N7778
7-Nitroindazole
≥98%
Synonym(s):
7-NI
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About This Item
Empirical Formula (Hill Notation):
C7H5N3O2
CAS Number:
Molecular Weight:
163.13
NACRES:
NA.77
PubChem Substance ID:
UNSPSC Code:
12352200
EC Number:
220-934-4
MDL number:
Quality Level
assay
≥98%
form
powder
solubility
DMF: 50 mg/mL, clear, yellow to orange
storage temp.
−20°C
SMILES string
[O-][N+](=O)c1cccc2cn[nH]c12
InChI
1S/C7H5N3O2/c11-10(12)6-3-1-2-5-4-8-9-7(5)6/h1-4H,(H,8,9)
InChI key
PQCAUHUKTBHUSA-UHFFFAOYSA-N
Gene Information
human ... NOS1(4842), NOS2(4843), NOS2B(201288), NOS2C(645740), NOS3(4846)
rat ... Nos1(24598)
Biochem/physiol Actions
Selective inhibitor of nitric oxide synthase from mouse brain.
Features and Benefits
This compound is featured on the Nitric Oxide Synthases page of the Handbook of Receptor Classification and Signal Transduction. To browse other handbook pages, click here.
signalword
Danger
hcodes
Hazard Classifications
Acute Tox. 3 Oral - Carc. 2 - Eye Irrit. 2 - 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, Faceshields, Gloves, type P3 (EN 143) respirator cartridges
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Morten Hedetoft et al.
Undersea & hyperbaric medicine : journal of the Undersea and Hyperbaric Medical Society, Inc, 45(3), 335-350 (2018-07-22)
Experiments have shown that hyperbaric oxygen (HBO2) therapy reduces cyanide-induced cerebral distress. The exact mechanism behind HBO2's neuroprotective effect is unknown, but has been proposed to be mediated by an increased neuronal nitric oxide (NO) bioavailability, which may compete with
Geoffrey E Ciarlone et al.
American journal of physiology. Cell physiology, 311(6), C1014-C1026 (2016-10-14)
Central CO2-chemosensitive neurons in the caudal solitary complex (cSC) are stimulated not only by hypercapnic acidosis, but by hyperoxia as well. While a cellular mechanism for the CO2 response has yet to be isolated, previous data show that a redox-sensitive
Anita J Turner et al.
American journal of physiology. Renal physiology, 313(4), F864-F873 (2017-07-07)
Via developmental programming, prenatal perturbations, such as exposure to glucocorticoids and maternal malnutrition alter kidney development and contribute to the development of hypertension. To examine the possibility that alterations in tubuloglomerular feedback (TGF) contribute to the development of hypertension in