20(S)-Ginsenoside Rh2CAS# 78214-33-2 |
- 20(R)-Ginsenoside Rh2
Catalog No.:BCN2484
CAS No.:112246-15-8
Quality Control & MSDS
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| Cas No. | 78214-33-2 | SDF | Download SDF |
| PubChem ID | 119307 | Appearance | White powder |
| Formula | C36H62O8 | M.Wt | 622.87 |
| Type of Compound | Triterpenoids | Storage | Desiccate at -20°C |
| Synonyms | 20(S)-Ginsenoside Rh2; 20(S)-Rh2; Ginsenoside-Rh2 | ||
| Solubility | DMSO : ≥ 300 mg/mL (481.64 mM) *"≥" means soluble, but saturation unknown. | ||
| Chemical Name | (2R,3R,4S,5S,6R)-2-[[(3S,5R,8R,9R,10R,12R,13R,14R,17S)-12-hydroxy-17-[(2S)-2-hydroxy-6-methylhept-5-en-2-yl]-4,4,8,10,14-pentamethyl-2,3,5,6,7,9,11,12,13,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthren-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)O)C)C)O)C)O)C | ||
| Standard InChIKey | CKUVNOCSBYYHIS-IRFFNABBSA-N | ||
| Standard InChI | InChI=1S/C36H62O8/c1-20(2)10-9-14-36(8,42)21-11-16-35(7)27(21)22(38)18-25-33(5)15-13-26(32(3,4)24(33)12-17-34(25,35)6)44-31-30(41)29(40)28(39)23(19-37)43-31/h10,21-31,37-42H,9,11-19H2,1-8H3/t21-,22+,23+,24-,25+,26-,27-,28+,29-,30+,31-,33-,34+,35+,36-/m0/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 Rh2 has memory-enhancing ,anti-osteoporosis, antitumor, antidiabetic, antiallergic, and anti-inflammatory effects, it potently protects ischemia-reperfusion brain injury, also inhibits prostaglandin-E_2 synthesis in lipopolysaccharide-stimulated RAW264.7 cells. It can inhibit the tendency of apoptosis, and reverse the impaired β-cell growth potential by modulating Akt/Foxo1/PDX-1 signaling pathway and regulating cell cycle proteins; it suppresses RANKL-induced osteoclast differentiation in vitro and in vivo through the regulation of c-Fos and NFATc1 expressions, not excluding the involvement of NF-κB and ERK. |
| Targets | HDAC | CDK | p21 | Caspase | MMP(e.g.TIMP) | P-gp | P450 (e.g. CYP17) | c-Fos | NFATc1 | PGE2 | Aldose reductase |
| In vitro | [Regulatory effect of ginsenoside Rh2 on HDAC1/2 activity and cyclin in human erythroleukemia K562 cells].[Pubmed: 25270209]Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2014 Oct;30(10):1062-6.To investigate the effects of the 20(S)-Ginsenoside Rh2 [Rh2(S)]on cell proliferation, histone deacetylase 1 (HDAC1) and HDAC2 activity, and expression of cyclin in human erythroleukemia K562 cells.
20S-Ginsenoside Rh2 induces apoptosis in human Leukaemia Reh cells through mitochondrial signaling pathways.[Pubmed: 24492721]Biol Pharm Bull. 2014;37(2):248-54.20(S)-Ginsenoside Rh2 (GRh2) and ginsenoside Rg3 (GRg3) are members of the protopanaxadiol family and have been investigated for possible chemopreventive activity. This study explored the biological and apoptotic mechanisms induced by 20(S)-GRh2 in human acute leukaemia line-Reh cells.
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| Kinase Assay | 20(S)-Ginsenoside Rh2 as aldose reductase inhibitor from Panax ginseng.[Pubmed: 25152999]Bioorg Med Chem Lett. 2014 Sep 15;24(18):4407-9.The root of Panax ginseng C. A. Meyer (Araliaceae) is a well-known herbal medicine in East Asia. The major bioactive metabolites in this root are commonly identified as ginsenosides.
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| Cell Research | Pharmacokinetic interactions between 20(S)-ginsenoside Rh2 and the HIV protease inhibitor ritonavir in vitro and in vivo.[Pubmed: 23892274]Acta Pharmacol Sin. 2013 Oct;34(10):1349-58.20(S)-Ginsenoside Rh2 (Rh2) has shown potent inhibition on P-glycoprotein (P-gp), while most HIV protease inhibitors are both substrates and inhibitors of P-gp and CYP3A4.
The aim of this study was to investigate the potential pharmacokinetic interactions between Rh2 and the HIV protease inhibitor ritonavir.
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20(S)-Ginsenoside Rh2 Dilution Calculator
20(S)-Ginsenoside Rh2 Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 1.6055 mL | 8.0274 mL | 16.0547 mL | 32.1094 mL | 40.1368 mL |
| 5 mM | 0.3211 mL | 1.6055 mL | 3.2109 mL | 6.4219 mL | 8.0274 mL |
| 10 mM | 0.1605 mL | 0.8027 mL | 1.6055 mL | 3.2109 mL | 4.0137 mL |
| 50 mM | 0.0321 mL | 0.1605 mL | 0.3211 mL | 0.6422 mL | 0.8027 mL |
| 100 mM | 0.0161 mL | 0.0803 mL | 0.1605 mL | 0.3211 mL | 0.4014 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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Ginsenoside Rh2 is isolated from the root of Ginseng. Ginsenoside Rh2 induces the activation of caspase-8 and caspase-9. Ginsenoside Rh2 induces cancer cell apoptosis in a multi-path manner.
In Vitro:Ginsenoside Rh2 induces the activation of two initiator caspases, caspase-8 and caspase-9 in human cancer cells. Ginsenoside Rh2 induces cancer cell apoptosis in a multi-path manner and is therefore a promising candidate for anti-tumor drug development. Ginsenoside Rh2 triggers p53-dependent Fas expression and consequent activation of caspase-8 and p53-independent caspase-9-mediated intrinsic pathway to cause cancer cell death.The cytotoxic activity of Ginsenoside Rh2 in the human tumor cell lines HeLa, SK-HEP-1, SW480, and PC-3 is assessed by MTT. The cell viability of HeLa cells is remarkably inhibited by Ginsenoside Rh2, with an IC50 value of 2.52 μg/mL, whereas SK-HEP-1 and SW480 cells are less sensitive to Ginsenoside Rh2, with IC50 values of 3.15 μg/mL and 4.06 μg/mL, respectively. PC-3 cells are the least vulnerable to Ginsenoside Rh2, with an IC50 value of 7.85 μg/mL, 3-fold higher than HeLa cells[1].
In Vivo:A total of 15 days following B16-F10 cell injection, tumor sizes from the 3 tumor bearing groups are measured. The tumor sizes in the G-L group and G-H group (G-L and G-H refer to a low or high dose of ginsenoside Rh2 injection) are reduced compared with the tumor group (P<0.05). The survival analysis reveals that the Ginsenoside Rh2 treated groups survive longer than the untreated tumor group and the effect is dose-dependent (P<0.05)[2].
References:
[1]. Guo XX, et al. p53-dependent Fas expression is critical for Ginsenoside Rh2 triggered caspase-8 activation in HeLa cells. Protein Cell. 2014 Mar;5(3):224-34.
[2]. Wang M, et al. Ginsenoside Rh2 enhances the antitumor immunological response of a melanoma mice model. Oncol Lett. 2017 Feb;13(2):681-685.
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[Regulatory effect of ginsenoside Rh2 on HDAC1/2 activity and cyclin in human erythroleukemia K562 cells].[Pubmed:25270209]
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2014 Oct;30(10):1062-6.
OBJECTIVE: To investigate the effects of the 20(S)-Ginsenoside Rh2 [Rh2(S)]on cell proliferation, histone deacetylase 1 (HDAC1) and HDAC2 activity, and expression of cyclin in human erythroleukemia K562 cells. METHODS: The K562 cells were treated with Rh2(S) at various concentrations (10-80 mumol/L). Cell proliferation activity was detected by CCK-8 assay. Flow cytometry (FCM) was used to detect cell cycle and apoptotic changes. The HDAC activity of cells was measured by chemical colorimetry. The protein expressions of HDAC1, HDAC2, cyclin D1, CDK4, p16INK4A and p21 after 48 hour-treatment of Rh2 (S) (10, 20, 40, 60 mumol/L) were examined by Western blotting. RESULTS: The proliferation of K562 cells was inhibited by Rh2 (S) (20-80 mumol/L) in dose-and time-dependent manner. FCM analyses revealed that the number of the K562 cells treated with 60 mumol/L Rh2(S) was arrested in G0/G1 phase. The apoptosis rates of K562 cells were respectively (8.09+/-0.86)%, (9.44+/-0.53)% and (22.80+/-2.16)% after induced by 20, 40, 60 mumol/L Rh2(S), which showed statistically significant difference (P<0.05) compared with the control group (2.63+/-0.14)%. HDAC activity of the cells treated with Rh2(S) (40, 60 mumol/L) was reduced. Western blotting showed that the expressions of HDAC1, HDAC2, cyclin D1 and CDK4 decreased after induced by Rh2(S), and p16INK4A, p21 proteins were enhanced significantly. CONCLUSION: The Rh2(S) can inhibit the proliferation of K562 cells and induce its cycle arrest and apoptosis through inhibiting HDAC1 and HDAC2 activity, down-regulating the expression of cyclin D1 and activating p16INK4A and p21.
Pharmacokinetic interactions between 20(S)-ginsenoside Rh2 and the HIV protease inhibitor ritonavir in vitro and in vivo.[Pubmed:23892274]
Acta Pharmacol Sin. 2013 Oct;34(10):1349-58.
AIM: 20(S)-Ginsenoside Rh2 (Rh2) has shown potent inhibition on P-glycoprotein (P-gp), while most HIV protease inhibitors are both substrates and inhibitors of P-gp and CYP3A4. The aim of this study was to investigate the potential pharmacokinetic interactions between Rh2 and the HIV protease inhibitor ritonavir. METHODS: The effects of Rh2 on the cellular accumulation and transepithelial transport of ritonavir were studied in Caco-2 and MDCK-MDR1 cells. Male rats were administered Rh2 (25 or 60 mg/kg, po) or Rh2 (5 mg/kg, iv), followed by ritonavir (25 mg/kg, po). The P-gp inhibitors verapamil (20 mg/kg, po) or GF120918 (5 mg/kg, po) were used as positive controls. The concentrations of ritonavir in plasma, bile, urine, feces and tissue homogenates were analyzed using LC-MS. RESULTS: Rh2 (10 mumol/L) significantly increased the accumulation and inhibited the efflux of ritonavir in Caco-2 and MDCK-MDR1 cells, as verapamil did. But Rh2 did not significantly alter ritonavir accumulation or transport in MDCK-WT cells. Intravenous Rh2 significantly increased the plasma exposure of ritonavir while reducing its excretion in the bile, and oral verapamil or GF120918 also increased plasma exposure of ritonavir but without changing its excretion in the bile. Interestingly, oral Rh2 at both doses did not significantly change the plasma profile of ritonavir. Moreover, oral Rh2 (25 mg/kg) significantly elevated the ritonavir concentration in the hepatic portal vein, and markedly increased its urinary excretion and tissue distribution, which might counteract the elevated absorption of ritonavir. CONCLUSION: Rh2 inhibits the efflux of ritonavir through P-gp in vitro. The effects of Rh2 on ritonavir exposure in vivo depend on the administration route of Rh2: intravenous, but not oral, administration of Rh2 significantly increased the plasma exposure of ritonavir.
20S-Ginsenoside Rh2 induces apoptosis in human Leukaemia Reh cells through mitochondrial signaling pathways.[Pubmed:24492721]
Biol Pharm Bull. 2014;37(2):248-54.
20(S)-Ginsenoside Rh2 (GRh2) and ginsenoside Rg3 (GRg3) are members of the protopanaxadiol family and have been investigated for possible chemopreventive activity. This study explored the biological and apoptotic mechanisms induced by 20(S)-GRh2 in human acute leukaemia line-Reh cells. Reh cells were treated with different concentration of 20(S)-GRh2 in vitro. Cell viability was determined by Cell Counting Kit-8 and Annexin V/7-AAD assays. Mitochondrial membrane potential (MMP) was examined through JC-1 staining. Activation of caspases associated with the mitochondria-mediated apoptosis pathway was determined by Western blot. We observed that survival of Reh cells decreased after exposure to 20(S)-GRh2 in a concentration-dependent manner. Moreover, 20(S)-GRh2 can induce mitochondria depolarization of Reh cells as evident in the shift in JC-1 fluorescence from red to green. In addition, 20(S)-GRh2 induced the release of mitochondrial cytochrome c and activation of caspase-9 and caspase-3 in Reh cells. These results indicate that 20(S)-GRh2 could induce apoptosis through the mitochondrial pathway, demonstrating its potential as a chemotherapeutic agent for leukaemia therapy.
20(S)-Ginsenoside Rh2 as aldose reductase inhibitor from Panax ginseng.[Pubmed:25152999]
Bioorg Med Chem Lett. 2014 Sep 15;24(18):4407-4409.
The root of Panax ginseng C. A. Meyer (Araliaceae) is a well-known herbal medicine in East Asia. The major bioactive metabolites in this root are commonly identified as ginsenosides. A series of ginsenosides were determined for in vitro human recombinant aldose reductase. This Letter aims to clarify the structural requirement for aldose reductase inhibition. We discovered that only ginsenoside 20(S)-Rh2 showed potent against aldose reductase, with an IC50 of 147.3 muM. These results implied that the stereochemistry of the hydroxyl group at C-20 may play an important role in aldose reductase inhibition. An understanding of these requirements is considered necessary in order to develop a new type of aldose reductase inhibitor. Furthermore, P. ginseng might be an important herbal medicine in preventing diabetic complications.
