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Lacosamide: Wikis


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Systematic (IUPAC) name
N2-acetyl-N-benzyl- D-homoserinamide
CAS number 175481-36-4
ATC code N03AX18
PubChem 219078
Chemical data
Formula C 13H18N2O3  
Mol. mass 250.294 g/mol
Synonyms (2R)-2-(acetylamino)-N-benzyl-3-methoxypropanamide
Pharmacokinetic data
Bioavailability High
Metabolism  ?
Half life 13 hours
Excretion  ?
Therapeutic considerations
Pregnancy cat.  ?
Legal status Schedule V (U.S.)
Routes Oral, intravenous

Lacosamide (INN, formerly known as erlosamide) is a medication developed by UCB for the adjunctive treatment of partial-onset seizures and diabetic neuropathic pain marketed under the trade name Vimpat.

The U.S. Food and Drug Administration accepted UCB's New Drug Application for lacosamide as of November 29, 2007, beginning the approval process for the drug.[1][2] UCB also filed for marketing approval in the European Union; the European Medicines Agency accepted the marketing application for review in May 2007.[1][3]

The drug was approved in the EU on September 3, 2008.[4] It was approved in the US on October 29, 2008.[5] Lacosamide release was delayed owing to an objection about its placement into schedule V of the Controlled Substances Act. The FDA issued their final rule of placement into Schedule V on June 22, 2009[6].

Mechanism of action

Lacosamide acts by enhancing slow inactivation of voltage gated sodium channels[7] . Voltage gated sodium channels are the membrane proteins responsible for generating the neuronal action potential, the all or none electrical event which causes neurons to release neurotransmitter. During an action potential voltage gated sodium channels undergo fast inactivation, a process which takes a few milliseconds. This inactivation prevents the channel from opening, and helps end the action potential. Many typical antiepileptic drugs, like carbamazepine or lamotrigine, slow the recovery from inactivation and hence reduce the ability of neurons to fire action potentials. As inactivation only occurs in neurons firing action potentials, this means that drug that modulate fast inactivation selectively reduce the firing in active cells.

Slow inactivation is a similar processes, except that it does not produce complete blockade of voltage gated sodium channels, and it occurs over the course of hundreds of milliseconds or more, and recovery from this state takes equally as long. Lacosamide makes this inactivation happen at less depolarized membrane potentials. This means that lacosamide only effects neurons which are depolarized or active for long periods of time, typical of neurons at the focus of an epileptic focus.[7]

Lacosamide does not affect AMPA, kainate, NMDA, GABAA, GABAB or a variety of dopaminergic, serotonergic, adrenergic, muscarinic or cannabinoid receptors and does not block potassium or calcium currents [8]

Clinical trials

In a large double-blind, randomized clinical trial of people with poorly controlled partial-onset seizures, lacosamide was found to significantly reduce seizure frequency when given in addition to other antiepileptics, at doses of 400 and 600 milligrams a day.[9] In a smaller trial of people with diabetic neuropathy, lacosamide also provided significantly better pain relief when compared to placebo.[10]


  1. ^ a b UCB (2007-11-29). "UCB Announces FDA Filing for lacosamide in the Treatment of Diabetic Neuropathic Pain". Press release. Retrieved 2007-11-29.  
  2. ^ UCB (2007-11-29). "UCB Announces FDA Filing for lacosamide in the Treatment of Partial Onset Seizures in Adults with Epilepsy". Press release. Retrieved 2007-11-29.  
  3. ^ Wan, Yuet (August 17, 2007). "Marketing application for lacosamide (Vimpat) filed in EU for treatment of diabetic neuropathic pain". PharmaTimes through the UK National electronic Library for Medicines. Retrieved 2007-11-30.  
  4. ^ UCB (2008-09-03). "Vimpat Approved in Europe". Press release. Retrieved 2008-09-17.  
  5. ^ UCB (2008-10-29). "UCB's Vimpat approved by U.S. FDA as adjunctive therapy for partial onset seizures in adults". Press release. Retrieved 2008-11-25.  
  6. ^ FDA (2009-06-22). "FDA places lacosamide in Schedule V". Press release. Retrieved 2009-06-28.  
  7. ^ a b Errington AC, Stöhr T, Heers C, Lees G (January 2008). "The investigational anticonvulsant lacosamide selectively enhances slow inactivation of voltage-gated sodium channels". Molecular pharmacology 73 (1): 157–69. doi:10.1124/mol.107.039867. PMID 17940193.  
  8. ^ Errington AC, Coyne L, Stöhr T, Selve N, Lees G (June 2006). "Seeking a mechanism of action for the novel anticonvulsant lacosamide". Neuropharmacology 50 (8): 1016–29. doi:10.1016/j.neuropharm.2006.02.002. PMID 16620882.  
  9. ^ Ben-Menachem E, Biton V, Jatuzis D, Abou-Khalil B, Doty P, Rudd GD (2007). "Efficacy and safety of oral lacosamide as adjunctive therapy in adults with partial-onset seizures". Epilepsia 48 (7): 1308–17. doi:10.1111/j.1528-1167.2007.01188.x. PMID 17635557.  
  10. ^ Rauck RL, Shaibani A, Biton V, Simpson J, Koch B (2007). "Lacosamide in painful diabetic peripheral neuropathy: a phase 2 double-blind placebo-controlled study". Clin J Pain 23 (2): 150–8. doi:10.1097/01.ajp.0000210957.39621.b2. PMID 17237664.  


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