Product Name Phillyrin
CAS No.: 487-41-2
Catalog No.: CFN99998
Molecular Formula: C27H34O11
Molecular Weight: 534.56 g/mol
Purity: >=98%
Type of Compound: Lignans
Physical Desc.: Powder
Targets: Fatty Acid Synthase | AMPK | ROS | Bcl-2/Bax | TNF-α | IL Receptor | MAPK | NF-kB
Source: The fruits of Forsythia suspensa
Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
Price: $40/20mg
Phillyrin is a novel AMPK activator, has anti-obesity effects in nutritive obesity mice, it can prevent lipid accumulation in HepG2 cells by blocking the expression of SREBP-1c and FAS through LKB1/AMPK activation. Phillyrin may be a new preventive agent of acute lung injury in the clinical setting, it potentially contributes to the suppression of the activation of MAPK and NF-κB pathways, it also has protective effects on H2O2-induced oxidative stress and apoptosis in PC12 cells.
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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:

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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    Food Chem. 2013 Jan 15;136(2):415-25.
    Phillyrin attenuates high glucose-induced lipid accumulation in human HepG2 hepatocytes through the activation of LKB1/AMP-activated protein kinase-dependent signalling.[Pubmed: 23122079]
    Phillyrin, an active constituent found in many medicinal plants and certain functional foods, has anti-obesity activity in vivo. The aim of our study was to provide new data on the molecular mechanism(s) underlying the role of Phillyrin in the prevention of high glucose-induced lipid accumulation in human HepG2 hepatocytes.
    We found that Phillyrin suppressed high glucose-induced lipid accumulation in HepG2 cells. Phillyrin strongly inhibited high glucose-induced fatty acid synthase (FAS) expression by modulating sterol regulatory element-binding protein-1c (SREBP-1c) activation. Moreover, use of the pharmacological AMP-activated protein kinase (AMPK) inhibitor compound C revealed that AMPK is essential for suppressing SREBP-1c expression in Phillyrin-treated cells. Finally, we found that liver kinase B1 (LKB1) phosphorylation is required for the Phillyrin-enhanced activation of AMPK in HepG2 hepatocytes.
    These results indicate that Phillyrin prevents lipid accumulation in HepG2 cells by blocking the expression of SREBP-1c and FAS through LKB1/AMPK activation, suggesting that Phillyrin is a novel AMPK activator with a role in the prevention and treatment of obesity.
    Zhong Yao Cai. 2005 Feb;28(2):123-4.
    [Effect of phillyrin on the anti-obesity in nutritive obesity mice].[Pubmed: 15981888]
    To study on the anti-obesity effect of Phillyrin in nutritive obesity mice.
    The alimentary obesity model was established by hyperalimentation. The wet weight of fat, fat index, number of fat cells per unit visual field, Lee's index, jejunum microvillus area, serum triglyceride and cholesterol were selected to observe the anti-obesity effect of Phillyrin. Phillyrin could lower wet weight of fat (P < 0.01), fat index (P < 0.05 or P < 0.01), diameter of fat cell and Lee's index (P < 0.05), decrease the jejunum microvillus area, lower the level of serum triglyceride and cholesterol.
    Phillyrin has anti-obesity effect in nutritive obesity mice.
    Cell Mol Neurobiol. 2014 Nov;34(8):1165-73.
    Protective effects of phillyrin on H2O 2-induced oxidative stress and apoptosis in PC12 cells.[Pubmed: 25146667]
    Oxidative stress is a major component of harmful cascades activated in neurodegenerative disorders. We sought to elucidate possible effects of Phillyrin, an active constituent isolated from the Chinese medicinal herb Forsythia suspense, on hydrogen peroxide (H2O2)-induced cell death and determine the underlying molecular mechanisms in neuron-like PC12 cells.
    By MTT assay and lactate dehydrogenase (LDH) leakage assay, we found that Phillyrin treatment effectively protected PC12 cells against H2O2-induced cell damage. H2O2 exposure induced oxidative stress in PC12 cells, as revealed by enhanced oxidative stress and decreased activities of antioxidative enzymes, which were inhibited by Phillyrin pretreatment. ROS activated mitochondria-dependent apoptosis. The anti-apoptotic effects of Phillyrin were also confirmed by acridine orange/ethidium bromide (AO/EB) staining. Mitochondrial membrane potential decrease, cytochrome c release, caspases activation, activation of AIF and Endo G were observed in H2O2-treated cells by rhodamine 123 or western blot. Interestingly, Phillyrin effectively suppressed these changes. Moreover, Phillyrin could inhibit H2O2-induced up-regulation of Bax/Bcl-2 ratio.
    In conclusion, Phillyrin effectively inhibited H2O2-induced oxidative stress and apoptosis in PC12 cells.
    Eur J Drug Metab Pharmacokinet. 2009 Apr-Jun;34(2):79-83.
    Pharmacokinetics of phillyrin and forsythiaside following iv administration to Beagle dog.[Pubmed: 19645216]
    The objective of the present study was to firstly investigate the in vivo pharmacokinetics of Phillyrin and forsythiaside in beagle dog.
    On I.V. administration, a rapid distribution was observed and followed by a slower elimination for Phillyrin and forsythiaside. The mean t(1/2Z) was 49.99, 34.87 and 43.81 min for 0.19, 0.70 and 1.43 mg/kg of Phillyrin, and 60.90, 64.30, 57.99 min for 0.62, 1.39 and 5.52 mg/kg of forsythiaside respectively. And the AUC(o-t) increased linearly from 36.51 to 160.22 microg x min/ml of Phillyrin and from 50.63 to 681.08 microg x min/ml after the three dosage administrated. In the range of the dose examined, the pharmacokinetics of Phillyrin and forsythiaside in beagle dog was based on first order kinetics.
    Although both drugs were widely distributed to various tissues in the dog, no concerns about extensive binding to tissues that may be consumed by the public should a dog be exposed to Phillyrin and forsythiaside according to the rapid elimination.
    Fitoterapia. 2013 Oct;90:132-9.
    Phillyrin attenuates LPS-induced pulmonary inflammation via suppression of MAPK and NF-κB activation in acute lung injury mice.[Pubmed: 23751215]
    Phillyrin (Phil) is one of the main chemical constituents of Forsythia suspensa (Thunb.), which has shown to be an important traditional Chinese medicine. We tested the hypothesis that Phil modulates pulmonary inflammation in an ALI model induced by LPS.
    Male BALB/c mice were pretreated with or without Phil before respiratory administration with LPS, and pretreated with dexamethasone as a control. Cytokine release (TNF-α, IL-1β, and IL-6) and amounts of inflammatory cell in bronchoalveolar lavage fluid (BALF) were detected by ELISA and cell counting separately. Pathologic changes, including neutrophil infiltration, interstitial edema, hemorrhage, hyaline membrane formation, necrosis, and congestion during acute lung injury in mice were evaluated via pathological section with HE staining. To further investigate the mechanism of Phil anti-inflammatory effects, activation of MAPK and NF-κB pathways was tested by western blot assay. Phil pretreatment significantly attenuated LPS-induced pulmonary histopathologic changes, alveolar hemorrhage, and neutrophil infiltration. The lung wet-to-dry weight ratios, as the index of pulmonary edema, were markedly decreased by Phil pretreatment. In addition, Phil decreased the production of the proinflammatory cytokines including (TNF-α, IL-1β, and IL-6) and the concentration of myeloperoxidase (MPO) in lung tissues. Phil pretreatment also significantly suppressed LPS-induced activation of MAPK and NF-κB pathways in lung tissues.
    Taken together, the results suggest that Phil may have a protective effect on LPS-induced ALI, and it potentially contributes to the suppression of the activation of MAPK and NF-κB pathways. Phil may be a new preventive agent of ALI in the clinical setting.

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