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VX is an extremely toxic synthetic chemical compound in the organophosphorus class, specifically, a thiophosphonate. In the class of nerve agents, it was developed for military use in chemical warfare after translation of earlier discoveries of organophosphate toxicity in pesticide research. In recent years, VX was found to be the agent used in the assassination of Kim Jong-nam. In its pure form, VX is an oily, relatively non-volatile liquid that is amber-like in colour.[4] Because of its low volatility, VX persists in environments where it is dispersed.[5]
VX, short for "venomous agent X",[6] is one of the best known of the V nerve agents and was first discovered at Porton Down by Ranajit Ghosh in England during the early 1950s based on research first done by Gerhard Schrader, a chemist working for IG Farben in Germany during the 1930s. It is now one of a broader V-series of agents which are classified as nerve agents and have been used as a chemical weapon in various recorded deadly attacks. VX fatalities occur with exposure to tens of milligram quantities via inhalation or absorption through skin; VX is thus more potent than sarin, another nerve agent with a similar mechanism of action. On such exposure, these agents severely disrupt the body's signaling between the nervous and muscular systems, leading to a prolonged neuromuscular blockade, flaccid paralysis of all the muscles in the body including the diaphragm, and death by asphyxiation.[7]
The extreme toxicity of VX is partly due to the fact that the inhibitor was designed to be an excellent structural mimic for the transition state of the natural substrate (acetylcholine) of acetylcholinesterase. VX has a very high "on-rate" to react with the target enzyme and form a stable P-O-C bond (phosphorylation).[21] However, compared with other highly toxic nerve agents like soman or sarin, VX undergoes relatively slow "aging". Aging is a time-dependent side reaction (loss of an alkoxyl group) that occurs on nerve agents after phosphonylation and renders the nerve agent-acetylcholinesterase complex highly resistant to regeneration by any known antidote. Slower aging by VX suggests it should be possible to develop more effective antidotes and treatments.[22]
Early symptoms of percutaneous exposure (skin contact) include local sweating and muscular twitching at the area of exposure, followed by nausea or vomiting. Early symptoms of exposure to VX vapor include rhinorrhea (runny nose) and/or tightness in the chest with shortness of breath (bronchial constriction). Miosis (pinpointing of the pupils) may be an early sign of agent exposure, but is not usually used as the only indicator of exposure.[29]
When treating VX exposure, primary consideration is given to removal of the liquid agent from the skin, before removal of the individual to an uncontaminated area or atmosphere. After this, the victim is decontaminated by washing the contaminated areas with household bleach and flushing with clean water, followed by removal of contaminated clothing and further skin decontamination. When possible, decontamination is completed before the casualty is taken for further medical treatment.[32][33][34]
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