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B2050

Sigma-Aldrich

3-Bromo-7-nitroindazole

≥98% (TLC), powder

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About This Item

Formule empirique (notation de Hill):
C7H4BrN3O2
Numéro CAS:
74209-34-0
Poids moléculaire :
242.03
Numéro MDL:
MFCD00159910
Code UNSPSC :
12352202
ID de substance PubChem :
24278258

Pureté

≥98% (TLC)

Forme

powder

Couleur

light yellow

Solubilité

ethanol: 25 mg/mL
DMSO: soluble

Température de stockage

2-8°C

Chaîne SMILES 

[O-][N+](=O)c1cccc2c(Br)n[nH]c12

InChI

1S/C7H4BrN3O2/c8-7-4-2-1-3-5(11(12)13)6(4)9-10-7/h1-3H,(H,9,10)

Clé InChI

NFSTZPMYAZRZPC-UHFFFAOYSA-N

Actions biochimiques/physiologiques

A potent inhibitor of all nitric oxide synthase isoforms. Shows substantial neuroprotective effects against hypoxic damage (such as stroke) and animal models of Parkinson′s disease. Crystallographic studies show that inhibition of eNOS is due to an induced cascade of conformation changes that ultimately dissociates the tetrahydrobiopterin cofactor from the enzyme.

Pictogrammes

Health hazard
GHS08

Mention d'avertissement

Danger

Mentions de danger

H360

Classification des risques

Repr. 1B

Code de la classe de stockage

6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

Équipement de protection individuelle

Eyeshields, Gloves, type P3 (EN 143) respirator cartridges

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Consulter la Bibliothèque de documents

N E Stagliano et al.
Brain research, 759(1), 32-40 (1997-06-06)
Although nitric oxide (NO) has been shown to play an important role in the pathophysiology of cerebral ischemia, its contribution to the pathogenesis of experimentally induced thromboembolic stroke is unknown. In this study, we pharmacologically manipulated NO levels in the
Saurav Bhowmick et al.
Free radical biology & medicine, 113, 203-211 (2017-10-01)
Cerebral ischemia-reperfusion (I/R) injury initiates a cascade of events, generating nitric oxide (NO) and superoxide(O
K Wada et al.
Journal of neurosurgery, 89(5), 807-818 (1998-11-17)
Although nitric oxide (NO) has been shown to play an important role in the pathophysiological process of cerebral ischemia, its contribution to the pathogenesis of traumatic brain injury (TBI) remains to be clarified. The authors investigated alterations in constitutive nitric
Carmen R Sunico et al.
Proceedings of the National Academy of Sciences of the United States of America, 113(47), E7564-E7571 (2016-11-09)
Recent studies have pointed to protein S-nitrosylation as a critical regulator of cellular redox homeostasis. For example, S-nitrosylation of peroxiredoxin-2 (Prx2), a peroxidase widely expressed in mammalian neurons, inhibits both enzymatic activity and protective function against oxidative stress. Here, using
M J O'Neill et al.
Brain research, 760(1-2), 170-178 (1997-06-20)
Recent studies have shown that the novel antioxidant LY231617 protects against ischaemia-induced neuronal damage in rat models of global cerebral ischaemia. In the present studies we have examined the effects of LY231617 in the gerbil model of global cerebral ischaemia.
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