12-Ketodeoxycholic acid
(Synonyms: 胆酸杂质9) 目录号 : GC60443
12-Ketodeoxycholic acid是次级胆汁酸脱氧胆酸(deoxycholic acid)的代谢产物。
Cas No.:5130-29-0
Sample solution is provided at 25 µL, 10mM.
12-Ketodeoxycholic acid is a metabolite of the secondary bile acid deoxycholic acid[1]. Bile acids are primarily synthesized from cholesterol in the liver and then secreted into the intestine through bile. In the intestine, some bile acids are metabolized by gut microbiota and reabsorbed into the liver through the enterohepatic circulation. Additionally, some bile acids and their metabolites are filtered by the kidneys and excreted in urine[2]. 12-Ketodeoxycholic acid can be used as potential metabolite biomarkers or therapeutic approaches for metabolic diseases such as atherosclerosis and non-alcoholic fatty liver disease (NAFLD)[3][4]. The level changes of 12-Ketodeoxycholic acid can also serve as a biomarker for kidney injury[5]. 12-Ketodeoxycholic acid is usually used in the research of intestinal inflammation[6].
In vitro, treatment of LPS-stimulated 293T cells with 12-Ketodeoxycholic acid (50, 75, and 100µM; 24h) significantly reduced the levels of pro-inflammatory cytokines IL-6, IL-1β, and TNF-α and increased anti-inflammatory IL-10 levels[7].
In vivo, 12-Ketodeoxycholic acid (50mg/kg/day; 7 days; oral administration) alleviated colonic inflammation, reduced the expression of pro-inflammatory cytokines IL-6, IL-1β, and TNF-α, increased anti-inflammatory IL-10 levels, and inhibited the mTORC1 signaling pathway in the colon of DSS-induced colitis mice[7].
References:
[1] Franco P, Porru E, Fiori J, et al. Identification and quantification of oxo-bile acids in human faeces with liquid chromatography-mass spectrometry: A potent tool for human gut acidic sterolbiome studies. J Chromatogr A. 2019;1585:70-81.
[2] Cai J, Rimal B, Jiang C, Chiang JYL, Patterson AD. Bile acid metabolism and signaling, the microbiota, and metabolic disease. Pharmacol Ther. 2022;237:108238.
[3] Xue J, Allaband C, Zuffa S, et al. Gut Microbiota and Derived Metabolites Mediate Obstructive Sleep Apnea Induced Atherosclerosis. Preprint. bioRxiv. 2024;2024.11.18.624205.
[4] Ahmad MI , Umair Ijaz M , Hussain M , et al. High fat diet incorporated with meat proteins changes biomarkers of lipid metabolism, antioxidant activities, and the serum metabolomic profile in Glrx1-/- mice. Food Funct. 2020;11(1):236-252.
[5] Chen H, Cao G, Chen DQ, et al. Metabolomics insights into activated redox signaling and lipid metabolism dysfunction in chronic kidney disease progression. Redox Biol. 2016;10:168-178.
[6] Feng P, Li Q, Liu L, et al. Crocetin Prolongs Recovery Period of DSS-Induced Colitis via Altering Intestinal Microbiome and Increasing Intestinal Permeability. Int J Mol Sci. 2022;23(7):3832.
[7] Zhang K, Xu Y, Zheng Y, et al. Bifidobacterium pseudolongum-Derived Bile Acid from Dietary Carvacrol and Thymol Supplementation Attenuates Colitis via cGMP-PKG-mTORC1 Pathway. Adv Sci (Weinh). 2024;11(43):e2406917.
12-Ketodeoxycholic acid是次级胆汁酸脱氧胆酸(deoxycholic acid)的代谢产物[1]。胆汁酸主要在肝脏中由胆固醇合成,随后通过胆汁分泌到肠道。在肠道中,部分胆汁酸被肠道微生物群代谢,并通过肠肝循环重吸收回肝脏。此外,部分胆汁酸及其代谢产物会通过肾脏滤过并排泄到尿液中[2]。12-Ketodeoxycholic acid可以作为代谢性疾病(如动脉粥样硬化和非酒精性脂肪性肝病,NAFLD)的潜在代谢标志物或治疗手段[3][4]。12-Ketodeoxycholic acid的水平变化也可以作为肾脏损伤的标志物[5]。12-Ketodeoxycholic acid通常用于肠道炎症相关研究[6]。
在体外实验中,用 12-Ketodeoxycholic acid( 50、75和100µM;24 小时)处理 LPS刺激的293T细胞,显著降低了促炎细胞因子IL-6、IL-1β和TNF-α的水平,并增加了抗炎细胞因子IL-10的水平[7]。
在体内实验中,12-Ketodeoxycholic acid(50mg/kg/天;连续给药7天;口服)显著减轻了DSS诱导的结肠炎小鼠的结肠炎症,降低了结肠中促炎细胞因子IL-6、IL-1β和TNF-α的表达,增加了抗炎细胞因子IL-10的水平,并抑制了mTORC1信号通路[7]。
| Cell experiment [1]: | |
Cell lines | HEK293T cells |
Preparation Method | HEK293T cells were cultured in Dulbecco’s modified eagle medium (DMEM) supplemented with 10% fetal bovine serum at 37°C in 5% CO2. Cells were maintained in a humidified incubator under standard cell culture conditions. To assess the anti-inflammatory effects of 12-Ketodeoxycholic acid, cells were stimulated with lipopolysaccharide (LPS) at a concentration of 5μg/mL for 24h. After 24h, the culture medium was replaced with LPS-free medium, and the cells were treated with different concentrations (50, 75, and 100μM) of 12-Ketodeoxycholic acid for 24h. Then cytokine levels in cell culture supernatants were determined by ELISA kits. |
Reaction Conditions | 50, 75, and 100µM; 24h |
Applications | Treatment of LPS-stimulated 293T cells with 12-Ketodeoxycholic acid significantly reduced the levels of pro-inflammatory cytokines IL-6, IL-1β, and TNF-α and increased anti-inflammatory IL-10 levels. |
| Animal experiment [1]: | |
Animal models | Seven-week-old female SPF C57BL/6J mice |
Preparation Method | Seven-week-old female SPF C57BL/6J mice were individually housed in an independent ventilation cage for 1 week to acclimatize to the laboratory environment. During this acclimatization period, mice had ad libitum access to standard rodent chow and water. To induce chemical colitis in mice, a 2.5% (wt/vol) solution of DSS with a molecular weight range of 36 000-50 000 was prepared and provided ad libitum in the drinking water. At the onset of apparent diarrhea and significant weight loss compared to the control group, the DSS treatment was discontinued and the following experimental procedures were initiated. To evaluate the therapeutic effects of 12-Ketodeoxycholic acid in DSS-induced colitis, mice were randomly allocated into three groups: a normal control group receiving regular drinking water, a DSS+PBS group receiving 3% DSS in the drinking water for 7 days followed by PBS administration every other day, and a DSS+12-Ketodeoxycholic acid group receiving 50mg/kg/d of 12-Ketodeoxycholic acid. Body weights were recorded every 2 days, and diarrhea occurrence was monitored daily. At the conclusion of the experiment, mice were euthanized, and spleen weights were recorded. Serum, colonic contents, and colonic tissues were collected for further analyses, with serum stored at -20°C and colonic contents/tissues preserved in liquid nitrogen for subsequent analyses. |
Dosage form | 50mg/kg/day; 7 days; oral administration |
Applications | 12-Ketodeoxycholic acid alleviated colonic inflammation, reduced the expression of pro-inflammatory cytokines IL-6, IL-1β, and TNF-α, increased anti-inflammatory IL-10 levels, and inhibited the mTORC1 signaling pathway in the colon of DSS-induced colitis mice. |
References: | |
| Cas No. | 5130-29-0 | SDF | |
| 别名 | 胆酸杂质9 | ||
| Canonical SMILES | C[C@H](CCC(O)=O)[C@H]([C@]12C)CC[C@@]1([H])[C@]3([H])CC[C@]4([H])C[C@H](O)CC[C@]4(C)[C@@]3([H])CC2=O | ||
| 分子式 | C24H38O4 | 分子量 | 390.56 |
| 溶解度 | DMF: 30 mg/ml,DMSO: 30 mg/ml,Ethanol: 30 mg/ml,Ethanol:PBS (pH 7.2) (1:3): 0.25 mg/ml | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液;一旦配成溶液,请分装保存,避免反复冻融造成的产品失效。 储备液的保存方式和期限:-80°C 储存时,请在 6 个月内使用,-20°C 储存时,请在 1 个月内使用。 为了提高溶解度,请将管子加热至37℃,然后在超声波浴中震荡一段时间。 |
||
| Shipping Condition | 评估样品解决方案:配备蓝冰进行发货。所有其他可用尺寸:配备RT,或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
![]() |
1 mg | 5 mg | 10 mg |
| 1 mM | 2.5604 mL | 12.8021 mL | 25.6043 mL |
| 5 mM | 512.1 μL | 2.5604 mL | 5.1209 mL |
| 10 mM | 256 μL | 1.2802 mL | 2.5604 mL |
| 第一步:请输入基本实验信息(考虑到实验过程中的损耗,建议多配一只动物的药量) | ||||||||||
| 给药剂量 | mg/kg | 动物平均体重 | g | 每只动物给药体积 | ul | 动物数量 | 只 | |||
| 第二步:请输入动物体内配方组成(配方适用于不溶于水的药物;不同批次药物配方比例不同,请联系GLPBIO为您提供正确的澄清溶液配方) | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度: mg/ml;
DMSO母液配制方法: mg 药物溶于 μL DMSO溶液(母液浓度 mg/mL,
体内配方配制方法:取 μL DMSO母液,加入 μL PEG300,混匀澄清后加入μL Tween 80,混匀澄清后加入 μL saline,混匀澄清。
1. 首先保证母液是澄清的;
2.
一定要按照顺序依次将溶剂加入,进行下一步操作之前必须保证上一步操作得到的是澄清的溶液,可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
















