Poncirin prevents bone loss in glucocorticoid-induced osteoporosis in vivo and in vitro.[Pubmed: 22407507]
    Poncirin, a flavonoid isolated from the fruit of Poncirus trifoliata, possesses anti-bacterial and anti-inflammatory activities. However, the action of Poncirin in bone biology is unclear. In this study, the in vivo and in vitro effects of Poncirin in a glucocorticoid-induced osteoporosis (GIO) mouse model were investigated.
    Seven-month-old male mice were assigned to the following five groups: (1) sham-implantation (sham), (2) prednisolone 2.1 mg/kg/day (GC), (3) GC treated with 10 mg/kg/day of genistein, (4) GC treated with 3 mg/kg/day of Poncirin, (5) and GC treated with 10 mg/kg/day of strontium (GC + SrCl(2)). After 8 weeks, bone loss was measured by microcomputed tomography. Osteocalcin (OC) and C-terminal telopeptides of type I collagen (CTX) were evaluated in sera. Runx2 protein, OC and osteoprotegerin (OPG) mRNA expression, alkaline phosphatase (ALP) activity, and mineral nodule assay were performed in C3H10T1/2 or primary bone marrow stromal cells. Poncirin significantly increased the bone mineral density and improved the microarchitecture. Poncirin increased serum OC, Runx2 protein production, expression of OC and OPG mRNA, ALP activity, and mineral nodule formation; and decreased serum CTX. These effects were more prominent in the Poncirin group compared to the other positive control groups (genistein and strontium).
    The Poncirin-mediated restoration of biochemical bone markers, increased bone mineral density, and improved trabecular microarchitecture likely reflect increased bone formation and decreased bone resorption in GIO mice.
    Eur J Pharmacol. 2011 Aug 16;664(1-3):54-9.
    Poncirin promotes osteoblast differentiation but inhibits adipocyte differentiation in mesenchymal stem cells.[Pubmed: 21550337]
    Poncirin, flavanone glycoside, isolated from the fruit of Poncirus trifoliata, has anti-bacterial and anti-inflammatory activities.
    In this study, the effects of Poncirin on the differentiation of mesenchymal stem cells were investigated. The C3H10T1/2 mesenchymal stem cells and primary bone marrow mesenchymal stem cells were studied. In the C3H10T1/2 cells, Poncirin prevented adipocyte differentiation, as demonstrated by inhibition of cytoplasm lipid droplet accumulation and peroxisome proliferator-activating receptor-γ (PPAR-γ) and CCAAT-enhancer-binding protein-β (C/EBP-β) mRNA expression. By contrast, Poncirin enhanced the expression of the key osteogenic transcription factors, runt-related transcription factor 2 (Runx2) and transcriptional coactivator with PDZ-binding motif (TAZ). Poncirin also enhanced expression of the osteogenic marker genes including alkaline phosphatase (ALP) and osteocalcin (OC). Poncirin increased mineral nodule formation in primary bone marrow mesenchymal stem cells.
    These results suggest that Poncirin prevents adipogenesis and enhances osteoblast differentiation in mesenchymal stem cells.
    Biol Pharm Bull. 2007 Dec;30(12):2345-51.
    Inhibition of LPS-induced iNOS, COX-2 and cytokines expression by poncirin through the NF-kappaB inactivation in RAW 264.7 macrophage cells.[Pubmed: 18057724]
    We previously reported that Poncirin, a flavanone glycoside isolated from the EtOAc extract of the dried immature fruits of Poncirus trifoliata, is an anti-inflammatory compound that inhibits PGE(2) and IL-6 production.
    The present work was undertaken to investigate the molecular actions of Poncirin in RAW 264.7 macrophage cell line. Poncirin reduced lipopolysaccharide (LPS)-induced protein levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) and the mRNA expressions of iNOS, COX-2, tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) in a concentration-dependent manner, as determined by Western blotting and RT-PCR, respectively. Furthermore, Poncirin inhibited the LPS-induced DNA binding activity of nuclear factor-kappaB (NF-kappaB). Moreover, this effect was accompanied by a parallel reduction in IkappaB-alpha degradation and phosphorylation that in by nuclear translocations of p50 and p65 NF-kappaB subunits.
    Taken together, our data indicate that anti-inflammatory properties of Poncirin might be the result from the inhibition iNOS, COX-2, TNF-alpha and IL-6 expression via the down-regulation of NF-kappaB binding activity.

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