DCPIBSelective blocker of VSAC/ICl, swell. Inhibits glucose-stimulated insulin release CAS# 82749-70-0 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 82749-70-0 | SDF | Download SDF |
PubChem ID | 10071166 | Appearance | Powder |
Formula | C22H28Cl2O4 | M.Wt | 427.37 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | DMSO : ≥ 125 mg/mL (292.49 mM) *"≥" means soluble, but saturation unknown. | ||
Chemical Name | 4-[(2-butyl-6,7-dichloro-2-cyclopentyl-1-oxo-3H-inden-5-yl)oxy]butanoic acid | ||
SMILES | CCCCC1(CC2=CC(=C(C(=C2C1=O)Cl)Cl)OCCCC(=O)O)C3CCCC3 | ||
Standard InChIKey | KHKGTPJPBOQECW-UHFFFAOYSA-N | ||
Standard 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) | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Description | Potent, selective blocker of the volume-sensitive anion channel (VSAC) in rat pancreatic β-cells (IC50 ~ 2 μM) and ICl,swell in various cardiovascular tissues (IC50 = 4.1 μM in CPAE cells); blockade is voltage-independent. Displays minimal inhibition of other Cl- and K+ currents (< 10% inhibition at 10 μM). Inhibits glucose-stimulated insulin secretion in intact β-cells via VSAC inhibition and indirect KATP channel activation. Reverses cell swelling-induced action potential duration shortening in atrial myocytes and inhibits astroglial swelling in vitro. |
DCPIB Dilution Calculator
DCPIB Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.3399 mL | 11.6995 mL | 23.3989 mL | 46.7979 mL | 58.4973 mL |
5 mM | 0.468 mL | 2.3399 mL | 4.6798 mL | 9.3596 mL | 11.6995 mL |
10 mM | 0.234 mL | 1.1699 mL | 2.3399 mL | 4.6798 mL | 5.8497 mL |
50 mM | 0.0468 mL | 0.234 mL | 0.468 mL | 0.936 mL | 1.1699 mL |
100 mM | 0.0234 mL | 0.117 mL | 0.234 mL | 0.468 mL | 0.585 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
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DCPIB, a potent volume-regulated anion channel antagonist, attenuates microglia-mediated inflammatory response and neuronal injury following focal cerebral ischemia.[Pubmed:24189520]
Brain Res. 2014 Jan 13;1542:176-85.
Accumulating evidence indicates that extensive microglia activation-mediated local inflammation contributes to neuronal injury in cerebral ischemia. We have previously shown that 4-(2-butyl-6, 7-dichloro-2-cyclopentyl-indan-1-on-5-yl) oxobutyric acid (DCPIB), a potent volume-regulated anion channel (VRAC) inhibitor, suppresses pathological glutamate release and excitatory neurotoxicity in reversible middle cerebral artery occlusion (rMCAO) model in vivo. In the present study, we sought to determine whether DCPIB also attenuates microglia activation that could contribute to neuronal injury in the cerebral ischemia/reperfusion pathology. We show that oxygen-glucose deprivation (OGD) induced microglia proliferation, migration, and secretion of cytokines and all these pathological changes were effectively inhibited by DCPIB in vitro. In the microglia/neuron co-cultures, OGD induced neuronal damage was reduced markedly in the presence of DCPIB. In rat rMCAO animal model, DCPIB significantly attenuated microglia activation and neuronal death. Activation of mitogen-activated protein kinase (MAPK) signaling pathway is known to be a critical signaling pathway for microglia activation. We further explored a potential involvement of DCPIB in this pathway by western blot analysis. Under the conditions that MAPK pathway was activated either by lipopolysaccharides (LPS) or OGD, the levels of phosphorylated ERK1/2, JNK and p38 were reduced significantly in the presence of DCPIB. Altogether, our study demonstrated that DCPIB inhibits microglia activation potently under ischemic conditions both in vitro and in vivo. The DCPIB effect is likely attributable to both direct inhibition VRAC and indirect inhibition of MAPK pathway in microglia that are beneficial for the survival of neurons in cerebral ischemic conditions.
Neuroprotective effects of volume-regulated anion channel blocker DCPIB on neonatal hypoxic-ischemic injury.[Pubmed:23202801]
Acta Pharmacol Sin. 2013 Jan;34(1):113-8.
AIM: To evaluate the role of swelling-induced activation of volume-regulated anion channels (VRACs) in a neonatal hypoxic-ischemic injury model using the selective VRAC blocker 4-(2-butyl-6,7-dichloro-2-cyclopentyl-indan-1-on5-yl) oxobutyric acid (DCPIB). METHODS: Cerebral hypoxic-ischemic injury was induced in 7-day-old mouse pups with Rice-Vannucci method. Prior to the onset of ischemia, the animals were ip administered DCPIB (10 mg/kg). The animals were sacrificed 24 h afterwards, coronal sections of the brains were cut and the areas of infarct were examined using TTC staining and an image-analysis system. Cultured PC12 cells were subjected to oxygen-glucose deprivation (OGD) for 4 h. The cellular viability was assessed using Cell Counting Kit 8. Intracellular chloride concentration [Cl(-)](i) was measured using 6-methoxy-N-ethylquinolinium iodide. RESULTS: DCPIB-treated mice showed a significant reduction in hemispheric corrected infarct volume (26.65%+/-2.23%) compared to that in vehicle-treated mice (45.52%+/-1.45%, P<0.001). DCPIB-treated mice also showed better functional recovery as they were more active than vehicle-treated mice at 4 and 24 h post injury. In cultured PC12 cells, DCPIB (10 mumol/L) significantly reduced OGD-induced cell death. Moreover, DCPIB (20 mumol/L) blocked hypotonic-induced decrease in [Cl(-)](i) in PC12 cells of both control and OGD groups. CONCLUSION: The results further support the pathophysiological role of VRACs in ischemic brain injury, and suggest DCPIB as a potential, easily administrable agent targeting VRACs in the context of perinatal and neonatal hypoxic-ischemic brain injury.
The ICl,swell inhibitor DCPIB blocks Kir channels that possess weak affinity for PIP2.[Pubmed:26837888]
Pflugers Arch. 2016 May;468(5):817-24.
Inwardly rectifying K(+) (Kir) channels are important contributors to the resting membrane potential and regulate cellular excitability. The activity of Kir channels depends critically on the phospholipid PIP2. Several modulators of the activity of Kir channels alter the apparent affinity of the channel to PIP2. Channels with high apparent affinity to PIP2 may not respond to a given modulator, but mutations that decrease such affinity can render the channel susceptible to modulation. Here, we identify a known inhibitor of the swelling-activated Cl(-) current, DCPIB, as an effective inhibitor of a number of Kir channels both in native cardiac cells and in heterologous expression systems. We show that the apparent affinity to PIP2 determines whether DCPIB will serve as an efficient blocker of Kir channels. These effects are consistent with a model in which DCPIB competes with PIP2 for a common binding site.
Inhibition of gastric H+,K+-ATPase by 4-(2-butyl-6,7-dichloro-2-cyclopentylindan-1-on-5-yl)oxybutyric acid (DCPIB), an inhibitor of volume-regulated anion channel.[Pubmed:26277321]
Eur J Pharmacol. 2015 Oct 15;765:34-41.
4-(2-Butyl-6,7-dichloro-2-cyclopentylindan-1-on-5-yl)oxybutyric acid (DCPIB) has been used as an inhibitor of volume-regulated anion channel (VRAC), which is expressed in almost all cells (IC50 is around 4 microM). Here, we found that DCPIB significantly inhibited the activities of gastric proton pump (H+,K+-ATPase) in isolated gastric tubulovesicles and the membrane sample of the H+,K+-ATPase-expressing cells, and their IC50 values were around 9 microM. In the tubulovesicles, no significant expression of leucine rich repeat containing 8 family member A (LRRC8A), an essential component of VRAC, was observed. The inhibitory effect of DCPIB was also found in the membrane sample obtained from the cells in which LRRC8A had been knocked down. On the other hand, DCPIB had no significant effect on the activity of Na+,K+-ATPase or Ca2+-ATPase. In the H+,K+-ATPase-expressing cells, DCPIB inhibited the 86Rb+ transport activity of H+,K+-ATPase but not that of Na+,K+-ATPase. DCPIB had no effect on the activity of Cl- channels other than VRAC in the cells. These results suggest that DCPIB directly inhibits H+,K+-ATPase activity. DCPIB may be a beneficial tool for studying the H+,K+-ATPase function in vitro.
Inhibition of glucose-induced electrical activity in rat pancreatic beta-cells by DCPIB, a selective inhibitor of volume-sensitive anion currents.[Pubmed:15063150]
Eur J Pharmacol. 2004 Apr 5;489(1-2):13-9.
We have investigated the effects of the ethacrynic acid derivative 4-(2-butyl-6,7-dichloro-2-cyclopentyl-indan-1-on-5-yl) oxobutyric acid (DCPIB), an inhibitor of the volume-sensitive anion channel (VSAC), on electrical activity and insulin secretion in rat pancreatic beta-cells. DCPIB inhibited whole-cell VSAC currents in beta-cells with IC50 values of 2.2 and 1.7 microM for inhibition of outward and inward currents, respectively. DCPIB also inhibited the VSAC at the single channel level in cells activated by glucose. In intact cells, DCPIB caused a net increase in beta-cell input conductance and evoked an outward current that was sensitive to inhibition by tolbutamide, suggesting KATP channel activation. However, no KATP channel activation was evident under conventional whole-cell conditions, suggesting that the drug might activate the channel in intact cells via an indirect mechanism, possibly involving nutrient metabolism. DCPIB suppressed glucose-induced electrical activity in beta-cells, hyperpolarised the cell membrane potential at a substimulatory glucose concentration and prevented depolarisation when the glucose concentration was raised to stimulatory levels. The suppression of electrical activity by DCPIB was associated with a marked inhibition of glucose-stimulated insulin release from intact islets. It is concluded that DCPIB inhibits electrical and secretory activity in the beta-cell as a combined result of a reciprocal inhibition of VSAC and activation of KATP channel activities, thus producing a marked hyperpolarisation of the beta-cell membrane potential.
DCPIB is a novel selective blocker of I(Cl,swell) and prevents swelling-induced shortening of guinea-pig atrial action potential duration.[Pubmed:11724753]
Br J Pharmacol. 2001 Dec;134(7):1467-79.
1. We identified the ethacrynic-acid derivative DCPIB as a potent inhibitor of I(Cl,swell), which blocks native I(Cl,swell) of calf bovine pulmonary artery endothelial (CPAE) cells with an IC(50) of 4.1 microM. Similarly, 10 microM DCPIB almost completely inhibited the swelling-induced chloride conductance in Xenopus oocytes and in guinea-pig atrial cardiomyocytes. Block of I(Cl,swell) by DCPIB was fully reversible and voltage independent. 2. DCPIB (10 microM) showed selectivity for I(Cl,swell) and had no significant inhibitory effects on I(Cl,Ca) in CPAE cells, on chloride currents elicited by several members of the CLC-chloride channel family or on the human cystic fibrosis transmembrane conductance regulator (hCFTR) after heterologous expression in Xenopus oocytes. DCPIB (10 microM) also showed no significant inhibition of several native anion and cation currents of guinea pig heart like I(Cl,PKA), I(Kr), I(Ks), I(K1), I(Na) and I(Ca). 3. In all atrial cardiomyocytes (n=7), osmotic swelling produced an increase in chloride current and a strong shortening of the action potential duration (APD). Both swelling-induced chloride conductance and AP shortening were inhibited by treatment of swollen cells with DCPIB (10 microM). In agreement with the selectivity for I(Cl,swell), DCPIB did not affect atrial APD under isoosmotic conditions. 4. Preincubation of atrial cardiomyocytes with DCPIB (10 microM) completely prevented both the swelling-induced chloride currents and the AP shortening but not the hypotonic cell swelling. 5. We conclude that swelling-induced AP shortening in isolated atrial cells is mainly caused by activation of I(Cl,swell). DCPIB therefore is a valuable pharmacological tool to study the role of I(Cl,swell) in cardiac excitability under pathophysiological conditions leading to cell swelling.
Adenosine-stimulated astroglial swelling in cat cerebral cortex in vivo with total inhibition by a non-diuretic acylaryloxyacid derivative.[Pubmed:6267227]
J Neurosurg. 1981 Sep;55(3):364-70.
The intact cerebral cortices of cats were exposed in vivo under normothermic conditions and superfused with isotonic artificial cerebrospinal fluid containing added 0.125 mM adenosine. This resulted in chloridecation-rich cerebrocortical swelling which was shown by electron microscopy to be associated with an expanded astroglial compartment. The addition of DCPIB, a non-diuretic acylaryloxyacid analogue of ethacrynic acid and an inhibitor of coupled chloride-cation transport in cerebral cortex in vitro, totally blocked astroglial swelling and the concomitant increases in tissue ion contents. These studies support our previous experiments on the mechanism of formation of astroglial swelling. The pathological consequences of astroglial swelling and the clinical applications of these findings are discussed.