GSK5182

SKU: orb1940952

Description

GSK5182 is a highly selective inverse estrogen-related receptor γ agonist (IC50 : 79 nM) .(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.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.(In Vivo):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.

Key Properties

• CAS Number: 877387-37-6
• MW: 417.55
• Purity: >98% (HPLC)
• Formula: C₂₇H₃₁NO₃
• SMILES: CN(C)CCOc1ccc(cc1)C(\c1ccc(O)cc1)=C(\CCCO)c1ccccc1
• Target: Estrogen Receptor/ERR
• Solubility: In Vitro: DMSO : 25 mg/mL (59.87 mM)

Bioactivity

• In Vivo:
  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.
• 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. 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. Cell Proliferation Assay 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. 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 Cell line: The human hepatoma cell line PLC/PRF/5. Concentration: 10 μM, 20 μM. Incubation time: Result: Induced cell cycle arrest.

Storage & Handling

• Storage: Storage temperature: -20°C. Stability: ≥ 2 years
• Expiration Date: 12 months from date of receipt.
• Disclaimer: For research use only

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Gene Symbol

Estrogen Receptor/ERR