Chenodeoxycholic Acid
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| Pack Size | Price | Availability | Quantity | Action |
|---|---|---|---|---|
| 10mM (in 1mL DMSO) | $33.00 | In Stock | 1 | |
| 100mg | $30.00 | In Stock | 1 | |
| 500mg | $42.00 | In Stock | 1 | |
| 1g | $54.00 | In Stock | 1 | |
| 5g | $78.00 | In Stock | 1 | |
| 10g | $117.00 | In Stock | 1 | |
| 25g | $187.00 | In Stock | 1 | |
| 50g | $243.00 | In Stock | 1 | |
| 100g | $306.00 | In Stock | 1 |
Citations
2 publicationsPublications de chercheurs utilisant ce produitDescription
Chenodeoxycholic Acid is a natural primary bile acid with multiple biological activities. Chenodeoxycholic Acid activates the FXR nuclear receptor to regulate cholesterol and bile acid metabolism, and simultaneously reduces inflammation by redirecting the bile acid synthesis pathway and inhibiting NF-κB/CXCL2 signaling. Chenodeoxycholic Acid can be used in research on cholesterol gallstones and cerebrotendinous xanthomatosis[1-4].
In vitro, Chenodeoxycholic Acid (0.5mM) treated Hep G2 human hepatocytes for 6h, and Chenodeoxycholic Acid significantly upregulated the mRNA levels of LDL receptor, HMG-CoA synthase, and HMG-CoA reductase[5]. Chenodeoxycholic Acid (25-200μM) treated GES-1 human gastric epithelial cells for 24h, and Chenodeoxycholic Acid inhibited cell viability, increased apoptosis rate, upregulated BAX and CDX2 protein expression, and downregulated BCL-2 protein expression[6].
In vivo, Chenodeoxycholic Acid (2.5-40mg/kg) was intraperitoneally injected into C57BL/6J mice with acute pancreatitis and severe acute pancreatitis for 3 weeks. Chenodeoxycholic Acid alleviated pancreatic histopathological injury, reduced serum amylase and lipase levels, decreased acinar cell necrosis, and relieved pancreatic necrosis[7]. Chenodeoxycholic Acid (100mg/kg) was administered by gavage to Wistar rats induced by a 35% high-fructose diet for 16 weeks. Chenodeoxycholic Acid improved serum triglycerides, very low-density lipoprotein, and uric acid levels, reduced the urinary albumin-to-creatinine ratio, decreased renal cortical triglyceride accumulation, alleviated glomerular mesangial expansion, irregular basement membrane thickening, and podocyte foot process fusion, downregulated the mRNA and protein expression of TGF-β1, PAI-I, TNF-α, IL-6, Nox2, and p22phox in kidney tissue, upregulated the mRNA and protein expression of FXR and SHP, downregulated the mRNA and protein expression of SREBP-1 and SCD-1, and improved renal fibrosis, inflammation, and oxidative stress[8].
References:
[1] Chen J, Yu Q, Patterson E, et al. Dinitroaniline Herbicide Resistance and Mechanisms in Weeds. Front Plant Sci. 2021 Mar 25;12:634018.
[2] Singh B, Yun S, Gil Y, et al. The Role of Colchicine in Plant Breeding. Int J Mol Sci. 2025 Jul 14;26(14):6743.
[3] Basit A, Lim KB. Systematic approach of polyploidy as an evolutionary genetic and genomic phenomenon in horticultural crops. Plant Sci. 2024 Nov;348:112236.
[4] Gantait S, Mukherjee E. Induced autopolyploidy-a promising approach for enhanced biosynthesis of plant secondary metabolites: an insight. J Genet Eng Biotechnol. 2021 Jan 8;19(1):4.
[5] Kawabe Y, Shimokawa T, Matsumoto A, et al. The molecular mechanism of the induction of the low density lipoprotein receptor by chenodeoxycholic acid in cultured human cells. Biochem Biophys Res Commun. 1995 Mar 8;208(1):405-11.
[6] Peng S, Sun R, Liu H,et al. Chenodeoxycholic acid triggers gastric mucosal injury by inducing apoptosis and FXR activation. PLoS One. 2025 Jul 15;20(7):e0328000.
[7] Zhu Q, Yuan C, Dong X, et al. Bile acid metabolomics identifies chenodeoxycholic acid as a therapeutic agent for pancreatic necrosis. Cell Rep Med. 2023 Dec 19;4(12):101304.
[8] Hu Z, Ren L, Wang C, et al. Effect of chenodeoxycholic acid on fibrosis, inflammation and oxidative stress in kidney in high-fructose-fed Wistar rats. Kidney Blood Press Res. 2012;36(1):85-97.
Protocole (Protocol)
| Cell experiment [1]: | |
Cell lines | GES-1 cells (human gastric epithelial cell line) |
Preparation Method | GES-1 cells were maintained in RPMI-1640 medium supplemented with 10% fetal bovine serum (FBS) at 37°C, 5% CO₂. For viability assessment, GES-1 cells were treated with Chenodeoxycholic Acid at 25, 50, 100, 200 and 400μM for 24h. For apoptosis and FXR-inhibition assays, GES-1 cells were treated with Chenodeoxycholic Acid (200μM). |
Reaction Conditions | 25–400μM, 24h |
Applications | Chenodeoxycholic Acid dose-dependently inhibited GES-1 cell viability with an IC₅₀ of 252.47μM at 24h. Chenodeoxycholic Acid (200μM, 24h) increased apoptotic rate, upregulated BAX and CDX2 protein expression while downregulating BCL-2 protein expression in GES-1 cells. |
| Animal experiment [2]: | |
Animal models | Male Wistar rats |
Preparation Method | 24 male Wistar rats (~200g) were maintained on 12h light/12h dark cycle and randomly allocated into 3 groups (n=8 per group): normal control group fed standard chow diet, high-fructose group fed 35% fructose diet, Chenodeoxycholic Acid group fed 35% fructose diet plus Chenodeoxycholic Acid (100mg/kg) via gavage once daily, control groups received equivalent volume of physiological saline via gavage. All rats were sacrificed at the end of 16-week feeding, fasting blood and spot urine were collected, kidneys were harvested for related detection. |
Dosage form | 100mg/kg; oral gavage; once daily for 16 weeks |
Applications | Chenodeoxycholic Acid reduced kidney/body weight ratio, serum triglyceride, very low density lipoprotein and uric acid levels, and urinary albumin-to-creatinine ratio in high-fructose-fed Wistar rats. Chenodeoxycholic Acid decreased renal cortical triglyceride accumulation, alleviated renal structural injuries including mesangial expansion, irregular glomerular basement membrane thickening and podocyte foot process effacement, upregulated renal FXR and SHP mRNA and protein expression while downregulating SREBP-1 and SCD-1 expression. Chenodeoxycholic Acid downregulated renal profibrotic (TGF-β1, PAI-I), proinflammatory (TNF-α, IL-6) and oxidative stress-related (Nox2, p22phox) mRNA and protein expression in high-fructose-fed Wistar rats. |
References: | |
Documents produit (Product Documents)
Propriétés chimiques (Chemical Properties)
Utilisez les solutions mères dans les 6 mois si elles sont conservées à -80°C, ou dans le mois si elles sont conservées à -20°C.
Pour améliorer la solubilité, réchauffez le tube à 37°C et soniquez-le pendant une durée appropriée.
Calculateurs (Calculators)Molarité / Dilution / Masse moléculaire / Conversion d’unités / Formulation in vivo / Solubilité
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