Cat. No.: HY-N20708

Chiisanogenin

Chiisanogenin is an orally active triterpenoid. Chiisanogenin reduces postprandial blood glucose by promoting GLUT4 translocation and glucose uptake via activation of the IRS-1/PI3K/Akt signaling pathway. Chiisanogenin binds to MLKL and inhibits its phosphorylation and oligomerization, maintains lysosomal integrity, restores autophagic flux, and suppresses NLRP3 inflammasome activation and pyroptosis. Chiisanogenin inhibits xanthine oxidase activity and regulates oxidative stress and ion pump activity. Chiisanogenin binds to or inhibits PKA, H⁺/K⁺-ATPase and β-glucuronidase. Chiisanogenin possesses multiple pharmacological activities, including broad-spectrum antibacterial activity, anticancer, anti-inflammatory, antirheumatic, renoprotective, cardioprotective and antiarrhythmic effects. Chiisanogenin can be used in research related to type 2 diabetes, rheumatoid arthritis, myocardial injury, hepatocellular carcinoma and ventricular arrhythmia^.

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CAS No.: 89353-99-1
Formule: C₃₀H₄₄O₅
Masse moléculaire:484.68

Stockage:

Please store the product under the recommended conditions in the Certificate of Analysis.

Chiisanogenin Chemical Structure

CAS No.: 89353-99-1

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Activité biologique
- Description
- IC₅₀ & Target
- In Vitro
- Parmacokinetics
- In Vivo
Chemical Information
Pureté et documentation
Références
Calculators
Help & FAQs
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Activité biologique

Description

IC₅₀ & Target

NLRP3

GLUT4

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In Vitro

Chiisanogenin (10-40 μM; 24 h) exhibits no cytotoxicity in differentiated L6-GLUT4myc cells^[1].
Chiisanogenin (40 μM; 15 min) induces intracellular calcium influx (with an amplitude of 2.4-fold) in L6-GLUT4myc cells. This influx mainly originates from the extracellular space and can further promote AS160 phosphorylation and glucose uptake via the calcium signaling pathway^[1].
Chiisanogenin (10 μM) exhibits high permeability across Caco-2 cell monolayers without significant active efflux, with an efflux ratio of 1.31^[1].
Chiisanogenin binds to the human insulin receptor (PDB ID: 8VJB) with high affinity, with a predicted binding energy of -6.96 kcal/mol and a K_d of 0.318 μM. Its binding mode involves hydrophobic interactions and hydrogen bond formation with key residues of the receptor^[1].
Chiisanogenin (20-40 μM; 15 min) enhances glucose uptake in differentiated L6-GLUT4myc cells in a dose-dependent manner, increasing glucose uptake by 1.8-fold and 2.6-fold at concentrations of 20 μM and 40 μM, respectively^[1].
Chiisanogenin (20-40 μM; 15 min) promotes the translocation of GLUT4 to the plasma membrane in differentiated L6-GLUT4myc cells, significantly increasing the levels of GLUT4 in the plasma membrane and on the cell surface. Specifically, the plasma membrane GLUT4 levels increase by 2.1-fold and 2.3-fold at concentrations of 20 μM and 40 μM, respectively^[1].
Chiisanogenin (20-40 μM; 15 min) activates the IRS1/PI3K/Akt/AS160 insulin signaling pathway in differentiated L6-GLUT4myc cells, and this activation as well as the subsequent GLUT4 translocation depends on the activity of PI3K^[1].
Chiisanogenin (12.5-50 μM) restores normal autophagic flux in H/R-treated HK-2 cells by enhancing autophagosome synthesis and autophagosome-lysosome fusion^[3].
Chiisanogenin (12.5-50 μM) promotes the nuclear translocation of TFEB in H/R-treated HK-2 cells, enhances autophagosome-lysosome fusion, and restores autophagy-lysosome homeostasis^[3].
Chiisanogenin (12.5-50 μM; 2 h) maintains the integrity of lysosomal membranes in H/R-treated HK-2 cells, prevents CTSB leakage, and inhibits subsequent NLRP3 inflammasome activation and pyroptosis^[3].
Chiisanogenin (12.5-50 μM; 2 h) inhibits H/R-induced pyroptosis in HK-2 cells by suppressing NLRP3 inflammasome activation, as well as downstream GSDMD cleavage, cytokine release and membrane damage^[3].
Chiisanogenin (12.5-50 μM; 2 h for Co-IP; 12 h for CETSA) binds directly to MLKL with high affinity, inhibits its phosphorylation and oligomerization, and disrupts its interaction with LAMP1, thereby preventing lysosomal membrane damage in H/R-treated HK-2 cells^[3].
Chiisanogenin (12.5-50 μM; 48 h) inhibits TGF-β1-induced fibrotic transdifferentiation and inflammatory response in HK-2 cells by negatively regulating the MLKL signaling pathway^[3].
Chiisanogenin (up to 100 μM) exhibits no anti-rotavirus activity in MA-104 cells^[4].
Chiisanogenin (0.2-0.5 mg/mL) exhibits in vitro cytotoxicity against P-388, L-1210, A549 and SNU C4 tumor cell lines, with ED₅₀ values ranging from 0.2 to 0.5 mg/mL, and shows the strongest activity against SNU C4 cells^[4].
Chiisanogenin (6.25-200 μM) exhibits low cytotoxicity against normal L02 hepatocytes, with only a slight decrease in cell viability observed at 200 μM, and it dose-dependently inhibits the growth of HepG2 hepatocellular carcinoma cells^[8].
Chiisanogenin (overnight) exhibits broad-spectrum antibacterial activity against Bacillus subtilis ATCC 6633 (MIC = 50 μg/mL), Staphylococcus epidermidis ATCC 12228, Staphylococcus aureus ATCC 65389, Proteus vulgaris ATCC 3851, and Salmonella typhimurium ATCC 14028 (all with an MIC of 100 μg/mL), but shows no inhibitory effect on *Escherichia coli* ATCC 35218 (>200 μg/mL)^[5]. Chiisanogenin (12.5-100 μM; 2 h) potently protects HK-2 cells against H/R-induced injury, with 25 μM being the optimal concentration for cytoprotection^[3].
Chiisanogenin binds to MLKL with high affinity in cell-free molecular docking assays, forming specific and stable interactions with key active site residues^[3].
Chiisanogenin (0.5 mg/mL) weakly inhibits β-glucuronidase, potently inhibits partially purified rat gastric H⁺/K⁺-ATPase with an IC₅₀ of 0.5 mg/mL, and shows no inhibitory effect on HP urease at concentrations up to 0.5 mg/mL^[4].
Chiisanogenin (5.00-500 ng/mL) can be reliably quantified in spiked rat plasma using this UPLC-MS/MS method. It shows linearity within the range of 5.00-500 ng/mL, with an LLOQ of 5.00 ng/mL, precision below 11%, accuracy within 8%, and good stability under sample processing and storage conditions^[6].
Chiisanogenin (5-800 μM; 24 h) exerts no significant effect on the viability of H9c2 rat cardiomyocytes at concentrations up to 100 μM, promotes cell proliferation at 50 μM, and inhibits cell viability at concentrations of 200 μM and above^[7].
Pretreatment with chiisanogenin (2.5-50 μM; 2 h pretreatment followed by 24 h aconitine exposure) significantly increases the survival rate of H9c2 rat cardiomyocytes damaged by aconitine within the concentration range of 2.5 μM to 50 μM, though its protective effect is weaker than that of divaroside^[7].
Chiisanogenin (20 μmol/L; 24 h) significantly inhibits TNF-α-induced proliferation of HFLS-RA cells, with no cytotoxicity observed within this concentration range^[9].
Chiisanogenin (0-1000 μM for 24 h) exhibits low cytotoxicity against H9c2 rat cardiomyocytes, showing no obvious toxicity at concentrations up to 50 μM, while significantly inhibiting cell viability at 400 μM and higher concentrations^[10].
Chiisanogenin (50 μM; 2 h pre-incubation; 24 h co-incubation with 50 μM BaCl₂) significantly protects H9c2 rat cardiomyocytes against cytotoxic damage induced by 50 μM BaCl₂^[10].
Chiisanogenin exhibits high binding affinity for PKA with a predicted binding energy of -7.8 kcal/mol, indicating the superiority of its ligand-receptor interaction^[10].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Viability Assay^[1]

Cell Line:

differentiated L6-GLUT4myc rat skeletal muscle cells
Concentration:

10, 20 and 40 μM
Incubation Time:

24 h
Result:

Maintained >95% cell viability relative to control at all tested concentrations.

Western Blot Analysis^[1]

Cell Line:

differentiated L6-GLUT4myc rat skeletal muscle cells
Concentration:

20 and 40 μM
Incubation Time:

15 min
Result:

Increased total GLUT4 in the plasma membrane fraction by 2.1-fold at 20 μM relative to control.
Increased total GLUT4 in the plasma membrane fraction by 2.3-fold at 40 μM relative to control.

Western Blot Analysis^[1]

Cell Line:

differentiated L6-GLUT4myc rat skeletal muscle cells
Concentration:

20 and 40 μM
Incubation Time:

15 min
Result:

Increased phosphorylation of IRS1 (Tyr612), PI3K (Tyr458), Akt (Thr308), and AS160 (Thr642).
Inhibited chiisanogenin-induced phosphorylation of PI3K, Akt, and AS160, and reduced GLUT4 levels in the plasma membrane when pretreated with wortmannin.

Western Blot Analysis^[1]

Cell Line:

differentiated L6-GLUT4myc rat skeletal muscle cells
Concentration:

40 μM
Incubation Time:

15 min
Result:

Increased AS160 phosphorylation.
Reduced chiisanogenin-induced AS160 phosphorylation when pretreated with BAPTA-AM.

Cell Viability Assay^[3]

Cell Line:

human proximal tubular epithelial HK-2 cells (exposed to hypoxia/reoxygenation (H/R) injury)
Concentration:

12.5, 25, 50 and 100 μM
Incubation Time:

2 h (pretreatment before H/R injury)
Result:

Exhibited the most significant cytoprotective effect against H/R-induced injury compared to other candidate compounds.
Provided optimal protection at 25 μM with stable, consistent effects and no observable toxicity or morphological abnormalities.
Showed reduced efficacy at higher doses (e.g., 50 μM) due to mild compound-induced cytotoxicity.

Cell Viability Assay^[7]

Cell Line:

H9c2 rat cardiomyocytes (non-injury baseline)
Concentration:

5 μM, 10 μM, 25 μM, 50 μM, 100 μM, 200 μM, 400 μM and 800 μM
Incubation Time:

24 h
Result:

Showed no significant effect on cell viability at concentrations up to 100 μM compared to the control group.
Significantly promoted cell proliferation at 50 μM (p < 0.01).
Significantly inhibited cell viability at 200 μM, 400 μM, and 800 μM (p < 0.01 or p < 0.001).

Cell Viability Assay^[7]

Cell Line:

aconitine-injured H9c2 rat cardiomyocytes
Concentration:

2.5 μM, 5 μM, 10 μM, 25 μM and 50 μM
Incubation Time:

2 h (pretreatment); 24 h (aconitine exposure)
Result:

Significantly increased the viability of aconitine-injured H9c2 cells at all tested concentrations (p < 0.01 or p < 0.001).
Exhibited a relatively weak protective effect compared to divaroside (DVS).

Cell Viability Assay^[9]

Cell Line:

TNF-α-induced human fibroblast-like synoviocyte rheumatoid arthritis (HFLS-RA) cells
Concentration:

20 μmol/L
Incubation Time:

24 h
Result:

Significantly inhibited the proliferation of TNF-α-induced HFLS-RA cells, with cell proliferation activity percentage within the range of 53.73 to 94.4% compared to the TNF-α induction group.
Showed no toxicity to HFLS-RA cells.

Cell Cytotoxicity Assay^[10]

Cell Line:

H9c2 rat cardiomyocytes
Concentration:

0, 2.5, 5, 10, 25, 50, 100, 200, 400, 800 and
1000 μM
Incubation Time:

24 h
Result:

Exhibited no inhibitory effect on H9c2 cell viability and did not affect cell proliferation at concentrations up to 50 μM.
Significantly inhibited H9c2 cell viability at concentrations of 400 μM and above.

Cell Cytotoxicity Assay^[10]

Cell Line:

BaCl₂-injured H9c2 rat cardiomyocytes
Concentration:

50 μM
Incubation Time:

2 h pre-incubation; 24 h co-incubation with 50 μM BaCl₂
Result:

Significantly protected H9c2 cells against cytotoxicity induced by 50 μM BaCl₂.

Parmacokinetics

Species	Dose	Route	C_max	T_max	T_1/2	AUC_0-t	AUC_0-∞
Rat^[6]	2 mg/kg	p.o.	89.8 ng/mL	1.83 h	3.66 h	359.6 ng·h/mL	402.2 ng·h/mL

In Vivo

Chiisanogenin (250-500 mg/kg; p.o.; single dose) dose-dependently lowers postprandial blood glucose levels in mice, with 250 mg/kg and 500 mg/kg doses reducing peak postprandial glucose by 32% and 46%, respectively^[1].
Chiisanogenin (10-30 mg/kg; p.o.; daily; 7 days) exerts dose-dependent antiinflammatory effects in carrageenan-induced rat edema, with 30 mg/kg reducing paw edema by 30.4% at 3 hours, reducing dye leakage by 50.1%, inhibiting trypsin activity by 37.1%, and attenuating oxidative stress markers^[2].
Chiisanogenin (50-200 mg/kg; i.g.; daily; 7 days) attenuates the AKI-to-CKD transition and chronic renal fibrosis in male C57BL/6 mice by regulating MLKL-mediated inflammatory responses, with efficacy comparable to NAC^[3].
Chiisanogenin (25 mg/kg; i.p.; single dose; 30 minutes before arrhythmia induction) exerts potent anti-arrhythmic activity in BaCl₂-induced ventricular arrhythmia in rats, reducing total arrhythmia duration to 59.33 seconds and normalizing oxidative stress markers and myocardial ion pump activities^[10].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:

ICR mice (female, 5 weeks old, 18–22 g) were orally administered D-(+)-glucose (2 g/kg in PBS) to induce postprandial hyperglycemia^[1]
Dosage:

250 mg/kg; 500 mg/kg
Administration:

p.o.; single dose
Result:

Reduced postprandial blood glucose levels by 32% at 30 minutes after glucose challenge (250 mg/kg dose) compared to the control group.
Reduced postprandial blood glucose levels by 46% at 30 minutes after glucose challenge (500 mg/kg dose) compared to the control group.
Confirmed significant reductions in overall blood glucose levels via area under the curve (AUC) analysis for both doses relative to the control group.

Animal Model:

Sprague-Dawley (4-week-old male, 250–300 g, carrageenan-induced hind paw edema)^[2]
Dosage:

10 mg/kg; 30 mg/kg
Administration:

p.o.; daily; 7 days
Result:

Reduced paw edema by 30.4% at 3 hours post-carrageenan injection at 30 mg/kg.
Reduced pontamine sky blue dye leakage into the peritoneal cavity by 37.5% and inhibited trypsin activity by 27.4% at 10 mg/kg.
Reduced pontamine sky blue dye leakage into the peritoneal cavity by 50.1% and inhibited trypsin activity by 37.1% at 30 mg/kg.
Reduced serum lipid peroxide levels to 50.0 nmole/mL MDA, hydroxy radical levels to 5.51 nmole/mg protein, and increased serum SOD activity to 2.97 units/mg protein at 10 mg/kg.
Reduced serum lipid peroxide levels to 41.8 nmole/mL MDA, hydroxy radical levels to 5.08 nmole/mg protein, and increased serum SOD activity to 3.21 units/mg protein at 30 mg/kg.
Reduced RA factor from 10 to 6 and CRP factor from 10 to 7 at 10 mg/kg.
Reduced RA factor to 5 and CRP factor to 5 at 30 mg/kg.
Reduced hepatic XO activity to 11.7 nmoles uric acid/mg protein/min, increased SOD activity to 4.98 units/mg protein, GPX activity to 1.69 nmoles NADPH oxidized/mg protein/min, and catalase activity to 170.7 nmoles H2O2 dissipated/mg protein at 10 mg/kg.
Reduced hepatic XO activity to 10.8 nmoles uric acid/mg protein/min, increased SOD activity to 6.17 units/mg protein, GPX activity to 1.90 nmoles NADPH oxidized/mg protein/min, and catalase activity to 183.5 nmoles H2O2 dissipated/mg protein at 30 mg/kg.

Animal Model:

C57BL/6 (male, 20–22 g, SPF conditions) underwent left nephrectomy followed by 40 min of right renal pedicle clamping to induce renal ischemia, then the clamp was released for reperfusion.^[3]
Dosage:

50 mg/kg; 100 mg/kg; 200 mg/kg
Administration:

i.g.; daily; 7 days
Result:

Significantly reversed IRI-induced elevations in serum creatinine and blood urea nitrogen levels at 100 mg/kg, with efficacy equivalent to MLKL siRNA knockdown and comparable to positive control NAC.
Significantly reduced acute renal injury pathological scores and suppressed expression of renal injury markers KIM-1 and NGAL.
Reversed IRI-induced increases in p-MLKL levels and downregulation of LAMP1, promoted nuclear translocation of TFEB, alleviated accumulation of LC3-II and p62, and restored autophagic flux.
Inhibited IRI-induced pyroptosis, reducing extracellular LDH release, lowering IL-1β and IL-18 levels, suppressing cytosolic CTSB leakage, and blocking activation of the NLRP3/GSDMD-N axis.
Significantly reduced IRI-induced elevations in serum creatinine and blood urea nitrogen levels at 14 days postreperfusion.
Significantly decreased interstitial collagen deposition (measured via Masson's trichrome and Sirius red staining) and downregulated expression of fibrotic markers α-SMA, fibronectin, and Collagen I, with efficacy comparable to positive control NAC.

Animal Model:

Wistar rats (male, SPF grade, 220-250 g, ventricular arrhythmia induced by BaCl₂)^[10]
Dosage:

25 mg/kg
Administration:

i.p.; single dose; 30 minutes before arrhythmia induction
Result:

Shortened the total duration of ventricular arrhythmia to 59.33 seconds, the duration of ventricular premature contractions to 5 seconds, and the duration of ventricular tachycardia to 54.33 seconds (all p < 0.001).
Increased serum SOD levels and decreased serum MDA levels (p < 0.001).
Increased myocardial Na⁺-K⁺-ATPase (p < 0.01) and Ca²⁺-Mg²⁺-ATPase (p < 0.01) activities.
Reduced myocardial cell disorder, interstitial edema, and focal vacuolar degeneration compared with the model group.

Chemical Information

CAS No. 89353-99-1
Masse moléculaire 484.68
Formule C₃₀H₄₄O₅
SMILES

C[C@]12[C@]3([C@](C)([C@H](C(C)=C)CC1)[C@H](O)CC(=O)O[C@@]3(C[C@]4([C@@]2(C)CC[C@]5(C(O)=O)[C@@]4([C@H](C(C)=C)CC5)[H])[H])[H])[H]
Structure Classification
- Steroids
Initial Source
Livraison

Room temperature in continental US; may vary elsewhere.
Stockage

Please store the product under the recommended conditions in the Certificate of Analysis.

Pureté et documentation

Instruction de manipulation (2659 KB)

Références

[1]. Kwon EB, et al. Chiisanogenin enhances glucose uptake and lowers blood glucose via insulin signaling activation. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie. 2025 Aug;189:118281. [Content Brief]

[2]. Jung HJ, et al. Antiinflammatory effects of chiisanoside and chiisanogenin obtained from the leaves of Acanthopanax chiisanensis in the carrageenan- and Freund's complete adjuvant-induced rats. Journal of ethnopharmacology. 2005 Feb 28;97(2):359-67. [Content Brief]

[3]. Qu S, et al. Chiisanogenin Targets MLKL to Restore Autophagy and Suppress Pyroptosis in Renal Ischemia-Reperfusion Injury. Journal of agricultural and food chemistry. 2026 Jun 10;74(22):17099-17128. [Content Brief]

[4]. Bae EA, et al. Metabolism of chiisanoside from Acanthopanax divaricatus var. albeofructus by human intestinal bacteria and its relation to some biological activities. Biological & pharmaceutical bulletin. 2001 May;24(5):582-5. [Content Brief]

[5]. Lee S, et al. Antibacterial compounds from the leaves of Acanthopanax senticosus. Archives of pharmacal research. 2003 Jan;26(1):40-2. [Content Brief]

[6]. Yang C, et al. Determination and pharmacokinetic study of chiisanogenin in rat plasma by ultra performance liquid chromatography-tandem mass spectrometry. Phytochemical analysis : PCA. 2011;22(3):225-9. [Content Brief]

[7]. Wang H, et al. Potential Myocardial Protection of 3,4-seco-Lupane Triterpenoids from Acanthopanax sessiliflorus Leaves. Chemistry & biodiversity. 2021 Jan;18(1):e2000830. [Content Brief]

[8]. Wang H, et al. Cytotoxic and anti-tumor effects of 3,4-seco-lupane triterpenoids from the leaves of Eleutherococcus sessiliflorus against hepatocellular carcinoma. Nat Prod Res. 2022 Feb;36(4):1062-1066. [Content Brief]

[9]. Liu Y, et al. Triterpenoids from the leaves of Eleutherococcus sessiliflorus, and their antiproliferative activities in TNF-α induced HFLS-RA cells. Phytochemistry. 2024 Jul;223:114133. [Content Brief]

[10]. Zhao Y, et al. Protective Effects of 3,4-Seco-Lupane Triterpenes from Food Raw Materials of the Leaves of Eleutherococcus Senticosus and Eleutherococcus Sessiliflorus on Arrhythmia Induced by Barium Chloride. Chemistry & biodiversity. 2021 Apr;18(4):e2001021. [Content Brief]

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Chiisanogenin

Voir tous les produits spécifiques à Isoform PI3K

Voir tous les produits spécifiques à Isoform Akt

Voir tous les produits spécifiques à Isoform NOD-like Receptor (NLR)

Voir tous les produits spécifiques à Isoform PKA

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Activité biologique

Chemical Information

Pureté et documentation

Références

Calculators

Help & FAQs

Chiisanogenin Related Classifications

HY-N20708 Related Classifications