VX (nerve agent)

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Stereo structural formula VX ((S)-phosphinate)
SP-(–)-VX enantiomer
Ball and stick model of VX ((R)-phosphinate)
IUPAC name
Ethyl ({2-[bis(propan-2-yl)amino]ethyl}sulfanyl)(methyl)phosphinate
Systematic IUPAC name
Ethyl ({2-[bis(propan-2-yl)amino]ethyl}sulfanyl)(methyl)phosphinate
Other names
[2-(Diisopropylamino)ethyl]-O-ethyl methylphosphonothioate
Ethyl {[2-(diisopropylamino)ethyl]sulfanyl}(methyl)phosphinate
Ethyl N-2-diisopropylaminoethyl methylphosphonothiolate
50782-69-9 YesY[2]
51848-47-6 YesY[2]
53800-40-1 YesY[2]
65143-05-7 N[2]
ChEBI CHEBI:609247 N
ChEMBL ChEMBL483105 YesY
ChemSpider 36386 YesY
Jmol 3D model Interactive image
Interactive image
PubChem 39793
Molar mass 267.37 g·mol−1
Density 1.0083 g cm−3
Melting point −3.90 °C (24.98 °F; 269.25 K)
Boiling point 300 °C (572 °F; 573 K)
log P 2.047
Vapor pressure 0.09 Pa
Vapor pressure {{{value}}}
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
N verify (what is YesYN ?)
Infobox references

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 its pure form, VX is a colorless, relatively non-volatile liquid, taking on a yellowish to brown color when impure.[3] Because of its low volatility, VX persists in environments where it is dispersed.[3]

VX, short for "venomous agent X",[4] is the best known of Tammelin's esters, named for the member of the Swedish National Defence Research Institute who first studied them; now one of a broader V-series of agents, they are classified as nerve agents and have been used as a chemical weapon in various recorded deadly attacks. VX fatalities occur with exposure to low 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.[5]

The danger of VX, in particular, lies in direct exposure to agent persisting where it was dispersed, and not through its evaporating and being distributed as a vapor (i.e., it is not a "vapor hazard"). VX is considered an area denial weapon due to these physical and biochemical characteristics.[6] As a chemical weapon, it is categorized as a weapon of mass destruction and is banned by the Chemical Weapons Convention of 1993,[7] where production and stockpiling of VX exceeding 100 grams (3.53 oz) per year is outlawed. The only exception is for "research, medical or pharmaceutical purposes outside a single small-scale facility in aggregate quantities not exceeding 10 kg [22 lb] per year per facility".[8]

Physical properties

It is of low molecular weight (FW 267), a liquid under standard and ambient temperate and tropical environmental conditions at most times (m.p. about −51°C),[9] with a density about that of water.[10] It is relatively hydrophobic—with about 100-fold more partitioning into octanol, over water, in this biphase[citation needed]—and is relatively high boiling (b.p. about 300°C).[11] In this regard, as a chemical warfare agent, its physical properties are considered somewhat exceptional, for instance, in that its low volatility gives it a high persistence in the environment.[12]

VX is odorless and tasteless,[13] and can be dispersed as a liquid, as an aerosol, or as a mixture with a clay or talc in the form of thickened agent.[12]

Mechanism of action

VX is an acetylcholinesterase inhibitor, i.e., it works by blocking the function of the enzyme known as acetylcholinesterase (AChE). Normally, when a motor neuron is stimulated, it releases a neurotransmitter into the space between the neuron and an adjacent muscle cell; that neurotransmitter is the chemical compound acetylcholine (ACh, abbreviation not used here, for clarity). 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 (hydrolysed) into the inactive substances, acetic acid and choline, by the AChe enzyme. VX blocks the action of AChe, resulting in an accumulation of acetylcholine in the space between the neuron and muscle cell. On a molecular level, this leads to this ongoing stimulation and eventual "fatigue" of all affected muscarinic and nicotinic ACh receptors.

Clinically, the consequence of ongoing stimulation is uncontrolled muscle contraction. This results in initial violent contractions, followed by "sustained supercontraction restricted to the fluid (sarcoplasm) of the subjunctional endplate and prolonged, depolarizing neuromuscular blockade."[this quote needs a citation] The prolonged blockade results in flaccid paralysis of all the muscles in the body, and it is such sustained paralysis of the diaphragm muscle that causes death by asphyxiation.



VX is chiral at its phosporus atom. The individual enantiomers are identified as SP-(–)-VX, and RP-(+)-VX (where the "P" subscript highlights that the chirality is at phosphorus).[1]

VX is produced via the transester process, which gives a racemic mixture of the two enantiomers. This entails a series of steps whereby phosphorus trichloride is methylated to produce methyl phosphonous dichloride. The resulting material is reacted with ethanol to form a diester. This is then transesterified with N,N-diisopropylaminoethanol to produce the mixed phosphonite. Finally, this immediate precursor is reacted with sulfur to form VX.

VX TransesterProcess.png

VX can also be delivered in binary chemical weapons which mix in-flight to form the agent prior to release. Binary VX is referred to as VX2,[14] and is created by mixing O-(2-diisopropylaminoethyl) O′-ethyl methylphosphonite (Agent QL) with elemental sulfur (Agent NE) as is done in the Bigeye aerial chemical bomb. It may also be produced by mixing with sulfur compounds, as with the liquid dimethyl polysulfide mixture (Agent NM) in the canceled XM736 8-inch projectile program.[15]


Like other organophosphorus nerve agents, VX may be destroyed by reaction with strong nucleophiles. The reaction of VX with concentrated aqueous sodium hydroxide results in competing cleavage of the P–O and P–S esters, with P–S cleavage dominating. This is problematic, however, as the product of P–O bond cleavage (named EA 2192) remains toxic. In contrast, reaction with the hydroperoxide anion (hydroperoxidolysis) leads to exclusive cleavage of the P–S bond.[16][17]

P–S cleavage (non-toxic products)
P-O cleavage (EA 2192 product is still toxic)

Medical aspects

Symptoms of exposure

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.[18]


VX is a "particularly toxic nerve agent"; as the Federation of American Scientists notes, doses of the agent

[that] are potentially life-threatening may be only slightly larger than those producing least effects. Death usually occurs within 15 minutes after absorption of a fatal VX dosage.[3]

The median lethal exposure—the exposure required to kill half of a tested population—as estimated for 70 kg human males has been reported: the median lethal dose (LD50) via exposure to the skin is reported to be 10 mg (0.00035 oz), and the lethal concentration time (LCt50), measuring the concentration of the vapor in milligrams per cubic meter (m3) per length of time exposed in minutes, is estimated for VX to be 30–50 mg·min/m3.[3]


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.[citation needed] 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.[citation needed] When possible, decontamination is completed before the casualty is taken for further medical treatment.[citation needed]

An individual known to have been exposed to a nerve-agent, or who exhibits definite signs or symptoms of nerve-agent exposure are generally given the antidotes atropine and pralidoxime (2-PAM), as well an injected sedative/antiepileptic such as diazepam.[citation needed] 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.[18]

Atropine blocks a subset of acetylcholine receptors known as muscarinic acetylcholine receptors (mAchRs), so that the buildup of acetylcholine produced by loss of the acetylcholinesterase function has a reduced effect on their target receptor.[citation needed] 2-PAM reactivates the acetylcholinesterase enzyme (AChE), thus reversing the effects of VX.[citation needed][19]

Ethyl methylphosphonic acid. R1 = ethyl, R2 = methyl.

However, if 2-PAM is not given soon enough, the inactivated enzyme will "age", resulting in a much stronger AChE-phosphate binding, that 2-PAM treatment cannot reverse.[20] The basis of this "aging" process in protein structure—a possible conformational isomerism—has been studied using X-ray crystallography focused on the AChE active site of relevant enzymes, where possible implications for the two enantiomers in the VX chemical agent are also discussed.[21]

Diagnostic tests

Controlled studies in humans have shown that minimally toxic doses cause 70–75% depression of erythrocyte cholinesterase within several hours of exposure. The serum level of ethyl methylphosphonic acid (EMPA), a VX hydrolysis product, was measured to confirm exposure in one poisoning victim. There also exist procedures for determination of VX hydrolysis products in urine and of VX adducts to albumin in blood.[22]



The chemists Ranajit Ghosh and J.F. Newman discovered the V-series nerve agents at the British firm ICI in 1952, patenting diethyl S-2-diethylaminoethyl phosphono- thioate (agent VG) in November 1952. Further commercial research on similar compounds ceased in 1955 when its lethality to humans was discovered. The U.S. went into production of large amounts of VX in 1961 at Newport Chemical Depot.

The discovery occurred when the chemists were investigating a class of organophosphate compounds (organophosphate esters of substituted aminoethanethiols).[23] Like Gerhard Schrader, an earlier investigator of organophosphates, Ghosh found that they were quite effective pesticides. In 1954, ICI put one of them on the market under the trade name Amiton. It was subsequently withdrawn, as it was too toxic for safe use. The toxicity did not go unnoticed, and samples of it had been sent to the British Armed Forces research facility at Porton Down for evaluation. After the evaluation was complete, several members of this class of compounds became a new group of nerve agents, the V agents. The best-known of these is probably VX, assigned the UK Rainbow Code Purple Possum, with the Russian V-Agent (VR) coming a close second (Amiton is largely forgotten as VG). This class of compounds is also sometimes known as Tammelin's esters, after Lars-Erik Tammelin of the Swedish National Defence Research Institute. Tammelin was also conducting research on this class of compounds in 1952, but did not widely publicize his work. The name is a contraction of the words "venomous agent X".[24]

Beginning in 1959, the United States Army began volunteer testing of VX in humans. Dr. Van M. Sim underwent an intravenous infusion of VX to evaluate its effects and to establish a baseline for future experimentation. After approximately 3.5 hours following initial administration of the agent, Dr. Sim suddenly became pale and delirious. The experiment was immediately terminated to preserve his life. In their conclusion, the researchers estimated that 2.12 μg/kg of VX delivered intravenously over the course of several hours would be the maximum tolerable dosage and that any more would risk death in a human subject.[25]

Instances of VX use

There was evidence of a combination of chemical agents having been used by Iraq against the Kurds in the Halabja chemical attack in 1988 under Saddam Hussein.[26] Hussein later testified to UNSCOM that Iraq had researched VX, but had failed to weaponize the agent due to production failure. After U.S. and allied forces had invaded Iraq, no VX agent or production facilities were found. However, UNSCOM laboratories detected traces of VX on warhead remnants.[27][28]

In December 1994 and January 1995, Masami Tsuchiya of Aum Shinrikyo synthesized 100 to 200 grams (3.5 to 7.1 oz) of VX which was used to attack three people. Two people were injured and one 28-year-old man died, who was the first victim of VX ever documented in the world at that time. The VX victim, whom Shoko Asahara had suspected as a spy, was attacked at 7:00 am on December 12, 1994 on the street in Osaka by Tomomitsu Niimi and another AUM member, who sprinkled the nerve agent on his neck. He chased them for about 100 yards (90 metres) before collapsing, dying 10 days later without ever coming out of a deep coma. Doctors in the hospital suspected at the time he had been poisoned with an organophosphate pesticide, but the cause of death was pinned down only after cult members arrested for the subway attack confessed to the killing. Metabolites of VX such as ethyl methylphosphonate, methylphosphonic acid and diisopropyl-2-(methylthio)ethylamine were later found in samples of the victim's blood seven months after his murder.[29] Unlike the cases for sarin gas (the Matsumoto incident and the attack on the Tokyo subway), VX was not used for mass murder.

On February 13, 2017, Kim Jong-nam, half-brother of North Korean leader Kim Jong-un, died after an assault in Kuala Lumpur International Airport in Malaysia. According to the authorities he was murdered by poisoning with VX which was found on his face.[30][31] The authorities further reported that one of the women suspected of applying the nerve agent experienced some physical symptoms of VX-poisoning.[32] The director of a non-proliferation research program of the Middlebury Institute of International Studies at Monterey stated that VX fumes would have killed the suspected attackers even if they had been wearing gloves, suggesting that the VX was applied as two non-lethal components that would mix to form VX only on the victim's face.[33]

Worldwide stockpiles

Some countries known to possess VX are the United States, Russia,[34] and Syria.[35] A Sudanese pharmaceutical facility, the Al-Shifa pharmaceutical factory, was bombed by the U.S. in 1998 acting on information that it produced VX and that the origin of the agent was associated with both Iraq and Al Qaeda.[27] The U.S. had obtained soil samples identified as containing O-ethyl hydrogen methylphosphonothioate (EMPTA), a chemical used in the production of VX which may also have commercial applications. Chemical weapons experts later suggested that the widely used fonofos organophosphate insecticide could have been mistaken for EMPTA.[36]

In 1969, the U.S. government canceled its chemical weapons programs, banned the production of VX in the United States, and began the destruction of its stockpiles of agents by a variety of methods. Early disposal included the U.S. Army's CHASE (Cut Holes And Sink 'Em) program, in which old ships were filled with chemical weapons stockpiles and then scuttled. CHASE 8 was conducted on June 15, 1967, in which the steamship Cpl. Eric G. Gibson was filled with 7,380 VX rockets and scuttled in 2,200 m (7,200 ft) of water off the coast of Atlantic City, New Jersey. Incineration was used for VX stockpile destruction starting in 1990 with Johnston Atoll Chemical Agent Disposal System in the North Pacific with other incineration plants following at Deseret Chemical Depot, Pine Bluff Arsenal, Umatilla Chemical Depot and Anniston Army Depot with the last of the VX inventory destroyed on December 24, 2008.[37]

Stockpile elimination

Worldwide, VX disposal has continued since 1997 under the mandate of the Chemical Weapons Convention. When the convention entered force, the parties declared worldwide stockpiles of 19,586 tonnes (21,590 short tons) of VX. As of December 2015, 98% of the stockpiles had been destroyed.[38]

In fiscal year 2008, the U.S. Department of Defense released a study finding that the United States had dumped at least 112 tonnes (124 short tons) of VX into the Atlantic Ocean off the coasts of New York/New Jersey and Florida between 1969 and 1970. This material consisted of nearly 22,000 M55 rockets, 19 bulk containers holding 640 kg (1,400 lb) each, and one M23 chemical landmine.[39]

The Newport Chemical Depot began VX stockpile elimination using chemical neutralization in 2005. VX was hydrolyzed to much less toxic byproducts by using concentrated caustic solution, and the resulting waste was then shipped off-site for further processing. Technical and political issues regarding this secondary byproduct resulted in delays, but the depot completed their VX stockpile destruction in August 2008.[40]

The remaining VX stockpile in the U.S. will be treated by the Blue Grass Chemical Agent-Destruction Pilot Plant in Kentucky, part of the Program Executive Office, Assembled Chemical Weapons Alternatives program. The program was established as an alternative to the incineration process successfully used by the Army Chemical Materials Agency, which completed its stockpile destruction activities in March 2012. The Blue Grass Pilot Plant has been plagued by repeated cost over-runs and schedule slippages since its inception.[41]

In Russia, the U.S. is providing support for these destruction activities with the Nunn-Lugar Global Cooperation Initiative.[42] The Initiative has been able to convert a former chemical weapons depot at Shchuchye, Kurgan Oblast, into a facility to destroy those chemical weapons. The new facility, which opened in May 2009, has been working on eliminating the nearly 5,400 tonnes (5,950 short tons) of nerve agents held at the former storage complex. However, this facility only holds about 14% of Russian chemical weapons, which are stored at seven sites.[43]

Popular culture

One of the best-known references to VX in popular culture is its use in the 1996 film The Rock,[44][45] which centers on a threatened VX attack on San Francisco from the island of Alcatraz. The film uses artistic license, notably with VX being ascribed corrosive powers it does not possess, permitting an early scene in which a VX victim is shown with his face melting, rather than dying through asphyxiation. It also shows the hero applying an intracardiac injection of atropine as a defense against VX contamination, rather than the more usual intramuscular injection (e.g. into the thigh) of a combination of atropine and pralidoxime.

In the BBC One spy drama Spooks, an episode named "I Spy Apocalypse" (Series 2, Episode 5) features an EERE (Extreme Emergency Response Exercise) turned real life emergency. A dirty bomb was reported to have exploded in Parliament Square and later the Morningside area of Edinburgh. The bomb was confirmed to have dispersed VX in quantities that exceeded the lethal dose across much of the southeast of England. It is later found that the emergency is a well constructed and believable exercise designed to test the MI5 officers to their limits.[citation needed]

In the CBS American science-based drama television series Eleventh Hour, an episode named Subway (Episode 16); Dr Hood, a science advisor to the FBI is called in to determine the cause of a poison cluster, which is killing people in Philadelphia.[46]

VX agent was featured on the History Channel's television series Modern Marvels in the episode Deadliest Weapons (Season 11, Episode 10).[47]

See also


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External links