329-99-7 Usage
Description
Cyclohexyl methylphosphonofluoridate, also known as cyclosarin, is a highly toxic colorless liquid with an odorless to fruity smell. It is a synthetic organophosphate compound and belongs to the G-series of nerve agents. Cyclosarin was discovered in 1949 and was the fourth of the G-series nerve agents to be described. It is a fluorinated organophosphorus compound with the chemical formula C7H14FO2P, a relative density of 1.13, a melting point of -30°C, and a boiling point of 239°C.
Uses
Used in Chemical Warfare and Terrorism:
Cyclohexyl methylphosphonofluoridate is used as a chemical warfare agent for its highly toxic properties. It was developed as a nerve agent and has been used in conflicts such as the Gulf War. Its use in warfare and terrorism is due to its ability to disrupt the nervous system, leading to severe health effects and potentially death.
Used in International Arms Control and Disarmament Efforts:
Cyclohexyl methylphosphonofluoridate is used as a subject of international concern and regulation. The Chemical Weapons Convention (CWC) enacted in 1997 banned the production, stockpiling, and use of chemical weapons, including cyclosarin. The CWC is administered by the Organisation for the Prohibition of Chemical Weapons (OPCW), which works to eliminate chemical weapons and prevent their re-emergence. The use of cyclosarin in this context is to ensure the destruction of existing stockpiles and prevent its future use in warfare and terrorism.
Air & Water Reactions
Likely hydrolyzed by water, rapidly hydrolyzed by dilute aqueous sodium hydroxide.
Reactivity Profile
Acidic conditions produce hydrogen fluoride; alkaline conditions produce isopropyl alcohol and polymers. When heated to decomposition or reacted with steam, cyclohexyl methylphosphonofluoridate emits very toxic fumes of fluorides and oxides of phosphorus. Slightly corrosive to steel. Hydrolyzed by water.
Health Hazard
Median lethal dose (mg-min/m3): 2500 by skin (vapor) or 350 (liquid); 35 inhaled. Median incapacitating dose: 25 inhaled. Eye/skin toxicity: Very high. Rate of action: Very rapid. Physiological action: Cessation of breath-death may follow. Detoxification rate: Low. (ANSER)
Health Hazard
GF is a highly toxic nerve agent. It is a potent inhibitor of acetylcholinesterase and a neurotoxicant. The toxic symptoms are characteristics of sarin and other similar organophosphates. The toxicity is lower than GA, GB, GD, and VX.LD50 value, subcutaneous (guinea pigs): 0.1 mg/kg (NIOSH 1986) LD50 value,subcutaneous(rats):0.225mg/kg (NIOSH 1986).
Shipping
UN2810 Toxic liquids, organic, n.o.s., Hazard
Class: 6.1; Labels: 6.1-Poisonous materials, Technical
Name Required.
Toxicity evaluation
Cyclosarin and other nerve agents are irreversible cholinesterase
inhibitors. Clinical effects of exposure result primarily
from inhibition of acetylcholinesterase (AChE) and butyrylcholinesterase
(BuChE). Normally, AChE is responsible for
the degradation of neurotransmitter acetylcholine, in both
the peripheral and central nervous systems (CNS). Acetylcholine
stimulates contraction of skeletal muscles and
hydrolysis by AChE prevents continual overstimulation of
the acetylcholine receptors. Inhibition of AChE blocks
degradation of acetylcholine, resulting in an accumulation of
acetylcholine and cholinergic overstimulation of the target
tissues. AChE inhibition can have muscarinic, nicotinic, and
CNS effects resulting in a variety of symptoms including
involuntary muscle contractions, seizures, and increased
fluid secretion (e.g., tears, saliva). The cause of death is
typically respiratory dysfunction resulting from paralysis of
the respiratory muscles, bronchoconstriction, buildup of
pulmonary secretions, and depression of the brain’s respiratory
center.
Cholinesterases in the blood are often used to approximate
AChE tissue levels following exposure to a nerve agent. Red
blood cell cholinesterase (RBC-ChE) is found on erythrocytes
and BuChE in blood plasma. Affinities of cholinesterase
inhibitors for BuChE or RBC-ChE vary. The turnover rate for
RBC-ChE enzyme activity is the same as that for red blood cell
turnover at w1% per day. Tissue AChE and plasma BuChE
activities return with synthesis of new enzymes, the rate of
which differs between plasma and tissues as well as between
different tissues.
Binding of nerve agents to AChE is generally considered to
be irreversible unless removed by therapy. Oximes are used as
therapeutics to reactivate the enzyme prior to ‘aging’ or the
point at which the agent–enzyme complex is covalently linked
and the enzyme cannot be reactivated. Spontaneous reactivation
in the absence of oximes is possible but is unlikely to
occur at a rate sufficient to be clinically important. The time
required for 50% of the enzyme to become resistant to reactivation
varies by nerve agent. For cyclosarin, the t1/2 for AChE
is ～7 h and for RBC-ChE is ～2.2 h.
It is known that OP cholinesterase inhibitors exert their
toxic effects through mechanisms other than AChE inhibition.
A 1978 study by Van Meter, Karczamar, and Fiscus showed
that administering a second dose of sarin to rabbits still
induced seizures even though the brain AChE was already
inhibited by the previous dose of sarin. Further, pretreatment
protection of AChE with physostigmine still resulted in death
upon high dose treatment with nerve agent. Finally, it has been
shown that mice lacking AChE are actually more sensitive to
OP poisoning (including sarin) than wild-type mice, supporting
the fact that inhibition of AChE is not the only cause of
toxic effects.
One of the noncholinergic effects that results from treatment
with OP nerve agents is changes in the levels of neurotransmitters
other than acetylcholine. These include g-amino-butyric
acid, dopamine, serotonin, and norepinephrine. While the exact
mechanism by which nerve agent exposure alters the levels of
these neurotransmitters is not known, it is thought that these
changes may be due to a compensatory mechanism in response
to overstimulation of the cholinergic system, direct action of the
OP on the proteins responsible for noncholinergic neurotransmission,
or perhaps both. Nerve agents have also been shown to
inhibit a family of enzymes called serine esterases, which play an
important role in the metabolism and persistence of neuropeptides
such as endorphins and enkephalins. Neuroinflammation
as a result of nerve agent exposure is another
possible mechanism for noncholinergic toxicity effects. OPs
have also been shown to have direct toxic effects on cells via
induction of cellular oxidative stress and mitochondrial
dysfunction. Specifically, OP-induced disruption of mitochondrial
oxidative phosphorylation occurs through a variety of
mechanisms including reduction of electron transport chain
enzyme complexes, reduction in ATP synthesis, increased
hydrolysis of ATP, and disruption of the mitochondrial
membrane potential. Accumulation of reactive oxygen species
induces oxidative damage and cell death via caspase-induced
apoptosis.
The pharmacological and toxicological effects of the nerve
agents are dependent on their stability, rates of absorption by
the various routes of exposure, distribution, ability to cross the
blood–brain barrier, and rate of reaction.
Check Digit Verification of cas no
The CAS Registry Mumber 329-99-7 includes 6 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 3 digits, 3,2 and 9 respectively; the second part has 2 digits, 9 and 9 respectively.
Calculate Digit Verification of CAS Registry Number 329-99:
(5*3)+(4*2)+(3*9)+(2*9)+(1*9)=77
77 % 10 = 7
So 329-99-7 is a valid CAS Registry Number.
InChI:InChI=1/C7H14FO2P/c1-11(8,9)10-7-5-3-2-4-6-7/h7H,2-6H2,1H3
