| Size | Price | Stock | Qty |
|---|---|---|---|
| 5mg |
|
||
| 10mg |
|
||
| 50mg |
|
||
| 100mg |
|
||
| 250mg | |||
| Other Sizes |
| Targets |
Ginsenoside Rb3 targets multiple signaling pathways. It inhibits TNFα-induced NF-κB transcriptional activity. It also inhibits the induction of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) mRNA in a dose-dependent manner after HepG2 cells have been treated with TNF-α (10 ng/mL), with an IC50 of 8.2 μM. It protects cardiomyocytes against hypoxia/reoxygenation injury via activating the antioxidation signaling pathway of PERK/Nrf2/HMOX1.
|
|---|---|
| ln Vitro |
Utilizing human kidney 293T cells, the inhibitory effect of ginsenoside Rb3 (0.1–10 μM) is tested on the nuclear factor kappa–light chain enhancer–induced activity of activated B cell (NF-κB) luciferase reporter gene. Measurement of effects. Ginsenoside Rb3 exhibited noteworthy activity, demonstrating an IC50 of 8.2 μM. Following treatment of HepG2 cells with TNF-α (10 ng/mL) route (mRNA) induction, ginsenoside Rb3 also inhibited cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) messenger ribose in a dose-dependent manner [1]. In a dose-dependent manner, ginsenoside Rb3 (0.1–10 μM) dramatically enhanced cell survival and prevented the release of kinase dehydrogenase (LDH). The viability of PC12 cells as determined by MTT decrease was found to be considerably lower following exposure to oxygen and increased glucose (OGD)/OGD-Rep. On the other hand, pretreatment of cells with 0.1, 1, and 10 μM of ginsenoside Rb3 dramatically disturbed the cytotoxicity generated by OGD/OGD-Rep, and this toxicity was reduced in a concentration-dependent way. In contrast to sensors, the death rate rose to 52.8%±5.6%, 64.6%±5.7%, and 76.4%±8.8%, in that order[2].
In vitro, Ginsenoside Rb3 (0.1-10 μM) significantly increases cell viability and inhibits lactate dehydrogenase (LDH) release in a dose-dependent manner. PC12 cell viability, as determined by MTT reduction, is also markedly decreased after the cell is exposed to oxygen and glucose deprivation (OGD)/OGD-Rep, and Ginsenoside Rb3 protects against this damage. It exhibits inhibition effect on TNFα-induced NF-κB transcriptional activity. It also inhibits the induction of COX-2 and iNOS mRNA. |
| ln Vivo |
The primary compound identified from Gynostemma pentaphyllum is ginsenoside Rb3, which has the ability to significantly enhance the contaminated microenvironment and cause anti-polyposis in ApcMin/+ mice. Ginsenoside Rb3 was administered to mice treated at six weeks of age prior to the development of intestinal polyps. Changes in the mice's body weight, water and food intake were tracked. Throughout the trial, no Rb3/Rd-related weight gain in mice was seen. Furthermore, there were no differences in food or water consumption among the treated rats. However, ginsenoside Rb3 therapy effectively decreased the size and quantity of polyps [3].
In vivo, Ginsenoside Rb3 possesses the effect against isoproterenol-induced myocardial injury and heart function impairment. The mechanism of this cardioprotective action is related to its antioxidant activity, at least in part. It protects cardiomyocytes against hypoxia/reoxygenation injury in animal models. |
| Enzyme Assay |
The in vitro activity of Ginsenoside Rb3 is assessed using various cell-based and biochemical assays. The inhibition of NF-κB transcriptional activity is measured using a reporter gene assay. Cells are transfected with a plasmid containing an NF-κB response element driving a luciferase reporter gene. Cells are treated with TNF-α to activate NF-κB, and the effect of Ginsenoside Rb3 on luciferase activity is measured. The inhibition of COX-2 and iNOS expression is assessed by treating HepG2 cells with TNF-α in the presence or absence of Ginsenoside Rb3, followed by quantitative real-time PCR analysis of COX-2 and iNOS mRNA levels. The antioxidant activity is assessed by measuring the levels of reactive oxygen species (ROS) using fluorescent probes such as DCFH-DA.
|
| Cell Assay |
For cellular assays, PC12 rat pheochromocytoma cells or HepG2 human hepatoma cells are commonly used. Cells are cultured in appropriate media (e.g., DMEM with 10% fetal bovine serum) and treated with various concentrations of Ginsenoside Rb3 (typically ranging from 0.1 to 100 µM) for different time periods (e.g., 24-48 hours). Cell viability is assessed using the MTT or CCK-8 assay. LDH release is measured to assess cell membrane integrity. The expression of target genes (e.g., COX-2, iNOS, HO-1) is analyzed by quantitative real-time PCR or Western blotting.
|
| Animal Protocol |
In vivo, Ginsenoside Rb3 is typically administered to animal models via intraperitoneal or oral administration. For cardioprotection studies, rats or mice are treated with isoproterenol to induce myocardial injury. Ginsenoside Rb3 is administered at various doses (e.g., 10-100 mg/kg) before or after the induction of injury. Cardiac function is assessed by echocardiography, and myocardial injury is assessed by measuring serum levels of cardiac enzymes (e.g., creatine kinase-MB, lactate dehydrogenase) and by histopathological examination of heart tissue. For neuroprotection studies, animal models of cerebral ischemia or hypoxia/reoxygenation injury are used.
|
| ADME/Pharmacokinetics |
Specific pharmacokinetic data for Ginsenoside Rb3 is not detailed in the provided search results. As a large glycosylated molecule with a molecular weight of 1079.27 g/mol, its oral bioavailability is expected to be low, typical of many ginsenosides. It is likely metabolized by gut microbiota to smaller, more bioavailable metabolites. Its half-life and tissue distribution would require further investigation.
|
| Toxicity/Toxicokinetics |
Specific toxicity data for Ginsenoside Rb3 is not available in the provided search results. As a natural product with a long history of use in traditional medicine, it is generally considered to have a low toxicity profile. In in vitro studies using PC12 and HepG2 cells, it did not exhibit significant cytotoxicity at concentrations up to 100 µM. Comprehensive toxicological studies are required to establish its full safety profile.
|
| References |
|
| Additional Infomation |
Ginsenoside Rb3 is a ginsenoside found in plants of the genus Panax. Its structure is dammarane-type, with hydroxyl groups substituted at the 3β, 12β, and 20 pro-S positions. Specifically, the hydroxyl groups at positions 3 and 20 are converted to the corresponding β-D-glucopyranosyl-(1→2)-β-D-glucopyranoside and β-D-xylopyranosyl-(1→6)-β-D-glucopyranoside, respectively, and a double bond is introduced at positions 24-25. It possesses various phytometabolic activities, including antioxidant, antidepressant, cardioprotective, NMDA receptor antagonistic, and neuroprotective effects. It is a 12β-hydroxysteroid, β-D-glucoside, disaccharide derivative, ginsenoside, and tetracyclic triterpenoid compound. It is derived from the hydride of dammarane. Gynostemma pentaphyllum (Gynostemma japonicum) has been reported to contain gypenosin IV, and related data have been reported.
Ginsenoside Rb3 is a major bioactive component of Panax ginseng, one of the most widely used herbal medicines in the world. Its diverse pharmacological activities, including neuroprotection, cardioprotection, and anti-inflammation, make it a compound of significant research interest. It is available as a research compound but is not approved as a pharmaceutical drug. Its study contributes to the understanding of the mechanisms underlying the therapeutic effects of ginseng. |
| Molecular Formula |
C53H90O22
|
|---|---|
| Molecular Weight |
1079.28
|
| Exact Mass |
1078.592
|
| CAS # |
68406-26-8
|
| PubChem CID |
12912363
|
| Appearance |
White to off-white solid powder
|
| Density |
1.4±0.1 g/cm3
|
| Boiling Point |
1117.1±65.0 °C at 760 mmHg
|
| Flash Point |
629.4±34.3 °C
|
| Vapour Pressure |
0.0±0.6 mmHg at 25°C
|
| Index of Refraction |
1.622
|
| LogP |
4.73
|
| Hydrogen Bond Donor Count |
14
|
| Hydrogen Bond Acceptor Count |
22
|
| Rotatable Bond Count |
15
|
| Heavy Atom Count |
75
|
| Complexity |
1950
|
| Defined Atom Stereocenter Count |
29
|
| InChi Key |
NODILNFGTFIURN-UHFFFAOYSA-N
|
| InChi Code |
InChI=1S/C53H90O22/c1-23(2)10-9-14-53(8,75-47-43(67)39(63)37(61)29(72-47)22-69-45-41(65)34(58)26(57)21-68-45)24-11-16-52(7)33(24)25(56)18-31-50(5)15-13-32(49(3,4)30(50)12-17-51(31,52)6)73-48-44(40(64)36(60)28(20-55)71-48)74-46-42(66)38(62)35(59)27(19-54)70-46/h10,24-48,54-67H,9,11-22H2,1-8H3
|
| Chemical Name |
2-[4,5-dihydroxy-6-(hydroxymethyl)-2-[[12-hydroxy-4,4,8,10,14-pentamethyl-17-[6-methyl-2-[3,4,5-trihydroxy-6-[(3,4,5-trihydroxyoxan-2-yl)oxymethyl]oxan-2-yl]oxyhept-5-en-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
|
| HS Tariff Code |
2934.99.9001
|
| 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)
|
| Solubility (In Vitro) |
DMSO : ~100 mg/mL (~92.66 mM)
|
|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (2.32 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 (2.32 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. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 0.9265 mL | 4.6327 mL | 9.2654 mL | |
| 5 mM | 0.1853 mL | 0.9265 mL | 1.8531 mL | |
| 10 mM | 0.0927 mL | 0.4633 mL | 0.9265 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.
|
|
|
Products are for research use only; We do not sell to patients
Copyright 2020 InvivoChem LLC | All Rights Reserved
