ArticleCNS neuroscience & therapeutics2012
Drug binding assays do not reveal specific binding of lacosamide to collapsin response mediator protein 2 (CRMP-2).
Article in CNS neuroscience & therapeutics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 38 citations in OpenAlex.
- Expanding the Phenotype ofAnnals of the Child Neurology Society · 2025Article
- Efficacy and Blood Levels of Lacosamide in Patients with Focal Epilepsy.Journal of clinical medicine · 2024Article
- The therapeutic effects of lacosamide on epilepsy-associated comorbidities.Frontiers in neurology · 2023Review
- Role of Sodium Channels in Epilepsy.Cold Spring Harbor perspectives in medicine · 2016Review
- Review
- Specific binding of lacosamide to collapsin response mediator protein 2 (CRMP2) and direct impairment of its canonical function: implications for the therapeutic potential of lacosamide.Molecular neurobiology · 2015Review
- Current understanding of the mechanism of action of the antiepileptic drug lacosamide.Epilepsy research · 2015Review
- Lacosamide: a review of its use as adjunctive therapy in the management of partial-onset seizures.CNS drugs · 2013Review
- CRMP2 protein SUMOylation modulates NaV1.7 channel trafficking.The Journal of biological chemistry · 2013Article
- Development of lacosamide for the treatment of partial-onset seizures.Annals of the New York Academy of Sciences · 2013Review
- Use of lacosamide in children with refractory epilepsy.The journal of pediatric pharmacology and therapeutics : JPPT : the official journal of PPAG · 2012Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsLacosamide (LCM; SPM 927, Vimpat®) 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.
methodsLCM binding to native and cloned human CRMP-2 was determined using radioligand binding experiments and surface plasmon resonance measurements.
resultsNo specific binding of [(3) H]LCM (free concentration 100-1450 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 0.39-100 μM, does not specifically bind to human CRMP-2.
conclusionThe 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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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.