<?xml version="1.0" encoding="UTF-8"?>
<compound>
  <id type="integer">3824</id>
  <title>T3D3770</title>
  <common-name>Moniliformin</common-name>
  <description>Moniliformin is a mycotoxin produced by a number of fungi of the Fusarium species. It can by found in contaminated cereal crops and is known to be a lethal food contaminant to fowl as well as a cause of Kashin-Beck disease in humans. (L1969, A3075)</description>
  <cas>71376-34-6</cas>
  <pubchem-id>40452</pubchem-id>
  <chemical-formula>C4H2O3</chemical-formula>
  <weight nil="true"/>
  <appearance>White powder.</appearance>
  <melting-point>158°C</melting-point>
  <boiling-point nil="true"/>
  <density nil="true"/>
  <solubility nil="true"/>
  <specific-gravity nil="true"/>
  <flash-point nil="true"/>
  <vapour-pressure nil="true"/>
  <route-of-exposure>Oral, dermal, inhalation, and parenteral (contaminated drugs). (A3101)</route-of-exposure>
  <target nil="true"/>
  <mechanism-of-toxicity>Moniliformin reversibly inhibits the enzymes pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase by competing for the binding site of pyruvate. This interferes with the tricarboxylic acid cycle by preventing the necessary incorporation of pyruvate and oxidation of the alpha-ketoglutarate intermediate. Moniliformin has also been shown to interfere with carbohydrate metabolism by inhibiting transketolase and aldose reductase. 

Moniliformin causes the necrosis of human chondrocytes in cartilage. It does so by increasing the expression of matrix catabolic enzymes, such as MMP-1 and MMP-13, and decreasing the syntheses of extracellular matrix components such as aggrecan and type II collage. This accelerates the catabolism of the extracellular matrix in articular cartilages, inducing a loss of cartilage function and eventually leading to cartilage degradation. Moniliformin is also known to cause DNA damage, inducing chromatid breaks, chromosome breaks, and chromatid exchanges. (A3075, A3076, A3077)</mechanism-of-toxicity>
  <metabolism nil="true"/>
  <toxicity nil="true"/>
  <lethaldose>LD50: 20.9 mg/kg (Mouse, Intraperitoneal) (A3077)</lethaldose>
  <carcinogenicity>No indication of carcinogenicity to humans (not listed by IARC).</carcinogenicity>
  <use-source>Moniliformin is a mycotoxin produced by a number of fungi of the Fusarium species. It can by found in contaminated cereal crops. (L1969, A3075)</use-source>
  <min-risk-level nil="true"/>
  <health-effects>Moniliformin is believed to be a cause of Kashin-Beck disease, which causes joint destruction and deformity. It may also have immunosuppressive properties and can cause fungal infections such as mycotic keratitis. (A3021, A3075, A3076, L1970)</health-effects>
  <symptoms>The main symptoms of acute moniliformin toxication in animals are muscular weakness, respiratory stress, myocardial degeneration, as well as some histopathological changes in organs such as the kidneys, the lungs and the pancreas, followed by coma and death. Kashin-Beck disease is characterized by joint pain, with restriction of movement and joint enlargement. (A3077)</symptoms>
  <treatment>Kashin-Beck disease cannot be cured but can be treated with physical therapy and corrective surgery. Natamycin ophthalmic suspension is the drug of choice for filamentous fungal infections such as mycotic keratitis. (L1964, L1828)</treatment>
  <created-at type="dateTime">2010-05-25T14:32:14Z</created-at>
  <updated-at type="dateTime">2026-04-06T13:27:20Z</updated-at>
  <interacting-proteins nil="true"/>
  <wikipedia>http://en.wikipedia.org/wiki/Moniliformin</wikipedia>
  <uniprot-id nil="true"/>
  <kegg-compound-id nil="true"/>
  <omim-id nil="true"/>
  <chebi-id nil="true"/>
  <biocyc-id nil="true"/>
  <ctd-id nil="true"/>
  <stitch-id nil="true"/>
  <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>OC1=CC(=O)C1=O</moldb-smiles>
  <moldb-formula>C4H2O3</moldb-formula>
  <moldb-inchi>InChI=1S/C4H2O3/c5-2-1-3(6)4(2)7/h1,5H</moldb-inchi>
  <moldb-inchikey>KGPQKNJSZNXOPV-UHFFFAOYSA-N</moldb-inchikey>
  <moldb-average-mass type="decimal">98.0569</moldb-average-mass>
  <moldb-mono-mass type="decimal">98.00039393</moldb-mono-mass>
  <origin>Exogenous</origin>
  <state>Solid</state>
  <logp nil="true"/>
  <hmdb-id nil="true"/>
  <chembl-id nil="true"/>
  <chemspider-id nil="true"/>
  <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>CHEM002737</chemdb-id>
  <dsstox-id nil="true"/>
  <toxcast-id nil="true"/>
  <stoff-ident-origin nil="true"/>
  <stoff-ident-id nil="true"/>
  <susdat-id>NS00126115</susdat-id>
  <iupac nil="true"/>
  <moldb-polar-surface-area>54.370000000000005</moldb-polar-surface-area>
  <moldb-refractivity>22.8278</moldb-refractivity>
  <moldb-polarizability>8.085928311089098</moldb-polarizability>
  <moldb-rotatable-bond-count>0</moldb-rotatable-bond-count>
  <moldb-acceptor-count>3</moldb-acceptor-count>
  <moldb-donor-count>1</moldb-donor-count>
  <moldb-pka-strongest-acidic>6.3164639937134135</moldb-pka-strongest-acidic>
  <moldb-pka-strongest-basic>-4.965438649149751</moldb-pka-strongest-basic>
  <moldb-physiological-charge>-1</moldb-physiological-charge>
  <moldb-number-of-rings>1</moldb-number-of-rings>
  <moldb-alogps-logp>-0.21</moldb-alogps-logp>
  <moldb-alogps-logs>0.19</moldb-alogps-logs>
  <moldb-alogps-solubility>1.50e+02 g/l</moldb-alogps-solubility>
</compound>
