DCPIB

DCPIB is a selective, reversible and potent inhibitor of volume-regulated anion channels (VRAC). DCPIB voltage-dependently activates potassium channels TREK1 and TRAAK, and inhibits TRESK, TASK1 and TASK3 (IC₅₀s: 0.14, 0.95, 50.72 μM, respectively). DCPIB is also a selective blocker of swelling-induced chloride current (I_Cl,swell), with an IC₅₀ of 4.1 μM. DCPIB is a useful tool for investigating structure-function studies of K2P channels^[1][2]. IC50 & Target: IC50：0.14 μM (TRESK), 0.95 μM (TASK1), 50.72 μM (TASK3)^[1], 4.1 μM (I_Cl,swell, CPAE cells)^[2] In Vitro: DCPIB (10 μM) activates TREK1 and enhances TRAAK currents in COS-7 cells^[1].
DCPIB (10 μM) prominently and reversibly suppresses TRESK currents in COS-7 cells, with an IC₅₀ of 0.14 μM^[1].
DCPIB (10 μM) displays selectivity for I_Cl,swell and has no significant inhibitory effects on I_Cl,Ca in CPAE cells^[2].
DCPIB (10 μM, 5 min) has no effect on attenuate subsequent swelling in cardiomyocytes^[2].
DCPIB (10 μM, 3 h) inhibits LPS-induced MAPK activation in BV2 cells^[3].
In Vivo: LDN-212854 (intracerebroventricular infusion, 1 mM, 10 μL) suppresses microglial activation and ameliorates neuronal damage in rMCAO rats^[3].