<?xml version="1.0" encoding="UTF-8"?>
<compound>
  <id type="integer">4839</id>
  <title>T3D4784</title>
  <common-name>Clofibrate</common-name>
  <description>A fibric acid derivative used in the treatment of hyperlipoproteinemia type III and severe hypertriglyceridemia.</description>
  <cas>637-07-0</cas>
  <pubchem-id>2796</pubchem-id>
  <chemical-formula>C12H15ClO3</chemical-formula>
  <weight nil="true"/>
  <appearance>White powder.</appearance>
  <melting-point>118-119°C</melting-point>
  <boiling-point>149°C at 2.00E+01 mm Hg</boiling-point>
  <density nil="true"/>
  <solubility>Insoluble</solubility>
  <specific-gravity nil="true"/>
  <flash-point nil="true"/>
  <vapour-pressure nil="true"/>
  <route-of-exposure>Completely but slowly absorbed from the intestine. Between 95% and 99% of an oral dose of clofibrate is excreted in the urine as free and conjugated clofibric acid; thus, the absorption of clofibrate is virtually complete.</route-of-exposure>
  <target nil="true"/>
  <mechanism-of-toxicity>Clofibrate increases the activity of extrahepatic lipoprotein lipase (LL), thereby increasing lipoprotein triglyceride lipolysis. Chylomicrons are degraded, VLDLs are converted to LDLs, and LDLs are converted to HDL. This is accompanied by a slight increase in secretion of lipids into the bile and ultimately the intestine. Clofibrate also inhibits the synthesis and increases the clearance of apolipoprotein B, a carrier molecule for VLDL. Also, as a fibrate, Clofibrate is an agonist of the PPAR-‘± receptor[4] in muscle, liver, and other tissues. This agonism ultimately leads to modification in gene expression resulting in increased beta-oxidation, decreased triglyceride secretion, increased HDL, increased lipoprotein lipase activity.</mechanism-of-toxicity>
  <metabolism>Hepatic and gastrointestinal: rapid de-esterification occurs in the gastrointestinal tract and/or on first-pass metabolism to produce the active form, clofibric acid (chlorophenoxy isobutyric acid [CPIB]).Half Life: Half-life in normal volunteers averages 18 to 22 hours (range 14 to 35 hours) but can vary by up to 7 hours in the same subject at different times.</metabolism>
  <toxicity>Oral, mouse: LD&lt;sub&gt;50&lt;/sub&gt; = 1220 mg/kg; Oral, rabbit: LD&lt;sub&gt;50&lt;/sub&gt; = 1370 mg/kg; Oral, rat: LD&lt;sub&gt;50&lt;/sub&gt; = 940 mg/kg.</toxicity>
  <lethaldose nil="true"/>
  <carcinogenicity>3, not classifiable as to its carcinogenicity to humans. (L135)</carcinogenicity>
  <use-source>For Primary Dysbetalipoproteinemia (Type III hyperlipidemia) that does not respond adequately to diet. This helps control high cholesterol and high triglyceride levels. </use-source>
  <min-risk-level nil="true"/>
  <health-effects nil="true"/>
  <symptoms nil="true"/>
  <treatment nil="true"/>
  <created-at type="dateTime">2014-09-11T05:16:26Z</created-at>
  <updated-at type="dateTime">2026-04-03T01:08:46Z</updated-at>
  <interacting-proteins nil="true"/>
  <wikipedia>Clofibrate</wikipedia>
  <uniprot-id nil="true"/>
  <kegg-compound-id>C06916</kegg-compound-id>
  <omim-id nil="true"/>
  <chebi-id>3750</chebi-id>
  <biocyc-id nil="true"/>
  <ctd-id nil="true"/>
  <stitch-id nil="true"/>
  <drugbank-id>DB00636</drugbank-id>
  <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>CCOC(=O)C(C)(C)OC1=CC=C(Cl)C=C1</moldb-smiles>
  <moldb-formula>C12H15ClO3</moldb-formula>
  <moldb-inchi>InChI=1S/C12H15ClO3/c1-4-15-11(14)12(2,3)16-10-7-5-9(13)6-8-10/h5-8H,4H2,1-3H3</moldb-inchi>
  <moldb-inchikey>KNHUKKLJHYUCFP-UHFFFAOYSA-N</moldb-inchikey>
  <moldb-average-mass type="decimal">242.699</moldb-average-mass>
  <moldb-mono-mass type="decimal">242.070972053</moldb-mono-mass>
  <origin>Exogenous</origin>
  <state>Solid</state>
  <logp>3.3</logp>
  <hmdb-id>HMDB14774</hmdb-id>
  <chembl-id>CHEMBL565</chembl-id>
  <chemspider-id>2694</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>&lt;p&gt;Jones, W.G.M.,Thorp, J.M. and Waring, W.S.; U.S. Patent 3,262,850; July 26, 1966; assigned to Imperial Chemical Industries Limited, England.&lt;/p&gt;</synthesis-reference>
  <structure-image-caption nil="true"/>
  <chemdb-id>CHEM003741</chemdb-id>
  <dsstox-id>DTXSID3020336</dsstox-id>
  <toxcast-id nil="true"/>
  <stoff-ident-origin nil="true"/>
  <stoff-ident-id nil="true"/>
  <susdat-id>NS00015389</susdat-id>
  <iupac>ethyl 2-(4-chlorophenoxy)-2-methylpropanoate</iupac>
</compound>
