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9-Anthracenecarboxylic acid

$63

  • Brand : BIOFRON

  • Catalogue Number : BN-O1078

  • Specification : 98%(HPLC)

  • CAS number : 723-62-6

  • Formula : C15H10O2

  • Molecular Weight : 222.24

  • PUBCHEM ID : 2201

  • Volume : 5mg

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Catalogue Number

BN-O1078

Analysis Method

Specification

98%(HPLC)

Storage

-20℃

Molecular Weight

222.24

Appearance

Powder

Botanical Source

Structure Type

Category

SMILES

C1=CC=C2C(=C1)C=C3C=CC=CC3=C2C(=O)O

Synonyms

9-Anthroic acid/9-Carboxyanthracene/ANCA/anthracene-9-carboxylic acid/9-Anthracene carboxylic acid/anthracenecarboxylic acid/9-Anthracenecarboxylic acid/Polyoxyethylenesorbitan monolaurate

IUPAC Name

Density

1.3±0.1 g/cm3

Solubility

Flash Point

206.1±14.8 °C

Boiling Point

467.5±14.0 °C at 760 mmHg

Melting Point

213-217 °C(lit.)

InChl

InChl Key

XGWFJBFNAQHLEF-UHFFFAOYSA-N

WGK Germany

RID/ADR

HS Code Reference

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:723-62-6) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.

PMID

28668303

Abstract

The role of Ca2+-activated Cl- current (ICl(Ca)) in cardiac arrhythmias is still controversial. It can generate delayed afterdepolarizations in Ca2+-overloaded cells while in other studies incidence of early afterdepolarization (EAD) was reduced by ICl(Ca). Therefore our goal was to examine the role of ICl(Ca) in spatial and temporal heterogeneity of cardiac repolarization and EAD formation. Experiments were performed on isolated canine cardiomyocytes originating from various regions of the left ventricle; subepicardial, midmyocardial and subendocardial cells, as well as apical and basal cells of the midmyocardium. ICl(Ca) was blocked by 0.5mmol/L 9-anthracene carboxylic acid (9-AC). Action potential (AP) changes were tested with sharp microelectrode recording. Whole-cell 9-AC-sensitive current was measured with either square pulse voltage-clamp or AP voltage-clamp (APVC). Protein expression of TMEM16A and Bestrophin-3, ion channel proteins mediating ICl(Ca), was detected by Western blot. 9-AC reduced phase-1 repolarization in every tested cell. 9-AC also increased AP duration in a reverse rate-dependent manner in all cell types except for subepicardial cells. Neither ICl(Ca) density recorded with square pulses nor the normalized expressions of TMEM16A and Bestrophin-3 proteins differed significantly among the examined groups of cells. The early outward component of ICl(Ca) was significantly larger in subepicardial than in subendocardial cells in APVC setting. Applying a typical subepicardial AP as a command pulse resulted in a significantly larger early outward component in both subepicardial and subendocardial cells, compared to experiments when a typical subendocardial AP was applied. Inhibiting ICl(Ca) by 9-AC generated EADs at low stimulation rates and their incidence increased upon beta-adrenergic stimulation. 9-AC increased the short-term variability of repolarization also. We suggest a protective role for ICl(Ca) against risk of arrhythmias by reducing spatial and temporal heterogeneity of cardiac repolarization and EAD formation.

KEYWORDS

Bestrophin-3; Ca(2+)-activated Cl(−) current; Early afterdepolarization; Short-term variability of repolarization; Spatial heterogeneity of repolarization; TMEM16A.

Title

Ca 2+-activated Cl - Current Is Antiarrhythmic by Reducing Both Spatial and Temporal Heterogeneity of Cardiac Repolarization

Author

Bence Hegyi 1, Balazs Horvath 2, Krisztina Vaczi 3, Monika Gonczi 4, Kornel Kistamas 3, Ferenc Ruzsnavszky 3, Roland Veress 3, Leighton T Izu 5, Ye Chen-Izu 6, Tamas Banyasz 3, Janos Magyar 7, Laszlo Csernoch 3, Peter P Nanasi 8, Norbert Szentandrassy 9

Publish date

Aug-17

PMID

29771515

Abstract

Prediction of membrane permeability to small molecules represents an important aspect of drug discovery. First-principles calculations of this quantity require an accurate description of both the thermodynamics and kinetics that underlie translocation of the permeant across the lipid bilayer. In this contribution, the membrane permeability to three drugs, or drug-like molecules, namely, 9-anthroic acid (ANA), 2′,3′-dideoxyadenosine (DDA), and hydrocortisone (HYL), are estimated in a pure 1-palmitoyl-2-oleoylphosphatidylcholine (POPC) and in a POPC:cholesterol (2:1) mixture. On the basis of independent 2-5-μs free-energy calculations combined with a time-fractional Smoluchowski determination of the diffusivity, the estimated membrane permeabilities to these chemically diverse permeants fall within an order of magnitude from the experimental values obtained in egg-lecithin bilayers, with the exception of HYL in pure POPC. This exception is particularly interesting because the calculated permeability of the sterol-rich bilayer to HYL, in close agreement with the experimental value, is about 600 times lower than that of the pure POPC bilayer to HYL. In contrast, the permeabilities to ANA and DDA differ by less than a factor of 10 between the pure POPC and POPC:cholesterol bilayers. The unusual behavior of HYL, a large, amphiphilic compound, may be linked with the longer range perturbation of the lipid bilayer it induces, compared to ANA and DDA, suggestive of a possibly different translocation mechanism. We find that the tendency of lower permeabilities of the POPC:cholesterol bilayer relative to those of the pure POPC one is a consequence of increased free-energy barriers. Beyond reporting accurate estimates of the membrane permeability, the present contribution also demonstrates that rigorous free-energy calculations and a fractional-diffusion model are key in revealing the molecular phenomena linking the composition of a membrane to its permeability to drugs.

Title

Link Between Membrane Composition and Permeability to Drugs

Author

Chi Hang Tse 1 2, Jeffrey Comer 3, Yi Wang 1 2, Christophe Chipot 4 5 6

Publish date

2018 Jun 12

PMID

29500929

Abstract

Background and purpose: Although chloride channels are involved in several physiological processes and acquired diseases, the availability of compounds selectively targeting CLC proteins is limited. ClC-1 channels are responsible for sarcolemma repolarization after an action potential in skeletal muscle and have been associated with myotonia congenita and myotonic dystrophy as well as with other muscular physiopathological conditions. To date only a few ClC-1 blockers have been discovered, such as anthracene-9-carboxylic acid (9-AC) and niflumic acid (NFA), whereas no activator exists. The absence of a ClC-1 structure and the limited information regarding the binding pockets in CLC channels hamper the identification of improved modulators.

Experimental approach: Here we provide an in-depth characterization of drug binding pockets in ClC-1 through an integrated in silico and experimental approach. We first searched putative cavities in a homology model of ClC-1 built upon an eukaryotic CLC crystal structure, and then validated in silico data by measuring the blocking ability of 9-AC and NFA on mutant ClC-1 channels expressed in HEK 293 cells.

Key results: We identified four putative binding cavities in ClC-1. 9-AC appears to interact with residues K231, R421 and F484 within the channel pore. We also identified one preferential binding cavity for NFA and propose R421 and F484 as critical residues.

Conclusions and implications: This study represents the first effort to delineate the binding sites of ClC-1. This information is fundamental to discover compounds useful in the treatment of ClC-1-associated dysfunctions and might represent a starting point for specifically targeting other CLC proteins.

© 2018 The British Pharmacological Society.

Title

Mapping Ligand Binding Pockets in Chloride ClC-1 Channels Through an Integrated in Silico and Experimental Approach Using anthracene-9-carboxylic Acid and Niflumic Acid

Author

C Altamura 1, G F Mangiatordi 1, O Nicolotti 1, D Sahbani 1, A Farinato 1, F Leonetti 1, M R Carratù 2, D Conte 1, J-F Desaphy 2, P Imbrici 1

Publish date

2018 May;


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