<?xml version="1.0" encoding="UTF-8"?>
<compound>
  <id type="integer">963</id>
  <title>T3D0959</title>
  <common-name>Diethofencarb</common-name>
  <description>Diethofencarb is an exogenous solid with the formula C14H21NO4 and an average molecular weight of 267.32 g/mol. Diethofencarb belongs to the phenylcarbamic acid esters, a subclass of benzene and substituted derivatives within the organic compounds. It is used biologically as a fungicide (PMC10922816, PMC7941040).

The compound has been recorded in five sources, including agriculture and land management pesticides, drinking water and water supply, food processing and cookware specifically in the preparation of malt, and building and construction materials such as tents, canopies, and floors. Exposure routes include touch, oral, and inhalation. Diethofencarb targets two proteins: acetylcholinesterase (ACHE) and cholinesterase (BCHE). Its mode of action is the inhibition of cholinesterase enzymes, which affects nerve impulse transmission in a manner similar to organophosphates.</description>
  <cas>87130-20-9</cas>
  <pubchem-id>91742</pubchem-id>
  <chemical-formula>C14H21NO4</chemical-formula>
  <weight>267.147060</weight>
  <appearance>White powder.</appearance>
  <melting-point>100.3°C</melting-point>
  <boiling-point nil="true"/>
  <density nil="true"/>
  <solubility>0.0266 mg/mL at 20°C [TOMLIN,C (1994)]</solubility>
  <specific-gravity nil="true"/>
  <flash-point nil="true"/>
  <vapour-pressure nil="true"/>
  <route-of-exposure>Inhalation  (L793) ; oral (L793); dermal (L793)</route-of-exposure>
  <target nil="true"/>
  <mechanism-of-toxicity>Diethofencarb 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.</mechanism-of-toxicity>
  <metabolism>The carbamates are hydrolyzed enzymatically by the liver; degradation products are excreted by the kidneys and the liver. (L793)</metabolism>
  <toxicity nil="true"/>
  <lethaldose nil="true"/>
  <carcinogenicity>No indication of carcinogenicity to humans (not listed by IARC).</carcinogenicity>
  <use-source>Diethofencarb is widely used as an insecticide or pesticide in homes, gardens and agricultural applications. It is a synthetic compound.</use-source>
  <min-risk-level nil="true"/>
  <health-effects>Acute 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 (&gt;10 years) exposure leads to neuropsychological consequences including disturbances in perception and visuo-motor processing (A15321).</health-effects>
  <symptoms>As 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. (L795)</symptoms>
  <treatment>If 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.</treatment>
  <created-at type="dateTime">2009-06-17T23:53:02Z</created-at>
  <updated-at type="dateTime">2026-08-19T07:12:41Z</updated-at>
  <interacting-proteins nil="true"/>
  <wikipedia nil="true"/>
  <uniprot-id nil="true"/>
  <kegg-compound-id>C11077</kegg-compound-id>
  <omim-id></omim-id>
  <chebi-id>4520</chebi-id>
  <biocyc-id></biocyc-id>
  <ctd-id>C070961</ctd-id>
  <stitch-id>Diethofencarb</stitch-id>
  <drugbank-id nil="true"/>
  <pdb-id nil="true"/>
  <actor-id nil="true"/>
  <organism nil="true"/>
  <export type="boolean">true</export>
  <metabolizing-proteins nil="true"/>
  <transporting-proteins nil="true"/>
  <moldb-smiles>CCOC1=CC=C(NC(=O)OC(C)C)C=C1OCC</moldb-smiles>
  <moldb-formula>C14H21NO4</moldb-formula>
  <moldb-inchi>InChI=1S/C14H21NO4/c1-5-17-12-8-7-11(9-13(12)18-6-2)15-14(16)19-10(3)4/h7-10H,5-6H2,1-4H3,(H,15,16)</moldb-inchi>
  <moldb-inchikey>LNJNFVJKDJYTEU-UHFFFAOYSA-N</moldb-inchikey>
  <moldb-average-mass type="decimal">267.3208</moldb-average-mass>
  <moldb-mono-mass type="decimal">267.147058165</moldb-mono-mass>
  <origin>Exogenous</origin>
  <state>Solid</state>
  <logp>2.8</logp>
  <hmdb-id nil="true"/>
  <chembl-id>CHEMBL1880404</chembl-id>
  <chemspider-id>82840</chemspider-id>
  <structure-image-file-name nil="true"/>
  <structure-image-content-type nil="true"/>
  <structure-image-file-size type="integer" nil="true"/>
  <structure-image-updated-at type="dateTime" nil="true"/>
  <biodb-id nil="true"/>
  <synthesis-reference></synthesis-reference>
  <structure-image-caption nil="true"/>
  <chemdb-id>CHEM000820</chemdb-id>
  <dsstox-id>DTXSID5037527</dsstox-id>
  <toxcast-id nil="true"/>
  <stoff-ident-origin nil="true"/>
  <stoff-ident-id nil="true"/>
  <susdat-id>NS00010585</susdat-id>
  <iupac>propan-2-yl N-(3,4-diethoxyphenyl)carbamate</iupac>
  <moldb-polar-surface-area>56.790000000000006</moldb-polar-surface-area>
  <moldb-refractivity>74.13560000000001</moldb-refractivity>
  <moldb-polarizability>29.242710008383774</moldb-polarizability>
  <moldb-rotatable-bond-count>7</moldb-rotatable-bond-count>
  <moldb-acceptor-count>4</moldb-acceptor-count>
  <moldb-donor-count>1</moldb-donor-count>
  <moldb-pka-strongest-acidic>13.098443175964576</moldb-pka-strongest-acidic>
  <moldb-pka-strongest-basic>-0.8913942005659905</moldb-pka-strongest-basic>
  <moldb-physiological-charge>0</moldb-physiological-charge>
  <moldb-number-of-rings>1</moldb-number-of-rings>
  <moldb-alogps-logp>3.06</moldb-alogps-logp>
  <moldb-alogps-logs>-3.03</moldb-alogps-logs>
  <moldb-alogps-solubility>2.48e-01 g/l</moldb-alogps-solubility>
  <kingdom>Organic compounds</kingdom>
  <superklass>Benzenoids</superklass>
  <klass>Benzene and substituted derivatives</klass>
  <subklass>Phenylcarbamic acid esters</subklass>
  <paper-count type="integer">79</paper-count>
  <sync-id>CED0014104</sync-id>
  <structure-inchikey>LNJNFVJKDJYTEU-UHFFFAOYSA-N</structure-inchikey>
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  <structure-indexed-at type="dateTime">2026-09-19T03:59:55Z</structure-indexed-at>
</compound>
