DCPIB

Research use only, not for human use.

DCPIB, a known specific and potent inhibitor of volume-regulated anion channels (VRAC),DCPIB displayed superior selectivity toward TRESK with an IC50 of 0.14 μM, demonstrating at least 100-fold higher affinity over TREK1/TRAAK channels. DCPIB, a known specific and potent inhibitor of volume-regulated anion channels (VRAC), has been reported to activate TREK1 and TREK2 in astrocytes and in vitro recently.

DCPIB, a known specific and potent inhibitor of volume-regulated anion channels (VRAC),DCPIB displayed superior selectivity toward TRESK with an IC50 of 0.14 μM, demonstrating at least 100-fold higher affinity over TREK1/TRAAK channels. DCPIB, a known specific and potent inhibitor of volume-regulated anion channels (VRAC), has been reported to activate TREK1 and TREK2 in astrocytes and in vitro recently. In the present study, we demonstrated DCPIB also voltage dependently activated TRAAK besides TREK1/TREK2, showing DCPIB activated all TREK subfamily members. In contrast, the compound potently inhibited several other K2P channels with no voltage dependence, including TRESK, TASK1, and TASK3. DCPIB displayed superior selectivity toward TRESK with an IC50 of 0.14 μM, demonstrating at least 100-fold higher affinity over TREK1/TRAAK channels. Furthermore, the impaired ion selectivity filter region greatly impaired the activating effect of DCPIB on TREK1 but not the inhibitory effect of DCPIB on TRESK. This indicates distinct molecular determinants underlying the effect of DCPIB on TREK1 or TRESK channels. DCPIB played diverse effects on K2P channels and could be a useful tool for further investigating structure-function studies of K2P channels.

Immunofluorescence Cell Line:BV2 cells Concentration:10 μM Incubation Time:3 h Result:Significantly decreased Ki67 positive staining microglia and pro-inflammatory cytokine (TNF-α, IL-1β) secretion.Western Blot Analysis Cell Line:BV2 cells Concentration:10 μM Incubation Time:3 h Result:Inhibited migratory potential of transient OGD (Oxygen-glucose deprivation) exposed BV2 cells.

Animal Model:Reversible middle cerebral artery occlusion (rMCAO) model Dosage:1 mM, 10 μL Administration:Administered manually for 20s by intracerebroventricular infusion Result:Diminished Pyramidal neurons injury induced by rMCAO in the CA1 region.

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Membrane Transporter/Ion Channel

Chloride Channel

VRAC|TRESK|TASK-1|TASK-3

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82749-70-0

427.36

C22H28Cl2O4

>98% (HPLC)

DMSO:125 mg/mL (292.49 mM)

O=C(O)CCCOC1=CC2=C(C(C(C3CCCC3)(CCCC)C2)=O)C(Cl)=C1Cl

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(-20℃)

With Ice Pack

≥ 2 years