产品
编 号：F493538
分子式：C27H31NO3
分子量：417.55
分子式：C27H31NO3
分子量：417.55
产品类型
规格
价格
是否有货
10mM*1mL in DMSO
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1mg
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5mg
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10mg
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25mg
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50mg
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100mg
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结构图
CAS No: 877387-37-6
产品详情
生物活性：
GSK5182 is a highly selective and orally active inverse agonist of estrogen-related receptor γ (ERRγ) with an IC50 of 79 nM. GSK5182 does not interact with other nuclear receptors, including ERRα or ERα. GSK5182 also induces reactive oxyen species (ROS) generation in hepatocellular carcinoma (HCC).
体内研究：
GSK5182 (40 mg/kg; intraperitoneal injection; every day; 25 or 30 days; db/db mice, 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.Animal Model:db/db mice (male, 7-12-week-old), diet-induced obesity (DIO) mice
Dosage:40 mg/kg
Administration:Intraperitoneal injection; every day; 30 days for db/db mice, 25 days for DIO mice
Result:Inhibited the transcriptional activity of ERRγ, suppressed hepatic glucose production through inhibition of hepatic gluconeogenesis.
体外研究：
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.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).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.
GSK5182 is a highly selective and orally active inverse agonist of estrogen-related receptor γ (ERRγ) with an IC50 of 79 nM. GSK5182 does not interact with other nuclear receptors, including ERRα or ERα. GSK5182 also induces reactive oxyen species (ROS) generation in hepatocellular carcinoma (HCC).
体内研究：
GSK5182 (40 mg/kg; intraperitoneal injection; every day; 25 or 30 days; db/db mice, 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.Animal Model:db/db mice (male, 7-12-week-old), diet-induced obesity (DIO) mice
Dosage:40 mg/kg
Administration:Intraperitoneal injection; every day; 30 days for db/db mice, 25 days for DIO mice
Result:Inhibited the transcriptional activity of ERRγ, suppressed hepatic glucose production through inhibition of hepatic gluconeogenesis.
体外研究：
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.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).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.
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