Evans Blue tetrasodium salt

potent inhibitor of AMPA and kainate receptor-mediated currents (GluRl and GIuR6) CAS# 314-13-6

Evans Blue tetrasodium salt

Catalog No. BCC6815----Order now to get a substantial discount!

Product Name & Size Price Stock
Evans Blue tetrasodium salt:1g $73.00 In stock
Evans Blue tetrasodium salt:2g $124.00 In stock
Evans Blue tetrasodium salt:5g $292.00 In stock
Evans Blue tetrasodium salt:10g $511.00 In stock
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Chemical structure

Evans Blue tetrasodium salt

3D structure

Chemical Properties of Evans Blue tetrasodium salt

Cas No. 314-13-6 SDF Download SDF
PubChem ID 5359386 Appearance Powder
Formula C34H24N6Na4O14S4 M.Wt 960.82
Type of Compound N/A Storage Desiccate at -20°C
Synonyms Direct Blue 53; C.I. 23860
Solubility Soluble to 10 mM in water
Chemical Name 6,6-[(3,3'-Dimethyl[1,1'-biphenyl]-4,4'-diyl)bis(azo)bis[4-amino- 5-hydroxy-1,3-naphthalenedisulphonic acid] tetrasodium salt
SMILES [Na+].[Na+].[Na+].[Na+].Cc1cc(ccc1NN=C2C=Cc3c(cc(c(N)c3C2=O)[S]([O-])(=O)=O)[S]([O-])(=O)=O)c4ccc(NN=C5C=Cc6c(cc(c(N)c6C5=O)[S]([O-])(=O)=O)[S]([O-])(=O)=O)c(C)c4
Standard InChIKey KBNIFDASRCWYGC-GXNXWABVSA-J
Standard InChI InChI=1S/C34H28N6O14S4.4Na/c1-15-11-17(3-7-21(15)37-39-23-9-5-19-25(55(43,44)45)13-27(57(49,50)51)31(35)29(19)33(23)41)18-4-8-22(16(2)12-18)38-40-24-10-6-20-26(56(46,47)48)14-28(58(52,53)54)32(36)30(20)34(24)42;;;;/h3-14,37-38H,35-36H2,1-2H3,(H,43,44,45)(H,46,47,48)(H,49,50,51)(H,52,53,54);;;;/q;4*+1/p-4/b39-23+,40-24+;;;;
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.
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.
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.

Biological Activity of Evans Blue tetrasodium salt

DescriptionPotent inhibitor of L-glutamate uptake into synaptic vesicles. Also inhibits AMPA and kainate receptor-mediated currents (IC50 values are 220 and 150 nM respectively). P2X-selective purinoceptor antagonist.

Evans Blue tetrasodium salt Dilution Calculator

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Evans Blue tetrasodium salt Molarity Calculator

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Preparing Stock Solutions of Evans Blue tetrasodium salt

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 1.0408 mL 5.2039 mL 10.4078 mL 20.8156 mL 26.0194 mL
5 mM 0.2082 mL 1.0408 mL 2.0816 mL 4.1631 mL 5.2039 mL
10 mM 0.1041 mL 0.5204 mL 1.0408 mL 2.0816 mL 2.6019 mL
50 mM 0.0208 mL 0.1041 mL 0.2082 mL 0.4163 mL 0.5204 mL
100 mM 0.0104 mL 0.052 mL 0.1041 mL 0.2082 mL 0.2602 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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Background on Evans Blue tetrasodium salt

IC50: 220 and 150 nM for GluRl and GIuR6, respectively.

Evans Blue tetrasodium salt is a potent inhibitor of AMPA and kainate receptor-mediated currents (GluRl and GIuR6).

Pharmacologically, the glutamate transporter is specific for glutamate and the closely related analogue L-aspartate does not block the uptake, whereas agents like L-homocysteate and La- aminoadipate block the vesicular L-glutamate uptake poorly.

In vitro: Evans blue inhibits the kainate-mediated responses of the non-NMDA receptor subunits (GIuRl, G1uR1,2, G1uRl,3, and G1uR2,3) expressed in Xenopus oocytes without the response of GluR3 and G1uR6 at low concentrations (IC50= 355 nM for the subunit combination GluR1,2). This pocess was partially reversible without competing with kainate for the agonist binding site [1]. In whole-cell patch clamp recordings of transfected human embryonic kidney 293 cells, Evans blue is a potent inhibitor of glutamate-evoked currents mediated by the kainate-type receptor GIuR6 as long as the AMPA-type receptor GluRl. Interestingly, pretreating with the lectin concanavalin cells recorded relatively little EB inhibition of GIuR6 currents, eliminating kainate receptor desensitization. In addition to decreasing GluR6-mediated peak current amplitude, EB significantly changed receptor desensitization by slowing the rate of onset by ~2-fold (1 M EB) and the rate of recovery by ~2-fold (0.1 p.M EB), and enhancing the steady state to peak current amplitude ratio by ~50-fold (1 M EB) [2].

In vivo: So far, no study in vivo has been conducted.

Clinical trial: So far, no clinical study has been conducted.

References:
[1] Roseth S, Fykse EM, Fonnum F.  Uptake of L-glutamate into rat brain synaptic vesicles: effect of inhibitors that bind specifically to the glutamate transporter. J Neurochem. 1995 Jul;65(1):96-103.
[2] Price CJ, Raymond LA.  Evans blue antagonizes both alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate and kainate receptors and modulates receptor desensitization. Mol Pharmacol. 1996 Dec; 50 (6):1665-71.

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References on Evans Blue tetrasodium salt

Differential modulation of AMPA receptor mediated currents by evans blue in postnatal rat hippocampal neurones.[Pubmed:9154333]

Br J Pharmacol. 1997 May;121(2):237-47.

1. The modulation of non-N-methyl-D-aspartate (NMDA) receptor-mediated whole cell currents and of glutamatergic synaptic transmission by purified Evans Blue (EB) was investigated in rat cultured postnatal hippocampal neurones by use of patch clamp recordings and a fast drug application system. 2. Three different groups of neurones could be distinguished with respect to the type of modulation obtained with 10 microM EB: EB was either a predominant inhibitor of desensitization (13% of the neurones), a predominant inhibitor of current amplitudes (42%) or a mixed inhibitor of both properties (45%). Both effects were not use-dependent and reached maximal levels after 30 s of pre-equilibration with the diazo dye. 3. Dose-response curves obtained from glutamate activated whole cell currents yielded an IC50 value for EB of 13.3 microM (Hill coefficient: 1.3) for the inhibition of desensitization, and an IC50 value of 10.7 microM (Hill coefficient: 1.2) for the inhibition of current amplitudes. 4. Chicago acid SS (100 microM) which is one of the synthesis precursors of EB had no effect on current amplitudes of glutamate activated whole cell currents but was a weak inhibitor of desensitization in all hippocampal neurones investigated, irrespective of the type of modulation obtained with EB in the same neurone. 5. Oxidatively modified EB (the so-called VIMP (10 microM)) had no effect on the kinetics but was a partial inhibitor of glutamate-activated whole cell currents in all hippocampal neurones investigated. 6. EB (10 microM) inhibited the amplitudes of non-NMDA receptor mediated autaptic currents to the same extent (to 39 +/- 19% of control) as observed for glutamate activated whole cell currents (to 41 +/- 17% and 56 +/- 20%). However, the decay of the autaptic responses remained uninfluenced upon EB application, indicating that either receptor desensitization does not dominate the time course of the synaptic response or that the non-NMDA receptors sensitive to modulation of desensitization by EB are not present in the postsynaptic membrane. 7. In conclusion, EB differentially modulates alpha-amino-3-hydroxy-5-methyl -4-isoxazole propionic acid (AMPA) receptor gating in different subsets of neurones. Upon identification of the cellular determinants for the differential modulation (e.g. AMPA receptor subunit composition) EB could become a useful tool to investigate receptor subtypes during electrophysiological recordings.

Evans blue antagonizes both alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate and kainate receptors and modulates receptor desensitization.[Pubmed:8967991]

Mol Pharmacol. 1996 Dec;50(6):1665-71.

The biphenyl derivative of 1,3-naphthalene disulfonic acid, known as Evans blue (EB), has been shown previously to specifically antagonize currents mediated by the alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) subtype of glutamate receptors (1). In contrast, we demonstrate herein that EB potently inhibits glutamate-evoked currents mediated by the kainate-type receptor GluR6 (IC50 150 nM) as well as the AMPA-type receptor GluR1 (IC50 = 220 nM) in whole-cell patch clamp recordings from transfected human embryonic kidney 293 cells. In addition to diminishing GluR6-mediated peak current amplitude, EB significantly altered receptor desensitization by slowing the rate of onset by approximately 2-fold (1 microM EB), slowing the rate of recovery by approximately 2-fold (0.1 microM EB), and increasing the steady state to peak current amplitude ratio by approximately 50-fold (1 microM EB). Interestingly, relatively little EB inhibition of GluR6 currents was observed in recordings from cells pretreated with the lectin concanavalin A, which eliminates kainate receptor desensitization. Similarly, currents recorded from GluR1-transfected cells were also relatively insensitive to EB inhibition if desensitization was first blocked by cyclothiazide. Moreover, for both GluR6 and GluR1, EB inhibition of agonist-evoked current was largely reversed if transfected cells were subsequently exposed to concanavalin A or cyclothiazide, respectively. Although EB may not be as selective an antagonist as previously believed, the relationship between EB-induced peak current inhibition and effects on receptor desensitization may be useful in further elucidating structures or mechanisms involved in the rapid desensitization of AMPA- and kainate-type glutamate receptors.

P2-purinoceptor antagonists: II. Blockade of P2-purinoceptor subtypes and ecto-nucleotidases by compounds related to Evans blue and trypan blue.[Pubmed:8897453]

Naunyn Schmiedebergs Arch Pharmacol. 1996 Oct;354(4):491-7.

Effects of Evans blue and four derivatives as well as of trypan blue and four derivatives, mostly smaller fragments but two compounds with an additional ethylene bridge in the center of the molecule, were studied on contractions of the rat vas deferens elicited by alpha, beta-methylene ATP (alpha, beta-MeATP; mediated by P2X-purinoceptors), relaxations of the carbachol-precontracted guinea-pig taenia coli elicited by adenosine 5'-O-(2-thiodiphosphate) (ADP beta S; mediated by P2Y-purinoceptors), and the degradation of ATP by rat vas deferens tissue. All compounds shifted the concentration-response curve of alpha, beta-MeATP in the rat vas deferens to the right, and most compounds increased the maximum of the curve. Each member of the Evans blue series was similar in potency to the corresponding member of the trypan blue series. Where three concentrations were tested, the Arunlakshana-Schild regression was linear, and the slope did not differ from 1. The apparent Kd values were between 0.8 and 385 microM. In the guinea-pig taenia coli, only the members of the trypan blue group were relatively potent, shifting the concentration-response curve of ADP beta S to the right in a surmountable manner. In 2 of 3 cases where three concentrations were tested, the slope of the Arunlakshana-Schild regression was lower than 1. Apparent Kd values in the trypan blue group were between 5.2 and 324 microM. The removal of ATP from the medium by vas deferens tissue was decreased mainly by the members of the Evans blue group, with IC25% values between 13 and 158 (in 1 case > 1000) microM. The results indicate that the position of the sulphonate residues at the terminal naphthalene rings of these compounds hardly influences P2X purinoceptor affinity but greatly influences P2Y affinity and ecto-nucleotidase blockade. Among active compounds, apparent purinoceptor affinity and ecto-nucleotidase blockade increase with the size of the molecules up to Evans blue and trypan blue themselves; introduction of a central ethylene bridge does not result in a further gain in potency. NH01, the desmethyl derivative of Evans blue, seems to be interesting because it is the compound with the highest P2X- versus P2Y-selectivity presently available.

Uptake of L-glutamate into rat brain synaptic vesicles: effect of inhibitors that bind specifically to the glutamate transporter.[Pubmed:7790899]

J Neurochem. 1995 Jul;65(1):96-103.

In this study we have described a series of new and potent inhibitors of the vesicular uptake of glutamate. The two most efficient inhibitors were the dyes Evans blue and Chicago Skye Blue 6B, which are structurally related to glutamate and were competitive inhibitors in the nanomolar range. The anion channel blocker 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (SITS) and the diuretics furosemide and bumetanide are inhibitors of chloride transport in other organs but were competitive inhibitors of glutamate and noncompetitive with respect to chloride ions. Evans blue, Chicago Skye Blue 6B, SITS, furosemide, and bumetanide are all large organic acids with two centers of negative charge and an electron-donating group at close vicinity of the negative charge at physiological pH. The inhibition of the glutamate uptake with these inhibitors was noncompetitive with respect to Cl-. The inhibitors, therefore, probably interact directly with the glutamate carrier. Bafilomycin A1, which is a specific vacuolar ATPase inhibitor, was used as a control and inhibited the vesicular dopamine, glutamate, and GABA uptake to the same extent. None of the inhibitors had any effect on the plasma membrane carrier, which is therefore clearly different from the vesicular carrier.

Description

Selective P2X purinergic antagonist,Evans Blue is a potent inhibitor of L-glutamate uptake via the membrane bound excitatory amino acid transporter (EAAT).

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