Ethosuximide, sold under the brand name Zarontin among others, is a medication used to treat absence seizures. It may be used by itself or with other antiseizure medications such as valproic acid. Ethosuximide is taken by mouth.[1]
Clinical data
Trade names Zarontin
AHFS/ Monograph
MedlinePlus a682327
  • AU: D
  • US: C (Risk not ruled out)
Routes of
by mouth (capsules, solution)
ATC code N03AD01 (WHO)
Legal status
Legal status
Pharmacokinetic data
Bioavailability 93%[1]
Metabolism liver (CYP3A4, CYP2E1)
Biological half-life 53 hours
Excretion kidney (20%)
CAS Number 77-67-8 YesY
PubChem (CID) 3291
DrugBank DB00593 YesY
ChemSpider 3175 YesY
KEGG D00539 YesY
ECHA InfoCard 100.000.954
Chemical and physical data
Formula C7H11NO2
Molar mass 141.168 g/mol
3D model (Jmol) Interactive image
Chirality Racemic mixture

Ethosuximide, sold under the brand name Zarontin among others, is a medication used to treat absence seizures. It may be used by itself or with other antiseizure medications such as valproic acid. Ethosuximide is taken by mouth.[1]

Side effects are generally minimal.[2] Common side effects include loss of appetite, abdominal pain, diarrhea, and feeling tired.[1] Serious side effects include suicidal thoughts, low blood cell levels, and lupus erythematosus.[1][2] It is unclear if use during pregnancy or under the age of three is safe for the baby. Ethosuximide is in the succinimide family of medications. How exactly it works is unclear.[1]

Ethosuximide was approved for medical use in the United States in 1960.[1] It is on the World Health Organization's List of Essential Medicines, the most important medications needed in a basic health system.[3] Ethosuximide is available as a generic medication.[1] The wholesale cost in the developing world is about 27.77 USD per month.[4] In the United States the wholesale cost as of 2016 is about 41.55 USD per month for a typical dose.[5]

Medical uses

It is approved for absence seizures.[2] Ethosuximide is considered the first choice drug for treating absence seizures in part because it lacks the idiosyncratic hepatotoxicity of the alternative anti-absence drug, valproic acid.[3]

Adverse effects

Central nervous system






The following can occur with or without bone marrow loss:




Drug interactions

Valproates can either decrease or increase the levels of ethosuximide; however, combinations of valproates and ethosuximide had a greater protective index than either drug alone.[4]

It may elevate serum phenytoin levels.

Mechanism of action

The mechanism by which ethosuximide affects neuronal excitability includes block of T-type calcium channels, and may include effects of the drug on other classes of ion channel. The primary finding that ethosuximide is a T-type calcium channel blocker gained widespread support, but initial attempts to replicate the finding were inconsistent. Subsequent experiments on recombinant T-type channels in cell lines demonstrated conclusively that ethosuximide blocks all T-type calcium channel isoforms.[citation needed] Significant T-type calcium channel density occurs in dendrites of neurons, and recordings from reduced preparations that strip away this dendritic source of T-type calcium channels may have contributed to reports of ethosuximide ineffectiveness.

In March 1989, Coulter, Huguenard and Prince showed that ethosuximide and dimethadione, both effective anti-absence agents, reduced low-threshold Ca2+ currents in T-type calcium channels in freshly removed thalamic neurons.[5] In June of that same year, they also found the mechanism of this reduction to be voltage-dependent, using acutely dissociated neurons of rats and guinea pigs; it was also noted that valproic acid, which is also used in absence seizures, did not do that.[6] The next year, they showed that anticonvulsant succinimides did this and that the pro-convulsant ones did not.[7] The first part was supported by Kostyuk et al. in 1992, who reported a substantial reduction in current in dorsal root ganglia at concentrations ranging from 7 µmol/L to 1 mmol/L.[8]

That same year, however, Herrington and Lingle found no such effect at concentrations of up to 2.5 mmol/L.[9] The year after, a study conducted on human neocortical cells removed during surgery for intractable epilepsy, the first to use human tissue, found that ethosuximide had no effect on Ca2+ currents at the concentrations typically needed for a therapeutic effect.[10]

In 1998, Slobodan M. Todorovic and Christopher J. Lingle of Washington University reported a 100% block of T-type current in dorsal root ganglia at 23.7 ± 0.5 mmol/L, far higher than Kostyuk reported.[11] That same year, Leresche et al. reported that ethosuximide had no effect on T-type currents, but did decrease noninactivating Na+ current by 60% and the Ca2+-activated K+ currents by 39.1 ± 6.4% in rat and cat thalamocortical cells. It was concluded that the decrease in Na+ current is responsible for the anti-absence properties.[12]

In the introduction of a paper published in 2001, Dr. Juan Carlos Gomora and colleagues at the University of Virginia in Charlottesville pointed out that past studies were often done in isolated neurons that had lost most of their T-type channels.[13] Using cloned α1G, α1H, and α1I T-type calcium channels, Gomora's team found that ethosuximide blocked the channels with an IC50 of 12 ± 2 mmol/L and that of N-desmethylmethsuximide (the active metabolite of mesuximide) is 1.95 ± 0.19 mmol/L for α1G, 1.82 ± 0.16 mmol/L for α1I, and 3.0 ± 0.3 mmol/L for α1H. It was suggested that the blockade of open channels is facilitated by ethosuximide's physically plugging the channels when current flows inward.


Ethosuximide is marketed under the trade names Emeside and Zarontin. However, both capsule preparations were discontinued from production, leaving only generic preparations available. Emeside capsules were discontinued by their manufacturer, Laboratories for Applied Biology, in 2005.[6] Similarly, Zarontin capsules were discontinued by Pfizer in 2007.[7] Syrup preparations of both brands remained available.

See also


  1. ^ a b c d e f "Ethosuximide". The American Society of Health-System Pharmacists. Retrieved 8 December 2016. 
  2. ^ a b WHO Model Formulary 2008 (PDF). World Health Organization. 2009. pp. 69, 74–75. ISBN 9789241547659. Retrieved 8 December 2016. 
  3. ^ "WHO Model List of Essential Medicines" (PDF). World Health Organization. October 2013. Retrieved 22 April 2014. 
  4. ^ "Ethosuximide". International Drug Price Indicator Guide. Retrieved 8 December 2016. 
  5. ^ "NADAC as of 2016-12-07 |". Centers for Medicare and Medicaid Services. Retrieved 13 December 2016. 
  6. ^ "Concern over ethosuximide capsule discontinuation". Pharm J. Oct 29, 2005. p. 539. Retrieved 2008-08-31.  (paywalled archive)
  7. ^ "Zarontin capsules discontinued". Retrieved 2012-10-24. 


  1. ^ Patsalos, P. N. (November 2005). "Properties of Antiepileptic Drugs in the Treatment of Idiopathic Generalized Epilepsies". Epilepsia. 46 (s9): 140–144. doi:10.1111/j.1528-1167.2005.00326.x. PMID 16302888. 
  2. ^ Pharmaceutical Associates, Incorporated (2000). "Ethosuximide Approval Label" (PDF). Label and Approval History. Food and Drug Administration Center for Drug Evaluation and Research. Retrieved 2006-02-05. 
  3. ^ Katzung, B., ed. (2003). "Drugs used in generalized seizures". Basic and Clinical Pharmacology (9th ed.). Lange Medical Books/McGraw-Hill. ISBN 0071410929. 
  4. ^ Andrulonis, P. A.; J. Donnelly; B. C. Glueck; C. F. Stroebel; B. L. Szabek (November 1980). "Preliminary data on ethosuximide and the Episodic dyscontrol syndrome". American Journal of Psychiatry. 137 (11): 1455–6. PMID 7435689. 
  5. ^ Coulter DA, Huguenard JR, Prince DA (Mar 13, 1989). "Specific petit mal anticonvulsants reduce calcium currents in thalamic neurons". Neurosci Lett. 98 (1): 74–8. doi:10.1016/0304-3940(89)90376-5. PMID 2710401. 
  6. ^ Coulter DA, Huguenard JR, Prince DA (June 1989). "Characterization of ethosuximide reduction of low-threshold calcium current in thalamic neurons". Annals of Neurology. 25 (6): 582–93. doi:10.1002/ana.410250610. PMID 2545161. 
  7. ^ Coulter DA, Huguenard JR, Prince DA (August 1990). "Differential effects of petit mal anticonvulsants and convulsants on thalamic neurones: calcium current reduction". British Journal of Pharmacology. 100 (4): 800–6. doi:10.1111/j.1476-5381.1990.tb14095.x. PMC 1917607Freely accessible. PMID 2169941. 
  8. ^ Kostyuk PG, Molokanova EA, Pronchuk NF, Savchenko AN, Verkhratsky AN (December 1992). "Different action of ethosuximide on low- and high-threshold calcium currents in rat sensory neurons". Neuroscience. 51 (4): 755–8. doi:10.1016/0306-4522(92)90515-4. PMID 1336826. 
  9. ^ Herrington J, Lingle CJ (July 1992). "Kinetic and pharmacological properties of low voltage-activated Ca2+ current in rat clonal (GH3) pituitary cells". Journal of Neurophysiology. 68 (1): 213–32. PMID 1325546. 
  10. ^ Sayer RJ, Brown AM, Schwindt PC, Crill WE. "Calcium currents in acutely isolated human neocortical neurons." Journal of Neurophysiology. 1993 May;69(5):1596-606. PMID 8389832 Fulltext
  11. ^ Todorovic SM, Lingle CJ (January 1, 1998). "Pharmacological properties of T-type Ca2+ current in adult rat sensory neurons: effects of anticonvulsant and anesthetic agents". Journal of Neurophysiology. 79 (1): 240–52. PMID 9425195. 
  12. ^ Leresche N, Parri HR, Erdemli G, Guyon A, Turner JP, Williams SR, Asprodini E, Crunelli V (July 1, 1998). "On the action of the anti-absence drug ethosuximide in the rat and cat thalamus". Journal of Neuroscience. 18 (13): 4842–53. PMID 9634550. 
  13. ^ Gomora JC, Daud AN, Weiergraber M, Perez-Reyes E (2001). "Block of cloned human T-type calcium channels by succinimide antiepileptic drugs". Molecular Pharmacology. 60 (5): 1121–32. PMID 11641441. 
  14. ^ Bourgeois, BF (December 1988). "Combination of valproate and ethosuximide: antiepileptic and neurotoxic interaction". The Journal of Pharmacology and Experimental Therapeutics. 247 (3): 1128–32. PMID 3144596. 

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