Enoximone

Enoximone
Clinical data
Trade namesPerfan
AHFS/Drugs.comInternational Drug Names
Routes of
administration		Intravenous
ATC code
Legal status
Legal status
  • UK: POM (Prescription only)
Pharmacokinetic data
Bioavailability50% (oral)
Protein binding85%[1]
MetabolismLiver (oxidation)
Elimination half-life4 to 10 hours[1]
ExcretionRenal (60 to 70%)
Identifiers
  • 4-Methyl-5-{[4-(methylsulfanyl)phenyl]carbonyl}-2,3-dihydro-1H-imidazol-2-one
CAS Number
PubChem CID
DrugBank
ChemSpider
UNII
KEGG
ChEMBL
CompTox Dashboard (EPA)
ECHA InfoCard100.419.380
Chemical and physical data
FormulaC12H12N2O2S
Molar mass248.30 g·mol−1
3D model (JSmol)
Melting point255 to 258 °C (491 to 496 °F) (decomposes)
  • O=C(/C1=C(/NC(=O)N1)C)c2ccc(SC)cc2
  • InChI=1S/C12H12N2O2S/c1-7-10(14-12(16)13-7)11(15)8-3-5-9(17-2)6-4-8/h3-6H,1-2H3,(H2,13,14,16) checkY
  • Key:ZJKNESGOIKRXQY-UHFFFAOYSA-N checkY
  (verify)

Enoximone (INN, trade name Perfan) is an imidazolinone phosphodiesterase inhibitor.[2] It is used in the treatment of congestive heart failure and is selective for phosphodiesterase 3.

Medical uses

Enoximone produces haemodynamic improvement and a fall in pulmonary wedge pressure and vascular resistance. It is used as short-term treatment in acute decompensated heart failure and as a bridge to cardiac transplantation.[3]

However a systematic review of oral phosphodiesterase 3 inhibitors in chronic heart failure, found that longer-term use of enoximone was associated with an increased risk of arrhythmia and mortality, which has limited its role to short-term, intravenous therapy rather than chronic oral treatment.[4][5]

Pharmacology

Pharmacokinetics

Enoximone has an elimination half-life in the range of 4–10 hours with about 85% plasma protein binding.[1]

Pharmacodynamics

Enoximone is a imidazolone derivative that acts as a selective phosphodiesterase 3 (and, to a lesser extent, 4) inhibitor, raising intracellular cyclic AMP in cardiac and vascular smooth muscle to produce positive inotropic and vasodilator effects without significantly increasing cardiac oxygen demand.[5][3]

References

  1. 1 2 3 "Enoximone". DrugBank.
  2. ↑ Vernon MW, Heel RC, Brogden RN (1991). "Enoximone". Drugs. 42 (6): 997–1017. doi:10.2165/00003495-199142060-00008. PMID 1724645.
  3. 1 2 Liam AM, Davidson JC (2002). "The evolving role of the cardiac inotrope, enoximone, in heart failure" (PDF). The British Journal of Cardiology (Acute & Interventional Cardiology). 9 (1): 26–31.
  4. ↑ Amsallem E, Kasparian C, Haddour G, Boissel JP, Nony P (January 2005). "Phosphodiesterase III inhibitors for heart failure". The Cochrane Database of Systematic Reviews. 2005 (1) CD002230. doi:10.1002/14651858.CD002230.pub2. PMC 8407097. PMID 15674893.
  5. 1 2 Vernon MW, Heel RC, Brogden RN (December 1991). "Enoximone. A review of its pharmacological properties and therapeutic potential". Drugs. 42 (6): 997–1017. doi:10.2165/00003495-199142060-00008. PMID 1724645.
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