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<compound>
  <id type="integer">2103</id>
  <title>T3D2099</title>
  <common-name>1,2,3,7,9-Pentachlorodibenzo-p-dioxin</common-name>
  <description>1,2,3,7,9-Pentachlorodibenzo-p-dioxin is an exogenous organic compound with the formula C12H3Cl5O2 and an average molecular weight of 356.42 g/mol. It exists as a solid at room temperature. 1,2,3,7,9-Pentachlorodibenzo-p-dioxin belongs to the benzo-p-dioxins, a subclass of benzodioxins within the organic compounds.

This compound targets several proteins to exert its effects. It binds to the aryl hydrocarbon receptor (AHR), which alters the transcription of certain genes. It also causes endocrine disruption in humans by binding to and inhibiting the estrogen receptor (ESR1) and estrogen receptor beta (ESR2). Additionally, metabolites of chlorinated dibenzo-p-dioxins are believed to disrupt the production, transport, and disposition of thyroid hormones by competing with thyroxine to bind to transthyretin (TTR). This interaction decreases serum thyroid hormone levels and has been linked to neurobehavioral alterations and thyroid toxicity.</description>
  <cas>71925-17-2</cas>
  <pubchem-id>51456</pubchem-id>
  <chemical-formula>C12H3Cl5O2</chemical-formula>
  <weight>353.857570</weight>
  <appearance>Colorless solid.</appearance>
  <melting-point></melting-point>
  <boiling-point nil="true"/>
  <density nil="true"/>
  <solubility></solubility>
  <specific-gravity nil="true"/>
  <flash-point nil="true"/>
  <vapour-pressure nil="true"/>
  <route-of-exposure>Oral (L177) ; inhalation(L177) ; dermal (L177)</route-of-exposure>
  <target nil="true"/>
  <mechanism-of-toxicity>CDDs cause their toxic effects by binding to the aryl hydrocarbon receptor and subsequently altering the trascription of certain genes. The affinity for the Ah receptor depends on the structure of the specific CDD. The change in gene expression may result from the direct interaction of the Ah receptor and its heterodimer-forming partner, the aryl hydrocarbon receptor nuclear translocator, with gene regulatory elements or the initiation of a phosphorylation/dephosphorylation cascade that subsequently activates other transcription factors. The affected genes include several oncogenes, growth factors, receptors, hormones, and drug-metabolizing enzymes. The change in transcription/translation of these genes is believed to be the cause of most of the toxic effects of CDDs. (L177)</mechanism-of-toxicity>
  <metabolism>CDDs are absorbed through oral, inhalation, and dermal routes of exposure. CDDs are carried in the plasma by serum lipids and lipoproteins, distributing mainly to the liver and adipose tissue. CDDs are very slowly metabolized by the microsomal monooxygenase system to polar metabolites that can undergo conjugation with glucuronic acid and glutathione. They may increase the rate of their own metabolism by inducing both phase I and phase II enzymes. The major routes of excretion of CDDs are the bile and the faeces, though smaller amounts are excreted in the urine and via lactation. (L177)</metabolism>
  <toxicity nil="true"/>
  <lethaldose nil="true"/>
  <carcinogenicity>3, not classifiable as to its carcinogenicity to humans. (L135)</carcinogenicity>
  <use-source>Dioxins occur as by-products from the manufacture of organochlorides, the bleaching of paper, chlorination by waste and drinking water treatment plants, municipal solid waste and industrial incinerators, and natural sources such as volcanoes and forest fires. (L177, L178) </use-source>
  <min-risk-level>Acute Oral: 0.0002 ug/kg/day (L134) 
Intermediate Oral: 0.00002 ug/kg/day (L134) 
Chronic Oral: 0.000001 ug/kg/day (L134) </min-risk-level>
  <health-effects>Exposure to large amounts of CDDs causes chloracne, a severe skin disease with acne-like lesions that occur mainly on the face and upper body. CDDs may also cause liver damage and induce long-term alterations in glucose metabolism and subtle changes in hormonal levels. In addition, studies have shown that CDDs may disrupt the endocrine system and weaken the immune system, as well as cause reproductive damage and birth defects, central and peripheral nervous system pathology, thyroid disorders, endometriosis, and diabetes. (L177, L178) </health-effects>
  <symptoms>In addition to chloracne, CDD exposure causes skin rashes, discoloration, and excessive body hair. (L177) </symptoms>
  <treatment>Treatment of CDD exposure may include washing the area of contact, GI decontamination, administering an IV, or forced alkaline diuresis. (L346) </treatment>
  <created-at type="dateTime">2009-06-24T17:37:28Z</created-at>
  <updated-at type="dateTime">2026-08-18T21:10:32Z</updated-at>
  <interacting-proteins nil="true"/>
  <wikipedia nil="true"/>
  <uniprot-id nil="true"/>
  <kegg-compound-id></kegg-compound-id>
  <omim-id></omim-id>
  <chebi-id></chebi-id>
  <biocyc-id></biocyc-id>
  <ctd-id nil="true"/>
  <stitch-id>1,2,3,7,9-Pentachlorodibenzo-p-dioxin</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>ClC1=CC(Cl)=C2OC3=C(OC2=C1)C=C(Cl)C(Cl)=C3Cl</moldb-smiles>
  <moldb-formula>C12H3Cl5O2</moldb-formula>
  <moldb-inchi>InChI=1S/C12H3Cl5O2/c13-4-1-6(15)11-7(2-4)18-8-3-5(14)9(16)10(17)12(8)19-11/h1-3H</moldb-inchi>
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  <moldb-average-mass type="decimal">356.416</moldb-average-mass>
  <moldb-mono-mass type="decimal">353.857567875</moldb-mono-mass>
  <origin>Exogenous</origin>
  <state>Solid</state>
  <logp>6.5</logp>
  <hmdb-id nil="true"/>
  <chembl-id nil="true"/>
  <chemspider-id>46607</chemspider-id>
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  <structure-image-updated-at type="dateTime" nil="true"/>
  <biodb-id nil="true"/>
  <synthesis-reference></synthesis-reference>
  <structure-image-caption nil="true"/>
  <chemdb-id>CHEM001842</chemdb-id>
  <dsstox-id nil="true"/>
  <toxcast-id nil="true"/>
  <stoff-ident-origin nil="true"/>
  <stoff-ident-id nil="true"/>
  <susdat-id>NS00125577</susdat-id>
  <iupac>1,2,3,7,9-pentachlorodibenzo-p-dioxin</iupac>
  <moldb-polar-surface-area>18.46</moldb-polar-surface-area>
  <moldb-refractivity>76.5056</moldb-refractivity>
  <moldb-polarizability>30.604140865773545</moldb-polarizability>
  <moldb-rotatable-bond-count>0</moldb-rotatable-bond-count>
  <moldb-acceptor-count>0</moldb-acceptor-count>
  <moldb-donor-count>0</moldb-donor-count>
  <moldb-pka-strongest-acidic nil="true"/>
  <moldb-pka-strongest-basic>-9.29469330090832</moldb-pka-strongest-basic>
  <moldb-physiological-charge>0</moldb-physiological-charge>
  <moldb-number-of-rings>3</moldb-number-of-rings>
  <moldb-alogps-logp>7.07</moldb-alogps-logp>
  <moldb-alogps-logs>-6.37</moldb-alogps-logs>
  <moldb-alogps-solubility>1.50e-04 g/l</moldb-alogps-solubility>
  <kingdom>Organic compounds</kingdom>
  <superklass>Organoheterocyclic compounds</superklass>
  <klass>Benzodioxins</klass>
  <subklass>Benzo-p-dioxins</subklass>
  <paper-count type="integer">0</paper-count>
  <sync-id>CED0097268</sync-id>
  <structure-inchikey>UAOYHTXYVWEPIB-UHFFFAOYSA-N</structure-inchikey>
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  <structure-indexed-at type="dateTime">2026-09-19T04:00:22Z</structure-indexed-at>
</compound>
