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Ginsenoside Rg1


  • Brand : BIOFRON

  • Catalogue Number : BF-G1013

  • Specification : 98%

  • CAS number : 22427-39-0

  • Formula : C42H72O14

  • Molecular Weight : 801.01

  • PUBCHEM ID : 441923

  • 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




(2R,3R,4S,5S,6R)-2-({(3S,5R,6S,8R,9R,10R,12R,13R,14R,17S)-3,12-Dihydroxy-4,4,8,10,14-pentamethyl-17-[(2S)-6-methyl-2-{[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)tetrahydro-2H-pyran-2-yl]oxy}-5-hepten-2-yl]hexadecahydro-1H-cyclopenta[a]phenanthren-6-yl}oxy)-6-(hydroxymethyl)tetrahydro-2H-pyran-3,4,5-triol/GINSENOSIDE RGL/PANAXOSIDE A/Ginsenoside Rg1/ginsenoside-Rg2/(3β,6α,12β)-20-(β-D-Glucopyranosyloxy)-3,12-dihydroxydammar-24-en-6-yl β-D-glucopyranoside/panaxosiderg1/(2R,3R,4S,5S,6R)-2-({(3S,5R,6S,8R,9R,10R,12R,13R,14R,17S)-3,12-Dihydroxy-4,4,8,10,14-pentamethyl-17-[(2S)-6-methyl-2-{[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)tetrahydro-2H-pyran-2-yl]oxy}-5-hepten-2-yl]hexadecahydro-1H-cyclopenta[a]phenanthren-6-yl}oxy)-6-(hydroxymethyl)tetrahydro-2H-pyran-3,4,5-triol/(3β,6α,12β)-20-(β-D-Glucopyranosyloxy)-3,12-dihydroxydammar-24-en-6-yl-β-D-glucopyranoside/Gensenoside Rg1/ginsenosidea2/GinsenosideRg1/Rg1/β-D-Glucopyranoside, (3β,6α,12β)-20-(β-D-glucopyranosyloxy)-3,12-dihydroxydammar-24-en-6-yl/SANCHINOSIDE C1/ginsenosideg1/ginsinoside Rg1




1.3±0.1 g/cm3


Methanol; Water; DMSO

Flash Point

497.2±34.3 °C

Boiling Point

898.5±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#:22427-39-0) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Ginsenoside Rg1, a saponin that is a primary component of ginseng, has been demonstrated to protect hearts from diverse cardiovascular diseases with regulating multiple cellular signal pathways. In the present study, we investigated the protective role of ginsenoside Rg1 on doxorubicin-induced cardiotoxicity and its effects on endoplasmic reticulum stress and autophagy. After pre-treatment with ginsenoside Rg1 (50 mg/kg i.g.) for 7 days, male C57BL/6J mice were intraperitoneally injected with a single dose of doxorubicin (6 mg/kg) every 3 days for four injections. Echocardiographic and pathological findings showed that ginsenoside Rg1 could significantly reduce the cardiotoxicity induced by doxorubicin. Ginsenoside Rg1 significantly inhibited doxorubicin-induced formation of autophagosome. At the same time, ginsenoside Rg1 decreased the doxorubicin-induced cardiac microtubule-associated protein-light chain 3 and autophagy related 5 expression. Ginsenoside Rg1 can reduce endoplasmic reticulum dilation caused by doxorubicin. Compared with the doxorubicin group, the expression of cleaved activating transcription factor 6 and inositol-requiring enzyme 1 decreased in group ginsenoside Rg1. Treatment with ginsenoside Rg1 reduces the expression of TIF1 and increases the expression of glucose-regulated protein 78. In the ginsenoside Rg1 group, the expression of p-P70S6K, c-Jun N-terminal kinases 1 and Beclin1 declined. These results indicate that ginsenoside Rg1 may improve doxorubicin-induced cardiac dysfunction by inhibiting endoplasmic reticulum stress and autophagy.


autophagy; cardiotoxicity; doxorubicin; endoplasmic reticulum stress; ginsenoside Rg1.


Ginsenoside Rg1 Prevents Doxorubicin-Induced Cardiotoxicity Through the Inhibition of Autophagy and Endoplasmic Reticulum Stress in Mice


Zhi-Meng Xu 1 , Cheng-Bin Li 2 , Qing-Ling Liu 3 , Ping Li 4 , Hua Yang 5

Publish date

2018 Nov 20




Background/aims: Ginsenoside Rg1 has been demonstrated to exhibit neuroprotective effects in various studies. This study aimed to investigate the neuronal mechanisms underlying the neuroprotective and antidepressant-like effects of ginsenoside Rg1 in a rat model of depression.
Methods: Chronic unpredictable mild stress was used to induce depression-like behaviors in rats. Transmission electron microscopy was used to observe neuronal synapses within the basolateral amygdala (BLA). The expression of microRNA (miR)-134 in the BLA was verified by real-time quantitative PCR. Finally, the synaptic plasticity-associated proteins CAMP-response element binding protein (CREB) and brain-derived neurotrophic factor (BDNF) were detected by immunoblotting.
Results: Results showed that chronic stress effectively induced depression-like behaviors in rats, which were associated with significant ultrastructural changes within BLA neurons. Moreover, chronic stress decreased the expression of miR-134 in the BLA, which was accompanied by decreased phosphorylation of CREB and decreased expression of BDNF. Remarkably, chronic administration of ginsenoside Rg1 (40 mg/kg, i.p., 5 weeks) significantly ameliorated the neuronal structural abnormalities and biochemical changes induced by chronic stress, as well as preventing depression-like behaviors in these rats.
Conclusion: Results suggested that ginsenoside Rg1 may exhibit neuroprotection and antidepressant-like effects by activating the CREB-BDNF system within the BLA in this rat model of depression. Amelioration of depression-like behaviors by ginsenoside Rg1 appears to involve modulation of the synapse-associated factor miR-134 within the BLA. Therefore, these findings demonstrate some of the neuronal mechanisms associated with depression and the therapeutic potential of ginsenoside Rg1 for use in the treatment of depression in clinical trials.


autophagy; cardiotoxicity; doxorubicin; endoplasmic reticulum stress; ginsenoside Rg1.


Ginsenoside Rg1 Prevents Chronic Stress-Induced Depression-Like Behaviors and Neuronal Structural Plasticity in Rats


Hongluan Yu 1 , Cuiqin Fan 2 , Lejin Yang 1 , Shuyan Yu 2 , Qiqi Song 2 , Peng Wang 2 , Xueqin Mao 1

Publish date





Epithelial-mesenchymal transition (EMT) is a process associated with airway remodeling in chronic obstructive pulmonary disease (COPD), which leads to progressive pulmonary destruction. Panax ginseng is a traditional herbal medicine that has been shown to improve pulmonary function and exercise capacity in patients with COPD. Ginsenoside Rg1 is one of the main active components and was shown to inhibit oxidative stress and inflammation. The present study investigated the hypothesis that ginsenoside Rg1 attenuates EMT in COPD rats induced by cigarette smoke (CS) and human bronchial epithelial (HBE) cells exposed to cigarette smoke extract (CSE). Our data showed that CS or CSE exposure increased expression of the mesenchymal marker α-smooth muscle actin (α-SMA) and decreased expression of the epithelial marker epithelial cadherin (E-cad) in both lung tissues and HBE cells, which was markedly suppressed by ginsenoside Rg1. Importantly, CS-induced upregulation of TGF-β1/Smad pathway components, including TGF-β1, TGF-βR1, phospho-Smad2, and phospho-Smad3, was also inhibited by ginsenoside Rg1. Additionally, ginsenoside Rg1 mimicked the effect of SB525334, a TGF-βR1-Smad2/3 inhibitor, on suppression of EMT in CSE-induced HBE cells. Collectively, we concluded that ginsenoside Rg1 alleviates CS-induced pulmonary EMT, in both COPD rats and HBE cells, via inhibition of the TGF-β1/Smad pathway.


Ginsenoside Rg1 Attenuates Cigarette Smoke-Induced Pulmonary Epithelial-Mesenchymal Transition via Inhibition of the TGF- β 1/Smad Pathway


Sibin Guan # 1 , Weiguo Xu # 1 , Fengfeng Han 1 , Wen Gu 1 , Lin Song 1 , Wenjing Ye 1 , Qian Liu 1 , Xuejun Guo 1

Publish date


Description :

Ginsenoside Rg1 is one of the major active components of ginseng. Ginsenoside Rg1 displays promising effects by reducing cerebral Aβ levels. Ginsenoside Rg1 also reduces NF-κB nuclear translocation.