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Organophosphorus nerve agents are a chemical class of highly toxic compounds developed as chemical warfare agents. The most common representatives are tabun (GA), sarin (GB), soman (GD), VX, and cyclosarin (GF)[2][4][5]. They function by **irreversibly inhibiting the enzyme acetylcholinesterase (AChE)**, resulting in accumulation of acetylcholine in synapses and neuromuscular junctions, which causes continuous nerve transmission, paralysis, and potentially death due to respiratory failure[2][4][6]. These agents are not a single molecular target or receptor but are instead a group of chemically related toxins designed to disrupt normal neurotransmission. Nerve agents can enter the body by inhalation, skin contact, or ingestion and have been used as weapons in warfare and terrorism. The clinical syndrome caused by exposure is known as the “cholinergic toxidrome," characterized by salivation, lacrimation, urination, diarrhea, gastrointestinal upset, emesis (SLUDGE), muscle twitching, seizures, and eventually paralysis and death if untreated[5][6]. Treatment involves rapid administration of antimuscarinic agents (e.g., atropine) and oxime reactivators of AChE (e.g., pralidoxime), and in severe cases, benzodiazepines to control seizures. Note: There is a fundamental problem with this entry as a target: “Organophosphorus nerve agents” is not a single biological molecule or canonical drug target (such as a receptor, enzyme, transporter, etc.), but rather a class of toxic small molecules that interact with biological targets—mainly acetylcholinesterase (the canonical therapeutic target in nerve agent poisoning)[2][4][6]. For structured data and meaningful target-based analysis, “acetylcholinesterase” should be the listed canonical target for this context, while nerve agents would be classified as inhibitors of that enzyme.
Irreversible inhibition of acetylcholinesterase (AChE), leading to accumulation of acetylcholine and overstimulation of cholinergic receptors in the nervous system[2][4][5][6]
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