Product Name Polydatin
CAS No.: 27208-80-6
Catalog No.: CFN99159
Molecular Formula: C20H22O8
Molecular Weight: 390.40 g/mol
Purity: >=98%
Type of Compound: Polyphenols
Physical Desc.: White powder
Targets: NF-kB | NOS | MAPK | TNF-α | IL Receptor | LTR | Akt | Bcl-2/Bax | NO
Source: The rhizomes of Polygonum cuspidatum Sieb. et Zucc.
Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
Price: $30/20mg
Polydatin has antioxidant, anti-inflammatory, neuroprotection and anti-cancer activities, which has favorable potency to develop a hypolipemic and/or hepatoprotective agent in clinic. It is a mitochondria protector for acute severe hemorrhagic shock treatment, the neuronal mitochondrial injury is involved in the genesis of severe shock. Polydatin has a protective effect against ischemia/reperfusion injury in rat heart, the cardioprotection of polydatin is mainly mediated by cNOS which leading to an increase in NO production.
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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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    Inflammation. 2015 Jan 8.
    Inhibitory Effects of Polydatin on Lipopolysaccharide-Stimulated RAW 264.7 Cells.[Pubmed: 25567371]
    The purpose of this study was to evaluate the effects of Polydatin (PD) on cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) expressions at protein and transcriptional levels, as well as the production of prostaglandin E2 (PGE2) and nitric oxide (NO) in lipopolysaccharide (LPS)-induced macrophage RAW 264.7 cells.
    To elucidate the underlying mechanism responsible for these symptoms, we investigated the phosphorylation of mitogen-activated protein kinase (MAPK) pathway and nuclear factor-κB (NF-κB) expression. NO was analyzed with the Griess method. PGE2 was measured by enzyme-linked immunosorbent assay (ELISA). iNOS and COX-2 messenger RNA (mRNA) were identified by qPCR assay. iNOS, COX-2, NF-κB, extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 protein expressions were detected with Western blot. The results revealed that PD effectively inhibited NO and PGE2 production, and it is not surprising that PD reduced iNOS and COX-2 expression at protein and transcriptional levels. Additionally, PD significantly ameliorated the activation of NF-κB and the phosphorylation of MAPKs in LPS-induced RAW 264.7 macrophages.
    These findings suggested that PD exerted potent anti-inflammatory activity in macrophages.
    Zhongguo Zhong Yao Za Zhi. 2014 Aug;39(16):3157-61.
    Inhibitory effect of polydatin on expression of toll-like receptor 4 in ischemia-reperfusion injured NRK-52E cells.[Pubmed: 25509306]
    Polydatin is a monocrystaline compound isolated from Polygonum cuspidatum Sieb. et Zucc. (Polygonaceae) with biological properties, such as anti-inflammation, anti-oxidative and nephroprotective effects. Increasing number of studies have demonstrated the protective effect of Polydatin on renal ischemia reperfusion injury. However, the possible mechanisms of this protection are not fully elucidated.
    This study aimed to investigate the effect of Polydatin on ischemia-reperfusion induced expression of toll-like receptor4 (TLR4) in rat renal tubular epithelia cells (NRK-52E), and analyze the mechanism of Polydatin on TLR4 signal pathway. The cultured NRK-52E cells were incubated in three gas incubators for a period of 6 h at hypoxia and 24h at reoxygenation to simulate the ischemia-reperfusion injury in vitro. TLR4 mRNA level was analyzed by real-time-PCR, and the protein expression of TLR4 and NF-κB by Western blotting, while TNF-α and IL-1β proteins expressions were detected by ELISA. Polydatin downregulated I/R induced mRNA and protein expressions of TLR4, and decreased the protein expression of NF-κB, TNF-α and IL-1β. The TLR4 blocker partially antagonized the effect of I/R on NF-κB signaling, and such inhibitory effect was markedly enhanced by Polydatin.
    In the present study, Polydatin protects NRK-52E cells from I/R injury possibly by relieving the inflammatory response through regulation of TLR4/NF-κB signaling pathway.
    Biomed Pharmacother. 2009 Aug;63(7):457-62.
    Effects of polydatin from Polygonum cuspidatum on lipid profile in hyperlipidemic rabbits.[Pubmed: 18657948]
    Hyperlipidemia is one of the vital coronary risk factors and is positively related to morbidity and mortality of coronary heart disease. There are numerous herbal medicines which are reported to exert good hypolipidemic actions with few side effects.
    In the present study, the hypolipidemic effects of Polydatin, a compound from Polygonum cuspidatum Sieb. et Zucc, on hyperlipidemic rabbits were evaluated. Thirty-two male rabbits were fed a high fat/cholesterol diet for 6 weeks and another eight male rabbits fed a basic diet served as normal control. Three weeks after a high fat/cholesterol diet, the animals were orally administrated Polydatin (25, 50, and 100 mg kg(-1) per day) by intubation for 3 weeks. The results showed that Polydatin markedly decreased the serum levels of total cholesterol (TC), triglyceride (TG), and low-density lipoprotein cholesterol (LDL-C) in hyperlipidemic rabbits. The ratio of TC to high-density lipoprotein cholesterol (HDL-C) and the liver coefficient were also reduced. But both Polydatin and high fat/cholesterol diet did not evidently affect body weight in hyperlipidemic rabbits.
    All these results suggest that Polydatin from Polygonum cuspidatum has favorable potency to develop a hypolipemic and/or hepatoprotective agent in clinic. However the mechanism of hypolipemic action of Polydatin is in need of further clarity.
    Sheng Li Xue Bao. 2008 Apr 25;60(2):161-8.
    Protective effect of polydatin against ischemia/reperfusion injury in rat heart.[Pubmed: 18425301]
    The aim of the present study was to investigate the protective effect of Polydatin against myocardial ischemia/reperfusion injury in rats and the underlying mechanism.
    In anesthetized rats, ischemia and reperfusion arrhythmia produced by ligating and loosing the coronary artery was recorded and myocardial infarct size was measured. In Langendorff isolated rat heart, cardiac function was recorded before and after 30 min of global ischemia followed by 60 min of reperfusion. The parameters of cardiac function include left ventricular developed pressure (LVDP), maximal differentials of LVDP (±LVdp/dt(max)) and coronary flow (CF) were measured. Myocardial superoxide dismutase (SOD) activity, the contents of myocardial malondialdehyde (MDA) and nitric oxide (NO) as well as the activity of nitric oxide synthase (NOS) were measured in isolated heart. The results showed: (1) Arrhythmia score and myocardial infarct size were significantly lower in Polydatin group than that in the control group (P<0.05, P<0.01); (2) The recovery of LVDP, ±LVdp/dt(max) and CF during reperfusion in Polydatin group were significantly better than that in the control rats (P<0.05, P<0.01); (3) SOD activity in Polydatin group was significantly higher than that in the control group, but MDA content was lower in Polydatin group than that in the control group (P<0.05); (4) NO content and NOS activity, especially constitutive nitric oxide synthase (cNOS) activity in Polydatin group were higher than that in the control group (P<0.05); (5) L-NAME, the NOS inhibitor, reversed the protective effect of Polydatin against ischemia/reperfusion injury.
    The results suggest that Polydatin has a protective effect against ischemia/reperfusion injury in rat heart. The cardioprotection of Polydatin is mainly mediated by cNOS which leading to an increase in NO production.
    Oncol Lett. 2014 Jan;7(1):295-301. Epub 2013 Nov 21.
    Polydatin inhibits growth of lung cancer cells by inducing apoptosis and causing cell cycle arrest.[Pubmed: 24348867]
    Polydatin (PD), a small natural compound from Polygonum cuspidatum, has a number of biological functions. However, the anticancer activity of PD has been poorly investigated.
    In the present study, thiazolyl blue tetrazolium bromide assay was used to evaluate the inhibitory effect of PD on cell growth. Cell cycle distribution and apoptosis were investigated by flow cytometry. In addition, the expression of several proteins associated with apoptosis and cell cycle were analyzed by western blot analysis. The results demonstrated that PD significantly inhibits the proliferation of A549 and NCI-H1975 lung cancer cell lines and causes dose-dependent apoptosis. Cell cycle analysis revealed that PD induces S phase cell cycle arrest. Western blot analysis showed that the expression of Bcl-2 decreased as that of Bax increased, and the expression of cyclin D1 was also suppressed.
    The results suggest that PD has potential therapeutic applications in the treatment of lung cancer.
    Eur J Pharmacol. 2014 Dec 15;745:152-65.
    Polydatin improves glucose and lipid metabolism in experimental diabetes through activating the Akt signaling pathway.[Pubmed: 25310908]
    Recently, the effect of Polydatin on lipid regulation has gained considerable attention. And previous study has demonstrated that Polydatin has hypoglycemic effect on experimental diabetic rats. Repressed Akt pathway contributes to glucose and lipid disorders in diabetes. Thus, whether Polydatin regulates glucose and lipid metabolism in experimental diabetic models through the Akt pathway arouses interest.
    The purpose was to explore the regulatory mechanism of polydain on glucose and lipid through Akt pathway. We used a diabetic rat model induced by high-fat and -sugar diet with low-dose of streptozocin and an insulin resistant HepG2 cell model induced by palmitic acid to clarify the role of Polydatin on glucose and lipid metabolism. Here, we found that Polydatin significantly attenuated fasting blood–glucose, glycosylated hemoglobin, glycosylated serum protein, total cholesterol, triglyceride, and low-density lipoprotein cholesterol in diabetic rats. Furthermore, Polydatin significantly increased glucose uptake and consumption and decreased lipid accumulation in insulin resistant HepG2 cells. Polydatin markedly increased serum insulin levels in diabetic rats, and obviously activated the Akt signaling pathway in diabetic rat livers and insulin resistant HepG2 cells. Polydatin markedly increased phosphorylated GSK-3β, decreased the protein levels of G6Pase and SREBP-1c, and increased protein levels of GCK, LDLR, and phosphorylated IRS in livers and HepG2 cells.
    Overall, the results indicate that Polydatin regulates glucose and lipid metabolism in experimental diabetic models, the underlying mechanism is probably associated with regulating the Akt pathway. The effect of Polydatin on increased Akt phosphorylation is independent of prompting insulin secretion, but dependent of increasing IRS phosphorylation.
    Expert Opin Investig Drugs. 2013 Feb;22(2):169-79.
    Polydatin--a new mitochondria protector for acute severe hemorrhagic shock treatment.[Pubmed: 23241098 ]
    The aim of the study was find out whether neuronal mitochondrial injury does take place in severe shock and to explore effective therapy for severe shock.
    Rats were divided in the following group: sham, shock + normal saline (NS), shock + cyclosporine A (CsA), shock + resveratrol (Res) and shock + Polydatin (PD). Rats were subjected to shock for 2 h, followed by administration of NS, CsA, Res and PD, and infusion of shed blood. Morphology, metabolism and function of mitochondria were measured. Increased lipid peroxides (LPO) levels, lysosomal injury and mitochondrial permeability transition pore opening took place in neurons, resulting in swollen mitochondria with poorly defined cristae, decreased mitochondrial membrane potential (ΔΨ) and reduced ATP content in shock + NS group, indicating mitochondrial dysfunction. Mitochondrial protectors, such as CsA, Res and PD, partially inhibited these alterations, especially following PD protection, ATP level increased from 44.14 ± 13.81% in shock + NS group to 89.57 ± 9.21% and the survival time was prolonged from 6.3 ± 5.9 h in the shock + NS group to 31.6 ± 13.7 h in shock + PD group.
    The study shows that neuronal mitochondrial injury is involved in the genesis of severe shock and PD may be the best choice for protection of neuron against mitochondrial injury in severe shock.
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