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SML2692

DCPIB

Name: DCPIB
Brand: SIGMA

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

Sinonimo/i:

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

Formula empirica (notazione di Hill):

C₂₂H₂₈Cl₂O₄

Numero CAS:

82749-70-0

Peso molecolare:

427.36

Numero MDL:

MFCD07783995

Codice UNSPSC:

12352200

NACRES:

NA.77

product name

DCPIB, ≥98% (HPLC)

Saggio

≥98% (HPLC)

Forma fisica

powder

Colore

white to beige

Solubilità

DMSO: 2 mg/mL, clear

Temperatura di conservazione

−20°C

Stringa SMILE

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)
KHKGTPJPBOQECW-UHFFFAOYSA-N

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Azioni biochim/fisiol

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 I_Cl,_Ca; hCFTR; nor guinea pig I_Cl,PKA, I_Kr, I_Ks,I_Kl, I_Na and I_Ca. 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 I_Cl,swell at 4.1/10 μM in calf pulmonary artery endothelial (CPAE) cells vs. 4.1% inhibition of Ca²⁺-activated I_Cl,Ca or CaCC at 10 μM) with little or no inhibition against hminK (I_Ks), hCFTR, hCLC-1/2/4/5, rCLC-K1, hKv1.5, hKv4.3, HERG (≤5.9% at 10 μM; transpected xenopus oocytes), nor I_Ks, I_Kr, I_K1, I_Na, I_Ca, or I_Cl,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.

Codice della classe di stoccaggio

11 - Combustible Solids

Classe di pericolosità dell'acqua (WGK)

WGK 3

Punto d’infiammabilità (°F)

Not applicable

Punto d’infiammabilità (°C)

Not applicable

Certificati d'analisi (COA)

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Activation of volume-sensitive Cl- channel mediates autophagy-related cell death in myocardial ischaemia/reperfusion injury.

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

DCPIB is a novel selective blocker of I(Cl,swell) and prevents swelling-induced shortening of guinea-pig atrial action potential duration.

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

Injection of mRNA isolated from trophozoites of Giardia intestinalis induces expression of three types of chloride currents in Xenopus laevis oocytes.

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

Involvement of the TREK-1 channel in human alveolar cell membrane potential and its regulation by inhibitors of the chloride current.

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

LRRCA8A and ANO1 contribute to serum-induced VRAC in a Ca2+-dependent manners.

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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