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    Ginsenoside Rd
    CAS No. 52705-93-8 Price $60 / 20mg
    Catalog No.CFN99975Purity>=98%
    Molecular Weight947.2Type of CompoundTriterpenoids
    FormulaC48H82O18Physical DescriptionWhite powder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Size /Price /Stock 10 mM * 1 mL in DMSO / $39.0 / In-stock
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  • Biological Activity
    Description: Ginsenoside Rd, a minor ginseng saponin, has several pharmacological activities such as immunosuppressive activity, anti-inflammatory activity, immunological adjuvant, anti-cancer activity and wound-healing activity. Rd inhibits TNFα-induced NF-κB transcriptional activity with an IC50 of 12.05±0.82 μM in HepG2 cells. Rd inhibits expression of COX-2 and iNOS mRNA. Rd also inhibits Ca2+ influx. Rd inhibits CYP2D6, CYP1A2, CYP3A4, and CYP2C9, with IC50s of 58.0±4.5 μM, 78.4±5.3 μM, 81.7±2.6 μM, and 85.1±9.1 μM, respectively.
    Targets: VEGFR | Akt | ERK | PI3K | Calcium Channel | IL Receptor | IFN-γ | COX | NOS | CYP2D6 | CYP1A2 | CYP3A4 | CYP2C9
    In vitro:
    J Ethnopharmacol. 2012 Aug 1;142(3):754-61.
    Promotive effect of ginsenoside Rd on proliferation of neural stem cells in vivo and in vitro.[Pubmed: 22683911 ]
    Ginseng, the root of Panax ginseng C. A. MEYER (Araliaceae), is reputedly known for its nootropic and anti-aging functions and has been widely used to treat various diseases and enhance health for thousands of years in Asia. Recent studies revealed that ginsenoside, responsible for the pharmacological effects of ginseng, can prevent memory loss and improve spatial learning in mice, but underlying mechanisms are still largely unknown. Active neurogenesis in adult hippocampus is closely related to animals' learning and memory ability. The present study aimed to investigate the possible effects of Ginsenoside Rd, one of the most effective ingredients in ginseng, on neurogenesis in vivo and in vitro.
    Adult rats and cultured neural stem cells were treated with Ginsenoside Rd at different doses, and the changes in the proliferation and differentiation of neural stem cells were examined by immunohistochemistry and immunocytochemistry. Ginsenoside Rd significantly increased the numbers of BrdU(+) and DCX(+) cells in the hippocampal dentate gyrus but did not affect the ratio of NeuN/BrdU double-labeled cells to the total number of BrdU(+) cells. For cultured neural stem cells, Ginsenoside Rd promoted the size and number of neurospheres, increased the number of BrdU(+) and Ki67(+) cells but did not affect the differentiation of neural stem cells into neurons, astrocytes and oligodendrocytes.
    These results indicate that Ginsenoside Rd can enhance the proliferation but not affect the differentiation of neural stem cells in vivo and in vitro.
    In vivo:
    Acta Pharmacol Sin. 2015 Apr;36(4):421-8.
    Ginsenoside Rd promotes neurogenesis in rat brain after transient focal cerebral ischemia via activation of PI3K/Akt pathway.[Pubmed: 25832422]
    To investigate the effects of Ginsenoside Rd (Rd) on neurogenesis in rat brain after ischemia/reperfusion injury (IRI).
    Male SD rats were subjected to transient middle cerebral artery occlusion (MCAO) followed by reperfusion. The rats were injected with Rd (1, 2.5, and 5 mg·kg(-1)·d(-1), ip) from d 1 to d 3 after MCAO, and with BrdU (50 mg·kg(-1)·d(-1), ip) from d 3 to d 6, then sacrificed on 7 d. The infarct size and neurological scores were assessed. Neurogenesis in the brains was detected by BrdU, DCX, Nestin, and GFAP immunohistochemistry staining. PC12 cells subjected to OGD/reperfusion were used as an in vitro model of brain ischemia. VEGF and BDNF levels were assessed with ELISA, and Akt and ERK phosphorylation was measured using Western blotting. Rd administration dose-dependently decreased the infarct size and neurological scores in the rats with IRI. The high dose of Rd 5 (mg·kg(-1)·d(-1)) significantly increased Akt phosphorylation in ipsilateral hemisphere, and markedly increased the number of BrdU/DCX and Nestin/GFAP double-positive cells in ischemic area, which was partially blocked by co-administration of the PI3 kinase inhibitor LY294002. Treatment with Rd (25, 50, and 100 μmol/L) during reperfusion significantly increased the expression of VEGF and BDNF in PC12 cells with IRI. Furthermore, treatment with Rd dose-dependently increased the phosphorylation of Akt and ERK, and significantly decreased PC12 cell apoptosis, which were blocked by co-application of LY294002.
    Rd not only attenuates ischemia/reperfusion injury in rat brain, but also promotes neurogenesis via increasing VEGF and BDNF expression and activating the PI3K/Akt and ERK1/2 pathways.
    Expert Rev Neurother. 2013 Jun;13(6):603-13.
    Ginsenoside Rd for acute ischemic stroke: translating from bench to bedside.[Pubmed: 23738998]
    Numerous studies have identified pathophysiological mechanisms of acute ischemic stroke and have provided proof-of-principle evidence that strategies designed to impede the ischemic cascade, namely neuroprotection, can protect the ischemic brain. However, the translation of these therapeutic agents to the clinic has not been successful. Ginsenoside Rd, a dammarane-type steroid glycoside extracted from ginseng plants, has exhibited an encouraging neuroprotective efficacy in both laboratory and clinical studies. This article attempts to provide a synopsis of the physiochemical profile, pharmacokinetics, pharmacodynamics, clinical efficacy, safety and putative therapeutic mechanisms of Rd. Finally, the authors discuss the validity of Rd as a neuroprotective agent for acute ischemic stroke.
    Vaccine. 2007 Jan 2;25(1):161-9.
    Ginsenoside Rd elicits Th1 and Th2 immune responses to ovalbumin in mice.[Pubmed: 16950547]
    Ginsenoside Rd (Rd), a saponin isolated from the roots of panax notoginseng, was evaluated for inducing Th1 or Th2 immune responses in mice against ovalbumin (OVA).
    ICR mice were immunized subcutaneously with OVA 100 microg alone or with OVA 100 microg dissolved in saline containing alum (200 microg), or Rd (10, 25 or 50 microg) on days 1 and 15. Two weeks later (day 28), concanavalin A (Con A)-, lipopolysaccharide (LPS)- and OVA-stimulated splenocyte proliferation was determined using MTT assay, and OVA-specific antibody titers and levels of cytokines in serum were measured by ELISA and microparticle-based flow cytometric immunoassay, as well as peripheral blood T-lymphocyte subsets analyzed using flow cytometer. Rd significantly enhanced the Con A-, LPS-, and OVA-induced splenocyte proliferation in the OVA-immunized mice. OVA-specific IgG, IgG1, and IgG2b antibody titers in serum were significantly enhanced by Rd compared with OVA control group. Meanwhile, Rd also significantly promoted the production of the Th1 and Th2 cytokines in OVA-immunized mice. Further, the effects of Rd on expression of cytokine mRNA in Con A-stimulated mice splenocytes were evaluated by RT-PCR analysis. Rd significantly enhanced the interleukin-2 (IL-2), interferon-gamma (IFN-gamma), IL-4, and IL-10 mRNA expression in mice splenocyte induced by Con A.
    These results suggested that Rd had immunological adjuvant activity, and elicited a Th1 and Th2 immune response by regulating production and gene expression of Th1 cytokines and Th2 cytokines.
    Ginsenoside Rd 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 1.0557 mL 5.2787 mL 10.5574 mL 21.1149 mL 26.3936 mL
    5 mM 0.2111 mL 1.0557 mL 2.1115 mL 4.223 mL 5.2787 mL
    10 mM 0.1056 mL 0.5279 mL 1.0557 mL 2.1115 mL 2.6394 mL
    50 mM 0.0211 mL 0.1056 mL 0.2111 mL 0.4223 mL 0.5279 mL
    100 mM 0.0106 mL 0.0528 mL 0.1056 mL 0.2111 mL 0.2639 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:
    Clin Exp Pharmacol Physiol. 2010 Feb;37(2):199-204.
    Ginsenoside Rd prevents glutamate-induced apoptosis in rat cortical neurons.[Pubmed: 19719747]
    1. The role of voltage-independent Ca(2+) entry in cell apoptosis has recently received considerable attention. It has been found that Ginsenoside Rd significantly inhibits voltage-independent Ca(2+) entry. The aim of the present study was to investigate the protective effects of Ginsenoside Rd against glutamate-induced apoptosis of rat cortical neurons.
    2. Ginsenoside Rd significantly reduced glutamate-induced apoptotic morphological changes and DNA laddering. In comparison, nimodipine only had a weak effect. 3. Ginsenoside Rd (1, 3 and 10 micromol/L) concentration-dependently inhibited caspase 3 activation and expression of the p20 subunit of active caspase 3 (by 30 +/- 10%, 41 +/- 9% and 62 +/- 19%, respectively, compared with glutamate alone; P < 0.05), whereas 1 micromol/L nimodipine had no effect. 4. Glutamate decreased cell viability to 37.4 +/- 4.7 (n = 8) and evoked cell apoptosis. Ginsenoside Rd (1, 3, 10 and 30 micromol/L) concentration-dependently inhibited glutamate-induced cell death, increased cell viability and reduced apoptotic percentage (from 47.5 +/- 4.9% to 37.4 +/- 6.9%, 28.3 +/- 5.2% and 22.5 +/- 5.6%, respectively; P < 0.05). At 1 micromol/L, nimodipine had no effect on cell viability. Furthermore, although 1, 3, 10, 30 and 60 micromol/L Ginsenoside Rd concentration-dependently inhibited glutamate-induced Ca(2+) entry by 8 +/- 2%, 24 +/- 4%, 40 +/- 7%, 49 +/- 8% and 50 +/- 8% (P < 0.05), respectively, nimodipine had no effect. 5.
    In conclusion, the results indicate that Ginsenoside Rd prevents glutamate-induced apoptosis in rat cortical neurons and provide further evidence of the potential of voltage-independent Ca(2+) channel blockers as new neuroprotective drugs for the prevention of neuronal apoptosis and death induced by cerebral ischaemia.
    Animal Research:
    Eur J Pharmacol. 2009 Mar 15;606(1-3):142-9.
    Ginsenoside-Rd, a new voltage-independent Ca2+ entry blocker, reverses basilar hypertrophic remodeling in stroke-prone renovascular hypertensive rats.[Pubmed: 19374845 ]
    The total saponins of Panax notoginseng have been clinically used for the treatment of cardiovascular diseases and stroke in China. Our recent study has identified ginsenoside-Rd, a purified component of total saponins of P. notoginseng, as an inhibitor to remarkably inhibit voltage-independent Ca(2+) entry. We deduced a hypothesis that the inhibition of voltage-independent Ca(2+) entry might contribute to its cerebrovascular benefits.
    Ginsenoside Rd was administered to two-kidney, two-clip (2k2c) stroke-prone hypertensive rats to examine its effects on blood pressure, cerebrovascular remodeling and Ca(2+) entry in freshly isolated basilar arterial vascular smooth muscle cells (BAVSMCs). Its effects on endothelin-1 induced Ca(2+) entry and cellular proliferation were assessed in cultured BAVSMCs. The results showed that, in vivo, ginsenoside-Rd treatment attenuated basilar hypertrophic inward remodeling in 2k2c hypertensive rats without affecting systemic blood pressure.During the development of hypertension, there were time-dependent increases in receptor-operated Ca(2+) channel (ROCC)-, store-operated Ca(2+) channel (SOCC)- and voltage dependent Ca(2+) channel (VDCC)-mediated Ca(2+) entries in freshly isolated BAVSMCs. Ginsenoside-Rd reversed the increase in SOCC- or ROCC- but not VDCC-mediated Ca(2+) entry. In vitro, ginsenoside-Rd concentration-dependently inhibited endothelin-1 induced BAVSMC proliferation and Mn(2+) quenching rate within the same concentration range as required for inhibition of increased SOCC- or ROCC-mediated Ca(2+) entries during hypertension.
    These results provide in vivo evidence showing attenuation of hypertensive cerebrovascular remodeling after ginsenoside-Rd treatment. The underlying mechanism might be associated with inhibitory effects of ginsenoside-Rd on voltage-independent Ca(2+) entry and BAVSMC proliferation, but not with VDCC-mediated Ca(2+) entry.
    J Pharm Pharmacol. 2004 Jan;56(1):107-13.
    Ginsenoside-Rd attenuates oxidative damage related to aging in senescence-accelerated mice.[Pubmed: 14980007 ]
    Among the various theories of the aging process, the free radical theory, which proposes that deleterious actions of free radicals are responsible for the functional deterioration associated with aging, has received widespread attention. The theory suggests that enhancement of the antioxidative defence system to attenuate free-radical-induced damage will counteract the aging process.
    We used senescence-accelerated mice (SAM) to investigate the relationship between aging and the antioxidative defence system and evaluated the effects of Ginsenoside Rd, the saponin from ginseng, by measuring antioxidative defence system parameters, including the glutathione (GSH)/glutathione disulfide (GSSG) redox status, antioxidative enzyme activity and level of lipid peroxidation. SAM at 11 months of age (old SAM) showed a significantly lower hepatic GSH/GSSG ratio, due to decreased GSH and increased GSSG levels, than SAM at 5 weeks of age (young SAM). However, the administration of Ginsenoside Rd at a dose of 1 or 5 mg kg(-1) daily for 30 days to 10-month-old SAM significantly increased GSH, but decreased GSSG, resulting in elevation of the GSH/GSSG ratio. In addition, Ginsenoside Rd increased the activity of glutathione peroxidase (GSH-Px) and glutathione reductase that were both significantly lower in old SAM than in young SAM. This suggests that Ginsenoside Rd could play a crucial role in enhancing the defence system through regulation of the GSH/GSSG redox status. Moreover, decreases in the superoxide dismutase (SOD) and catalase activity in old SAM compared with young SAM were also revealed, indicating that the aging process resulted in suppression of the antioxidative defence system. However, Ginsenoside Rd did not affect SOD and catalase activity. As catalase is localized in peroxisome granules and GSH-Px is present in the cytoplasm and mitochondrial matrix, the site of Ginsenoside Rd action may be the cytoplasm and mitochondrial matrix. Furthermore, the serum and liver malondialdehyde levels, indicators of lipid peroxidation, were elevated with aging, while ginsenoside-Rd inhibited lipid peroxidation.
    This study indicates that the aging process leads to suppression of the antioxidative defence system and accumulation of lipid peroxidation products, while Ginsenoside Rd attenuates the oxidative damage, which may be responsible for the intervention of GSH/GSSG redox status.