All Photos(1)
About This Item
Linear Formula:
NaNO2
CAS Number:
Molecular Weight:
69.00
EC Number:
MDL number:
UNSPSC Code:
12352300
PubChem Substance ID:
Recommended Products
assay
99.5%
autoignition temp.
914 °F
mp
271 °C (lit.)
SMILES string
[Na+].[O-]N=O
InChI
1S/HNO2.Na/c2-1-3;/h(H,2,3);/q;+1/p-1
InChI key
LPXPTNMVRIOKMN-UHFFFAOYSA-M
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signalword
Danger
hcodes
Hazard Classifications
Acute Tox. 3 Oral - Aquatic Acute 1 - Eye Irrit. 2 - Ox. Sol. 3
Storage Class
5.1B - Oxidizing hazardous materials
wgk_germany
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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Paul J Shami et al.
Journal of medicinal chemistry, 49(14), 4356-4366 (2006-07-11)
The literature provides evidence that metabolic nitric oxide (NO) release mediates the cytotoxic activities (against human leukemia and prostate cancer xenografts in mice) of JS-K, a compound of structure R(2)N-N(O)=NO-Ar for which R(2)N is 4-(ethoxycarbonyl)piperazin-1-yl and Ar is 2,4-dinitrophenyl. Here
Lucas C Pinheiro et al.
Free radical biology & medicine, 53(4), 701-709 (2012-06-23)
The new pathway nitrate-nitrite-nitric oxide (NO) has emerged as a physiological alternative to the classical enzymatic pathway for NO formation from l-arginine. Nitrate is converted to nitrite by commensal bacteria in the oral cavity and the nitrite formed is then
Rustem F Dautov et al.
Nitric oxide : biology and chemistry, 40, 36-44 (2014-05-27)
Previous studies in non-human blood vessels and in platelets have demonstrated that under hypoxic conditions release of NO from nitrite (NO2(-)) is potentiated by deoxyhaemoglobin. In the current study, we characterized hypoxic potentiation of NO2(-) effects in human vasculature and
Edward H Oldfield et al.
Journal of neurosurgery, 119(3), 634-641 (2013-05-28)
Intravenous sodium nitrite has been shown to prevent and reverse cerebral vasospasm in a primate model of subarachnoid hemorrhage (SAH). The present Phase IIA dose-escalation study of sodium nitrite was conducted to determine the compound's safety in humans with aneurysmal
Borja Ibáñez et al.
Journal of the American College of Cardiology, 65(14), 1454-1471 (2015-04-11)
The damage inflicted on the myocardium during acute myocardial infarction is the result of 2 processes: ischemia and subsequent reperfusion (ischemia/reperfusion injury). During the last 3 decades, therapies to reduce ischemic injury (mainly reperfusion strategies) have been widely incorporated into
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