180270
N-tert-Butyl-α-phenylnitrone
98%
Synonym(s):
N-Benzylidene-tert-butylamine N-oxide, PBN, Phenyl N-t-butylnitrone
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About This Item
Linear Formula:
C6H5CH=N(O)C(CH3)3
CAS Number:
Molecular Weight:
177.24
Beilstein/REAXYS Number:
2044028
EC Number:
MDL number:
UNSPSC Code:
12352202
PubChem Substance ID:
Recommended Products
assay
98%
mp
73-74 °C (lit.)
SMILES string
CC(C)(C)[N+](\[O-])=C\c1ccccc1
InChI
1S/C11H15NO/c1-11(2,3)12(13)9-10-7-5-4-6-8-10/h4-9H,1-3H3/b12-9-
InChI key
IYSYLWYGCWTJSG-XFXZXTDPSA-N
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Biochem/physiol Actions
N-tert-butyl-α-phenylnitrone (PBN) is a commonly used free-radical spin trap.
N-tert-butyl-α-phenylnitrone (PBN) is a commonly used free-radical spin trap. It has been shown to reduce the number of emboli-induced cerebral microinfarctions in the rabbit cortex and prevent neoplasia by its radical scavenging activity and its ability to inhibit cyclooxygenase-2 activity. Reported to inhibit the induction of nitric oxide synthase (iNOS), thereby preventing the overproduction of nitric oxide (NO). PBN in a dose of 100 mg/kg i.p. reduced necrosis of the substantia nigra, pars reticulate in flurothyl-induced status epilepticus in rats. It protects against some types of post-trauma epileptogenic events in an animal model of epilepsy. The lethal dose of PBN in rats was found to be approximately 100 mg/100 g body weight (0.564 mmol/100Å g).
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Product No.
Description
Pricing
Storage Class
13 - Non Combustible Solids
wgk_germany
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
Eyeshields, Gloves, type N95 (US)
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Bulletin of the Chemical Society of Japan, 67, 165-165 (1994)
Appl. Magn. Res., 3, 1021-1021 (1992)
Aldrichimica Acta, 12, 23-23 (1979)
Jiwon Yang et al.
Journal of neurochemistry, 124(4), 523-535 (2012-12-04)
Oxidative stress after stroke is associated with the inflammatory system activation in the brain. The complement cascade, especially the degradation products of complement component 3, is a key inflammatory mediator of cerebral ischemia. We have shown that pro-inflammatory complement component
Jian-Jun Wen et al.
Journal of the American College of Cardiology, 55(22), 2499-2508 (2010-06-01)
The purpose of this study was to determine the pathological importance of oxidative stress-induced injurious processes in chagasic heart dysfunction. Trypanosoma cruzi-induced inflammatory pathology and a feedback cycle of mitochondrial dysfunction and oxidative stress may contribute to Chagas disease. Sprague-Dawley
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