Sodium Nitrite API Manufacturers & Suppliers
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Nitrous acid | CAS No: 7782-77-6 | GMP-certified suppliers
A medication that treats acute life-threatening cyanide poisoning when used sequentially with sodium thiosulfate, providing rapid detoxification in emergency care settings.
Therapeutic categories
Primary indications
- For sequential use with sodium thiosulfate for the treatment of acute cyanide poisoning that is judged to be life-threatening
Product Snapshot
- Nitrous acid is available in multiple formulations including paste, dentifrice, and injection solutions suitable for dental and intravenous administration
- It is primarily indicated for the treatment of acute cyanide poisoning in combination with sodium thiosulfate
- The product holds approved or investigational status in key markets including the US and Canada
Clinical Overview
Pharmacologically, sodium nitrite acts by inducing the formation of methemoglobin through oxidation of hemoglobin iron from the ferrous (Fe2+) to the ferric (Fe3+) state. Methemoglobin has a higher affinity for cyanide than mitochondrial cytochrome oxidase a3, the enzyme inhibited by cyanide. Binding of cyanide to methemoglobin facilitates cyanide removal from cytochrome oxidase a3, restoring oxidative phosphorylation and cellular energy production. The cyanide-methemoglobin complex then undergoes hepatic detoxification via rhodanese enzymes. Additionally, methemoglobin is enzymatically reduced back to hemoglobin, preserving red blood cell function. Sodium nitrite is also associated with the generation of nitric oxide during reduction, contributing to vasodilation through activation of soluble guanylate cyclase and downstream cyclic GMP signaling pathways.
Key pharmacokinetic data on absorption, distribution, metabolism, and excretion are limited; however, intravenous administration enables rapid systemic availability essential for emergency treatment. Sodium nitrite’s safety profile mandates careful dosing to avoid excessive methemoglobinemia and hypotension. Adverse effects primarily involve cardiovascular and hematologic parameters; monitoring during administration is critical.
Beyond approved indications, investigational research is exploring nitrite’s potential in managing heart attacks, brain aneurysms, pulmonary hypertension in neonates, and infections caused by Pseudomonas aeruginosa, although these are not established clinical uses.
For API procurement, sourcing high-purity sodium nitrite is essential, given its critical therapeutic role and narrow therapeutic index. Suppliers should provide material compliant with pharmacopeial standards and supported by rigorous quality control to ensure safety and efficacy in clinical applications.
Identification & chemistry
| Generic name | Nitrous acid |
|---|---|
| Molecule type | Small molecule |
| CAS | 7782-77-6 |
| UNII | T2I5UM75DN |
| DrugBank ID | DB09112 |
Pharmacology
| Summary | Sodium nitrite functions primarily as an antidote for acute cyanide poisoning by oxidizing hemoglobin to methemoglobin, which sequesters cyanide from cytochrome oxidase a3, restoring mitochondrial oxidative phosphorylation. Additionally, nitrite reduction by hemoglobin generates nitric oxide, inducing vasodilation through activation of guanylate cyclase signaling pathways. The compound’s pharmacodynamics involve interaction with hemoglobin subunits and myoglobin to facilitate cyanide detoxification and vascular smooth muscle relaxation. |
|---|---|
| Mechanism of action | Cyanide has a high affinity for the oxidized form of iron (Fe3+) such as that found in cytochrome oxidase a3 . Cyanide binds to and inhibits cytochrome oxidase a3, preventing oxidative phophorylation from occuring. The resultant lack of ATP cannot support normal cellular processes, particularly in the brain. Compensatory increases in anaerobic respiration result in rising levels of lactic acid and subsequent acidosis. Nitrite primarily acts by oxidizing hemoglobin to methemoglobin . The now oxidized Fe3+ in methemoglobin also binds cyanide with high affinity and accepts cyanide from cytochrome a3. This leaves cytochrome a3 free to resume its function in oxidative phosphorylation. The slow dissociation of cyanide from methemoglobin allows hepatic enzymes such as rhodanese to detoxify the compound without further systemic toxicity occuring. Methemoglobin is reduced back to hemoglobin by methemoglobin reductase allowing the affected blood cells to resume normal functioning. The reduction of nitrite by hemoglobin results in the formation of nitric oxide . Nitric oxide acts as a powerful vasodilator, producing vascular smooth muscle relaxation through activation of soluble guanylate cyclase and the subsequent cyclic guanylyl triphosphate mediated signalling cascade . |
| Pharmacodynamics | Sodium nitrite reverses cyanide toxicity and produces blood vessel dilation . |
Targets
| Target | Organism | Actions |
|---|---|---|
| Hemoglobin subunit alpha | Humans | oxidizer |
| Hemoglobin subunit beta | Humans | oxidizer |
| Myoglobin | Humans | oxidizer |
ADME / PK
| Half-life | Half life of 0.4-0.78h . |
|---|---|
| Metabolism | Reduced by deoxyhemoglobin to form nitric oxide . Nitrite is also reduced to nitric oxide and further reduced to ammonia by gut bacteria . Nitrite can be oxidized to nitrate by oxyhemoglobin. |
Formulation & handling
- Nitrous acid is a small molecule suitable for both dental paste formulations and intravenous injectable solutions.
- Due to its low LogP and small molecular weight, aqueous solubility is expected, facilitating solution-based formulations for IV use.
- Handling should consider stability issues common to nitrous acid derivatives, including potential decomposition in solution, requiring controlled storage conditions.
Regulatory status
| Lifecycle | The API is currently under patent protection in the United States until 2031, limiting generic competition in the US and Canadian markets. Its market presence remains in the growth phase with patent expiry anticipated in 2031. |
|---|
| Markets | US, Canada |
|---|
Supply Chain
| Supply chain summary | The supply landscape for nitrous acid includes multiple originator companies marketing branded products primarily in the US and Canadian markets. Several patents are active in the United States with expiry dates in 2031, indicating that branded exclusivity is maintained and generic competition is not yet present but may emerge post-patent expiration. |
|---|
Safety
| Toxicity | Oral LD50 of 157.9mg/kg observed in rats and 175mg/kg observed in mice [MSDS]. Estimated oral LD50 of 35mg/kg in humans . Sodium nitrite toxicity manifests as cardiovascular collapse following severe hypotension due to nitrite's vasodilatory action. |
|---|
- Exhibits high acute toxicity with estimated oral LD50 of approximately 35 mg/kg in humans
- Handle with appropriate precautions to minimize exposure
- Exposure risk includes severe hypotension and cardiovascular collapse attributed to nitrite-induced vasodilation
Sodium Nitrite is a type of Antidotes
Antidotes are a vital subcategory of pharmaceutical active pharmaceutical ingredients (APIs) that play a crucial role in counteracting the toxic effects of certain substances or drugs. These specialized substances are developed to treat and reverse the harmful effects caused by accidental or intentional poisonings, drug overdoses, or adverse reactions.
Antidotes work through various mechanisms to neutralize or counteract the toxic effects of specific substances. They may function by binding to the toxin directly, preventing it from interacting with its target receptors or enzymes. Alternatively, they may stimulate enzymatic pathways that metabolize and eliminate the toxic substance from the body more rapidly.
The development of antidotes involves rigorous research and testing to ensure their safety and efficacy. Clinical trials are conducted to evaluate their effectiveness in treating poisoning cases and to establish appropriate dosing regimens. Furthermore, antidotes are subject to stringent regulatory guidelines to ensure their quality, purity, and consistency.
Medical professionals, particularly toxicologists and emergency healthcare providers, rely on antidotes to manage and treat poisoning emergencies effectively. Antidotes are essential tools in the emergency department and poison control centers, where timely administration can be life-saving.
In summary, antidotes are specialized pharmaceutical APIs designed to counteract the toxic effects of specific substances. Their development, testing, and regulatory compliance are crucial to ensure their efficacy and safety. These critical medications are indispensable in the field of emergency medicine and play a pivotal role in saving lives affected by poisoning incidents.
Sodium Nitrite (Antidotes), classified under Antidotes, Deterrents, and Toxicologic Agents
Antidotes, Deterrents, and Toxicologic Agents are an important category of pharmaceutical Active Pharmaceutical Ingredients (APIs) that play a critical role in healthcare and toxicology. These substances are designed to counteract the effects of poisons, toxins, and overdoses, thereby saving lives and preventing severe health consequences.
Antidotes are substances that neutralize the toxic effects of certain drugs, chemicals, or poisons. They work by either directly binding to the toxic substance or by blocking its harmful actions on the body. Antidotes are administered in emergency situations to quickly reverse the effects of poisoning and restore normal physiological functions.
Deterrents, on the other hand, are pharmaceutical agents used to discourage or prevent harmful behaviors, such as substance abuse. They are designed to make the ingestion or misuse of certain substances unpleasant or less desirable. Deterrents can be formulated to cause unpleasant side effects, such as nausea or vomiting, when a particular substance is consumed in excessive amounts.
Toxicologic agents encompass a broad range of pharmaceutical APIs used in toxicology studies and research. These substances are employed to investigate the toxicity, metabolism, and mechanisms of action of various chemicals and compounds. Toxicologic agents are vital for understanding the potential hazards and risks associated with certain substances, ensuring the safety of drugs, and developing effective treatments for poisoning cases.
In conclusion, Antidotes, Deterrents, and Toxicologic Agents are essential categories of pharmaceutical APIs that address poisoning emergencies, deter harmful behaviors, and enable toxicological research. Their development and availability are crucial for safeguarding public health, enhancing patient care, and advancing our understanding of toxicology.
