P0043
PNU-120596
≥98% (HPLC)
Synonym(s):
N-(5-Chloro-2,4-dimethoxyphenyl)-N′-(5-methyl-3-isoxazolyl)-urea, NSC 216666
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About This Item
Empirical Formula (Hill Notation):
C13H14ClN3O4
CAS Number:
Molecular Weight:
311.72
NACRES:
NA.77
PubChem Substance ID:
UNSPSC Code:
12352200
MDL number:
InChI key
CEIIEALEIHQDBX-UHFFFAOYSA-N
SMILES string
O=C(NC1=NOC(C)=C1)NC2=CC(Cl)=C(OC)C=C2OC
InChI
1S/C13H14ClN3O4/c1-7-4-12(17-21-7)16-13(18)15-9-5-8(14)10(19-2)6-11(9)20-3/h4-6H,1-3H3,(H2,15,16,17,18)
assay
≥98% (HPLC)
form
solid
color
white to off-white
solubility
DMSO: >10 mg/mL
storage temp.
room temp
Quality Level
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Biochem/physiol Actions
An allosteric modulator of α7 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 acetylcholinePNU-120596 is a positive allosteric modulator selective for the α7 nicotinic acetylcholine receptor. PNU-120596 produces no detectable change in currents mediated by α4β2, α3β4, α9α10 nAChRs. It increases channel mean open time, but does not affect ion selectivity. It does not bind at the agonist binding site, but induces conformational changes similar to the natural effector.
PNU-120596 is a positive allosteric modulator of the α7 nicotinic acetylcholine receptor.
Storage Class
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
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Shakir D AlSharari et al.
Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco, 19(4), 460-468 (2016-11-01)
α7 nicotinic acetylcholine receptors (nAChRs) play an important role in vagus nerve-based cholinergic anti-inflammatory effects. This study was designed to assess the role of α7 nAChRs in dextran sodium sulfate (DSS)-induced colitis in male and female mouse. We first compared
Jean-Rémi Godin et al.
Brain, behavior, and immunity, 87, 286-300 (2019-12-25)
Nicotinic acetylcholine receptors (nAChRs) are best known to function as ligand-gated ion channels in the nervous system. However, recent evidence suggests that nicotine modulates inflammation by desensitizing non-neuronal nAChRs, rather than by inducing channel opening. Silent agonists are molecules that
Kateryna Uspenska et al.
Neuroscience letters, 656, 43-50 (2017-07-13)
Several nicotinic acetylcholine receptor (nAChR) subtypes are expressed in mitochondria to regulate the internal pathway of apoptosis in ion channel-independent manner. However, the mechanisms of nAChR activation in mitochondria and targeting to mitochondria are still unknown. Nicotine has been shown
C Morel et al.
Molecular psychiatry, 23(7), 1597-1605 (2017-11-21)
Epidemiological studies report strong association between mood disorders and tobacco addiction. This high comorbidity requires adequate treatment but the underlying mechanisms are unknown. We demonstrate that nicotine exposure, independent of drug withdrawal effects, increases stress sensitivity, a major risk factor
Kateryna Uspenska et al.
The international journal of biochemistry & cell biology, 99, 226-235 (2018-04-29)
Mitochondrial nicotinic acetylcholine receptors (nAChRs) regulate the early stage of mitochondria-driven apoptosis, including cytochrome c release. Mitochondrial nAChR signaling is mainly mediated by intra-mitochondrial kinases, in an ion-independent manner. To determine the relationship between specific nAChR subtypes and mitochondrial kinases
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