Molecular Weight(MW): 69
Sodium nitrite is a myeloperoxidase inhibitor with IC50 of 1.3 μM.
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|Description||Sodium nitrite is a myeloperoxidase inhibitor with IC50 of 1.3 μM.|
Sodium nitrite is well known for its role in inhibiting the growth of Clostridium botulinum by inhibiting iron-sulfur clusters essential to energy metabolism. Sodium nitrite slows chlorination by univalently reducing myeloperoxidase to an inactive form and as a consequence is oxidized to nitrogen dioxide. Myeloperoxidase oxidizes free tyrosine to tyrosyl radicals that exchange with tyrosyl residues in peptides. These peptide radicals then couple with nitrogen dioxide to form 3-nitrotyrosyl residues. With neutrophils, myeloperoxidase-dependent nitration required a high concentration of nitrite (1 mM), is doubled by tyrosine, and increases 4-fold by superoxide dismutase. Superoxide is likely to inhibit nitration by reacting with nitrogen dioxide and/or tyrosyl radicals.  Sodium nitrite results in intoxication of white mice with decrease of red cell superoxide dismutase (SOD) and catalase activity. The total activity of glucose-6-phosphate dehydrogenase and dehydrogenase of 6-phosphogluconate as well as the activity of glutathione reductase are higher in the group of mice that receive sodium nitrite in comparison with the control group. 
|In vivo||Peak plasma levels of nitrite are achieved in both sexes approximately 30 min after oral exposure. The model predicts that 10% of the hemoglobin is oxidized to the ferric form after oral doses of 15.9 mg/kg in male rats and 11.0 mg/kg in female rats and after intravenous doses of 8.9 and 7.1 mg/kg in male and female rats, respectively. The t1/2 for recovery from methemoglobinemia is 60 to 120 min depending on dose and route of administration. Replacement of the Vmax of methemoglobin reductase with a value representative of humans predicted a 10% methemoglobinemia following an intravenous dose of 5.8 mg/kg, in close agreement with an observed value of 5.7 mg/kg for humans. |
H2O2 uptake assay:Reactions are started by adding 10 nM myeloperoxidase to 30 μM H 2 O 2 and varying concentrations of nitrite, in 100 mM phosphate buffer, pH 7.4, containing 20 μM DTPA. Steady state rates of H 2 O 2 loss at 21°C are calculated over the first minute. Data are means and ranges of at least duplicate experiments.
|In vitro||DMSO||13 mg/mL warmed (188.4 mM)|
|Water||13 mg/mL warmed (188.4 mM)|
|In vivo||Add solvents individually and in order:
30% propylene glycol, 5% Tween 80, 65% D5W
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT01316796||Completed||Sickle Cell Anemia|Sickle Cell Disease|Chronic Hemolytic Disorders||National Heart, Lung, and Blood Institute (NHLBI)|National Institutes of Health Clinical Center (CC)||March 9, 2011||Phase 1|
|NCT00105222||Terminated||Healthy|Healthy Volunteer|HV||National Heart, Lung, and Blood Institute (NHLBI)|National Institutes of Health Clinical Center (CC)||March 8, 2005||Phase 1|
|NCT00103025||Completed||Healthy||National Institute of Neurological Disorders and Stroke (NINDS)|National Institutes of Health Clinical Center (CC)||February 4, 2005||Phase 1|
|NCT00098072||Completed||Hypertension, Pulmonary||National Institutes of Health Clinical Center (CC)||November 30, 2004||Phase 1|
|NCT03015402||Not yet recruiting||Pulmonary Hypertension Secondary|Heart Failure||University of Pittsburgh|National Heart, Lung, and Blood Institute (NHLBI)||June 2017||Phase 2|
|NCT02517697||Not yet recruiting||Metabolic Syndrome|Hypertension||University of Pittsburgh||June 2017||Phase 2|
Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.
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