Ginsenoside Rk3CAS# 364779-15-7 |
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| Cas No. | 364779-15-7 | SDF | Download SDF |
| PubChem ID | 75412555 | Appearance | Powder |
| Formula | C36H60O8 | M.Wt | 620.9 |
| Type of Compound | Triterpenoids | Storage | Desiccate at -20°C |
| Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
| Chemical Name | (2R,3R,4S,5S,6R)-2-[[(3S,5R,6S,8R,9R,10R,12R,13R,14R,17S)-3,12-dihydroxy-4,4,8,10,14-pentamethyl-17-(6-methylhepta-1,5-dien-2-yl)-2,3,5,6,7,9,11,12,13,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthren-6-yl]oxy]-6-(hydroxymethyl)oxane-3,4,5-triol | ||
| SMILES | CC(=CCCC(=C)C1CCC2(C1C(CC3C2(CC(C4C3(CCC(C4(C)C)O)C)OC5C(C(C(C(O5)CO)O)O)O)C)O)C)C | ||
| Standard InChIKey | AVXFIVJSCUOFNT-QXPABTKOSA-N | ||
| Standard InChI | InChI=1S/C36H60O8/c1-19(2)10-9-11-20(3)21-12-15-35(7)27(21)22(38)16-25-34(6)14-13-26(39)33(4,5)31(34)23(17-36(25,35)8)43-32-30(42)29(41)28(40)24(18-37)44-32/h10,21-32,37-42H,3,9,11-18H2,1-2,4-8H3/t21-,22-,23+,24-,25-,26+,27+,28-,29+,30-,31+,32-,34-,35-,36-/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. |
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| 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. |
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| 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. | ||
| Description | Ginsenoside Rk3 is often used as a major ingredient of the compound preparation for ischemic heart diseases, it could have a role in treating inflammatory diseases. Ginsenoside Rk3 significantly inhibits TNF-α-induced NF-κB transcriptional activity, with an IC50 of 14.24±1.30 μM in HepG2 cells. |
| Targets | Bcl-2/Bax | Caspase | Akt | Nrf2 | HO-1 | MAPK | NF-κB |
| In vitro | Ginsenoside RK3 Prevents Hypoxia-Reoxygenation Induced Apoptosis in H9c2 Cardiomyocytes via AKT and MAPK Pathway.[Pubmed: 23935671 ]Evid Based Complement Alternat Med. 2013;2013:690190.Cardiac hypertrophy is a thickening of the heart muscle that is associated with cardiovascular diseases such as hypertension and myocardial infarction. It occurs initially as an adaptive process against increased workloads and often leads to sudden arrhythmic deaths. Studies suggest that the lethal arrhythmia is attributed to hypertrophy-induced destabilization of cardiac electrical activity, especially the prolongation of the action potential. The reduced activity of Ito is demonstrated to be responsible for the ionic mechanism of prolonged action potential duration and arrhythmogeneity. Isosteviol (STV), a derivative of stevioside, plays a protective role in a variety of stress-induced cardiac diseases. |
| Structure Identification | Biol Pharm Bull. 2011;34(6):898-900.Anti-complementary ginsenosides isolated from processed ginseng.[Pubmed: 21628891]
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Ginsenoside Rk3 Dilution Calculator
Ginsenoside Rk3 Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 1.6106 mL | 8.0528 mL | 16.1057 mL | 32.2113 mL | 40.2641 mL |
| 5 mM | 0.3221 mL | 1.6106 mL | 3.2211 mL | 6.4423 mL | 8.0528 mL |
| 10 mM | 0.1611 mL | 0.8053 mL | 1.6106 mL | 3.2211 mL | 4.0264 mL |
| 50 mM | 0.0322 mL | 0.1611 mL | 0.3221 mL | 0.6442 mL | 0.8053 mL |
| 100 mM | 0.0161 mL | 0.0805 mL | 0.1611 mL | 0.3221 mL | 0.4026 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. | |||||
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Anti-complementary ginsenosides isolated from processed ginseng.[Pubmed:21628891]
Biol Pharm Bull. 2011;34(6):898-900.
As part of an ongoing search for immunomodulatory components aimed at the anti-complementary effect, ginsenosides isolated from processed ginseng were found to have inhibitory activity on complement activation through classical pathways. Activity-guided fractionation was used to isolate four ginsenosides, namely ginsenoside Rg(6), F(4), Rk(3), and Rh(4). Ginsenoside Rk(3) and Rh(4) had a 3 fold higher inhibition activity than rosmarinic acid which was used as a positive control while ginsenoside Rg(6) and F(4) showed only mild effects similar to that of the positive control. The results suggest that the activity of the corresponding ginsenosides may be increased by the glycosyl moiety at the C(6) position rather than the double bond conformation at C(2)(0), and ginsenoside Rk(3) and Rh(4) could have a role in treating inflammatory diseases.
Ginsenoside RK3 Prevents Hypoxia-Reoxygenation Induced Apoptosis in H9c2 Cardiomyocytes via AKT and MAPK Pathway.[Pubmed:23935671]
Evid Based Complement Alternat Med. 2013;2013:690190.
Reperfusion therapy is widely utilized for acute myocardial infarction (AMI), but further injury induced by rapidly initiating reperfusion of the heart is often encountered in clinical practice. Ginsenoside Rk3 (RK3) is reportedly present in the processed Radix notoginseng that is often used as a major ingredient of the compound preparation for ischemic heart diseases. This study aimed to investigate the possible protective effect of RK3 against hypoxia-reoxygenation (H/R) induced H9c2 cardiomyocytes damage and its underlying mechanisms. Our results showed that RK3 pretreatment caused increased cell viability and decreased levels of LDH leakage compared with the H/R group. Moreover, RK3 pretreatment inhibited cell apoptosis, as evidenced by decreased caspase-3 activity, TUNEL-positive cells, and Bax expression, as well as increased Bcl-2 level. Further mechanism investigation revealed that RK3 prevented H9c2 cardiomyocytes injury and apoptosis induced by H/R via AKT/Nrf-2/HO-1 and MAPK pathways. These observations indicate that RK3 has the potential to exert cardioprotective effects against H/R injury, which might be of great importance to clinical efficacy for AMI treatment.
