<?xml version="1.0" encoding="UTF-8"?>
<compound>
  <id type="integer">3071</id>
  <title>T3D3029</title>
  <common-name>Sevoflurane</common-name>
  <description>Sevoflurane is only found in individuals that have used or taken this drug. Sevoflurane (2,2,2-trifluoro-1-[trifluoromethyl]ethyl fluoromethyl ether), also called fluoromethyl, is a sweet-smelling, non-flammable, highly fluorinated methyl isopropyl ether used for induction and maintenance of general anesthesia. Together with desflurane, it is replacing isoflurane and halothane in modern anesthesiology. [Wikipedia] Sevoflurane induces a reduction in junctional conductance by decreasing gap junction channel opening times and increasing gap junction channel closing times. Sevoflurane also activates calcium dependent ATPase in the sarcoplasmic reticulum by increasing the fluidity of the lipid membrane. It also appears to bind the D subunit of ATP synthase and NADH dehydogenase and also binds to the GABA receptor, the large conductance Ca&lt;sup&gt;2+&lt;/sup&gt; activated potassium channel, the glutamate receptor, and the glycine receptor.</description>
  <cas>28523-86-6</cas>
  <pubchem-id>5206</pubchem-id>
  <chemical-formula>C4H3F7O</chemical-formula>
  <weight>200.007210</weight>
  <appearance nil="true"/>
  <melting-point>&lt; 25°C</melting-point>
  <boiling-point>58.5°C</boiling-point>
  <density nil="true"/>
  <solubility>Very slightly soluble</solubility>
  <specific-gravity nil="true"/>
  <flash-point nil="true"/>
  <vapour-pressure nil="true"/>
  <route-of-exposure>Rapidly absorbed into circulation via the lungs, however solubility in the blood is low.</route-of-exposure>
  <target nil="true"/>
  <mechanism-of-toxicity>Sevoflurane induces a reduction in junctional conductance by decreasing gap junction channel opening times and increasing gap junction channel closing times. Sevoflurane also activates calcium dependent ATPase in the sarcoplasmic reticulum by increasing the fluidity of the lipid membrane. It also appears to bind the D subunit of ATP synthase and NADH dehydogenase and also binds to the GABA receptor, the large conductance Ca&lt;sup&gt;2+&lt;/sup&gt; activated potassium channel, the glutamate receptor, and the glycine receptor.</mechanism-of-toxicity>
  <metabolism>Relatively little biotransformation, only 5% is metabolized by cytochrome P450 CYP2E1 to hexafluoroisopropanol (HFIP) with release of inorganic fluoride and CO2. No other metabolic pathways have been identified for sevoflurane.Route of Elimination: The low solubility of sevoflurane facilitates rapid elimination via the lungs. In vivo metabolism studies suggest that approximately 5% of the sevoflurane dose may be metabolized. Up to 3.5% of the sevoflurane dose appears in the urine as inorganic fluoride.Half Life: 15-23 hours</metabolism>
  <toxicity>LD50: 10.8 g/kg (Rat) (A308)LC50: 49881 ppm/hr (Inhalation, Rat) (A308)</toxicity>
  <lethaldose nil="true"/>
  <carcinogenicity>No indication of carcinogenicity to humans (not listed by IARC).</carcinogenicity>
  <use-source>Used for induction and maintenance of general anesthesia in adult and pediatric patients for inpatient and outpatient surgery.</use-source>
  <min-risk-level nil="true"/>
  <health-effects nil="true"/>
  <symptoms></symptoms>
  <treatment>In the event of overdosage, or what may appear to be overdosage, the following action should be taken: discontinue administration of sevoflurane, maintain a patent airway, initiate assisted or controlled ventilation with oxygen, and maintain adequate cardiovascular function. (L1712)</treatment>
  <created-at type="dateTime">2009-07-21T20:28:42Z</created-at>
  <updated-at type="dateTime">2014-12-24T20:25:56Z</updated-at>
  <interacting-proteins nil="true"/>
  <wikipedia>Sevoflurane</wikipedia>
  <uniprot-id></uniprot-id>
  <kegg-compound-id>C07520</kegg-compound-id>
  <omim-id></omim-id>
  <chebi-id>9130</chebi-id>
  <biocyc-id></biocyc-id>
  <ctd-id nil="true"/>
  <stitch-id>Sevoflurane</stitch-id>
  <drugbank-id>DB01236</drugbank-id>
  <pdb-id></pdb-id>
  <actor-id nil="true"/>
  <organism nil="true"/>
  <export type="boolean">true</export>
  <metabolizing-proteins nil="true"/>
  <transporting-proteins nil="true"/>
  <moldb-smiles>FCOC(C(F)(F)F)C(F)(F)F</moldb-smiles>
  <moldb-formula>C4H3F7O</moldb-formula>
  <moldb-inchi>InChI=1S/C4H3F7O/c5-1-12-2(3(6,7)8)4(9,10)11/h2H,1H2</moldb-inchi>
  <moldb-inchikey>InChIKey=DFEYYRMXOJXZRJ-UHFFFAOYSA-N</moldb-inchikey>
  <moldb-average-mass type="decimal">200.0548</moldb-average-mass>
  <moldb-mono-mass type="decimal">200.007212153</moldb-mono-mass>
  <origin>Exogenous</origin>
  <state>Liquid</state>
  <logp>2.4</logp>
  <hmdb-id>HMDB15366</hmdb-id>
  <chembl-id>CHEMBL1200694</chembl-id>
  <chemspider-id>5017</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;Ross C. Terrell, &amp;#8220;Method for the preparation of sevoflurane.&amp;#8221; U.S. Patent US5969193, issued December, 1979.&lt;/p&gt;</synthesis-reference>
  <structure-image-caption nil="true"/>
</compound>
