GSK5182 是一种高效选择性，具有口服活性的ERRγ反向激动剂，其IC50值为 79 nM。GSK5182 不与其他核受体相互作用，包括 ERRα 和 ERα。GSK5182 还能增加肝癌细胞中reactive oxyen species (ROS)的产生。
| 生物活性 | GSK5182 is a highly selective and orally active inverse agonist ofestrogen-related receptor γ (ERRγ)with anIC50of 79 nM. GSK5182 does not interact with other nuclear receptors, includingERRαorERα. GSK5182 also inducesreactive oxyen species (ROS)generation in hepatocellular carcinoma (HCC)[1][2][3]. |
| IC50& Target | ERRγ 79 nM (IC50) | Reactive Oxygen Species |
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体外研究
(In Vitro) | GSK5182 (0-20 μM; 0-hours; PLC/PRF/5 cells) treatment leads to a significant and dose-dependent reduction in the number of proliferating PLC/PRF/5 cells[1].
GSK5182 (0-20 μM; 24 hours; PLC/PRF/5 cells) treatment also causes a dose-dependent increase in the expression of p21 and p27 while at the same time reducing the level of phosphorylated retinoblastoma protein (p-pRb)[1].
GSK5182 (10-20 μM; PLC/PRF/5 cells) treatment induces cell cycle arrest at G1 phase, which in turn induces a corresponding dose-dependent reduction in the percentage of cells in S phase[1].
Cell Proliferation Assay[1] | Cell Line: | The human hepatoma cell line PLC/PRF/5 | | Concentration: | 0 μM, 10 μM, 20 μM | | Incubation Time: | 0 hour, 24 hours, 48 hours, 72 hours | | Result: | Led to a significant and dose-dependent reduction in the number of proliferating PLC/PRF/5 cells. |
Western Blot Analysis[1] | Cell Line: | The human hepatoma cell line PLC/PRF/5 | | Concentration: | 0 μM, 10 μM, 20 μM | | Incubation Time: | 24 hours | | Result: | Caused a dose-dependent increase in the expression of p21 and p27 while at the same time reducing the level of p-pRb. |
Cell Cycle Analysis[1] | Cell Line: | The human hepatoma cell line PLC/PRF/5 | | Concentration: | 10 μM, 20 μM | | Incubation Time: | | | Result: | Induced cell cycle arrest. |
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体内研究
(In Vivo) | GSK5182 (40 mg/kg; intraperitoneal injection; every day; 25 or 30 days;db/dbmice, diet-induced obesity mice) specifically inhibits the transcriptional activity of ERRγ, and suppresses hepatic glucose production through inhibition of hepatic gluconeogenesis. GSK5182 elicits anti-diabetic effects in mouse models via negative regulation of the hepatic gluconeogenesis program. GSK5182 normalizes hyperglycemia mainly through inhibition of hepatic glucose production[3].
| Animal Model: | db/dbmice (male, 7-12-week-old), diet-induced obesity (DIO) mice[3] | | Dosage: | 40 mg/kg | | Administration: | Intraperitoneal injection; every day; 30 days fordb/dbmice, 25 days for DIO mice | | Result: | Inhibited the transcriptional activity of ERRγ, suppressed hepatic glucose production through inhibition of hepatic gluconeogenesis. |
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| 运输条件 | Room temperature in continental US; may vary elsewhere. |
| 储存方式 | | Powder | -20°C | 3 years | | 4°C | 2 years | | In solvent | -80°C | 6 months | | -20°C | 1 month |
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| 溶解性数据 | In Vitro: DMSO : 25 mg/mL(59.87 mM;ultrasonic and warming and heat to 80℃) 配制储备液 | 1 mM | 2.3950 mL | 11.9749 mL | 23.9498 mL | | 5 mM | 0.4790 mL | 2.3950 mL | 4.7900 mL | | 10 mM | 0.2395 mL | 1.1975 mL | 2.3950 mL |
*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℃, 6 months; -20℃, 1 month。-80℃ 储存时，请在 6 个月内使用，-20℃ 储存时，请在 1 个月内使用。 |
