Record Information
Version2.0
Creation Date2009-06-17 23:53:02 UTC
Update Date2014-12-24 20:22:59 UTC
Accession NumberT3D0947
Identification
Common NameChlorbufam
ClassSmall Molecule
DescriptionCarbamate pesticides are derived from carbamic acid and kill insects in a similar fashion as organophosphate insecticides. They are widely used in homes, gardens and agriculture. The first carbamate, carbaryl, was introduced in 1956 and more of it has been used throughout the world than all other carbamates combined. Because of carbaryl's relatively low mammalian oral and dermal toxicity and broad control spectrum, it has had wide use in lawn and garden settings. Most of the carbamates are extremely toxic to Hymenoptera, and precautions must be taken to avoid exposure to foraging bees or parasitic wasps. Some of the carbamates are translocated within plants, making them an effective systemic treatment. (2)
Compound Type
  • Amine
  • Carbamate
  • Ester
  • Ether
  • Organic Compound
  • Organochloride
  • Pesticide
  • Synthetic Compound
Chemical Structure
Thumb
Synonyms
Synonym
1-Butyn-3-yl m-chlorophenylcarbamate
1-Methyl-2-propynyl 3-chlorophenylcarbamate
1-Methyl-2-propynyl m-chlorocarbanilate
1-Methyl-2-propynyl m-chlorophenylcarbamate
1-Methyl-2-propynyl N-(3-chlorophenyl)carbamate
1-Methylprop-2-ynyl 3-chlorocarbanilate
1-Methylprop-2-ynyl 3-chlorophenylcarbamate
1-Methylpropynyl 3-chlorophenylcarbamate
1-Methylpropynyl ester OF 3-chlorophenylcarbamic acid
3-Butyn-2-ol, m-chlorocarbanilate
3-Butynyl-m-chlorocarbanilate
3-Chlorophenylcarbamic acid 1-methylpropynyl ester
3-Chlorphenyl-carbamidsaure-butin-(1)-yl(3)-ester
BICP
BIPC
Bipc (the herbicide)
Butyn-1-ol-3-ester OF m-chlorophenylcarbamic acid
Carbamic acid, (3-chlorophenyl)-, 1-methyl-2-propynyl ester
Carbanilic acid, m-chloro-, 1-methyl-2-propynyl ester
Caswell No. 575A
Chlorbufame
Chlorbupham
Chlorobufam
Grisemin
Grisin
Isobutinyl-N-(3-chlorphenyl)-carbamat
Chemical FormulaC11H10ClNO2
Average Molecular Mass223.656 g/mol
Monoisotopic Mass223.040 g/mol
CAS Registry Number1967-16-4
IUPAC Namebut-3-yn-2-yl N-(3-chlorophenyl)carbamate
Traditional Namechlorbufam
SMILESCC(OC(=O)NC1=CC=CC(Cl)=C1)C#C
InChI IdentifierInChI=1S/C11H10ClNO2/c1-3-8(2)15-11(14)13-10-6-4-5-9(12)7-10/h1,4-8H,2H3,(H,13,14)
InChI KeyInChIKey=ULBXWWGWDPVHAO-UHFFFAOYSA-N
Chemical Taxonomy
Description belongs to the class of organic compounds known as chlorobenzenes. Chlorobenzenes are compounds containing one or more chlorine atoms attached to a benzene moiety.
KingdomOrganic compounds
Super ClassBenzenoids
ClassBenzene and substituted derivatives
Sub ClassHalobenzenes
Direct ParentChlorobenzenes
Alternative Parents
Substituents
  • Chlorobenzene
  • Aryl chloride
  • Aryl halide
  • Carboximidic acid derivative
  • Propargyl-type 1,3-dipolar organic compound
  • Organic 1,3-dipolar compound
  • Acetylide
  • Organooxygen compound
  • Organonitrogen compound
  • Organochloride
  • Organohalogen compound
  • Organopnictogen compound
  • Organic nitrogen compound
  • Organic oxygen compound
  • Hydrocarbon derivative
  • Aromatic homomonocyclic compound
Molecular FrameworkAromatic homomonocyclic compounds
External Descriptors
Biological Properties
StatusDetected and Not Quantified
OriginExogenous
Cellular Locations
  • Membrane
Biofluid LocationsNot Available
Tissue LocationsNot Available
PathwaysNot Available
ApplicationsNot Available
Biological RolesNot Available
Chemical RolesNot Available
Physical Properties
StateSolid
AppearanceWhite powder.
Experimental Properties
PropertyValue
Melting Point45.5°C
Boiling PointNot Available
Solubility0.54 mg/mL at 20°C [YALKOWSKY,SH & HE,Y (2003)]
LogPNot Available
Predicted Properties
PropertyValueSource
Water Solubility0.024 g/LALOGPS
logP2.81ALOGPS
logP3.08ChemAxon
logS-4ALOGPS
pKa (Strongest Acidic)12.85ChemAxon
pKa (Strongest Basic)-1.2ChemAxon
Physiological Charge0ChemAxon
Hydrogen Acceptor Count2ChemAxon
Hydrogen Donor Count1ChemAxon
Polar Surface Area38.33 ŲChemAxon
Rotatable Bond Count3ChemAxon
Refractivity59.35 m³·mol⁻¹ChemAxon
Polarizability22.45 ųChemAxon
Number of Rings1ChemAxon
Bioavailability1ChemAxon
Rule of FiveYesChemAxon
Ghose FilterYesChemAxon
Veber's RuleYesChemAxon
MDDR-like RuleYesChemAxon
Spectra
Spectra
Spectrum TypeDescriptionSplash KeyDeposition DateView
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 10V, Positivesplash10-00di-9850000000-b89177500b24cdfbbcc32016-08-01View Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 20V, Positivesplash10-0uk9-9300000000-6b6b5bfeb767b03d194c2016-08-01View Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 40V, Positivesplash10-0udi-9600000000-16aae65455933c8362a42016-08-01View Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 10V, Negativesplash10-0udi-4940000000-857e7a78aca5e3f350522016-08-03View Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 20V, Negativesplash10-0uxr-6920000000-72aebfe6d21bbf9639322016-08-03View Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 40V, Negativesplash10-0fb9-4900000000-355a5b43c9d463c24e892016-08-03View Spectrum
MSMass Spectrum (Electron Ionization)splash10-0udi-6900000000-87a4d8187e276a621c6a2014-09-20View Spectrum
Toxicity Profile
Route of ExposureInhalation (1) ; oral (1); dermal (1)
Mechanism of ToxicityChlorbufam is a cholinesterase or acetylcholinesterase (AChE) inhibitor. A cholinesterase inhibitor (or 'anticholinesterase') suppresses the action of acetylcholinesterase. Because of its essential function, chemicals that interfere with the action of acetylcholinesterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses, followed by muscle spasms and ultimately death. Nerve gases and many substances used in insecticides have been shown to act by binding a serine in the active site of acetylcholine esterase, inhibiting the enzyme completely. Acetylcholine esterase breaks down the neurotransmitter acetylcholine, which is released at nerve and muscle junctions, in order to allow the muscle or organ to relax. The result of acetylcholine esterase inhibition is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop. Among the most common acetylcholinesterase inhibitors are phosphorus-based compounds, which are designed to bind to the active site of the enzyme. The structural requirements are a phosphorus atom bearing two lipophilic groups, a leaving group (such as a halide or thiocyanate), and a terminal oxygen.
MetabolismThe carbamates are hydrolyzed enzymatically by the liver; degradation products are excreted by the kidneys and the liver. (1)
Toxicity ValuesNot Available
Lethal DoseNot Available
Carcinogenicity (IARC Classification)No indication of carcinogenicity to humans (not listed by IARC).
Uses/SourcesThis is a man-made compound that is used as a pesticide.
Minimum Risk LevelNot Available
Health EffectsAcute exposure to cholinesterase inhibitors can cause a cholinergic crisis characterized by severe nausea/vomiting, salivation, sweating, bradycardia, hypotension, collapse, and convulsions. Increasing muscle weakness is a possibility and may result in death if respiratory muscles are involved. Accumulation of ACh at motor nerves causes overstimulation of nicotinic expression at the neuromuscular junction. When this occurs symptoms such as muscle weakness, fatigue, muscle cramps, fasciculation, and paralysis can be seen. When there is an accumulation of ACh at autonomic ganglia this causes overstimulation of nicotinic expression in the sympathetic system. Symptoms associated with this are hypertension, and hypoglycemia. Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh, results in anxiety, headache, convulsions, ataxia, depression of respiration and circulation, tremor, general weakness, and potentially coma. When there is expression of muscarinic overstimulation due to excess acetylcholine at muscarinic acetylcholine receptors symptoms of visual disturbances, tightness in chest, wheezing due to bronchoconstriction, increased bronchial secretions, increased salivation, lacrimation, sweating, peristalsis, and urination can occur. Certain reproductive effects in fertility, growth, and development for males and females have been linked specifically to organophosphate pesticide exposure. Most of the research on reproductive effects has been conducted on farmers working with pesticides and insecticdes in rural areas. In females menstrual cycle disturbances, longer pregnancies, spontaneous abortions, stillbirths, and some developmental effects in offspring have been linked to organophosphate pesticide exposure. Prenatal exposure has been linked to impaired fetal growth and development. Neurotoxic effects have also been linked to poisoning with OP pesticides causing four neurotoxic effects in humans: cholinergic syndrome, intermediate syndrome, organophosphate-induced delayed polyneuropathy (OPIDP), and chronic organophosphate-induced neuropsychiatric disorder (COPIND). These syndromes result after acute and chronic exposure to OP pesticides.
SymptomsAs with organophosphates, the signs and symptoms are based on excessive cholinergic stimulation. Unlike organophosphate poisoning, carbamate poisonings tend to be of shorter duration because the inhibition of nervous tissue acetylcholinesterase is reversible, and carbamates are more rapidly metabolized. Muscle weakness, dizziness, sweating and slight body discomfort are commonly reported early symptoms. Headache, salivation, nausea, vomiting, abdominal pain and diarrhea are often prominent at higher levels of exposure. Contraction of the pupils with blurred vision, incoordination, muscle twitching and slurred speech have been reported. (2)
TreatmentIf the compound has been ingested, rapid gastric lavage should be performed using 5% sodium bicarbonate. For skin contact, the skin should be washed with soap and water. If the compound has entered the eyes, they should be washed with large quantities of isotonic saline or water. In serious cases, atropine and/or pralidoxime should be administered. Anti-cholinergic drugs work to counteract the effects of excess acetylcholine and reactivate AChE. Atropine can be used as an antidote in conjunction with pralidoxime or other pyridinium oximes (such as trimedoxime or obidoxime), though the use of '-oximes' has been found to be of no benefit, or possibly harmful, in at least two meta-analyses. Atropine is a muscarinic antagonist, and thus blocks the action of acetylcholine peripherally.
Normal Concentrations
Not Available
Abnormal Concentrations
Not Available
DrugBank IDNot Available
HMDB IDNot Available
PubChem Compound ID16073
ChEMBL IDNot Available
ChemSpider IDNot Available
KEGG IDNot Available
UniProt IDNot Available
OMIM ID
ChEBI IDNot Available
BioCyc IDNot Available
CTD IDC034326
Stitch IDChlorbufam
PDB IDNot Available
ACToR IDNot Available
Wikipedia LinkNot Available
References
Synthesis ReferenceNot Available
MSDST3D0947.pdf
General References
  1. IPCS Intox Database (1987). Antimony pentoxide. [Link]
  2. Fishel F (2009). Pesticide Toxicity Profile: Carbamate Pesticides. University of Florida, IFAS Extension. [Link]
Gene Regulation
Up-Regulated GenesNot Available
Down-Regulated GenesNot Available

Targets

General Function:
Identical protein binding
Specific Function:
Esterase with broad substrate specificity. Contributes to the inactivation of the neurotransmitter acetylcholine. Can degrade neurotoxic organophosphate esters.
Gene Name:
BCHE
Uniprot ID:
P06276
Molecular Weight:
68417.575 Da
References
  1. Fishel F (2009). Pesticide Toxicity Profile: Carbamate Pesticides. University of Florida, IFAS Extension. [Link]