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D4068

Sigma-Aldrich

DCPIB

≥98% (HPLC), solid

Synonym(s):

4-(2-butyl-6,7-dichloro-2-cyclopentylindan-1-on-5-yl)oxybutyric acid

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About This Item

Empirical Formula (Hill Notation):
C22H28Cl2O4
CAS Number:
82749-70-0
Molecular Weight:
427.36
MDL number:
MFCD07783995
UNSPSC Code:
12352200
PubChem Substance ID:
24724462

assay

≥98% (HPLC)

form

solid

storage condition

under inert gas

color

white

solubility

DMSO: >40 mg/mL

storage temp.

2-8°C

SMILES string

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)

InChI key

KHKGTPJPBOQECW-UHFFFAOYSA-N

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Biochem/physiol Actions

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.

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Faceshields, Gloves, type P2 (EN 143) respirator cartridges

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Certificates of Analysis (COA)

Lot/Batch Number
066K46095
066K46094
066K46093
066K46092
066K46091

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Marcelo A Catalán et al.
Proceedings of the National Academy of Sciences of the United States of America, 112(7), 2263-2268 (2015-02-04)
Activation of an apical Ca(2+)-activated Cl(-) channel (CaCC) triggers the secretion of saliva. It was previously demonstrated that CaCC-mediated Cl(-) current and Cl(-) efflux are absent in the acinar cells of systemic Tmem16A (Tmem16A Cl(-) channel) null mice, but salivation
M Shen et al.
Cell death & disease, 5, e1528-e1528 (2014-11-21)
Endoplasmic reticulum (ER) stress occurring in stringent conditions is critically involved in cardiomyocytes apoptosis and cardiac contractile dysfunction (CCD). However, the molecular machinery that mediates cardiac ER stress and subsequent cell death remains to be fully deciphered, which will hopefully
Hiroya Takada et al.
Journal of cell science, 127(Pt 19), 4159-4171 (2014-08-07)
Cutaneous wound healing is accelerated by exogenous mechanical forces and is impaired in TRPC6-knockout mice. Therefore, we designed experiments to determine how mechanical force and TRPC6 channels contribute to wound healing using HaCaT keratinocytes. HaCaT cells were pretreated with hyperforin
Preeti Dohare et al.
Free radical biology & medicine, 77, 168-182 (2014-09-17)
The contribution of oxidative stress to ischemic brain damage is well established. Nevertheless, for unknown reasons, several clinically tested antioxidant therapies have failed to show benefits in human stroke. Based on our previous in vitro work, we hypothesized that the
Dobrin Draganov et al.
Scientific reports, 5, 16222-16222 (2015-11-11)
Overexpression of P2X7 receptors correlates with tumor growth and metastasis. Yet, release of ATP is associated with immunogenic cancer cell death as well as inflammatory responses caused by necrotic cell death at sites of trauma or ischemia-reperfusion injury. Using an
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