VX Nerve Agent

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VX (IUPAC name: O-ethyl S-[2-(diisopropylamino)ethyl] methylphosphonothioate), an extremely toxic organophosphate, is a tasteless and odorless liquid with an amber-like color that severely disrupts the body’s nervous system and is used as a nerve agent in chemical warfare. Ten milligrams is sufficient for it to be fatal through skin contact and the median lethal dose for inhalation is estimated to be 30–50 mg·min/m3.

Chemical characteristics

With its high viscosity and low volatility, VX has the texture and feel of motor oil. This makes it especially dangerous, as it has a high persistence in the environment. It is odorless and tasteless, and can be distributed as a liquid, either pure or as a mixture with a polymer in the form of thickened agent, or as an aerosol.[citation needed]

VX is an acetylcholinesterase inhibitor, i.e., it works by blocking the function of the enzyme acetylcholinesterase. Normally, when a motor neuron is stimulated, it releases the neurotransmitter acetylcholine into the space between the neuron and an adjacent muscle cell. When this acetylcholine is taken up by the muscle cell, it stimulates muscle contraction. To avoid a state of constant muscle contraction, the acetylcholine is then broken down to non-reactive substances (acetic acid and choline) by the enzyme acetylcholinesterase. VX blocks the action of acetylcholinesterase, resulting in an accumulation of acetylcholine in the space between the neuron and muscle cell, leading to uncontrolled muscle contraction. This results in initial violent contractions, followed by sustained supercontraction restricted to the subjunctional endplate sarcoplasm and prolonged depolarizing neuromuscular blockade, the latter resulting in flaccid paralysis of all the muscles in the body. Sustained paralysis of the diaphragm muscle causes death by asphyxiation.

Early symptoms can include pinprick pupils, runny nose, wheezing and muscle twitching. Death can occur anywhere from within a few minutes to hours, depending on the dose and the method of contact.


Primary consideration should be given to removal of the liquid agent from the skin before removal of the individual to an uncontaminated area or atmosphere. After removal from the contaminated area, the casualty will be decontaminated by washing the contaminated areas with household bleach and flushing with clean water. After decontamination, the contaminated clothing is removed and skin contamination washed away. If possible, decontamination is completed before the casualty is taken for further medical treatment.

An individual who has received a known nerve-agent exposure or who exhibits definite signs or symptoms of nerve-agent exposure should immediately have the nerve agent antidote drugs atropine and pralidoxime (2-PAM), and a sedative/antiepileptic such as diazepam injected. In several nations the nerve agent antidotes are issued for military personnel in the form of an autoinjector such as the United States military Mark I NAAK.[11]

Atropine works by binding and blocking a subset of acetylcholine receptors (known as muscarinic acetylcholine receptor, mAchR), so that the buildup of acetylcholine produced by loss of the acetylcholinesterase function has a reduced effect on their target receptor.

VX (and other organophosphates) block the enzymatic activity of acetylcholinesterase (AChE) by binding to the active site of the enzyme. The phosphate group on VX is then transferred from VX to AChE, inactivating the enzyme and producing an inactive metabolite of VX. The injection of pralidoxime (2-PAM) removes the phosphate group from AChE, reactivating it, thereby reversing the effects of VX. If pralidoxime is not given soon enough, the inactivated enzyme will “age”, resulting in a much stronger AChEW-phosphate that pralidoxime cannot reverse.[12][13]

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