Drug class
Cyanide Poisoning Antidotes
Cyanide poisoning antidotes are a specialized functional class of emergency pharmacological agents indicated for the rapid treatment of known or suspected life-threatening acute cyanide toxicity, commonly arising from industrial exposures, smoke inhalation, or chemical emergencies. Read more about Cyanide Poisoning Antidotes
3 drugs in this class 2 manufacturers
Drugs in Cyanide Poisoning Antidotes
SODIUM THIOSULFATE
CYANOKIT (hydroxocobalamin)
Cyanide poisoning antidotes are a specialized functional class of emergency pharmacological agents indicated for the rapid treatment of known or suspected life-threatening acute cyanide toxicity, commonly arising from industrial exposures, smoke inhalation, or chemical emergencies.
These agents reverse cyanide's fatal inhibition of mitochondrial cytochrome c oxidase, thereby restoring aerobic cellular respiration and oxidative phosphorylation.
The class achieves this through distinct complementary mechanisms, including direct chemical chelation to form non-toxic cyanocobalamin (hydroxocobalamin), induction of methemoglobinemia to sequester cyanide away from mitochondrial enzymes (sodium nitrite), or provision of an exogenous sulfur substrate to accelerate enzymatic conversion into excretable thiocyanate via rhodanese (sodium thiosulfate).
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fda.gov
Cyanide poisoning antidotes are a specialized functional class of emergency pharmacological agents indicated for the rapid treatment of known or suspected life-threatening acute cyanide toxicity, commonly arising from industrial exposures, smoke inhalation, or chemical emergencies
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osha.gov
Cyanide poisoning antidotes are a specialized functional class of emergency pharmacological agents indicated for the rapid treatment of known or suspected life-threatening acute cyanide toxicity, commonly arising from industrial exposures, smoke inhalation, or chemical emergencies
-
fda.gov
These agents reverse cyanide's fatal inhibition of mitochondrial cytochrome c oxidase, thereby restoring aerobic cellular respiration and oxidative phosphorylation
-
nih.gov
The class achieves this through distinct complementary mechanisms, including direct chemical chelation to form non-toxic cyanocobalamin (hydroxocobalamin), induction of methemoglobinemia to sequester cyanide away from mitochondrial enzymes (sodium nitrite), or provision of an exogenous sulfur substrate to accelerate enzymatic conversion into excretable thiocyanate via rhodanese (sodium thiosulfate)
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drugs.com
The class achieves this through distinct complementary mechanisms, including direct chemical chelation to form non-toxic cyanocobalamin (hydroxocobalamin), induction of methemoglobinemia to sequester cyanide away from mitochondrial enzymes (sodium nitrite), or provision of an exogenous sulfur substrate to accelerate enzymatic conversion into excretable thiocyanate via rhodanese (sodium thiosulfate)
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