Journal
CNS NEUROSCIENCE & THERAPEUTICS
Volume 18, Issue 6, Pages 493-500Publisher
WILEY-BLACKWELL
DOI: 10.1111/j.1755-5949.2012.00313.x
Keywords
CRMP-2; Epilepsy; lacosamide; mechanism of action
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Aims: Lacosamide (LCM; SPM 927, Vimpat (R)) is an antiepileptic drug (AED) used as adjunctive treatment for adults with partial-onset seizures. LCM has a different mode of action from traditional sodium channel blocking AEDs in that it selectively enhances slow inactivation of sodium channels without affecting fast inactivation. Initial investigations suggested that LCM might have an additional mode of action by binding to the collapsin response mediator protein 2 (CRMP-2), which is further investigated here. Methods: LCM binding to native and cloned human CRMP-2 was determined using radioligand binding experiments and surface plasmon resonance measurements. Results: No specific binding of [3H]LCM (free concentration 1001450 nM) to isolated or membrane bound human CRMP-2 expressed in mammalian cell systems and bacteria was observed. Surface plasmon resonance analysis also showed that LCM, over a concentration range of 0.39100 mu M, does not specifically bind to human CRMP-2. Conclusion: The diverse drug binding methods employed here are well suited to detect specific binding of LCM to CRMP-2 in the micromolar range, yet the results obtained were all negative. Results of this study suggest that LCM does not specifically bind to CRMP-2.
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