B2050
3-Bromo-7-nitroindazole
≥98% (TLC), powder
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About This Item
Empirical Formula (Hill Notation):
C7H4BrN3O2
CAS Number:
Molecular Weight:
242.03
UNSPSC Code:
12352202
PubChem Substance ID:
MDL number:
assay
≥98% (TLC)
form
powder
color
light yellow
solubility
ethanol: 25 mg/mL, DMSO: soluble
storage temp.
2-8°C
SMILES string
[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)
InChI key
NFSTZPMYAZRZPC-UHFFFAOYSA-N
Biochem/physiol Actions
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.
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.
signalword
Danger
hcodes
Hazard Classifications
Repr. 1B
Storage Class
6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
Eyeshields, Gloves, type P3 (EN 143) respirator cartridges
Regulatory Information
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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
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
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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