<?xml version="1.0" encoding="UTF-8"?>
<compound>
  <id type="integer">2876</id>
  <title>T3D2834</title>
  <common-name>Ethosuximide</common-name>
  <description>Ethosuximide is only found in individuals that have used or taken this drug. It is an anticonvulsant especially useful in the treatment of absence seizures unaccompanied by other types of seizures. [PubChem]Binds to T-type voltage sensitive calcium channels. Voltage-sensitive calcium channels (VSCC) mediate the entry of calcium ions into excitable cells and are also involved in a variety of calcium-dependent processes, including muscle contraction, hormone or neurotransmitter release, gene expression, cell motility, cell division and cell death. The isoform alpha-1G gives rise to T-type calcium currents. T-type calcium channels belong to the low-voltage activated (LVA) group and are strongly blocked by mibefradil. A particularity of this type of channels is an opening at quite negative potentials and a voltage-dependent inactivation. T-type channels serve pacemaking functions in both central neurons and cardiac nodal cells and support calcium signaling in secretory cells and vascular smooth muscle. They may also be involved in the modulation of firing patterns of neurons which is important for information processing as well as in cell growth processes.</description>
  <cas>77-67-8</cas>
  <pubchem-id>3291</pubchem-id>
  <chemical-formula>C7H11NO2</chemical-formula>
  <weight>141.078980</weight>
  <appearance>White powder.</appearance>
  <melting-point>64.5°C</melting-point>
  <boiling-point nil="true"/>
  <density nil="true"/>
  <solubility>39.2 g/L</solubility>
  <specific-gravity nil="true"/>
  <flash-point nil="true"/>
  <vapour-pressure nil="true"/>
  <route-of-exposure>Bioavailability following oral administration is 93%.</route-of-exposure>
  <target nil="true"/>
  <mechanism-of-toxicity>Binds to T-type voltage sensitive calcium channels. Voltage-sensitive calcium channels (VSCC) mediate the entry of calcium ions into excitable cells and are also involved in a variety of calcium-dependent processes, including muscle contraction, hormone or neurotransmitter release, gene expression, cell motility, cell division and cell death. The isoform alpha-1G gives rise to T-type calcium currents. T-type calcium channels belong to the "low-voltage activated (LVA)" group and are strongly blocked by mibefradil. A particularity of this type of channels is an opening at quite negative potentials and a voltage-dependent inactivation. T-type channels serve pacemaking functions in both central neurons and cardiac nodal cells and support calcium signaling in secretory cells and vascular smooth muscle. They may also be involved in the modulation of firing patterns of neurons which is important for information processing as well as in cell growth processes.</mechanism-of-toxicity>
  <metabolism>Hepatic, via CYP3A4 and CYP2E1.Half Life: 53 hours</metabolism>
  <toxicity nil="true"/>
  <lethaldose nil="true"/>
  <carcinogenicity>No indication of carcinogenicity to humans (not listed by IARC).</carcinogenicity>
  <use-source>For the treatment of petit mal epilepsy.</use-source>
  <min-risk-level nil="true"/>
  <health-effects>May cause a potentially dangerous rash that may develop into Stevens Johnson syndrome, an extremely rare but potentially fatal skin disease.</health-effects>
  <symptoms>Acute overdoses may produce nausea, vomiting, and CNS depression including coma with respiratory depression.</symptoms>
  <treatment>Treatment should include emesis (unless the patient is or could rapidly become obtunded, comatose, or convulsing) or gastric lavage, activated charcoal, cathartics, and general supportive measures. Hemodialysis may be useful to treat ethosuximide overdose. Forced diuresis and exchange transfusions are ineffective. (L1712)</treatment>
  <created-at type="dateTime">2009-07-21T20:27:13Z</created-at>
  <updated-at type="dateTime">2026-03-31T19:42:05Z</updated-at>
  <interacting-proteins nil="true"/>
  <wikipedia>Ethosuximide</wikipedia>
  <uniprot-id></uniprot-id>
  <kegg-compound-id>C07505</kegg-compound-id>
  <omim-id></omim-id>
  <chebi-id>4887</chebi-id>
  <biocyc-id></biocyc-id>
  <ctd-id nil="true"/>
  <stitch-id>Ethosuximide</stitch-id>
  <drugbank-id>DB00593</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>CCC1(C)CC(=O)NC1=O</moldb-smiles>
  <moldb-formula>C7H11NO2</moldb-formula>
  <moldb-inchi>InChI=1S/C7H11NO2/c1-3-7(2)4-5(9)8-6(7)10/h3-4H2,1-2H3,(H,8,9,10)</moldb-inchi>
  <moldb-inchikey>HAPOVYFOVVWLRS-UHFFFAOYSA-N</moldb-inchikey>
  <moldb-average-mass type="decimal">141.1677</moldb-average-mass>
  <moldb-mono-mass type="decimal">141.078978601</moldb-mono-mass>
  <origin>Exogenous</origin>
  <state>Solid</state>
  <logp>0.38</logp>
  <hmdb-id>HMDB14731</hmdb-id>
  <chembl-id>CHEMBL696</chembl-id>
  <chemspider-id>3175</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;Miller, C.A. and Long, L.M.; U.S. Patent 2,993,835; July 25,1961; assigned to Parke, Davis and Company.&lt;/p&gt;</synthesis-reference>
  <structure-image-caption nil="true"/>
  <chemdb-id>CHEM002226</chemdb-id>
  <dsstox-id>DTXSID7023019</dsstox-id>
  <toxcast-id nil="true"/>
  <stoff-ident-origin nil="true"/>
  <stoff-ident-id nil="true"/>
  <susdat-id>NS00010826</susdat-id>
  <iupac>3-ethyl-3-methylpyrrolidine-2,5-dione</iupac>
</compound>
