2-Ketoglutaric acid
(Synonyms: α-酮戊二酸; Alpha-Ketoglutaric acid) 目录号 : GC30136
2-Ketoglutaric acid是一种可逆的酪氨酸酶抑制剂，IC50值为15 ± 0.5mM。
Cas No.:328-50-7
Sample solution is provided at 25 µL, 10mM.
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2-Ketoglutaric acid is a reversible inhibitor of tyrosinase, with an IC50 value of 15 ± 0.5mM[1]. 2-Ketoglutaric acid is naturally found in organisms and is an intermediate in the production of ATP or GTP in the Krebs cycle[2]. Widely used as an antioxidant, 2-Ketoglutaric acid reduced cyanide-induced GSH depletion and DNA damage in rat in vitro and in vivo models[3].
In vitro, 2-Ketoglutaric acid treatment at 0.1mM for 8 days promoted cell growth in C2C12 cells and decreased intracellular glucose consumption and ammonia production[4]. Pretreatment of rabbit dermal papilla cells with 6mM 2-Ketoglutaric acid for 24h alleviated the H2O2-induced decrease in cell viability, reduced ROS accumulation, and restored mitochondrial membrane potential damaged by oxidative stress[5]. Pretreatment with 5mM 2-Ketoglutaric acid for 30min significantly prevented 5mM potassium cyanide-induced cell toxicity and attenuated mitochondrial dysfunction in rat thymocytes[6].
In vivo, 2-Ketoglutaric acid treatment via oral administration at a dose of 10mg/kg/day for 14 days significantly inhibited dextran sulfate sodium-induced intestinal injury, and prevented disruption of gut microbial homeostasis in a mouse model of colitis[7]. Oral administration of 2-Ketoglutaric acid at a dose of 10mg/kg daily for 10 days helped to repair the intestinal barrier damage induced by high altitude exposure in mice[8].
References:
[1] Gou L, Lee J, Yang J M, et al. The effect of alpha-ketoglutaric acid on tyrosinase activity and conformation: Kinetics and molecular dynamics simulation study[J]. International Journal of Biological Macromolecules, 2017, 105: 1654-1662.
[2] Huergo L F, Dixon R. The emergence of 2-oxoglutarate as a master regulator metabolite[J]. Microbiology and Molecular Biology Reviews, 2015, 79(4): 419-435.
[3] Liu S, He L, Yao K. The antioxidative function of alpha‐ketoglutarate and its applications[J]. BioMed research international, 2018, 2018(1): 3408467.
[4] Yang B, Liu Y, Steinacker J M. α-Ketoglutarate stimulates cell growth through the improvement of glucose and glutamine metabolism in C2C12 cell culture[J]. Frontiers in Nutrition, 2023, 10: 1145236.
[5] Wang X, Li S, Chen J, et al. Exogenous Alpha-Ketoglutaric Acid Alleviates the Rabbit Dermal Papilla Cell Oxidative Damage Caused by Hydrogen Peroxide Through the ERK/Nrf2 Signaling Pathway[J]. Antioxidants, 2025, 14(4): 455.
[6] Bhattacharya R, Rao P V L, Vijayaraghavan R. In vitro and in vivo attenuation of experimental cyanide poisoning by α-ketoglutarate[J]. Toxicology Letters, 2002, 128(1-3): 185-195.
[7] Kim S, Jang S H, Kim M J, et al. Hybrid nutraceutical of 2-ketoglutaric acid in improving inflammatory bowel disease: Role of prebiotics and TAK1 inhibitor[J]. Biomedicine & Pharmacotherapy, 2024, 171: 116126.
[8] Sun X, Li W, Chen G, et al. Faecalibacterium duncaniae Mitigates Intestinal Barrier Damage in Mice Induced by High-Altitude Exposure by Increasing Levels of 2-Ketoglutaric Acid[J]. Nutrients, 2025, 17(8): 1380.
2-Ketoglutaric acid是一种可逆的酪氨酸酶抑制剂，IC50值为15 ± 0.5mM[1]。2-Ketoglutaric acid天然存在于生物体内，是三羧酸循环中ATP或GTP生成的关键中间体[2]。作为抗氧化剂，2-Ketoglutaric acid在大鼠体外和体内模型中能减少氰化物诱导的谷胱甘肽（GSH）耗竭和DNA损伤[3]。
在体外，0.1mM的2-Ketoglutaric acid处理C2C12细胞8天可促进细胞生长，降低细胞内葡萄糖消耗和氨产量[4]。6mM的2-Ketoglutaric acid预处理兔真皮乳头细胞24小时能缓解H2O2诱导的细胞活力下降，减少ROS积累并恢复氧化应激损伤的线粒体膜电位[5]。5mM的2-Ketoglutaric acid预处理30分钟可显著防止5mM氰化钾诱导的大鼠胸腺细胞毒性，并减轻线粒体功能障碍[6]。
在体内，2-Ketoglutaric acid以10mg/kg/day的剂量口服给药14天，可显著抑制葡聚糖硫酸钠诱导的肠道损伤，并防止结肠炎小鼠肠道微生物稳态的破坏[7]。每日口服10mg/kg剂量的2-Ketoglutaric acid（持续10天）有助于修复高海拔暴露引起的小鼠肠道屏障损伤[8]。
| Cell experiment [1]: | |
Cell lines | IPEC-J2 cells |
Preparation Method | IPEC-J2 cells were cultured in plastic culture flasks (25cm2) in DMEM-H medium containing 10% FBS, 5mM L-glutamine, 100U/mL penicillin, and 100μg/mL streptomycin. When the cells reached 80% confluence, the cells were digested with trypsin and seeded in 6-well culture plates at 8×103 cells per well in a humidified incubator at 37 °C with 5% CO2. After overnight culture, the medium was replaced with basal medium (blank control, groups 1 and 3) and basal medium plus 0.1mM H2O2 (groups 2 and 4) for 4 hours. After that, 2mM 2-Ketoglutaric acid was added to groups 3 and 4, and cells were harvested after 2 days of culture to determine cell viability. |
Reaction Conditions | 2mM; 48h |
Applications | 2-Ketoglutaric acid treatment significantly alleviated the H2O2-induced decrease in cell viability of IPEC-J2 cells. |
| Animal experiment [2]: | |
Animal models | C57BL/6 mice |
Preparation Method | Female C57BL/6 mice (8 weeks of age) were housed in an air-conditioned room (23 °C ± 2 °C) with a 12-h light/dark cycle. Mice had free access to food and water. The nutrient composition of the feed was 60.7% nitrogenous extract, 15.2% protein, 12.1% water, 5.0% mineral ash, 4.1% cellulose and 2.9% lipid. Mice were randomly divided into three groups, with 10 mice in each group: control group, 2% dextran sulfate sodium (DSS) group, and 2% DSS+ 2-Ketoglutaric acid group (10mg/kg/day). The body weight of each mouse was assessed for 3 consecutive days, and 2-Ketoglutaric acid was administered orally for 14 days. On day 7, colitis was induced by supplementing the drinking water of mice with 2% DSS for 8 consecutive days. Mice were sacrificed after 15 days, and intestinal samples were collected for analysis. |
Dosage form | 10mg/kg/day for 14 days; p.o. |
Applications | 2-Ketoglutaric acid treatment significantly inhibited DSS-induced intestinal injury and abnormal intestinal dysfunction in mice. |
References: | |
| Cas No. | 328-50-7 | SDF | |
| 别名 | α-酮戊二酸; Alpha-Ketoglutaric acid | ||
| Canonical SMILES | OC(=O)CCC(=O)C(O)=O | ||
| 分子式 | C5H6O5 | 分子量 | 146.1 |
| 溶解度 | Water : 50 mg/mL (342.23 mM) | 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。 |
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| 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 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 6.8446 mL | 34.2231 mL | 68.4463 mL |
| 5 mM | 1.3689 mL | 6.8446 mL | 13.6893 mL |
| 10 mM | 0.6845 mL | 3.4223 mL | 6.8446 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。
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Quality Control & SDS
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- Purity: >98.00%
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