DCPIB

SKU: orb1309784

Description

DCPIB

Research Area

Pharmacology & Drug Discovery

Key Properties

• CAS Number: 82749-70-0
• MW: 427.36
• Purity: 99.87%
• Formula: C₂₂H₂₈Cl₂O₄
• SMILES: CCCCC1(Cc2cc(OCCCC(O)=O)c(Cl)c(Cl)c2C1=O)C1CCCC1
• Target: Potassium Channel,Chloride channel
• Solubility: 10% DMSO+40% PEG300+5% Tween 80+45% Saline:4 mg/mL (9.36 mM);DMSO:250 mg/mL (584.99 mM)

Bioactivity

• Target IC50:
  TRESK:0.14 μM |TASK1:0.95 μM |TASK3:50.72 μM
• In Vitro:
  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.

Storage & Handling

• Storage: Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice/Shipping at ambient temperature.
• Expiration Date: 12 months from date of receipt.
• Disclaimer: For research use only

Alternative Names

Cl-Channels, Chloride channel, Chloride Channel, Chloridechannel, cardiomyocytes, COS-7, CPAE cell, Inhibitor, DCPIB, inhibit, KcsA, ischemia, PotassiumChannel, Potassium Channel, TASK-1, TASK-3, swelling, rMCAO, TRESK, VRAC

Compound Identifiers

PubChem CID

10071166