6. Erlosamide [inn]
7. Spm 927
10. Add 234037
14. Propanamide, 2-(acetylamino)-3-methoxy-n-(phenylmethyl)-, (2r)-
19. Lacosamide [usan]
22. Lacosamide [usan:inn:ban]
23. Add 243037
25. Lacosamide Racemate
26. Vimpat (tn)
27. Lacosamide (usan/inn)
34. Lacosamide (jan/usan/inn)
35. Erlosamide, Vimpat, Lacosamide
40. Dea No. 2746
70. Bb 0260890
79. (r)-n-benzyl 2-acetamido-3-methoxypropionamide
80. (r)-n-benzyl 2-acetamido-3-methoxypropionamide,
93. ( )-(2r)-2-(acetylamino)-n-benzyl-3-methoxypropanamide
95. 2-(acetylamino)-3-methoxy-n-(phenylmethyl)propanamide, (2r)-
96. Lacosamide; Propanamide,2-(acetylamino)-3-methoxy-n-(phenylmethyl)-, (r)-
97. Propanamide 2-(acetylamino)-3-methoxy-n-(phenylmethyl)- (2r)-
98. Lacosamide Solution, 1.0 Mg/ml In Acetonitrile, Ampule Of 1 Ml, Certified Reference Material
|Molecular Weight||250.298 g/mol|
|Hydrogen Bond Donor Count||2|
|Hydrogen Bond Acceptor Count||3|
|Rotatable Bond Count||6|
|Exact Mass||250.132 g/mol|
|Monoisotopic Mass||250.132 g/mol|
|Topological Polar Surface Area||67.4 A^2|
|Heavy Atom Count||18|
|Isotope Atom Count||0|
|Defined Atom Stereocenter Count||1|
|Undefined Atom Stereocenter Count||0|
|Defined Bond Stereocenter Count||0|
|Undefined Bond Stereocenter Count||0|
|Covalently Bonded Unit Count||1|
|1 of 1|
|Company||UCB INC (Application Number: N022253. Patent: RE38551); UCB INC (Application Number: N022254. Patent: RE38551); UCB INC (Application Number: N022255. Patent: RE38551)|
Lacosamide is indicated for adjunctive therapy for partial onset seizures in patients with epilepsy over 17 years old. Injection is indicated for short term use when oral therapy is not feasible.
Adjunctive therapy in the treatment of partial-onset seizures with or without secondary generalisation in adult and adolescent (16-18 years) patients with epilepsy.
Lacosamide therapy is correlated with a decrease in seizure frequency. It should be noted that in group analyses, dosages above 400 mg/day do not appear to result in additional benefit.
Lacosamide is a functionalized amino acid compound specifically synthesized as an anticonvulsive drug to use as add-on therapy for partial-onset seizures with antinociceptive and neuroprotective activities. Lacosamide selectively enhances slow inactivation of voltage-gated sodium channels without affecting fast inactivation, thereby stabilizing hyperexcitabe neuronal membranes. Furthermore, this agent binds to collapsin response mediator protein 2 (CRMP2; DPYSL2), a cytosolic phosphoprotein expressed in most tissues. In the nervous system, CRMP2 acts as a mediator of growth cone collapse as well as modifies axon number, length, and neuronal polarity.
Established Pharmacologic Class [EPC]
Physiologic Effects [PE]
Decreased Central Nervous System Disorganized Electrical Activity
Anatomical main group: N - Nervous system
Therapeutic subgroup: N03 - Antiepileptics
Pharmacological subgroup: N03A - Antiepileptics
Chemical subgroup: N03AX - Other antiepileptics
Chemical substance: N03AX18 - lacosamide
N - Nervous system
N03 - Antiepileptics
N03A - Antiepileptics
N03AX - Other antiepileptics
N03AX18 - Lacosamide
Lacosamide has a negligible first pass effect with bioavailability of about 100%. The maximum Lacosamide plasma concentrations occur about 1-4 hours after oral administration, and the pharmacokinetics of Lacosamide are dose proportional. Food does not affect absorption.
Route of Elimination
Lacosamide is eliminated primarily from the systemic circulation by biotransformation and renal excretion.
Volume of Distribution
approximately 0.6 L/kg; thus close to the volume of total body water.
95% recovered in the urine 0.5% in the feces
Lacosamide is a CYP2C19 substrate. The relative contribution of other CYP isoforms or non-CYP enzymes in the metabolism of lacosamide is not known. Primary compounds excreted were unchanged lacosamide (approximately 40% of the dose), its O-desmethyl metabolite (approximately 30%), and a structurally unknown polar fraction (~20%). The plasma exposure of the major human metabolite, O-desmethyl-lacosamide, is approximately 10% of that of lacosamide. This metabolite has no known pharmacological activity.
It is proposed that lacosamide's inhibition of sodium channels is responsible for analgesia. Lacosamide may be selective for inhibiting depolarized neurons rather than neurons with normal resting potentials. Pain and nociceptor hyperexcitability are associated with neural membrane depolarization. Lacosamide binds to collapsin response mediator protein-2 (CRMP-2), a phosphoprotein which is expressed primarily in the nervous system and is involved in neuronal differentiation and control of axonal outgrowth. The role CRMP-2 of binding in seizure control is hasn't been elucidated.