Ginsenoside Rg5

CAS# 186763-78-0

Ginsenoside Rg5

Catalog No. BCN3551----Order now to get a substantial discount!

Product Name & Size Price Stock
Ginsenoside Rg5:10mg $188.00 In stock
Ginsenoside Rg5:20mg $320.00 In stock
Ginsenoside Rg5:50mg $752.00 In stock
Ginsenoside Rg5:100mg $1316.00 In stock

Quality Control of Ginsenoside Rg5

Number of papers citing our products

Chemical structure

Ginsenoside Rg5

3D structure

Chemical Properties of Ginsenoside Rg5

Cas No. 186763-78-0 SDF Download SDF
PubChem ID 11550001 Appearance White powder
Formula C42H70O12 M.Wt 767.0
Type of Compound Triterpenoids Storage Desiccate at -20°C
Solubility Soluble in DMSO; sparingly soluble in methanol; insoluble in water
Chemical Name (2S,3R,4S,5S,6R)-2-[(2R,3R,4S,5S,6R)-4,5-dihydroxy-6-(hydroxymethyl)-2-[[(3S,5R,8R,9R,10R,12R,13R,14R,17S)-12-hydroxy-4,4,8,10,14-pentamethyl-17-[(2E)-6-methylhepta-2,5-dien-2-yl]-2,3,5,6,7,9,11,12,13,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthren-3-yl]oxy]oxan-3-yl]oxy-6-(hydroxymethyl)oxane-3,4,5-triol
SMILES CC(=CCC=C(C)C1CCC2(C1C(CC3C2(CCC4C3(CCC(C4(C)C)OC5C(C(C(C(O5)CO)O)O)OC6C(C(C(C(O6)CO)O)O)O)C)C)O)C)C
Standard InChIKey NJUXRKMKOFXMRX-RNCAKNGISA-N
Standard InChI InChI=1S/C42H70O12/c1-21(2)10-9-11-22(3)23-12-16-42(8)30(23)24(45)18-28-40(6)15-14-29(39(4,5)27(40)13-17-41(28,42)7)53-38-36(34(49)32(47)26(20-44)52-38)54-37-35(50)33(48)31(46)25(19-43)51-37/h10-11,23-38,43-50H,9,12-20H2,1-8H3/b22-11+/t23-,24-,25-,26-,27+,28-,29+,30+,31-,32-,33+,34+,35-,36-,37+,38+,40+,41-,42-/m1/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.
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.
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.

Source of Ginsenoside Rg5

The roots of Panax ginseng C. A. Mey.

Biological Activity of Ginsenoside Rg5

Description1. Ginsenoside Rg5 could be a beneficial agent for the treatment of Alzheimer's disease. 2. Ginsenoside Rg5 suppresses LPS-induced nitric oxide (NO) production and proinflammatory TNF-α secretion. 3. Ginsenoside Rg5 can ameliorate lung inflammation possibly by inhibiting the binding of LPS to toll-like receptor (TLR)-4 on macrophages. 4. Ginsenoside Rg5 plays a novel role as an IGF-1R agonist, promoting therapeutic angiogenesis and improving hypertension without adverse effects in the vasculature. 5. Ginsenoside Rg5 blocks cell cycle of SK-HEP-1 cells at the Gl/S transition phase by down-regulating cyclin E-dependent kinase activity and that the down-regulation of cyclin E-dependent kinase activity is caused mainly by induced CDK2 inhibitor, p21Cip/WAF1 and decreased levels of cyclin E.
TargetsTNF-α | IL Receptor | AChR | COX | NOS | Beta Amyloid | ERK | FAK | Akt | MMP(e.g.TIMP) | NF-kB | AP-1 | ROS | HO-1 | TLR | CDK | p21

Protocol

Kinase Assay [1]
HUVECs are cultured in 24-well plates overnight. The cells are changed to serum-free M199 and incubated for 1 h. The medium is removed, and cells are incubated with fresh serum-free medium containing 0.1 μM-50 mM Ginsenoside Rg5 at 37°C for 20 min followed by the addition of 50 μL (1 μCi) of [125I]IGF-1 and then further incubated for 10 min. The medium is decanted, and cell plates are washed twice with serum-free medium. Cells are lysed in 300 μL of 0.1 N NaOH solution containing 0.1% SDS, transferred to scintillation vials, and mixed with 1 mL of Ultima Gold mixture solution. Cell-associated [125I]IGF-1 is analyzed in a scintillation counter. The nonspecific binding is determined by coincubation with unlabeled IGF-1 (50 nM)[1].

Cell Assay [3]
MCF-7 (HER2-/ER+) and MDA-MB-453 (HER2+/ER-) human breast cancer cell lines are maintained using RPMI 1640 medium supplemented with 10% (vol/vol) FBS plus 100 units/mL Penicillin and Streptomycin in a 5% carbon dioxide air incubator at 37°C. Cell cytotoxicity is measured by MTT assay. Cells are seeded in 96-well tissue culture plates at the density of 0.2×104 cells per well with 100 μL medium, and are allowed to become attached for 24 h. One hundred microliters of the medium with different concentrations of Ginsenoside Rg5 (e.g., 0 μM, 25 μM, 50 μM, and 100 μM) are added to each well. At indicated times, 30 μL MTT stock solution (3 mg/mL) are added to each well. After culturing the cells at 37°C for 2 h, DMSO is added to dissolve the formazan crystals. The absorbance is read at the wavelength of 540 nm with a microplate reader[3].

Animal Administration [2]
Mice[2] Male ICR mice (6 to 8 weeks old), weighing 25-27 g, are used. After acclimation for one week, mice are randomly assigned into 4 experimental groups with 8 mice in each group: normal control, Cisplatin control, and Cisplatin+Ginsenoside Rg5 groups (10 and 20 mg/kg, respectively). Ginsenoside Rg5 is administered intragastrically at the dose of 10 and 20 mg/kg for 10 days. On the 7th day, animals in Cisplatin control and Ginsenoside Rg5-treated groups receive a single intraperitoneal injection of Cisplatin (25 mg/kg) to induce nephrotoxicity in mice. Mice are anaesthetized with pentobarbital, subsequently sacrificed at 72 h after Cisplatin injection (Day 10). Blood samples are collected and then centrifuged at 3000 rpm to separate the serum and stored at -20 °C for determining blood urea nitrogen (BUN) and creatinine (CRE) levels.

References:
[1]. Cho YL, et al. Specific activation of insulin-like growth factor-1 receptor by ginsenoside Rg5 promotes angiogenesis and vasorelaxation. J Biol Chem. 2015 Jan 2;290(1):467-77. [2]. Li W, et al. Ginsenoside Rg5 Ameliorates Cisplatin-Induced Nephrotoxicity in Mice through Inhibition of Inflammation, Oxidative Stress, and Apoptosis. Nutrients. 2016 Sep 13;8(9). pii: E566. [3]. Kim SJ, et al. Anti-breast cancer activity of Fine Black ginseng (Panax ginseng Meyer) and ginsenoside Rg5. J Ginseng Res. 2015 Apr;39(2):125-34.

Ginsenoside Rg5 Dilution Calculator

Concentration (start)
x
Volume (start)
=
Concentration (final)
x
Volume (final)
 
 
 
C1
V1
C2
V2

calculate

Ginsenoside Rg5 Molarity Calculator

Mass
=
Concentration
x
Volume
x
MW*
 
 
 
g/mol

calculate

Preparing Stock Solutions of Ginsenoside Rg5

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 1.3038 mL 6.5189 mL 13.0378 mL 26.0756 mL 32.5945 mL
5 mM 0.2608 mL 1.3038 mL 2.6076 mL 5.2151 mL 6.5189 mL
10 mM 0.1304 mL 0.6519 mL 1.3038 mL 2.6076 mL 3.2595 mL
50 mM 0.0261 mL 0.1304 mL 0.2608 mL 0.5215 mL 0.6519 mL
100 mM 0.013 mL 0.0652 mL 0.1304 mL 0.2608 mL 0.3259 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.

Organizitions Citing Our Products recently

 
 
 

Calcutta University

University of Minnesota

University of Maryland School of Medicine

University of Illinois at Chicago

The Ohio State University

University of Zurich

Harvard University

Colorado State University

Auburn University

Yale University

Worcester Polytechnic Institute

Washington State University

Stanford University

University of Leipzig

Universidade da Beira Interior

The Institute of Cancer Research

Heidelberg University

University of Amsterdam

University of Auckland
TsingHua University
TsingHua University
The University of Michigan
The University of Michigan
Miami University
Miami University
DRURY University
DRURY University
Jilin University
Jilin University
Fudan University
Fudan University
Wuhan University
Wuhan University
Sun Yat-sen University
Sun Yat-sen University
Universite de Paris
Universite de Paris
Deemed University
Deemed University
Auckland University
Auckland University
The University of Tokyo
The University of Tokyo
Korea University
Korea University

Background on Ginsenoside Rg5

Ginsenoside Rg5 is the main component of Red ginseng. Ginsenoside blocks binding of IGF-1 to its receptor with an IC50 of ~90 nM. Ginsenoside Rg5 also inhibits the mRNA expression of COX-2 via suppression of the DNA binding activities of NF-κB p65.

In Vitro:Ginsenoside Rg5 plays a novel role as an IGF-1R agonist. Ginsenoside Rg5 binds to IGF-1R with an IC50 value of ~90 and its angiogenic activity is inhibited by IGF-1R knockdown. To investigate the possible interaction of Ginsenoside Rg5 with IGF-1R, a docking analysis is performed. Docking results show that Ginsenoside Rg5 binds strongly at two sites, A and B, with Kd values of 20 and 27 nM, respectively, to the cysteine-rich domain of IGF-1R. Pretreatment with Rg5 blocks the binding of radiolabeled IGF-1 to HUVECs with an IC50 value of ~90 μM, which is greater than an IC50 value of ~1.4 nM for unlabeled IGF-1[1]. The results from MTT assay show that MCF-7 cell proliferation is inhibited by Ginsenoside Rg5 treatment for 24, 48 and 72 h in a dose-dependent manner. Ginsenoside Rg5 at different concentrations (0, 25, 50 and 100 μM), induce cell cycle arrest in G0/G1 phase through regulation of cell cycle-related proteins in MCF-7 cells[3].

In Vivo:Ginsenoside Rg5 inhibits the mRNA expression of COX-2 via suppression of the DNA binding activities of NF-κB p65 in lipopolysaccharides (LPS)-stimulated BV2 microglial cells. Rg5 pretreated group mice show declined expression of NF-κB p65 and COX-2. In the group treated with low dose of Ginsenoside Rg5 (10 mg/kg), there is remarkable tubular damage and infiltration of inflammatory cells. However, at the higher dose of Ginsenoside Rg5 (20 mg/kg), tubules markedly appeare histologically normal and no inflammation and cast formation is observed in kidney tissues[2].

References:
[1]. Cho YL, et al. Specific activation of insulin-like growth factor-1 receptor by ginsenoside Rg5 promotes angiogenesis and vasorelaxation. J Biol Chem. 2015 Jan 2;290(1):467-77. [2]. Li W, et al. Ginsenoside Rg5 Ameliorates Cisplatin-Induced Nephrotoxicity in Mice through Inhibition of Inflammation, Oxidative Stress, and Apoptosis. Nutrients. 2016 Sep 13;8(9). pii: E566. [3]. Kim SJ, et al. Anti-breast cancer activity of Fine Black ginseng (Panax ginseng Meyer) and ginsenoside Rg5. J Ginseng Res. 2015 Apr;39(2):125-34.

Featured Products
New Products
 

References on Ginsenoside Rg5

Ginsenoside-Rg5 suppresses cyclin E-dependent protein kinase activity via up-regulating p21Cip/WAF1 and down-regulating cyclin E in SK-HEP-1 cells.[Pubmed:9137450]

Anticancer Res. 1997 Mar-Apr;17(2A):1067-72.

In the present study, we report that ginsenoside-Rg5 (G-Rg5), a newly discovered diol-containing ginsenoside, blocks the cell cycle of human hepatoma SK-HEP-1 cells via the down-regulation of cyclin E-dependent kinase activity. The results from flow cytometric analyses show that G-Rg5 arrests the cell cycle of SK-HEP-1 cells at the Gl/S transition phase. The cyclin E-dependent kinase activity that has been immunoprecipitated with cyclin E-specific antibody is down-regulated in response to G-Rg5. The results from immunoblottings show that the down-regulation of cyclin E-dependent kinase activity is related to increased protein levels of p21Cip/WAF1 and to decreased protein levels of cyclin E, CDK2, and CDC25A. Collectively, these data suggest that G-Rg5 blocks cell cycle of SK-HEP-1 cells at the Gl/S transition phase by down-regulating cyclin E-dependent kinase activity and that the down-regulation of cyclin E-dependent kinase activity is caused mainly by induced CDK2 inhibitor, p21Cip/WAF1 and decreased levels of cyclin E.

Ginsenoside Rg5 ameliorates lung inflammation in mice by inhibiting the binding of LPS to toll-like receptor-4 on macrophages.[Pubmed:22107725]

Int Immunopharmacol. 2012 Jan;12(1):110-6.

Heating and steaming processes have been applied to various natural medicines for either enhancing or altering their pharmacological activities, and the chemical compositions of the active components. While ginsenoside Rb1, which is the major constituent of raw ginseng, has been studied extensively for its anti-inflammatory effect, the biological activity of Ginsenoside Rg5, a major constituent of steamed ginseng, remains to be explored. Here, we isolated Rg5 and examined anti-inflammatory effect in lipopolysaccharide (LPS)-stimulated macrophages and on LPS-induced lung inflammation. Rg5 inhibited the expression of proinflammatory cytokines, IL-1beta and TNF-alpha, as well as inflammatory enzymes, COX-2 and iNOS in LPS-stimulated alveolar macrophages. Rg5 also reduced LPS-induced phosphorylation of IL-1 receptor-associated kinases (IRAK)-1 and IKK-beta, as well as the degradation of IRAK-1 and IRAK-4. Rg5 inhibited the phosphorylation of NF-kappaB as well as the translocation of p65 into the nucleus. When macrophages were treated with Alexa Fluor 594-conjugated LPS in the presence of Rg5, the fluorescence intensity of LPS observed outside the cell membrane was lower than that in LPS-stimulated alveolar macrophages alone. Rg5, inhibited the levels of protein and neutrophils in bronchoalveolar lavage fluid of LPS-stimulated mice, as well as pro-inflammatory cytokines, TNF-alpha and IL-1beta. Rg5 also inhibited iNOS and COX expressions, and NF-kappaB activation in LPS-stimulated lung inflammation of mice. The inhibitory effect of Rg5 (10 mg/kg) was comparable to that of dexamethasone (5 mg/kg). Based on these findings, Rg5 can ameliorate lung inflammation possibly by inhibiting the binding of LPS to toll-like receptor (TLR)-4 on macrophages.

Ginsenoside Rg5 improves cognitive dysfunction and beta-amyloid deposition in STZ-induced memory impaired rats via attenuating neuroinflammatory responses.[Pubmed:24503167]

Int Immunopharmacol. 2014 Apr;19(2):317-26.

Neuroinflammatory responses play a crucial role in the pathogenesis of Alzheimer's disease (AD). Ginsenoside Rg5 (Rg5), an abundant natural compound in Panax ginseng, has been found to be beneficial in treating AD. In the present study, we demonstrated that Rg5 improved cognitive dysfunction and attenuated neuroinflammatory responses in streptozotocin (STZ)-induced memory impaired rats. Cognitive deficits were ameliorated with Rg5 (5, 10 and 20mg/kg) treatment in a dose-dependent manner together with decreased levels of inflammatory cytokines TNF-alpha and IL-1beta (P<0.05) in brains of STZ rats. Acetylcholinesterase (AChE) activity was also significantly reduced by Rg5 whereas choline acetyltransferase (ChAT) activity was remarkably increased in the cortex and hippocampus of STZ-induced AD rats (P<0.05). In addition, Congo red and immunohistochemistry staining results showed that Rg5 alleviated Abeta deposition but enhanced the expressions of insulin-like growth factors 1 (IGF-1) and brain derived neurophic factor (BDNF) in the hippocampus and cerebral cortex (P<0.05). Western blot analysis also demonstrated that Rg5 increased remarkably BDNF and IGF-1 expressions whereas decreased significantly Abeta deposits (P<0.05). Furthermore, it was observed that the expressions of COX-2 and iNOS were significantly up-regulated in STZ-induced AD rats and down-regulated strongly (P<0.05) by Rg5 compared with control rats. These data demonstrated that STZ-induced learning and memory impairments in rats could be improved by Rg5, which was associated with attenuating neuroinflammatory responses. Our findings suggested that Rg5 could be a beneficial agent for the treatment of AD.

Specific activation of insulin-like growth factor-1 receptor by ginsenoside Rg5 promotes angiogenesis and vasorelaxation.[Pubmed:25391655]

J Biol Chem. 2015 Jan 2;290(1):467-77.

Ginsenoside Rg5 is a compound newly synthesized during the steaming process of ginseng; however, its biological activity has not been elucidated with regard to endothelial function. We found that Rg5 stimulated in vitro angiogenesis of human endothelial cells, consistent with increased neovascularization and blood perfusion in a mouse hind limb ischemia model. Rg5 also evoked vasorelaxation in aortic rings isolated from wild type and high cholesterol-fed ApoE(-/-) mice but not from endothelial nitric-oxide synthase (eNOS) knock-out mice. Angiogenic activity of Rg5 was highly associated with a specific increase in insulin-like growth factor-1 receptor (IGF-1R) phosphorylation and subsequent activation of multiple angiogenic signals, including ERK, FAK, Akt/eNOS/NO, and Gi-mediated phospholipase C/Ca(2+)/eNOS dimerization pathways. The vasodilative activity of Rg5 was mediated by the eNOS/NO/cGMP axis. IGF-1R knockdown suppressed Rg5-induced angiogenesis and vasorelaxation by inhibiting key angiogenic signaling and NO/cGMP pathways. In silico docking analysis showed that Rg5 bound with high affinity to IGF-1R at the same binding site of IGF. Rg5 blocked binding of IGF-1 to its receptor with an IC50 of approximately 90 nmol/liter. However, Rg5 did not induce vascular inflammation and permeability. These data suggest that Rg5 plays a novel role as an IGF-1R agonist, promoting therapeutic angiogenesis and improving hypertension without adverse effects in the vasculature.

Anti-inflammatory effect of ginsenoside Rg5 in lipopolysaccharide-stimulated BV2 microglial cells.[Pubmed:23698769]

Int J Mol Sci. 2013 May 8;14(5):9820-33.

Microglia are resident immune cells in the central nervous system. They play a role in normal brain development and neuronal recovery. However, overactivation of microglia causes neuronal death, which is associated with neurodegenerative diseases, such as Parkinson's disease and Alzheimer's disease. Therefore, controlling microglial activation has been suggested as an important target for treatment of neurodegenerative diseases. In the present study, we investigated the anti-inflammatory effect of Ginsenoside Rg5 in lipopolysaccharide (LPS)-stimulated BV2 microglial cells and rat primary microglia. The data showed that Rg5 suppressed LPS-induced nitric oxide (NO) production and proinflammatory TNF-alpha secretion. In addition, Rg5 inhibited the mRNA expressions of iNOS, TNF-alpha, IL-1b, COX-2 and MMP-9 induced by LPS. Further mechanistic studies revealed that Rg5 inhibited the phophorylations of PI3K/Akt and MAPKs and the DNA binding activities of NF-kB and AP-1, which are upstream molecules controlling inflammatory reactions. Moreover, Rg5 suppressed ROS production with upregulation of hemeoxygenase-1 (HO-1) expression in LPS-stimulated BV2 cells. Overall, microglial inactivation by Ginsenoside Rg5 may provide a therapeutic potential for various neuroinflammatory disorders.

Description

Ginsenoside Rg5 is the main component of Red ginseng. Ginsenoside blocks binding of IGF-1 to its receptor with an IC50 of ~90 nM. Ginsenoside Rg5 also inhibits the mRNA expression of COX-2 via suppression of the DNA binding activities of NF-κB p65.

Keywords:

Ginsenoside Rg5,186763-78-0,Natural Products, buy Ginsenoside Rg5 , Ginsenoside Rg5 supplier , purchase Ginsenoside Rg5 , Ginsenoside Rg5 cost , Ginsenoside Rg5 manufacturer , order Ginsenoside Rg5 , high purity Ginsenoside Rg5

Online Inquiry for:

      Fill out the information below

      • Size:Qty: - +

      * Required Fields

                                      Result: