GSK205 is a potent, selective TRPV4 antagonist with an IC 50 of 4.19 μM for inhibiting TRPV4 -mediated Ca 2+ influx In Vitro GSK205 (100 μM) potently antagonizes TRPV4 in 3T3-F442A adipocytes, as it effectively blocks the calcium influx caused by TRPV4 agonist. ?\nGSK205 (5 μM; 4 days; T3-F442A adipocytes) treatment results in increases expression of thermogenic genes (Mcp1, Mip1α, Mcp3, Rantes and Vcam, et al.) and is also accompanied by a decrease in the proinflammatory gene program. This shift resembles the gene expression changes seen in TRPV4-deficient adipocytes. MCE has not independently confirmed the accuracy of these methods. They are for reference only. RT-PCRCell Line: T3-F442A adipocytes Concentration: 5 μM Incubation Time: 4 days Result: Resulted in increased expression of thermogenic genes and is also accompanied by a decrease in the proinflammatory gene program. In Vivo GSK205 (10 mg/kg; intraperitoneal injection; twice daily; for 7 days; for 4 weeks; male C57BL/6J mice) treatment shows significantly increases expression of thermogenic genes such as Ucp1, Pgc1a, Cidea and Cox8b. GSK205 treatment causes a reduced expression of the proinflammatory chemokines, macrophage marker and Tnfa in the EPI fat. GSK205 treatment significantly improves glucose tolerance in diet-induced obese (DIO) mice. There are no apparent sign of sickness or weight loss . ?\nGSK205 has a relatively short half-life of 2 hours in the plasma and adipose tissues . MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: Male C57BL/6J mice with high-fat diet Dosage: 10 mg/kg Administration: Intraperitoneal injection; twice daily; for 7 days Result: Caused a reduced expression of the proinflammatory chemokines, macrophage marker and Tnfa in the EPI fat. Significantly improved glucose tolerance in diet-induced obese (DIO) mice. Form:Solid IC50& Target:IC50: 4.19 μM (TRPV4)