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Chikusetsu saponin IVa


  • Brand : BIOFRON

  • Catalogue Number : BF-C1007

  • Specification : 98%

  • CAS number : 51415-02-2

  • Formula : C42H66O14

  • Molecular Weight : 794.98

  • PUBCHEM ID : 13909684

  • Volume : 20mg

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Catalogue Number


Analysis Method






Molecular Weight



White crystalline powder

Botanical Source

herbs of Hemsleya amabilis Diels

Structure Type



Standards;Natural Pytochemical;API




Chikusetsusaponin/Chikusetsusaponin Iva/1-O-[(3α,5ξ,9ξ)-3-(β-D-Glucopyranuronosyloxy)-28-oxoolean-12-en-28-yl]-β-D-glucopyranose/GLUCOPYRANOSIDURONIC ACID/Silphioside G/Chikusetsu saponin Ⅳa/β-D-Glucopyranose, 1-O-[(3α,5ξ,9ξ)-3-(β-D-glucopyranuronosyloxy)-28-oxoolean-12-en-28-yl]-/β-D-Glucopyranose, 1-O-[(3β)-3-(β-D-glucopyranuronosyloxy)-28-oxoolean-12-en-28-yl]-/Chikusetsu Saponin IVa/1-O-[(3β)-3-(β-D-Glucopyranuronosyloxy)-28-oxoolean-12-en-28-yl]-β-D-glucopyranose/Calenduloside F/Chikusetsusaponin IV


(2S,3S,4S,5R,6R)-6-[[(3S,4aR,6aR,6bS,8aS,12aS,14aR,14bR)-4,4,6a,6b,11,11,14b-heptamethyl-8a-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxycarbonyl-1,2,3,4a,5,6,7,8,9,10,12,12a,14,14a-tetradecahydropicen-3-yl]oxy]-3,4,5-trihydroxyoxane-2-carboxylic acid


1.4±0.1 g/cm3


Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.

Flash Point

255.6±27.8 °C

Boiling Point

873.3±65.0 °C at 760 mmHg

Melting Point

218-220 ºC (methanol , water )



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#:51415-02-2) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Inhalation anesthetics isoflurane may increase the risk of neurotoxicity and cognitive deficiency at postnatal and childhood. Chikusetsu saponin IVa (chIV) is a plant extract compound, which could possessed extensive pharmacological actions of central nervous system, cardia-cerebrovascular system, immunologic system and treatment and prevention of tumor. In our study, we investigated the neuroprotective effect of chIV on isoflurane-induced hippocampal neurotoxicity and cognitive function impairment in neonatal rats. ChIV or saline intraperitoneal injected into seven-day old rats 30 min prior to isoflurane exposure. We found that, anesthesia with 1.8% isoflurane for 6 h significantly decreased the expression of SIRT1 in hippocampus. ChIV increased SIRT1, p-ERK1/2, PSD95 level in hippocampus, decreased hippocampal neuron apoptosis and lactate dehydrogenase (LDH) release after isoflurane exposure. Furthermore, chIV improved adolescent spatial memory of rats after their neonatal exposure to isoflurane by Morris Water Maze (MWM) test. In addition, SIRT1 inhibitor sirtinol decreased the expression of SIRT1 and its downstream of p-ERK1/2. Taken together, our date suggested that chIV could ameliorate isoflurane-induced neurotoxicity and cognitive impairment. The neuroprotective effect of chIV might be associated with up-regulation of SIRT1/ERK1/2. Moreover, chIV appeared to be a potential therapeutic target for isoflurane induced developmental neurotoxicity as well as subsequent cognitive impairment.


Chikusetsu saponin IVa; SIRT1; hippocampus; isoflurane; neurotoxicity


Chikusetsu saponin IVa attenuates isoflurane-induced neurotoxicity and cognitive deficits via SIRT1/ERK1/2 in developmental rats.


Fang X1, Han Q1, Li S1, Zhao Y1, Luo A1.

Publish date

2017 Sep 15




Hyperglycemia-induced reactive oxygen species (ROS) generation and Ca(2+) overload contribute to the development of diabetic cardiomyopathy. In this study, we aimed to study the protective effects of Chikusetsu saponin IVa (CHS) from Aralia taibaiensis against hyperglycemia-induced myocardial injuries. Treatment of H9c2 cells with high glucose (HG) for 24 h resulted in a loss of cell viability and increase of ROS, LDH and Ca(2+) levels, and also induced cell apoptosis, and those changes were all markedly reversed by the administration of CHS. In further studies, CHS dose-dependently increased the expression of Homer1a, ERK1/2 and SIRT1 in both H9c2 cells and rat primary cardiomyocytes. However, transfection of Homer1a-specific siRNA abolished the ability of CHS in controlling the ROS and Ca(2+) homeostasis. Moreover, specific SIRT1 inhibitors or siRNA significantly suppressed the enhanced phosphorylation of ERK1/2 and expression of Homer1a induced by CHS as well as its cytoprotective effect. CHS induced Homer1a expression was also suppressed by siERK1/2. Additionally, results in diabetic mice also showed that CHS protected myocardium from I/R-introduced apoptosis by activating the SIRT1/ERK1/2/Homer1a pathway. These results demonstrated that CHS protected against hyperglycemia-induced myocardial injury through SIRT1/ERK1/2 and Homer1a pathway in vivo and in vitro


Chikusetsu saponin IVa confers cardioprotection via SIRT1/ERK1/2 and Homer1a pathway.


Duan J1, Yin Y1, Wei G1, Cui J1, Zhang E2, Guan Y1, Yan J1, Guo C1, Zhu Y1, Mu F1, Weng Y1, Wang Y1, Wu X1, Xi M1, Wen A1.

Publish date

2015 Dec 9




Chronic metabolic inflammation in adipose tissue plays an important role in the development of obesity-associated diseases. Our previous study indicated that total saponins of Panax japonicus (SPJ) rhizoma and Chikusetsu saponin V, one main component of SPJ, could exert the anti-oxidative and anti-inflammatory effects. The present study aimed to investigate the in vivo and Ex vivo anti-inflammatory activities of another main component of SPJ, namely Chikusetsu saponin IVa (CS). CS could significantly inhibited HFD-induced lipid homeostasis, and inhibited inflammation in adipose tissue, as reflected by the decreased mRNA expression levels of inflammation-related genes and secretion of the chemokines/cytokines, inhibited the accumulation of adipose tissue macrophages (ATMs) and shifted their polarization from M1 to M2, suppressed HFD-induced expression of NLRP3 inflammasome component genes and decreased IL-1β and Caspase-1 production in mice. Moreover, CS treatment also inhibited the activation of NLRP3 inflammasome in bone marrow-derived macrophages (BMDMs). Meanwhile, CS treatment inhibited an NLRP3-induced ASC pyroptosome formation and lipopolysaccharide (LPS)-induced pyroptosis. Furthermore, CS treatment suppressed HFD-induced NF-κB signaling in vivo and LPS-induced NF-κB activation as reflected by the fact that their phosphorylated forms and the ratios of pNF-κB/NF-κB, pIKK/IKK, and pIκB/IκB were all decreased in EAT from HFD-fed mice treated with CS as compared with those of HFD mice. Taking together, this study has revealed that CS effectively inhibits HFD-induced inflammation in adipose tissue of mice through inhibiting both NLRP3 inflammasome activation and NF-κB signaling. Thus, CS can serve as a potential therapeutic drug in the prevention and treatment of inflammation-associated diseases.


ASC pyroptosome; Chikusetsu saponin IVa; NF-κB signaling; NLRP3 inflammasome; adipose tissue inflammation


Chikusetsu saponin IVa ameliorates high fat diet-induced inflammation in adipose tissue of mice through inhibition of NLRP3 inflammasome activation and NF-κB signaling.


Yuan C1, Liu C1, Wang T1, He Y1, Zhou Z1, Dun Y1, Zhao H1, Ren D1, Wang J2, Zhang C1, Yuan D2.

Publish date

2017 May 9

Description :

Chikusetsusaponin IVa a major active ingredient of triterpenoid saponins, exerts antithrombotic effects, including minor hemorrhagic events. This appears to be important for the development of new therapeutic agents. a novel AMPK activator that is capable of bypassing defective insulin signalling and could be useful for the treatment of T2DM or other metabolic disorders.IC50 Value: 199.4 ± 9.1 μM (inhibiting thrombin-induced fibrinogen clotting) Target: In vitro: Using biochemical and pharmacological methods, it proves that chikusetsusaponin IVa prolongs the recalcification time, prothrombin time, activated partial thromboplastin time, and thrombin time of normal human plasma in a dose-dependent manner; inhibits the amidolytic activity of thrombin and factor Xa upon synthetic substrates S2238 and S2222; inhibits thrombin-induced fibrinogen clotting (50% inhibition concentration, 199.4 ± 9.1 μM); inhibits thrombin- and collagen-induced platelet aggregation. Chikusetsusaponin IVa can also preferentially inhibits thrombin in a competitive manner (K(i)=219.6 μM) [1]. Chikusetsusaponin IVa suppresses the production of iNOS, COX-2, IL-1β, IL-6, and TNF-α in LPS-stimulated THP-1 cells likely by inhibiting NF-κB activation and ERK, JNK, and p38 signal pathway phosphorylation [2].In vivo: Studies were performed on type 2 diabetic mellitus (T2DM) rats given CHS for 28 days to test the antihyperglycemic activity. Oral administration of CHS dose-dependently increased the level of serum insulin and decreased the rise in blood glucose level [3].