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    Pseudoginsenoside F11
    Information
    CAS No. 69884-00-0 Price $100 / 20mg
    Catalog No.CFN99963Purity>=98%
    Molecular Weight801.01Type of CompoundTriterpenoids
    FormulaC42H72O14Physical DescriptionWhite powder
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    Pseudoginsenoside F11

    Pseudoginsenoside F11
    Product Name Pseudoginsenoside F11
    CAS No.: 69884-00-0
    Catalog No.: CFN99963
    Molecular Formula: C42H72O14
    Molecular Weight: 801.01 g/mol
    Purity: >=98%
    Type of Compound: Triterpenoids
    Physical Desc.: White powder
    Targets: Bcl-2/Bax | PPAR | NO | PGE | IL Receptor | TNF-伪 | ROS | TLR | IkB | NF-kB | MAPK | Akt | JNK | p53 | Caspase | Beta Amyloid | IKK
    Source: The roots of Panax ginseng C. A. Mey.
    Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
    Price: $100 / 20mg
    Inquire / Order: manager@chemfaces.com
    Technical Inquiries: service@chemfaces.com
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  • Invest New Drugs.2017, 35(2):166-179
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  • Biological Activity
    Description: Pseudoginsenoside F11, a novel partial PPAR γ agonist, can promote adiponectin oligomerization and secretion in 3T3-L1 adipocytes and inhibit obesity-linked phosphorylation of PPAR γ at Ser-273 by Cdk5. It possesses significant neuroprotective activity, has been demonstrated to antagonize the learning and memory deficits induced by scopolamine, morphine and methamphetamine in mice; it also antagonizes the development of analgesia tolerance to morphine and blocks the development of morphine-induced behavioral sensitization via its effect, at least partially, on the glutamatergic system in the mPFC.
    Targets: Bcl-2/Bax | PPAR | NO | PGE | IL Receptor | TNF-α | ROS | TLR | IkB | NF-kB | MAPK | Akt | JNK | p53 | Caspase | Beta Amyloid | IKK
    In vitro:
    Neuropharmacology. 2014 Apr;79:642-56.
    Pseudoginsenoside-F11 (PF11) exerts anti-neuroinflammatory effects on LPS-activated microglial cells by inhibiting TLR4-mediated TAK1/IKK/NF-κB, MAPKs and Akt signaling pathways.[Pubmed: 24467851 ]
    Pseudoginsenoside-F11 (PF11), an ocotillol-type ginsenoside, has been shown to possess significant neuroprotective activity. Since microglia-mediated inflammation is critical for induction of neurodegeneration, this study was designed to investigate the effect of PF11 on activated microglia.
    METHODS AND RESULTS:
    PF11 significantly suppressed the release of ROS and proinflammatory mediators induced by LPS in a microglial cell line N9 including NO, PGE2, IL-1β, IL-6 and TNF-α. Moreover, PF11 inhibited interaction and expression of TLR4 and MyD88 in LPS-activated N9 cells, resulting in an inhibition of the TAK1/IKK/NF-κB signaling pathway. PF11 also inhibited the phosphorylation of Akt and MAPKs induced by LPS in N9 cells. Importantly, PF11 significantly alleviated the death of SH-SY5Y neuroblastoma cells and primary cortical neurons induced by the conditioned-medium from activated microglia. At last, the effect of PF11 on neuroinflammation was confirmed in vivo: PF11 mitigated the microglial activation and proinflammatory factors expression obviously in both cortex and hippocampus in mice injected intrahippocampally with LPS.
    CONCLUSIONS:
    These findings indicate that PF11 exerts anti-neuroinflammatory effects on LPS-activated microglial cells by inhibiting TLR4-mediated TAK1/IKK/NF-κB, MAPKs and Akt signaling pathways, suggesting its therapeutic implication for neurodegenerative disease associated with neuroinflammation.
    In vivo:
    Sci Rep. 2014 May 16;4:4986.
    The pseudoginsenoside F11 ameliorates cisplatin-induced nephrotoxicity without compromising its anti-tumor activity in vivo.[Pubmed: 24832194]
    The clinical use of cisplatin was severely limited by its associated nephrotoxicity. In this study, we investigated whether the Pseudoginsenoside F11 had protective effects against cisplatin-induced nephrotoxicity.
    METHODS AND RESULTS:
    To clarify it, one in vivo model of cisplatin-induced acute renal failure was performed. The results showed that pretreatment with F11 reduced cisplatin-elevated blood urea nitrogen and creatinine levels, as well as ameliorated the histophathological damage. Further studies showed that F11 could suppress P53 activation, inverse the ratio of Bax/Bcl2 and the anti-oxidative and free radical levels induced by cisplatin, which in turn inhibited tubular cell apoptosis. Importantly, F11 enhanced rather than inhibited the anti-tumor activity of cispaltin in murine melanoma and Lewis lung cancer xenograft tumor models.
    CONCLUSIONS:
    Our findings suggested that administering F11 with cisplatin might alleviate the associated nephrotoxicity without compromising its therapeutic efficiency. This finding provides a novel potential strategy in the clinical treatment of cancer.
    Pharmacol Biochem Behav. 2007 Apr;86(4):660-6.
    Pseudoginsenoside-F11 decreases morphine-induced behavioral sensitization and extracellular glutamate levels in the medial prefrontal cortex in mice.[Pubmed: 17368734 ]
    Morphine produces a variety of behavioral and biochemical changes related to its abuse. Our previous studies showed that Pseudoginsenoside-F11 (PF11), an ocotillol-type saponin existing in American ginseng, can antagonize pharmacological effects of morphine.
    METHODS AND RESULTS:
    To further investigate the effects of PF11 on morphine abuse and the underlying mechanisms, we tested the effects of PF11 on morphine-induced development of behavioral sensitization and alterations in glutamate levels in the medial prefrontal cortex (mPFC) in freely moving mice by using in vivo microdialysis.
    CONCLUSIONS:
    As the results shown, PF11 antagonized the development of behavioral sensitization and decrease of glutamate in the mPFC induced by morphine. Therefore, these findings suggest that PF11 may block the development of morphine-induced behavioral sensitization via its effect, at least partially, on the glutamatergic system in the mPFC.
    Pseudoginsenoside F11 Description
    Source: The roots of Panax ginseng C. A. Mey.
    Solvent: DMSO, Pyridine, Methanol, Ethanol, 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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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 1.2484 mL 6.2421 mL 12.4842 mL 24.9685 mL 31.2106 mL
    5 mM 0.2497 mL 1.2484 mL 2.4968 mL 4.9937 mL 6.2421 mL
    10 mM 0.1248 mL 0.6242 mL 1.2484 mL 2.4968 mL 3.1211 mL
    50 mM 0.025 mL 0.1248 mL 0.2497 mL 0.4994 mL 0.6242 mL
    100 mM 0.0125 mL 0.0624 mL 0.1248 mL 0.2497 mL 0.3121 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.
    Protocol
    Kinase Assay:
    PPAR Res. 2013;2013:701017.
    Pseudoginsenoside F11, a Novel Partial PPAR γ Agonist, Promotes Adiponectin Oligomerization and Secretion in 3T3-L1 Adipocytes.[Pubmed: 24454336]
    PPAR γ is a nuclear hormone receptor that functions as a master regulator of adipocyte differentiation and development. Full PPAR γ agonists, such as the thiazolidinediones (TZDs), have been widely used to treat type 2 diabetes. However, they are characterized by undesirable side effects due to their strong agonist activities. Pseudoginsenoside F11 (p-F11) is an ocotillol-type ginsenoside isolated from Panax quinquefolium L. (American ginseng).
    METHODS AND RESULTS:
    In this study, we found that p-F11 activates PPAR γ with modest adipogenic activity. In addition, p-F11 promotes adiponectin oligomerization and secretion in 3T3-L1 adipocytes. We also found that p-F11 inhibits obesity-linked phosphorylation of PPAR γ at Ser-273 by Cdk5.
    CONCLUSIONS:
    Therefore, p-F11 is a novel partial PPAR γ agonist, which might have the potential to be developed as a new PPAR γ -targeted therapeutics for type 2 diabetes.
    Animal Research:
    Pharmacol Biochem Behav. 2013 May;106:57-67.
    Anti-amnesic effect of pseudoginsenoside-F11 in two mouse models of Alzheimer's disease.[Pubmed: 23541491]
    Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by amyloid β (Aβ) deposits, elevated oxidative stress, and apoptosis of the neurons. Pseudoginsenoside F11 (PF11), a component of Panax quinquefolium (American ginseng), has been demonstrated to antagonize the learning and memory deficits induced by scopolamine, morphine and methamphetamine in mice.
    METHODS AND RESULTS:
    In the present study, we investigated the effect of Pseudoginsenoside F11 on AD-like cognitive impairment both in mice induced by intracerebroventricular injection of Aβ1-42 (410 pmol) and in Tg-APPswe/PS1dE9 (APP/PS1) mice. It was found that oral treatment with Pseudoginsenoside F11 significantly mitigated learning and memory impairment in mice given Aβ1-42-treated mice for 15 days at doses of 1.6 and 8 mg/kg and APP/PS1 for 4 weeks at a dose of 8 mg/kg as measured by the Morris water maze and step-through tests. In APP/PS1 mice, Pseudoginsenoside F11 8 mg/kg significantly inhibited the expressions of β-amyloid precursor protein (APP) and Aβ1-40 in the cortex and hippocampus, restored the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and decreased the production of malondialdehyde (MDA) in the cortex. It also noticeably improved the histopathological changes in the cortex and hippocampus and downregulated the expressions of JNK 2, p53 and cleaved caspase 3 in the hippocampus.
    CONCLUSIONS:
    These findings suggested that the inhibitory effect on amyloidogenesis and oxidative stress and some beneficial effects on neuronal functions might contribute to the recognition improvement effect of Pseudoginsenoside F11 in APP/PS1 mice. Cumulatively, the present study indicated that Pseudoginsenoside F11 may serve as a potential therapeutic agent for the treatment of AD.
    Pharmacol Biochem Behav. 2000 Jul;66(3):595-601.
    Antagonistic effect of pseudoginsenoside F11 on the behavioral actions of morphine in mice.[Pubmed: 10899376]

    METHODS AND RESULTS:
    The antagonistic effect of pseudoginoside-F11 (PF(11)) on the various actions of morphine was studied in mice. The results demonstrated that PF(11), at the doses of 4 and 8 mg/kg, PO, significantly inhibited morphine (10 mg/kg, SC)-induced memory impairment in the Morris water maze test. PF(11), at 4 mg/kg, PO, did not influence conditioned place preference per se, yet markedly blocked the conditioned place preference to morphine. PF(11), at the doses of 4 and 8 mg/kg, PO, also significantly antagonized morphine (5 mg/kg, SC)-induced analgesia tested by tail pinch method. PF(11), at 4 mg/kg, PO, did not influence locomotor activity per se, yet inhibited the development of the reverse tolerance, as shown by the increase in locomotor activity, to morphine. At the doses of 4 and 8 mg/kg, PO, PF(11) significantly antagonized the development of analgesia tolerance to morphine in the tail pinch test.
    CONCLUSIONS:
    Thus, the above results demonstrate for the first time that PF(11) can antagonize some actions of morphine. However, the mechanism of action of PF(11) merits further evaluation.
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