Ginsenoside Rh2 - CAS 78214-33-2
Catalog number:
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
Molecular Weight:
Ginsenoside Rh2 is a bioactive metabolite of the ginsenoside component of Panax ginseng. It is a potent anti-inflammatory and anticancer drug and exhibits antibacterial effects in vitro. It also has antitumor, antidiabetic, antiallergic effects. It inhibited the growth of cultured human UL cells in vitro. It reduced the activity of oestrogen receptor alpha (ERα) and c-Src, increased p38 MAPK activity in UL cells by using ELISA, real-time RT-PCR and Western blot methods. It increased the levels of miR-497, which bound to 3′UTR of VEGF-A mRNA to inhibit its translation. It suppressed growth of uterine leiomyomas (ULs) in a rat model and decreased serum hormone levels in a dose-dependent manner. It can suppress RANKL-induced osteoclast differentiation in vitro and in vivo through the regulation of c-Fos and NFATc1 expressions. It potently reverses memory impairment caused by scopolamine, it might improve learning deficits, also have the memory-enhancing effects of RGB. It can suppress growth of uterine leiomyoma in vitro and in vivo and may regulate ERα/c-Src/p38 MAPK activity. 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.
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(2R,3R,4S,5R,6R)-2-[[(10S,12S,14R,17S)-12-hydroxy-17-[(2R)-2-hydroxy-6 -methyl-hept-5-en-2-yl]-4,4,10,14,17-pentamethyl-2,3,5,6,7,8,9,11,12,1 3,15,16-dodecahydro-1H-cyclopenta[a]phenanthren-3-yl]oxy]-6-(hydroxyme thyl)oxane-3,4,5-triol;(3beta,12beta,20R)-12,20-Dihydroxydammar-24-en-3-yl beta-D-glucopyranoside;b-D-Glucopyranoside, (3b,12b,20R)-12,20-dihydroxydammar-24-en-3-yl;20(S)-Ginsenoside Rh2;20(S)-Rh2
10 mM in DMSO
-20°C Freezer
It is a potent anti-inflammatory and anticancer drug and exhibits antibacterial effects in vitro. It also has antitumor, antidiabetic, antiallergic effects. It potently reverses memory impairment caused by scopolamine, it might improve learning deficits, also have the memory-enhancing effects of RGB. 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.
Quality Standard:
In-house standard
Shelf Life:
2 month in rt, long time
Boiling Point:
726.4±60.0 °C | Condition: Press: 760 Torr
Melting Point:
139-144 °C
1.19±0.1 g/cm3 | Condition: Temp: 20 °C Press: 760 Torr
Canonical SMILES:
1.The Octyl Ester of Ginsenoside Rh2 Induces Lysosomal Membrane Permeabilization via Bax Translocation.
Chen F1,2, Zhang B3, Sun Y4,5, Xiong ZX6,7, Peng H8,9, Deng ZY10,11, Hu JN12,13. Nutrients. 2016 Apr 25;8(5). pii: E244. doi: 10.3390/nu8050244.
Ginsenoside Rh2 is a potential pharmacologically active metabolite of ginseng. Previously, we have reported that an octyl ester derivative of ginsenoside Rh2 (Rh2-O), has been confirmed to possess higher bioavailability and anticancer effect than Rh2 in vitro. In order to better assess the possibility that Rh2-O could be used as an anticancer compound, the underlying mechanism was investigated in this study. The present results revealed that lysosomal destabilization was involved in the early stage of cell apoptosis in HepG2 cells induced by Rh2-O. Rh2-O could induce an early lysosomal membrane permeabilization with the release of lysosomal protease cathepsins to the cytosol in HepG2 cells. The Cat B inhibitor (leu) and Cat D inhibitor (pepA) inhibited Rh2-O-induced HepG2 apoptosis as well as tBid production and Δφm depolarization, indicating that lysosomal permeabilization occurred upstream of mitochondrial dysfunction. In addition, Rh2-O induced a significant increase in the protein levels of DRAM1 and Bax (p < 0.
2.Ginsenoside Rh2 inhibits hepatocellular carcinoma through β-catenin and autophagy.
Yang Z1, Zhao T2, Liu H2, Zhang L1. Sci Rep. 2016 Jan 19;6:19383. doi: 10.1038/srep19383.
Hepatocellular carcinoma (HCC) is the most common liver cancer, with a very poor prognosis. There is an urgent need for an effective therapy for HCC. Ginsenoside Rh2 (GRh2) has been shown to significantly inhibit growth of some types of cancer, whereas its effects on HCC have not been examined. Here, we treated human HCC cells with different doses of GRh2, and found that GRh2 dose-dependently reduced HCC viability, in either CCK-8 assay or MTT assay. The effects of GRh2 on the cancer stem cells (CSCs)-like cells were determined by aldefluor flow cytometry and by tumor sphere formation, showing that GRh2 dose-dependently decreased the number of these CSCs-like cells in HCC. Autophagy-associated protein and β-catenin level were measured in GRh2-treated HCC cells by Western blot, showing that GRh2 increased autophagy and inhibited β-catenin signaling. Expression of short hairpin small interfering RNA (shRNA) for Atg7 in HCC cells completely abolished the effects of GRh2 on β-catenin and cell viability, while overexpression of β-catenin abolished the effects of GRh2 on autophagy and cell viability.
3.Esterification of Ginsenoside Rh2 Enhanced Its Cellular Uptake and Antitumor Activity in Human HepG2 Cells.
Chen F1, Deng ZY1,2, Zhang B1, Xiong ZX2, Zheng SL2, Tan CL2, Hu JN1,2. J Agric Food Chem. 2016 Jan 13;64(1):253-61. doi: 10.1021/acs.jafc.5b05450. Epub 2015 Dec 28.
Our previous research had indicated that the octyl ester derivative of ginsenoside Rh2 (Rh2-O) might have a higher bioavailability than Rh2 in the Caco-2 cell line. The aim of this study was to investigate the cellular uptake and antitumor effects of Rh2-O in human HepG2 cells as well as its underlying mechanism compared with Rh2. Results showed that Rh2-O exhibited a higher cellular uptake (63.24%) than Rh2 (36.76%) when incubated with HepG2 cells for 24 h. Rh2-O possessed a dose- and time-dependent inhibitory effect against the proliferation of HepG2 cells. The IC50 value of Rh2-O for inhibition of HepG2 cell proliferation was 20.15 μM, which was roughly half the value of Rh2. Rh2-O induced apoptosis of HepG2 cells through a mitochondrial-mediated intrinsic pathway. In addition, the accumulation of ROS was detected in Rh2-O-treated HepG2 cells, which participated in the apoptosis of HepG2 cells. Conclusively, the findings above all suggested that Rh2-O as well as Rh2 inducing HepG2 cells apoptosis might involve similar mechanisms; however, Rh2-O had better antitumor activities than Rh2, probably due to its higher cellular uptake.
4.Anti-Inflammatory Effects of Ginsenoside-Rh2 Inhibits LPS-Induced Activation of Microglia and Overproduction of Inflammatory Mediators Via Modulation of TGF-β1/Smad Pathway.
Vinoth Kumar R1, Oh TW2, Park YK3,4. Neurochem Res. 2016 May;41(5):951-7. doi: 10.1007/s11064-015-1804-x. Epub 2016 Jan 6.
Microglia activation plays an important role in neuroinflammation and contributes to several neurological disorders. Hence, inhibition of both microglia activation and pro-inflammatory cytokines may lead to the effective treatment of neurodegenerative diseases. In this study, we found that GRh2 inhibited the inflammatory response to lipopolysaccharide (LPS) and prevented the LPS-induced neurotoxicity in microglia cells. GRh2 significantly decreased the generation of nitric oxide production, and tumor necrosis factor-α, interleukin (IL)-6, IL-1β, cyclooxygenase-2 and inducible nitric oxide synthase in LPS-induced activated microglia cells. Furthermore, GRh2 (20 and 50 μM) significantly increased TGF-β1 expression and reduced the expression of Smad. These results suggest that GRh2 effectively inhibits microglia activation and production of pro-inflammatory cytokines via modulating the TGF-β1/Smad pathway.
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CAS 78214-33-2 Ginsenoside Rh2

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