Repositioning Candidate Details
| Candidate ID: | R0115 |
| Source ID: | DB00325 |
| Source Type: | approved; investigational |
| Compound Type: | small molecule |
| Compound Name: | Nitroprusside |
| Synonyms: | Nitroferricyanide |
| Molecular Formula: | C5FeN6O |
| SMILES: | O=N[Fe--](C#N)(C#N)(C#N)(C#N)C#N |
| Structure: |
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| DrugBank Description: | Nitroprusside serves as a source of nitric oxide, a potent peripheral vasodilator that affects both arterioles and venules (venules more than arterioles). Nitroprusside is often administered intravenously to patients who are experiencing a hypertensive emergency. |
| CAS Number: | 15078-28-1 |
| Molecular Weight: | 215.938 |
| DrugBank Indication: | For immediate reduction of blood pressure of patients in hypertensive crises, reduce bleeding during surgery, and for the treatment of acute congestive heart failure |
| DrugBank Pharmacology: | Nitroprusside a powerful vasodilator relaxes the vascular smooth muscle and produce consequent dilatation of peripheral arteries and veins. Other smooth muscle (e.g., uterus, duodenum) is not affected. Sodium nitroprusside is more active on veins than on arteries. |
| DrugBank MoA: | One molecule of sodium nitroprusside is metabolized by combination with hemoglobin to produce one molecule of cyanmethemoglobin and four CN- ions; methemoglobin, obtained from hemoglobin, can sequester cyanide as cyanmethemoglobin; thiosulfate reacts with cyanide to produce thiocyanate; thiocyanate is eliminated in the urine; cyanide not otherwise removed binds to cytochromes. Cyanide ion is normally found in serum; it is derived from dietary substrates and from tobacco smoke. Cyanide binds avidly (but reversibly) to ferric ion (Fe+++), most body stores of which are found in erythrocyte methemoglobin (metHgb) and in mitochondrial cytochromes. When CN is infused or generated within the bloodstream, essentially all of it is bound to methemoglobin until intraerythrocytic methemoglobin has been saturated. Sodium nitroprusside is further broken down in the circulation to release nitric oxide (NO), which activates guanylate cyclase in the vascular smooth muscle. This leads to increased production of intracellular cGMP, which stimulates calcium ion movement from the cytoplasm to the endoplasmic reticulum, reducing the level of available calcium ions that can bind to calmodulin. This ultimately results in vascular smooth muscle relaxation and vessel dilation. |
| Targets: | Atrial natriuretic peptide receptor 1 agonist |
| Inclusion Criteria: | Indication associated |
