Loss of β1accessory Na+channel subunits causes failure of carbamazepine, but not of lacosamide, in blocking high-frequency firing via differential effects on persistent Na+currents

Development and Characterization of Novel Derivatives of the Antiepileptic Drug Lacosamide That Exhibit Far Greater Enhancement in Slow Inactivation of Voltage-Gated Sodium Channels

(2010) Yuying Wang et al.   ACS Chemical Neuroscience

Efficacy Loss of the Anticonvulsant Carbamazepine in Mice Lacking Sodium Channel   Subunits via Paradoxical Effects on Persistent Sodium Currents

(2010) M. Uebachs et al.   JOURNAL OF NEUROSCIENCE

Lacosamide as treatment for partial epilepsy: mechanisms of action, pharmacology, effects, and safety

(2010) Christoph Kellinghaus   Therapeutics and Clinical Risk Management

Lacosamide

(2009) Sarah A. Cross et al.   DRUGS

The external pore loop interacts with S6 and S3-S4 linker in domain 4 to assume an essential role in gating control and anticonvulsant action in the Na+channel

(2009) Ya-Chin Yang et al.   JOURNAL OF GENERAL PHYSIOLOGY

A Functional Null Mutation of SCN1B in a Patient with Dravet Syndrome

(2009) G. A. Patino et al.   JOURNAL OF NEUROSCIENCE

Differential Block of Sensory Neuronal Voltage-Gated Sodium Channels by Lacosamide [(2R)-2-(Acetylamino)-N-benzyl-3-methoxypropanamide], Lidocaine, and Carbamazepine

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