| Size | Price | Stock | Qty |
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| 10mg |
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| Targets |
R-Ginsenoside Rg3 targets multiple pathways including the PI3K/Akt pathway, γ2 GABA-A receptors, 7.1 K+ channels, and α10 nACh receptors. It causes an inhibition of phosphatidylinositol 3-kinase/Akt activation that results in modulations in Bcl-2 family proteins, regulating apoptosis of cancer cells. The compound inhibits vascular endothelial cell proliferation (IC50=10 nM). It modulates ion channels such as Ca²⁺ and K⁺ channels for neuronal protection.
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| ln Vitro |
(20R)-Ginsenoside Rg3 inhibits the growth of human venous endothelial cells (HUVEC) with an IC50 of 10 nM[1]. In either the presence of a simulated variable dilution matrix with 20 ng/mL VEGF or without it, (20R)-ginsenoside Rg3 significantly exfoliated VEGF-induced HUVEC. In isolated microvessel sprouting and (20R)-ginsenoside Rg3 chemical sensing in arterial aortic ring tests [1]. HUVEC capillaries form on the gel in the arterial Matrigel plug experiment [1]. Angiogenesis caused by basic fibroblast growth factor (bFGF) is dramatically inhibited by (20R)-ginsenoside Rg3 at 150 and 600 nM [1].
20(R)-Ginsenoside Rg3 inhibited proliferation of human umbilical vein endothelial cells (HUVEC) with an IC50 of 10 nM in Trypan blue exclusion assay. [1] It dose-dependently (1-10^3 nM) suppressed capillary tube formation of HUVEC on Matrigel in the absence or presence of VEGF (20 ng/ml). In the absence of VEGF, branch points reduced from 52±3 to 18±4 at 10 nM (p<0.001). In the presence of VEGF (25 ng/ml), branch points increased to 78±5, and Rg3 (10^3 nM) reduced them to 40±5 (p<0.001). [1] Rg3 (1-10^3 nM) inhibited VEGF-induced chemoinvasion of HUVEC through Matrigel-coated membrane, reducing migration by >50% (p<0.05 for 1-10^2 nM, p<0.01 for 10^3 nM). [1] Rg3 (10-10^3 nM) dose-dependently inhibited ECGS-induced microvascular sprouting in ex vivo rat aortic ring assay. [1] Rg3 reduced gelatinolytic activities of secreted MMP-9, proMMP-2, and MMP-2 from aortic explants in a dose-dependent manner (effective at concentrations >1 nM). [1] In vitro, R-Ginsenoside Rg3 inhibits the growth of U87 cells with an IC50 of 10 nM. It causes inhibition of PI3K/Akt activation, resulting in modulations in Bcl-2 family proteins and regulation of apoptosis. The compound elicits significant inhibition of in vitro cell adhesion and invasion of U87 cells. It has inhibitory effects on vascular endothelial cell proliferation. Its anti-cancer, anti-inflammatory, and neuroprotective effects have been characterized in various cell lines. |
| ln Vivo |
(20R)-Ginsenoside Rg3 (0.05-0.5 mg/kg; intranasal medicine; lasts for 2 weeks) has demonstrated anti-fatigue properties when administered as a spray [2].
In a mouse weight-loaded swimming test, intranasal administration of 20(R)-Ginsenoside Rg3 at intermediate dose (0.1 mg/kg) and high dose (0.5 mg/kg) significantly prolonged swimming time (p<0.05 and p<0.01, respectively) compared to negative control. Serum urea nitrogen (SUN) levels were significantly decreased in all three treatment groups (low 0.05 mg/kg, intermediate 0.1 mg/kg, high 0.5 mg/kg) with p<0.01. Hepatic glycogen level was significantly increased in the high-dose group (p<0.05). Blood lactic acid variance after swimming was significantly reduced in the low-dose group (p<0.05). No significant changes were observed in LDH, SOD, and MDA levels. The anti-fatigue effect was not dose-dependent. [2] In vivo, R-Ginsenoside Rg3 has been studied for its anti-tumor, immunity enhancement, and memory improvement activities. It has been considered as one of the most promising approaches for fatigue treatment. The compound has demonstrated anti-cancer effects in animal models, inhibiting tumor growth and metastasis. Its neuroprotective effects have been evaluated in models of excitotoxicity and neurodegeneration. Studies have examined its effects on immune function, cognitive performance, and fatigue. |
| Enzyme Assay |
Gelatin zymography was performed to measure matrix metalloproteinase (MMP) activity. Culture supernatants from rat aortic ring cultures treated with 20(R)-Ginsenoside Rg3 were collected on day 8. Samples were mixed with zymograph sample buffer (10% SDS, 40% glycerol, 0.25 M Tris-HCl pH6.8, 0.02% bromophenol blue) without heat denaturation. Electrophoresis was carried out on 8% (for MMP-9) and 10% (for MMP-2) polyacrylamide gels containing 1 mg/ml gelatin at 20 mA at 4°C for 2 hours. After electrophoresis, gels were washed twice in renaturing solution (50 mM Tris-HCl pH7.4, 2% Triton X-100). Gels were then incubated in substrate buffer (50 mM Tris-HCl pH7.4, 1% Triton X-100, 5 mM CaCl2, 0.02% Tween 20) at 37°C overnight. Gels were stained with 0.5% Coomassie Blue R-350 and destained with 10% acetic acid in 40% methanol. Gelatinolytic activity appeared as clear bands. The intensity of bands was quantified. [1]
In cell-free biochemical assays, R-Ginsenoside Rg3 is evaluated for its inhibitory activity against PI3K/Akt signaling and its binding affinity to various receptors. Enzyme activity assays measure the compound's ability to inhibit PI3K and Akt activity. Receptor binding assays characterize its interactions with GABA-A receptors, K+ channels, and nACh receptors. Its purity and molecular weight (785.02 g/mol) are characterized using analytical techniques. These assays confirm the compound's multi-target mechanism. |
| Cell Assay |
Cell Viability Assay[1]
Cell Types: HUVEC Tested Concentrations: 1 nM, 10 nM, 100 nM, 1000 nM Incubation Duration: 48 hrs (hours) Experimental Results: Inhibited HUVEC proliferation. Proliferation assay: HUVEC were plated at 2x10^4 cells/well in 24-well plates in growth medium with 20% FCS and ECGS (20 μg/ml) for 24 h, then treated with various concentrations of 20(R)-Ginsenoside Rg3 (1-10^4 nM) for 48 h. Viable cells were counted using Trypan blue exclusion method. [1] Tube formation assay: GFR-Matrigel diluted 1:3 in PBS was added to 24-well plates and solidified. HUVEC (8x10^4 cells/well) were seeded with medium containing 10% FCS, ECGS (20 μg/ml), and Rg3 (1-10^3 nM) with or without VEGF (20 ng/ml) for 16 h. Branch points of capillary tubes were counted from five microscopic fields per well using image analysis software. [1] Chemoinvasion assay: Transwell chambers with 8 μm pore size polycarbonate filters were coated with GFR-Matrigel (1:30 on upper surface, 1:100 on lower surface). HUVEC (5x10^4 cells/well) were loaded into upper wells with medium containing 1% serum and various concentrations of Rg3 (1-10^3 nM). Lower chambers contained medium with or without VEGF (25 ng/ml). After 5 h incubation at 37°C, migrated cells on the lower membrane side were fixed with methanol, stained with DAPI (1 μg/ml), and counted under fluorescence microscope. [1] Aortic ring sprouting assay: Rat aortic fragments were embedded in GFR-Matrigel in 96-well plates, overlaid with additional Matrigel, and cultured in serum-free endothelial growth medium containing ECGS (200 μg/ml) with or without Rg3 (1-10^3 nM) for 8 days. Microvascular sprouting area was quantified using Image J software. [1] Cellular assays for R-Ginsenoside Rg3 involve evaluating its effects on cell proliferation, apoptosis, adhesion, and invasion in cancer cell lines such as U87 glioblastoma cells. The compound's ability to inhibit PI3K/Akt signaling and modulate Bcl-2 family proteins is assessed. Its effects on vascular endothelial cell proliferation are evaluated. The compound's neuroprotective effects are studied in neuronal cell cultures. |
| Animal Protocol |
Animal/Disease Models: Male Kunming mice, body weight 18-22 g[2]
Doses: 0.05 mg/kg, 0.1 mg/kg, 0.5 mg/kg (5 μL per nostril) Route of Administration: intranasal administration; 2 weeks Experimental Results: Weight-bearing swimming time was Dramatically prolonged, and liver glycogen levels were also increased. Male Kunming mice (18-22 g) were divided into 4 groups (n=30 each): negative control (normal saline), low-dose (0.05 mg/kg), intermediate-dose (0.1 mg/kg), high-dose (0.5 mg/kg) of 20(R)-Ginsenoside Rg3. All mice received intranasal administration of 10 μl of drug solution daily for two weeks. Weight-loaded swimming test: 30 min after last administration, mice (10 per group) were placed in a pool (90x45x45 cm) filled with water at 30±1°C, depth ~35 cm, with a lead block (5% body weight) attached to tail root. Swimming time until exhaustion was recorded. For biochemical measurements: 30 min after last administration, mice (10 per group) swam for 90 min without weight, then after 60 min rest, blood collected by heart puncture under ether anesthesia. Liver was dissected. Serum was separated by centrifugation at 3000 rpm for 10 min. Contents of SUN, LDH, hepatic glycogen, SOD, and MDA were analyzed with commercial kits. For blood lactic acid: 30 min after last administration, 20 μl blood collected via retroorbital bleeding method, then mice swam for 10 min without weight, blood collected immediately after and 20 min after swimming. LA levels were analyzed with commercial kits. [2] Animal models for R-Ginsenoside Rg3 include models of cancer, neurodegeneration, and fatigue. The compound is typically administered orally or via injection. Studies have examined its effects on tumor growth, cognitive function, immune response, and physical performance. Its anti-tumor activity has been demonstrated in xenograft models. Its neuroprotective effects have been evaluated in models of excitotoxicity. |
| ADME/Pharmacokinetics |
Pharmacokinetic data for R-Ginsenoside Rg3 show that the compound has a molecular weight of 785.02 g/mol with a molecular formula of C42H72O13. The CAS number is 38243-03-7. The compound is a saponin and should be stored under appropriate conditions. Standard handling procedures for ginsenoside research compounds apply.
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| Toxicity/Toxicokinetics |
The toxicity profile of R-Ginsenoside Rg3 indicates that it is generally well-tolerated at research doses. As a natural product from ginseng, it has a history of traditional use. Standard safety precautions for handling laboratory chemicals apply. The compound is for research use only and not for human use. No significant toxicity has been reported at research doses.
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| References | |
| Additional Infomation |
(20S)-Ginsenoside Rg3 is a ginsenoside found in ginseng (Panax ginseng) and Japanese ginseng (Panax japonicus var. major). It belongs to the dammarane type, with its 3β, 12β, and 20 prothiophosphate sites replaced by hydroxyl groups. Specifically, the 3-hydroxyl group is converted to the corresponding β-D-glucopyranosyl-β-D-glucopyranoside, and a double bond is introduced at positions 24-25. It possesses apoptosis-inducing, antitumor, plant metabolite, and angiogenesis-regulating effects. It is a ginsenoside, a tetracyclic triterpenoid, and a glycoside. Its function is related to (20S)-protopanaxadiol. It is derived from the hydride of dammarane. Ginsenoside Rg3 has been reported to exist in Panax notoginseng, ginseng, and other organisms with relevant data.
The study demonstrated that intranasal administration of 20(R)-Ginsenoside Rg3 has anti-fatigue effect in mice. The mechanism is related to increased hepatic glycogen storage and decreased accumulation of metabolites such as lactic acid and serum urea nitrogen. The anti-fatigue effect was not dose-dependent. The intranasal route avoids first-pass effect and has potential application prospect. [2] R-Ginsenoside Rg3 (20(R)-Ginsenoside Rg3) is a minor ginsenoside from Panax ginseng with anti-tumor, immunity enhancement, and memory improvement activities. It inhibits PI3K/Akt signaling (IC50=10 nM) and modulates Bcl-2 family proteins. The compound has a molecular weight of 785.02 g/mol and formula C42H72O13. The CAS number is 38243-03-7. |
| Molecular Formula |
C42H72O13
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|---|---|
| Molecular Weight |
785.01328
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| Exact Mass |
1078.592
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| CAS # |
38243-03-7
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| Related CAS # |
20(S)-Ginsenoside Rg3;14197-60-5
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| PubChem CID |
9918693
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| Appearance |
White to off-white solid powder
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| Density |
1.4±0.1 g/cm3
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| Boiling Point |
1117.1±65.0 °C at 760 mmHg
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| Melting Point |
315-318ºC
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| Flash Point |
629.4±34.3 °C
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| Vapour Pressure |
0.0±0.6 mmHg at 25°C
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| Index of Refraction |
1.622
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| LogP |
4.73
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| Hydrogen Bond Donor Count |
9
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| Hydrogen Bond Acceptor Count |
13
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| Rotatable Bond Count |
10
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| Heavy Atom Count |
55
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| Complexity |
1370
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| Defined Atom Stereocenter Count |
20
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| SMILES |
CC(=CCC[C@@](C)([C@H]1CC[C@@]2([C@@H]1[C@@H](C[C@H]3[C@]2(CC[C@@H]4[C@@]3(CC[C@@H](C4(C)C)O[C@H]5[C@@H]([C@H]([C@@H]([C@H](O5)CO)O)O)O[C@H]6[C@@H]([C@H]([C@@H]([C@H](O6)CO)O)O)O)C)C)O)C)O)C
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| InChi Key |
RWXIFXNRCLMQCD-JBVRGBGGSA-N
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| InChi Code |
InChI=1S/C42H72O13/c1-21(2)10-9-14-42(8,51)22-11-16-41(7)29(22)23(45)18-27-39(5)15-13-28(38(3,4)26(39)12-17-40(27,41)6)54-37-35(33(49)31(47)25(20-44)53-37)55-36-34(50)32(48)30(46)24(19-43)52-36/h10,22-37,43-51H,9,11-20H2,1-8H3/t22-,23+,24+,25+,26-,27+,28-,29-,30+,31+,32-,33-,34+,35+,36-,37-,39-,40+,41+,42-/m0/s1
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| Chemical Name |
(2S,3R,4S,5S,6R)-2-[(2R,3R,4S,5S,6R)-4,5-dihydroxy-2-[[(3S,5R,8R,9R,10R,12R,13R,14R,17S)-12-hydroxy-17-[(2S)-2-hydroxy-6-methylhept-5-en-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-3-yl]oxy]-6-(hydroxymethyl)oxan-3-yl]oxy-6-(hydroxymethyl)oxane-3,4,5-triol
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO : ~41.67 mg/mL (~53.08 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 4.17 mg/mL (5.31 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 41.7 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.2739 mL | 6.3693 mL | 12.7387 mL | |
| 5 mM | 0.2548 mL | 1.2739 mL | 2.5477 mL | |
| 10 mM | 0.1274 mL | 0.6369 mL | 1.2739 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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