Tmic
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Record Information
Version2.0
Creation Date2009-06-17 23:53:02 UTC
Update Date2014-12-24 20:22:59 UTC
Accession NumberT3D0955
Identification
Common NameDesmedipham
ClassSmall Molecule
DescriptionDesmedipham is a selective, systemic post-emergence herbicide of the phenyl carbamate and biscarbamate classes. Carbamate 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. Desmedipham was developed by Schering AG and approved for use in the United States in 1970. It is commonly used in beet and strawberry crops to protect against weeds, often in comination with Phenmedipham under the trade names Betanal or Betamax. (3)
Compound Type
  • Amine
  • Carbamate
  • Ester
  • Ether
  • Herbicide
  • Organic Compound
  • Pesticide
  • Synthetic Compound
Chemical Structure
Thumb
Synonyms
Synonym
3-((Ethoxycarbonyl)amino)phenyl phenylcarbamate
3-Ethoxycarbonylaminophenyl-N-phenylcarbamate
Bentanex
Betamix
Betanal
Betanal am
Betanex
Carbamic acid, phenylcarbamoyloxyphenyl-, ethyl ester
Carbanilic acid, m-carbaniloyloxy-, ethyl ester
Caswell No. 447AAA
Ethyl (3-(((phenylamino)carbonyl)oxy)phenyl)carbamate
Ethyl 3'-phenylcarbamoyloxycarbanilate
Ethyl 3-phenylcarbamoyloxyphenylcarbamate
Ethyl m-hydroxycarbanilate carbanilate
Ethyl m-hydroxycarbanilate carbanilate (ester)
Ethyl meta-hydroxycarbanilate carbanilate
Ethyl N-[3-(N'-phenylcarbamoyloxy)phenyl]carbamate
Ethyl N-[3-(N-phenylcarbamoyloxy)phenyl]carbamate
Ethyl phenylcarbamoyloxyphenylcarbamate
Ethyl-3-phenylcarbamoyloxyphenylcarbamate
Synbetan d
[3-(ethoxycarbonylamino) phenyl] phenylcarbamate
Chemical FormulaC16H16N2O4
Average Molecular Mass300.309 g/mol
Monoisotopic Mass300.111 g/mol
CAS Registry Number13684-56-5
IUPAC Name1-3-{[ethoxy(hydroxy)methylidene]amino}phenoxy-N-phenylmethanimidic acid
Traditional Name1-3-{[ethoxy(hydroxy)methylidene]amino}phenoxy-N-phenylmethanimidic acid
SMILESCCOC(O)=NC1=CC(OC(O)=NC2=CC=CC=C2)=CC=C1
InChI IdentifierInChI=1S/C16H16N2O4/c1-2-21-15(19)18-13-9-6-10-14(11-13)22-16(20)17-12-7-4-3-5-8-12/h3-11H,2H2,1H3,(H,17,20)(H,18,19)
InChI KeyInChIKey=WZJZMXBKUWKXTQ-UHFFFAOYSA-N
Chemical Taxonomy
Description belongs to the class of organic compounds known as phenylcarbamic acid esters. These are ester derivatives of phenylcarbamic acids.
KingdomOrganic compounds
Super ClassBenzenoids
ClassBenzene and substituted derivatives
Sub ClassPhenylcarbamic acid esters
Direct ParentPhenylcarbamic acid esters
Alternative Parents
Substituents
  • Phenylcarbamic acid ester
  • Phenoxy compound
  • Carbamic acid ester
  • Carbonic acid derivative
  • Organic nitrogen compound
  • Organic oxygen compound
  • Organopnictogen compound
  • Organic oxide
  • Hydrocarbon derivative
  • Organooxygen compound
  • Organonitrogen compound
  • Carbonyl group
  • 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
Pathways
NameSMPDB LinkKEGG Link
Metabolic PathwaysNot AvailableNot Available
ApplicationsNot Available
Biological RolesNot Available
Chemical RolesNot Available
Physical Properties
StateSolid
AppearanceColorless and odorless powder.
Experimental Properties
PropertyValue
Melting Point120 ° C
Boiling PointNot Available
SolubilityPractically insoluble in water (0.07 g/L at 20 °C)
LogPNot Available
Predicted Properties
PropertyValueSource
Water Solubility0.021 g/LALOGPS
logP2.54ALOGPS
logP5.12ChemAxon
logS-4.2ALOGPS
pKa (Strongest Acidic)2.87ChemAxon
pKa (Strongest Basic)-2.7ChemAxon
Physiological Charge0ChemAxon
Hydrogen Acceptor Count6ChemAxon
Hydrogen Donor Count2ChemAxon
Polar Surface Area83.64 ŲChemAxon
Rotatable Bond Count6ChemAxon
Refractivity85.34 m³·mol⁻¹ChemAxon
Polarizability30.64 ųChemAxon
Number of Rings2ChemAxon
Bioavailability1ChemAxon
Rule of FiveYesChemAxon
Ghose FilterYesChemAxon
Veber's RuleYesChemAxon
MDDR-like RuleYesChemAxon
Spectra
Spectra
Spectrum TypeDescriptionSplash Key
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 10V, Positivesplash10-0f89-4943000000-3fd4093da639e3680508View in MoNA
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 20V, Positivesplash10-002f-8960000000-c26de169b4253bbc54aaView in MoNA
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 40V, Positivesplash10-02fx-9520000000-a315f8835bc4cbb1219cView in MoNA
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 10V, Negativesplash10-0uxr-3690000000-a9d14dbb5e775161c3f3View in MoNA
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 20V, Negativesplash10-0gbc-5960000000-48147b8c2835b8e0a2abView in MoNA
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 40V, Negativesplash10-0006-9610000000-13b3f0753c692c69e05bView in MoNA
MSMass Spectrum (Electron Ionization)splash10-015c-9600000000-48cec14e9ec64efc8aefView in MoNA
1D NMR1H NMR SpectrumNot AvailableView in JSpectraViewer
1D NMR13C NMR SpectrumNot AvailableView in JSpectraViewer
Toxicity Profile
Route of ExposureInhalation (2) ; oral (2); dermal (2)
Mechanism of ToxicityDesmedipham is a cholinesterase or acetylcholinesterase (AChE) inhibitor. Carbamates form unstable complexes with chlolinesterases by carbamoylation of the active sites of the enzymes. This inhibition is reversible. A cholinesterase inhibitor suppresses the action of acetylcholine esterase. Because of its essential function, chemicals that interfere with the action of acetylcholine esterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses. Headache, salivation, nausea, vomiting, abdominal pain and diarrhea are often prominent at higher levels of exposure. 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.
MetabolismThe carbamates are hydrolyzed enzymatically by the liver; degradation products are excreted by the kidneys and the liver. (2)
Toxicity ValuesLD50: 9600 mg/kg (Rat, oral); LD50: >2000 mg/kg (Rabbits, transdermally)
Lethal DoseNot Available
Carcinogenicity (IARC Classification)No indication of carcinogenicity to humans (not listed by IARC).
Uses/SourcesDesmedipham is a selective, systemic post-emergence herbicide commonly used in beet and strawberry crops to protect against weeds, often in comination with Phenmedipham.
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. Chronically high (>10 years) exposure leads to neuropsychological consequences including disturbances in perception and visuo-motor processing. (1)
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. (3)
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 ID24743
ChEMBL IDCHEMBL16024
ChemSpider ID23133
KEGG IDC18417
UniProt IDNot Available
OMIM ID
ChEBI IDNot Available
BioCyc IDNot Available
CTD IDC001984
Stitch IDDesmedipham
PDB IDNot Available
ACToR ID7885
Wikipedia LinkNot Available
References
Synthesis ReferenceNot Available
MSDSNot Available
General References
  1. Roldan-Tapia L, Nieto-Escamez FA, del Aguila EM, Laynez F, Parron T, Sanchez-Santed F: Neuropsychological sequelae from acute poisoning and long-term exposure to carbamate and organophosphate pesticides. Neurotoxicol Teratol. 2006 Nov-Dec;28(6):694-703. Epub 2006 Aug 30. [17029710 ]
  2. IPCS Intox Database (1987). Antimony pentoxide. [Link]
  3. 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:
Serine hydrolase activity
Specific Function:
Terminates signal transduction at the neuromuscular junction by rapid hydrolysis of the acetylcholine released into the synaptic cleft. Role in neuronal apoptosis.
Gene Name:
ACHE
Uniprot ID:
P22303
Molecular Weight:
67795.525 Da
References
  1. Fishel F (2009). Pesticide Toxicity Profile: Carbamate Pesticides. University of Florida, IFAS Extension. [Link]
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]
General Function:
Norepinephrine:sodium symporter activity
Specific Function:
Amine transporter. Terminates the action of noradrenaline by its high affinity sodium-dependent reuptake into presynaptic terminals.
Gene Name:
SLC6A2
Uniprot ID:
P23975
Molecular Weight:
69331.42 Da
Binding/Activity Constants
TypeValueAssay TypeAssay Source
AC503.28 uMNVS_TR_hNETNovascreen
References
  1. Sipes NS, Martin MT, Kothiya P, Reif DM, Judson RS, Richard AM, Houck KA, Dix DJ, Kavlock RJ, Knudsen TB: Profiling 976 ToxCast chemicals across 331 enzymatic and receptor signaling assays. Chem Res Toxicol. 2013 Jun 17;26(6):878-95. doi: 10.1021/tx400021f. Epub 2013 May 16. [23611293 ]
General Function:
Zinc ion binding
Specific Function:
Ligand-activated transcription factor. Receptor for bile acids such as chenodeoxycholic acid, lithocholic acid and deoxycholic acid. Represses the transcription of the cholesterol 7-alpha-hydroxylase gene (CYP7A1) through the induction of NR0B2 or FGF19 expression, via two distinct mechanisms. Activates the intestinal bile acid-binding protein (IBABP). Activates the transcription of bile salt export pump ABCB11 by directly recruiting histone methyltransferase CARM1 to this locus.
Gene Name:
NR1H4
Uniprot ID:
Q96RI1
Molecular Weight:
55913.915 Da
Binding/Activity Constants
TypeValueAssay TypeAssay Source
AC506.92 uMOT_SRC1_SRC1FXR_1440Odyssey Thera
References
  1. Sipes NS, Martin MT, Kothiya P, Reif DM, Judson RS, Richard AM, Houck KA, Dix DJ, Kavlock RJ, Knudsen TB: Profiling 976 ToxCast chemicals across 331 enzymatic and receptor signaling assays. Chem Res Toxicol. 2013 Jun 17;26(6):878-95. doi: 10.1021/tx400021f. Epub 2013 May 16. [23611293 ]