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Merck

SML2692

Sigma-Aldrich

DCPIB

≥98% (HPLC), powder, VRAC or VSOAC blocker

Sinónimos:

4-(2-Butyl-6,7-dichloro-2-cyclopentyl-1-oxo-2,3-dihydro-1H-inden-5-yloxy)butanoic acid, 4-[(2-Butyl-6,7-dichloro-2-cyclopentyl-2,3-dihydro-1-oxo-1H-inden-5-yl)oxy]butanoic acid, 4-(2-butyl-6,7-dichloro-2-cyclopentylindan-1-on-5-yl)oxybutyric acid

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About This Item

Fórmula empírica (notación de Hill):
C22H28Cl2O4
Número de CAS:
Peso molecular:
427.36
Número MDL:
Código UNSPSC:
12352200
NACRES:
NA.77

Nombre del producto

DCPIB, ≥98% (HPLC)

Ensayo

≥98% (HPLC)

Formulario

powder

color

white to beige

solubilidad

DMSO: 2 mg/mL, clear

temp. de almacenamiento

−20°C

cadena SMILES

CCCCC1(Cc2cc(OCCCC(O)=O)c(Cl)c(Cl)c2C1=O)C3CCCC3

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)

Clave InChI

KHKGTPJPBOQECW-UHFFFAOYSA-N

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Acciones bioquímicas o fisiológicas

DCPIB is a potent inhibitor of the volume-sensitive anion channel (VSAC). IC50 = 4.1μM
DCPIB is a potent inhibitor of the volume-sensitive anion channel (VSAC). IC50 = 4.1μM ) versus ICl,swell in calf pulmonary artery endothelial (CPAE) cells. DCPIB does not inhibit CPAE cell ICl,Ca; hCFTR; nor guinea pig ICl,PKA, IKr, IKs,IKl, INa and ICa. DCPIB inhibition is reversible and voltage independent. ICl,swell is believed to be important in cardiovascular function. Studies have been limited by the lack of specific ligands.
DCPIB is a reversible and highly selective volume-regulated anion channel (VRAC or VSOAC) blocker (by 50/98.7% of hypotonic solution-induced Cl current or ICl,swell at 4.1/10 μM in calf pulmonary artery endothelial (CPAE) cells vs. 4.1% inhibition of Ca2+-activated ICl,Ca or CaCC at 10 μM) with little or no inhibition against hminK (IKs), hCFTR, hCLC-1/2/4/5, rCLC-K1, hKv1.5, hKv4.3, HERG (≤5.9% at 10 μM; transpected xenopus oocytes), nor IKs, IKr, IK1, INa, ICa, or ICl,PKA in isolated guinea pig cardiomyocytes. When applied in rats in vivo (10 mg/kg ip.), DCPIB is shown to protect against myocardial ischaemia/reperfusion injury.

Código de clase de almacenamiento

11 - Combustible Solids

Clase de riesgo para el agua (WGK)

WGK 3

Punto de inflamabilidad (°F)

Not applicable

Punto de inflamabilidad (°C)

Not applicable


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Yuesheng Xia et al.
Oncotarget, 7(26), 39345-39362 (2016-10-26)
Excessive reactive oxygen species (ROS) plays an important role in myocardial ischemia/reperfusion (I/R) injury, which triggers not only myocardial cellular apoptosis but also autophagy-related cell death, in which volume-sensitive outwardly rectifying (VSOR) Cl- channel-activated by ROS contributes to cell apoptotic
N Decher et al.
British journal of pharmacology, 134(7), 1467-1479 (2001-11-29)
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
Arturo Ponce et al.
Physiological reports, 7(11), e14029-e14029 (2019-06-13)
Giardia lamblia is one of the most important worldwide causes of intestinal infections, yet little is known about its cellular physiology, especially the diversity of ionic channels that this parasite expresses. In this work, we show that injection of mRNA
Rita Canella et al.
Journal of cellular physiology, 234(10), 17704-17713 (2019-02-26)
K+ channels of the alveolar epithelium control the driving force acting on the ionic and solvent flow through the cell membrane contributing to the maintenance of cell volume and the constitution of epithelial lining fluid. In the present work, we analyze
Huiran Zhang et al.
Journal of pharmacological sciences, 143(3), 176-181 (2020-05-11)
The volume-regulated anion channel (VRAC) plays a central role in maintaining cell volume in response to osmotic stress. Leucine-rich repeat-containing 8A (LRRC8A) was recently identified as an essential component of VRAC although other Cl- channels were also suggested to contribute

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