Nsc 216666
N-(5-CHLORO-2,4-DIMETHOXYPHENYL)-N'-(5-METHYL-3-ISOXAZOLYL)-UREA
CAS: 501925-31-1
Molecular Formula: C13H14ClN3O4
Nsc 216666 - Names and Identifiers
| Name | N-(5-CHLORO-2,4-DIMETHOXYPHENYL)-N'-(5-METHYL-3-ISOXAZOLYL)-UREA |
| Synonyms | CS-224 PNU120596 PNU 120596 PNU-120596 Nsc 216666 NSC 216666 1-(5-Chloro-2,4-dimethoxyphenyl)-3-(5-methylisoxazol-3-yl)urea N-(5-Chloro-2,4-dimethoxphenyl)-N'-(5-methyl-3-isoxazolyl)-urea N-(5-CHLORO-2,4-DIMETHOXYPHENYL)-N'-(5-METHYL-3-ISOXAZOLYL)-UREA Urea, N-(5-chloro-2,4-dimethoxyphenyl)-N'-(5-methyl-3-isoxazolyl)- |
| CAS | 501925-31-1 |
Nsc 216666 - Physico-chemical Properties
| Molecular Formula | C13H14ClN3O4 |
| Molar Mass | 311.72 |
| Density | 1.403 |
| Solubility | 30mg/ml DMSO mother liquor storage: sub-package and freeze storage to avoid repeated freezing and thawing;-20 ℃,1 month;-80 ℃,6 months (after dilution, the solution temperature is low and storage may precipitate, try to use it now) Cell experiment: Dissolve with DMSO first: dilute with culture medium, and the dilution process is recommended to be carried out in stages to avoid excessive concentration changes leading to compound precipitation. If the compound is precipitated during the dilution process, it can be redissolved by ultrasound. During dilution, ensure that the final concentration of DMSO in the working fluid should be below 0.1% as far as possible, and the maximum should not exceed 0.5%, and set up a DMSO control group with corresponding concentration. Animal experiment: Dissolve with DMSO first: dilute with water or normal saline, etc. The dilution process is recommended to be carried out in sections to avoid excessive concentration changes leading to compound precipitatio |
| Appearance | White solid |
| Color | white to off-white |
| Storage Condition | room temp |
| MDL | MFCD00095313 |
| Use | PNU-120596 (NSC 216666) is an effective selective α7 nAChR positive allosteric modulator with EC50 of 216 nM. PNU-120596 were inactive for α4β2,α3β4 and α9α10 nAChRs. PNU-120596 can be used for the study of psychosis and neurological diseases. |
| In vitro study | PNU-12059 increases calcium ion flux regulated by agonist (Ach)-induced human α7 nAChR variants. PNU-120596 acts on Xenopus oocytes to increase the current evoked by wild-type receptor-regulated agonists (choline and ACh) and, in the presence of persistent agonists, also causes a prolonged excitation response. PNU-120596 increases the average open time of the α7 nAChRs channel, but has no effect on ion selectivity and little effect on single conduction. PNU-120596 acts on acute hippocampal slices to increase Ach-induced gabaeric postsynaptic current frequency, which can be inhibited by TTX, indicating that PNU-120596 regulates α7 nAChRs function located on the synaptic membrane of hippocampal neurons. In addition to the positive modulation of α7 nAChR, PNU-120596 significantly inhibited desensitization kinetics, increasing Ca2-induced toxicity potential by over-stimulation of α7 nAChR. In the internal beta fold, transition zone, and stimulant binding, in combination with the Alpha 7 nAChR, PNU-120596 can change the accessibility to cysteine. PNU-120596 of the binding sites are not in the agonist binding site, and PNU-120596 enhance the agonist-induced nicotinic receptor gating by inducing a conformational effect, which is similar to but not identical to the Ach-promoted gating conformation. PNU-12059 increases calcium ion flux regulated by agonist (Ach)-induced human α7 nAChR variants. PNU-120596 acts on Xenopus oocytes to increase the current evoked by wild-type receptor-regulated agonists (choline and ACh) and, in the presence of persistent agonists, also causes a prolonged excitation response. PNU-120596 increases the average open time of the α7 nAChRs channel, but has no effect on ion selectivity and little effect on single conduction. PNU-120596 acts on acute hippocampal slices to increase Ach-induced gabaeric postsynaptic current frequency, which can be inhibited by TTX, indicating that PNU-120596 regulates α7 nAChRs function located on the synaptic membrane of hippocampal neurons. In addition to the positive regulation of α7 nAChR, PNU-120596 significantly inhibits desensitization kinetics by overstimulating α7 nAChR, while increasing Ca binding to α7 nAChR at the internal β-fold, transition zone, and stimulant binding, PNU-120596 can change the rate of arrival of cysteine. PNU-120596 of the binding sites are not in the agonist binding site, and PNU-120596 enhance the agonist-induced nicotinic receptor gating by inducing a conformational effect, which is similar to but not identical to the Ach-promoted gating conformation. |
| In vivo study | Treatment with 30 mg/kg PNU-1230596 followed by treatment with carrageenan now attenuates mechanical hyperalgesia for up to 4 hours. PNU-120596 treatment of inflammatory edema, reduced the carrageenan-induced increase in TNF-α and IL-6 levels, whereas dicofenac reduced only IL-6 levels. PNU-120596 may also partially reverse the mechanical hyperalgesia induced by carrageenan or CFA. treatment with 30 mg/kg PNU-1230596 followed by treatment with carrageenan now attenuates mechanical hyperalgesia for up to 4 hours. PNU-120596 treatment of inflammatory edema, reduced the carrageenan-induced increase in TNF-α and IL-6 levels, whereas dicofenac reduced only IL-6 levels. PNU-120596 may also partially reverse the mechanical hyperalgesia induced by carrageenan or CFA. |
Nsc 216666 - Risk and Safety
| WGK Germany | 3 |
Nsc 216666 - Reference
| Reference Show more | [1]. Hurst RS, et al. A novel positive allosteric modulator of the alpha7 neuronal nicotinic acetylcholine receptor: in vitro and in vivo characterization. J Neurosci, 2005, 25(17), 4396-4405.[2]. Barron SC, et al. An allosteric modulator of alpha7 nicotinic receptors, N-(5-Chloro-2,4-dimethoxyphenyl)-N'-(5-methyl-3-isoxazolyl)-urea (PNU-120596), causes conformational changes in the extracellular ligand binding domain similar to those caused by acetylcholine. Mol Pharmacol, 2009 76(2), 253-263.[3]. Munro G, et al. The α7 nicotinic ACh receptor agonist compound B and positive allosteric modulator PNU-120596 both alleviate inflammatory hyperalgesia and cytokine release in the rat. Br J Pharmacol, 2012, doi: 10.1111/j.1476-5381.2012.02003.x |
Nsc 216666 - Preparation solution concentration reference
| 1mg | 5mg | 10mg | |
|---|---|---|---|
| 1 mM | 3.208 ml | 16.04 ml | 32.08 ml |
| 5 mM | 0.642 ml | 3.208 ml | 6.416 ml |
| 10 mM | 0.321 ml | 1.604 ml | 3.208 ml |
| 5 mM | 0.064 ml | 0.321 ml | 0.642 ml |
Last Update：2024-01-02 23:10:35
Nsc 216666 - Reference Information
| biological activity | PNU-120596 is an effective α7 nAChR allosteric regulator, EC50 is 216 nM. PNU-120596 (Nsc 216666) is an effective α7 nAChR allosteric regulator with EC50 of 216 nM. |
| In vitro study | PNU-12059 enhance the calcium ion flow regulated by human α7 nAChR variant induced by stimulant (Ach). PNU-120596 acts on Xenopus oocytes to increase the current induced by wild-type receptor-regulated stimulants (choline and ACh), and also causes prolonged excitation response in the presence of persistent stimulants. PNU-120596 increase the average opening time of the α7 nAChRs channel, it has no effect on ion selectivity and has little effect on single conduction. PNU-120596 acts on acute hippocampal slices to increase the frequency of Ach-induced GABAergic postsynaptic currents. This effect can be inhibited by TTX, indicating that PNU-120596 regulates the function of α7 nAChRs located on the synaptic membrane of hippocampal neurons. In addition to positive regulation of α7 nAChR, PNU-120596 significantly inhibited desensitization kinetics and increased Ca2 +-induced toxicity potential by over-stimulating α7 nAChR. At the internal β-fold, transition zone, and stimulant binding, binding to α7 nAChR, PNU-120596 can change the accessibility to cysteine. The binding site of the PNU-120596 is not at the doping binding site, PNU-120596 enhances the doping-induced nicotinic receptor gating by initiating a conformational effect, which is similar but not identical to the Ach-promoted gating conformation. PNU-12059 enhances the calcium ion flow regulated by human α7 nAChR variant induced by stimulant (Ach). PNU-120596 acts on Xenopus oocytes to increase the current induced by wild-type receptor-regulated stimulants (choline and ACh), and also causes prolonged excitation response in the presence of persistent stimulants. PNU-120596 increase the average opening time of the α7 nAChRs channel, it has no effect on ion selectivity and has little effect on single conduction. PNU-120596 acts on acute hippocampal slices to increase the frequency of Ach-induced GABAergic postsynaptic currents. This effect can be inhibited by TTX, indicating that PNU-120596 regulates the function of α7 nAChRs located on the synaptic membrane of hippocampal neurons. In addition to the positive regulation of α7 nAChR, PNU-120596 significantly inhibited the desensitization kinetics. By overstimulating α7 nAChR, it increased Ca in the internal β fold, transition zone, and stimulant binding, and the binding of α7 nAChR, PNU-120596 can change the available rate of cysteine. The binding site of the PNU-120596 is not at the doping binding site, PNU-120596 enhances the doping-induced nicotinic receptor gating by initiating a conformational effect, which is similar but not identical to the Ach-promoted gating conformation. |
| in vivo study | 30 mg/kg PNU-1230596 administration treatment, then carrageenan treatment, now reduces mechanical hyperalgesia for up to 4 hours. PNU-120596 treatment of inflammatory edema reduces carrageenan-induced TNF-α and IL-6 levels, while diclofenac only reduces IL-6 levels. PNU-120596 can also partially reverse mechanical hyperalgesia induced by carrageenan or CFA. 30 mg/kg PNU-1230596 administration, then carrageenan treatment, now attenuates mechanical hyperalgesia for up to 4 hours. PNU-120596 treatment of inflammatory edema reduces carrageenan-induced TNF-α and IL-6 levels, while diclofenac only reduces IL-6 levels. PNU-120596 can also partially reverse mechanical hyperalgesia induced by carrageenan or CFA. |
| target | TargetValue α7 nAChR 216 nM(EC50) |
| Target | Value |
| α7 nAChR | 216 nM(EC50) |
Last Update：2024-04-09 21:49:45
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CAS: 501925-31-1
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