Pseudoginsenoside F11CAS# 69884-00-0 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 69884-00-0 | SDF | Download SDF |
| PubChem ID | 5458669 | Appearance | White powder |
| Formula | C42H72O14 | M.Wt | 801.01 |
| Type of Compound | Triterpenoids | Storage | Desiccate at -20°C |
| Synonyms | Ginsenoside A1 | ||
| Solubility | DMSO : 100 mg/mL (124.84 mM; Need ultrasonic) H2O : 0.67 mg/mL (0.84 mM; Need ultrasonic) | ||
| Chemical Name | 2-[2-[[(3S,6S,8R,10R,12R,13R,14R,17S)-3,12-dihydroxy-17-[(2S,5R)-5-(2-hydroxypropan-2-yl)-2-methyloxolan-2-yl]-4,4,8,10,14-pentamethyl-2,3,5,6,7,9,11,12,13,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthren-6-yl]oxy]-4,5-dihydroxy-6-(hydroxymethyl)oxan-3-yl]oxy-6-methyloxane-3,4,5-triol | ||
| SMILES | CC1C(C(C(C(O1)OC2C(C(C(OC2OC3CC4(C(CC(C5C4(CCC5C6(CCC(O6)C(C)(C)O)C)C)O)C7(C3C(C(CC7)O)(C)C)C)C)CO)O)O)O)O)O | ||
| Standard InChIKey | JBGYSAVRIDZNKA-GSXRAQGCSA-N | ||
| Standard InChI | InChI=1S/C42H72O14/c1-19-28(46)30(48)32(50)35(52-19)55-33-31(49)29(47)23(18-43)54-36(33)53-22-17-41(8)24(39(6)13-11-25(45)37(2,3)34(22)39)16-21(44)27-20(10-14-40(27,41)7)42(9)15-12-26(56-42)38(4,5)51/h19-36,43-51H,10-18H2,1-9H3/t19?,20-,21+,22-,23?,24?,25-,26+,27-,28?,29?,30?,31?,32?,33?,34?,35?,36?,39+,40+,41+,42-/m0/s1 | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| 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 | 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 ]Neuropharmacology. 2014 Apr;79:642-56.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.
|
| In vivo | The pseudoginsenoside F11 ameliorates cisplatin-induced nephrotoxicity without compromising its anti-tumor activity in vivo.[Pubmed: 24832194]Sci Rep. 2014 May 16;4:4986.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.
Pseudoginsenoside-F11 decreases morphine-induced behavioral sensitization and extracellular glutamate levels in the medial prefrontal cortex in mice.[Pubmed: 17368734 ]Pharmacol Biochem Behav. 2007 Apr;86(4):660-6.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.
|
| Kinase Assay | Pseudoginsenoside F11, a Novel Partial PPAR γ Agonist, Promotes Adiponectin Oligomerization and Secretion in 3T3-L1 Adipocytes.[Pubmed: 24454336]PPAR Res. 2013;2013:701017.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). |
| Animal Research | Antagonistic effect of pseudoginsenoside F11 on the behavioral actions of morphine in mice.[Pubmed: 10899376]Anti-amnesic effect of pseudoginsenoside-F11 in two mouse models of Alzheimer's disease.[Pubmed: 23541491]Pharmacol Biochem Behav. 2013 May;106:57-67.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.
Pharmacol Biochem Behav. 2000 Jul;66(3):595-601.
|
Pseudoginsenoside F11 Dilution Calculator
Pseudoginsenoside F11 Molarity Calculator
| 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 necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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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. IC50 value: Inhibition of diprenorphine binding with an IC50 of 6.1 μM Target: In vitro: Biochemical experiments revealed that PF11 could inhibit diprenorphine (DIP) binding with an IC50 of 6.1 μM and reduced the binding potency of morphine in Chinese hamster ovary (CHO)-μ cells [2]. In vivo: One in vivo model of cisplatin-induced acute renal failure was performed. The results showed that pretreatment with Pseudoginsenoside F11 reduced cisplatin-elevated blood urea nitrogen and creatinine levels, as well as ameliorated the histophathological damage [1]. We tested the effects of Pseudoginsenoside F11 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. As the results shown, Pseudoginsenoside F11 antagonized the development of behavioral sensitization and decrease of glutamate in the mPFC induced by morphine [3].
References:
[1]. Wang H, et al. The pseudoginsenoside F11 ameliorates cisplatin-induced nephrotoxicity without compromising its anti-tumor activity in vivo. Scientific Reports [2014, 4:4986]
[2]. Li Zhu, et al. Pseudoginsenoside-F11 attenuates morphine-induced signalling in Chinese hamster ovary-μ cells. Neuroreport, 25 May 2001 - Volume 12 - Issue 7 - pp 1453-1456
[3]. Yue Hao, et al. Pseudoginsenoside-F11 decreases morphine-induced behavioral sensitization and extracellular glutamate levels in the medial prefrontal cortex in mice. Pharmacology Biochemistry and Behavior Volume 86, Issue 4, April 2007, Pages 660–666
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Pseudoginsenoside-F11 decreases morphine-induced behavioral sensitization and extracellular glutamate levels in the medial prefrontal cortex in mice.[Pubmed:17368734]
Pharmacol Biochem Behav. 2007 Apr;86(4):660-6.
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. 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. 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.
Anti-amnesic effect of pseudoginsenoside-F11 in two mouse models of Alzheimer's disease.[Pubmed:23541491]
Pharmacol Biochem Behav. 2013 May;106:57-67.
Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by amyloid beta (Abeta) 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. In the present study, we investigated the effect of PF11 on AD-like cognitive impairment both in mice induced by intracerebroventricular injection of Abeta1-42 (410 pmol) and in Tg-APPswe/PS1dE9 (APP/PS1) mice. It was found that oral treatment with PF11 significantly mitigated learning and memory impairment in mice given Abeta1-42-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, PF11 8 mg/kg significantly inhibited the expressions of beta-amyloid precursor protein (APP) and Abeta1-40 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. 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 PF11 in APP/PS1 mice. Cumulatively, the present study indicated that PF11 may serve as a potential therapeutic agent for the treatment of AD.
Pseudoginsenoside F11, a Novel Partial PPAR gamma Agonist, Promotes Adiponectin Oligomerization and Secretion in 3T3-L1 Adipocytes.[Pubmed:24454336]
PPAR Res. 2013;2013:701017.
PPAR gamma is a nuclear hormone receptor that functions as a master regulator of adipocyte differentiation and development. Full PPAR gamma 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). In this study, we found that p-F11 activates PPAR gamma 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 gamma at Ser-273 by Cdk5. Therefore, p-F11 is a novel partial PPAR gamma agonist, which might have the potential to be developed as a new PPAR gamma -targeted therapeutics for type 2 diabetes.
The pseudoginsenoside F11 ameliorates cisplatin-induced nephrotoxicity without compromising its anti-tumor activity in vivo.[Pubmed:24832194]
Sci Rep. 2014 May 16;4:4986.
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. 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. 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.
Pseudoginsenoside-F11 (PF11) exerts anti-neuroinflammatory effects on LPS-activated microglial cells by inhibiting TLR4-mediated TAK1/IKK/NF-kappaB, MAPKs and Akt signaling pathways.[Pubmed:24467851]
Neuropharmacology. 2014 Apr;79:642-56.
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. PF11 significantly suppressed the release of ROS and proinflammatory mediators induced by LPS in a microglial cell line N9 including NO, PGE2, IL-1beta, IL-6 and TNF-alpha. Moreover, PF11 inhibited interaction and expression of TLR4 and MyD88 in LPS-activated N9 cells, resulting in an inhibition of the TAK1/IKK/NF-kappaB 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. These findings indicate that PF11 exerts anti-neuroinflammatory effects on LPS-activated microglial cells by inhibiting TLR4-mediated TAK1/IKK/NF-kappaB, MAPKs and Akt signaling pathways, suggesting its therapeutic implication for neurodegenerative disease associated with neuroinflammation.
Antagonistic effect of pseudoginsenoside-F11 on the behavioral actions of morphine in mice.[Pubmed:10899376]
Pharmacol Biochem Behav. 2000 Jul;66(3):595-601.
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. 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.
