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Trade namesFelbatol
  • (3-carbamoyloxy-2-phenylpropyl) carbamate
Clinical data
Drug classAnticonvulsant
Main usesPartial seizures, Lennox–Gastaut syndrome[1]
Side effectsNausea, trouble sleeping, headache, aplastic anemia, liver failure, Stevens-Johnson syndrome, suicide[1]
  • US: C (Risk not ruled out)
Routes of
By mouth (tablets, suspension)
External links
Legal status
  • In general: ℞ (Prescription only)
Elimination half-life20–23 hours
Chemical and physical data
Molar mass238.24 g·mol−1
3D model (JSmol)
  • O=C(N)OCC(c1ccccc1)COC(N)=O
  • InChI=1S/C11H14N2O4/c12-10(14)16-6-9(7-17-11(13)15)8-4-2-1-3-5-8/h1-5,9H,6-7H2,(H2,12,14)(H2,13,15) checkY

Felbamate, sold under the brand name Felbatol, is medication used to treat epilepsy.[1] It is specifically used to treat partial seizures and Lennox–Gastaut syndrome.[1] It is only recommended with safer options are not effective.[1] It is taken by mouth.[1]

Common side effects include loss of appetite, nausea, trouble sleeping, and headache.[1] Side effects may include aplastic anemia, liver failure, Stevens-Johnson syndrome, and suicide.[1] Safety in pregnancy is unclear.[1] How it works is not clear.[1]

Felbamate was approved for medical use in the United States in 1993.[1] It is not approved in the United Kingdom, but can be acquired if other option are not effective.[2] In the United States 30 tablets of 600 mg cost about 95 USD as of 2021.[3]

Medical uses

  • Adults: Monotherapy or adjunctive therapy in the treatment of partial seizures, with and without generalization.
  • Children: Adjunctive therapy in the treatment of partial and generalized seizures associated with Lennox-Gastaut syndrome.


Felbamate is available in tablets (400 mg and 600 mg) and as a peach-coloured oral suspension (600 mg/5 mL).

  • Adults (≥ 14 years): begin with 1,200 mg daily, divided into every 6 to 8 hours
  • Children (2–14 years): 15 to 45 mg per kg per day given every 6 to 8 hours

Side effects

Adverse reactions include decreased appetite, vomiting, insomnia, nausea, dizziness, somnolence, and headache. Many patients report increased alertness with the drug. Two rare but very serious effects include aplastic anemia and serious liver damage. The risk of aplastic anemia is between 1:3,600 and 1:5,000, of which 30% of cases are fatal. The risk of liver damage is between 1:24,000 to 1:34,000, of which 40% of cases are fatal.[citation needed]


Felbamate is an inhibitor of CYP2C19 - an enzyme involved in the metabolism of several commonly used medications.[4] Felbamate interacts with several other AEDs, including phenytoin, valproate, and carbamazepine; dosage adjustments may be necessary to avoid adverse effects. Concomitant administration of felbamate and carbamazepine decreases blood levels of both drugs, while increasing the level of carbamazepine-10,11 epoxide, the active metabolite of carbamazepine.[5]

Mechanism of action

Felbamate has been proposed to have a unique dual mechanism of action as a positive modulator of GABAA receptors[6][7] and as a blocker of NMDA receptors, particularly isoforms containing the NR2B subunit.[8][9][10][11] Although it is clear that felbamate does cause pharmacological inhibition of NMDA receptors, the relevance of NMDA receptor blockade as a strategy for the treatment of human epilepsy has been questioned.[12] Therefore, the importance of the effects of felbamate on NMDA receptors to its therapeutic action in epilepsy is uncertain.


Felbamate was discovered by Frank Berger at Wallace Laboratories.[13]

United States

  • August 1993. Felbamate was approved for partial seizures with and without secondary generalization in adults and for Lennox–Gastaut Syndrome, a serious form of childhood epilepsy. Over the following year 150,000 people were started on felbamate therapy and a third of these became established.
  • August 1, 1994. It was urgently withdrawn after 10 cases of aplastic anemia.[14] A "Dear Doctor" letter was sent to 240,000 physicians.
  • September 27, 1994. Felbamate had a limited redemption in another "Dear Doctor" letter sent to 260,000 physicians. It was recommended that the drug remain available only for patients with severe epilepsy for whom the benefits outweigh the risks, and that changes be made to the product's labelling to reflect the newly recognized risk.[15] This redemption came with an additional warning since there had been 10 cases acute liver failure (4 of which were fatal). At this point, 10,000 to 12,000 people remained on the drug.

United Kingdom

  • The drug is only available on a limited named-patient basis.


  1. 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 "Felbamate Monograph for Professionals". Drugs.com. Archived from the original on 6 November 2021. Retrieved 10 December 2021.
  2. BNF 81: March-September 2021. BMJ Group and the Pharmaceutical Press. 2021. p. 324. ISBN 978-0857114105.
  3. "Felbamate Prices, Coupons & Patient Assistance Programs". Drugs.com. Retrieved 10 December 2021.
  4. Flockhart DA (2007). "Drug Interactions: Cytochrome P450 Drug Interaction Table". Indiana University School of Medicine. Archived from the original on 2007-10-10. Retrieved 2020-11-29. Retrieved on December 25, 2008.
  5. Curry WJ, Kulling DL (February 1998). "Newer Antiepileptic Drugs: Gabapentin, Lamotrigine, Felbamate, Topiramate and Fosphenytoin". Am Fam Physician. 57 (3): 513–20. PMID 9475899. Archived from the original on 2011-09-27. Retrieved 2020-11-29.
  6. Rho JM, Donevan SD, Rogawski MA (Feb 1994). "Mechanism of Action of the Anticonvulsant Felbamate: Opposing Effects on N-Methyl-D-aspartate and Gamma-Aminobutyric Acid A Receptors". Annals of Neurology. 35 (2): 229–34. doi:10.1002/ana.410350216. PMID 8109904. S2CID 33913077.
  7. Kume A, Greenfield LJ, Macdonald RL, Albin RL (June 1996). "Felbamate Inhibits [3H]t-Butylbicycloorthobenzoate (TBOB) Binding and Enhances Cl Current at the Gamma-Aminobutyric Acid A (GABAA) Receptor". J. Pharmacol. Exp. Ther. 277 (3): 1784–92. PMID 8667250. Archived from the original on 2021-10-31. Retrieved 2020-11-29.
  8. Subramaniam S, Rho JM, Penix L, Donevan SD, Fielding RP, Rogawski MA (May 1995). "Felbamate Block of the N-Methyl-D-aspartate Receptor". The Journal of Pharmacology and Experimental Therapeutics. 273 (2): 878–86. PMID 7752093.
  9. Kleckner NW, Glazewski JC, Chen CC, Moscrip TD (May 1999). "Subtype-Selective Antagonism of N-Methyl-D-aspartate Receptors by Felbamate: Insights into the Mechanism of Action". The Journal of Pharmacology and Experimental Therapeutics. 289 (2): 886–894. PMID 10215667.
  10. Harty TP, Rogawski MA (March 2000). "Felbamate Block of Recombinant N-Methyl-D-aspartate Receptors: Selectivity for the NR2B Subunit". Epilepsy Research. 39 (1): 47–55. doi:10.1016/s0920-1211(99)00108-4. PMID 10690753. S2CID 25467576. Archived from the original on 2021-10-31. Retrieved 2020-11-29.
  11. Chang HR, Chung-Chin Kuo CC (March 2008). "Molecular determinants of the anticonvulsant felbamate binding site in the N-methyl-D-aspartate receptor". Journal of Medicinal Chemistry. 51 (6): 1534–45. doi:10.1021/jm0706618. PMID 18311896.
  12. Rogawski MA (March 2011). "Revisiting AMPA Receptors as an Antiepileptic Drug Target". Epilepsy Currents. 11 (2): 56–63. doi:10.5698/1535-7511-11.2.56. PMC 3117497. PMID 21686307.
  13. "Frank Berger". Daily Telegraph. 2008-04-07. ISSN 0307-1235. Archived from the original on 2018-09-22. Retrieved 2018-09-22.
  14. "www.fda.gov". Archived from the original on November 2, 2008. Retrieved 2008-11-15.
  15. "www.fda.gov". Archived from the original on September 29, 2007. Retrieved 2008-11-15.

External links