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:
Pricing and availability is not currently available.
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
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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