| Bioactivity | GSK205 is a potent, selective TRPV4 antagonist with an IC50 of 4.19 μM for inhibiting TRPV4-mediated Ca2+ influx[1][2]. |
| Target | IC50: 4.19 μM (TRPV4) |
| Invitro | GSK205 (100 μM) potently antagonizes TRPV4 in 3T3-F442A adipocytes, as it effectively blocks the calcium influx caused by TRPV4 agonist[1].GSK205 (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[1]. RT-PCR[1] Cell Line: |
| 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[1]. GSK205 has a relatively short half-life of 2 hours in the plasma and adipose tissues[1]. Animal Model: |
| Name | GSK205 |
| CAS | 1263068-83-2 |
| Formula | C24H25BrN4S |
| Molar Mass | 481.45 |
| Appearance | Solid |
| Transport | Room temperature in continental US; may vary elsewhere. |
| Storage | 4°C, sealed storage, away from moisture *In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture) |
| Reference | [1]. Ye L, et al. TRPV4 is a regulator of adipose oxidative metabolism, inflammation, and energy homeostasis. Cell. 2012 Sep 28;151(1):96-110. [2]. Kanju P, et al. Small molecule dual-inhibitors of TRPV4 and TRPA1 for attenuation of inflammation and pain. Sci Rep. 2016 Jun 1;6:26894. |