For research use only. Not for therapeutic Use.
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 (ICl,swell), with an IC50 of 4.1 μM. DCPIB is a useful tool for investigating structure-function studies of K2P channels[1][2].
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 ICl,swell and has no significant inhibitory effects on ICl,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].
LDN-212854 (intracerebroventricular infusion, 1 mM, 10 μL) suppresses microglial activation and ameliorates neuronal damage in rMCAO rats[3].
| Catalog Number | I010427 |
| CAS Number | 82749-70-0 |
| Synonyms | 4-[(2-butyl-6,7-dichloro-2-cyclopentyl-1-oxo-3H-inden-5-yl)oxy]butanoic acid |
| Molecular Formula | C22H28Cl2O4 |
| Purity | ≥95% |
| InChI | InChI=1S/C22H28Cl2O4/c1-2-3-10-22(15-7-4-5-8-15)13-14-12-16(28-11-6-9-17(25)26)19(23)20(24)18(14)21(22)27/h12,15H,2-11,13H2,1H3,(H,25,26) |
| InChIKey | KHKGTPJPBOQECW-UHFFFAOYSA-N |
| SMILES | CCCCC1(CC2=CC(=C(C(=C2C1=O)Cl)Cl)OCCCC(=O)O)C3CCCC3 |
| Reference | [1]. Lv J, et al. DCPIB, an Inhibitor of Volume-Regulated Anion Channels, Distinctly Modulates K2P Channels. ACS Chem Neurosci. 2019 Apr 17. [2]. Decher N, et al. DCPIB is a novel selective blocker of I(Cl,swell) and prevents swelling-induced shortening of guinea-pig atrial action potential duration. Br J Pharmacol. 2001 Dec;134(7):1467-79. [3]. Qingdong Han, et al. DCPIB, a potent volume-regulated anion channel antagonist, attenuates microglia-mediated inflammatory response and neuronal injury following focal cerebral ischemia. Brain Res. 2014 Jan 13;1542:176-85. |
