An antidote is a drug, chelating substance, or a chemical that counteracts (neutralizes) the effects of another drug or a poison.
Acetaminophen (Tylenol) toxicity-N-acetylcysteine (Mucomyst) Acetylcysteine replenishes glutathione stores, enhancing the non-toxic metabolism of acetaminophen, thereby preventing liver damage.
Various oral poisonings and overdoses except for cyanide, iron, lithium, caustics, and alcohol. Activated charcoal Activated charcoal adsorbs toxins in the gastrointestinal tract, reducing their systemic absorption.
Cholinergic crisis, Organophosphate or carbamate insecticide poisoning, certain mushroom poisonings-Atropine Atropine blocks acetylcholine receptors, reversing cholinergic effects like salivation, bronchial secretions, and bradycardia.
Magnesium Sulfate overdose, hyperkalemia, calcium channel blocker overdose-Calcium gluconate Calcium gluconate stabilizes cardiac membranes and counteracts the effects of hyperkalemia and calcium channel blockers.
Fluoride ingestion-Calcium chloride or calcium gluconate Calcium chloride binds to fluoride ions, forming insoluble calcium fluoride, reducing fluoride toxicity, especially on the cardiovascular and nervous systems.
Iron poisoning Deferoxamine (Desferal) Deferoxamine binds free iron in the bloodstream, forming a complex that can be excreted in the urine.
Digoxin toxicity Digoxin immune fab (DigiFab/Digibind)Digoxin immune fab binds to digoxin molecules, forming a complex that is then excreted by the kidneys, thereby neutralizing its effects.
Heavy metal poisoning, such as lead, arsenic, mercury, copper, and thallium. Dimercaprol (BAL) Dimercaprol chelates heavy metals, forming stable complexes that can be excreted in the urine, thereby reducing their toxicity.
Extrapyramidal symptoms (EPS) Diphenhydramine (Benadryl) Diphenhydramine blocks histamine (H1) and muscarinic (M1) receptors, which reduces the excessive cholinergic activity in the central nervous system that contributes to EPS.
Heavy metal poisoning, such as lead, copper, and mercury D-penicillamine (Cuprimine) D-penicillamine works by forming stable complexes with the metal ions, which are then excreted from the body.
Lead poisoning Edetate calcium disodium (Calcium EDTA), dimercaprol (BAL), Succimer Dimercaptosuccinate (DMSA) EDTA: Chelates lead by binding to it, forming a water-soluble complex that is excreted in the urine.
Benzodiazepine overdose Flumazenil (Romazicon) Flumazenil competitively inhibits benzodiazepine binding at the GABA receptor, reversing sedation and respiratory depression.
Ethylene glycol (antifreeze), Methanol poisoning Fomepizole (Antizol) Ethanol, Hemodialysis Fomepizole inhibits alcohol dehydrogenase, preventing the metabolism of toxic alcohols into their harmful metabolites.
Beta-blockers overdose, calcium channel blockers overdose, hypoglycemia Glucagon Glucagon increases cyclic AMP in cardiac cells, improving heart contractility and counteracting the effects of beta-blockers. Insulin reaction Glucose (Dextrose 50%) Glucose rapidly raises blood sugar levels, providing immediate energy to counteract insulin-induced hypoglycemia and alleviate symptoms like dizziness and weakness.
Cyanide poisoning Hydroxocobalamin (1st line) Nitrites and thiosulfate (2nd line) Hydroxocobalamin binds to cyanide to form cyanocobalamin, a non-toxic compound that is excreted by the body.
Methotrexate toxicity Leucovorin Calcium (folinic acid) Leucovorin calcium acts as a folate precursor, counteracting methotrexate toxicity by restoring normal cell function, especially in rapidly dividing tissues like the bone marrow and GI tract.
Cyclophosphamide toxicity Mesna Mesna works by binding to acrolein, a toxic metabolite of cyclophosphamide, preventing damage to the bladder and reducing the risk of hemorrhagic cystitis.
Chemical producing severe methemoglobinemia. Ifosamide-induced encephalopathy. Methylene blue Methylene blue works by reducing methemoglobin back to hemoglobin, restoring the oxygen-carrying capacity of the blood.
Opioids (Narcotic) overdose Naloxone (Narcan) Naloxone competitively binds to opioid receptors, reversing the effects of opioids like respiratory depression and sedation.
Anticholinergics Neostigmine Anticholinesterase which causes accumulation of acetylcholine at cholinergic receptor sites.
Carbon Monoxide poisoning 100% Oxygen Administering high-flow oxygen helps to rapidly displace carbon monoxide from hemoglobin, restoring oxygen delivery to tissues and reducing the risk of tissue hypoxia and organ damage.
Hypertensive crisis due to catecholamine excess (e.g., pheochromocytoma) Phentolamine (Regitine) Phentolamine blocks alpha-adrenergic receptors, causing vasodilation and reducing blood pressure.
Anticholinergic toxicity, Tricyclic antidepressants, anticholinergic, diphenhydramine dimehydrinate overdose Physostigmine A reversible anticholinesterase which effectively increases the concentration of acetylcholine at the sites of cholinergic transmission.
Warfarin (Coumadin) overdose Phytomenadione ( Vitamin K) Vitamin K is essential for the synthesis of clotting factors II, VII, IX, and X, reversing the anticoagulant effects of warfarin.
Organophosphate poisoning Pralidoxime (2-PAM, Protopam) Pralidoxime reactivates acetylcholinesterase that has been inactivated by organophosphates, restoring normal neuromuscular function.
Heparin overdose Protamine sulfate Protamine sulfate binds to heparin, forming a stable complex that neutralizes its anticoagulant effect.
Isoniazid overdose, monomethyl hydrazine poisoning. Adjunctive therapy in ethylene glycol poisoning. Pyridoxine (Vitamin B6) Vitamin B6 serves as a cofactor for pyridoxal kinase, converting isoniazid (INH) into less toxic metabolites, thereby decreasing the risk of neurological side effects from INH overdose.
Cobra bite Snake antivenom Neutralizes venom by binding with circulating venom components and with locally deposited venom by accumulating at the bite site.
Tricyclic Antidepressant (TCA) overdose, salicylate poisoning, metabolic acidosis, hyperkalemia, chlorine gas inhalation Sodium Bicarbonate Sodium bicarbonate alkalinizes the blood and urine, enhancing the elimination of certain drugs and counteracting metabolic acidosis.
Alcohol-induced Wernicke-Korsakoff syndrome, acute thiamine deficiency Thiamine (Vitamin B1) Thiamine replenishes deficient levels, crucial for glucose metabolism, preventing and treating neurological damage in Wernicke-Korsakoff syndrome and acute thiamine deficiency.