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    CAS No. 19666-76-3 Price $40 / 20mg
    Catalog No.CFN99981Purity>=98%
    Molecular Weight460.73Type of CompoundTriterpenoids
    FormulaC30H52O3Physical DescriptionWhite powder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Ganoderol A

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    Biological Activity
    Description: Panaxadiol, an anti-hepatitis B virus inhibitor, exhibits anticancer, cardioprotective, anti-arrhythmic, and antioxidative activities. It inhibits Ca2+ channels, decreasing channel open time and open state probability in vitro and displaying anti-arrhythmic potential. Panaxadiol selectively interferes with the cell cycle in human cancer cell lines, it inhibits DNA synthesis in a dose-dependent manner with IC50 values ranging from 0.8 to 1.2 μM in SK-HEP-1 cells and HeLa cells, it selectively elevates p21WAF1/CIP1 levels and thereby arrests the cell cycle at G1/S phase by down-regulating Cyclin A–Cdk2 activity.
    Targets: ATPase | p21 | CDK | SOD | HBV | DNA synthesis | WAF1 | CIP1 | Calcium Channel
    In vitro:
    Cancer Chemother Pharmacol. 2009 Nov;64(6):1097-104.
    Panaxadiol, a purified ginseng component, enhances the anti-cancer effects of 5-fluorouracil in human colorectal cancer cells.[Pubmed: 19277659]
    Colorectal cancer is a major cause of morbidity and mortality for cancer worldwide. Although 5-fluorouracil (5-FU) is one of the most widely used chemotherapeutic agents in first-line therapy for colorectal cancer, serious side effects limit its clinical usefulness. Panaxadiol (PD) is the purified sapogenin of ginseng saponins, which exhibit anti-tumor activity. In this study, we investigated the possible synergistic anti-cancer effects of PD and 5-FU on a human colorectal cancer cell line, HCT-116.
    Cell viability was evaluated by an MTS cell proliferation assay. Morphological observation was performed by crystal violet cell viability staining assay. Cell cycle distribution and apoptotic effects were analyzed by flow cytometry after staining with PI/RNase or Annexin V/PI. Cell growth was markedly suppressed in HCT-116 cells treated by 5-FU (20-100 microM) for 24 or 48 h with time-dependent effects. The significant suppression on HCT-116 cell proliferation was observed after treatment with PD (25 microM) for 24 and 48 h. Panaxadiol (25 microM) markedly (P < 0.05) enhanced the anti-proliferative effects of 5-FU (5, 10, 20 microM) on HCT-116 cells compared to single treatment of 5-FU for 24 and 48 h. Flow cytometric analysis on DNA indicated that PD and 5-FU selectively arrested cell cycle progression in the G1 phase and S phase (P < 0.01), respectively, compared to the control condition. Combination use of 5-FU with PD significantly (P < 0.001) increased cell cycle arrest in the S phase compared to that treated by 5-FU alone. The combination of 5-FU and PD significantly enhanced the percentage of apoptotic cells when compared with the corresponding cell groups treated by 5-FU alone (P < 0.001).
    Panaxadiol enhanced the anti-cancer effects of 5-FU on human colorectal cancer cells through the regulation of cell cycle transition and the induction of apoptotic cells.
    Nat Prod Bioprospect. 2014 Jun;4(3):163-74.
    Panaxadiol and panaxatriol derivatives as anti-hepatitis B virus inhibitors.[Pubmed: 24955298]
    28 Derivatives of Panaxadiol (PD) and panaxatriol were synthesized and evaluated for their anti-HBV activity on HepG 2.2.15 cells, of which 17 derivatives inhibited HBV DNA replication.
    Compounds 4, 9, 10, 14, and 15 showed moderate activity against HBV DNA replication with IC50 values ranged from 7.27 to 28.21 μM compared with PD. In particular, 3-O-2'-thenoyl Panaxadiol (4) inhibited not only HBV DNA replication (IC50 = 16.5 μM, SI > 115.7) but also HBsAg (IC50 = 30.8 μM, SI > 62.0) and HBeAg (IC50 = 18.2 μM, SI > 105.14) secretions.
    Their structure-activity relationships were discussed for guiding future research toward the discovery of new anti-HBV agents.
    Phytother Res. 1999 Dec;13(8):641-4.
    Transcriptional activation of Cu/Zn superoxide dismutase and catalase genes by panaxadiol ginsenosides extracted from Panax ginseng.[Pubmed: 10594930]
    Superoxide dismutase (SOD) converts superoxide radical to H(2)O(2), which is in turn broken down to water and oxygen by catalase. Thus, SOD and catalase constitute the first coordinated unit of defence against reactive oxygen species. A wide variety of chemical and environmental factors are known to induce these antioxidant enzymes.
    Here, we examined the effect of ginseng saponins on the induction of SOD and catalase gene expression. To explore this possibility, the upstream regulatory promoter region of Cu/Zn superoxide dismutase (SOD1) and catalase genes were linked to the chloramphenicol acetyltransferase (CAT) structural gene and introduced into human hepatoma HepG2 cells. Total saponin and panaxatriol did not activate the transcription of SOD1 and catalase genes but Panaxadiol increased the transcription of these genes about 2-3 fold. Among the Panaxadiol ginsenosides, the Rb(2) subfraction appeared to be a major inducer of SOD1 and catalase genes. The specificity of the Rb(2) effect was further confirmed by time course- and dose-dependent induction experiments.
    These results suggest that the Panaxadiol fraction and its ginsenosides could induce the antioxidant enzymes which are important for maintaining cell viability by lowering the level of oxygen radical generated from intracellular metabolism.
    In vivo:
    Food Chem Toxicol. 2010 Jun;48(6):1516-20.
    The effects of ginseng total saponin, panaxadiol and panaxatriol on ischemia/reperfusion injury in isolated rat heart.[Pubmed: 20353807]
    The aim of the present study was to evaluate the protective effect of ginseng total saponin, Panaxadiol and panaxatriol, which are the major components of Panax ginseng, against myocardial ischemia/reperfusion (I/R) injury in isolated rat hearts.
    Rats were orally administered once a day with total saponin (20 mg/kg), Panaxadiol (5 mg/kg) and panaxatriol (5 mg/kg) for consecutive 7 days. On day 8, the hearts were isolated and perfused with Krebs-Henseleit bicarbonate buffer solution using Langendorff apparatus. After 30 min of global ischemia, hearts were reperfused for 30 min. Myocardial function, coronary flow and biochemical parameters, such as lactate dehydrogenase (LDH), creatine kinase (CK), adenosine triphosphate (ATP), malondialdehyde (MDA) and reduced glutathione (GSH) were measured. Total saponin and panaxatriol significantly improved I/R-induced myocardial dysfunction by increasing left ventricular development pressure, (-dP/dt)/(+dP/dt) and time to contracture. Moreover, the increases in the levels of LDH, CK and MDA and the decrease in the levels of GSH were attenuated by total saponin and panaxatriol. However, the ATP levels did not affected by total saponin, Panaxadiol and panaxatriol pretreatment.
    Our findings suggest that pretreatment with ginseng total saponin, especially panaxatriol, ameliorates I/R-induced myocardial damage and this protection is caused by reducing oxidative stress.
    Panaxadiol Description
    Source: The roots of Panax ginseng C. A. Mey.
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
    Storage: 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

    After receiving: 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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    Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals

    Cell. 2018 Jan 11;172(1-2):249-261.e12.
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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 2.1705 mL 10.8523 mL 21.7047 mL 43.4094 mL 54.2617 mL
    5 mM 0.4341 mL 2.1705 mL 4.3409 mL 8.6819 mL 10.8523 mL
    10 mM 0.217 mL 1.0852 mL 2.1705 mL 4.3409 mL 5.4262 mL
    50 mM 0.0434 mL 0.217 mL 0.4341 mL 0.8682 mL 1.0852 mL
    100 mM 0.0217 mL 0.1085 mL 0.217 mL 0.4341 mL 0.5426 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    Cell Research:
    Carcinogenesis. 2003 Nov;24(11):1767-72.
    Panaxadiol selectively inhibits cyclin A-associated Cdk2 activity by elevating p21WAF1/CIP1 protein levels in mammalian cells.[Pubmed: 12819186]
    We show that Panaxadiol (PD), a ginseng saponin with a dammarane skeleton, selectively interferes with the cell cycle in human cancer cell lines.
    PD inhibited DNA synthesis in a dose-dependent manner with IC50 values ranging from 0.8 to 1.2 micro M in SK-HEP-1 cells and HeLa cells. PD-treated cells were arrested at G1/S phase, which coincided well with decreases in Cyclin A-Cdk2 activity, but not in Cyclin E-Cdk2 and Cdc2 activities. The intracellular levels of p21WAF1/CIP1 were significantly and selectively elevated in a dose- and time-dependent manner in PD-treated HeLa cells. Similarly, levels of the p21WAF1/CIP1 protein that is associated with the Cyclin A-Cdk2 complex increased, and these increases correlated well with the down-regulation of Cyclin A-Cdk2 activity.
    Thus, PD selectively elevates p21WAF1/CIP1 levels and thereby arrests the cell cycle at G1/S phase by down-regulating Cyclin A-Cdk2 activity.