Ginsenoside Rk1CAS# 494753-69-4 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 494753-69-4 | SDF | Download SDF |
| PubChem ID | 11499198 | Appearance | Powder |
| Formula | C42H70O12 | M.Wt | 767.0 |
| Type of Compound | Triterpenoids | Storage | Desiccate at -20°C |
| Solubility | Soluble in methan | ||
| 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-(6-methylhepta-1,5-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(=CCCC(=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 | KWDWBAISZWOAHD-MHOSXIPRSA-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/h10,23-38,43-50H,3,9,11-20H2,1-2,4-8H3/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. |
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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 Rk1, one of the main elements of Sung Ginseng, has been confirmed as a new endothelial barrier enhancer recently and has anti-cancer activity, the mechanism involves coordination between inhibition of telomerase activity and induction of apoptosis. |
| Targets | Caspase | p53 | Bcl-2/Bax | c-Myc | ERK | Autophagy |
| In vitro | Induction of apoptosis by ginsenoside Rk1 in SK-MEL-2-human melanoma.[Pubmed: 22553065]Arch Pharm Res. 2012 Mar;35(4):717-22.Ginsenosides are active compounds isolated from Panax ginseng Meyer. Among these ginsenosides, less polar ginsenosides such as ginsenoside Rg3 and ginsenoside Rh2 have been demonstrated to have tumor inhibitory effects because of their cytotoxicity. Anti-tumor activity of the ginsenoside Rk1 in human hepatocellular carcinoma cells through inhibition of telomerase activity and induction of apoptosis.[Pubmed: 18451501]Biol Pharm Bull. 2008 May;31(5):826-30.The Ginsenoside Rk1 is one of major components of heat-processed Panax ginseng C. A. MEYER, Sun Ginseng (SG). |
| Cell Research | Autophagy inhibition enhances apoptosis induced by ginsenoside Rk1 in hepatocellular carcinoma cells.[Pubmed: 19809182]Biosci Biotechnol Biochem. 2009 Oct;73(10):2183-9.Our previous study indicated that Ginsenoside Rk1 has anti-tumor activity and that its mode of action in HepG2 cells treated for 48 h involves coordinated inhibition of telomerase and induction of apoptosis. |
| Structure Identification | Bioorg Med Chem Lett. 2010 Dec 1;20(23):7102-5.Cholesterol-derived novel anti-apoptotic agents on the structural basis of ginsenoside Rk1.[Pubmed: 20971002]Design and synthesis of cholesterol-derived anti-apoptotic agents were described. |
Ginsenoside Rk1 Dilution Calculator
Ginsenoside Rk1 Molarity Calculator
| 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. | |||||
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Induction of apoptosis by ginsenoside Rk1 in SK-MEL-2-human melanoma.[Pubmed:22553065]
Arch Pharm Res. 2012 Mar;35(4):717-22.
Ginsenosides are active compounds isolated from Panax ginseng Meyer. Among these ginsenosides, less polar ginsenosides such as ginsenoside Rg3 and ginsenoside Rh2 have been demonstrated to have tumor inhibitory effects because of their cytotoxicity. In this study, we evaluated the apoptotic effects of Ginsenoside Rk1 in SK-MEL-2 human melanoma. Ginsenoside Rk1 isolated from red ginseng is one of the novel ginsenosides that shows strong cytotoxicity compared to ginsenoside Rg3 in dose- and time-dependent manners. The results of DNA fragmentation, 4',6-diamidino-2-phenylindole staining, and flow cytometric analysis are corroborated that Ginsenoside Rk1 induced apoptosis in SK-MEL-2 cells. Western blot analysis revealed up-regulation of Fas, FasL, and Bax protein expression and down-regulation of procaspase-8, procaspase-3, mutant p53 and Bcl-2 protein expression. These findings suggest that Ginsenoside Rk1 might be a promising compound to induce apoptosis through both extrinsic and intrinsic pathways in SK-MEL-2 cells.
Autophagy inhibition enhances apoptosis induced by ginsenoside Rk1 in hepatocellular carcinoma cells.[Pubmed:19809182]
Biosci Biotechnol Biochem. 2009 Oct;73(10):2183-9. Epub 2009 Oct 7.
Our previous study indicated that Ginsenoside Rk1 has anti-tumor activity and that its mode of action in HepG2 cells treated for 48 h involves coordinated inhibition of telomerase and induction of apoptosis. In the present study, we found that Rk1 induces both G(1) phase arrest and autophagy, but not apoptosis, at an earlier stage of treatment. A 24-h incubation of HepG2cells with Rk1 induced G(1) phase arrest. Rk1-induced autophagy was documented by the conversion of microtubule associated protein light chain 3 (LC3)-I to LC3-II, an autophagosome marker, and monodansylcadaverine (MDC) incorporation into autolysosomes. Combination of Rk1 with an autophagy inhibitor, such as bafilomycin A1 or beclin 1 siRNA, enhanced the anti-tumor effect of Rk1. These results imply that autophagy functions as a survival mechanism in HepG2 cells against Rk1-induced apoptosis. Taken together, our results support the use of autophagy inhibitors in combination with Rk1 as an effective anti-cancer regimen in HepG2 cells.
Cholesterol-derived novel anti-apoptotic agents on the structural basis of ginsenoside Rk1.[Pubmed:20971002]
Bioorg Med Chem Lett. 2010 Dec 1;20(23):7102-5.
Design and synthesis of cholesterol-derived anti-apoptotic agents were described. The synthesized cholesterol analogs designed on the structural basis of Ginsenoside Rk1 inhibited the undesirable apoptosis of human endothelial cells, which are induced by a vascular injury. In particular, analogue 1 possessing 4,6-di-O-acetyl-2,3-dideoxyhex-2-enopyran linked to hydroxyl group of cholesterol exhibited the most effective anti-apoptotic activities at both 5 and 10 mug/ml.
Anti-tumor activity of the ginsenoside Rk1 in human hepatocellular carcinoma cells through inhibition of telomerase activity and induction of apoptosis.[Pubmed:18451501]
Biol Pharm Bull. 2008 May;31(5):826-30.
The Ginsenoside Rk1 is one of major components of heat-processed Panax ginseng C. A. MEYER, Sun Ginseng (SG). Here, we investigated the mechanisms underlying the anti-tumor activity of Rk1 in human hepatocellular carcinoma HepG2 cells in vitro. Rk1 markedly inhibited telomerase activity and cell growth along with significant morphological change. The expression levels of telomerase reverse transcriptase (hTERT) and c-Myc mRNA were obviously decreased with Rk1 treatment, while that of telomerase RNA (hTR) was not. Furthermore, Rk1 induced apoptosis through activation of caspases-8 and -3. However, Fas-associated death domain (FADD) expression decreased with Rk1 treatment, though it was known that the signaling cascade of FADD was associated with caspase-8 activity. Interestingly, activation of extracellular-regulated kinase (ERK) increased with Rk1 treatment. In conclusion, these results represent the first identification of the biological activity of Rk1 against HepG2 cell growth and show that the mechanism underlying the anti-tumor activity of Rk1 involves coordination between inhibition of telomerase activity and induction of apoptosis.
