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Ginsenoside Rg5 is an IGF-1R-angiogenic agent. Ginsenoside Rg5 exhibits angiogenic activity, which can be reduced by IGF-1R knockdown. Docking analysis was used to investigate the potential interaction of ginsenoside Rg5 with IGF-1R. The docking results indicated that ginsenoside Rg5 may interact with IGF-1R, and docking analysis was carried out. Rg5 binds to the cysteine-docking domain of IGF-1R at two locations, A and B, with Kd values of 20 and 27 nM, respectively. Using Rg5 as a transferable label for IGF-1 and HUVEC, the IC50 value was ~90 μM, which was higher than the IC50 value of ~1.4 nM for unlabeled IGF-1 [1]. The MTT assay results revealed that after 24, 48, and 72 hours of treatment with ginsenoside Rg5, dose-related parameters influenced MCF-7 cell growth. Various concentrations (0, 25, 50, and 100 μM) of ginsenoside Rg5 influenced MCF-7 cell cycle-related cosmetics. The induced cell cycle appears to be in the G0/G1 phase [3].
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| ln Vitro |
Ginsenoside Rg5 is an IGF-1R-angiogenic agent. Ginsenoside Rg5 exhibits angiogenic activity, which can be reduced by IGF-1R knockdown. Docking analysis was used to investigate the potential interaction of ginsenoside Rg5 with IGF-1R. The docking results indicated that ginsenoside Rg5 may interact with IGF-1R, and docking analysis was carried out. Rg5 binds to the cysteine-docking domain of IGF-1R at two locations, A and B, with Kd values of 20 and 27 nM, respectively. Using Rg5 as a transferable label for IGF-1 and HUVEC, the IC50 value was ~90 μM, which was higher than the IC50 value of ~1.4 nM for unlabeled IGF-1 [1]. The MTT assay results revealed that after 24, 48, and 72 hours of treatment with ginsenoside Rg5, dose-related parameters influenced MCF-7 cell growth. Various concentrations (0, 25, 50, and 100 μM) of ginsenoside Rg5 influenced MCF-7 cell cycle-related cosmetics. The induced cell cycle appears to be in the G0/G1 phase [3].
Ginsenoside Rg5 stimulates human umbilical vein endothelial cell (HUVEC) proliferation in a dose-dependent manner, with 20 μM Rg5 showing stronger activity than 10 ng/mL VEGF. It promotes HUVEC chemotactic migration and tube formation on Matrigel. Rg5 increases phosphorylation of ERK, Akt, eNOS, Src, FAK, and paxillin in a time-dependent manner. It elevates intracellular NO and cGMP levels, which are inhibited by L-NAME (NOS inhibitor) and IGF-1R knockdown. Rg5 enhances eNOS dimerization and Ca²⁺ mobilization via Gi protein and PLC-γ1 pathways. It does not increase VEGF mRNA expression, promoter activity, or vascular inflammation markers (ICAM-1, VCAM-1). Rg5 does not promote monocyte adhesion to endothelial cells or increase endothelial permeability. [1] |
| ln Vivo |
By blocking NF-κB p65's ability to bind DNA in response to lipopolysaccharide (LPS) stimulation in BV2 astrocytes, ginsenoside Rg5 suppresses the mRNA expression of COX-2. COX-2 and NF-κB p65 expression in the Rg5 model group. Acute cellular respiration occurred and renal tubular injury was evident in the group treated with low-dose ginsenoside Rg5 (10 mg/kg). Nevertheless, while appearing to have histologically normal renal tubules, no inflammation or cast formation was seen in the renal tissue in another group of ginsenoside Rg5 (20 mg/kg) [2].
Ginsenoside Rg5 promotes neovascularization in a Matrigel plug assay in mice, with increased hemoglobin content indicating blood vessel formation. It enhances vessel sprouting in ex vivo rat aortic ring assays. In a mouse hind limb ischemia model, Rg5 improves blood flow recovery and increases capillary density in ischemic muscle. Rg5 induces vasorelaxation in aortic rings from wild-type and high-cholesterol-fed ApoE⁻/⁻ mice, but not in eNOS⁻/⁻ mice. It does not increase vascular permeability in a Miles assay. [1] |
| Enzyme Assay |
IGF-1 binding assay: HUVECs were pretreated with Rg5 (10⁻⁷–5×10⁻² M) for 20 min, followed by incubation with ¹²⁵I-labeled IGF-1 for 10 min. Cell-bound radioactivity was measured by scintillation counting. Rg5 inhibited IGF-1 binding with an IC₅₀ of ~90 nmol/L. [1]
Molecular docking simulation: Blind docking of Rg5 to IGF-1R (PDB: 11GR) was performed using Autodock 4.2 with a Lamarckian genetic algorithm. The grid box covered the entire IGF-1R molecule, and 50 million energy evaluations were performed. Binding sites and interactions were visualized using Chimera software. [1] |
| Cell Assay |
Cell proliferation: HUVECs were treated with Rg5 or VEGF for 30 h, then pulsed with ³H-thymidine for 6 h. Incorporated radioactivity was measured by scintillation counting.
Cell migration: HUVECs were placed in Transwell inserts coated with gelatin. Rg5 or VEGF was added to the lower chamber. After 4 h, migrated cells were stained and counted. Tube formation: HUVECs were plated on growth factor-reduced Matrigel and treated with Rg5 or VEGF. Tube networks were imaged and quantified after 20 h. NO measurement: HUVECs were loaded with DAF-FM diacetate, treated with Rg5 ± L-NAME, and fluorescence was measured by confocal microscopy. Ca²⁺ measurement: HUVECs were loaded with Fluo-4 AM, treated with Rg5 ± inhibitors, and Ca²⁺ flux was monitored by confocal microscopy. Western blot and immunoprecipitation: Phosphorylation of signaling proteins and eNOS dimerization were analyzed using specific antibodies and low-temperature SDS-PAGE. VEGF expression: VEGF mRNA was measured by RT-PCR, and promoter activity was assessed using a luciferase reporter assay. [1] |
| Animal Protocol |
Matrigel plug assay: C57BL/6 mice were injected subcutaneously with 400 μL Matrigel containing 200 nmol Rg5 or 100 ng VEGF. After 7 days, plugs were excised and hemoglobin content was measured.
Hind limb ischemia model: C57BL/6 mice underwent femoral artery ligation, followed by intramuscular injection of Rg5 (300 μmol/100 μL per mouse). Blood flow was monitored by laser-Doppler perfusion imaging at days 7, 14, and 21. Aortic ring vasorelaxation assay: Thoracic aortas from mice were cut into rings and mounted in a myograph system. Rings were preconstricted with U46619 or phenylephrine, then treated with Rg5 or acetylcholine. Relaxation responses were recorded. Miles permeability assay: Evans blue dye was injected intravenously into mice, followed by intradermal injection of Rg5 or VEGF. Dye leakage in skin was quantified spectrophotometrically. [1] |
| References |
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| Additional Infomation |
Ginsenoside Rg5 is a triterpenoid saponin with the function of a metabolite. It has been reported that ginsenoside Rg5 exists in Panax notoginseng and Centella asiatica, and there are related data reports. Ginsenoside Rg5 is a saponin synthesized during the steaming process of ginseng. It is a novel non-biological IGF-1R agonist that can promote angiogenesis and vasodilation without the adverse reactions associated with VEGF therapy. Its mechanism of action involves multiple signaling pathways: PI3K/Akt/eNOS, MEK/ERK, Src/FAK/paxillin and Gi/PLC/Ca²⁺/eNOS dimerization. It may have the potential to treat ischemic vascular disease and hypertension. [1]
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| Molecular Formula |
C42H70O12
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|---|---|
| Molecular Weight |
766.9980
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| Exact Mass |
766.486
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| CAS # |
186763-78-0
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| PubChem CID |
11550001
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| Appearance |
White to off-white solid powder
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| Density |
1.3±0.1 g/cm3
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| Boiling Point |
855.6±65.0 °C at 760 mmHg
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| Flash Point |
471.2±34.3 °C
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| Vapour Pressure |
0.0±0.6 mmHg at 25°C
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| Index of Refraction |
1.592
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| LogP |
6.81
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| Hydrogen Bond Donor Count |
8
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| Hydrogen Bond Acceptor Count |
12
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| Rotatable Bond Count |
9
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| Heavy Atom Count |
54
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| Complexity |
1380
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| Defined Atom Stereocenter Count |
19
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| SMILES |
CC(=CC/C=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)C
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| InChi Key |
NJUXRKMKOFXMRX-RNCAKNGISA-N
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| InChi Code |
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
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| 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
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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 : ~50 mg/mL (~65.19 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (3.26 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (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 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.5 mg/mL (3.26 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (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 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (3.26 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.3038 mL | 6.5189 mL | 13.0378 mL | |
| 5 mM | 0.2608 mL | 1.3038 mL | 2.6076 mL | |
| 10 mM | 0.1304 mL | 0.6519 mL | 1.3038 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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