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Ginsenoside Rk1
ChemFaces products have been cited in many studies from excellent and top scientific journals
Product Name Ginsenoside Rk1
Price: $188 / 20mg
CAS No.: 494753-69-4
Catalog No.: CFN92644
Molecular Formula: C42H70O12
Molecular Weight: 767.0 g/mol
Purity: >=98%
Type of Compound: Triterpenoids
Physical Desc.: Powder
Source: The roots of Panax ginseng C. A. Mey.
Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
Download: COA    MSDS    SDF    Manual
Similar structural: Comparison (Web)  (SDF)
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Related Screening Libraries
Size /Price /Stock 10 mM * 100 uL in DMSO / Inquiry / In-stock
10 mM * 1 mL in DMSO / Inquiry / In-stock
Related Libraries
Biological Activity
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:
Arch Pharm Res. 2012 Mar;35(4):717-22.
Induction of apoptosis by ginsenoside Rk1 in SK-MEL-2-human melanoma.[Pubmed: 22553065]
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.
METHODS AND RESULTS:
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.
CONCLUSIONS:
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.
Biol Pharm Bull. 2008 May;31(5):826-30.
Anti-tumor activity of the ginsenoside Rk1 in human hepatocellular carcinoma cells through inhibition of telomerase activity and induction of apoptosis.[Pubmed: 18451501]
The Ginsenoside Rk1 is one of major components of heat-processed Panax ginseng C. A. MEYER, Sun Ginseng (SG).
METHODS AND RESULTS:
Here, we investigated the mechanisms underlying the anti-tumor activity of Ginsenoside 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 Ginsenoside Rk1 treatment, while that of telomerase RNA (hTR) was not. Furthermore, Ginsenoside Rk1 induced apoptosis through activation of caspases-8 and -3. However, Fas-associated death domain (FADD) expression decreased with Ginsenoside 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 Ginsenoside Rk1 treatment.
CONCLUSIONS:
In conclusion, these results represent the first identification of the biological activity of Ginsenoside Rk1 against HepG2 cell growth and show that the mechanism underlying the anti-tumor activity of Ginsenoside Rk1 involves coordination between inhibition of telomerase activity and induction of apoptosis.
Toxicology . 2019 Apr 15;418:22-31.
Ginsenoside Rk1 induces cell cycle arrest and apoptosis in MDA-MB-231 triple negative breast cancer cells[Pubmed: 30797898]
Ginsenoside Rk1 (Rk1) is a component found in processed ginseng that exhibits anti-insulin resistance, anti-inflammation and anti-cancer activities. However, there are few reports of Rk1 activity against triple negative breast cancer (TNBC). In this study, the anti-proliferation and potential mechanisms of Rk1 in MDA-MB-231 cells were investigated. Xenograft model exhibited that Rk1 significantly repressed tumor growth with low toxicity to major organs. Moreover, Rk1 dramatically inhibited cell proliferation, colony formation, promoted LDH release, and induced G0/G1 phase arrest. Rk1 also triggered intracellular reactive oxygen species (ROS) generation and mitochondrial membrane potential reduction. Western blot results revealed that Rk1 increased the expression of Bax, cytochrome C, cleaved caspase 3, 8 and 9 levels and decreased Bcl-2 level and blocked the PI3K/Akt pathway. Pretreatment with the pan-caspase inhibitor Z-VAD-FMK, PI3K/Akt pathway activator insulin or ROS scavenger N-acetylcysteine (NAC) further demonstrated that ROS/PI3K/Akt pathway was responsible for Rk1-induced apoptosis. Overall, this is the first study to illustrate the anti-triple negative breast cancer effects and mechanisms of Rk1 and Ginsenoside Rk1 could be a new promising anti-tumor drug for TNBC.
PeerJ . 2017 Nov 17;5:e3993.
Ginsenoside Rk1 bioactivity: a systematic review[Pubmed: 29158964]
Ginsenoside Rk1 (G-Rk1) is a unique component created by processing the ginseng plant (mainly Sung Ginseng (SG)) at high temperatures. The aim of our study was to systematically review the pharmacological effects of G-Rk1. We utilized and manually searched eight databases to select in vivo and in vitro original studies that provided information about biological, pharmaceutical effects of G-Rk1 and were published up to July 2017 with no restriction on language or study design. Out of the 156 papers identified, we retrieved 28 eligible papers in the first skimming phase of research. Several articles largely described the G-Rk1 anti-cancer activity investigating "cell viability", "cell proliferation inhibition", "apoptotic activity", and "effects of G-Rk1 on G1 phase and autophagy in tumor cells" either alone or in combination with G-Rg5. Others proved that it has antiplatelet aggregation activities, anti-inflammatory effects, anti-insulin resistance, nephroprotective effect, antimicrobial effect, cognitive function enhancement, lipid accumulation reduction and prevents osteoporosis. In conclusion, G-Rk1 has a significant anti-tumor effect on liver cancer, melanoma, lung cancer, cervical cancer, colon cancer, pancreatic cancer, gastric cancer, and breast adenocarcinoma against in vitro cell lines. In vivo experiments are further warranted to confirm these effects.
Chin J Nat Med . 2017 Oct;15(10):751-757.
Ginsenoside Rk1 suppresses pro-inflammatory responses in lipopolysaccharide-stimulated RAW264.7 cells by inhibiting the Jak2/Stat3 pathway[Pubmed: 29103460]
The saponin Ginsenoside Rk1 is a major compound isolated from ginseng. Ginsenoside Rk1 has been reported to have anti-inflammatory and anti-tumor properties and to be involved in the regulation of metabolism. However, the effect and mechanism of anti-inflammatory action of Ginsenoside Rk1 has not been fully clarified. We investigated whether Ginsenoside Rk1 could suppress the inflammatory response in lipopolysaccharide-stimulated RAW264.7 macrophages and to explore its mechanism of the action. RAW264.7 cells were treated with LPS (1 μg·mL-1) in the absence or the presence of Ginsenoside Rk1 (10, 20, and 40 μmol·L-1). Then the inflammatory factors were tested with Griess reagents, ELISA, and RT-PCR. The proteins were analyzed by Western blotting. Ginsenoside Rk1 inhibited lipopolysaccharide-induced expression of nitric oxide (NO), interleukin (IL)-6, IL-1β, tumor necrosis factor (TNF)-α, and monocyte chemotactic protein (MCP)-1. Ginsenoside Rk1 inhibited the lipopolysaccharide-stimulated phosphorylation of NF-κB and janus kinase (Jak)2 and signal transducer and activator of transcription (Stat)3 at Ser727 and Tyr705. These data suggested that Ginsenoside Rk1 could inhibit expression of inflammatory mediators and suppress inflammation further by blocking activation of NF-κB and the Jak2/Stat3 pathway in LPS-stimulated RAW264.7 cells.
Ginsenoside Rk1 Description
Source: The roots of Panax ginseng C. A. Mey.
Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

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After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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Cell. 2018 Jan 11;172(1-2):249-261.e12.
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Calculate Dilution Ratios(Only for Reference)
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 need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
Protocol
Cell Research:
Biosci Biotechnol Biochem. 2009 Oct;73(10):2183-9.
Autophagy inhibition enhances apoptosis induced by ginsenoside Rk1 in hepatocellular carcinoma cells.[Pubmed: 19809182]
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.
METHODS AND RESULTS:
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.
CONCLUSIONS:
Taken together, our results support the use of autophagy inhibitors in combination with Rk1 as an effective anti-cancer regimen in HepG2 cells.
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.
METHODS AND RESULTS:
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 μg/ml.
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