Nisoxetine hydrochlorideNoradrenalin re-uptake inhibitor CAS# 57754-86-6 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 57754-86-6 | SDF | Download SDF |
PubChem ID | 134453 | Appearance | Powder |
Formula | C17H22ClNO2 | M.Wt | 307.82 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | Soluble to 100 mM in water | ||
Chemical Name | (±)-γ-(2-Methoxyphenoxy)-N-methylbenz | ||
SMILES | [H+].[Cl-].CNCCC(Oc1ccccc1OC)c2ccccc2 | ||
Standard InChIKey | LCEURBZEQJZUPV-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C17H21NO2.ClH/c1-18-13-12-15(14-8-4-3-5-9-14)20-17-11-7-6-10-16(17)19-2;/h3-11,15,18H,12-13H2,1-2H3;1H | ||
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. |
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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. |
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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. |
Description | A potent and selective inhibitor of noradrenalin uptake with little or no affinity for a range of other neurotransmitter receptors. |
Nisoxetine hydrochloride Dilution Calculator
Nisoxetine hydrochloride Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 3.2487 mL | 16.2433 mL | 32.4865 mL | 64.973 mL | 81.2163 mL |
5 mM | 0.6497 mL | 3.2487 mL | 6.4973 mL | 12.9946 mL | 16.2433 mL |
10 mM | 0.3249 mL | 1.6243 mL | 3.2487 mL | 6.4973 mL | 8.1216 mL |
50 mM | 0.065 mL | 0.3249 mL | 0.6497 mL | 1.2995 mL | 1.6243 mL |
100 mM | 0.0325 mL | 0.1624 mL | 0.3249 mL | 0.6497 mL | 0.8122 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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Norepinephrine transporters in rat placenta labeled with [3H]nisoxetine.[Pubmed:9454822]
J Pharmacol Exp Ther. 1998 Feb;284(2):736-43.
Previous research has identified a norepinephrine (NE) transporter in brush-border membranes from human placental syncytiotrophoblastic cells. In the present study, we used the selective ligand [3H]nisoxetine to demonstrate the presence of an NE transporter in rat placental membranes, determine the binding characteristics of the transporter and ascertain its localization by means of in vitro film and dry-emulsion autoradiography. Additional membrane binding studies were performed with [3H]GBR 12935 to determine whether a dopamine transporter also was present in rat placenta. Saturation analyses carried out on washed membrane fractions from whole rat placentas at gestational day 20 showed saturable [3H]nisoxetine binding (mean Kd = 1.00 nM, Bmax = 1.24 pmol/mg of protein) but no saturable binding of [3H]GBR 12935. When various monoamine uptake inhibitors were tested for their potency to inhibit placental [3H]nisoxetine binding, the results supported the conclusion that the radioligand was labeling an NE transporter. Autoradiographic studies showed the presence of [3H]nisoxetine binding in all three cellular zones of the rat placenta: the decidua, junctional zone and labyrinth. Binding was greatest in the junctional zone, particularly in the giant trophoblastic cells. These findings indicate the presence of a high density of NE transporters in the late-gestation rat placenta. Catecholamine uptake probably has a multifunctional role in placental physiology, and blockade of the NE transporter by certain drugs such as cocaine may therefore contribute to the adverse effects of such compounds on pregnancy outcome and offspring development.
Down-regulation of norepinephrine transporters on PC12 cells by transporter inhibitors.[Pubmed:8978719]
J Neurochem. 1997 Jan;68(1):134-41.
To investigate the regulation of norepinephrine transporters (NETs) in vitro, we measured the binding of the NET-selective ligand [3H]nisoxetine in homogenates of PC12 cells after exposure of intact cells to the NET inhibitor desipramine (DMI). A 3-day exposure of PC12 cells to DMI robustly reduced the Bmax, but not the KD, of [3H]nisoxetine binding to NETs. Reduction of the binding of [3H]nisoxetine was dependent on both the concentration of DMI and the time of exposure to DMI. Reduction of [3H]nisoxetine binding to NETs produced by a 1-day exposure to DMI reverted to preexposure levels 48 h after cessation of DMI exposure. Similar down-regulation of NETs was found when PC12 cells were exposed to another NET-selective drug, nisoxetine, which is structurally unrelated to DMI. In contrast, exposure of cells to the serotonin transporter-selective drug citalopram, or the NET substrate norepinephrine, had no effects on the binding of [3H]nisoxetine to NETs. The down-regulation of NETs was paralleled by a DMI-induced reduction in the uptake of [3H]norepinephrine in intact PC12 cells. It can be inferred from these data that inhibitors of the NET can down-regulate NETs directly, and do so in the absence of changes in the synaptic concentration of norepinephrine.
[3H]nisoxetine--a radioligand for noradrenaline reuptake sites: correlation with inhibition of [3H]noradrenaline uptake and effect of DSP-4 lesioning and antidepressant treatments.[Pubmed:8684598]
Neuropharmacology. 1996 Jan;35(1):63-70.
Nisoxetine is a potent and selective inhibitor of noradrenaline uptake into noradrenergic neurones. [3H]Nisoxetine binding to rat frontal cortical membranes was of high affinity. The binding data of both competition and saturation studies fitted a single site binding model. [3H]Nisoxetine binding was potently inhibited by the selective noradrenaline uptake inhibitors desipramine and protriptyline. In addition, a very good correlation was obtained between the ability of 25 monoamine reuptake inhibitors and related compounds both to inhibit [3H]nisoxetine binding and to inhibit [3H]noradrenaline uptake in rat frontal cortex. DSP-4 (10-100 mg/kg, i.p.) dose-dependently depleted cortical noradrenaline concentrations (51-100%), with no significant effects on 5-HT and dopamine. These depletions, which were used as a marker of loss of noradrenergic nerve terminals, were associated with a dose-dependent decrease in the number of [3H]nisoxetine binding sites (20-97%) with no change in binding affinity. Furthermore, a good correlation was obtained between cortical noradrenaline concentrations and the number of [3H]nisoxetine binding sites. These data support the view that [3H]nisoxetine binds to a single population of homogeneous sites associated with the noradrenaline transporter complex. Using this ligand, the effects of repeated administration of both antidepressant drugs with a range of pharmacological actions and of electroconvulsive shock on noradrenaline reuptake sites were examined. The number and affinity of [3H]nisoxetine binding sites were unaltered by all treatments. It is unlikely, therefore, that antidepressant therapy would produce adaptive changes in noradrenaline uptake sites.