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Ginsenoside Rg2


  • Brand : BIOFRON

  • Catalogue Number : BF-G1014

  • Specification : 98%

  • CAS number : 52286-74-5

  • Formula : C42H72O13

  • Molecular Weight : 785.01

  • PUBCHEM ID : 21599924

  • Volume : 20mg

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Catalogue Number


Analysis Method






Molecular Weight



White crystalline powder

Botanical Source

Panax ginseng,Panax notoginseng

Structure Type



Standards;Natural Pytochemical;API




CHIKUSETSUSAPONIN I/(3β,6α,12β)-3,12,20-Trihydroxydammar-24-en-6-yl-2-O-(6-deoxy-α-L-mannopyranosyl)-β-D-glucopyranoside/(3β,6α,12β)-3,12,20-Trihydroxydammar-24-en-6-yl 2-O-(6-deoxy-α-L-mannopyranosyl)-β-D-glucopyranoside/Ginsenoside Rg2/(2S,3R,4R,5R,6S)-2-{[(2R,3R,4S,5S,6R)-2-({(3S,5R,6S,8R,9R,10R,12R,13R,14R,17S)-3,12-Dihydroxy-17-[(2S)-2-hydroxy-6-methyl-5-hepten-2-yl]-4,4,8,10,14-pentamethylhexadecahydro-1H-cyclopenta[a]phenanthren-6-yl}oxy)-4,5-dihydroxy-6-(hydroxymethyl)tetrahydro-2H-pyran-3-yl]oxy}-6-methyltetrahydro-2H-pyran-3,4,5-triol/GINSENOSIDE Rg2(SH)/mannopyranosyl)/β-D-Glucopyranoside, (3β,6α,12β)-3,12,20-trihydroxydammar-24-en-6-yl 2-O-(6-deoxy-α-L-mannopyranosyl)-/Ginsenoside 20(s)-Rg2/GinsesideRg2/GinsenosideRg2/(2S,3R,4R,5R,6S)-2-{[(2R,3R,4S,5S,6R)-2-({(3S,5R,6S,8R,9R,10R,12R,13R,14R,17S)-3,12-Dihydroxy-17-[(2S)-2-hydroxy-6-methyl-5-hepten-2-yl]-4,4,8,10,14-pentamethylhexadecahydro-1H-cyclopenta[a]phenanthren-6-yl}oxy)-4,5-dihydroxy-6-(hydroxymethyl)tetrahydro-2H-pyran-3-yl]oxy}-6-methyltetrahydro-2H-pyran-3,4,5-triol/anaxatriol/PROSAPOGENIN C2/iGInsenoside Rg2




1.3±0.1 g/cm3



Flash Point

486.6±34.3 °C

Boiling Point

881.0±65.0 °C at 760 mmHg

Melting Point


InChl Key

WGK Germany


HS Code Reference


Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:52286-74-5) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Alzheimer’s disease (AD) is one of the most debilitating neurodegenerative diseases in an aging population. Excessive accumulation of β-amyloid (Aβ) has been proposed as a pivotal event in the pathogenesis of AD. Ginsenoside Rg2 has been reported to exert neuroprotective effects. However, the underlying mechanism for its neuroprotection is not well-understood. In this study, we investigated the protective effects of ginsenoside Rg2 on Aβ25-35-induced neurotoxicity in PC12 cells and identified a potential molecular signaling pathway involved. The results showed that pretreatment of PC12 cells with ginsenoside Rg2 followed by Aβ25-35 increased cell viability in a concentration-dependent manner compared to cells that were not pretreated. In addition, ginsenoside Rg2 pretreatment attenuated Aβ25-35-induced increases in the release of lactate dehydrogenase, the intracellular calcium concentration, and levels of reactive oxygen species. Pretreatment with ginsenoside Rg2 increased the Bcl-2/Bax ratio. Moreover, ginsenoside Rg2 attenuated the cleavage of caspase-3 induced by Aβ25-35 thereby improving cell survival. Ginsenoside Rg2 significantly enhanced the phosphorylation of Akt in PC12 cells. Additionally, pretreatment with the phosphoinositide 3-kinase (PI3K) inhibitor, LY294002, completely abolished the protective effects of ginsenoside Rg2 against Aβ25-35-induced neuronal cell apoptosis. These findings unambiguously suggested that the protective effect of ginsenoside Rg2 against Aβ25-35-induced apoptosis in PC12 cells was associated with enhancement of the PI3K/Akt signaling pathway.

Copyright © 2017 Elsevier B.V. All rights reserved.


Alzheimer's disease; Ginsenoside Rg2; PC12 cells; Phosphoinositide 3-kinase/Akt; β-amyloid


Ginsenoside Rg2 protects PC12 cells against β-amyloid25-35-induced apoptosis via the phosphoinositide 3-kinase/Akt pathway.


Cui J1, Wang J2, Zheng M3, Gou D2, Liu C4, Zhou Y5.

Publish date

2017 Sep 25




Ginsenoside Rg2 is one of the specific ginsenosides in red ginseng, and has been reported to exhibit protective effects against neurotoxicity and memory impairment, and also inhibition of hepatic glucose production. However, the effect of Rg2 on the prevention of obesity has not been investigated. In this study, we evaluated the anti-obesity and anti-adipogenic effects of Rg2 in high-fat diet-induced obese mice (HFD mice) and 3T3-L1 preadipocytes. Oral administration of Rg2 (10 mg kg-1) to HFD mice significantly decreased body weight gain, total triglycerides, and free fatty acid levels. In 3T3-L1 preadipocytes, Rg2 (80 μM) inhibited adipocyte differentiation and reduced the accumulation of intracellular lipids. Quantitative PCR and western blot analysis revealed that Rg2 decreased the expression levels of adipogenic transcription factors (PPARγ, C/EBPα, and SREBP1-c), and then regulated target genes such as acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS). Rg2 significantly promoted AMP-activated protein kinase (AMPK) both in vivo and in vitro, which is known to suppress adipogenesis. It was also found that pretreating with compound C, a typical inhibitor of AMPK, attenuated the inhibitory effect of Rg2 on AMPK phosphorylation. These findings suggested that Rg2-induced activation of AMPK leads to a decrease in the expression of adipogenic transcription factors, and suppression of adipogenesis in vivo and in vitro. Hence, Rg2 has the potential for the development of healthy foods and the prevention of obesity.


Ginsenoside Rg2 inhibits adipogenesis in 3T3-L1 preadipocytes and suppresses obesity in high-fat-diet-induced obese mice through the AMPK pathway.


Liu H 1, Liu M , Jin Z , Yaqoob S , Zheng M , Cai D , Liu J , Guo S .

Publish date

2019 Jun 19




Ginsenoside Rg2 has been previously reported to reduce glucose production and adipogenesis in adipose tissue. However, the effects of ginsenosides Rg2 on hepatic lipid metabolism remain vacant. In this study, we found that ginsenoside Rg2 treatment significantly attenuated oleic acid and palmitic acid (OA&PA)-induced intracellular lipid deposition and oxidative stress in mouse primary hepatocytes. C57BL/6J mice that are fed with a high-fat diet (HFD) and treated with ginsenosides Rg2 displayed decreased body weight, reversed hepatic steatosis, and improved glucose tolerance and insulin sensitivity. Ginsenoside Rg2 administration significantly ameliorated HFD-induced hepatic oxidative stress and apoptosis. Moreover, Ginsenoside Rg2 had a good affinity with Sirtuin1 (SIRT1) and regulated its expression in vivo and in vitro. Deficiency of SIRT1 eliminated the therapeutic effect of ginsenoside Rg2 on lipid accumulation and overproduction of reactive oxygen species (ROS) in OA&PA-induced mice primary hepatocytes. Ginsenoside Rg2 treatment failed to alter the lipid and glucose disorder in hepatic SIRT1 deficient mice feeding on HFD. SIRT1 deficiency dissolves the therapeutic effect of ginsenoside Rg2 on oxidative stress and hepatocyte apoptosis induced by HFD. In summary, ginsenoside Rg2 plays a therapeutic role in HFD-induced hepatosteatosis of mice by decreasing the lipogenesis process and improving antioxidant capacity in an SIRT1-dependent manner.


SIRT1; antioxidant; ginsenosides Rg2; lipid metabolism; non-alcoholic fatty liver disease


Ginsenoside Rg2 Ameliorates High-Fat Diet-Induced Metabolic Disease through SIRT1.


Cheng B1,2, Gao W1, Wu X3, Zheng M4, Yu Y5, Song C1, Miao W1, Yang Z6, He Y1, Liu C7, Yang W8, Yang X4, Li Y1, Zhang F3, Gao Y1,2.

Publish date

2020 Apr 8

Description :

Ginsenoside Rg2 is one of the major active components of ginseng. Ginsenoside Rg2 acts as a NF-κB inhibitor. Ginsenoside Rg2 also reduces Aβ1-42 accumulation.