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Ginsenoside Rb1


Catalogue Number : BF-G1007
Specification : 98%
CAS number : 41753-43-9
Formula : C54H92O23
Molecular Weight : 1109.29
PUBCHEM ID : 9898279
Volume : 20mg

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Ginsenoside rb1 (Synonyms: Gypenoside III)

Ginsenoside Rb1 (Gypenoside Ⅲ) is a protopanaxadiol that has diverse in vitro and in vivo effects, including neuroprotective, anti-inflammatory, and anti-obesity actions. Ginsenoside Rb1, a main constituent of the root of Panax ginseng, inhibits Na+, K+-ATPase activity with IC50 of 6.3±1.0 μM. Ginsenoside also inhibits IRAK-1 activation and phosphorylation of NF-κB p65. Ginsenoside Rb1 reduces the expressions of TLR3, TLR4 and TRAF-6, and down-regulates the levels of TNF-α, IFN-β and iNOS.

Catalogue Number


Analysis Method






Molecular Weight



White crystalline powder

Botanical Source

Panax ginseng,Panax notoginseng

Structure Type



Standards;Natural Pytochemical;API




gypenosideiii/(3β,12β)-20-{[6-O-(β-D-Glucopyranosyl)-β-D-glucopyranosyl]oxy}-12-hydroxydammar-24-en-3-yl 2-O-β-D-glucopyranosyl-β-D-glucopyranoside/β-D-Glucopyranoside, (3β,12β)-20-[(6-O-β-D-glucopyranosyl-β-D-glucopyranosyl)oxy]-12-hydroxydammar-24-en-3-yl 2-O-β-D-glucopyranosyl-/Ginsenoside-Rb1/arasaponine1/gynosaponinc/ginseng Rb1/Gypenoside I/ginsenoside Rb1/Panaxoside Rb1/GYPENOSIDE/panaxsaponine/GinsenosideRb1/Ginsenoside-Rb1 from Panax ginseng (Korean ginseng) root/SANCHINOSIDE E1/ginsinoside Rb1




1.4±0.1 g/cm3



Flash Point

646.8±34.3 °C

Boiling Point

1145.9±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#:41753-43-9) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Panax ginseng and Panax notoginseng, two well-known medical plants with economic value, have a long history of use for managing various diseases in Asian countries. Accumulating clinical and experimental evidence suggests that notoginsenosides and ginsenosides, which are the major bioactive components of the plants, have a variety of beneficial effects on several types of disease, including metabolic, vascular, and central nervous system disease. Considerable attention has been focused on ginsenoside Rb1 derived from their common ownership as an anti-diabetic agent that can attenuate insulin resistance and various complications. Particularly, in vitro and in vivo models have suggested that ginsenoside Rb1 exerts various pharmacological effects on metabolic disorders, including attenuation of glycemia, hypertension, and hyperlipidemia, which depend on the modulation of oxidative stress, inflammatory response, autophagy, and anti-apoptosis effects. Regulation of these pathophysiological mechanisms can improve blood glucose and insulin resistance and protect against macrovascular/microvascular related complications. This review summarizes the pharmacological effects and mechanisms of action of ginsenoside Rb1 in the management of diabetes or diabetic complications. Moreover, a multi-target effect and mechanism analysis of its antidiabetic actions were performed to provide a theoretical basis for further pharmacological studies and new drug development for clinical treatment of type 2 diabetes. In conclusion, ginsenoside Rb1 exerts significant anti-obesity, anti-hyperglycemic, and anti-diabetic effects by regulating the effects of glycolipid metabolism and improving insulin and leptin sensitivities. All of these findings suggest ginsenoside Rb1 exerts protective effects on diabetes and diabetic complications by the regulation of mitochondrial energy metabolism, improving insulin resistance and alleviating the occurrence complications, which should be further explored. Hence, ginsenoside Rb1 may be developed as a potential anti-obesity, anti-hyperglycemic, and anti-diabetic agent with multi-target effects.


diabetes; diabetic complication; ginsenoside Rb1; multi-target effects.


Ginsenoside Rb1 as an Anti-Diabetic Agent and Its Underlying Mechanism Analysis


Ping Zhou 1 2 3 4 , Weijie Xie 5 6 7 8 , Shuaibing He 9 10 11 12 , Yifan Sun 13 , Xiangbao Meng 14 15 16 17 , Guibo Sun 18 19 20 21 , Xiaobo Sun 22 23 24 25

Publish date

2019 Feb




We investigated the effect of ginsenoside Rb1 on cardiac function and remodeling in heart failure (HF). Four weeks after HF induction, the rats were administrated with ginsenoside Rb1 (35 and 70 mg/kg) and losartan (4.5 mg/kg) for 8 weeks. Losartan was used as a positive control. Cardiac function was assessed by measuring hemodynamic parameters. Histological changes were analyzed by HE and Masson’s trichrome staining. Cardiac hypertrophy, fibrosis, mitochondrial membrane potential and glucose transporter type 4 (GLUT4) levels were evaluated. In the present study, high dose of (H-) ginsenoside Rb1 decreased heart rate, improved cardiac function and alleviated histological changes induced by HF. H-ginsenoside Rb1 attenuated cardiac hypertrophy and myocardial fibrosis by decreasing left ventricular (LV) weight/heart weight ratio and cardiomyocyte cross-sectional area and reducing the levels of atrial natriuretic factor (ANF), β-myosin heavy chain (β-MHC), periostin, collagen I, Angiotensin II (Ang II), Angiotensin converting enzyme (ACE) and Ang II type 1 (AT1) receptor. Moreover, H-ginsenoside Rb1 decreased mitochondrial membrane potential and enhanced the translocation of GLUT4 to plasma membrane. The TGF-β1/Smad and ERK signaling pathways were inhibited and the Akt pathway was activated. These findings suggest that ginsenoside Rb1 might restore cardiac/mitochondrial function, increase glucose uptake and protect against cardiac remodeling via the TGF-β1/Smad, ERK and Akt signaling pathways.


diabetes; diabetic complication; ginsenoside Rb1; multi-target effects.


Ginsenoside Rb1 Improves Cardiac Function and Remodeling in Heart Failure


Xian Zheng 1 , Shuai Wang 2 , Xiaoming Zou 1 , Yating Jing 2 , Ronglai Yang 2 , Siqi Li 3 , Fengrong Wang 2

Publish date

2017 Aug 5




Atherosclerosis (AS) is characterized as progressive arterial plaque, which is easy to rupture under low stability. Macrophage polarization and inflammation response plays an important role in regulating plaque stability. Ginsenoside Rb1 (Rb1), one of the main active principles of Panax Ginseng, has been found powerful potential in alleviating inflammatory response. However, whether Rb1 could exert protective effects on AS plaque stability remains unclear. This study investigated the role of Rb1 on macrophage polarization and atherosclerotic plaque stability using primary peritoneal macrophages isolated from C57BL/6 mice and AS model in ApoE-/- mice. In vitro, Rb1 treatment promoted the expression of arginase-I (Arg-I) and macrophage mannose receptor (CD206), two classic M2 macrophages markers, while the expression of iNOS (M1 macrophages) was decreased. Rb1 increased interleukin-4 (IL-4) and interleukin-13 (IL-13) secretion in supernatant and promoted STAT6 phosphorylation. IL-4 and/or IL-13 neutralizing antibodies and leflunomide, a STAT6 inhibitor attenuated the up-regulation of M2 markers induced by Rb1. In vivo, the administration of Rb1 promoted atherosclerotic lesion stability, accompanied by increased M2 macrophage phenotype and reduced MMP-9 staining. These data suggested that Rb1 enhanced atherosclerotic plaque stability through promoting anti-inflammatory M2 macrophage polarization, which is achieved partly by increasing the production of IL-4 and/or IL-13 and STAT6 phosphorylation. Our study provides new evidence for possibility of Rb1 in prevention and treatment of atherosclerosis.


Ginsenoside Rb1; M2 macrophages; atherosclerotic plaque stability; inflammation.


Ginsenoside Rb1 Enhances Atherosclerotic Plaque Stability by Skewing Macrophages to the M2 Phenotype


Xue Zhang 1 2 , Ming-Hao Liu 1 , Lei Qiao 1 , Xin-Yu Zhang 1 , Xiao-Ling Liu 1 , Mei Dong 1 , Hong-Yan Dai 2 , Mei Ni 1 , Xiao-Rong Luan 1 , Jun Guan 2 , Hui-Xia Lu 1

Publish date

2018 Jan