Page last updated: 2024-11-08

lacosamide

Description Research Excerpts Clinical Trials Roles Classes Pathways Study Profile Bioassays Related Drugs Related Conditions Protein Interactions Research Growth Market Indicators

Description

Lacosamide: An acetamide derivative that acts as a blocker of VOLTAGE-GATED SODIUM CHANNELS. It is used as an anticonvulsant, for adjunctive or monotherapy, in the treatment of PARTIAL SEIZURES. [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

Cross-References

ID SourceID
PubMed CID219078
CHEMBL ID58323
CHEBI ID135939
SCHEMBL ID35330
MeSH IDM0356576
PubMed CID21634109
CHEMBL ID57293
SCHEMBL ID223961
MeSH IDM0356576

Synonyms (118)

Synonym
2-(acetylamino)-3-methoxy-n-(phenylmethyl)-, (2r)-
ertosamide
(+)-(2r)-2-(acetylamino)-n-benzyl-3-methoxypropanamide
dea no. 2746
unii-563ks2pqy5
lacosamide [usan:inn:ban]
563ks2pqy5 ,
HY-13015
BB 0260890
erlosamide
lacosamide
harkoseride
vimpat
add-234037
spm-927
spm-929
vimpat (tn)
D07299
175481-36-4
lacosamide (jan/usan/inn)
add 234037
spm 927
propanamide, 2-(acetylamino)-3-methoxy-n-(phenylmethyl)-, (2r)-
(2r)-2-(acetylamino)-n-benzyl-3-methoxypropanamide
erlosamide [inn]
CHEBI:135939
(r)-2-acetamido-n-benzyl-3-methoxypropanamide
lacosamide cv
CHEMBL58323 ,
(r)-lacosamide 1
add-243037
add 243037
AKOS005146274
(2r)-2-(acetylamino)-3-methoxy-n-(phenylmethyl)propanamide
(r)-n-benzyl 2-acetamido-3-methoxypropionamide
(2r)-2-acetylamino-n-benzyl-3-methoxypropanamide
(r)-n-benzyl 2-acetamido-3-methoxypropionamide,
(r)-2-acetylamino-n-benzyl-3-methoxy-propionamide
bdbm50300204
A3897
(2r)-2-acetamido-n-benzyl-3-methoxypropanamide
lacosamide [usp monograph]
lacosamide [ep monograph]
lacosamide [usp-rs]
spm927
add243037
lacosamide [orange book]
lacosamide [mart.]
lacosamide [jan]
lacosamide [ema epar]
lacosamide [vandf]
lacosamide [inn]
lacosamide [usan]
lacosamide [mi]
lacosamide [who-dd]
motpoly
CS-0529
DB06218
AM808141
SCHEMBL35330
dtxcid2031455
NCGC00253740-01
dtxsid1057666 ,
cas-175481-36-4
tox21_113857
KS-1227
harkeroside
gtpl7472
(2r)-2-acetamido-3-methoxy-n-(phenylmethyl)propanamide
VPPJLAIAVCUEMN-GFCCVEGCSA-N
(r)-n-benzyl-2-acetamido-3-methoxypropanamide
(r)-n-benzyl-2-acetamido-3-methoxypropionamide
(r)-2-acetamido-n-benzyl-3-methoxypropionamide
(r)-2-acetylamino-n-benzyl-3-methoxypropionamide
AB01559947-01
lacosamide racemate
AC-22750
sr-01000942286
SR-01000942286-1
lacosamide 1.0 mg/ml in acetonitrile
Q420077
BCP02197
AR-270/11402703
(r)-2-acetamido-n-benzyl-3-methoxypropionamide.
BL164605
lacosamide- bio-x
lacosamide (usp monograph)
motpoly xr
lacosamide (mart.)
lacosamida
lacosamide oral solution
n03ax18
lacosamide (ep monograph)
lacosamide cv (usp-rs)
lacosamidum
()-(2r)-2-(acetylamino)-n-benzyl-3-methoxypropanamide
n~2~-acetyl-n-benzyl-o-methyl-d-serinamide
LQO ,
LS-14226
CHEMBL57293
175481-26-2
BCP9000832
AKOS015852404
SCHEMBL223961
HY-13015A
lacosamide (racemate)
2-acetamino-n-benzyl-3-methoxypropanamide
n-benzyl-2-acetamido-3-methoxypropionamide
ec 700-539-8
2-(acetylamino)-n-benzyl-3-methoxypropanamide
FT-0770536
2-acetamido-n-benzyl-3-methoxypropionamide
SB18905
SY265474
mfcd16620493
2-acetamido-n-benzyl-3-methoxypropanamide
DTXSID00861451
AT39553

Research Excerpts

Overview

Lacosamide (LCM) is a new generation antiepileptic drug that affects the slow inactivation of voltage-gated sodium channels. Previous studies have reported an efficacy of LCM as add-on treatment in brain tumor-related epilepsy (BTRE)

ExcerptReferenceRelevance
"Lacosamide is a third-generation antiepileptic drug."( Lacosamide monotherapy for the treatment of childhood epilepsy with centrotemporal spikes.
Enoki, H; Fujii, Y; Fujimoto, A; Motoi, H; Okanishi, T; Sakuma, S; Shiraishi, H; Yazaki, K, 2022
)
2.89
"Lacosamide (LCM) is a new generation antiepileptic drug that affects the slow inactivation of voltage-gated sodium channels. "( The effect of chronic treatment with sodium channel blocker lacosamide on early development of absence seizures in genetic absence epilepsy rats.
Akat, Ş; Akman, Ö; Çarçak, N; Karanfil, C; Onat, F, 2022
)
2.41
"Lacosamide (LCM) is a third-generation anti-seizure medication (ASM) approved for focal onset epilepsy in patients aged ≥ 4.378 Previous studies have reported an efficacy of LCM as add-on treatment in brain tumor-related epilepsy (BTRE). "( Lacosamide in monotherapy in BTRE (brain tumor-related epilepsy): results from an Italian multicenter retrospective study.
Belcastro, V; Bello, L; Bruno, F; Cavallieri, F; Conti Nibali, M; Dainese, F; Di Gennaro, G; Florindo, I; Gigli, GL; Giovannini, G; Mascia, A; Meletti, S; Mo, F; Napolitano, M; Pauletto, G; Pellerino, A; Pisanello, A; Polosa, M; Quadri, S; Rudà, R; Scarpelli, M; Sessa, M, 2022
)
3.61
"Lacosamide (LCM), is a third-generation antiseizure medicine, with limited clinical evidence for use in pediatric populations. "( Efficacy and safety of lacosamide in pediatric patients with epilepsy: A systematic review and meta-analysis.
Peng, Y; Yang, C; Yang, Y; Yu, D; Zhang, L, 2022
)
2.47
"Lacosamide is a novel antiepileptic drug. "( [Case Report on a Woman with Epilepsy Who Took Lacosamide during Pregnancy and Gave Birth to a Healthy Infant].
Kitamura, S; Nishimura, A; Saito, Y; Sugawara, M; Takekuma, Y; Umazume, T, 2022
)
2.42
"Lacosamide is an antiepileptic drug that acts on voltage-gated sodium channels and was approved as an antiepileptic by the Food and Drug Administration in 2008. "( Lacosamide Intoxication-induced Wide QRS Tachycardia Successfully Treated with Veno-arterial Extracorporeal Membrane Oxygenation.
Hagiwara, Y; Kadoya, T; Kaito, D; Kimura, T; Kobayashi, T; Koinuma, T; Misumi, K; Nishida, H; Ogura, T; Takai, C; Yamada, S; Yoshii, M, 2023
)
3.8
"Lacosamide (LCM) is a third-generation antiepileptic drug (AED) that affects sodium channel inactivation. "( Effect of Lacosamide therapy on blood cells and IgA levels in children and adolescents with epilepsy in a clinical setting.
Eguchi, Y; Ishikawa, N; Izumo, H; Kobayashi, Y; Okada, S; Tateishi, Y, 2022
)
2.57
"Lacosamide (LCM) is a third-generation anti-seizure drug approved in Europe and the United States, either as a monotherapy or adjunctive therapy, to treat partial-onset seizures in adults, adolescents, and children. "( Use of lacosamide in children: experience of a tertiary medical care center in Brazil.
Angelim, AIM; D'Andrea-Meira, I; Fernandes, AR; Fontana, RDS; Goes, FV; Pires, LC; Pires, MEP; Prado, HJPD; Romão, TT, 2022
)
2.62
"Lacosamide (LCM) is a third-generation antiseizure medication (ASM), and its effect on sleep architecture was supported by a few studies in patients with drug-resistant epilepsy in which LCM was used as an add-on treatment. "( The effect of lacosamide monotherapy on sleep architecture in patients with epilepsy: a preliminary evidence.
Carnovale, C; Di Gioia, B; Fernandes, M; Izzi, F; Liguori, C; Lupo, C; Mercuri, NB; Placidi, F; Sarbu, OE; Spanetta, M, 2023
)
2.71
"Lacosamide is a newer antiepileptic medication used in refractory neonatal seizures with limited safety and efficacy data. "( Tolerability and Safety of Lacosamide in Neonatal Population.
Bamgbose, O; Boyle, F; Kean, AC; Stefanescu, BM; Wing, S, 2023
)
2.65
"Lacosamide (LA) is an antiepileptic medicine that is used to treat tonic-clonic seizures, partial-onset seizures, mental problems, and pain. "( Stability-indicating normal-phase HPLC method development for separation and quantitative estimation of S-enantiomer of lacosamide in pharmaceutical drug substance and tablet dosage form.
Haridasyam, SB; Vadagam, N; Venkatanarayana, M, 2023
)
2.56
"Lacosamide (LCM) is a new-generation anti-seizure medication approved for monotherapy and add-on therapy for focal-onset epilepsy. "( Efficacy and tolerability of immediate switch from sodium channel blockers to Lacosamide.
Buluş, E; Çelebi, Ö; Duman, A; Gürses, C; Kandemir Yılmaz, M; Keskin Güler, S; Mert Atmaca, M; Talha Özgün, O, 2023
)
2.58
"Lacosamide is an antiepileptic drug with US Food and Drug Administration approval for the treatment of partial-onset seizures in patients older than one month. "( Neonatal Cardiac Arrest Following Lacosamide Treatment: A Case Report.
Huberman, MA; Kalika, PM; Mallar, C, 2023
)
2.63
"Lacosamide is a sodium-channel blocker that is efficacious in animal models of neuropathic pain."( Effect of lacosamide in peripheral neuropathic pain: study protocol for a randomized, placebo-controlled, phenotype-stratified trial.
Andersen, NT; Bach, FW; Carmland, ME; Finnerup, NB; Holbech, JV; Jensen, TS; Kreutzfeldt, M; Sindrup, SH, 2019
)
1.64
"Lacosamide (LCM) is a new generation antiepileptic drug. "( Efficacy upon 12-weeks after achievement of maximal dose and tolerability of lacosamide as an adjunctive therapy in epilepsy: Real world clinical experience.
Chang, RS; Leung, CYW; Leung, YHI; Lui, HKK; Lui, HTC; Wang, YO, 2020
)
2.23
"Lacosamide (LCM) is an antiepileptic drug (AED) with insufficient clinical experience in patients with intellectual disability (ID). "( Clinical experience combined with therapeutic drug monitoring of lacosamide.
Baftiu, A; Brodtkorb, E; Johannessen Landmark, C; Johannessen, SI; Lossius, MI; Nakken, KO; Svendsen, T, 2020
)
2.24
"Lacosamide is an antiepileptic drug (AED) that has linear pharmacokinetics, predictable blood concentrations, and few drug interactions, setting it apart from other AEDs that require vigorous therapeutic drug monitoring (TDM) such as phenytoin and carbamazepine. "( Is Therapeutic Drug Monitoring of Lacosamide Needed in Patients with Seizures and Epilepsy?
Mahmoud, SH; Schultz, L, 2020
)
2.28
"Lacosamide (LCM) is a well-tolerated and increasingly used second-generation AED, and side effects such as atrial fibrillation are rare and poorly characterized. "( Cardioembolic acute cerebral micro-infarcts in the context of atrial fibrillation after low-dose intravenous infusion of lacosamide.
Catevilla, FJB; Corbellini, ÁB; Díaz, PP; García, ACC; García, JLC; Hristova, VN; Jorge, FR; Sanz, BZ; Torre, PP, 2020
)
2.21
"Lacosamide (LCM) is a third-generation anti-epileptic drug (AED) for partial-onset epilepsy with minimal hepatic metabolism and drug-drug interactions. "( Racial variations in lacosamide serum concentrations in adult patients with epilepsy.
Basha, MM; Mahulikar, A; Seraji-Bozorgzad, N; Shah, AK; Yarraguntla, K; Zutshi, D, 2020
)
2.32
"Lacosamide appears to be an effective and well-tolerated symptomatic treatment against acute, painful OXAIPN."( Real world, open label experience with lacosamide against acute painful oxaliplatin-induced peripheral neurotoxicity.
Anastopoulou, GG; Argyriou, AA; Bruna, J; Kalofonos, HP; Kalofonou, F; Litsardopoulos, P; Psimaras, D, 2020
)
1.55
"Lacosamide (LCM) is a third-generation antiepileptic drug that interacts with collapsing response mediator protein 2, a protein that has been associated with neurodevelopmental diseases like schizophrenia."( Lacosamide intake during pregnancy increases the incidence of foetal malformations and symptoms associated with schizophrenia in the offspring of mice.
Álvarez Del Vayo, C; Caro-Vega, J; Carrión, MÁ; Fernández-Torres, R; González-Meneses, A; Hernández-Viñas, A; López-Escobar, B; Rivas-Infante, E; Rybkina, T; Sánchez-Alcázar, JA; Vargas-López, V; Villar-Navarro, M; Ybot-González, P, 2020
)
2.72
"Lacosamide (LCM) is a third-generation anticonvulsant with a mechanism of action that is not completely clear."( Lacosamide in trigeminal neuralgia: report of a case refractory to first- and second-generation anticonvulsants.
Adamo, D; Coppola, N; Mignogna, MD; Nicolò, M; Pecoraro, G, 2023
)
3.07
"Lacosamide is an effective and well tolerable drug for patients with focal epilepsy."( Efficacy and Tolerability of Lacosamide for Focal Epileptic Patients: Study from Epilepsy Clinic in Makkah.
Abualula, H; Alaa, A; Alkhotani, A; Almatrafi, Y; Ghomiem, S, 2021
)
2.36
"Lacosamide is a new-generation anticonvulsant acting on Na"( Inhibition of neuronal Na
Chen, JL; Kuo, CC; Lai, YC; Peng, YS; Wu, HT; Yang, YC, 2020
)
2
"Lacosamide is a novel anticonvulsant that acts by enhancing sodium channel slow inactivation. "( Therapeutic Monitoring of Lacosamide in Japanese Patients With Epilepsy: Clinical Response, Tolerability, and Optimal Therapeutic Range.
Araki, Y; Fukushima, Y; Imai, K; Kagawa, Y; Takahashi, Y; Terada, K; Yamamoto, Y, 2020
)
2.3
"Lacosamide is a novel antiepileptic with neuroprotective properties. "( Effectiveness of Lacosamide on everyday cognitive deficits, psychiatric symptoms and resilience in patients with epilepsy.
Gul, A; Mehreen, S, 2020
)
2.34
"Lacosamide is a third-generation anti-seizure drug that stands out due to its good efficacy and safety profile."( Pharmacology of lacosamide: From its molecular mechanisms and pharmacokinetics to future therapeutic applications.
Bicker, J; Carona, A; Falcão, A; Fonseca, C; Fortuna, A; Silva, R, 2021
)
1.69
"Lacosamide (LCM) is an anticonvulsant compound approved for the adjunctive treatment of partial-onset seizures and neuropathic pain."( Therapeutic effects of Lacosamide in a rat model of traumatic brain injury: A histological, biochemical and electroencephalography monitoring study.
Alpay, S; Aydemir, I; Collu, F; Duransoy, YK; Kutlu, N; Mete, M; Özel, HF; Tuglu, Mİ; Unsal, UU, 2021
)
1.65
"Lacosamide is an antiepileptic agent with a novel mechanism of sodium channel inhibition and has the potential to cause cardiac sodium channel blockade."( Lacosamide induced Brugada I morphology in the setting of septicemia: A case report.
Badea, A; Geier, C; Goodnough, R; LeSaint, KT; Lynch, KL, 2021
)
2.79
"Lacosamide (LCM) is a new antiseizure medication, and intravenous (IV) loading of LCM is recently used against status epilepticus. "( Cardiac effects of rapid intravenous loading of lacosamide in patients with epilepsy.
Bae, EK; Kim, DW; Kim, HK; Lee, H, 2021
)
2.32
"Lacosamide is a new-generation antiepileptic drug (AED) most commonly used adjunctively in the setting of partial-onset seizures refractory to traditional therapy. "( Lacosamide-Induced Recurrent Ventricular Tachycardia in the Acute Care Setting.
Almquist, AK; Berei, TJ; Lillyblad, MP, 2018
)
3.37
"Lacosamide (LCM) is a new antiepileptic drug (AED). "( Therapeutic Drug Monitoring of Lacosamide in Norway: Focus on Pharmacokinetic Variability, Efficacy and Tolerability.
Baftiu, A; Brodtkorb, E; Burns, ML; Johannessen Landmark, C; Johannessen, SI; Svendsen, T, 2017
)
2.18
"Lacosamide (LCM) is a new antiepileptic drug (AED) used as adjunctive therapy in patients with partial seizures with or without secondary generalization, with a favorable pharmacokinetic profile that seems to be effective and well tolerated."( Quality of life, mood and seizure control in patients with brain tumor related epilepsy treated with lacosamide as add-on therapy: A prospective explorative study with a historical control group.
Fabi, A; Giannarelli, D; Maialetti, A; Maschio, M; Vidiri, A; Villani, V; Zarabla, A, 2017
)
1.39
"Lacosamide is an antiepileptic drug (AED), which has proven to be effective to control seizures, including acute conditions such as status epilepticus. "( Outcome of cancer-related seizures in patients treated with lacosamide.
Martinez-Ricarte, F; Martínez-Saez, E; Molins, A; Quintana, M; Salas-Puig, J; Santamarina, E; Toledo, M, 2018
)
2.17
"Lacosamide is an AED to consider in cases of cancer-related seizures. "( Outcome of cancer-related seizures in patients treated with lacosamide.
Martinez-Ricarte, F; Martínez-Saez, E; Molins, A; Quintana, M; Salas-Puig, J; Santamarina, E; Toledo, M, 2018
)
2.17
"Lacosamide (LCM) is a third-generation antiepileptic drug (AED) for which there is limited experience in the treatment of elderly patients with epilepsy. "( Clinical management of elderly patients with epilepsy; the use of lacosamide in a single center setting.
Mäkinen, J; Peltola, J; Rainesalo, S; Raitanen, J, 2017
)
2.13
"Lacosamide (LCM) is an effective antiepileptic drug (AED) approved for the treatment of focal epilepsy in both children and adults. "( Lacosamide treatment of childhood refractory focal epilepsy: the first reported side effect in paediatric patients.
Aydinli, N; Bektas, G; Caliskan, M; Ozkan, MU; Ozmen, M; Uzunhan, TA; Yildiz, EP, 2017
)
3.34
"Lacosamide is a new-generation antiepileptic drug (AED) that is eliminated by both hepatic and renal mechanisms. "( Lacosamide Pharmacokinetics in a Critically Ill Patient Receiving Continuous Venovenous Hemofiltration.
Armahizer, MJ; Badjatia, N; Franquiz, MJ; Gopalakrishnan, M; Kalaria, SN; McCarthy, PJ, 2018
)
3.37
"Lacosamide is a potentially efficacious adjunctive therapy in patients with refractory sleep-related hypermotor epilepsy."( A case series of lacosamide as adjunctive therapy in refractory sleep-related hypermotor epilepsy (previously nocturnal frontal lobe epilepsy).
Berkovic, SF; Samarasekera, SR; Scheffer, IE, 2018
)
1.54
"Lacosamide is an antiepileptic drug whose exact mechanism of action remains unknown. "( [Lacosamide associated with high-degree block in a patient with trigeminal neuralgia].
Cantero-Lozano, D; Garces-Anton, E; Garces-Redondo, M; Garrido-Fernandez, A; Lopez-Bravo, A; Marin-Gracia, M; Navarro-Perez, MP; Santos-Lasaosa, S, 2018
)
2.83
"Lacosamide (LCM) is an effective and well-tolerated new-generation antiepileptic drug (AED), currently licensed as add-on therapy for partial-onset seizures."( A novel action of lacosamide on GABA
Aronica, E; Cifelli, P; Di Bonaventura, C; Fattouch, J; Giallonardo, AT; Limatola, C; Morano, A; Palma, E; Roseti, C; Ruffolo, G, 2018
)
1.54
"Lacosamide may prove to be a useful, 'broad-spectrum' antiepileptic medication in children for focal and generalised epilepsies and in association with comorbidities."( Lacosamide in children with drug-resistant epilepsy.
Freeman, JL; Harvey, AS; Rüegger, AD, 2019
)
2.68
"Lacosamide (LCM) is a new antiepileptic drug (AED). "( Influence of Dose and Antiepileptic Comedication on Lacosamide Serum Concentrations in Patients With Epilepsy of Different Ages.
Bien, CG; Brandt, C; Helmer, R; May, TW, 2018
)
2.17
"Lacosamide (LCM) is a new AED that could be a valid therapeutic choice in patients with brain tumor-related epilepsy (BTRE)."( Lacosamide on background eeg activity in brain tumor-related epilepsy patients: A case series study.
Cantelmi, T; Dinapoli, L; Dispenza, S; Maialetti, A; Maschio, M; Petreri, G; Sperati, F; Zarabla, A, 2018
)
2.64
"Lacosamide is a cost-effective option at a willingness-to-pay threshold of €30,000 per QALY, representing a valuable monotherapy treatment option for patients with focal epileptic seizures in the Greek setting."( Lacosamide as a first-line treatment option in focal epilepsy: a cost-utility analysis for the Greek healthcare system.
Charokopou, M; Christou, P; Geitona, M; Giannakodimos, S; Kimiskidis, VK; Kountouris, V; Stamuli, E, 2019
)
3.4
"Lacosamide (LCM) is a recently developed sodium channel blocker (SCB), which acts mainly on the slow activation state in sodium channels. "( Switching from traditional sodium channel blockers to lacosamide in patients with epilepsy.
Bae, EK; Kim, DW; Kim, HK, 2019
)
2.21
"Lacosamide is a third-generation antiepileptic drug. "( Lacosamide Overdose: A Case of QRS Prolongation and Seizure.
Ng, PC; Schimmel, J; Wang, GS, 2019
)
3.4
"Lacosamide (Vimpat®) is an anticonvulsant used to treat partial-onset seizures. "( Lacosamide: a Study of Exposures Reported to US Poison Centers over a 9-Year Period.
Borys, D; Kempf, D; Laubach, E; Teijido, J; Zosel, A, 2019
)
3.4
"Lacosamide ((R)-1) is a recently marketed, first-in-class, antiepileptic drug. "( Discovery of lacosamide affinity bait agents that exhibit potent voltage-gated sodium channel blocking properties.
Dustrude, ET; Khanna, R; Kohn, H; Lee, H; Park, KD; Wang, Y; Yang, XF, 2013
)
2.2
"Lacosamide (LCM) is a new AED, holding promise as a potent treatment option for RSE."( Safety and efficacy of intravenous lacosamide for adjunctive treatment of refractory status epilepticus: a comparative cohort study.
Marsch, S; Rüegg, S; Sutter, R, 2013
)
1.39
"Lacosamide (LCM, Vimpat) is an anticonvulsant with a unique mode of action. "( Synergism of lacosamide with established antiepileptic drugs in the 6-Hz seizure model in mice.
Kaschenko, O; Matagne, A; Shandra, A; Shandra, P; Stöhr, T, 2013
)
2.2
"Lacosamide (LCM) is a recently licensed antiepileptic drug available in the UK since 2008. "( Long-term retention of lacosamide in a large cohort of people with medically refractory epilepsy: a single centre evaluation.
Bartolini, E; Bell, GS; Duncan, JS; Novy, J; Sander, JW, 2013
)
2.14
"Lacosamide is an antiepileptic drug (AED) available in multiple formulations that was first approved in 2008 as adjunctive therapy for partial-onset seizures (POS) in adults. "( Development of lacosamide for the treatment of partial-onset seizures.
Byrnes, W; Doty, P; Hebert, D; Mathy, FX; Simontacchi, K; Zackheim, J, 2013
)
2.19
"Lacosamide (LCM) is a new anticonvulsant available in intravenous (IV) form, but its optimal dosing regimen for the treatment of RSE is unknown."( Intravenous lacosamide in refractory seizure clusters and status epilepticus: comparison of 200 and 400 mg loading doses.
Depondt, C; Gaspard, N; Legros, B; Levy-Nogueira, M; Ligot, N; Mavroudakis, N; Naeije, G, 2014
)
1.5
"Lacosamide is a third-generation antiepileptic drug that has been proven to be effective, safe and with few side effects. "( [Lacosamide as an alternative in the treatment of post-surgery neuropathic pain in an allergic patient].
Márquez-Rivas, J; Mayorga-Buiza, MJ; Monge-Márquez, ME; Rivero-Garvía, M, 2013
)
2.74
"Lacosamide (LCM) is a treatment option for status epilepticus (SE) described in several series. "( Usefulness of intravenous lacosamide in status epilepticus.
Ailouti, N; Alvarez-Sabín, J; De Gracia, R; Lainez, E; Porta, I; Quintana, M; Raspall, M; Santamarina, E; Sueiras, M; Toledo, M; Xavier Salas Puig, XS, 2013
)
2.13
"Lacosamide (Vimpat(®)) is a functionalized amino acid available orally (as a syrup or tablet) and as an intravenous infusion. "( Lacosamide: a review of its use as adjunctive therapy in the management of partial-onset seizures.
Hoy, SM, 2013
)
3.28
"Lacosamide is an anticonvulsant hypothesized to enhance slow inactivation of neuronal Na(+) channels for its therapeutic action. "( Block of human cardiac sodium channels by lacosamide: evidence for slow drug binding along the activation pathway.
Wang, GK; Wang, SY, 2014
)
2.11
"Lacosamide is an anticonvulsant drug which presents carbonic anhydrase inhibition. "( Lacosamide derivatives with anticonvulsant activity as carbonic anhydrase inhibitors. Molecular modeling, docking and QSAR analysis.
Andrada, MF; Duchowicz, PR; Estrada, MR; Garro Martinez, JC; Torrens, F; Vega-Hissi, EG, 2014
)
3.29
"Lacosamide is an anticonvulsant drug approved for adjunctive therapy of partial-onset seizures in adults. "( High-throughput method for the quantification of lacosamide in serum using ultrafast SPE-MS/MS.
Jannetto, PJ; Korman, E; Langman, LJ, 2015
)
2.11
"Lacosamide is a new antiepileptic as adjunctive therapy in partial seizures with or without generalization."( [Effect of lacosamide on the quality of life of patients with epilepsy].
Alfaro, A; Asensio-Asensio, M; García, C; García-Escrivá, A; Lezcano-Rodas, M; Llorca, V; López-Hernández, N; Medrano, V; Palao, S, 2014
)
1.51
"Lacosamide (LCM) is a functionalized amino acid specifically developed for use as an antiepileptic drug (AED) and is currently indicated as adjunctive treatment for partial-onset seizures in adults with focal epilepsy (maximum approved dose 400 mg/day). "( Advances in epilepsy treatment: lacosamide pharmacokinetic profile.
Andreas, JO; Cawello, W; Dimova, S; Stockis, A, 2014
)
2.13
"Lacosamide is an effective add-on antiepileptic drug for children with refractory partial epilepsy and is well tolerated."( Efficacy and tolerability of lacosamide as an adjunctive therapy in children with refractory partial epilepsy.
Didagi, SK; Kamate, M; Pasha, I, 2014
)
2.14
"Lacosamide (LCM) is a novel anticonvulsant that enhances the slow inactivation state of VGSCs."( Antinociceptive effects of lacosamide on spinal neuronal and behavioural measures of pain in a rat model of osteoarthritis.
Dickenson, AH; Rahman, W, 2014
)
1.42
"Lacosamide (LCM) is a novel antiepileptic drug (AED) with potential benefit as adjunctive treatment in patients with partial-onset seizures. "( Cognitive effects of lacosamide as adjunctive therapy in refractory epilepsy.
Aldenkamp, AP; de Louw, AJ; IJff, DM; Jansen, JF; Majoie, HJ; van Veenendaal, TM, 2015
)
2.18
"Lacosamide (LCM) is a novel anti-epileptic drug (AED) that enhances the slow inactivation of voltage-gated sodium channels. "( Lacosamide as adjunctive therapy in treatment-resistant epilepsy in childhood.
Bint, L; Cannell, P; Ghia, T; Ghosh, S; Gulati, P; Nagarajan, L; Walsh, P, 2015
)
3.3
"Lacosamide is an effective add-on antiepileptic drug in difficult-to treat adult partial epilepsy patients. "( [The efficacy of lacosamide in relation to antiepileptic drug history. Clinical experiences in adult partial epilepsy].
Horváth, A; Kamondi, A; Szűcs, A, 2015
)
2.2
"Lacosamide is a novel antiepileptic drug that acts mainly via the selective enhancement of slow inactivation of voltage-gated sodium channels. "( A case of lacosamide-induced hepatotoxicity.
Byun, JI; Lee, SK; Sunwoo, JS, 2015
)
2.26
"Lacosamide is an antiepileptic drug that has been licensed as an add-on treatment for partial epilepsy."( Lacosamide add-on therapy for partial epilepsy.
Marson, AG; McKay, AJ; Shukralla, A; Weston, J, 2015
)
2.58
"Lacosamide is a relatively new AED and the intravenous formulation has shown promise for treatment of SE."( Observational study of intravenous lacosamide in patients with convulsive versus non-convulsive status epilepticus.
Bondy Peña, EC; Domínguez Lorenzo, JM; Fernandez Peleteiro, M; Fernández, A; Moreno Morales, EY; Pardellas Santiago, E, 2015
)
1.42
"Lacosamide (LCM) is an antiepileptic medication used as an adjunctive treatment for partial seizures. "( Lacosamide Induced Psychosis: Case Report, Review of Differential Diagnosis and Relevant Pharmacokinetics.
Cohen, H; Friedman, M; Hayes, D; Lam, T; Pinkhasov, A; Singh, D,
)
3.02
"Lacosamide (LCM) is a novel AED that stabilizes hyperexcitable neuronal membranes by selectively enhancing the slow inactivation of voltage-gated sodium channels (VGSCs)."( Differential effects of lacosamide, phenytoin and topiramate on peripheral nerve excitability: An ex vivo electrophysiological study.
Kagiava, A; Karlovasitou, A; Kimiskidis, VK; Kosmidis, EK; Krikonis, K; Spilioti, M; Zafeiridou, G, 2016
)
1.46
"Lacosamide (Vimpat(®)) is a functionalized amino acid available orally (as a solution or tablets) and as an intravenous infusion for use as monotherapy (only in the USA) or adjunctive therapy for the treatment of focal seizures in adult and adolescent (aged ≥17 years in the USA) patients with epilepsy. "( Lacosamide: A Review in Focal Seizures in Patients with Epilepsy.
Scott, LJ, 2015
)
3.3
"Lacosamide is an antiepileptic drug approved for the treatment of focal epilepsy in adult patients. "( Efficacy and safety of lacosamide as an adjunctive therapy for refractory focal epilepsy in paediatric patients: a retrospective single-centre study.
Birca, A; Carmant, L; D'Anjou, G; Diadori, P; Larbrisseau, A; Lortie, A; Major, P; Perreault, S; Rossignol, E; Toupin, JF; Vanasse, M, 2015
)
2.17
"Lacosamide is a sodium channel blocker antiepileptic drug authorized as an adjunctive therapy for focal seizures in adolescents and adults."( [Clinical experience with lacosamide in Galicia: the GALACO study].
Abella-Corral, J; Amigo-Jorrin, MC; Castro-Vilanova, MD; Cebrian-Perez, E; Corredera-Garcia, E; Lopez-Gonzalez, FJ; Marey-Lopez, J; Pato-Pato, A; Pego-Reigosa, R; Rodriguez-Osorio, X; Rodriguez-Regal, A; Rubio-Nazabal, E, 2015
)
2.16
"Lacosamide is an approved antiepileptic drug that also shows antinociceptive activity in animal models, including analgesic efficacy in central and trigeminal pain."( Lacosamide inhibits calcitonin gene-related peptide production and release at trigeminal level in the rat.
Capuano, A; Greco, MC; Navarra, P; Tringali, G, 2016
)
2.6
"Lacosamide is a new antiepileptic drug which is widely used to treat partial-onset seizures. "( Increases of Catalase and Glutathione Peroxidase Expressions by Lacosamide Pretreatment Contributes to Neuroprotection Against Experimentally Induced Transient Cerebral Ischemia.
Ahn, JH; Chen, BH; Cho, JH; Choi, HY; Hwang, IK; Kim, IH; Kim, SK; Kim, YM; Lee, JC; Lee, TK; Lee, YL; Park, JH; Shin, BN; Tae, HJ; Won, MH; Yan, BC, 2016
)
2.12
"Lacosamide is an antiepilepsy drug approved by the Food and Drug Administration for patients aged 17 years and older for partial-onset seizures as monotherapy or adjunctive therapy. "( Intravenous Lacosamide in Pediatric Status Epilepticus: An Open-Label Efficacy and Safety Study.
Ng, YT; Poddar, K; Sharma, R, 2016
)
2.26
"Lacosamide is an anti-epileptic drug that is also used for the treatment of painful diabetic neuropathy acting through voltage-gated sodium channels. "( Lacosamide diminishes dryness-induced hyperexcitability of corneal cold sensitive nerve terminals.
Acosta, MC; Belmonte, C; Dienes, L; Gallar, J; Kovács, I; Luna, C; Mizerska, K; Perényi, K; Quirce, S, 2016
)
3.32
"Lacosamide is an anticonvulsant, which blocks Nav1.3, Nav1.7, and Nav1.8, and stabilizes channels in the slow-inactivation state."( Efficacy, safety, and tolerability of lacosamide in patients with gain-of-function Nav1.7 mutation-related small fiber neuropathy: study protocol of a randomized controlled trial-the LENSS study.
de Greef, BT; Faber, CG; Geerts, M; Hoeijmakers, JG; Merkies, IS, 2016
)
1.43
"Lacosamide is a newer-generation AED, not known to induce or strongly inhibit cytochrome P450 (CYP450) enzymes."( Changes in hormone and lipid levels in male patients with focal seizures when switched from carbamazepine to lacosamide as adjunctive treatment to levetiracetam: A small phase IIIb, prospective, multicenter, open-label trial.
Brandt, C; De Backer, M; Dedeken, P; Eckhardt, K; Elger, CE; Elmoufti, S; Rademacher, M; Tennigkeit, F, 2016
)
1.37
"Lacosamide is a safe and effective treatment option for patients with epilepsy and psychiatric comorbidities."( LAM study: Effects of lacosamide on behaviour and quality of life in patients with epilepsy.
Alfaro, A; Asensio, M; Berenguer, L; Buendía, JF; Cerdán, M; García-Escrivá, A; Giner, JC; Lezcano, M; Medrano, V; Navarro, M; Palao, S; Salom, JM; Tortosa, D,
)
1.89
"Lacosamide is an antiseizure agent that targets voltage-dependent sodium channels. "( Lacosamide Inhibition of Nav1.7 Voltage-Gated Sodium Channels: Slow Binding to Fast-Inactivated States.
Bean, BP; Jo, S, 2017
)
3.34
"Lacosamide (Vimpat) is an aniepileptic drug with a new, dual mode of action. "( [Lacosamide. A new antiepileptic drug as adjunctive therapy in patients with partial-onset seizures].
Saussele, T, 2008
)
2.7
"Lacosamide is a novel chemical entity with anticonvulsant and analgesic properties that is being developed to treat epilepsy and neuropathic pain conditions. "( Lacosamide for the treatment of diabetic neuropathic pain.
Biton, V, 2008
)
3.23
"Lacosamide is an antiepileptic drug approved in the USA and Europe as adjunctive therapy for partial-onset seizures. "( Lacosamide: pharmacology, mechanisms of action and pooled efficacy and safety data in partial-onset seizures.
Beydoun, A; D'Souza, J; Doty, P; Hebert, D, 2009
)
3.24
"Lacosamide is a novel anticonvulsant drug that is available as infusion solution."( Intravenous lacosamide as successful treatment for nonconvulsive status epilepticus after failure of first-line therapy.
Berning, S; Besselmann, M; Kellinghaus, C, 2009
)
1.45
"Lacosamide is a functionalized amino acid, the antiepileptic effects of which appear to be due to a novel mode of action, namely the selective enhancement of slow inactivation of voltage-gated sodium channels. "( Lacosamide: in partial-onset seizures.
Cross, SA; Curran, MP, 2009
)
3.24
"Lacosamide is a functionalised amino acid that affects voltage-gated sodium channels in a novel way by enhancing the slow inactivating 'braking' state of these channels."( Effects of lacosamide, a novel sodium channel modulator, on dorsal horn neuronal responses in a rat model of neuropathy.
Bee, LA; Dickenson, AH, 2009
)
1.46
"Lacosamide (Vimpat) is a newly licensed novel antiepileptic drug. "( Successful treatment for refractory convulsive status epilepticus by non-parenteral lacosamide.
Eggers, C; Hofer, T; Resch, R; Tilz, C, 2010
)
2.03
"Lacosamide is a new antiepileptic drug for adjunctive treatment of adult partial-onset seizures. "( No pharmacokinetic interaction between lacosamide and carbamazepine in healthy volunteers.
Cawello, W; Eggert-Formella, A; Nickel, B, 2010
)
2.07
"Lacosamide is a functionalized amino acid molecule that selectively enhances the slow inactivation of voltage-gated sodium channels and interacts with the collapsin-response mediator protein-2. "( Lacosamide: an adjunctive agent for partial-onset seizures and potential therapy for neuropathic pain.
Harris, JA; Murphy, JA, 2009
)
3.24
"Lacosamide is an effective agent for adjunctive treatment of refractory partial-onset seizures. "( Lacosamide: an adjunctive agent for partial-onset seizures and potential therapy for neuropathic pain.
Harris, JA; Murphy, JA, 2009
)
3.24
"Lacosamide is a new antiepileptic drug effective for adjunctive treatment of partial-onset seizures. "( Intravenous lacosamide as short-term replacement for oral lacosamide in partial-onset seizures.
Ben-Menachem, E; Brock, M; Johnson, ME; Krauss, G; Mameniskiene, R; Vaiciene-Magistris, N; Whitesides, JG, 2010
)
2.18
"Lacosamide (LCM) is a recently approved anticonvulsant in Europe and the USA which offers new mechanisms of action and favorable safety profiles."( Lacosamide: new adjunctive treatment option for partial-onset seizures.
Chung, SS, 2010
)
2.52
"Lacosamide (LCM) is a novel antiepileptic drug that exerts a strong antiepileptic effect via slow inactivation of voltage-gated sodium channels. "( Atrial flutter/atrial fibrillation associated with lacosamide for partial seizures.
Degiorgio, CM, 2010
)
2.06
"Lacosamide (LCM) is a newer antiepileptic drug with a dual mode of action. "( Lacosamide, a newer antiepileptic.
Medhi, B; Patyar, S, 2010
)
3.25
"Lacosamide is a new antiepileptic drug that has a novel mechanism of action, linear pharmacokinetics, and proven efficacy in the adjunctive treatment of partial-onset seizures. "( Saliva and serum lacosamide concentrations in patients with epilepsy.
Greenaway, C; Patsalos, PN; Ratnaraj, N; Sander, JW, 2011
)
2.15
"Lacosamide is a new antiepileptic drug recently approved for the treatment of partial-onset seizures."( Does lacosamide aggravate Lennox-Gastaut syndrome? Report on three consecutive cases.
Bramanti, P; Calabrò, RS; Cuzzola, A; Ferlazzo, E; Genton, P; Italiano, D, 2010
)
1.6
"Lacosamide is a new antiepileptic drug (AED) apparently devoid of major pharmacokinetic interactions. "( Lacosamide neurotoxicity associated with concomitant use of sodium channel-blocking antiepileptic drugs: a pharmacodynamic interaction?
Novy, J; Patsalos, PN; Sander, JW; Sisodiya, SM, 2011
)
3.25
"Lacosamide is an antiepileptic drug (AED) approved for the adjunctive treatment of partial-onset seizures in adults. "( Examining the clinical utility of lacosamide: pooled analyses of three phase II/III clinical trials.
Ben-Menachem, E; Benbadis, S; Chung, S; Doty, P; Fountain, NB; Hebert, D; Isojärvi, J; Rosenfeld, W; Sperling, MR, 2010
)
2.08
"Lacosamide (LCM) is a novel antiepileptic drug (AED) recently approved as an adjunctive therapy in the treatment of partial seizures in adults. "( Efficacy and safety of intravenous lacosamide in refractory nonconvulsive status epilepticus.
Azar, NJ; Estephan, B; Koubeissi, MZ; Mayor, CL; Rashid, S, 2011
)
2.09
"Lacosamide is a novel anticonvulsant drug that is available as infusion solution."( Intravenous lacosamide--an effective add-on treatment of refractory status epilepticus.
Albers, JM; Dittrich, R; Dziewas, R; Möddel, G; Ringelstein, EB; Steidl, C; Suntrup, S, 2011
)
1.47
"Lacosamide (LCM) is a novel anticonvulsant that modulates voltage-dependent sodium channels. "( Atrioventricular block following lacosamide intoxication.
Brodowski, KO; Kellinghaus, C; Krause, LU, 2011
)
2.09
"Lacosamide is a newly approved medication for treatment of partial onset seizures in adults, which has a novel mechanism of action."( Successful treatment of childhood prolonged refractory status epilepticus with lacosamide.
Fan, Z; Greenwood, R; Shiloh-Malawsky, Y; Tennison, M, 2011
)
1.32
"Lacosamide appears to be a safe, efficacious and cost-effective adjunctive therapy for partial-onset epileptic seizures in adult patients."( Lacosamide as adjunctive therapy for partial-onset epileptic seizures: a review of the clinical and economic literature.
Simoens, S, 2011
)
2.53
"Lacosamide (LCM) is an antiepileptic drug (AED) that has demonstrated a good efficacy in controlling seizures as an add-on in adult epilepsy. "( Lacosamide as add-on in brain tumor-related epilepsy: preliminary report on efficacy and tolerability.
Carapella, CM; Dinapoli, L; Maschio, M; Mingoia, M; Muti, P; Pace, A; Pompili, A; Sperati, F; Vidiri, A, 2011
)
3.25
"Lacosamide is a functionalized amino acid, and selectively enhances voltage-gated sodium channel slow inactivation."( [New antiepileptic drugs, and therapeutic considerations].
Szupera, Z, 2011
)
1.09
"Lacosamide (Vimpat®) is an antiepileptic drug approved in the USA, Europe and several other countries as adjunctive therapy for partial-onset seizures. "( A simple HPLC-UV method for the determination of lacosamide in human plasma.
Boekens, H; Boulanger, P; Dell'Aiera, S; Higuet, N; Kestelyn, C; Lastelle, M; Smith, S; Staelens, L, 2011
)
2.07
"Lacosamide (LCM) is a new AED which is available in parental form although few studies have evaluated the safety and efficacy of LCM in critically ill patients."( Safety and efficacy of lacosamide in the intensive care unit.
Cherry, S; Elzawahry, H; Judd, L; LaRoche, S; Muniz, JC, 2012
)
1.41
"Lacosamide is a new antiepileptic drug with a novel mechanism of action, as it selectively promotes the slow inactivation of voltage-dependent sodium channels without affecting fast inactivation. "( [Treatment of neuropathic pain with lacosamide].
García-Escrivá, A; Gil-Cortés, C; López-Hernández, N, 2012
)
2.1
"Lacosamide is an antiepileptic drug that has recently been investigated for neuropathic pain relief, although it failed to get approval for painful diabetic peripheral neuropathy from either the Food and Drug Administration or the European Medicines Agency."( Lacosamide for neuropathic pain and fibromyalgia in adults.
Derry, S; Hearn, L; Moore, RA, 2012
)
2.54
"Lacosamide is a third-generation antiepilepsy drug approved for adjunctive treatment of partial-onset seizures in adults. "( Lacosamide for the treatment of epilepsy.
Edwards, HB; Krauss, GL; Lin, B, 2012
)
3.26
"Lacosamide is an anti-epileptic drug, indicated as adjunctive therapy for patients with focal seizures with or without secondary generalization. "( Cost effectiveness of lacosamide in the adjunctive treatment of patients with refractory focal epilepsy in Belgium.
De Naeyer, L; Dedeken, P; Simoens, S, 2012
)
2.14
"Lacosamide is a new antiepileptic drug that is currently approved by the US Food and Drug Administration (FDA) for adults 17 years or older for partial-onset seizures. "( Lacosamide in refractory mixed pediatric epilepsy: a prospective add-on study.
Ng, YT; Rastogi, RG, 2012
)
3.26
"Lacosamide (LCM) is a new AED recently approved for treatment of partial onset seizures with or without secondary generalization."( Lacosamide in Lennox-Gastaut syndrome: case report.
Andrade-Machado, R; Benjumea-Cuartas, V; Jaramillo-Jimenez, E,
)
2.3
"Lacosamide (LCM) is an antiepileptic drug approved as adjunctive therapy for partial-onset seizures in adults. "( Lacosamide for the treatment of partial-onset seizures.
Biton, V, 2012
)
3.26
"Lacosamide (LCS) is a new antiepileptic drug (AED) licensed in the European Union (EU) and United States (US) in 2008."( Clinical experience with oral lacosamide as adjunctive therapy in adult patients with uncontrolled epilepsy: a multicentre study in epilepsy clinics in the United Kingdom (UK).
Colbeck, K; Elwes, R; Flores, L; Goulding, P; Kemp, S; Moran, N; Nashef, L; Quirk, J; Ramkolea, P; Richardson, MP; von Oertzen, TJ, 2012
)
2.11
"Lacosamide is a third generation antiepileptic drug, available in France since 2008. "( [Therapeutic drug monitoring of lacosamide].
Bentué-Ferrer, D; Tribut, O; Verdier, MC,
)
1.86
"Lacosamide is a novel antiepileptic drug licensed in the US and Europe as adjunctive therapy for partial-onset seizures in adults. "( Lacosamide in patients with pharmacoresistant epilepsy.
Loiacono, G; Olivieri, C; Verrotti, A; Zaccara, G; Zulli, E, 2012
)
3.26
"Lacosamide (LCM) is a novel AED with a unique mode of action in that it selectively enhances slow inactivation of fast transient Na(+) channels."( Loss of β1 accessory Na+ channel subunits causes failure of carbamazepine, but not of lacosamide, in blocking high-frequency firing via differential effects on persistent Na+ currents.
Albus, C; Beck, H; Isom, L; Niespodziany, I; Opitz, T; Uebachs, M; Wolff, C, 2012
)
1.32
"Lacosamide is a US Food and Drug Administration (FDA)-approved antiepileptic drug for patients 17 years or older with partial epilepsy. "( Efficacy of lacosamide as adjunctive therapy in children with refractory epilepsy.
Carvalho, KS; Hardison, HH; Khurana, DS; Legido, A; Valencia, I; Yorns, WR, 2014
)
2.22
"Lacosamide is a novel anti-epileptic drug that enhances the slow- and not fast-inactivating state of voltage-gated sodium channels. "( Analgesic ineffectiveness of lacosamide after spinal nerve ligation and its sodium channel activity in injured neurons.
Büsselberg, D; Hagenacker, T; Schäfer, N; Schäfers, M, 2013
)
2.12
"Lacosamide (LCM) is a newer antiepileptic drug with a favorable safety profile used in partial epilepsy as adjunctive therapy. "( First case of lacosamide-induced psychosis.
Chatzistefanidis, D; Karvouni, E; Kyritsis, AP; Markoula, S,
)
1.93
"Lacosamide is a functionalized amino acid which was initially synthesized as an antiepileptic drug. "( Lacosamide displays potent antinociceptive effects in animal models for inflammatory pain.
Krause, E; Selve, N; Stöhr, T, 2006
)
3.22
"Lacosamide is a new chemical entity being investigated as an adjunctive treatment for epilepsy, as well as monotherapy for diabetic neuropathic pain. "( Lacosamide.
Doty, P; Rudd, GD; Stoehr, T; Thomas, D, 2007
)
3.23

Effects

Lacosamide has a neuroprotective effect in SCI in rats that is related to its ability to decrease the production of reactive oxygen species. It also increases antioxidant enzyme expression, inhibit lipid peroxidation and attenuate glial cell activation. Lacosamide has a well-characterized and favorable pharmacokinetic profile.

Lacosamide has been reported to have been successfully used for non-convulsive status epilepticus after benzodiazepine failure. It has limited efficacy in the treatment of peripheral diabetic neuropathy. The lacosamide dose has been 200 mg/day with excellent tolerability.

ExcerptReferenceRelevance
"Lacosamide has a neuroprotective effect in SCI in rats that is related to its ability to decrease the production of reactive oxygen species by increasing antioxidant enzyme expression, inhibit lipid peroxidation and attenuate glial cell activation."( Neuroprotective Effects of Lacosamide in Experimental Traumatic Spinal Cord Injury in Rats.
Bengu, AS; Demiroz, S; Erdem, S; Gergin, OO; Ulucan, A; Ur, FD; Ur, K, 2019
)
2.25
"Lacosamide has a well-characterized and favorable pharmacokinetic profile, including a fast absorption rate, minimal or no interaction with cytochrome P-450 izoenzymes, and a low potential for drug-drug interactions."( Development of lacosamide for the treatment of partial-onset seizures.
Byrnes, W; Doty, P; Hebert, D; Mathy, FX; Simontacchi, K; Zackheim, J, 2013
)
1.46
"Lacosamide has a novel mechanism of action that seems to be different in relation to other conventional AEDs."( Lacosamide in Lennox-Gastaut syndrome: case report.
Andrade-Machado, R; Benjumea-Cuartas, V; Jaramillo-Jimenez, E,
)
2.3
"Lacosamide has a low potential for drug-drug interactions."( Lacosamide: an investigational drug for adjunctive treatment of partial-onset seizures.
Ben-Menachem, E, 2008
)
2.51
"Lacosamide has been submitted for regulatory approval in the United States and Europe for the treatment of epilepsy. "( Synthesis and anticonvulsant activities of N-benzyl (2R)-2-acetamido-3-oxysubstituted propionamide derivatives.
Kohn, H; Morieux, P; Stables, JP, 2008
)
1.79
"Lacosamide has been suggested as a valid option."( Oral lacosamide for the treatment of refractory trigeminal neuralgia: A retrospective analysis of 86 cases.
Campoy, S; García-Parra, B; Huerta-Villanueva, M; Martínez-Yélamos, S; Muñoz-Vendrell, A; Prat, J; Tena-Cucala, R, 2023
)
2.15
"Lacosamide (LCM) has been shown to possess complex anticonvulsant and neuroprotective actions, being an enhancer of the slow inactivation of voltage-gated sodium channels, and it has the potential to prevent epileptogenesis."( Role of Lacosamide in Preventing Pentylenetetrazole Kindling-Induced Alterations in the Expression of the Gamma-2 Subunit of the GABAA Receptor in Rats.
Gáll, Z; Kelemen, K; Kolcsár, M; Mihály, I; Miklóssy, I; Salamon, P; Zsigmond, B, 2020
)
1.71
"Lacosamide has very few clinically relevant drug-drug interactions; however, there seems to be a significant drug interaction between lacosamide and enzyme-inducer AEDs."( Is Therapeutic Drug Monitoring of Lacosamide Needed in Patients with Seizures and Epilepsy?
Mahmoud, SH; Schultz, L, 2020
)
1.56
"Lacosamide has limited impact on cognitive and mood status in this review. "( The effects of lacosamide on cognitive function and psychiatric profiles in patients with epilepsy.
Chang, YP; Huang, LC; Li, KY; Yang, YH, 2020
)
2.35
"Lacosamide has been licenced as an add-on therapy for drug-resistant focal epilepsy."( Lacosamide add-on therapy for focal epilepsy.
Babar, RK; Bresnahan, R; Gillespie, CS; Michael, BD, 2021
)
2.79
"Lacosamide has shown positive effects against neuroinflammation-mediated model of seizures comorbid with depression by reducing hippocampal kynurenine levels."( Effect of lacosamide on neuroinflammation-mediated seizures comorbid with depression in C57BL/6 mice- Role of kynurenine pathway.
Agarwal, S; Nirwan, N; Vohora, D; Vyas, P, 2021
)
1.75
"Lacosamide has been recently introduced as adjunctive treatment for partial epilepsy."( Clinical stabilisation with lacosamide of mood disorder comorbid with PTSD and fronto-temporal epilepsy.
Cuomo, I; De Filippis, S; Kotzalidis, GD, 2017
)
1.47
"Lacosamide has not been tested in BD."( Lacosamide in bipolar disorder: A 30-day comparison to a retrospective control group treated with other antiepileptics.
Cuomo, I; De Filippis, S; Kotzalidis, GD; Lionetto, L; Piacentino, D, 2018
)
2.64
"Lacosamide has been recently approved by the European Medicines Agency as monotherapy for the treatment of focal seizures."( Lacosamide as a first-line treatment option in focal epilepsy: a cost-utility analysis for the Greek healthcare system.
Charokopou, M; Christou, P; Geitona, M; Giannakodimos, S; Kimiskidis, VK; Kountouris, V; Stamuli, E, 2019
)
2.68
"Lacosamide has a neuroprotective effect in SCI in rats that is related to its ability to decrease the production of reactive oxygen species by increasing antioxidant enzyme expression, inhibit lipid peroxidation and attenuate glial cell activation."( Neuroprotective Effects of Lacosamide in Experimental Traumatic Spinal Cord Injury in Rats.
Bengu, AS; Demiroz, S; Erdem, S; Gergin, OO; Ulucan, A; Ur, FD; Ur, K, 2019
)
2.25
"Lacosamide has a well-characterized and favorable pharmacokinetic profile, including a fast absorption rate, minimal or no interaction with cytochrome P-450 izoenzymes, and a low potential for drug-drug interactions."( Development of lacosamide for the treatment of partial-onset seizures.
Byrnes, W; Doty, P; Hebert, D; Mathy, FX; Simontacchi, K; Zackheim, J, 2013
)
1.46
"Lacosamide has shown efficacy in many animal models of chronic pain and in several short- and long-term Phase II/III clinical trials in humans with diabetic neuropathic pain."( Lacosamide for the treatment of diabetic neuropathic pain.
Biton, V, 2008
)
2.51
"Lacosamide has been reported to have been successfully used for non-convulsive status epilepticus after benzodiazepine failure, and convulsive status epilepticus after benzodiazepine and levetiracetam failure. "( Successful treatment of refractory simple motor status epilepticus with lacosamide and levetiracetam.
Chen, LL; Dorsch, A; Haneef, Z; Keselman, I; Stern, JM, 2011
)
2.04
"Lacosamide has recently been approved by the European Medicines Agency (EMEA) and its United States counterpart (FDA) as an adjuctive AED in partial onset seizures in adults over the age of 16, thus making it a novel option in the treatment of epilepsy."( [Lacosamide: a new generation in the treatment of epilepsy].
Gil-Nagel, A; Marin, H, 2011
)
2
"Lacosamide has been shown to exert its anticonvulsant effects predominantly by enhancement of the slow inactivation of voltage-gated sodium channels."( Review of therapeutic options for adjuvant treatment of focal seizures in epilepsy: focus on lacosamide.
Becerra, JL; Corredera, E; Ojeda, J; Ruiz Giménez, J, 2011
)
1.31
"The lacosamide dose has been 200 mg/day with excellent tolerability."( [Treatment of neuropathic pain with lacosamide].
García-Escrivá, A; Gil-Cortés, C; López-Hernández, N, 2012
)
1.13
"Lacosamide has limited efficacy in the treatment of peripheral diabetic neuropathy. "( Lacosamide for neuropathic pain and fibromyalgia in adults.
Derry, S; Hearn, L; Moore, RA, 2012
)
3.26
"Lacosamide has a novel mechanism of action that seems to be different in relation to other conventional AEDs."( Lacosamide in Lennox-Gastaut syndrome: case report.
Andrade-Machado, R; Benjumea-Cuartas, V; Jaramillo-Jimenez, E,
)
2.3
"Lacosamide has demonstrated analgesic efficacy in several animal studies but preclinical studies on neuropathic pain models are rare, and recent clinical trials showed no superior analgesic effects."( Analgesic ineffectiveness of lacosamide after spinal nerve ligation and its sodium channel activity in injured neurons.
Büsselberg, D; Hagenacker, T; Schäfer, N; Schäfers, M, 2013
)
1.4
"Lacosamide has a low potential for drug-drug interactions."( Lacosamide: an investigational drug for adjunctive treatment of partial-onset seizures.
Ben-Menachem, E, 2008
)
2.51

Actions

Lacosamide did not increase total or neuronal apoptosis in the neocortex in vitro or in vivo. Lacosamide was able to inhibit pain at days 3, 7 and 14 after induction of arthritis.

ExcerptReferenceRelevance
"Lacosamide did not increase total or neuronal apoptosis in the neocortex in vitro or in vivo."( Lacosamide decreases neonatal seizures without increasing apoptosis.
Bassuk, AG; Glykys, J; Langton, RL; Sharma, S; Tiarks, GC, 2022
)
2.89
"As lacosamide did not increase QTcI, the trial is considered a negative QTc trial."( Lacosamide cardiac safety: a thorough QT/QTc trial in healthy volunteers.
Cawello, W; Horstmann, R; Johnson, M; Kropeit, D; Rudd, GD, 2015
)
2.37
"Lacosamide was able to inhibit pain at days 3, 7 and 14 after induction of arthritis."( Antinociceptive efficacy of lacosamide in the monosodium iodoacetate rat model for osteoarthritis pain.
Beyreuther, B; Callizot, N; Stöhr, T, 2007
)
1.35

Treatment

Lacosamide (LCM) is a treatment option for status epilepticus (SE) described in several series. Lacosamide treats partial seizures by enhancing slow inactivation of voltage-gated sodium channels. Treatment at a dose of 400 mg/day reduced diabetic neuropathic pain.

ExcerptReferenceRelevance
"Lacosamide treatment improved everyday cognition, reduced psychiatric symptoms and improved resilience in patients with epilepsy."( Effectiveness of Lacosamide on everyday cognitive deficits, psychiatric symptoms and resilience in patients with epilepsy.
Gul, A; Mehreen, S, 2020
)
1.62
"Lacosamide treatment after SE mitigated the increased levels of IL-1β and TNF-α in the hippocampus and exerted strong neuroprotection both in the dorsal and ventral hippocampus, basolateral amygdala, and partially in the piriform cortex."( Effects of Lacosamide Treatment on Epileptogenesis, Neuronal Damage and Behavioral Comorbidities in a Rat Model of Temporal Lobe Epilepsy.
Atanasova, D; Marinov, P; Peychev, L; Shishmanova-Doseva, M; Tchekalarova, J; Uzunova, Y; Yoanidu, L, 2021
)
1.73
"The lacosamide treatment pathway was associated with higher costs (i.e. "( Lacosamide as a first-line treatment option in focal epilepsy: a cost-utility analysis for the Greek healthcare system.
Charokopou, M; Christou, P; Geitona, M; Giannakodimos, S; Kimiskidis, VK; Kountouris, V; Stamuli, E, 2019
)
2.51
"Lacosamide treatment appeared beneficial for children and adults experiencing tonic-clonic and myoclonic seizures."( Role of observational studies in supporting extrapolation of efficacy data from adults to children with epilepsy - A systematic review of the literature using lacosamide as an example.
Anamoo, MA; Arzimanoglou, A; Bozorg, A; Cooney, M; Golembesky, A; Kalilani, L; Taeter, C; Tofighy, A; Wheless, J, 2019
)
1.43
"Lacosamide (LCM) is a treatment option for status epilepticus (SE) described in several series. "( Usefulness of intravenous lacosamide in status epilepticus.
Ailouti, N; Alvarez-Sabín, J; De Gracia, R; Lainez, E; Porta, I; Quintana, M; Raspall, M; Santamarina, E; Sueiras, M; Toledo, M; Xavier Salas Puig, XS, 2013
)
2.13
"Lacosamide treats partial seizures by enhancing slow inactivation of voltage-gated sodium channels. "( Cardiac sodium channel blockade after an intentional ingestion of lacosamide, cyclobenzaprine, and levetiracetam: Case report.
Cao, D; Chua-Tuan, JL; Hoyte, CO; Iwanicki, JL, 2015
)
2.1
"Lacosamide pre-treatment increased expressions of CAT and GPX, not SOD1 and 2, in the CA1 pyramidal neurons compared with controls, and their expressions induced by lacosamide pre-treatment were maintained after transient cerebral ischemia."( Increases of Catalase and Glutathione Peroxidase Expressions by Lacosamide Pretreatment Contributes to Neuroprotection Against Experimentally Induced Transient Cerebral Ischemia.
Ahn, JH; Chen, BH; Cho, JH; Choi, HY; Hwang, IK; Kim, IH; Kim, SK; Kim, YM; Lee, JC; Lee, TK; Lee, YL; Park, JH; Shin, BN; Tae, HJ; Won, MH; Yan, BC, 2016
)
1.39
"Lacosamide treatment at a dose of 400 mg/day reduced diabetic neuropathic pain with a favorable safety and tolerability profile that may be suitable for patients with diabetes."( Lacosamide in painful diabetic neuropathy: an 18-week double-blind placebo-controlled trial.
Arslanian, A; Bongardt, S; Fares, S; Selam, JL; Sen, D; Shaibani, A; Simpson, J, 2009
)
2.52
"Treatment with lacosamide led to significant improvement in pain in all three patients."( Lacosamide for refractory trigeminal neuralgia and other facial pain-Case report.
Masrour, S, 2022
)
2.5
"Treatment with lacosamide was also associated with effective seizure control."( Adjunctive lacosamide for focal epilepsy: an open-label trial evaluating the impact of flexible titration and dosing on safety and seizure outcomes.
Bartolomei, F; Baulac, M; Coulbaut, S; De Backer, M; Doty, P; McShea, C; Vlaicu, M, 2017
)
1.18
"Treatment with lacosamide in neuropathic pain due to different causes could be considered an effective and well-tolerated alternative for patients who fail to respond to standard treatments."( [Effectiveness of lacosamide in the treatment of refractory neuropathic pain: an open observational trial].
Almajano, J; Aragón, E; Bermejo, PE; Blanco, MV; Ceballos, MÁ; Colás, J; Costa-Frossard, L; García del Carrizo, F; Gómez-Argüelles, JM; Lara, M; Latorre-González, G; Morin-Martin, Mdel M; Sánchez-Del Valle, O; Toribio-Díaz, ME; Valenzuela-Rojas, FJ, 2014
)
1.09
"Treatment with lacosamide in neuropathic pain of various etiologies could be considered as an effective alternative for patients who do not respond or not tolerate standard treatments. "( [Lacosamide and neuropathic pain, a review].
Alcántara-Montero, A; Sánchez-Carnerero, CI, 2016
)
1.7
"Treatment with lacosamide for 6months resulted in a 30.8% seizure-free rate, and 66.3% of patients had a ≥50% seizure reduction (responders)."( NEOPLASM study: Real-life use of lacosamide in patients with brain tumor-related epilepsy.
Arcediano, A; Bonet, M; Castillo, A; Gago, A; Garcés, M; Gómez-Ibáñez, A; González de la Aleja, J; López-González, FJ; Mauri, JA; Palao-Duarte, S; Palau, J; Piera, A; Rodríguez-Osorio, X; Rodriguez-Uranga, JJ; Ruiz-Giménez, J; Saiz-Diaz, R; Toledo, M; Villanueva, V, 2016
)
1.06
"Treatment with lacosamide met the predefined non-inferiority criteria when compared with carbamazepine-CR. "( Efficacy, safety, and tolerability of lacosamide monotherapy versus controlled-release carbamazepine in patients with newly diagnosed epilepsy: a phase 3, randomised, double-blind, non-inferiority trial.
Baulac, M; Brock, M; De Backer, M; Li, T; Rosenow, F; Terada, K; Toledo, M; Werhahn, KJ, 2017
)
1.08
"Rats treated with lacosamide, in contrast to vehicle treated rats, did not develop vincristine-induced cold allodynia."( Lacosamide has protective disease modifying properties in experimental vincristine neuropathy.
Beyreuther, BK; Geis, C; Sommer, C; Stöhr, T, 2011
)
2.14

Toxicity

Lacosamide is licensed for the treatment of focal seizures in both adults and children. There is little information available on its adverse reactions. A total of 10,226 adverse reaction reports with Lacosamide as the primary suspect drug were obtained.

ExcerptReferenceRelevance
" Adverse events that appeared dose-related included dizziness, nausea, fatigue, ataxia, vision abnormal, diplopia, and nystagmus."( Efficacy and safety of oral lacosamide as adjunctive therapy in adults with partial-onset seizures.
Abou-Khalil, B; Ben-Menachem, E; Biton, V; Doty, P; Jatuzis, D; Rudd, GD, 2007
)
0.63
" Clinical trials show that lacosamide is well tolerated; the most common adverse events were dizziness, nausea and vomiting."( Lacosamide: pharmacology, mechanisms of action and pooled efficacy and safety data in partial-onset seizures.
Beydoun, A; D'Souza, J; Doty, P; Hebert, D, 2009
)
2.09
" Dose-related adverse events (AEs) included dizziness, nausea, and vomiting."( Adjunctive lacosamide for partial-onset seizures: Efficacy and safety results from a randomized controlled trial.
Doty, P; Halász, P; Hebert, D; Kälviäinen, R; Mazurkiewicz-Beldzińska, M; Rosenow, F; Sullivan, T, 2009
)
0.74
" This was probably secondary to a relatively high-premature withdrawal rate due to adverse events that occurred during the titration phase in that group."( Efficacy and safety of lacosamide in diabetic neuropathic pain: an 18-week double-blind placebo-controlled trial of fixed-dose regimens.
Bongardt, S; Sen, D; Simpson, J; Wymer, JP, 2009
)
0.66
"Intravenous LCM may be safe and efficacious as an add-on AED for the treatment of NCSE when standard therapy fails."( Efficacy and safety of intravenous lacosamide in refractory nonconvulsive status epilepticus.
Azar, NJ; Estephan, B; Koubeissi, MZ; Mayor, CL; Rashid, S, 2011
)
0.65
"Lacosamide seems to be effective and safe according to the data in our small cohort."( Preliminary efficacy and safety of lacosamide in children with refractory epilepsy.
Berkovitch, M; Gandelman-Marton, R; Heyman, E; Lahat, E; Levin, N, 2012
)
2.1
"We performed a retrospective study in patients with poorly controlled epilepsy treated with add-on lacosamide (LCM) to investigate the relationship of LCM-related adverse events with LCM serum concentration and weight-dependent dosage."( Add-on lacosamide: a retrospective study on the relationship between serum concentration, dosage, and adverse events.
Hillenbrand, B; Jürges, U; Steinhoff, BJ; Wisniewski, I, 2011
)
1.04
" Traditional anti-epileptic drugs (AEDs) in this setting are not always effective and are associated with adverse events and drug interactions."( Safety and efficacy of lacosamide in the intensive care unit.
Cherry, S; Elzawahry, H; Judd, L; LaRoche, S; Muniz, JC, 2012
)
0.69
" Adverse effects were also recorded."( Safety and efficacy of lacosamide in the intensive care unit.
Cherry, S; Elzawahry, H; Judd, L; LaRoche, S; Muniz, JC, 2012
)
0.69
"This preliminary data suggests that LCM may be a safe and effective alternative for treatment of seizures in critically ill patients."( Safety and efficacy of lacosamide in the intensive care unit.
Cherry, S; Elzawahry, H; Judd, L; LaRoche, S; Muniz, JC, 2012
)
0.69
" Treatment-emergent adverse events (TEAEs), vital signs, body weight, clinical laboratory data, electrocardiography studies, and seizure frequency were evaluated."( Long-term safety and efficacy in patients with uncontrolled partial-onset seizures treated with adjunctive lacosamide: results from a Phase III open-label extension trial.
Chung, S; Doty, P; Faught, E; Husain, A; Isojarvi, J; McShea, C, 2012
)
0.59
" Primary reasons for discontinuation were lack of efficacy (26%) and adverse events (11%)."( Long-term safety and efficacy in patients with uncontrolled partial-onset seizures treated with adjunctive lacosamide: results from a Phase III open-label extension trial.
Chung, S; Doty, P; Faught, E; Husain, A; Isojarvi, J; McShea, C, 2012
)
0.59
" Safety evaluations included treatment-emergent adverse events (TEAEs), patient withdrawals due to TEAEs, and changes in vital signs, 12-lead electrocardiography (ECG) studies, laboratory parameters, and clinical examinations."( Safety and tolerability of adjunctive lacosamide intravenous loading dose in lacosamide-naive patients with partial-onset seizures.
Dilley, D; Doty, P; Fountain, NB; Isojarvi, J; Krauss, G; Rudd, GD, 2013
)
0.66
" We aimed to identify any adverse event (AE) associated with LCM treatment by conducting a systematic review and meta-analysis of all available randomized controlled trials (RCTs)."( The adverse event profile of lacosamide: a systematic review and meta-analysis of randomized controlled trials.
Giovannelli, F; Loiacono, G; Perucca, P; Verrotti, A; Zaccara, G, 2013
)
0.68
"Lacosamide may be a useful and safe pharmacological treatment option for both pediatric and adult patients with uncontrolled seizures."( Lacosamide in pediatric and adult patients: comparison of efficacy and safety.
Aloisi, P; Bruni, O; Cappanera, S; Coppola, G; Curatolo, P; Cusmai, R; Elia, M; Ferretti, A; Franzoni, E; Gobbi, G; Grosso, S; Janello, C; Kluger, G; Loiacono, G; Luchetti, A; Parisi, P; Pavone, P; Pizzolorusso, A; Romeo, A; Savasta, S; Spalice, A; Striano, P; Verrotti, A; Viri, M; Zamponi, N, 2013
)
3.28
" We collected the following variables: gender, aetiology of epilepsy, epileptogenic area, reason for switch to ESL, clinical response after initiation of ESL, adverse effects of ESL, refractoriness criteria and treatment discontinuation."( [Eslicarbazepine acetate in clinical practice. Efficacy and safety results].
Cimadevilla, JM; Fernández-Pérez, J; Payán-Ortiz, M; Quiroga-Subirana, P; Serrano-Castro, PJ, 2013
)
0.39
" There were no serious LCM-related adverse events."( Safety and efficacy of intravenous lacosamide for adjunctive treatment of refractory status epilepticus: a comparative cohort study.
Marsch, S; Rüegg, S; Sutter, R, 2013
)
0.67
"Analysis of overall tolerability and neurological adverse effects (AEs) of eslicarbazepine acetate (ESL), lacosamide (LCM) and oxcarbazepine (OXC) from double-blind, placebo-controlled trials."( Neurological adverse events of new generation sodium blocker antiepileptic drugs. Meta-analysis of randomized, double-blinded studies with eslicarbazepine acetate, lacosamide and oxcarbazepine.
Fadda, V; Giovannelli, F; Maratea, D; Verrotti, A; Zaccara, G, 2013
)
0.8
" Adverse events were seen in 8 (33%) patients."( Efficacy and safety of lacosamide in infants and young children with refractory focal epilepsy.
Balestri, P; Grosso, S; Parisi, P; Spalice, A; Verrotti, A, 2014
)
0.71
" Common treatment-emergent adverse events (TEAEs) were dizziness (39."( Safety and efficacy of adjunctive lacosamide among patients with partial-onset seizures in a long-term open-label extension trial of up to 8 years.
Ben-Menachem, E; Doty, P; Fountain, NB; Isojarvi, J; Kaubrys, G; McShea, C; Rosenfeld, W, 2014
)
0.68
" Liver function tests should be prompted in patients with symptoms suggestive of adverse effects after the initiation of lacosamide."( A case of lacosamide-induced hepatotoxicity.
Byun, JI; Lee, SK; Sunwoo, JS, 2015
)
1.03
" Adverse events (AEs) were dose related and most commonly involved the nervous and gastrointestinal systems."( Lacosamide cardiac safety: a thorough QT/QTc trial in healthy volunteers.
Cawello, W; Horstmann, R; Johnson, M; Kropeit, D; Rudd, GD, 2015
)
1.86
"Post-randomization changes from baseline for electrocardiographic (ECG) measurements, diagnostic findings, and relevant adverse events (AEs) were compared for pooled data from three randomized, placebo-controlled trials of adjunctive lacosamide for the treatment of POS."( Lacosamide cardiac safety: clinical trials in patients with partial-onset seizures.
Doty, P; Haverkamp, W; Hebert, D; Horstmann, R; Jay, G; Mason, JW; Rudd, GD; Wenger, T, 2015
)
2.04
"4 mg/kg/min is safe and will produce levels of 15 μg/ml and higher."( Safety & pK of IV loading dose of lacosamide in the ICU.
Dave, H; Irland, M; Kafai, C; Khan, F; Ramsay, RE; Sabharwal, V; Shumate, R, 2015
)
0.7
" Most common treatment-emergent adverse events (TEAEs) were dizziness (31."( Efficacy and safety of lacosamide as first add-on or later adjunctive treatment for uncontrolled partial-onset seizures: A multicentre open-label trial.
Borghs, S; Byrnes, W; De Backer, M; Dedeken, P; Escartin, A; Li, T; Tennigkeit, F; Zadeh, WW, 2015
)
0.73
" Safety outcomes included treatment-emergent adverse events (TEAEs) of particular relevance to patients with POS, overall TEAEs, and discontinuations due to TEAEs."( Safety and tolerability of lacosamide as adjunctive therapy for adults with partial-onset seizures: Analysis of data pooled from three randomized, double-blind, placebo-controlled clinical trials.
Biton, V; Doty, P; Fountain, NB; Gil-Nagel, A; Hebert, D; Isojarvi, J, 2015
)
0.71
" Treatment-emergent adverse events (TEAEs) were reported by 48."( A noninterventional study evaluating the effectiveness and safety of lacosamide added to monotherapy in patients with epilepsy with partial-onset seizures in daily clinical practice: The VITOBA study.
Arnold, S; Brandt, C; Dedeken, P; Isensee, K; Kühn, F; Lauterbach, T; Mayer, T; Noack-Rink, M; Ramirez, F; Reinhardt, F; Runge, U, 2015
)
0.65
" Adverse effects were reported in 11 patients and none were severe."( Efficacy and safety of lacosamide as an adjunctive therapy for refractory focal epilepsy in paediatric patients: a retrospective single-centre study.
Birca, A; Carmant, L; D'Anjou, G; Diadori, P; Larbrisseau, A; Lortie, A; Major, P; Perreault, S; Rossignol, E; Toupin, JF; Vanasse, M, 2015
)
0.73
"Our study adds evidence that lacosamide appears to be a safe and effective adjunctive therapy for children with refractory focal epilepsy."( Efficacy and safety of lacosamide as an adjunctive therapy for refractory focal epilepsy in paediatric patients: a retrospective single-centre study.
Birca, A; Carmant, L; D'Anjou, G; Diadori, P; Larbrisseau, A; Lortie, A; Major, P; Perreault, S; Rossignol, E; Toupin, JF; Vanasse, M, 2015
)
1.02
"This noninterventional, observational, postauthorization safety study (SP0942, NCT00771927) evaluated the incidence of predefined cardiovascular- (CV) and psychiatric-related treatment-emergent adverse events (TEAEs), in patients with epilepsy and uncontrolled partial-onset seizures, when initiating adjunctive therapy with lacosamide or another approved antiepileptic drug (AED) according to standard medical practice."( A long-term noninterventional safety study of adjunctive lacosamide therapy in patients with epilepsy and uncontrolled partial-onset seizures.
Brunnert, M; De Backer, M; Doty, P; Eckhardt, K; Schulze-Bonhage, A; Steinhoff, BJ, 2016
)
0.85
" In addition, no significant adverse reactions were observed."( Intravenous Lacosamide in Pediatric Status Epilepticus: An Open-Label Efficacy and Safety Study.
Ng, YT; Poddar, K; Sharma, R, 2016
)
0.81
"0% of patients reported treatment-emergent adverse events, of which the most common were dizziness (27."( Long-term exposure and safety of lacosamide monotherapy for the treatment of partial-onset (focal) seizures: Results from a multicenter, open-label trial.
Byrnes, W; Therriault, S; Vossler, DG; Wechsler, RT; Williams, P, 2016
)
0.72
" Treatment-emergent adverse events reported by ≥10% of all lacosamide-treated patients occurring at ≥2% difference compared with placebo were dizziness (25."( Efficacy and safety of adjunctive lacosamide for the treatment of partial-onset seizures in Chinese and Japanese adults: A randomized, double-blind, placebo-controlled study.
Du, X; Hong, Z; Inoue, Y; Liao, W; Meng, H; Tennigkeit, F; Wang, W; Wang, X; Zhang, L; Zhou, L, 2016
)
0.96
"IV LCM appears safe short term in critically ill patients with SE."( The Safety and Effectiveness of Intravenous Lacosamide for Refractory Status Epilepticus in the Critically Ill.
Ahrens, C; Hantus, S; Le, NM; Newey, CR; Sahota, P, 2017
)
0.72
" Treatment-emergent adverse events were reported in 328 (74%) patients receiving lacosamide and 332 (75%) receiving carbamazepine-CR."( Efficacy, safety, and tolerability of lacosamide monotherapy versus controlled-release carbamazepine in patients with newly diagnosed epilepsy: a phase 3, randomised, double-blind, non-inferiority trial.
Baulac, M; Brock, M; De Backer, M; Li, T; Rosenow, F; Terada, K; Toledo, M; Werhahn, KJ, 2017
)
0.95
" Primary outcomes were incidence of treatment-emergent adverse events (TEAEs) and withdrawal due to TEAEs."( Adjunctive lacosamide for focal epilepsy: an open-label trial evaluating the impact of flexible titration and dosing on safety and seizure outcomes.
Bartolomei, F; Baulac, M; Coulbaut, S; De Backer, M; Doty, P; McShea, C; Vlaicu, M, 2017
)
0.84
" Common adverse side effects included dizziness, ataxia, nausea, and vomiting."( Lacosamide treatment of childhood refractory focal epilepsy: the first reported side effect in paediatric patients.
Aydinli, N; Bektas, G; Caliskan, M; Ozkan, MU; Ozmen, M; Uzunhan, TA; Yildiz, EP, 2017
)
1.9
" These patients would benefit from intravenous anti-seizure medications with few adverse effects."( Safety of intravenous lacosamide in critically ill children.
Abend, NS; Lin, N; Topjian, AA; Welsh, SS, 2017
)
0.77
" Adverse effects were defined by predefined criteria, and most were evaluated during the full admission."( Safety of intravenous lacosamide in critically ill children.
Abend, NS; Lin, N; Topjian, AA; Welsh, SS, 2017
)
0.77
" No other adverse effects were identified, including no evidence of PR interval prolongation."( Safety of intravenous lacosamide in critically ill children.
Abend, NS; Lin, N; Topjian, AA; Welsh, SS, 2017
)
0.77
" Safety findings were generally similar to those of pivotal trials, with no major safety risks identified and with several specific adverse drug effects, such as hyponatremia, reported."( Comparing Safety and Efficacy of "Third-Generation" Antiepileptic Drugs: Long-Term Extension and Post-marketing Treatment.
Johnson, EL; Krauss, GL; Kwok, CS, 2017
)
0.46
" The most common adverse events were seizure number increased (14."( The effectiveness and safety of lacosamide in children with epilepsy in a clinical practice setting.
Díaz-Gómez, A; Sanmartí-Vilaplana, F, 2018
)
0.76
"Lacosamide use in children with refractory focal epilepsy can result in a reduction in seizure rate that improves progressively over time with few adverse effects, making lacosamide a promising option in these patients."( The effectiveness and safety of lacosamide in children with epilepsy in a clinical practice setting.
Díaz-Gómez, A; Sanmartí-Vilaplana, F, 2018
)
2.21
"Administration of lacosamide via IV push results in similar adverse effect rates to IV piggyback preparations with more efficient time to administration."( Safety and Efficiency of Intravenous Push Lacosamide Administration.
Alsherbini, K; Davidson, KE; Jones, GM; Krushinski, J; Newell, J, 2018
)
1.08
" Treatment-emergent adverse events (TEAEs) were reported by 42/47 (89."( Safety and tolerability of adjunctive lacosamide in a pediatric population with focal seizures - An open-label trial.
Abdelmoity, AT; Byrnes, W; Daniels, T; Dedeken, P; Dilley, D; Ferreira, JA; Le Pichon, JB, 2019
)
0.78
" Primary outcomes of the extension were treatment-emergent adverse events (TEAEs), serious TEAEs, and discontinuations due to TEAEs."( Long-term safety and efficacy of lacosamide and controlled-release carbamazepine monotherapy in patients with newly diagnosed epilepsy.
Ben-Menachem, E; Biton, V; Brock, M; De Backer, M; Gasalla, T; Grebe, HP; Jensen, L; Li, T; Steiniger-Brach, B; Terada, K, 2019
)
0.8
"d) as an effective and safe symptomatic treatment against acute painful oxaliplatin-induced peripheral neurotoxicity (OXAIPN)."( Real world, open label experience with lacosamide against acute painful oxaliplatin-induced peripheral neurotoxicity.
Anastopoulou, GG; Argyriou, AA; Bruna, J; Kalofonos, HP; Kalofonou, F; Litsardopoulos, P; Psimaras, D, 2020
)
0.83
"There are limited data regarding the incidence of adverse events associated with administering lacosamide by intravenous push (IVP) compared with IV piggyback (IVPB)."( Safety of Intravenous Push Lacosamide Compared With Intravenous Piggyback at a Tertiary Academic Medical Center.
Anger, KE; Carabetta, S; Hunt, N; McLaughlin, K; Schuler, BR; Szumita, PM; Ting, C; Tran, LK, 2021
)
1.14
"IVP lacosamide was associated with a similar incidence of cardiovascular, neurological, and infusion site-related adverse events compared with IVPB, in which nearly every adverse event was deemed clinically insignificant."( Safety of Intravenous Push Lacosamide Compared With Intravenous Piggyback at a Tertiary Academic Medical Center.
Anger, KE; Carabetta, S; Hunt, N; McLaughlin, K; Schuler, BR; Szumita, PM; Ting, C; Tran, LK, 2021
)
1.48
"3%) patients on lacosamide had treatment-emergent adverse events (placebo 79/121 (65."( Efficacy and safety of adjunctive lacosamide in the treatment of primary generalised tonic-clonic seizures: a double-blind, randomised, placebo-controlled trial.
Brock, M; Knake, S; O'Brien, TJ; Roebling, R; Steiniger-Brach, B; Vossler, DG; Watanabe, M; Williams, P, 2020
)
1.18
"Lacosamide was efficacious and generally safe as adjunctive treatment for uncontrolled PGTCS in patients with IGE."( Efficacy and safety of adjunctive lacosamide in the treatment of primary generalised tonic-clonic seizures: a double-blind, randomised, placebo-controlled trial.
Brock, M; Knake, S; O'Brien, TJ; Roebling, R; Steiniger-Brach, B; Vossler, DG; Watanabe, M; Williams, P, 2020
)
2.28
" The primary safety variable was treatment-emergent adverse events (TEAEs) spontaneously reported to, or observed by, the treating physician."( A prospective, multicenter, noninterventional study in Taiwan to evaluate the safety and tolerability of lacosamide as adjunctive therapy for epilepsy in clinical practice.
Chang, CW; Cheng, MY; Chuang, YC; Du, X; Hellot, S; Hsieh, HY; Hsieh, PF; Huang, HC; Hung, C; Jou, SB; Lee, WT; Lim, SN; McClung, C; Tsai, MH; Wu, T, 2020
)
0.77
"Results of this prospective, noninterventional study suggest that adjunctive LCM was generally safe and well tolerated in this patient group in real-world practice in Taiwan."( A prospective, multicenter, noninterventional study in Taiwan to evaluate the safety and tolerability of lacosamide as adjunctive therapy for epilepsy in clinical practice.
Chang, CW; Cheng, MY; Chuang, YC; Du, X; Hellot, S; Hsieh, HY; Hsieh, PF; Huang, HC; Hung, C; Jou, SB; Lee, WT; Lim, SN; McClung, C; Tsai, MH; Wu, T, 2020
)
0.77
" Safety variables included the incidence and type of adverse reactions."( Safety, efficacy, and tolerability of lacosamide for the treatment of epilepsy in pediatric patients in Uygur, China.
Feng, J; Li, HJ; Ma, L; Sun, L; Sun, Y; Wang, TT; Yu, J; Yu, LH; Zhao, T, 2021
)
0.89
"5%) experienced at least one adverse reaction."( Safety, efficacy, and tolerability of lacosamide for the treatment of epilepsy in pediatric patients in Uygur, China.
Feng, J; Li, HJ; Ma, L; Sun, L; Sun, Y; Wang, TT; Yu, J; Yu, LH; Zhao, T, 2021
)
0.89
"This retrospective study of 72 pediatric patients with epilepsy in Uygur, China, showed that LCM therapy is safe and effective for epilepsy in children, resulting in a reduction in the seizure rate."( Safety, efficacy, and tolerability of lacosamide for the treatment of epilepsy in pediatric patients in Uygur, China.
Feng, J; Li, HJ; Ma, L; Sun, L; Sun, Y; Wang, TT; Yu, J; Yu, LH; Zhao, T, 2021
)
0.89
" Safety variables were treatment-emergent adverse events (TEAEs) and discontinuations due to TEAEs."( Safety and efficacy of adjunctive lacosamide in Chinese and Japanese adults with epilepsy and focal seizures: A long-term, open-label extension of a randomized, controlled trial.
Du, X; Hong, Z; Hoshii, N; Inoue, Y; Liao, W; Osakabe, T; Sasamoto, H; Tennigkeit, F; Wang, X; Yuen, N, 2021
)
0.9
" Primary safety outcomes were treatment-emergent adverse events (TEAEs), discontinuations due to TEAEs, and serious TEAEs."( Long-term safety and tolerability of lacosamide monotherapy in patients with epilepsy: Results from a multicenter, open-label trial.
Beller, C; Ben-Menachem, E; Dominguez, J; Howerton, C; Jensen, L; McClung, C; Roebling, R; Steiniger-Brach, B; Szász, J, 2021
)
0.89
" Although oxcarbazepine (OXC) is often considered efficacious for focal seizures in NCC, due to adverse effects, newer ASMs like levetiracetam (LCM) and lacosamide are also being explored."( Comparative Efficacy and Safety of Lacosamide and Oxcarbazepine for Seizure Control in Children with Newly Diagnosed Solitary Neurocysticercosis.
Kumar, V; Panda, PK; Sharawat, IK; Sherwani, P, 2022
)
1.2
" Seizure control, electroencephalographic abnormalities, resolution of inflammatory granulomas and adverse effects were compared between two arms at 12 and 24 weeks."( Comparative Efficacy and Safety of Lacosamide and Oxcarbazepine for Seizure Control in Children with Newly Diagnosed Solitary Neurocysticercosis.
Kumar, V; Panda, PK; Sharawat, IK; Sherwani, P, 2022
)
1
" Patients receiving OXC had more frequent treatment-emergent adverse events (p = 0."( Comparative Efficacy and Safety of Lacosamide and Oxcarbazepine for Seizure Control in Children with Newly Diagnosed Solitary Neurocysticercosis.
Kumar, V; Panda, PK; Sharawat, IK; Sherwani, P, 2022
)
1
"Lacosamide appears to be efficacious and safe for achieving seizure freedom in patients with solitary viable parenchymal neurocysticercosis."( Comparative Efficacy and Safety of Lacosamide and Oxcarbazepine for Seizure Control in Children with Newly Diagnosed Solitary Neurocysticercosis.
Kumar, V; Panda, PK; Sharawat, IK; Sherwani, P, 2022
)
2.44
" The most common adverse events (AEs) were drowsiness (15."( Efficacy and safety of lacosamide in pediatric patients with epilepsy: A systematic review and meta-analysis.
Peng, Y; Yang, C; Yang, Y; Yu, D; Zhang, L, 2022
)
1.03
" The mainstay of treatment is with multiple anti-seizure medications (ASMs); however, the ASMs themselves can be associated with psychobehavioural adverse events, and effects (negative or positive) on cognition and sleep."( Psychobehavioural and Cognitive Adverse Events of Anti-Seizure Medications for the Treatment of Developmental and Epileptic Encephalopathies.
Schubert-Bast, S; Strzelczyk, A, 2022
)
0.72
" The primary outcomes were treatment-emergent adverse events (TEAEs) and discontinuations due to TEAEs."( Safety and tolerability of short-term infusions of intravenous lacosamide in pediatric patients with epilepsy: An open-label, phase 2/3 trial.
Beller, C; Bozorg, A; Farkas, MK; Makedonska, I; McClung, C; Roebling, R; Yates, T; Yuen, N, 2023
)
1.15
"The aim of this study was to compare the safety profile of newer ASMs with older ASMs through an analysis of the US Food and Drug Administration Adverse Event Reporting System (FAERS) database, with a focus on suicidality."( Newer Antiseizure Medications and Suicidality: Analysis of the Food and Drug Administration Adverse Event Reporting System (FAERS) Database.
Doughty, BJ; Hurd, KL; Leppien, EE; McCall, KL; Piper, BJ; Strong, KN, 2023
)
0.91
" The results of this case control study of FDA adverse event reports spanning 10 years and 6309 cases of suicidality expand our understanding of the safety profile of newer ASMs."( Newer Antiseizure Medications and Suicidality: Analysis of the Food and Drug Administration Adverse Event Reporting System (FAERS) Database.
Doughty, BJ; Hurd, KL; Leppien, EE; McCall, KL; Piper, BJ; Strong, KN, 2023
)
0.91
" The response rate, retention rate, and adverse effects were calculated."( Investigation of the efficacy and adverse effects of lacosamide over 36 months.
Ikeda, T; Kuwajima, M; Matsumoto, A; Muramatsu, K; Osaka, H; Wakabayashi, K; Yamagata, T; Yamagishi, H, 2023
)
1.16
" The most common adverse effects were somnolence in 21 patients (16."( Investigation of the efficacy and adverse effects of lacosamide over 36 months.
Ikeda, T; Kuwajima, M; Matsumoto, A; Muramatsu, K; Osaka, H; Wakabayashi, K; Yamagata, T; Yamagishi, H, 2023
)
1.16
"Seizures are common in critically ill children and neonates, and these patients would benefit from intravenous (IV) antiseizure medications with few adverse effects."( Safety of intravenous lacosamide in hospitalized children and neonates.
Abend, NS; Dickinson, K; Fong, SL; Forrest, CB; Foskett, N; Grande, KM; Guerriero, RM; Jain, B; Kaur, M; Maltenfort, M; McDonald, J; Rao, S; Roebling, R; Stoltenberg, M; Utidjian, L; Wainwright, MS; Williams, P; Yuen, N, 2023
)
1.22
" There were no reports of PR interval prolongation or severe cutaneous adverse reactions."( Safety of intravenous lacosamide in hospitalized children and neonates.
Abend, NS; Dickinson, K; Fong, SL; Forrest, CB; Foskett, N; Grande, KM; Guerriero, RM; Jain, B; Kaur, M; Maltenfort, M; McDonald, J; Rao, S; Roebling, R; Stoltenberg, M; Utidjian, L; Wainwright, MS; Williams, P; Yuen, N, 2023
)
1.22
" This literature review evaluated whether lacosamide is effective and safe for the treatment of poststroke seizures and epilepsy."( Effectiveness and Safety of Lacosamide, A Third-generation Anti-seizure Medication, for Poststroke Seizure and Epilepsy: A Literature Review.
Chen, TS; Chen, YS; Huang, CW; Lai, MC; Li, YJ; Tseng, YH, 2023
)
1.47
"Lacosamide is licensed for the treatment of focal seizures in both adults and children, however there is little information available on its adverse reactions."( Real-world safety of Lacosamide: A pharmacovigilance study based on spontaneous reports in the FDA adverse event reporting system.
He, M; He, Y; Liu, B; Liu, P; Xu, X; Yao, W, 2023
)
2.67
"A total of 10,226 adverse reaction reports with Lacosamide as the primary suspect drug were obtained, with 30,960 reported cases, detecting 232 valuable positive signals, involving a total of 20 SOCs, of which the most frequently reported SOCs were nervous system disorders (6537 cases, 55."( Real-world safety of Lacosamide: A pharmacovigilance study based on spontaneous reports in the FDA adverse event reporting system.
He, M; He, Y; Liu, B; Liu, P; Xu, X; Yao, W, 2023
)
1.48
" Treatment-emergent adverse events (TEAEs) were reported by 49 patients (89."( Safety, tolerability, and efficacy of adjunctive lacosamide in pediatric patients with epilepsy syndromes associated with generalized seizures: Phase 2, open-label exploratory trial.
Arzimanoglou, A; Auvin, S; Beller, C; Bozorg, A; Daniels, T; Floricel, F, 2023
)
1.16

Pharmacokinetics

The pharmacokinetic parameters of area under the concentration-time curve (AUC), maximum steady-state plasma drug concentration (Cmax ), and time to maximum concentration (tmax ) were measured for the OC components and lacosamide. Two open-label, multiple-dose clinical trials were conducted.

ExcerptReferenceRelevance
" Two open-label, multiple-dose clinical trials were conducted to evaluate the potential for pharmacokinetic interaction between lacosamide and carbamazepine."( No pharmacokinetic interaction between lacosamide and carbamazepine in healthy volunteers.
Cawello, W; Eggert-Formella, A; Nickel, B, 2010
)
0.84
"Lacosamide is a new antiepileptic drug (AED) apparently devoid of major pharmacokinetic interactions."( Lacosamide neurotoxicity associated with concomitant use of sodium channel-blocking antiepileptic drugs: a pharmacodynamic interaction?
Novy, J; Patsalos, PN; Sander, JW; Sisodiya, SM, 2011
)
3.25
" The developed analytical method was successfully applied to the pharmacokinetic study of lacosamide in rats."( Liquid chromatography-tandem mass spectrometry for quantification of lacosamide, an antiepileptic drug, in rat plasma and its application to pharmacokinetic study.
Baek, M; Ha, DJ; Kim, SJ; Koo, TS; Lee, SK; Moon, H; Shin, DS, 2012
)
0.83
"A method for analysis of lacosamide [(R)-2-acetamido-N-benzyl-3-methoxypropionamide] is needed for both human and veterinary pharmacokinetic investigations."( High-performance liquid chromatographic analysis of lacosamide in canine serum using ultraviolet detection: application to pre-clinical pharmacokinetics in dogs.
Bowen, KA; Chen-Allen, AV; Davies, NM; Martinez, SE; Remsberg, CM; Takemoto, JK; Wright, HM, 2012
)
0.93
"To determine whether pharmacodynamic interactions between high doses of lacosamide (400-800 mg/day) and concomitant sodium channel antiepilepsy drugs (AEDs) can be minimized in patients with drug-resistant partial-onset seizures."( Minimizing pharmacodynamic interactions of high doses of lacosamide.
Bean, A; Cole, AG; Edwards, HB; Griffiths, AS; Krauss, GL; Lin, B, 2012
)
0.86
"Two open-label, randomized, multiple-dose clinical studies evaluated the potential for pharmacokinetic interaction between the antiepileptic drugs lacosamide and valproic acid."( No pharmacokinetic interaction between lacosamide and valproic acid in healthy volunteers.
Bonn, R; Cawello, W, 2012
)
0.85
" However, the time to peak concentration and the dose-normalized peak concentration for 30 mg/kg were significantly different with those for other doses."( Pharmacokinetics, brain distribution, and plasma protein binding of the antiepileptic drug lacosamide in rats.
Baek, M; Ha, DJ; Kim, SJ; Koo, TS; Moon, H, 2011
)
0.59
" The developed method was successfully used for the preclinical pharmacokinetic study of lacosamide in rats."( Development of a sensitive bioanalytical method for the quantification of lacosamide in rat plasma. Application to preclinical pharmacokinetics studies in rats.
Arumugam, K; Desai, N; Muddukrishna, BS; Shah, S; Vasantharaju, SG, 2012
)
0.83
" Additional objectives were to compare the pharmacokinetic profile of lacosamide in saliva and plasma, and to evaluate its tolerability."( Tolerability, pharmacokinetics, and bioequivalence of the tablet and syrup formulations of lacosamide in plasma, saliva, and urine: saliva as a surrogate of pharmacokinetics in the central compartment.
Andreas, JO; Bökens, H; Cawello, W; Halabi, A; Nickel, B, 2013
)
0.84
" Plasma and saliva samples for evaluation of pharmacokinetic parameters of lacosamide and the major metabolite O-desmethyl lacosamide (SPM 12809) were taken over 15 time points (0."( Tolerability, pharmacokinetics, and bioequivalence of the tablet and syrup formulations of lacosamide in plasma, saliva, and urine: saliva as a surrogate of pharmacokinetics in the central compartment.
Andreas, JO; Bökens, H; Cawello, W; Halabi, A; Nickel, B, 2013
)
0.84
" The pharmacokinetic parameters of area under the concentration-time curve (AUC), maximum steady-state plasma drug concentration (Cmax ), and time to maximum concentration (tmax ) were measured for the OC components and lacosamide."( Pharmacodynamic and pharmacokinetic evaluation of coadministration of lacosamide and an oral contraceptive (levonorgestrel plus ethinylestradiol) in healthy female volunteers.
Cawello, W; Rosenkranz, B; Schmid, B; Wierich, W, 2013
)
0.81
" In each of the 31 volunteers who completed the trial (through cycle 3), pharmacodynamic assessment showed progesterone serum concentration was <5."( Pharmacodynamic and pharmacokinetic evaluation of coadministration of lacosamide and an oral contraceptive (levonorgestrel plus ethinylestradiol) in healthy female volunteers.
Cawello, W; Rosenkranz, B; Schmid, B; Wierich, W, 2013
)
0.62
" Pharmacokinetic end points were area under the plasma concentration-time curve (AUC(0,last) and AUC(0,∞) ) and maximum plasma concentration (Cmax ) for S- and R-warfarin."( Lack of effect of lacosamide on the pharmacokinetic and pharmacodynamic profiles of warfarin.
Cawello, W; Eckhardt, K; Kumke, T; Stockis, A; van Lier, JJ, 2013
)
0.72
"Following warfarin and lacosamide coadministration, Cmax and AUC of S- and R-warfarin, as well as peak value and AUC of PT and INR, were equivalent to those after warfarin alone."( Lack of effect of lacosamide on the pharmacokinetic and pharmacodynamic profiles of warfarin.
Cawello, W; Eckhardt, K; Kumke, T; Stockis, A; van Lier, JJ, 2013
)
1.03
" Therefore, an evaluation of the impact of renal impairment on its pharmacokinetic profile is an important component of its safety assessment."( Impact of impaired renal function on the pharmacokinetics of the antiepileptic drug lacosamide.
Cawello, W; Fuhr, U; Halabi, A; Hering, U; Maatouk, H, 2013
)
0.61
" Terminal half-life and systemic exposure were increased with renal impairment, while total body clearance, renal clearance, and urinary excretion were decreased."( Impact of impaired renal function on the pharmacokinetics of the antiepileptic drug lacosamide.
Cawello, W; Fuhr, U; Halabi, A; Hering, U; Maatouk, H, 2013
)
0.61
"This phase I, randomized, open-label, two-way crossover trial evaluated the pharmacokinetic effects of lacosamide and omeprazole coadministration."( Pharmacokinetics of lacosamide and omeprazole coadministration in healthy volunteers: results from a phase I, randomized, crossover trial.
Cawello, W; Fichtner, A; Mueller-Voessing, C, 2014
)
0.94
" Area under the concentration-time curve (AUC) and peak concentration (C(max)) were the primary pharmacokinetic parameters measured for lacosamide or omeprazole administered alone (reference) or in combination (test)."( Pharmacokinetics of lacosamide and omeprazole coadministration in healthy volunteers: results from a phase I, randomized, crossover trial.
Cawello, W; Fichtner, A; Mueller-Voessing, C, 2014
)
0.93
"Frequent plasma sampling to monitor pharmacokinetic (PK) profile of antiepileptic drugs (AEDs), is invasive, costly and time consuming."( A system of equations to approximate the pharmacokinetic parameters of lacosamide at steady state from one plasma sample.
Cawello, W; Schäfer, C, 2014
)
0.64
"05 h(-1), corresponding to half-life of 13 h) was calculated to reach Cpeak,ss after ∼1 h (tmax,ss)."( A system of equations to approximate the pharmacokinetic parameters of lacosamide at steady state from one plasma sample.
Cawello, W; Schäfer, C, 2014
)
0.64
" Characterization of the pharmacokinetic profile is an important aspect in the development of LCM."( Advances in epilepsy treatment: lacosamide pharmacokinetic profile.
Andreas, JO; Cawello, W; Dimova, S; Stockis, A, 2014
)
0.69
"Age- and sex-related differences in body composition could affect the pharmacokinetic parameters of administered drugs."( Effect of age and sex on lacosamide pharmacokinetics in healthy adult subjects and adults with focal epilepsy.
Cawello, W; Elshoff, JP; Schaefer, C; Waitzinger, J, 2015
)
0.72
"This post hoc analysis used pharmacokinetic data taken at steady state from (i) two phase I studies of oral lacosamide in healthy adult subjects (n = 66), and (ii) a population pharmacokinetic analysis carried out using data from two phase III studies of adjunctive oral lacosamide in adults (n = 565) with focal epilepsy taking 1-3 concomitant anti-epileptic drugs."( Effect of age and sex on lacosamide pharmacokinetics in healthy adult subjects and adults with focal epilepsy.
Cawello, W; Elshoff, JP; Schaefer, C; Waitzinger, J, 2015
)
0.93
" The pharmacokinetic profile of lacosamide was unaffected by age or sex in adults with focal epilepsy."( Effect of age and sex on lacosamide pharmacokinetics in healthy adult subjects and adults with focal epilepsy.
Cawello, W; Elshoff, JP; Schaefer, C; Waitzinger, J, 2015
)
1
" Variability in pharmacokinetic parameters is low (coefficients of variation almost all <20 %)."( Clinical pharmacokinetic and pharmacodynamic profile of lacosamide.
Cawello, W, 2015
)
0.66
" The possible differential diagnosis and pharmacokinetic nuances are discussed."( Lacosamide Induced Psychosis: Case Report, Review of Differential Diagnosis and Relevant Pharmacokinetics.
Cohen, H; Friedman, M; Hayes, D; Lam, T; Pinkhasov, A; Singh, D,
)
1.57
"The knowledge of pharmacokinetic and pharmacodynamic properties of antiepileptic drugs is helpful in optimizing drug therapy for epilepsy."( Evaluation of Brain Pharmacokinetic and Neuropharmacodynamic Attributes of an Antiepileptic Drug, Lacosamide, in Hepatic and Renal Impairment: Preclinical Evidence.
Kumar, B; Medhi, B; Modi, M; Saikia, B, 2017
)
0.67
" The purpose of this study is to evaluate the pharmacokinetic variability of LCM in relation to efficacy and tolerability in patients with refractory epilepsy in a real-life setting."( Therapeutic Drug Monitoring of Lacosamide in Norway: Focus on Pharmacokinetic Variability, Efficacy and Tolerability.
Baftiu, A; Brodtkorb, E; Burns, ML; Johannessen Landmark, C; Johannessen, SI; Svendsen, T, 2017
)
0.74
" It is focused on the pharmacokinetic properties of lacosamide (LCM) for the treatment of partial-onset seizures."( Pharmacokinetic drug evaluation of lacosamide for the treatment of partial-onset seizures.
de Biase, S; Gigli, GL; Merlino, G; Valente, M, 2017
)
0.98
"69 L/kg, elimination half-life of 13."( Lacosamide Pharmacokinetics in a Critically Ill Patient During Continuous Renal Replacement Therapy.
Albright, RC; Barreto, EF; Fugate, JE; Lopez-Ruiz, A; Wieruszewski, PM, 2020
)
2
"A pediatric population pharmacokinetic model including covariate effects was developed using data from 2 clinical trials in pediatric patients with epilepsy (SP0847 and SP1047)."( Population Pharmacokinetics of Adjunctive Lacosamide in Pediatric Patients With Epilepsy.
Schoemaker, R; Stockis, A; Winkler, J, 2019
)
0.78
" The purpose of this study was to investigate the use of LCM in this patient group in relation to age, comedication, dose, serum concentrations and duration of treatment, and to examine pharmacokinetic variability."( Pharmacokinetic Variability and Clinical Use of Lacosamide in Children and Adolescents in Denmark and Norway.
Baftiu, A; Borg Rasmussen, J; Johannessen Landmark, C; Johannessen, SI; Larsen Burns, M; Nikanorova, M, 2019
)
0.77
"The study demonstrates pharmacokinetic variability in and between age groups, which indicates usefulness of therapeutic drug monitoring."( Pharmacokinetic Variability and Clinical Use of Lacosamide in Children and Adolescents in Denmark and Norway.
Baftiu, A; Borg Rasmussen, J; Johannessen Landmark, C; Johannessen, SI; Larsen Burns, M; Nikanorova, M, 2019
)
0.77
" Serum and brain levels of antiepileptic drugs and cannabidiol were determined by using HPLC in order to ascertain any pharmacokinetic contribution to the observed behavioral effects."( Acute effect of cannabidiol on the activity of various novel antiepileptic drugs in the maximal electroshock- and 6 Hz-induced seizures in mice: Pharmacodynamic and pharmacokinetic studies.
Nieoczym, D; Socała, K; Szafarz, M; Wlaź, P; Wyska, E, 2019
)
0.51
"This narrative review aimed to provide critical findings of the available literature about the role of pharmacodynamic AEDs' interactions in patients whose epilepsies were treated with polytherapy."( Pharmacodynamic interactions of antiepileptic drugs: From bench to clinical practice.
Brigo, F; Lattanzi, S; Verrotti, A; Zaccara, G, 2020
)
0.56
"Electronic databases, Medical Literature Analysis and Retrieval System Online (MEDLINE) and Excerpta Medica dataBASE (EMBASE), were systematically searched to identify relevant studies on pharmacodynamic AEDs' interactions in patients with epilepsy."( Pharmacodynamic interactions of antiepileptic drugs: From bench to clinical practice.
Brigo, F; Lattanzi, S; Verrotti, A; Zaccara, G, 2020
)
0.56
" Conversely, the combination of AEDs may cause pharmacodynamic synergistic effects that may result in not only increased efficacy but also more adverse effects."( Pharmacodynamic interactions of antiepileptic drugs: From bench to clinical practice.
Brigo, F; Lattanzi, S; Verrotti, A; Zaccara, G, 2020
)
0.56
" The validated method was successfully applied to a pharmacokinetic study with three lacosamide formulations (50, 100, and 200 mg) in 36 healthy subjects."( Selective quantification of lacosamide in human plasma using UPLC-MS/MS: Application to pharmacokinetic study in healthy subjects with different doses.
Bharwad, KD; Shah, PA; Sharma, VS; Shrivastav, PS, 2020
)
1.08
" Although its treatment is currently symptomatic, the last generation of anti-seizure drugs is characterized by better pharmacokinetic profiles, efficacy, tolerability and safety."( Pharmacology of lacosamide: From its molecular mechanisms and pharmacokinetics to future therapeutic applications.
Bicker, J; Carona, A; Falcão, A; Fonseca, C; Fortuna, A; Silva, R, 2021
)
0.97
"We present pharmacokinetic data during pregnancy and lactation for brivaracetam, lacosamide and perampanel based on two case studies."( Pharmacokinetic data on brivaracetam, lacosamide and perampanel during pregnancy and lactation.
Brodtkorb, E; Burns, ML; Johannessen, SI; Landmark, CJ; Rektorli, L; Revdal, E, 2021
)
1.12
"Many pharmacokinetic studies of lacosamide (LCM) have been reported, but no large-scale clinical study has been conducted on genetic polymorphisms that affect the metabolism of LCM."( Effects of CYP2C19 genetic polymorphisms on the pharmacokinetics of lacosamide in Korean patients with epilepsy.
Ahn, SJ; Chu, K; Hwang, S; Jung, KH; Jung, KY; Kim, DY; Kim, EY; Lee, HS; Lee, S; Lee, SK; Lee, ST; Lee, WJ; Moon, J; Oh, J; Park, KI; Shin, HR; Son, H; Yu, KS, 2022
)
1.24
" In the pharmacodynamic subgroup analysis, patients in the ineffective LCM group had significantly lower serum concentrations (6."( Effects of CYP2C19 genetic polymorphisms on the pharmacokinetics of lacosamide in Korean patients with epilepsy.
Ahn, SJ; Chu, K; Hwang, S; Jung, KH; Jung, KY; Kim, DY; Kim, EY; Lee, HS; Lee, S; Lee, SK; Lee, ST; Lee, WJ; Moon, J; Oh, J; Park, KI; Shin, HR; Son, H; Yu, KS, 2022
)
0.96

Bioavailability

Lacosamide has a favorable pharmacokinetic profile. The bioavailability of lacosamide is 100% and is unaffected by food intake. protein binding is low; it is metabolized by CYP2C19 into inactive O-desmethyl Lacosamide.

ExcerptReferenceRelevance
" The bioavailability of the oral lacosamide tablet was similar to that of a 30- or 60-minute intravenous infusion of lacosamide administered at the same dosage."( Lacosamide: in partial-onset seizures.
Cross, SA; Curran, MP, 2009
)
2.08
" The AUC(tau,ss) and C(max,ss) point estimates (combined vs sole treatment) showed relative bioavailability of approximately 100% for both drugs."( No pharmacokinetic interaction between lacosamide and carbamazepine in healthy volunteers.
Cawello, W; Eggert-Formella, A; Nickel, B, 2010
)
0.63
" With its bioavailability of approximately 100%, minimal protein binding, and few drug-drug interactions, lacosamide has a favorable pharmacokinetic profile."( Lacosamide: an adjunctive agent for partial-onset seizures and potential therapy for neuropathic pain.
Harris, JA; Murphy, JA, 2009
)
2.01
" It has a high oral bioavailability of approximately 100%."( Lacosamide, a newer antiepileptic.
Medhi, B; Patyar, S, 2010
)
1.8
" Following oral administration, absolute oral bioavailability was not dose dependent and was at 93."( Pharmacokinetics, brain distribution, and plasma protein binding of the antiepileptic drug lacosamide in rats.
Baek, M; Ha, DJ; Kim, SJ; Koo, TS; Moon, H, 2011
)
0.59
" The bioavailability of lacosamide is 100% and is unaffected by food intake; protein binding is low; it is metabolized by CYP2C19 into inactive O-desmethyl lacosamide."( [Therapeutic drug monitoring of lacosamide].
Bentué-Ferrer, D; Tribut, O; Verdier, MC,
)
0.72
"5-72 h) and used to statistically compare bioavailability of the two."( Tolerability, pharmacokinetics, and bioequivalence of the tablet and syrup formulations of lacosamide in plasma, saliva, and urine: saliva as a surrogate of pharmacokinetics in the central compartment.
Andreas, JO; Bökens, H; Cawello, W; Halabi, A; Nickel, B, 2013
)
0.61
" Studies in healthy subjects and in patients with focal epilepsy have established that LCM has several favorable pharmacokinetic characteristics, including rapid absorption and high oral bioavailability not affected by food, linear and dose-proportional pharmacokinetics, low inter- and intraindividual variability, low plasma protein binding, renal elimination, and a low potential for clinically relevant pharmacokinetic drug-drug interactions both with AEDs and other common medications."( Advances in epilepsy treatment: lacosamide pharmacokinetic profile.
Andreas, JO; Cawello, W; Dimova, S; Stockis, A, 2014
)
0.69
" Following normalization by lean body weight or volume of distribution, an analysis of relative bioavailability resulted in 90 % confidence intervals of the ratios for AUCτ,ss and C max,ss for age (elderly to younger) or sex (male to female) falling within the range accepted for equivalence (80-125 %); without normalization, the 90 % confidence intervals were outside this range."( Effect of age and sex on lacosamide pharmacokinetics in healthy adult subjects and adults with focal epilepsy.
Cawello, W; Elshoff, JP; Schaefer, C; Waitzinger, J, 2015
)
0.72
" Oral bioavailability is high (100 %) for a dose up to 800 mg."( Clinical pharmacokinetic and pharmacodynamic profile of lacosamide.
Cawello, W, 2015
)
0.66
" Because the bioavailability and tolerability of oral and intravenous LCM are comparable, LCM offers the advantage of direct conversion from oral to intravenous administration, and vice versa, without the need for titration or dose adjustment."( Pharmacokinetic drug evaluation of lacosamide for the treatment of partial-onset seizures.
de Biase, S; Gigli, GL; Merlino, G; Valente, M, 2017
)
0.73
"The ATP-binding cassette transporter P-glycoprotein (P-gp) is known to limit both brain penetration and oral bioavailability of many chemotherapy drugs."( A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
Ambudkar, SV; Brimacombe, KR; Chen, L; Gottesman, MM; Guha, R; Hall, MD; Klumpp-Thomas, C; Lee, OW; Lee, TD; Lusvarghi, S; Robey, RW; Shen, M; Tebase, BG, 2019
)
0.51

Dosage Studied

Lacosamide (LCM) is a new anticonvulsant available in intravenous (IV) form. Its optimal dosing regimen for the treatment of RSE is unknown.

ExcerptRelevanceReference
" Pharmacokinetic parameters, area under the concentration-time curve during a dosage interval at steady state (AUC(tau,ss)), and maximum steady-state plasma drug concentration during a dosage interval (C(max,ss)) of lacosamide, carbamazepine, and carbamazepine-10,11-epoxide were measured and compared for each drug alone and together."( No pharmacokinetic interaction between lacosamide and carbamazepine in healthy volunteers.
Cawello, W; Eggert-Formella, A; Nickel, B, 2010
)
0.82
" Lacosamide was found to be efficacious with significant reduction in seizure frequency dosed 400-600 mg daily."( Lacosamide and epilepsy.
Harris, JA; Murphy, JA, 2011
)
2.72
" Lacosamide mean dosage was of 332."( Lacosamide as add-on in brain tumor-related epilepsy: preliminary report on efficacy and tolerability.
Carapella, CM; Dinapoli, L; Maschio, M; Mingoia, M; Muti, P; Pace, A; Pompili, A; Sperati, F; Vidiri, A, 2011
)
2.72
" Currently, no dosing regimen for the drug exists in dogs."( High-performance liquid chromatographic analysis of lacosamide in canine serum using ultraviolet detection: application to pre-clinical pharmacokinetics in dogs.
Bowen, KA; Chen-Allen, AV; Davies, NM; Martinez, SE; Remsberg, CM; Takemoto, JK; Wright, HM, 2012
)
0.63
" Efficacy was determined according to seizure frequency during the week prior to treatment initiation and the week after the maximal dosage of lacosamide was attained."( Preliminary efficacy and safety of lacosamide in children with refractory epilepsy.
Berkovitch, M; Gandelman-Marton, R; Heyman, E; Lahat, E; Levin, N, 2012
)
0.86
" Area under the concentration-time curve during a 12-hour dosing interval at steady state (AUC(τ,ss)) and maximum steady-state plasma drug concentration (C(max,ss)) were measured for each drug alone and together and tested for equivalence."( No pharmacokinetic interaction between lacosamide and valproic acid in healthy volunteers.
Bonn, R; Cawello, W, 2012
)
0.65
" Subsequent dosage adjustments of lacosamide (100-800 mg/day) and/or concomitant AEDs were allowed to optimize tolerability and seizure reduction."( Long-term safety and efficacy in patients with uncontrolled partial-onset seizures treated with adjunctive lacosamide: results from a Phase III open-label extension trial.
Chung, S; Doty, P; Faught, E; Husain, A; Isojarvi, J; McShea, C, 2012
)
0.87
" We used risk differences to evaluate the association of any (99% confidence intervals [CIs]) or serious AEs (95% CIs) with LCM and to investigate dose-response relationships of identified AEs."( The adverse event profile of lacosamide: a systematic review and meta-analysis of randomized controlled trials.
Giovannelli, F; Loiacono, G; Perucca, P; Verrotti, A; Zaccara, G, 2013
)
0.68
" Lacosamide (LCM) is a new anticonvulsant available in intravenous (IV) form, but its optimal dosing regimen for the treatment of RSE is unknown."( Intravenous lacosamide in refractory seizure clusters and status epilepticus: comparison of 200 and 400 mg loading doses.
Depondt, C; Gaspard, N; Legros, B; Levy-Nogueira, M; Ligot, N; Mavroudakis, N; Naeije, G, 2014
)
1.69
" The 2 groups were comparable for age, gender, weight, LCM daily dose, and dosing frequency."( Lacosamide therapeutic monitoring in patients with epilepsy: effect of concomitant antiepileptic drugs.
Albani, F; Baruzzi, A; Candela, C; Contin, M; Mohamed, S; Riva, R, 2013
)
1.83
" The steady-state area under concentration-time curve over the dosing interval (AUC(24,ss)) and maximum steady-state plasma concentration (C(max,ss)) of digoxin were measured; ratios of these parameters for co-administration of digoxin + lacosamide versus digoxin alone were used to evaluate potential DDIs."( Effect of lacosamide on the steady-state pharmacokinetics of digoxin: results from a phase I, multiple-dose, double-blind, randomised, placebo-controlled, crossover trial.
Andreas, JO; Cawello, W; Mueller-Voessing, C, 2014
)
0.99
"Equations were derived to approximate steady-state peak and trough lacosamide plasma concentrations (Cpeak,ss and Ctrough,ss, respectively) and area under concentration-time curve during dosing interval (AUCτ,ss) from one plasma sample."( A system of equations to approximate the pharmacokinetic parameters of lacosamide at steady state from one plasma sample.
Cawello, W; Schäfer, C, 2014
)
0.87
" Dosage adjustments of lacosamide (100-800 mg/day) and/or concomitant antiepileptic drugs were allowed to optimize tolerability and seizure reduction."( Safety and efficacy of adjunctive lacosamide among patients with partial-onset seizures in a long-term open-label extension trial of up to 8 years.
Ben-Menachem, E; Doty, P; Fountain, NB; Isojarvi, J; Kaubrys, G; McShea, C; Rosenfeld, W, 2014
)
0.99
"Monitoring lacosamide (LCM) helps optimize therapeutic dosing in some clinical settings."( A sensitive and rapid method for quantification of lacosamide and desmethyl lacosamide by LC-MS/MS.
Bruton, M; Foldvary-Schaefer, N; Payto, D; So, N; Wang, S, 2014
)
1.04
"Minor numerical differences between lacosamide exposure [the area under the concentration-time curve at steady state over the dosage interval (AUCτ,ss)] and the maximum plasma concentration at steady state (C max,ss) in subjects of different ages or sexes were noted."( Effect of age and sex on lacosamide pharmacokinetics in healthy adult subjects and adults with focal epilepsy.
Cawello, W; Elshoff, JP; Schaefer, C; Waitzinger, J, 2015
)
1
"Following intravenous dosing with lacosamide, dose-dependent PR and QRS prolongation and ECG abnormalities (loss of P waves, atrioventricular and intraventricular blocks, junctional premature contractions) were observed in anesthetized dogs and monkeys."( Cardiac safety of lacosamide: the non-clinical perspective.
Colomar, A; Cornet, M; Delaunois, A; Depelchin, BO, 2015
)
1.03
" In patients with epilepsy who follow a stable oral AED dosing regimen, lacosamide concentration in CSF is approximately 85% of that found in serum, suggesting that serum may be a valuable indicator of lacosamide concentration in the CNS."( Comparison of lacosamide concentrations in cerebrospinal fluid and serum in patients with epilepsy.
Bien, CG; Brandt, C; Cawello, W; Helmer, R; May, TW, 2015
)
1.01
" Higher mg/kg dosing had been used subsequently with doses up to 13 mg/kg."( Safety & pK of IV loading dose of lacosamide in the ICU.
Dave, H; Irland, M; Kafai, C; Khan, F; Ramsay, RE; Sabharwal, V; Shumate, R, 2015
)
0.7
"Although chronic dosing resulted in higher LCM concentrations in serum and CSF compared to drug-naive patients, the CSF/serum ratio was not affected by LCM pretreatment."( Acute or chronic use of lacosamide does not alter its distribution between serum and cerebrospinal fluid.
Basha, M; Michelhaugh, SK; Mittal, S; Rhoney, DH; Shah, AK, 2015
)
0.72
"Patients with POS (≥2 years' duration, ≥2 previous antiepileptic drugs [AEDs]) uncontrolled by a stable dosing regimen of 1-3 concomitant AEDs were randomized to treatment with lacosamide at doses of 200 mg/day, 400 mg/day, or 600 mg/day, or placebo."( Safety and tolerability of lacosamide as adjunctive therapy for adults with partial-onset seizures: Analysis of data pooled from three randomized, double-blind, placebo-controlled clinical trials.
Biton, V; Doty, P; Fountain, NB; Gil-Nagel, A; Hebert, D; Isojarvi, J, 2015
)
0.91
" The acute tolerability at this dosing range represents a positive trend and need confirmation from larger studies."( Clinical experience of intravenous lacosamide in infants and young children.
Arkilo, D; Gustafson, M; Ritter, FJ, 2016
)
0.71
" Increasing the dosage led to higher incidence of quitting the medication because of adverse events [400 vs."( Dose effects of lacosamide as add-on therapy for partial-onset seizure in adult.
Chen, D; Chen, T; Lin, Y; Liu, L; Si, Y; Xu, D; Zhang, Q; Zhang, WW, 2016
)
0.78
" For patients who fail low dose levetiracetam (LEV), a reasonable alternative to increasing dosage may be the addition of a low-dose adjunctive AED."( Open Label Trial of Add on Lacosamide Versus High Dose Levetiracetam Monotherapy in Patients With Breakthrough Seizures.
Alam, J; Bubrick, EB; Dworetzky, BA; Hurwitz, S; Lee, JW; Llewellyn, N; Pennell, PB; Putta, S; Sarkis, RA; Weisholtz, D; Yu, H,
)
0.43
" In this phase IIIb, prospective, multicenter, open-label, single-arm trial (NCT01375374), the serum concentrations of CYP-related reproductive hormones, thyroid hormones, and lipids were assessed in otherwise healthy male patients with focal seizures (N=11), before and after a switch from CBZ (600-1200mg/day at baseline) to lacosamide (target dose: 400mg/day by the end of titration) as adjunctive treatment to the nonenzyme-inducing AED levetiracetam (LEV, stable dosage of >1000mg/day throughout)."( Changes in hormone and lipid levels in male patients with focal seizures when switched from carbamazepine to lacosamide as adjunctive treatment to levetiracetam: A small phase IIIb, prospective, multicenter, open-label trial.
Brandt, C; De Backer, M; Dedeken, P; Eckhardt, K; Elger, CE; Elmoufti, S; Rademacher, M; Tennigkeit, F, 2016
)
0.82
"The aim of this review was to evaluate current literature for dosing recommendations for the use of antiepileptic medications in patients receiving renal replacement therapy (RRT)."( Antiepileptic dosing for critically ill adult patients receiving renal replacement therapy.
Bastin, ML; Cook, AM; Oyler, DR; Smetana, KS, 2016
)
0.43
" Micromedex® DRUGDEX as well as package inserts were used to obtain known pharmacokinetic properties and dosage adjustment recommendations in RRT if known."( Antiepileptic dosing for critically ill adult patients receiving renal replacement therapy.
Bastin, ML; Cook, AM; Oyler, DR; Smetana, KS, 2016
)
0.43
"Data regarding antiepileptic drug use in RRT are limited and mostly consist of case reports limiting our proposed dosing recommendations."( Antiepileptic dosing for critically ill adult patients receiving renal replacement therapy.
Bastin, ML; Cook, AM; Oyler, DR; Smetana, KS, 2016
)
0.43
"Additional studies are necessary before specific dosing recommendations can be made for most antiepileptic drugs in critically ill patients receiving RRT, specifically with newer agents."( Antiepileptic dosing for critically ill adult patients receiving renal replacement therapy.
Bastin, ML; Cook, AM; Oyler, DR; Smetana, KS, 2016
)
0.43
" Patients who continued to the extension study (SP0962; NCT01118962) then received ≤59 weeks of flexible treatment (100-800mg/day lacosamide with flexible dosing of concomitant antiepileptic drugs)."( Lacosamide for uncontrolled primary generalized tonic-clonic seizures: An open-label pilot study with 59-week extension.
Beller, C; Doty, P; Leroy, R; Messenheimer, J; Wechsler, RT; Yates, SL, 2017
)
2.1
" Criterion 2=the last drug introduced into the antiepileptic therapy within 72h before the cessation of SE and without changes in dosage or number of the co-medication."( The efficacy of different kinds of intravenously applied antiepileptic drugs in the treatment of status epilepticus. How can it be determined?
Redecker, J; Rösche, J; Wittstock, M, 2017
)
0.46
" Flexible lacosamide dosing in this open-label trial was associated with a favourable tolerability and safety profile; the nature of the TEAEs was consistent with that observed in previous pivotal trials."( Adjunctive lacosamide for focal epilepsy: an open-label trial evaluating the impact of flexible titration and dosing on safety and seizure outcomes.
Bartolomei, F; Baulac, M; Coulbaut, S; De Backer, M; Doty, P; McShea, C; Vlaicu, M, 2017
)
1.25
" LCM was added up to reach the maximum dosage of 400mg/die (mean final dose 300mg/die)."( Quality of life, mood and seizure control in patients with brain tumor related epilepsy treated with lacosamide as add-on therapy: A prospective explorative study with a historical control group.
Fabi, A; Giannarelli, D; Maialetti, A; Maschio, M; Vidiri, A; Villani, V; Zarabla, A, 2017
)
0.67
" Patients in whom LCM was added to their AED regimen for clinical indications comprised the LCM group (n=18), while the control group (n=32) comprised patients on ≥2 AEDs with anticipated stable dosing for the duration of the study."( Effects of adjunctive lacosamide on mood and quality of life in patients with epilepsy.
Arnedo, V; Coleman, M; Grant, AC; Kunnakkat, SD; Lushbough, C; Nakhutina, L; Soni, N, 2017
)
0.77
"Type I isobolographic analysis for nonparallel dose-response effects for the combination of retigabine with LCM (at the fixed-ratio of 1:1) in both the MES and chimney test in mice was performed."( Beneficial Combination of Lacosamide with Retigabine in Experimental Animals: An Isobolographic Analysis.
Adamczuk, P; Czuczwar, SJ; Florek-Luszczki, M; Kondrat-Wrobel, MW; Luszczki, JJ; Miziak, B; Wroblewska-Luczka, P; Zagaja, M; Zaluska, K, 2018
)
0.78
"Linear regression analysis revealed that retigabine had its dose-response effect line nonparallel to that of LCM in both the MES and chimney tests."( Beneficial Combination of Lacosamide with Retigabine in Experimental Animals: An Isobolographic Analysis.
Adamczuk, P; Czuczwar, SJ; Florek-Luszczki, M; Kondrat-Wrobel, MW; Luszczki, JJ; Miziak, B; Wroblewska-Luczka, P; Zagaja, M; Zaluska, K, 2018
)
0.78
" Dosing and prescribing practices were reviewed."( Safety of intravenous lacosamide in critically ill children.
Abend, NS; Lin, N; Topjian, AA; Welsh, SS, 2017
)
0.77
" Lacosamide was cleared by CVVH as demonstrated by the sieving coefficient, but plasma concentrations remained within goal range throughout the dosing interval."( Lacosamide Pharmacokinetics in a Critically Ill Patient Receiving Continuous Venovenous Hemofiltration.
Armahizer, MJ; Badjatia, N; Franquiz, MJ; Gopalakrishnan, M; Kalaria, SN; McCarthy, PJ, 2018
)
2.83
" AED extension studies evaluate treatment retention, drug tolerability, and drug safety during individualized treatment with flexible dosing and thus provide information not available in rigid pivotal trials."( Comparing Safety and Efficacy of "Third-Generation" Antiepileptic Drugs: Long-Term Extension and Post-marketing Treatment.
Johnson, EL; Krauss, GL; Kwok, CS, 2017
)
0.46
"A direct, eco-friendly, stability-indicating GC method was developed for the determination of Lacosamide (LCM) in tablet dosage forms in presence of its degradation products as well as in human urine in presence of the co-administered drug Zonisamide (ZON)."( Green gas chromatographic stability-indicating method for the determination of Lacosamide in tablets. Application to in-vivo human urine profiling.
Elmallah, OA; Haggag, RS; Korany, MA; Mahgoub, H; Ragab, MAA, 2018
)
0.93
" Not being dose-dependent (initiation dosage used), it seemed partially explained by drug-drug interaction with bisoprolol."( Complete Atrioventricular Block in an Elderly Patient Treated with Low-Dose Lacosamide.
Bézie, Y; Corny, J; Durand-Gasselin, B; Ferchichi, S; Lachuer, C, 2018
)
0.71
" Alternative GEE models confirmed the effect of comedication, whereas the effect of age, especially in children, depended on adjustment of LCM dosage to body weight, body surface area, or approximated volume of distribution."( Influence of Dose and Antiepileptic Comedication on Lacosamide Serum Concentrations in Patients With Epilepsy of Different Ages.
Bien, CG; Brandt, C; Helmer, R; May, TW, 2018
)
0.73
" Yet, we demonstrated that measuring serum lacosamide concentrations in the critically ill population during continuous renal replacement therapy may be useful to individualize dosing programs."( Lacosamide Pharmacokinetics in a Critically Ill Patient During Continuous Renal Replacement Therapy.
Albright, RC; Barreto, EF; Fugate, JE; Lopez-Ruiz, A; Wieruszewski, PM, 2020
)
2.26
"A combined adult and pediatric population pharmacokinetic model including covariate effects was developed; simulations were subsequently performed to guide intravenous pediatric dosing adaptations."( Modeling and simulation for the evaluation of dose adaptation rules of intravenous lacosamide in children.
Schoemaker, R; Stockis, A; Winkler, J, 2019
)
0.74
" Different dosing adaptation schemes by body weight bands were simulated to approximate, in pediatric patients aged 4 to 17 years, the same average plasma concentration as in adult patients receiving the maximum recommended lacosamide daily dose."( Population Pharmacokinetics of Adjunctive Lacosamide in Pediatric Patients With Epilepsy.
Schoemaker, R; Stockis, A; Winkler, J, 2019
)
0.96
" Findings from Cohort 1, aged 5-11 years, who received lacosamide ≤8 mg/kg/day, informed dosing for age-based cohorts 2-5, who then received ≤12 mg/kg/day (≤600 mg/day)."( Safety and tolerability of adjunctive lacosamide in a pediatric population with focal seizures - An open-label trial.
Abdelmoity, AT; Byrnes, W; Daniels, T; Dedeken, P; Dilley, D; Ferreira, JA; Le Pichon, JB, 2019
)
1.03
" Both, the type I isobolographic analysis and the test of parallelism of dose-response effects of the ASDs were used so as to properly classify interaction among three ASDs, administered in a fixed ratio combination of 1:1:1."( Sub-additive (antagonistic) interaction of lacosamide with lamotrigine and valproate in the maximal electroshock-induced seizure model in mice: an isobolographic analysis.
Bojar, H; Florek-Łuszczki, M; Karwan, S; Kondrat-Wróbel, M; Plewa, Z; Zagaja, M; Łuszczki, JJ, 2020
)
0.82
" The treatment dosage was 100 mg twice daily."( Lacosamide in trigeminal neuralgia: report of a case refractory to first- and second-generation anticonvulsants.
Adamo, D; Coppola, N; Mignogna, MD; Nicolò, M; Pecoraro, G, 2023
)
2.35
" We reviewed retrospectively weight-based dosing of IV LCM in patients admitted to ICU with acute seizures and status epilepticus."( Safety, tolerability, and pharmacokinetics of weight-based IV loading dose of lacosamide in the ICU.
Chimakurthy, AK; Menon, U; Ramsay, RE; Sabharwal, V, 2021
)
0.85
"9, 2-414) days, and the mean (SD, range) daily dosage of LCM was 205."( A prospective, multicenter, noninterventional study in Taiwan to evaluate the safety and tolerability of lacosamide as adjunctive therapy for epilepsy in clinical practice.
Chang, CW; Cheng, MY; Chuang, YC; Du, X; Hellot, S; Hsieh, HY; Hsieh, PF; Huang, HC; Hung, C; Jou, SB; Lee, WT; Lim, SN; McClung, C; Tsai, MH; Wu, T, 2020
)
0.77
"Currently recommended dosing of lacosamide often necessitates long titration periods."( Tolerability of lacosamide rapid dose titration: A randomized, multicenter, prospective, open-label study.
Chang, H; Cho, YW; Chu, K; Hong, SB; Jang, IJ; Jung, KH; Jung, KY; Kim, DW; Kim, DY; Kim, M; Lee, S; Lee, SK; Lee, ST; Moon, J; Park, KI; Shin, YW; Yoon, SH; Yu, KS, 2021
)
1.25
" Uptitration of lacosamide at shorter intervals to an effective target dosage may be feasible in appropriate clinical situations."( Tolerability of lacosamide rapid dose titration: A randomized, multicenter, prospective, open-label study.
Chang, H; Cho, YW; Chu, K; Hong, SB; Jang, IJ; Jung, KH; Jung, KY; Kim, DW; Kim, DY; Kim, M; Lee, S; Lee, SK; Lee, ST; Moon, J; Park, KI; Shin, YW; Yoon, SH; Yu, KS, 2021
)
1.31
" Based on the developed population pharmacokinetic model, simulations were performed in virtual pediatric patients to explore age-associated dose requirements to match lacosamide exposure in patient groups of different age with the exposure achieved in children ≥4 year of age with the weight-based dosing recommendations provided by the US Food and Drug Administration."( Use of Real-World Data and Pharmacometric Modeling in Support of Lacosamide Dosing in Pediatric Patients Under 4 Years of Age.
Chhim, R; Lukka, PB; Meibohm, B; Phelps, SJ; Wheless, JW; Woods, M, 2021
)
1.05
"Although the use of continuous renal replacement therapy (CRRT) has increased, limited dosing information exists on the effect of CRRT on antiepileptic drug pharmacokinetics."( A prospective, real-world, clinical pharmacokinetic study to inform lacosamide dosing in critically ill patients undergoing continuous venovenous haemofiltration (PADRE-02).
Armahizer, M; Badjatia, N; Gobburu, JV; Gopalakrishnan, M; Kalaria, SN; McCarthy, P, 2021
)
0.86
" Simulations of various doses suggest that effluent flow rate-based dosing regimens could be used to individualize lacosamide therapeutics."( A prospective, real-world, clinical pharmacokinetic study to inform lacosamide dosing in critically ill patients undergoing continuous venovenous haemofiltration (PADRE-02).
Armahizer, M; Badjatia, N; Gobburu, JV; Gopalakrishnan, M; Kalaria, SN; McCarthy, P, 2021
)
1.07
" Given that drug clearance increases with higher effluent flow rates, lacosamide dosing regimens should be increased to match exposures observed in patients with normal renal function."( A prospective, real-world, clinical pharmacokinetic study to inform lacosamide dosing in critically ill patients undergoing continuous venovenous haemofiltration (PADRE-02).
Armahizer, M; Badjatia, N; Gobburu, JV; Gopalakrishnan, M; Kalaria, SN; McCarthy, P, 2021
)
1.09
" Exposure to certain newer ASMs, such as lamotrigine and levetiracetam, does not thus far appear to impact certain aspects of neurodevelopment, but further delineation across the different neurodevelopmental domains and dosage levels is required."( Neurodevelopmental outcomes in children exposed to newer antiseizure medications: A systematic review.
Bromley, RL; Knight, R; Wittkowski, A, 2021
)
0.62
" The maintenance median dosage of LCM was 200 mg/day."( Lacosamide as first add-on or conversion monotherapy: A retrospective real-life study.
Casciato, S; D'Aniello, A; Di Gennaro, G; Gialluisi, A; Grammaldo, LG; Mascia, A; Quarato, PP, 2021
)
2.06
" The objectives of this study are to develop an ex-vivo in-vivo correlation (EVIVC) model to predict drug clearance for commonly used antiepileptics and to evaluate similarity in drug extraction across different CRRT modalities to extrapolate dosing recommendations."( Development and Use of an Ex-Vivo In-Vivo Correlation to Predict Antiepileptic Drug Clearance in Patients Undergoing Continuous Renal Replacement Therapy.
Armahizer, M; Badjatia, N; Gobburu, JV; Gopalakrishnan, M; Kalaria, SN; McCarthy, P, 2022
)
0.72
"After reviewing evidence, the conclusion was that pediatric efficacy trials would be impracticable to conduct but a waiver of the regulatory requirement to conduct any study would lead to an absence of information to guide dosing in a critical population."( Considerations for determining the efficacy of new antiseizure medications in children age 1 month to younger than 2 years.
Blum, D; Cleary, E; Dlugos, D; Farfel, G; Farrell, K; Fountain, N; French, JA; Gidal, B; Grzeskowiak, CL; Gurrell, R; Harden, C; Stalvey, TJ; Tsai, J; Wirrell, EC, 2022
)
0.72
" In clinical practice, ABCC2 polymorphisms should be identified before LCM treatment, and then, the dosage should be adjusted for pediatric patients with epilepsy accordingly."( Impact of ABCC2 1249G>A and -24C>T Polymorphisms on Lacosamide Efficacy and Plasma Concentrations in Uygur Pediatric Patients With Epilepsy in China.
Feng, J; Li, HJ; Sun, Y; Wang, TT; Yu, J; Yu, LH; Zhang, HL; Zhao, T, 2023
)
1.16
" Little evidence was available to guide lacosamide dosing during TPE."( The effect of plasma exchange on serum levels of lacosamide: A case report.
Brown, AE; Chalmers, SJ; Peters, BJ; Thornton, NM; Winters, JL, 2023
)
1.43
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Drug Classes (1)

ClassDescription
N-acyl-amino acidA carboxamide resulting from the formal condensation of a carboxylic acid with the amino group of an amino acid.
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Protein Targets (26)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
nuclear factor erythroid 2-related factor 2 isoform 1Homo sapiens (human)Potency34.48110.000627.21521,122.0200AID743202; AID743219
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Inhibition Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
ATP-binding cassette sub-family C member 3Homo sapiens (human)IC50 (µMol)133.00000.63154.45319.3000AID1473740
Multidrug resistance-associated protein 4Homo sapiens (human)IC50 (µMol)133.00000.20005.677410.0000AID1473741
Carbonic anhydrase 12Homo sapiens (human)Ki3.71300.00021.10439.9000AID441714
Bile salt export pumpHomo sapiens (human)IC50 (µMol)133.00000.11007.190310.0000AID1473738
Carbonic anhydrase 1Homo sapiens (human)Ki0.36200.00001.372610.0000AID441705
Carbonic anhydrase 2Homo sapiens (human)Ki0.33100.00000.72369.9200AID441706
Carbonic anhydrase 3Homo sapiens (human)Ki0.37400.00022.010210.0000AID441707
Sodium channel protein type 3 subunit alphaRattus norvegicus (Norway rat)IC50 (µMol)0.41500.00600.86052.9390AID1411523; AID726283
Potassium voltage-gated channel subfamily E member 1Homo sapiens (human)IC50 (µMol)251.18900.12004.048010.0000AID1207372
Carbonic anhydrase 4Homo sapiens (human)Ki0.52500.00021.97209.9200AID441708
Carbonic anhydrase 6Homo sapiens (human)Ki0.41200.00011.47109.9200AID441711
Carbonic anhydrase 5A, mitochondrialHomo sapiens (human)Ki4.56500.00001.27259.9000AID441709
Carbonic anhydrase 7Homo sapiens (human)Ki4.44600.00021.37379.9000AID441712
Potassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)IC50 (µMol)251.18900.12004.048010.0000AID1207372
Potassium voltage-gated channel subfamily H member 2Homo sapiens (human)IC50 (µMol)50,118.69920.00091.901410.0000AID1207526
Voltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)IC50 (µMol)50.11870.00032.25459.6000AID1207560
Sodium channel protein type 5 subunit alphaHomo sapiens (human)IC50 (µMol)501.18700.00033.64849.2000AID1207312
Sodium channel protein type 9 subunit alphaHomo sapiens (human)IC50 (µMol)0.18200.00602.77499.0000AID726282
Carbonic anhydrase 9Homo sapiens (human)Ki0.35300.00010.78749.9000AID441713
Sodium channel protein type 10 subunit alphaRattus norvegicus (Norway rat)IC50 (µMol)16.00000.04500.08500.1250AID726281
Carbonic anhydrase 13Homo sapiens (human)Ki1.21000.00031.23099.8000AID441715
Canalicular multispecific organic anion transporter 1Homo sapiens (human)IC50 (µMol)133.00002.41006.343310.0000AID1473739
Carbonic anhydrase 15Mus musculus (house mouse)Ki0.46100.00091.884610.0000AID441717
Carbonic anhydrase 14Homo sapiens (human)Ki0.47300.00021.50999.9000AID441716
Carbonic anhydrase 5B, mitochondrialHomo sapiens (human)Ki0.34100.00001.34129.9700AID441710
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (178)

Processvia Protein(s)Taxonomy
xenobiotic metabolic processATP-binding cassette sub-family C member 3Homo sapiens (human)
xenobiotic transmembrane transportATP-binding cassette sub-family C member 3Homo sapiens (human)
bile acid and bile salt transportATP-binding cassette sub-family C member 3Homo sapiens (human)
glucuronoside transportATP-binding cassette sub-family C member 3Homo sapiens (human)
xenobiotic transportATP-binding cassette sub-family C member 3Homo sapiens (human)
transmembrane transportATP-binding cassette sub-family C member 3Homo sapiens (human)
leukotriene transportATP-binding cassette sub-family C member 3Homo sapiens (human)
monoatomic anion transmembrane transportATP-binding cassette sub-family C member 3Homo sapiens (human)
transport across blood-brain barrierATP-binding cassette sub-family C member 3Homo sapiens (human)
prostaglandin secretionMultidrug resistance-associated protein 4Homo sapiens (human)
cilium assemblyMultidrug resistance-associated protein 4Homo sapiens (human)
platelet degranulationMultidrug resistance-associated protein 4Homo sapiens (human)
xenobiotic metabolic processMultidrug resistance-associated protein 4Homo sapiens (human)
xenobiotic transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
bile acid and bile salt transportMultidrug resistance-associated protein 4Homo sapiens (human)
prostaglandin transportMultidrug resistance-associated protein 4Homo sapiens (human)
urate transportMultidrug resistance-associated protein 4Homo sapiens (human)
glutathione transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
cAMP transportMultidrug resistance-associated protein 4Homo sapiens (human)
leukotriene transportMultidrug resistance-associated protein 4Homo sapiens (human)
monoatomic anion transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
export across plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
transport across blood-brain barrierMultidrug resistance-associated protein 4Homo sapiens (human)
guanine nucleotide transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
estrous cycleCarbonic anhydrase 12Homo sapiens (human)
chloride ion homeostasisCarbonic anhydrase 12Homo sapiens (human)
one-carbon metabolic processCarbonic anhydrase 12Homo sapiens (human)
fatty acid metabolic processBile salt export pumpHomo sapiens (human)
bile acid biosynthetic processBile salt export pumpHomo sapiens (human)
xenobiotic metabolic processBile salt export pumpHomo sapiens (human)
xenobiotic transmembrane transportBile salt export pumpHomo sapiens (human)
response to oxidative stressBile salt export pumpHomo sapiens (human)
bile acid metabolic processBile salt export pumpHomo sapiens (human)
response to organic cyclic compoundBile salt export pumpHomo sapiens (human)
bile acid and bile salt transportBile salt export pumpHomo sapiens (human)
canalicular bile acid transportBile salt export pumpHomo sapiens (human)
protein ubiquitinationBile salt export pumpHomo sapiens (human)
regulation of fatty acid beta-oxidationBile salt export pumpHomo sapiens (human)
carbohydrate transmembrane transportBile salt export pumpHomo sapiens (human)
bile acid signaling pathwayBile salt export pumpHomo sapiens (human)
cholesterol homeostasisBile salt export pumpHomo sapiens (human)
response to estrogenBile salt export pumpHomo sapiens (human)
response to ethanolBile salt export pumpHomo sapiens (human)
xenobiotic export from cellBile salt export pumpHomo sapiens (human)
lipid homeostasisBile salt export pumpHomo sapiens (human)
phospholipid homeostasisBile salt export pumpHomo sapiens (human)
positive regulation of bile acid secretionBile salt export pumpHomo sapiens (human)
regulation of bile acid metabolic processBile salt export pumpHomo sapiens (human)
transmembrane transportBile salt export pumpHomo sapiens (human)
one-carbon metabolic processCarbonic anhydrase 1Homo sapiens (human)
morphogenesis of an epitheliumCarbonic anhydrase 2Homo sapiens (human)
positive regulation of synaptic transmission, GABAergicCarbonic anhydrase 2Homo sapiens (human)
positive regulation of cellular pH reductionCarbonic anhydrase 2Homo sapiens (human)
angiotensin-activated signaling pathwayCarbonic anhydrase 2Homo sapiens (human)
regulation of monoatomic anion transportCarbonic anhydrase 2Homo sapiens (human)
secretionCarbonic anhydrase 2Homo sapiens (human)
regulation of intracellular pHCarbonic anhydrase 2Homo sapiens (human)
neuron cellular homeostasisCarbonic anhydrase 2Homo sapiens (human)
positive regulation of dipeptide transmembrane transportCarbonic anhydrase 2Homo sapiens (human)
regulation of chloride transportCarbonic anhydrase 2Homo sapiens (human)
carbon dioxide transportCarbonic anhydrase 2Homo sapiens (human)
one-carbon metabolic processCarbonic anhydrase 2Homo sapiens (human)
response to bacteriumCarbonic anhydrase 3Homo sapiens (human)
one-carbon metabolic processCarbonic anhydrase 3Homo sapiens (human)
epithelial cell maturationPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
sensory perception of soundPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
male gonad developmentPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
vestibular nucleus developmentPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
secretory granule organizationPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
regulation of ventricular cardiac muscle cell membrane repolarizationPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
cellular response to cAMPPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
cellular response to acidic pHPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
cellular response to light stimulusPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
potassium ion transmembrane transportPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
cardiac muscle cell action potential involved in contractionPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
cardiac muscle cell contractionPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
ventricular cardiac muscle cell action potentialPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
membrane repolarizationPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
membrane repolarization during action potentialPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
membrane repolarization during cardiac muscle cell action potentialPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
regulation of heart rate by cardiac conductionPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
negative regulation of protein targeting to membranePotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
potassium ion export across plasma membranePotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
membrane repolarization during ventricular cardiac muscle cell action potentialPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
regulation of potassium ion transmembrane transportPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
positive regulation of potassium ion transmembrane transportPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
regulation of delayed rectifier potassium channel activityPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
negative regulation of delayed rectifier potassium channel activityPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
bicarbonate transportCarbonic anhydrase 4Homo sapiens (human)
one-carbon metabolic processCarbonic anhydrase 4Homo sapiens (human)
detection of chemical stimulus involved in sensory perception of bitter tasteCarbonic anhydrase 6Homo sapiens (human)
one-carbon metabolic processCarbonic anhydrase 6Homo sapiens (human)
one-carbon metabolic processCarbonic anhydrase 5A, mitochondrialHomo sapiens (human)
positive regulation of synaptic transmission, GABAergicCarbonic anhydrase 7Homo sapiens (human)
positive regulation of cellular pH reductionCarbonic anhydrase 7Homo sapiens (human)
neuron cellular homeostasisCarbonic anhydrase 7Homo sapiens (human)
regulation of chloride transportCarbonic anhydrase 7Homo sapiens (human)
regulation of intracellular pHCarbonic anhydrase 7Homo sapiens (human)
one-carbon metabolic processCarbonic anhydrase 7Homo sapiens (human)
gastrin-induced gastric acid secretionPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
glucose metabolic processPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
heart developmentPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
sensory perception of soundPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
rhythmic behaviorPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
regulation of heart contractionPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
regulation of blood pressurePotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
positive regulation of heart ratePotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
iodide transportPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
erythrocyte differentiationPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
intracellular chloride ion homeostasisPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
response to insulinPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
social behaviorPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
corticosterone secretionPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
inner ear morphogenesisPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
inner ear developmentPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
intestinal absorptionPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
detection of mechanical stimulus involved in sensory perception of soundPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
potassium ion homeostasisPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
cardiac muscle contractionPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
auditory receptor cell developmentPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
regulation of membrane repolarizationPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
regulation of ventricular cardiac muscle cell membrane repolarizationPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
regulation of atrial cardiac muscle cell membrane repolarizationPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
positive regulation of cardiac muscle contractionPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
regulation of gastric acid secretionPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
stomach developmentPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
renal absorptionPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
renal sodium ion absorptionPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
cellular response to cAMPPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
cellular response to xenobiotic stimulusPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
potassium ion transmembrane transportPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
cellular response to epinephrine stimulusPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
adrenergic receptor signaling pathwayPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
cardiac muscle cell contractionPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
ventricular cardiac muscle cell action potentialPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
membrane repolarization during action potentialPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
membrane repolarization during cardiac muscle cell action potentialPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
atrial cardiac muscle cell action potentialPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
regulation of heart rate by cardiac conductionPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
cochlea developmentPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
potassium ion export across plasma membranePotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
membrane repolarization during atrial cardiac muscle cell action potentialPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
membrane repolarization during ventricular cardiac muscle cell action potentialPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
positive regulation of potassium ion transmembrane transportPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
non-motile cilium assemblyPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
potassium ion import across plasma membranePotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
action potentialPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
regulation of heart rate by cardiac conductionPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
regulation of heart rate by hormonePotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
regulation of membrane potentialPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
positive regulation of DNA-templated transcriptionPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
potassium ion homeostasisPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
cardiac muscle contractionPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
regulation of membrane repolarizationPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
regulation of ventricular cardiac muscle cell membrane repolarizationPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
cellular response to xenobiotic stimulusPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
potassium ion transmembrane transportPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
ventricular cardiac muscle cell action potentialPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
membrane repolarizationPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
membrane depolarization during action potentialPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
membrane repolarization during action potentialPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
membrane repolarization during cardiac muscle cell action potentialPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
regulation of heart rate by cardiac conductionPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
potassium ion export across plasma membranePotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
membrane repolarization during ventricular cardiac muscle cell action potentialPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
regulation of potassium ion transmembrane transportPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
negative regulation of potassium ion transmembrane transportPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
positive regulation of potassium ion transmembrane transportPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
negative regulation of potassium ion export across plasma membranePotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
potassium ion import across plasma membranePotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
immune system developmentVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
positive regulation of cytosolic calcium ion concentrationVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
heart developmentVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
regulation of cardiac muscle contraction by regulation of the release of sequestered calcium ionVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
embryonic forelimb morphogenesisVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
camera-type eye developmentVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
positive regulation of adenylate cyclase activityVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
positive regulation of muscle contractionVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
calcium ion transport into cytosolVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
cardiac conductionVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
calcium ion transmembrane transport via high voltage-gated calcium channelVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
calcium ion transmembrane transportVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
cardiac muscle cell action potential involved in contractionVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
membrane depolarization during cardiac muscle cell action potentialVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
membrane depolarization during AV node cell action potentialVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
cell communication by electrical coupling involved in cardiac conductionVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
regulation of heart rate by cardiac conductionVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
regulation of ventricular cardiac muscle cell action potentialVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
membrane depolarization during atrial cardiac muscle cell action potentialVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
calcium ion import across plasma membraneVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
regulation of heart rateSodium channel protein type 5 subunit alphaHomo sapiens (human)
cardiac conduction system developmentSodium channel protein type 5 subunit alphaHomo sapiens (human)
cardiac ventricle developmentSodium channel protein type 5 subunit alphaHomo sapiens (human)
brainstem developmentSodium channel protein type 5 subunit alphaHomo sapiens (human)
sodium ion transportSodium channel protein type 5 subunit alphaHomo sapiens (human)
positive regulation of sodium ion transportSodium channel protein type 5 subunit alphaHomo sapiens (human)
response to denervation involved in regulation of muscle adaptationSodium channel protein type 5 subunit alphaHomo sapiens (human)
telencephalon developmentSodium channel protein type 5 subunit alphaHomo sapiens (human)
cerebellum developmentSodium channel protein type 5 subunit alphaHomo sapiens (human)
sodium ion transmembrane transportSodium channel protein type 5 subunit alphaHomo sapiens (human)
odontogenesis of dentin-containing toothSodium channel protein type 5 subunit alphaHomo sapiens (human)
positive regulation of action potentialSodium channel protein type 5 subunit alphaHomo sapiens (human)
positive regulation of epithelial cell proliferationSodium channel protein type 5 subunit alphaHomo sapiens (human)
membrane depolarizationSodium channel protein type 5 subunit alphaHomo sapiens (human)
cardiac muscle contractionSodium channel protein type 5 subunit alphaHomo sapiens (human)
regulation of ventricular cardiac muscle cell membrane repolarizationSodium channel protein type 5 subunit alphaHomo sapiens (human)
regulation of atrial cardiac muscle cell membrane depolarizationSodium channel protein type 5 subunit alphaHomo sapiens (human)
regulation of atrial cardiac muscle cell membrane repolarizationSodium channel protein type 5 subunit alphaHomo sapiens (human)
regulation of ventricular cardiac muscle cell membrane depolarizationSodium channel protein type 5 subunit alphaHomo sapiens (human)
cellular response to calcium ionSodium channel protein type 5 subunit alphaHomo sapiens (human)
cardiac muscle cell action potential involved in contractionSodium channel protein type 5 subunit alphaHomo sapiens (human)
regulation of cardiac muscle cell contractionSodium channel protein type 5 subunit alphaHomo sapiens (human)
ventricular cardiac muscle cell action potentialSodium channel protein type 5 subunit alphaHomo sapiens (human)
membrane depolarization during action potentialSodium channel protein type 5 subunit alphaHomo sapiens (human)
membrane depolarization during cardiac muscle cell action potentialSodium channel protein type 5 subunit alphaHomo sapiens (human)
atrial cardiac muscle cell action potentialSodium channel protein type 5 subunit alphaHomo sapiens (human)
SA node cell action potentialSodium channel protein type 5 subunit alphaHomo sapiens (human)
AV node cell action potentialSodium channel protein type 5 subunit alphaHomo sapiens (human)
bundle of His cell action potentialSodium channel protein type 5 subunit alphaHomo sapiens (human)
membrane depolarization during AV node cell action potentialSodium channel protein type 5 subunit alphaHomo sapiens (human)
membrane depolarization during SA node cell action potentialSodium channel protein type 5 subunit alphaHomo sapiens (human)
membrane depolarization during Purkinje myocyte cell action potentialSodium channel protein type 5 subunit alphaHomo sapiens (human)
membrane depolarization during bundle of His cell action potentialSodium channel protein type 5 subunit alphaHomo sapiens (human)
AV node cell to bundle of His cell communicationSodium channel protein type 5 subunit alphaHomo sapiens (human)
regulation of heart rate by cardiac conductionSodium channel protein type 5 subunit alphaHomo sapiens (human)
membrane depolarization during atrial cardiac muscle cell action potentialSodium channel protein type 5 subunit alphaHomo sapiens (human)
regulation of sodium ion transmembrane transportSodium channel protein type 5 subunit alphaHomo sapiens (human)
sodium ion transportSodium channel protein type 9 subunit alphaHomo sapiens (human)
inflammatory responseSodium channel protein type 9 subunit alphaHomo sapiens (human)
circadian rhythmSodium channel protein type 9 subunit alphaHomo sapiens (human)
response to toxic substanceSodium channel protein type 9 subunit alphaHomo sapiens (human)
post-embryonic developmentSodium channel protein type 9 subunit alphaHomo sapiens (human)
sensory perception of painSodium channel protein type 9 subunit alphaHomo sapiens (human)
sodium ion transmembrane transportSodium channel protein type 9 subunit alphaHomo sapiens (human)
behavioral response to painSodium channel protein type 9 subunit alphaHomo sapiens (human)
detection of temperature stimulus involved in sensory perception of painSodium channel protein type 9 subunit alphaHomo sapiens (human)
detection of mechanical stimulus involved in sensory perceptionSodium channel protein type 9 subunit alphaHomo sapiens (human)
cardiac muscle cell action potential involved in contractionSodium channel protein type 9 subunit alphaHomo sapiens (human)
response to hypoxiaCarbonic anhydrase 9Homo sapiens (human)
morphogenesis of an epitheliumCarbonic anhydrase 9Homo sapiens (human)
response to xenobiotic stimulusCarbonic anhydrase 9Homo sapiens (human)
response to testosteroneCarbonic anhydrase 9Homo sapiens (human)
secretionCarbonic anhydrase 9Homo sapiens (human)
one-carbon metabolic processCarbonic anhydrase 9Homo sapiens (human)
one-carbon metabolic processCarbonic anhydrase 13Homo sapiens (human)
xenobiotic metabolic processCanalicular multispecific organic anion transporter 1Homo sapiens (human)
xenobiotic transmembrane transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
negative regulation of gene expressionCanalicular multispecific organic anion transporter 1Homo sapiens (human)
bile acid and bile salt transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
bilirubin transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
heme catabolic processCanalicular multispecific organic anion transporter 1Homo sapiens (human)
xenobiotic export from cellCanalicular multispecific organic anion transporter 1Homo sapiens (human)
transmembrane transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
transepithelial transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
leukotriene transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
monoatomic anion transmembrane transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
transport across blood-brain barrierCanalicular multispecific organic anion transporter 1Homo sapiens (human)
xenobiotic transport across blood-brain barrierCanalicular multispecific organic anion transporter 1Homo sapiens (human)
one-carbon metabolic processCarbonic anhydrase 14Homo sapiens (human)
response to bacteriumCarbonic anhydrase 5B, mitochondrialHomo sapiens (human)
one-carbon metabolic processCarbonic anhydrase 5B, mitochondrialHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (71)

Processvia Protein(s)Taxonomy
ATP bindingATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type xenobiotic transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
glucuronoside transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type bile acid transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ATP hydrolysis activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ATPase-coupled transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
xenobiotic transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
icosanoid transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
guanine nucleotide transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
protein bindingMultidrug resistance-associated protein 4Homo sapiens (human)
ATP bindingMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type xenobiotic transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
prostaglandin transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
urate transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
purine nucleotide transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type bile acid transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
efflux transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
15-hydroxyprostaglandin dehydrogenase (NAD+) activityMultidrug resistance-associated protein 4Homo sapiens (human)
ATP hydrolysis activityMultidrug resistance-associated protein 4Homo sapiens (human)
glutathione transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ATPase-coupled transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
xenobiotic transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
zinc ion bindingCarbonic anhydrase 12Homo sapiens (human)
carbonate dehydratase activityCarbonic anhydrase 12Homo sapiens (human)
protein bindingBile salt export pumpHomo sapiens (human)
ATP bindingBile salt export pumpHomo sapiens (human)
ABC-type xenobiotic transporter activityBile salt export pumpHomo sapiens (human)
bile acid transmembrane transporter activityBile salt export pumpHomo sapiens (human)
canalicular bile acid transmembrane transporter activityBile salt export pumpHomo sapiens (human)
carbohydrate transmembrane transporter activityBile salt export pumpHomo sapiens (human)
ABC-type bile acid transporter activityBile salt export pumpHomo sapiens (human)
ATP hydrolysis activityBile salt export pumpHomo sapiens (human)
arylesterase activityCarbonic anhydrase 1Homo sapiens (human)
carbonate dehydratase activityCarbonic anhydrase 1Homo sapiens (human)
protein bindingCarbonic anhydrase 1Homo sapiens (human)
zinc ion bindingCarbonic anhydrase 1Homo sapiens (human)
hydro-lyase activityCarbonic anhydrase 1Homo sapiens (human)
cyanamide hydratase activityCarbonic anhydrase 1Homo sapiens (human)
arylesterase activityCarbonic anhydrase 2Homo sapiens (human)
carbonate dehydratase activityCarbonic anhydrase 2Homo sapiens (human)
protein bindingCarbonic anhydrase 2Homo sapiens (human)
zinc ion bindingCarbonic anhydrase 2Homo sapiens (human)
cyanamide hydratase activityCarbonic anhydrase 2Homo sapiens (human)
carbonate dehydratase activityCarbonic anhydrase 3Homo sapiens (human)
protein bindingCarbonic anhydrase 3Homo sapiens (human)
zinc ion bindingCarbonic anhydrase 3Homo sapiens (human)
nickel cation bindingCarbonic anhydrase 3Homo sapiens (human)
voltage-gated potassium channel activityPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
delayed rectifier potassium channel activityPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
voltage-gated potassium channel activity involved in cardiac muscle cell action potential repolarizationPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
voltage-gated potassium channel activity involved in ventricular cardiac muscle cell action potential repolarizationPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
delayed rectifier potassium channel activityPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
protein bindingPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
potassium channel regulator activityPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
telethonin bindingPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
protein-containing complex bindingPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
transmembrane transporter bindingPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
protein bindingCarbonic anhydrase 4Homo sapiens (human)
zinc ion bindingCarbonic anhydrase 4Homo sapiens (human)
carbonate dehydratase activityCarbonic anhydrase 4Homo sapiens (human)
zinc ion bindingCarbonic anhydrase 6Homo sapiens (human)
carbonate dehydratase activityCarbonic anhydrase 6Homo sapiens (human)
carbonate dehydratase activityCarbonic anhydrase 5A, mitochondrialHomo sapiens (human)
zinc ion bindingCarbonic anhydrase 5A, mitochondrialHomo sapiens (human)
zinc ion bindingCarbonic anhydrase 7Homo sapiens (human)
carbonate dehydratase activityCarbonic anhydrase 7Homo sapiens (human)
voltage-gated potassium channel activityPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
delayed rectifier potassium channel activityPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
voltage-gated potassium channel activityPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
delayed rectifier potassium channel activityPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
protein bindingPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
calmodulin bindingPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
phosphatidylinositol-4,5-bisphosphate bindingPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
protein phosphatase 1 bindingPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
outward rectifier potassium channel activityPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
protein kinase A catalytic subunit bindingPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
protein kinase A regulatory subunit bindingPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
transmembrane transporter bindingPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
voltage-gated potassium channel activity involved in cardiac muscle cell action potential repolarizationPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
voltage-gated potassium channel activity involved in atrial cardiac muscle cell action potential repolarizationPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
scaffold protein bindingPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
voltage-gated potassium channel activity involved in ventricular cardiac muscle cell action potential repolarizationPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
transcription cis-regulatory region bindingPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
inward rectifier potassium channel activityPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
voltage-gated potassium channel activityPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
delayed rectifier potassium channel activityPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
protein bindingPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
ubiquitin protein ligase bindingPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
identical protein bindingPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
protein homodimerization activityPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
C3HC4-type RING finger domain bindingPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
voltage-gated potassium channel activity involved in cardiac muscle cell action potential repolarizationPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
scaffold protein bindingPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
voltage-gated potassium channel activity involved in ventricular cardiac muscle cell action potential repolarizationPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
high voltage-gated calcium channel activityVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
voltage-gated calcium channel activity involved in cardiac muscle cell action potentialVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
voltage-gated calcium channel activityVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
protein bindingVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
calmodulin bindingVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
high voltage-gated calcium channel activityVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
metal ion bindingVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
alpha-actinin bindingVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
voltage-gated calcium channel activity involved in cardiac muscle cell action potentialVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
voltage-gated calcium channel activity involved in AV node cell action potentialVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
voltage-gated sodium channel activitySodium channel protein type 5 subunit alphaHomo sapiens (human)
protein bindingSodium channel protein type 5 subunit alphaHomo sapiens (human)
calmodulin bindingSodium channel protein type 5 subunit alphaHomo sapiens (human)
fibroblast growth factor bindingSodium channel protein type 5 subunit alphaHomo sapiens (human)
enzyme bindingSodium channel protein type 5 subunit alphaHomo sapiens (human)
protein kinase bindingSodium channel protein type 5 subunit alphaHomo sapiens (human)
protein domain specific bindingSodium channel protein type 5 subunit alphaHomo sapiens (human)
ankyrin bindingSodium channel protein type 5 subunit alphaHomo sapiens (human)
ubiquitin protein ligase bindingSodium channel protein type 5 subunit alphaHomo sapiens (human)
transmembrane transporter bindingSodium channel protein type 5 subunit alphaHomo sapiens (human)
nitric-oxide synthase bindingSodium channel protein type 5 subunit alphaHomo sapiens (human)
voltage-gated sodium channel activity involved in cardiac muscle cell action potentialSodium channel protein type 5 subunit alphaHomo sapiens (human)
voltage-gated sodium channel activity involved in AV node cell action potentialSodium channel protein type 5 subunit alphaHomo sapiens (human)
voltage-gated sodium channel activity involved in bundle of His cell action potentialSodium channel protein type 5 subunit alphaHomo sapiens (human)
voltage-gated sodium channel activity involved in Purkinje myocyte action potentialSodium channel protein type 5 subunit alphaHomo sapiens (human)
voltage-gated sodium channel activity involved in SA node cell action potentialSodium channel protein type 5 subunit alphaHomo sapiens (human)
scaffold protein bindingSodium channel protein type 5 subunit alphaHomo sapiens (human)
voltage-gated sodium channel activitySodium channel protein type 9 subunit alphaHomo sapiens (human)
protein bindingSodium channel protein type 9 subunit alphaHomo sapiens (human)
carbonate dehydratase activityCarbonic anhydrase 9Homo sapiens (human)
protein bindingCarbonic anhydrase 9Homo sapiens (human)
zinc ion bindingCarbonic anhydrase 9Homo sapiens (human)
molecular function activator activityCarbonic anhydrase 9Homo sapiens (human)
protein bindingCarbonic anhydrase 13Homo sapiens (human)
zinc ion bindingCarbonic anhydrase 13Homo sapiens (human)
carbonate dehydratase activityCarbonic anhydrase 13Homo sapiens (human)
protein bindingCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ATP bindingCanalicular multispecific organic anion transporter 1Homo sapiens (human)
organic anion transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ABC-type xenobiotic transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
bilirubin transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ATP hydrolysis activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ATPase-coupled transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
xenobiotic transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ABC-type transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
zinc ion bindingCarbonic anhydrase 14Homo sapiens (human)
carbonate dehydratase activityCarbonic anhydrase 14Homo sapiens (human)
carbonate dehydratase activityCarbonic anhydrase 5B, mitochondrialHomo sapiens (human)
zinc ion bindingCarbonic anhydrase 5B, mitochondrialHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (65)

Processvia Protein(s)Taxonomy
plasma membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
basal plasma membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
basolateral plasma membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
nucleolusMultidrug resistance-associated protein 4Homo sapiens (human)
Golgi apparatusMultidrug resistance-associated protein 4Homo sapiens (human)
plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
membraneMultidrug resistance-associated protein 4Homo sapiens (human)
basolateral plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
apical plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
platelet dense granule membraneMultidrug resistance-associated protein 4Homo sapiens (human)
external side of apical plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
plasma membraneCarbonic anhydrase 12Homo sapiens (human)
membraneCarbonic anhydrase 12Homo sapiens (human)
basolateral plasma membraneCarbonic anhydrase 12Homo sapiens (human)
apical plasma membraneCarbonic anhydrase 12Homo sapiens (human)
plasma membraneCarbonic anhydrase 12Homo sapiens (human)
basolateral plasma membraneBile salt export pumpHomo sapiens (human)
Golgi membraneBile salt export pumpHomo sapiens (human)
endosomeBile salt export pumpHomo sapiens (human)
plasma membraneBile salt export pumpHomo sapiens (human)
cell surfaceBile salt export pumpHomo sapiens (human)
apical plasma membraneBile salt export pumpHomo sapiens (human)
intercellular canaliculusBile salt export pumpHomo sapiens (human)
intracellular canaliculusBile salt export pumpHomo sapiens (human)
recycling endosomeBile salt export pumpHomo sapiens (human)
recycling endosome membraneBile salt export pumpHomo sapiens (human)
extracellular exosomeBile salt export pumpHomo sapiens (human)
membraneBile salt export pumpHomo sapiens (human)
cytosolCarbonic anhydrase 1Homo sapiens (human)
extracellular exosomeCarbonic anhydrase 1Homo sapiens (human)
cytoplasmCarbonic anhydrase 2Homo sapiens (human)
cytosolCarbonic anhydrase 2Homo sapiens (human)
plasma membraneCarbonic anhydrase 2Homo sapiens (human)
myelin sheathCarbonic anhydrase 2Homo sapiens (human)
apical part of cellCarbonic anhydrase 2Homo sapiens (human)
extracellular exosomeCarbonic anhydrase 2Homo sapiens (human)
cytoplasmCarbonic anhydrase 2Homo sapiens (human)
plasma membraneCarbonic anhydrase 2Homo sapiens (human)
apical part of cellCarbonic anhydrase 2Homo sapiens (human)
cytosolCarbonic anhydrase 3Homo sapiens (human)
cytosolCarbonic anhydrase 3Homo sapiens (human)
cytoplasmCarbonic anhydrase 3Homo sapiens (human)
voltage-gated potassium channel complexPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
lysosomePotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
plasma membranePotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
cell surfacePotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
apical plasma membranePotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
Z discPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
membrane raftPotassium voltage-gated channel subfamily E member 1Homo sapiens (human)
basolateral plasma membraneCarbonic anhydrase 4Homo sapiens (human)
rough endoplasmic reticulumCarbonic anhydrase 4Homo sapiens (human)
endoplasmic reticulum-Golgi intermediate compartmentCarbonic anhydrase 4Homo sapiens (human)
Golgi apparatusCarbonic anhydrase 4Homo sapiens (human)
trans-Golgi networkCarbonic anhydrase 4Homo sapiens (human)
plasma membraneCarbonic anhydrase 4Homo sapiens (human)
external side of plasma membraneCarbonic anhydrase 4Homo sapiens (human)
cell surfaceCarbonic anhydrase 4Homo sapiens (human)
membraneCarbonic anhydrase 4Homo sapiens (human)
apical plasma membraneCarbonic anhydrase 4Homo sapiens (human)
transport vesicle membraneCarbonic anhydrase 4Homo sapiens (human)
secretory granule membraneCarbonic anhydrase 4Homo sapiens (human)
brush border membraneCarbonic anhydrase 4Homo sapiens (human)
perinuclear region of cytoplasmCarbonic anhydrase 4Homo sapiens (human)
extracellular exosomeCarbonic anhydrase 4Homo sapiens (human)
plasma membraneCarbonic anhydrase 4Homo sapiens (human)
extracellular regionCarbonic anhydrase 6Homo sapiens (human)
extracellular spaceCarbonic anhydrase 6Homo sapiens (human)
cytosolCarbonic anhydrase 6Homo sapiens (human)
extracellular exosomeCarbonic anhydrase 6Homo sapiens (human)
extracellular spaceCarbonic anhydrase 6Homo sapiens (human)
mitochondrial matrixCarbonic anhydrase 5A, mitochondrialHomo sapiens (human)
mitochondrionCarbonic anhydrase 5A, mitochondrialHomo sapiens (human)
cytoplasmCarbonic anhydrase 5A, mitochondrialHomo sapiens (human)
mitochondrionCarbonic anhydrase 5A, mitochondrialHomo sapiens (human)
cytosolCarbonic anhydrase 7Homo sapiens (human)
cytoplasmCarbonic anhydrase 7Homo sapiens (human)
early endosomePotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
endoplasmic reticulumPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
cytoplasmPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
lysosomePotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
early endosomePotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
late endosomePotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
endoplasmic reticulumPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
plasma membranePotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
voltage-gated potassium channel complexPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
membranePotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
basolateral plasma membranePotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
apical plasma membranePotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
transport vesiclePotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
cytoplasmic vesicle membranePotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
neuron projectionPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
neuronal cell bodyPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
membrane raftPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
ciliary basePotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
lumenal side of membranePotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
basolateral part of cellPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
monoatomic ion channel complexPotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
membranePotassium voltage-gated channel subfamily KQT member 1Homo sapiens (human)
plasma membranePotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
cell surfacePotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
perinuclear region of cytoplasmPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
voltage-gated potassium channel complexPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
inward rectifier potassium channel complexPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
plasma membranePotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
cytoplasmVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
plasma membraneVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
postsynaptic densityVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
membraneVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
Z discVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
dendriteVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
perikaryonVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
postsynaptic density membraneVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
L-type voltage-gated calcium channel complexVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
voltage-gated calcium channel complexVoltage-dependent L-type calcium channel subunit alpha-1CHomo sapiens (human)
caveolaSodium channel protein type 5 subunit alphaHomo sapiens (human)
nucleoplasmSodium channel protein type 5 subunit alphaHomo sapiens (human)
nucleolusSodium channel protein type 5 subunit alphaHomo sapiens (human)
endoplasmic reticulumSodium channel protein type 5 subunit alphaHomo sapiens (human)
plasma membraneSodium channel protein type 5 subunit alphaHomo sapiens (human)
caveolaSodium channel protein type 5 subunit alphaHomo sapiens (human)
cell surfaceSodium channel protein type 5 subunit alphaHomo sapiens (human)
intercalated discSodium channel protein type 5 subunit alphaHomo sapiens (human)
membraneSodium channel protein type 5 subunit alphaHomo sapiens (human)
lateral plasma membraneSodium channel protein type 5 subunit alphaHomo sapiens (human)
Z discSodium channel protein type 5 subunit alphaHomo sapiens (human)
T-tubuleSodium channel protein type 5 subunit alphaHomo sapiens (human)
sarcolemmaSodium channel protein type 5 subunit alphaHomo sapiens (human)
perinuclear region of cytoplasmSodium channel protein type 5 subunit alphaHomo sapiens (human)
voltage-gated sodium channel complexSodium channel protein type 5 subunit alphaHomo sapiens (human)
plasma membraneSodium channel protein type 9 subunit alphaHomo sapiens (human)
axonSodium channel protein type 9 subunit alphaHomo sapiens (human)
voltage-gated sodium channel complexSodium channel protein type 9 subunit alphaHomo sapiens (human)
nucleolusCarbonic anhydrase 9Homo sapiens (human)
plasma membraneCarbonic anhydrase 9Homo sapiens (human)
membraneCarbonic anhydrase 9Homo sapiens (human)
basolateral plasma membraneCarbonic anhydrase 9Homo sapiens (human)
microvillus membraneCarbonic anhydrase 9Homo sapiens (human)
plasma membraneCarbonic anhydrase 9Homo sapiens (human)
cytosolCarbonic anhydrase 13Homo sapiens (human)
myelin sheathCarbonic anhydrase 13Homo sapiens (human)
intracellular membrane-bounded organelleCarbonic anhydrase 13Homo sapiens (human)
cytoplasmCarbonic anhydrase 13Homo sapiens (human)
cytosolCarbonic anhydrase 13Homo sapiens (human)
plasma membraneCanalicular multispecific organic anion transporter 1Homo sapiens (human)
cell surfaceCanalicular multispecific organic anion transporter 1Homo sapiens (human)
apical plasma membraneCanalicular multispecific organic anion transporter 1Homo sapiens (human)
intercellular canaliculusCanalicular multispecific organic anion transporter 1Homo sapiens (human)
apical plasma membraneCanalicular multispecific organic anion transporter 1Homo sapiens (human)
plasma membraneCarbonic anhydrase 14Homo sapiens (human)
membraneCarbonic anhydrase 14Homo sapiens (human)
basolateral plasma membraneCarbonic anhydrase 14Homo sapiens (human)
apical plasma membraneCarbonic anhydrase 14Homo sapiens (human)
plasma membraneCarbonic anhydrase 14Homo sapiens (human)
mitochondrionCarbonic anhydrase 5B, mitochondrialHomo sapiens (human)
mitochondrial matrixCarbonic anhydrase 5B, mitochondrialHomo sapiens (human)
mitochondrionCarbonic anhydrase 5B, mitochondrialHomo sapiens (human)
cytoplasmCarbonic anhydrase 5B, mitochondrialHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (308)

Assay IDTitleYearJournalArticle
AID497227Anticonvulsant activity in ip dosed albino Carworth Farms number 1 mouse assessed as protection against maximal electroshock-induced seizure2010Journal of medicinal chemistry, Aug-12, Volume: 53, Issue:15
The structure-activity relationship of the 3-oxy site in the anticonvulsant (R)-N-benzyl 2-acetamido-3-methoxypropionamide.
AID687768Anticonvulsant activity in ip dosed NMRI mouse assessed as protection against 6 Hz psychomotor seizure after 30 mins2011Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13
Primary amino acid derivatives: compounds with anticonvulsant and neuropathic pain protection activities.
AID619708Protective index, ratio of TD50 for ip dosed NMRI mouse to ED50 for ip dosed NMRI mouse by maximal electroshock test2011Journal of medicinal chemistry, Oct-13, Volume: 54, Issue:19
Primary amino acid derivatives: substitution of the 4'-N'-benzylamide site in (R)-N'-benzyl 2-amino-3-methylbutanamide, (R)-N'-benzyl 2-amino-3,3-dimethylbutanamide, and (R)-N'-benzyl 2-amino-3-methoxypropionamide provides potent anticonvulsants with pain
AID443563Anticonvulsant activity in po dosed albino Sprague-Dawley rat seizure model assessed as protection against hind limb extension by MES test2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Synthesis and anticonvulsant activities of (R)-N-(4'-substituted)benzyl 2-acetamido-3-methoxypropionamides.
AID626747Anticonvulsant activity in po dosed albino Sprague-Dawley rat assessed as protection against maximal electroshock-induced seizure after 0.25 hrs2011European journal of medicinal chemistry, Oct, Volume: 46, Issue:10
Synthesis and anticonvulsant activity of novel 2,6-diketopiperazine derivatives. Part 1: perhydropyrrole[1,2-a]pyrazines.
AID1432520Anticonvulsant activity in ip dosed albino CD1 mouse assessed as protection against maximal electroshock-induced seizures2017Bioorganic & medicinal chemistry letters, 03-15, Volume: 27, Issue:6
Synthesis and evaluation of anticonvulsant properties of new N-Mannich bases derived from pyrrolidine-2,5-dione and its 3-methyl-, 3-isopropyl, and 3-benzhydryl analogs.
AID1207466Inhibition of rapid delayed inward rectifying potassium current (IKr) in Chinese hamster ovary (CHO) K1 cells stably expressing hERG measured using IonWorks Quattro automated patch clamp platform
AID1411523Inhibition of rat NaV1.3 expressed in HEK293 cells at -80V holding potential by whole-cell patch-Clamp method2017MedChemComm, Jun-01, Volume: 8, Issue:6
The discovery of a potent Na
AID1269442Anticonvulsant activity in ip dosed Swiss mouse assessed as protection against maximal electroshock-induced seizures at 0.5 hrs2016Bioorganic & medicinal chemistry, Feb-15, Volume: 24, Issue:4
New hybrid molecules with anticonvulsant and antinociceptive activity derived from 3-methyl- or 3,3-dimethyl-1-[1-oxo-1-(4-phenylpiperazin-1-yl)propan-2-yl]pyrrolidine-2,5-diones.
AID441711Inhibition of human recombinant CA6 by stopped flow CO2 hydrase assay2010Journal of medicinal chemistry, Jan-28, Volume: 53, Issue:2
The coumarin-binding site in carbonic anhydrase accommodates structurally diverse inhibitors: the antiepileptic lacosamide as an example and lead molecule for novel classes of carbonic anhydrase inhibitors.
AID626721Anticonvulsant activity in ip dosed albino Carworth Farms No.1 mouse assessed as time needs to show peak effect for electric-current for 3 secs-induced seizure after 0.25 hrs by 6Hz minimal clonic seizure test2011European journal of medicinal chemistry, Oct, Volume: 46, Issue:10
Synthesis and anticonvulsant activity of novel 2,6-diketopiperazine derivatives. Part 1: perhydropyrrole[1,2-a]pyrazines.
AID1059037Anticonvulsant activity in ip dosed albino CF-1 mouse assessed as protection against 6 Hz psychomotor seizure measured at 0.5 hrs2013Bioorganic & medicinal chemistry, Dec-15, Volume: 21, Issue:24
Benzyloxybenzylammonium chlorides: Simple amine salts that display anticonvulsant activity.
AID475784Neurotoxicity in ip dosed albino mouse assessed as time of peak effect by rotarod test2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Lacosamide isothiocyanate-based agents: novel agents to target and identify lacosamide receptors.
AID443565Protective index, ratio of TD50 for po dosed albino Sprague-Dawley rat to ED50 for po dosed albino Sprague-Dawley rat2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Synthesis and anticonvulsant activities of (R)-N-(4'-substituted)benzyl 2-acetamido-3-methoxypropionamides.
AID1161081Anticonvulsant activity in ip dosed hippocampal kindled albino Sprague-Dawley rat seizure model assessed as time of rest2014Bioorganic & medicinal chemistry, Oct-01, Volume: 22, Issue:19
Novel fluorinated pyrrolo[1,2-a]pyrazine-2,6-dione derivatives: synthesis and anticonvulsant evaluation in animal models of epilepsy.
AID189456Protective index between TD50/MES ED50 when administered orally to rat1996Journal of medicinal chemistry, Apr-26, Volume: 39, Issue:9
Synthesis and anticonvulsant activities of N-Benzyl-2-acetamidopropionamide derivatives.
AID1864028Binding affinity to TTX-sensitive sodium channel (unknown origin) at 100 uM
AID1229802Protective index, ratio of neurotoxic TD50 in Swiss mouse by by Chimney test to anticonvulsant ED50 in Swiss mouse measured at 0.5 hrs of time to peak effect by maximal electroshock test2015Journal of medicinal chemistry, Jul-09, Volume: 58, Issue:13
Design, synthesis, and anticonvulsant activity of new hybrid compounds derived from 2-(2,5-dioxopyrrolidin-1-yl)propanamides and 2-(2,5-dioxopyrrolidin-1-yl)butanamides.
AID480302Anticonvulsant activity in albino mouse assessed as protection against subcutaneous metrazole-induced seizures up to 300 mg/kg, ip after 0.5 hrs2010Journal of medicinal chemistry, May-13, Volume: 53, Issue:9
Merging the structural motifs of functionalized amino acids and alpha-aminoamides: compounds with significant anticonvulsant activities.
AID1720733Protection index, ratio of TD50 for toxicity in ip dosed mouse to ED50 for anticonvulsant activity in ip dosed mouse
AID1304288Anticonvulsant activity in albino Swiss mouse by maximal electroshock seizure test2016Bioorganic & medicinal chemistry, 07-01, Volume: 24, Issue:13
Design, synthesis and anticonvulsant activity of new hybrid compounds derived from N-phenyl-2-(2,5-dioxopyrrolidin-1-yl)-propanamides and -butanamides.
AID1517278Neurotoxicity against ip dosed Kunming mouse assessed as time remained in rod measured at 0.5 hrs by rotarod test2019European journal of medicinal chemistry, Dec-01, Volume: 183Polygala tenuifolia-Acori tatarinowii herbal pair as an inspiration for substituted cinnamic α-asaronol esters: Design, synthesis, anticonvulsant activity, and inhibition of lactate dehydrogenase study.
AID1517282Protective index, ratio of TD50 for neurotoxicity against ip dosed Kunming mouse assessed as time remained in rod measured at 0.5 hrs by rotarod test to ED50 for anticonvulsant activity in ip dosed Kunming mouse assessed as reduction in formalin-induced p2019European journal of medicinal chemistry, Dec-01, Volume: 183Polygala tenuifolia-Acori tatarinowii herbal pair as an inspiration for substituted cinnamic α-asaronol esters: Design, synthesis, anticonvulsant activity, and inhibition of lactate dehydrogenase study.
AID619699Protective index, ratio of TD50 for po dosed albino Sprague-Dawley rat to ED50 for po dosed albino Sprague-Dawley rat by maximal electroshock test2011Journal of medicinal chemistry, Oct-13, Volume: 54, Issue:19
Primary amino acid derivatives: substitution of the 4'-N'-benzylamide site in (R)-N'-benzyl 2-amino-3-methylbutanamide, (R)-N'-benzyl 2-amino-3,3-dimethylbutanamide, and (R)-N'-benzyl 2-amino-3-methoxypropionamide provides potent anticonvulsants with pain
AID1517280Protective index, ratio of TD50 for neurotoxicity against ip dosed Kunming mouse assessed as time remained in rod measured at 0.5 hrs by rotarod test to ED50 for anticonvulsant activity in ip dosed Kunming mouse assessed as reduction in ScPTZ-induced seiz2019European journal of medicinal chemistry, Dec-01, Volume: 183Polygala tenuifolia-Acori tatarinowii herbal pair as an inspiration for substituted cinnamic α-asaronol esters: Design, synthesis, anticonvulsant activity, and inhibition of lactate dehydrogenase study.
AID1863984Toxicity in CD-1 seizure mouse model assessed as effect on motor coordination administered ip measured after 0.5 hrs for 3 mins by rotarod test
AID1863981Antiseizure activity against ScPTZ-induced seizure in ip dosed CD-1 mouse model assessed as clonic seizures pretreated for 0.5 hrs and measured after 30 mins by subcutaneous pentylenetetrazole test
AID759085Toxicity in po dosed albino Sprague-Dawley rat assessed as behavioral toxicity2013Journal of medicinal chemistry, Jul-25, Volume: 56, Issue:14
(Biphenyl-4-yl)methylammonium chlorides: potent anticonvulsants that modulate Na+ currents.
AID626715Anticonvulsant activity in ip dosed albino Carworth Farms No.1 mouse assessed as protection against subcutaneous metrazol-induced seizure after 0.25 hrs2011European journal of medicinal chemistry, Oct, Volume: 46, Issue:10
Synthesis and anticonvulsant activity of novel 2,6-diketopiperazine derivatives. Part 1: perhydropyrrole[1,2-a]pyrazines.
AID475797Protective index, ratio of TD50 for po dosed Sprague-Dawley rat to ED50 for protection against maximal electroshock-induced seizures in po dosed Sprague-Dawley rat2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Lacosamide isothiocyanate-based agents: novel agents to target and identify lacosamide receptors.
AID1304292Protective index, ratio of TD50 for acute neurotoxicity in albino Swiss mouse to ED50 for anticonvulsant activity in albino Swiss mouse by maximal electroshock seizure test2016Bioorganic & medicinal chemistry, 07-01, Volume: 24, Issue:13
Design, synthesis and anticonvulsant activity of new hybrid compounds derived from N-phenyl-2-(2,5-dioxopyrrolidin-1-yl)-propanamides and -butanamides.
AID1452169Protection index, ratio of TD50 for neurotoxicity in ip dosed Albino Swiss CD-1 mouse to ED50 for ip dosed maximal electroshock induced seizure Albino Swiss CD-1 mouse
AID1195111Anticonvulsant activity in intraperitoneally dosed Albino Swiss CD1 mouse assessed as time to peak effect by maximal electroshock test2015Bioorganic & medicinal chemistry, May-15, Volume: 23, Issue:10
Design, synthesis and biological evaluation of new hybrid anticonvulsants derived from N-benzyl-2-(2,5-dioxopyrrolidin-1-yl)propanamide and 2-(2,5-dioxopyrrolidin-1-yl)butanamide derivatives.
AID1269475Neurotoxicity in ip dosed Swiss mouse seizure model assessed as motor impairment pretreated for 0.5 hrs measured within 60 s by chimney test2016Bioorganic & medicinal chemistry, Feb-15, Volume: 24, Issue:4
New hybrid molecules with anticonvulsant and antinociceptive activity derived from 3-methyl- or 3,3-dimethyl-1-[1-oxo-1-(4-phenylpiperazin-1-yl)propan-2-yl]pyrrolidine-2,5-diones.
AID475794Neurotoxicity in po dosed Sprague-Dawley rat by rotarod test2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Lacosamide isothiocyanate-based agents: novel agents to target and identify lacosamide receptors.
AID665941Anticonvulsant activity in ip dosed NMRI mouse assessed as protection against 6 Hz psychomotor seizure after 30 mins2012Bioorganic & medicinal chemistry, Jun-01, Volume: 20, Issue:11
Synthesis, anticonvulsant activity, and neuropathic pain-attenuating activity of N-benzyl 2-amino-2-(hetero)aromatic acetamides.
AID1195116Protective index, ratio of neurotoxic TD50 in Albino Swiss CD1 mouse by rotarod test to anticonvulsant ED50 in Albino Swiss CD1 mouse by maximal electroshock test2015Bioorganic & medicinal chemistry, May-15, Volume: 23, Issue:10
Design, synthesis and biological evaluation of new hybrid anticonvulsants derived from N-benzyl-2-(2,5-dioxopyrrolidin-1-yl)propanamide and 2-(2,5-dioxopyrrolidin-1-yl)butanamide derivatives.
AID687779Anticonvulsant activity in NMRI mouse assessed as protection against subcutaneous pentylenetetrazol-induced seizure at 30 to 300 mg/kg, ip after 0.5 to 4 hrs2011Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13
Primary amino acid derivatives: compounds with anticonvulsant and neuropathic pain protection activities.
AID1229804Anticonvulsant activity in ip dosed Swiss mouse assessed as protection against seizures measured at 0.5 hrs of time to peak effect by subcutaneous pentylenetetrazole seizure test2015Journal of medicinal chemistry, Jul-09, Volume: 58, Issue:13
Design, synthesis, and anticonvulsant activity of new hybrid compounds derived from 2-(2,5-dioxopyrrolidin-1-yl)propanamides and 2-(2,5-dioxopyrrolidin-1-yl)butanamides.
AID121999Neurotoxic toxicity in mice was evaluated by rotarod test after intraperitoneal administration1996Journal of medicinal chemistry, Apr-26, Volume: 39, Issue:9
Synthesis and anticonvulsant activities of N-Benzyl-2-acetamidopropionamide derivatives.
AID1207372Inhibition of slow delayed inward rectifying potassium current (Iks) in Chinese Hamster Ovary (CHO) cells expressing hKvLQT1/hminK measured using IonWorks Quattro automated patch clamp platform
AID480293Anticonvulsant activity in po dosed Sprague-Dawley albino rat assessed as inhibition of maximal electroshock-induced seizures after 2 hrs2010Journal of medicinal chemistry, May-13, Volume: 53, Issue:9
Merging the structural motifs of functionalized amino acids and alpha-aminoamides: compounds with significant anticonvulsant activities.
AID1195112Anticonvulsant activity in intraperitoneally dosed Albino Swiss CD1 mouse assessed as time to peak effect after 2 hrs by subcutaneous pentylenetetrazole test2015Bioorganic & medicinal chemistry, May-15, Volume: 23, Issue:10
Design, synthesis and biological evaluation of new hybrid anticonvulsants derived from N-benzyl-2-(2,5-dioxopyrrolidin-1-yl)propanamide and 2-(2,5-dioxopyrrolidin-1-yl)butanamide derivatives.
AID621624Neurotoxicity in ip dosed albino CF1 mouse assessed as minimal motor coordination impairment by rotarod test2011Journal of medicinal chemistry, Oct-13, Volume: 54, Issue:19
Defining the structural parameters that confer anticonvulsant activity by the site-by-site modification of (R)-N'-benzyl 2-amino-3-methylbutanamide.
AID1207312Inhibition of fast sodium current (INa) in Chinese Hamster Ovary (CHO) K1 cells transfected with human Nav1.5 measured using IonWorks Quattro automated patch clamp platform
AID475795Neurotoxicity in po dosed Sprague-Dawley rat assessed as time of peak effect by rotarod test2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Lacosamide isothiocyanate-based agents: novel agents to target and identify lacosamide receptors.
AID621654Neurotoxicity in ip dosed albino CF1 mouse assessed as time of peak effect by rotarod test2011Journal of medicinal chemistry, Oct-13, Volume: 54, Issue:19
Defining the structural parameters that confer anticonvulsant activity by the site-by-site modification of (R)-N'-benzyl 2-amino-3-methylbutanamide.
AID1161061Neurotoxicity in ip dosed albino CF1 mouse2014Bioorganic & medicinal chemistry, Oct-01, Volume: 22, Issue:19
Novel fluorinated pyrrolo[1,2-a]pyrazine-2,6-dione derivatives: synthesis and anticonvulsant evaluation in animal models of epilepsy.
AID1195115Neurological toxicity in intraperitoneally dosed Albino Swiss CD1 mouse by rotarod test2015Bioorganic & medicinal chemistry, May-15, Volume: 23, Issue:10
Design, synthesis and biological evaluation of new hybrid anticonvulsants derived from N-benzyl-2-(2,5-dioxopyrrolidin-1-yl)propanamide and 2-(2,5-dioxopyrrolidin-1-yl)butanamide derivatives.
AID1474167Liver toxicity in human assessed as induction of drug-induced liver injury by measuring verified drug-induced liver injury concern status2016Drug discovery today, Apr, Volume: 21, Issue:4
DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID441708Inhibition of human recombinant CA4 by stopped flow CO2 hydrase assay2010Journal of medicinal chemistry, Jan-28, Volume: 53, Issue:2
The coumarin-binding site in carbonic anhydrase accommodates structurally diverse inhibitors: the antiepileptic lacosamide as an example and lead molecule for novel classes of carbonic anhydrase inhibitors.
AID619700Anticonvulsant activity in ip dosed NMRI mouse assessed as protection against maximal electroshock seizure after 30 mins2011Journal of medicinal chemistry, Oct-13, Volume: 54, Issue:19
Primary amino acid derivatives: substitution of the 4'-N'-benzylamide site in (R)-N'-benzyl 2-amino-3-methylbutanamide, (R)-N'-benzyl 2-amino-3,3-dimethylbutanamide, and (R)-N'-benzyl 2-amino-3-methoxypropionamide provides potent anticonvulsants with pain
AID1711724Protection index, ratio of TD50 for neurotoxicity in ip dosed mouse to ED50 for anticonvulsant activity in ip dosed mouse measured after 0.5 hrs by 6 Hz limbic seizure test2016Bioorganic & medicinal chemistry letters, May-01, Volume: 26, Issue:9
Synthesis and evaluation of anticonvulsant properties of new N-Mannich bases derived from 3-(1-phenylethyl)- and 3-benzyl-pyrrolidine-2,5-dione.
AID687787Neurotoxicity in po dosed Sprague-Dawley rat assessed as minimal motor impairment after 30 mins by rotorod test2011Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13
Primary amino acid derivatives: compounds with anticonvulsant and neuropathic pain protection activities.
AID1304291Acute neurotoxicity in albino Swiss mouse pretreated for 2 hrs by rotorod test2016Bioorganic & medicinal chemistry, 07-01, Volume: 24, Issue:13
Design, synthesis and anticonvulsant activity of new hybrid compounds derived from N-phenyl-2-(2,5-dioxopyrrolidin-1-yl)-propanamides and -butanamides.
AID475790Anticonvulsant activity against maximal electroshock-induced seizures in ip dosed albino mouse assessed as time of peak effect2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Lacosamide isothiocyanate-based agents: novel agents to target and identify lacosamide receptors.
AID687789Protective index, ratio of TD50 for Sprague-Dawley rat to ED50 for Sprague-Dawley rat by maximal electroshock seizure test2011Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13
Primary amino acid derivatives: compounds with anticonvulsant and neuropathic pain protection activities.
AID443568Anticonvulsant activity against subcutaneous metrazole-induced seizures in albino Sprague-Dawley rat at 300 mg/kg, ip after 0.5 hrs2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Synthesis and anticonvulsant activities of (R)-N-(4'-substituted)benzyl 2-acetamido-3-methoxypropionamides.
AID619781Neurotoxicity in ip dosed albino CF1 mouse assessed as time of peak effect for median neurological impairing2011Journal of medicinal chemistry, Oct-13, Volume: 54, Issue:19
Primary amino acid derivatives: substitution of the 4'-N'-benzylamide site in (R)-N'-benzyl 2-amino-3-methylbutanamide, (R)-N'-benzyl 2-amino-3,3-dimethylbutanamide, and (R)-N'-benzyl 2-amino-3-methoxypropionamide provides potent anticonvulsants with pain
AID1452170Neurotoxicity in ip dosed Albino Swiss CD-1 mouse assessed as induction of motor impairment measured up to 60 secs by chimney test
AID1517274Anticonvulsant activity in ip dosed Kunming mouse assessed as MES-induced hind limb extension administered 0.5 hrs before MES stimulation2019European journal of medicinal chemistry, Dec-01, Volume: 183Polygala tenuifolia-Acori tatarinowii herbal pair as an inspiration for substituted cinnamic α-asaronol esters: Design, synthesis, anticonvulsant activity, and inhibition of lactate dehydrogenase study.
AID1229803Anticonvulsant activity in ip dosed Swiss mouse assessed as protection against seizures measured at 0.5 hrs of time to peak effect by maximal electroshock test2015Journal of medicinal chemistry, Jul-09, Volume: 58, Issue:13
Design, synthesis, and anticonvulsant activity of new hybrid compounds derived from 2-(2,5-dioxopyrrolidin-1-yl)propanamides and 2-(2,5-dioxopyrrolidin-1-yl)butanamides.
AID475792Anticonvulsant activity in po dosed Sprague-Dawley rat assessed as protection against maximal electroshock-induced seizures2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Lacosamide isothiocyanate-based agents: novel agents to target and identify lacosamide receptors.
AID1232867Protective index, ratio of TD50 for behavioural toxicity in po dosed albino Sprague-Dawley rat to ED50 for anticonvulsant activity in po dosed MES albino Sprague-Dawley rat model2015Bioorganic & medicinal chemistry, Jul-01, Volume: 23, Issue:13
Chimeric derivatives of functionalized amino acids and α-aminoamides: compounds with anticonvulsant activity in seizure models and inhibitory actions on central, peripheral, and cardiac isoforms of voltage-gated sodium channels.
AID626717Protective index, ratio of TD50 for albino Carworth Farms No.1 mouse to ED50 for albino Carworth Farms No.1 mouse by maximal electroshock-induced seizure test2011European journal of medicinal chemistry, Oct, Volume: 46, Issue:10
Synthesis and anticonvulsant activity of novel 2,6-diketopiperazine derivatives. Part 1: perhydropyrrole[1,2-a]pyrazines.
AID1517277Anticonvulsant activity in ip dosed Kunming mouse assessed as reduction in formalin-induced paw licking administered 0.5 hrs before formalin stimulation2019European journal of medicinal chemistry, Dec-01, Volume: 183Polygala tenuifolia-Acori tatarinowii herbal pair as an inspiration for substituted cinnamic α-asaronol esters: Design, synthesis, anticonvulsant activity, and inhibition of lactate dehydrogenase study.
AID1863999Protective index, ratio of TD50 for toxicity in CD-1 seizure mouse model assessed as effect on motor coordination administered ip measured after 0.5 hrs for 3 mins by rotarod test to ED50 for antiseizure activity against electrical stimulus induced seizur
AID497233Protective index, ratio of neurotoxicity TD50 to anticonvulsant ED50 for po dosed albino Spague-Dawley rat2010Journal of medicinal chemistry, Aug-12, Volume: 53, Issue:15
The structure-activity relationship of the 3-oxy site in the anticonvulsant (R)-N-benzyl 2-acetamido-3-methoxypropionamide.
AID1232848Anticonvulsant activity in ip dosed albino Carworth Farms No. 1 mouse measured at 0.5 hrs by 6Hz (32 mA) psychomotor seizure test2015Bioorganic & medicinal chemistry, Jul-01, Volume: 23, Issue:13
Chimeric derivatives of functionalized amino acids and α-aminoamides: compounds with anticonvulsant activity in seizure models and inhibitory actions on central, peripheral, and cardiac isoforms of voltage-gated sodium channels.
AID480286Toxicity in ip dosed albino mouse after 0.25 hrs by rotarod test2010Journal of medicinal chemistry, May-13, Volume: 53, Issue:9
Merging the structural motifs of functionalized amino acids and alpha-aminoamides: compounds with significant anticonvulsant activities.
AID665864Anticonvulsant activity in ip dosed NMRI mouse assessed as protection against maximal electroshock-induced seizure after 30 mins postdose2012Bioorganic & medicinal chemistry, Jun-01, Volume: 20, Issue:11
Synthesis, anticonvulsant activity, and neuropathic pain-attenuating activity of N-benzyl 2-amino-2-(hetero)aromatic acetamides.
AID1720732Toxicity in ip dosed mouse assessed as motor impairment by rotarod test
AID619693Anticonvulsant activity in ip dosed albino CF1 mouse assessed as protection against 6 Hz psychomotor seizure after 30 mins2011Journal of medicinal chemistry, Oct-13, Volume: 54, Issue:19
Primary amino acid derivatives: substitution of the 4'-N'-benzylamide site in (R)-N'-benzyl 2-amino-3-methylbutanamide, (R)-N'-benzyl 2-amino-3,3-dimethylbutanamide, and (R)-N'-benzyl 2-amino-3-methoxypropionamide provides potent anticonvulsants with pain
AID497230Protective index, ratio of neurotoxicity TD50 to anticonvulsant ED50 for ip dosed albino Carworth Farms number 1 mouse2010Journal of medicinal chemistry, Aug-12, Volume: 53, Issue:15
The structure-activity relationship of the 3-oxy site in the anticonvulsant (R)-N-benzyl 2-acetamido-3-methoxypropionamide.
AID619704Analgesic activity in ip dosed NMRI mouse assessed as reduction in formalin-induced neuropathic pain after 30 mins2011Journal of medicinal chemistry, Oct-13, Volume: 54, Issue:19
Primary amino acid derivatives: substitution of the 4'-N'-benzylamide site in (R)-N'-benzyl 2-amino-3-methylbutanamide, (R)-N'-benzyl 2-amino-3,3-dimethylbutanamide, and (R)-N'-benzyl 2-amino-3-methoxypropionamide provides potent anticonvulsants with pain
AID441717Inhibition of mouse recombinant CA15 by stopped flow CO2 hydrase assay2010Journal of medicinal chemistry, Jan-28, Volume: 53, Issue:2
The coumarin-binding site in carbonic anhydrase accommodates structurally diverse inhibitors: the antiepileptic lacosamide as an example and lead molecule for novel classes of carbonic anhydrase inhibitors.
AID190119Neurotoxic toxicity against Rat was evaluated by rotarod test afte oral administration1996Journal of medicinal chemistry, Apr-26, Volume: 39, Issue:9
Synthesis and anticonvulsant activities of N-Benzyl-2-acetamidopropionamide derivatives.
AID1232860Anticonvulsant activity in po dosed albino Sprague-Dawley rat measured at 2 hrs by maximal electroshock seizure test2015Bioorganic & medicinal chemistry, Jul-01, Volume: 23, Issue:13
Chimeric derivatives of functionalized amino acids and α-aminoamides: compounds with anticonvulsant activity in seizure models and inhibitory actions on central, peripheral, and cardiac isoforms of voltage-gated sodium channels.
AID117857Protective index between TD50/MES ED50 when administered intraperitoneally to mouse1996Journal of medicinal chemistry, Apr-26, Volume: 39, Issue:9
Synthesis and anticonvulsant activities of N-Benzyl-2-acetamidopropionamide derivatives.
AID621650Anticonvulsant activity in po dosed albino Sprague-Dawley rat assessed as time of peak effect by maximal electroshock seizures test in presence of 150 miliamperes of electric current2011Journal of medicinal chemistry, Oct-13, Volume: 54, Issue:19
Defining the structural parameters that confer anticonvulsant activity by the site-by-site modification of (R)-N'-benzyl 2-amino-3-methylbutanamide.
AID1161063Anticonvulsant activity in ip dosed albino CF1 mouse assessed as protection against maximal electroshock-induced seizures measured as time to peak effect2014Bioorganic & medicinal chemistry, Oct-01, Volume: 22, Issue:19
Novel fluorinated pyrrolo[1,2-a]pyrazine-2,6-dione derivatives: synthesis and anticonvulsant evaluation in animal models of epilepsy.
AID1415347Anticonvulsant activity in mouse assessed as current strength required to induce tonic hind-limb extension in 50% of the animals at 10 mg/kg, ip by maximal electroshock seizure threshold test (Rvb = 6.05 to 8.13 mA)2017MedChemComm, Jan-01, Volume: 8, Issue:1
Design, synthesis and anticonvulsant-analgesic activity of new
AID621622Anticonvulsant activity in ip dosed albino CF1 mouse assessed as protection against maximal electroshock-induced seizures in presence of 50 miliamperes of electric current2011Journal of medicinal chemistry, Oct-13, Volume: 54, Issue:19
Defining the structural parameters that confer anticonvulsant activity by the site-by-site modification of (R)-N'-benzyl 2-amino-3-methylbutanamide.
AID443567Anticonvulsant activity against subcutaneous metrazole-induced seizures in albino CF1 mouse at 300 mg/kg, ip after 0.5 hrs2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Synthesis and anticonvulsant activities of (R)-N-(4'-substituted)benzyl 2-acetamido-3-methoxypropionamides.
AID619695Neurotoxicity in ip dosed albino CF1 mouse assessed as median neurological impairing dose after 30 mins2011Journal of medicinal chemistry, Oct-13, Volume: 54, Issue:19
Primary amino acid derivatives: substitution of the 4'-N'-benzylamide site in (R)-N'-benzyl 2-amino-3-methylbutanamide, (R)-N'-benzyl 2-amino-3,3-dimethylbutanamide, and (R)-N'-benzyl 2-amino-3-methoxypropionamide provides potent anticonvulsants with pain
AID1269448Protective index, ratio of TD50 for neurotoxicity in ip dosed Swiss mouse to ED50 for anticonvulsant activity in ip dosed Swiss mouse 6 Hz psychomotor seizure model at 0.5 hrs2016Bioorganic & medicinal chemistry, Feb-15, Volume: 24, Issue:4
New hybrid molecules with anticonvulsant and antinociceptive activity derived from 3-methyl- or 3,3-dimethyl-1-[1-oxo-1-(4-phenylpiperazin-1-yl)propan-2-yl]pyrrolidine-2,5-diones.
AID626718Anticonvulsant activity in ip dosed albino Carworth Farms No.1 mouse assessed as time needs to show peak effect for protection against maximal electroshock-induced seizure2011European journal of medicinal chemistry, Oct, Volume: 46, Issue:10
Synthesis and anticonvulsant activity of novel 2,6-diketopiperazine derivatives. Part 1: perhydropyrrole[1,2-a]pyrazines.
AID441712Inhibition of human recombinant CA7 by stopped flow CO2 hydrase assay2010Journal of medicinal chemistry, Jan-28, Volume: 53, Issue:2
The coumarin-binding site in carbonic anhydrase accommodates structurally diverse inhibitors: the antiepileptic lacosamide as an example and lead molecule for novel classes of carbonic anhydrase inhibitors.
AID1161062Protective index, ratio of TD50 for neurotoxicity in ip dosed albino CF1 mouse to ED50 for anticonvulsant activity in ip dosed MES albino CF1 mouse model2014Bioorganic & medicinal chemistry, Oct-01, Volume: 22, Issue:19
Novel fluorinated pyrrolo[1,2-a]pyrazine-2,6-dione derivatives: synthesis and anticonvulsant evaluation in animal models of epilepsy.
AID1304287Anticonvulsant activity against albino Swiss mouse seizure model assessed as time to peak effect at 100 mg/kg, ip2016Bioorganic & medicinal chemistry, 07-01, Volume: 24, Issue:13
Design, synthesis and anticonvulsant activity of new hybrid compounds derived from N-phenyl-2-(2,5-dioxopyrrolidin-1-yl)-propanamides and -butanamides.
AID1432538Anticonvulsant in ip dosed CD1 mouse assessed as time to peak effect2017Bioorganic & medicinal chemistry letters, 03-15, Volume: 27, Issue:6
Synthesis and evaluation of anticonvulsant properties of new N-Mannich bases derived from pyrrolidine-2,5-dione and its 3-methyl-, 3-isopropyl, and 3-benzhydryl analogs.
AID1161059Anticonvulsant activity in ip dosed albino CF1 mouse assessed as protection against maximal electroshock-induced seizures2014Bioorganic & medicinal chemistry, Oct-01, Volume: 22, Issue:19
Novel fluorinated pyrrolo[1,2-a]pyrazine-2,6-dione derivatives: synthesis and anticonvulsant evaluation in animal models of epilepsy.
AID687777Protective index, ratio of TD50 for CF1 mouse to ED50 for CF1 mouse by maximal electroshock seizure test2011Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13
Primary amino acid derivatives: compounds with anticonvulsant and neuropathic pain protection activities.
AID441713Inhibition of human recombinant CA9 by stopped flow CO2 hydrase assay2010Journal of medicinal chemistry, Jan-28, Volume: 53, Issue:2
The coumarin-binding site in carbonic anhydrase accommodates structurally diverse inhibitors: the antiepileptic lacosamide as an example and lead molecule for novel classes of carbonic anhydrase inhibitors.
AID1517275Anticonvulsant activity in ip dosed Kunming mouse assessed as reduction in ScPTZ-induced seizure administered 0.5 hrs before ScPTZ stimulation2019European journal of medicinal chemistry, Dec-01, Volume: 183Polygala tenuifolia-Acori tatarinowii herbal pair as an inspiration for substituted cinnamic α-asaronol esters: Design, synthesis, anticonvulsant activity, and inhibition of lactate dehydrogenase study.
AID1207526Inhibition of rapid delayed inward rectifying potassium current (IKr) measured using manual patch clamp assay
AID626749Neurotoxicity in po dosed albino Sprague-Dawley rat assessed as motor impairment after 0.25 hrs by rotarod test2011European journal of medicinal chemistry, Oct, Volume: 46, Issue:10
Synthesis and anticonvulsant activity of novel 2,6-diketopiperazine derivatives. Part 1: perhydropyrrole[1,2-a]pyrazines.
AID443569Anticonvulsant activity against subcutaneous metrazole-induced seizures in albino CF1 mouse at 300 mg/kg, ip after 4 hrs2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Synthesis and anticonvulsant activities of (R)-N-(4'-substituted)benzyl 2-acetamido-3-methoxypropionamides.
AID1452171Protection index, ratio of TD50 for neurotoxicity in ip dosed Albino Swiss CD-1 mouse to ED50 for ip dosed Albino Swiss CD-1 mouse model of 6 Hz-induced siezures
AID619776Protective index, ratio of TD50 for ip dosed NMRI mouse to ED50 for ip dosed formalin-induced neuropathic pain model of NMRI mouse2011Journal of medicinal chemistry, Oct-13, Volume: 54, Issue:19
Primary amino acid derivatives: substitution of the 4'-N'-benzylamide site in (R)-N'-benzyl 2-amino-3-methylbutanamide, (R)-N'-benzyl 2-amino-3,3-dimethylbutanamide, and (R)-N'-benzyl 2-amino-3-methoxypropionamide provides potent anticonvulsants with pain
AID480278Anticonvulsant activity in ip dosed albino mouse assessed as inhibition of maximal electroshock-induced seizures after 0.5 hrs2010Journal of medicinal chemistry, May-13, Volume: 53, Issue:9
Merging the structural motifs of functionalized amino acids and alpha-aminoamides: compounds with significant anticonvulsant activities.
AID1473741Inhibition of human MRP4 overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 20 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID443561Neurological toxicity in ip dosed albino CF1 mouse assessed as neurological impairment by rotarod test2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Synthesis and anticonvulsant activities of (R)-N-(4'-substituted)benzyl 2-acetamido-3-methoxypropionamides.
AID226538Protective index as the ratio of TD50 value to that of ED50 value in mice.2002Journal of medicinal chemistry, Oct-10, Volume: 45, Issue:21
Design and evaluation of affinity labels of functionalized amino acid anticonvulsants.
AID1863988Protective index, ratio of TD50 for toxicity in CD-1 seizure mouse model assessed as effect on motor coordination administered ip measured after 0.5 hrs for 3 mins by rotarod test to ED50 for antiseizure activity against electrical stimulus induced seizur
AID1473738Inhibition of human BSEP overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-taurocholate in presence of ATP measured after 15 to 20 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID759083Inhibition of Na+ channel in mouse CAD cells assessed as slow inactivation by whole cell voltage clamp technique2013Journal of medicinal chemistry, Jul-25, Volume: 56, Issue:14
(Biphenyl-4-yl)methylammonium chlorides: potent anticonvulsants that modulate Na+ currents.
AID1304294Protective index, ratio of TD50 for acute neurotoxicity in albino Swiss mouse to ED50 for anticonvulsant activity in albino Swiss mouse by 6Hz psychomotor seizure test2016Bioorganic & medicinal chemistry, 07-01, Volume: 24, Issue:13
Design, synthesis and anticonvulsant activity of new hybrid compounds derived from N-phenyl-2-(2,5-dioxopyrrolidin-1-yl)-propanamides and -butanamides.
AID441706Inhibition of human recombinant CA2 by stopped flow CO2 hydrase assay2010Journal of medicinal chemistry, Jan-28, Volume: 53, Issue:2
The coumarin-binding site in carbonic anhydrase accommodates structurally diverse inhibitors: the antiepileptic lacosamide as an example and lead molecule for novel classes of carbonic anhydrase inhibitors.
AID1207432Inhibition of transient outward potassium current (Ito) current in Chinese Hamster Ovary (CHO) K1 cells expressing human Kv4.3 measured using IonWorks Quattro automated patch clamp platform
AID619698Toxicity in po dosed albino Sprague-Dawley rat assessed as behavioural toxicity2011Journal of medicinal chemistry, Oct-13, Volume: 54, Issue:19
Primary amino acid derivatives: substitution of the 4'-N'-benzylamide site in (R)-N'-benzyl 2-amino-3-methylbutanamide, (R)-N'-benzyl 2-amino-3,3-dimethylbutanamide, and (R)-N'-benzyl 2-amino-3-methoxypropionamide provides potent anticonvulsants with pain
AID497232Neurotoxicity in po dosed albino Sprague-Dawley rat by rotarod test2010Journal of medicinal chemistry, Aug-12, Volume: 53, Issue:15
The structure-activity relationship of the 3-oxy site in the anticonvulsant (R)-N-benzyl 2-acetamido-3-methoxypropionamide.
AID1269438Anticonvulsant activity in ip dosed Swiss mouse assessed as reduction in clonic seizures at 0.5 hrs by subcutaneous pentylenetetrazole seizure test2016Bioorganic & medicinal chemistry, Feb-15, Volume: 24, Issue:4
New hybrid molecules with anticonvulsant and antinociceptive activity derived from 3-methyl- or 3,3-dimethyl-1-[1-oxo-1-(4-phenylpiperazin-1-yl)propan-2-yl]pyrrolidine-2,5-diones.
AID1863974Antiseizure activity against electrical stimulus induced seizure in ip dosed CD-1 mouse model assessed as reduction in hindlimb tonic extension pretreated for 0.5 hrs by maximal electroshock seizure test
AID626748Anticonvulsant activity in po dosed albino Sprague-Dawley rat assessed as protection against subcutaneous metrazol-induced seizure after 0.25 hrs2011European journal of medicinal chemistry, Oct, Volume: 46, Issue:10
Synthesis and anticonvulsant activity of novel 2,6-diketopiperazine derivatives. Part 1: perhydropyrrole[1,2-a]pyrazines.
AID441710Inhibition of human recombinant CA5B by stopped flow CO2 hydrase assay2010Journal of medicinal chemistry, Jan-28, Volume: 53, Issue:2
The coumarin-binding site in carbonic anhydrase accommodates structurally diverse inhibitors: the antiepileptic lacosamide as an example and lead molecule for novel classes of carbonic anhydrase inhibitors.
AID687769Anticonvulsant activity in ip dosed CF1 mouse assessed as protection against 6 Hz psychomotor seizure after 30 mins2011Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13
Primary amino acid derivatives: compounds with anticonvulsant and neuropathic pain protection activities.
AID626719Anticonvulsant activity in ip dosed albino Carworth Farms No.1 mouse assessed as protection against electric-current for 3 secs-induced seizure after 0.25 hrs by 6Hz minimal clonic seizure test2011European journal of medicinal chemistry, Oct, Volume: 46, Issue:10
Synthesis and anticonvulsant activity of novel 2,6-diketopiperazine derivatives. Part 1: perhydropyrrole[1,2-a]pyrazines.
AID687776Protective index, ratio of TD50 for NMRI mouse to ED50 for NMRI mouse by maximal electroshock seizure test2011Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13
Primary amino acid derivatives: compounds with anticonvulsant and neuropathic pain protection activities.
AID621625Protective index, ratio of TD50 for albino CF1 mouse by rotarod test to ED50 for albino CF1 mouse by maximal electroshock seizures test2011Journal of medicinal chemistry, Oct-13, Volume: 54, Issue:19
Defining the structural parameters that confer anticonvulsant activity by the site-by-site modification of (R)-N'-benzyl 2-amino-3-methylbutanamide.
AID441705Inhibition of human recombinant CA1 by stopped flow CO2 hydrase assay2010Journal of medicinal chemistry, Jan-28, Volume: 53, Issue:2
The coumarin-binding site in carbonic anhydrase accommodates structurally diverse inhibitors: the antiepileptic lacosamide as an example and lead molecule for novel classes of carbonic anhydrase inhibitors.
AID223724Neurologic toxicity using rotarod test in rat after oral administration2002Journal of medicinal chemistry, Oct-10, Volume: 45, Issue:21
Design and evaluation of affinity labels of functionalized amino acid anticonvulsants.
AID1161080Anticonvulsant activity in ip dosed hippocampal kindled albino Sprague-Dawley rat seizure model2014Bioorganic & medicinal chemistry, Oct-01, Volume: 22, Issue:19
Novel fluorinated pyrrolo[1,2-a]pyrazine-2,6-dione derivatives: synthesis and anticonvulsant evaluation in animal models of epilepsy.
AID1229808Protective index, ratio of neurotoxic TD50 in Swiss mouse by by Chimney test to anticonvulsant ED50 in Swiss mouse measured at 0.5 hrs of time to peak effect by 6 Hz test by 6 Hz psychomotor seizure test2015Journal of medicinal chemistry, Jul-09, Volume: 58, Issue:13
Design, synthesis, and anticonvulsant activity of new hybrid compounds derived from 2-(2,5-dioxopyrrolidin-1-yl)propanamides and 2-(2,5-dioxopyrrolidin-1-yl)butanamides.
AID626714Anticonvulsant activity in ip dosed albino Carworth Farms No.1 mouse assessed as protection against maximal electroshock-induced seizure after 0.25 hrs2011European journal of medicinal chemistry, Oct, Volume: 46, Issue:10
Synthesis and anticonvulsant activity of novel 2,6-diketopiperazine derivatives. Part 1: perhydropyrrole[1,2-a]pyrazines.
AID759090Anticonvulsant activity against po dosed albino Sprague-Dawley rat after 2 hrs by maximal electroshock seizure test2013Journal of medicinal chemistry, Jul-25, Volume: 56, Issue:14
(Biphenyl-4-yl)methylammonium chlorides: potent anticonvulsants that modulate Na+ currents.
AID1452168Anticonvulsant activity in ip dosed Albino Swiss CD-1 mouse assessed as protection against 32 mA current-induced seizure treated up to 2 hrs prior to 6-Hz current induction measured at time to peak effect
AID1473740Inhibition of human MRP3 overexpressed in Sf9 insect cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 10 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID759104Toxicity in ip dosed albino CF1 mouse after 0.25 hrs by rotorod test2013Journal of medicinal chemistry, Jul-25, Volume: 56, Issue:14
(Biphenyl-4-yl)methylammonium chlorides: potent anticonvulsants that modulate Na+ currents.
AID1432518Anticonvulsant activity in ip dosed albino CD1 mouse assessed as protection against 32 mA current-induced seizure by 6 Hz psychomotor test2017Bioorganic & medicinal chemistry letters, 03-15, Volume: 27, Issue:6
Synthesis and evaluation of anticonvulsant properties of new N-Mannich bases derived from pyrrolidine-2,5-dione and its 3-methyl-, 3-isopropyl, and 3-benzhydryl analogs.
AID1517279Protective index, ratio of TD50 for neurotoxicity against ip dosed Kunming mouse assessed as time remained in rod measured at 0.5 hrs by rotarod test to ED50 for anticonvulsant activity in ip dosed Kunming mouse assessed as MES-induced hind limb extension2019European journal of medicinal chemistry, Dec-01, Volume: 183Polygala tenuifolia-Acori tatarinowii herbal pair as an inspiration for substituted cinnamic α-asaronol esters: Design, synthesis, anticonvulsant activity, and inhibition of lactate dehydrogenase study.
AID387784Anticonvulsant activity in ip dosed albino mouse by MES seizure test2008Bioorganic & medicinal chemistry, Oct-01, Volume: 16, Issue:19
Synthesis and anticonvulsant activities of N-benzyl (2R)-2-acetamido-3-oxysubstituted propionamide derivatives.
AID441715Inhibition of human recombinant CA13 by stopped flow CO2 hydrase assay2010Journal of medicinal chemistry, Jan-28, Volume: 53, Issue:2
The coumarin-binding site in carbonic anhydrase accommodates structurally diverse inhibitors: the antiepileptic lacosamide as an example and lead molecule for novel classes of carbonic anhydrase inhibitors.
AID1711719Anti-convulsant activity in ip dosed mouse assessed as protection against psychomotor seizures measured after 0.5 hrs by 6 Hz limbic seizure test2016Bioorganic & medicinal chemistry letters, May-01, Volume: 26, Issue:9
Synthesis and evaluation of anticonvulsant properties of new N-Mannich bases derived from 3-(1-phenylethyl)- and 3-benzyl-pyrrolidine-2,5-dione.
AID443570Anticonvulsant activity against subcutaneous metrazole-induced seizures in albino Sprague-Dawley rat at 300 mg/kg, ip after 4 hrs2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Synthesis and anticonvulsant activities of (R)-N-(4'-substituted)benzyl 2-acetamido-3-methoxypropionamides.
AID475789Anticonvulsant activity in ip dosed albino mouse assessed as protection against maximal electroshock-induced seizures2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Lacosamide isothiocyanate-based agents: novel agents to target and identify lacosamide receptors.
AID113858Effective dose against maximal electroshock seizure in mice after intraperitoneal administration1996Journal of medicinal chemistry, Apr-26, Volume: 39, Issue:9
Synthesis and anticonvulsant activities of N-Benzyl-2-acetamidopropionamide derivatives.
AID626751Anticonvulsant activity in po dosed albino Sprague-Dawley rat assessed as time needs to show peak effect for protection against maximal electroshock-induced seizure after 0.25 hrs2011European journal of medicinal chemistry, Oct, Volume: 46, Issue:10
Synthesis and anticonvulsant activity of novel 2,6-diketopiperazine derivatives. Part 1: perhydropyrrole[1,2-a]pyrazines.
AID687763Antinociceptive activity in ip dosed NMRI mouse assessed as inhibition of formalin-induced neuropathic pain after 30 mins2011Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13
Primary amino acid derivatives: compounds with anticonvulsant and neuropathic pain protection activities.
AID1232852Neurotoxicity in ip dosed albino Carworth Farms No. 1 mouse measured at 0.25 hrs by rotarod test2015Bioorganic & medicinal chemistry, Jul-01, Volume: 23, Issue:13
Chimeric derivatives of functionalized amino acids and α-aminoamides: compounds with anticonvulsant activity in seizure models and inhibitory actions on central, peripheral, and cardiac isoforms of voltage-gated sodium channels.
AID475798Anticonvulsant activity in ip dosed albino mouse assessed as protection against subcutaneous metrazole-induced seizures2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Lacosamide isothiocyanate-based agents: novel agents to target and identify lacosamide receptors.
AID1864057Cytotoxicity against human HepG2 cells assessed as cell viability at 100 uM measured for 72 hrs
AID1432534Neurotoxicity in ip dosed albino CD1 mouse assessed as motor impairment by rotarod test2017Bioorganic & medicinal chemistry letters, 03-15, Volume: 27, Issue:6
Synthesis and evaluation of anticonvulsant properties of new N-Mannich bases derived from pyrrolidine-2,5-dione and its 3-methyl-, 3-isopropyl, and 3-benzhydryl analogs.
AID687778Protective index, ratio of TD50 for NMRI mouse to ED50 for NMRI mouse formalin-induced neuropathic pain model2011Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13
Primary amino acid derivatives: compounds with anticonvulsant and neuropathic pain protection activities.
AID665942Antinociceptive activity in ip dosed NMRI mouse neuropathic pain model assessed as protection against formalin-induced nociceptive behaviour after 30 mins2012Bioorganic & medicinal chemistry, Jun-01, Volume: 20, Issue:11
Synthesis, anticonvulsant activity, and neuropathic pain-attenuating activity of N-benzyl 2-amino-2-(hetero)aromatic acetamides.
AID225116Anticonvulsant activity using MES test in rat after oral administration2002Journal of medicinal chemistry, Oct-10, Volume: 45, Issue:21
Design and evaluation of affinity labels of functionalized amino acid anticonvulsants.
AID1195114Anticonvulsant activity in intraperitoneally dosed Albino Swiss CD1 mouse by subcutaneous pentylenetetrazole test2015Bioorganic & medicinal chemistry, May-15, Volume: 23, Issue:10
Design, synthesis and biological evaluation of new hybrid anticonvulsants derived from N-benzyl-2-(2,5-dioxopyrrolidin-1-yl)propanamide and 2-(2,5-dioxopyrrolidin-1-yl)butanamide derivatives.
AID443560Anticonvulsant activity in ip dosed albino CF1 mouse seizure model assessed as protection against hind limb extension by MES test2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Synthesis and anticonvulsant activities of (R)-N-(4'-substituted)benzyl 2-acetamido-3-methoxypropionamides.
AID726282Binding affinity to human inactivated voltage-gated Na channel 1.7 expressed in HEK293 cells by patch-clamp technique2013Journal of medicinal chemistry, Feb-14, Volume: 56, Issue:3
Ion channels as therapeutic targets: a drug discovery perspective.
AID1863978Antiseizure activity against electrical stimulus induced seizure in ip dosed CD-1 mouse model assessed as normal behavior within 10 seconds after stimulation at 6 Hz and 32 mA for 3 secs pretreated for 0.5 hr by psychomotor seizure test
AID1415351Anticonvulsant activity in mouse assessed as increase in electroconvulsive threshold at 10 mg/kg, ip by maximal electroshock seizure threshold test relative to control2017MedChemComm, Jan-01, Volume: 8, Issue:1
Design, synthesis and anticonvulsant-analgesic activity of new
AID621623Anticonvulsant activity in ip dosed albino CF1 mouse assessed as time of peak effect by maximal electroshock seizures test in presence of 50 miliamperes of electric current2011Journal of medicinal chemistry, Oct-13, Volume: 54, Issue:19
Defining the structural parameters that confer anticonvulsant activity by the site-by-site modification of (R)-N'-benzyl 2-amino-3-methylbutanamide.
AID1161060Anticonvulsant activity in ip dosed albino CF1 mouse assessed as protection against subcutaneous metrazol-induced seizures2014Bioorganic & medicinal chemistry, Oct-01, Volume: 22, Issue:19
Novel fluorinated pyrrolo[1,2-a]pyrazine-2,6-dione derivatives: synthesis and anticonvulsant evaluation in animal models of epilepsy.
AID726281Binding affinity to voltage-gated Na channel 1.8 in Sprague-Dawley rat L4/L5 DRG neurons by patch-clamp technique2013Journal of medicinal chemistry, Feb-14, Volume: 56, Issue:3
Ion channels as therapeutic targets: a drug discovery perspective.
AID1269477Protective index, ratio of TD50 for neurotoxicity in ip dosed Swiss mouse to ED50 for anticonvulsant activity in ip dosed MES Swiss mouse model at 0.5 hrs2016Bioorganic & medicinal chemistry, Feb-15, Volume: 24, Issue:4
New hybrid molecules with anticonvulsant and antinociceptive activity derived from 3-methyl- or 3,3-dimethyl-1-[1-oxo-1-(4-phenylpiperazin-1-yl)propan-2-yl]pyrrolidine-2,5-diones.
AID475799Anticonvulsant activity in po dosed Sprague-Dawley rat assessed as protection against subcutaneous metrazole-induced seizures2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Lacosamide isothiocyanate-based agents: novel agents to target and identify lacosamide receptors.
AID1415327Neurotoxicity in ip dosed mouse assessed as motor impairment measured after 15 mins by rotarod test2017MedChemComm, Jan-01, Volume: 8, Issue:1
Design, synthesis and anticonvulsant-analgesic activity of new
AID1863997Antiseizure activity against electrical stimulus induced seizure in ip dosed CD-1 mouse model assessed as normal behavior within 10 seconds after stimulation at 6 Hz and 44 mA for 3 secs pretreated for 0.5 hr by psychomotor seizure test
AID1432535Protection index, ratio of TD50 for motor impairment in ip dosed albino CD1 mouse to ED50 for protection against maximal electroshock-induced seizures in ip dosed albino CD1 mouse2017Bioorganic & medicinal chemistry letters, 03-15, Volume: 27, Issue:6
Synthesis and evaluation of anticonvulsant properties of new N-Mannich bases derived from pyrrolidine-2,5-dione and its 3-methyl-, 3-isopropyl, and 3-benzhydryl analogs.
AID443571Anticonvulsant activity against in ip dosed albino Sprague-Dawley rat hippocampal kindled seizure model assessed as decrease in seizures after 0.5 hrs2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Synthesis and anticonvulsant activities of (R)-N-(4'-substituted)benzyl 2-acetamido-3-methoxypropionamides.
AID178377Effective dose against maximal electroshock seizure in rat after oral administration1996Journal of medicinal chemistry, Apr-26, Volume: 39, Issue:9
Synthesis and anticonvulsant activities of N-Benzyl-2-acetamidopropionamide derivatives.
AID626720Protective index, ratio of TD50 for albino Carworth Farms No.1 mouse to ED50 for albino Carworth Farms No.1 mouse by 6Hz minimal clonic seizure test2011European journal of medicinal chemistry, Oct, Volume: 46, Issue:10
Synthesis and anticonvulsant activity of novel 2,6-diketopiperazine derivatives. Part 1: perhydropyrrole[1,2-a]pyrazines.
AID687766Anticonvulsant activity in ip dosed NMRI mouse assessed as protection against maximal electroshock-induced seizure after 30 mins2011Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13
Primary amino acid derivatives: compounds with anticonvulsant and neuropathic pain protection activities.
AID1229805Anticonvulsant activity in ip dosed Swiss mouse assessed as protection against seizures measured at 0.5 hrs of time to peak effect by 6 Hz test by 6 Hz psychomotor seizure test2015Journal of medicinal chemistry, Jul-09, Volume: 58, Issue:13
Design, synthesis, and anticonvulsant activity of new hybrid compounds derived from 2-(2,5-dioxopyrrolidin-1-yl)propanamides and 2-(2,5-dioxopyrrolidin-1-yl)butanamides.
AID687775Neurotoxicity in ip dosed NMRI mouse assessed as time of peak effect for minimal motor impairment after 30 mins2011Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13
Primary amino acid derivatives: compounds with anticonvulsant and neuropathic pain protection activities.
AID619782Anticonvulsant activity in po dosed albino Sprague-Dawley rat assessed as time of peak effect for protection against maximal electroshock seizure2011Journal of medicinal chemistry, Oct-13, Volume: 54, Issue:19
Primary amino acid derivatives: substitution of the 4'-N'-benzylamide site in (R)-N'-benzyl 2-amino-3-methylbutanamide, (R)-N'-benzyl 2-amino-3,3-dimethylbutanamide, and (R)-N'-benzyl 2-amino-3-methoxypropionamide provides potent anticonvulsants with pain
AID687785Anticonvulsant activity in po dosed Sprague-Dawley rat assessed as protection against maximal electroshock-induced seizure after 30 mins2011Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13
Primary amino acid derivatives: compounds with anticonvulsant and neuropathic pain protection activities.
AID475785Neurotoxicity in ip dosed albino mouse by rotarod test2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Lacosamide isothiocyanate-based agents: novel agents to target and identify lacosamide receptors.
AID1269472Anticonvulsant activity against ip dosed Swiss mouse seizure model assessed as protection at 0.5 hrs by 6 Hz psychomotor seizure test2016Bioorganic & medicinal chemistry, Feb-15, Volume: 24, Issue:4
New hybrid molecules with anticonvulsant and antinociceptive activity derived from 3-methyl- or 3,3-dimethyl-1-[1-oxo-1-(4-phenylpiperazin-1-yl)propan-2-yl]pyrrolidine-2,5-diones.
AID619692Anticonvulsant activity in ip dosed albino CF1 mouse assessed as protection against maximal electroshock-induced seizure after 30 mins2011Journal of medicinal chemistry, Oct-13, Volume: 54, Issue:19
Primary amino acid derivatives: substitution of the 4'-N'-benzylamide site in (R)-N'-benzyl 2-amino-3-methylbutanamide, (R)-N'-benzyl 2-amino-3,3-dimethylbutanamide, and (R)-N'-benzyl 2-amino-3-methoxypropionamide provides potent anticonvulsants with pain
AID475793Anticonvulsant activity against maximal electroshock-induced seizures in po dosed Sprague-Dawley rat assessed as time of peak effect2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Lacosamide isothiocyanate-based agents: novel agents to target and identify lacosamide receptors.
AID687767Anticonvulsant activity in ip dosed CF1 mouse assessed as time of peak effect for protection against maximal electroshock-induced seizure2011Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13
Primary amino acid derivatives: compounds with anticonvulsant and neuropathic pain protection activities.
AID759121Anticonvulsant activity against ip dosed albino CF1 mouse after 0.5 hrs by maximal electroshock seizure test2013Journal of medicinal chemistry, Jul-25, Volume: 56, Issue:14
(Biphenyl-4-yl)methylammonium chlorides: potent anticonvulsants that modulate Na+ currents.
AID621649Anticonvulsant activity in po dosed albino Sprague-Dawley rat assessed as protection against maximal electroshock-induced seizures in presence of 150 miliamperes of electric current2011Journal of medicinal chemistry, Oct-13, Volume: 54, Issue:19
Defining the structural parameters that confer anticonvulsant activity by the site-by-site modification of (R)-N'-benzyl 2-amino-3-methylbutanamide.
AID443562Protective index, ratio of TD50 for ip dosed albino CF1 mouse to ED50 for ip dosed albino CF1 mouse2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Synthesis and anticonvulsant activities of (R)-N-(4'-substituted)benzyl 2-acetamido-3-methoxypropionamides.
AID619696Protective index, ratio of TD50 for ip dosed albino CF1 mouse to ED50 for ip dosed albino CF1 mouse by maximal electroshock test2011Journal of medicinal chemistry, Oct-13, Volume: 54, Issue:19
Primary amino acid derivatives: substitution of the 4'-N'-benzylamide site in (R)-N'-benzyl 2-amino-3-methylbutanamide, (R)-N'-benzyl 2-amino-3,3-dimethylbutanamide, and (R)-N'-benzyl 2-amino-3-methoxypropionamide provides potent anticonvulsants with pain
AID619702Anticonvulsant activity in ip dosed 6 Hz psychomotor seizure model of NMRI mouse assessed as protection against seizure after 30 minutes2011Journal of medicinal chemistry, Oct-13, Volume: 54, Issue:19
Primary amino acid derivatives: substitution of the 4'-N'-benzylamide site in (R)-N'-benzyl 2-amino-3-methylbutanamide, (R)-N'-benzyl 2-amino-3,3-dimethylbutanamide, and (R)-N'-benzyl 2-amino-3-methoxypropionamide provides potent anticonvulsants with pain
AID621651Neurotoxicity in po dosed albino Sprague-Dawley rat2011Journal of medicinal chemistry, Oct-13, Volume: 54, Issue:19
Defining the structural parameters that confer anticonvulsant activity by the site-by-site modification of (R)-N'-benzyl 2-amino-3-methylbutanamide.
AID687773Neurotoxicity in ip dosed CF1 mouse assessed as minimal motor impairment after 30 mins2011Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13
Primary amino acid derivatives: compounds with anticonvulsant and neuropathic pain protection activities.
AID1720726Anticonvulsant activity in ip dosed mouse assessed as protection against current-induced seizure by maximal electroshock seizure test
AID1474166Liver toxicity in human assessed as induction of drug-induced liver injury by measuring severity class index2016Drug discovery today, Apr, Volume: 21, Issue:4
DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID1232864Behavioural toxicity in po dosed albino Sprague-Dawley rat measured at 0.5 hrs2015Bioorganic & medicinal chemistry, Jul-01, Volume: 23, Issue:13
Chimeric derivatives of functionalized amino acids and α-aminoamides: compounds with anticonvulsant activity in seizure models and inhibitory actions on central, peripheral, and cardiac isoforms of voltage-gated sodium channels.
AID626750Protective index, ratio of TD50 for albino Sprague-Dawley rat to ED50 for albino Sprague-Dawley rat by maximal electroshock-induced seizure test2011European journal of medicinal chemistry, Oct, Volume: 46, Issue:10
Synthesis and anticonvulsant activity of novel 2,6-diketopiperazine derivatives. Part 1: perhydropyrrole[1,2-a]pyrazines.
AID480303Anticonvulsant activity in albino mouse assessed as protection against subcutaneous metrazole-induced seizures up to 300 mg/kg, ip after 4 hrs2010Journal of medicinal chemistry, May-13, Volume: 53, Issue:9
Merging the structural motifs of functionalized amino acids and alpha-aminoamides: compounds with significant anticonvulsant activities.
AID665954Protective index, ratio of TD50 for NMRI mouse to ED50 for anticonvulsant activity in ip dosed NMRI mouse by maximal electroshock seizure test2012Bioorganic & medicinal chemistry, Jun-01, Volume: 20, Issue:11
Synthesis, anticonvulsant activity, and neuropathic pain-attenuating activity of N-benzyl 2-amino-2-(hetero)aromatic acetamides.
AID1232844Anticonvulsant activity in ip dosed albino Carworth Farms No. 1 mouse measured at 0.5 hrs by maximal electroshock seizure test2015Bioorganic & medicinal chemistry, Jul-01, Volume: 23, Issue:13
Chimeric derivatives of functionalized amino acids and α-aminoamides: compounds with anticonvulsant activity in seizure models and inhibitory actions on central, peripheral, and cardiac isoforms of voltage-gated sodium channels.
AID226539Protective index as the ratio of TD50 value to that of ED50 value in rat.2002Journal of medicinal chemistry, Oct-10, Volume: 45, Issue:21
Design and evaluation of affinity labels of functionalized amino acid anticonvulsants.
AID619778Anticonvulsant activity in ip dosed albino CF1 mouse assessed as time of peak effect for protection against maximal electroshock-induced seizure2011Journal of medicinal chemistry, Oct-13, Volume: 54, Issue:19
Primary amino acid derivatives: substitution of the 4'-N'-benzylamide site in (R)-N'-benzyl 2-amino-3-methylbutanamide, (R)-N'-benzyl 2-amino-3,3-dimethylbutanamide, and (R)-N'-benzyl 2-amino-3-methoxypropionamide provides potent anticonvulsants with pain
AID441714Inhibition of human recombinant CA12 by stopped flow CO2 hydrase assay2010Journal of medicinal chemistry, Jan-28, Volume: 53, Issue:2
The coumarin-binding site in carbonic anhydrase accommodates structurally diverse inhibitors: the antiepileptic lacosamide as an example and lead molecule for novel classes of carbonic anhydrase inhibitors.
AID665955Protective index, ratio of TD50 for NMRI mouse to ED50 for antinociceptive activity in ip dosed NMRI mouse neuropathic pain model2012Bioorganic & medicinal chemistry, Jun-01, Volume: 20, Issue:11
Synthesis, anticonvulsant activity, and neuropathic pain-attenuating activity of N-benzyl 2-amino-2-(hetero)aromatic acetamides.
AID687765Anticonvulsant activity in ip dosed CF1 mouse assessed as protection against maximal electroshock-induced seizure after 30 mins2011Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13
Primary amino acid derivatives: compounds with anticonvulsant and neuropathic pain protection activities.
AID497231Anticonvulsant activity in po dosed albino Sprague-Dawley rat assessed as protection against maximal electroshock-induced seizure2010Journal of medicinal chemistry, Aug-12, Volume: 53, Issue:15
The structure-activity relationship of the 3-oxy site in the anticonvulsant (R)-N-benzyl 2-acetamido-3-methoxypropionamide.
AID1195113Anticonvulsant activity in intraperitoneally dosed Albino Swiss CD1 mouse by maximal electroshock test2015Bioorganic & medicinal chemistry, May-15, Volume: 23, Issue:10
Design, synthesis and biological evaluation of new hybrid anticonvulsants derived from N-benzyl-2-(2,5-dioxopyrrolidin-1-yl)propanamide and 2-(2,5-dioxopyrrolidin-1-yl)butanamide derivatives.
AID480311Antiinflammatory activity in albino mouse assessed as reduction in formalin-induced late inflammation at 16 mg/kg, ip2010Journal of medicinal chemistry, May-13, Volume: 53, Issue:9
Merging the structural motifs of functionalized amino acids and alpha-aminoamides: compounds with significant anticonvulsant activities.
AID497229Neurotoxicity in ip dosed albino Carworth Farms number 1 mouse by rotarod test2010Journal of medicinal chemistry, Aug-12, Volume: 53, Issue:15
The structure-activity relationship of the 3-oxy site in the anticonvulsant (R)-N-benzyl 2-acetamido-3-methoxypropionamide.
AID726283Binding affinity to rat inactivated voltage-gated Na channel 1.3 expressed in human HEK293 cells by patch-clamp technique2013Journal of medicinal chemistry, Feb-14, Volume: 56, Issue:3
Ion channels as therapeutic targets: a drug discovery perspective.
AID1304290Anticonvulsant activity in albino Swiss mouse assessed as protection against electrically-induced seizure by 6Hz psychomotor seizure test2016Bioorganic & medicinal chemistry, 07-01, Volume: 24, Issue:13
Design, synthesis and anticonvulsant activity of new hybrid compounds derived from N-phenyl-2-(2,5-dioxopyrrolidin-1-yl)-propanamides and -butanamides.
AID387785Neurotoxicity in ip dosed albino mouse by rotarod test2008Bioorganic & medicinal chemistry, Oct-01, Volume: 16, Issue:19
Synthesis and anticonvulsant activities of N-benzyl (2R)-2-acetamido-3-oxysubstituted propionamide derivatives.
AID443564Behavioral toxicity in po dosed albino Sprague-Dawley rat2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Synthesis and anticonvulsant activities of (R)-N-(4'-substituted)benzyl 2-acetamido-3-methoxypropionamides.
AID1473739Inhibition of human MRP2 overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 20 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID1415401Neurotoxicity in ip dosed mouse assessed as motor impairment measured after 30 mins by rotarod test2017MedChemComm, Jan-01, Volume: 8, Issue:1
Design, synthesis and anticonvulsant-analgesic activity of new
AID1711722Neurotoxicity activity in ip dosed mouse assessed as induction of motor impairment by rotarod test2016Bioorganic & medicinal chemistry letters, May-01, Volume: 26, Issue:9
Synthesis and evaluation of anticonvulsant properties of new N-Mannich bases derived from 3-(1-phenylethyl)- and 3-benzyl-pyrrolidine-2,5-dione.
AID387786Protective index, ratio of TD50 for albino mouse by rotarod test to ED50 for albino mouse by MES seizure test2008Bioorganic & medicinal chemistry, Oct-01, Volume: 16, Issue:19
Synthesis and anticonvulsant activities of N-benzyl (2R)-2-acetamido-3-oxysubstituted propionamide derivatives.
AID687774Neurotoxicity in ip dosed NMRI mouse assessed as minimal motor impairment after 30 mins2011Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13
Primary amino acid derivatives: compounds with anticonvulsant and neuropathic pain protection activities.
AID1304289Anticonvulsant activity in albino Swiss mouse measured after 30 mins by subcutaneous pentylenetetrazole seizure test2016Bioorganic & medicinal chemistry, 07-01, Volume: 24, Issue:13
Design, synthesis and anticonvulsant activity of new hybrid compounds derived from N-phenyl-2-(2,5-dioxopyrrolidin-1-yl)-propanamides and -butanamides.
AID619707Neurotoxicity in ip dosed NMRI mouse assessed as median neurological impairing dose after 30 mins by rotarod test2011Journal of medicinal chemistry, Oct-13, Volume: 54, Issue:19
Primary amino acid derivatives: substitution of the 4'-N'-benzylamide site in (R)-N'-benzyl 2-amino-3-methylbutanamide, (R)-N'-benzyl 2-amino-3,3-dimethylbutanamide, and (R)-N'-benzyl 2-amino-3-methoxypropionamide provides potent anticonvulsants with pain
AID687786Anticonvulsant activity in po dosed Sprague-Dawley rat assessed as time of peak effect for protection against maximal electroshock-induced seizure after 30 mins2011Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13
Primary amino acid derivatives: compounds with anticonvulsant and neuropathic pain protection activities.
AID626716Neurotoxicity in ip dosed albino Carworth Farms No.1 mouse assessed as motor impairment after 0.25 hrs by rotarod test2011European journal of medicinal chemistry, Oct, Volume: 46, Issue:10
Synthesis and anticonvulsant activity of novel 2,6-diketopiperazine derivatives. Part 1: perhydropyrrole[1,2-a]pyrazines.
AID1232854Protective index, ratio of TD50 for neurotoxicity in ip dosed albino Carworth Farms No. 1 mouse to ED50 for anticonvulsant activity in ip dosed MES albino Carworth Farms No. 1 mouse model2015Bioorganic & medicinal chemistry, Jul-01, Volume: 23, Issue:13
Chimeric derivatives of functionalized amino acids and α-aminoamides: compounds with anticonvulsant activity in seizure models and inhibitory actions on central, peripheral, and cardiac isoforms of voltage-gated sodium channels.
AID1229806Toxicity in ip dosed Swiss mouse assessed as induction of motor performance impairment measured within 60 seconds measured at 0.5 hrs of time to peak effect by Chimney test2015Journal of medicinal chemistry, Jul-09, Volume: 58, Issue:13
Design, synthesis, and anticonvulsant activity of new hybrid compounds derived from 2-(2,5-dioxopyrrolidin-1-yl)propanamides and 2-(2,5-dioxopyrrolidin-1-yl)butanamides.
AID475787Anticonvulsant activity in ip dosed albino mouse assessed as protection against 6 Hz electric shock-induced seizures2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Lacosamide isothiocyanate-based agents: novel agents to target and identify lacosamide receptors.
AID480300Behavioral toxicity in po dosed Sprague-Dawley albino rat2010Journal of medicinal chemistry, May-13, Volume: 53, Issue:9
Merging the structural motifs of functionalized amino acids and alpha-aminoamides: compounds with significant anticonvulsant activities.
AID665943Neurotoxicity in ip dosed NMRI mouse after 30 mins by rotorod test2012Bioorganic & medicinal chemistry, Jun-01, Volume: 20, Issue:11
Synthesis, anticonvulsant activity, and neuropathic pain-attenuating activity of N-benzyl 2-amino-2-(hetero)aromatic acetamides.
AID475791Protective index, ratio of TD50 for ip dosed albino mouse to ED50 for protection against maximal electroshock-induced seizures in ip dosed albino mouse2009Journal of medicinal chemistry, Nov-12, Volume: 52, Issue:21
Lacosamide isothiocyanate-based agents: novel agents to target and identify lacosamide receptors.
AID443572Anticonvulsant activity against in ip dosed albino Sprague-Dawley rat hippocampal kindled seizure model assessed as after-discharge duration after 0.5 hrs2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Synthesis and anticonvulsant activities of (R)-N-(4'-substituted)benzyl 2-acetamido-3-methoxypropionamides.
AID1452162Anticonvulsant activity in Albino Swiss CD-1 mouse assessed as protection against maximal electroshock-induced seizures by measuring time to peak effect at 100 mg/kg, ip pretreated up to 2 hrs followed by 50 Hz current induction for 2 secs
AID441716Inhibition of human recombinant CA14 by stopped flow CO2 hydrase assay2010Journal of medicinal chemistry, Jan-28, Volume: 53, Issue:2
The coumarin-binding site in carbonic anhydrase accommodates structurally diverse inhibitors: the antiepileptic lacosamide as an example and lead molecule for novel classes of carbonic anhydrase inhibitors.
AID441707Inhibition of human recombinant CA3 by stopped flow CO2 hydrase assay2010Journal of medicinal chemistry, Jan-28, Volume: 53, Issue:2
The coumarin-binding site in carbonic anhydrase accommodates structurally diverse inhibitors: the antiepileptic lacosamide as an example and lead molecule for novel classes of carbonic anhydrase inhibitors.
AID1207560Inhibition of long-lasting type calcium current (hICa) in Chinese Hamster Ovary (CHO) cells expressing hCav1.2 measured using IonWorks Quattro automated patch clamp platform
AID619697Anticonvulsant activity in po dosed albino Sprague-Dawley rat assessed as protection against maximal electroshock seizure2011Journal of medicinal chemistry, Oct-13, Volume: 54, Issue:19
Primary amino acid derivatives: substitution of the 4'-N'-benzylamide site in (R)-N'-benzyl 2-amino-3-methylbutanamide, (R)-N'-benzyl 2-amino-3,3-dimethylbutanamide, and (R)-N'-benzyl 2-amino-3-methoxypropionamide provides potent anticonvulsants with pain
AID1432537Protection index, ratio of TD50 for motor impairment in ip dosed albino CD1 mouse to ED50 for protection against 32 mA current-induced seizure in ip dosed albino CD1 mouse by 6 Hz psychomotor test2017Bioorganic & medicinal chemistry letters, 03-15, Volume: 27, Issue:6
Synthesis and evaluation of anticonvulsant properties of new N-Mannich bases derived from pyrrolidine-2,5-dione and its 3-methyl-, 3-isopropyl, and 3-benzhydryl analogs.
AID441709Inhibition of human recombinant CA5A by stopped flow CO2 hydrase assay2010Journal of medicinal chemistry, Jan-28, Volume: 53, Issue:2
The coumarin-binding site in carbonic anhydrase accommodates structurally diverse inhibitors: the antiepileptic lacosamide as an example and lead molecule for novel classes of carbonic anhydrase inhibitors.
AID223109Anticonvulsant activity using MES test in mice after intraperitoneal administration2002Journal of medicinal chemistry, Oct-10, Volume: 45, Issue:21
Design and evaluation of affinity labels of functionalized amino acid anticonvulsants.
AID221080Neurologic toxicity using rotarod test in mice after intraperitoneal administration2002Journal of medicinal chemistry, Oct-10, Volume: 45, Issue:21
Design and evaluation of affinity labels of functionalized amino acid anticonvulsants.
AID1452159Anticonvulsant activity in ip dosed Albino Swiss CD-1 mouse assessed as protection against maximal electroshock-induced seizures pretreated up to 2 hrs followed by 50 Hz current induction for 2 secs measured at time to peak effect
AID1508628Confirmatory qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome: Secreted ER Calcium Modulated Protein (SERCaMP) assay2021Cell reports, 04-27, Volume: 35, Issue:4
A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
AID1347083qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: Viability assay - alamar blue signal for LASV Primary Screen2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347097qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Saos-2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347114qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for DAOY cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347089qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for TC32 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1296008Cytotoxic Profiling of Annotated Libraries Using Quantitative High-Throughput Screening2020SLAS discovery : advancing life sciences R & D, 01, Volume: 25, Issue:1
Cytotoxic Profiling of Annotated and Diverse Chemical Libraries Using Quantitative High-Throughput Screening.
AID1347129qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for SK-N-SH cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347093qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-MC cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347082qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: LASV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347126qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Rh30 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347090qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for DAOY cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347092qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for A673 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347086qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lymphocytic Choriomeningitis Arenaviruses (LCMV): LCMV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347424RapidFire Mass Spectrometry qHTS Assay for Modulators of WT P53-Induced Phosphatase 1 (WIP1)2019The Journal of biological chemistry, 11-15, Volume: 294, Issue:46
Physiologically relevant orthogonal assays for the discovery of small-molecule modulators of WIP1 phosphatase in high-throughput screens.
AID1347104qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for RD cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347099qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB1643 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347123qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Rh41 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347095qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB-EBc1 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347118qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for TC32 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347407qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Pharmaceutical Collection2020ACS chemical biology, 07-17, Volume: 15, Issue:7
High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1347096qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for U-2 OS cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347111qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for SK-N-MC cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1346986P-glycoprotein substrates identified in KB-3-1 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1508630Primary qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome: Secreted ER Calcium Modulated Protein (SERCaMP) assay2021Cell reports, 04-27, Volume: 35, Issue:4
A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
AID1347122qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for U-2 OS cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347425Rhodamine-PBP qHTS Assay for Modulators of WT P53-Induced Phosphatase 1 (WIP1)2019The Journal of biological chemistry, 11-15, Volume: 294, Issue:46
Physiologically relevant orthogonal assays for the discovery of small-molecule modulators of WIP1 phosphatase in high-throughput screens.
AID1347124qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for RD cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347128qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for OHS-50 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347115qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for NB-EBc1 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347125qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Rh18 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347094qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-37 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID651635Viability Counterscreen for Primary qHTS for Inhibitors of ATXN expression
AID1347098qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-SH cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347154Primary screen GU AMC qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347113qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for LAN-5 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1745845Primary qHTS for Inhibitors of ATXN expression
AID1347116qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for SJ-GBM2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347101qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-12 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347119qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for MG 63 (6-TG R) cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347109qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for NB1643 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347108qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh41 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347110qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for A673 cells)2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347121qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for control Hh wild type fibroblast cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347107qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh30 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347127qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Saos-2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347105qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for MG 63 (6-TG R) cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347112qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for BT-12 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347091qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SJ-GBM2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1508627Counterscreen qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome: GLuc-NoTag assay2021Cell reports, 04-27, Volume: 35, Issue:4
A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
AID1347106qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for control Hh wild type fibroblast cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347103qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for OHS-50 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1346987P-glycoprotein substrates identified in KB-8-5-11 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1347117qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for BT-37 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1508629Cell Viability qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome2021Cell reports, 04-27, Volume: 35, Issue:4
A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
AID1347100qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for LAN-5 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347102qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh18 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347411qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Mechanism Interrogation Plate v5.0 (MIPE) Libary2020ACS chemical biology, 07-17, Volume: 15, Issue:7
High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1346731Rat Nav1.2 (Voltage-gated sodium channels)2013Frontiers in pharmacology, , Volume: 4A thermosensitive mutation alters the effects of lacosamide on slow inactivation in neuronal voltage-gated sodium channels, NaV1.2.
AID1346742Rat Nav1.3 (Voltage-gated sodium channels)2008The Journal of pharmacology and experimental therapeutics, Jul, Volume: 326, Issue:1
Differential block of sensory neuronal voltage-gated sodium channels by lacosamide [(2R)-2-(acetylamino)-N-benzyl-3-methoxypropanamide], lidocaine, and carbamazepine.
AID1346760Rat Nav1.8 (Voltage-gated sodium channels)2008The Journal of pharmacology and experimental therapeutics, Jul, Volume: 326, Issue:1
Differential block of sensory neuronal voltage-gated sodium channels by lacosamide [(2R)-2-(acetylamino)-N-benzyl-3-methoxypropanamide], lidocaine, and carbamazepine.
AID1346749Human Nav1.7 (Voltage-gated sodium channels)2008The Journal of pharmacology and experimental therapeutics, Jul, Volume: 326, Issue:1
Differential block of sensory neuronal voltage-gated sodium channels by lacosamide [(2R)-2-(acetylamino)-N-benzyl-3-methoxypropanamide], lidocaine, and carbamazepine.
AID225116Anticonvulsant activity using MES test in rat after oral administration2002Journal of medicinal chemistry, Oct-10, Volume: 45, Issue:21
Design and evaluation of affinity labels of functionalized amino acid anticonvulsants.
AID687775Neurotoxicity in ip dosed NMRI mouse assessed as time of peak effect for minimal motor impairment after 30 mins2011Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13
Primary amino acid derivatives: compounds with anticonvulsant and neuropathic pain protection activities.
AID117857Protective index between TD50/MES ED50 when administered intraperitoneally to mouse1996Journal of medicinal chemistry, Apr-26, Volume: 39, Issue:9
Synthesis and anticonvulsant activities of N-Benzyl-2-acetamidopropionamide derivatives.
AID113014In vivo anticonvulsant activity in male albino mice using the maximal electroshock seizure(MES) test upon intraperitoneal administration; value ranges from 7.9 to 9.82002Journal of medicinal chemistry, Jun-20, Volume: 45, Issue:13
Quantitative structure-activity relationship analysis of functionalized amino acid anticonvulsant agents using k nearest neighbor and simulated annealing PLS methods.
AID480286Toxicity in ip dosed albino mouse after 0.25 hrs by rotarod test2010Journal of medicinal chemistry, May-13, Volume: 53, Issue:9
Merging the structural motifs of functionalized amino acids and alpha-aminoamides: compounds with significant anticonvulsant activities.
AID114630Compound was evaluated for anticonvulsant activity by maximal electroshock seizure test, intraperitoneally in mice2004Journal of medicinal chemistry, Apr-22, Volume: 47, Issue:9
Application of predictive QSAR models to database mining: identification and experimental validation of novel anticonvulsant compounds.
AID687767Anticonvulsant activity in ip dosed CF1 mouse assessed as time of peak effect for protection against maximal electroshock-induced seizure2011Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13
Primary amino acid derivatives: compounds with anticonvulsant and neuropathic pain protection activities.
AID190119Neurotoxic toxicity against Rat was evaluated by rotarod test afte oral administration1996Journal of medicinal chemistry, Apr-26, Volume: 39, Issue:9
Synthesis and anticonvulsant activities of N-Benzyl-2-acetamidopropionamide derivatives.
AID124082In vivo anticonvulsant activity in male albino mice using the maximal electroshock seizure(MES) test upon intraperitoneal administration, expressed as logarithm of effective dose2002Journal of medicinal chemistry, Jun-20, Volume: 45, Issue:13
Quantitative structure-activity relationship analysis of functionalized amino acid anticonvulsant agents using k nearest neighbor and simulated annealing PLS methods.
AID687765Anticonvulsant activity in ip dosed CF1 mouse assessed as protection against maximal electroshock-induced seizure after 30 mins2011Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13
Primary amino acid derivatives: compounds with anticonvulsant and neuropathic pain protection activities.
AID221080Neurologic toxicity using rotarod test in mice after intraperitoneal administration2002Journal of medicinal chemistry, Oct-10, Volume: 45, Issue:21
Design and evaluation of affinity labels of functionalized amino acid anticonvulsants.
AID223724Neurologic toxicity using rotarod test in rat after oral administration2002Journal of medicinal chemistry, Oct-10, Volume: 45, Issue:21
Design and evaluation of affinity labels of functionalized amino acid anticonvulsants.
AID223109Anticonvulsant activity using MES test in mice after intraperitoneal administration2002Journal of medicinal chemistry, Oct-10, Volume: 45, Issue:21
Design and evaluation of affinity labels of functionalized amino acid anticonvulsants.
AID113858Effective dose against maximal electroshock seizure in mice after intraperitoneal administration1996Journal of medicinal chemistry, Apr-26, Volume: 39, Issue:9
Synthesis and anticonvulsant activities of N-Benzyl-2-acetamidopropionamide derivatives.
AID226539Protective index as the ratio of TD50 value to that of ED50 value in rat.2002Journal of medicinal chemistry, Oct-10, Volume: 45, Issue:21
Design and evaluation of affinity labels of functionalized amino acid anticonvulsants.
AID480288Protective index, ratio of TD50 for albino mouse to anticonvulsant ED50 for albino mouse2010Journal of medicinal chemistry, May-13, Volume: 53, Issue:9
Merging the structural motifs of functionalized amino acids and alpha-aminoamides: compounds with significant anticonvulsant activities.
AID122000Neurotoxic toxicity was evaluated by rotarod test after intraperitoneal administration1996Journal of medicinal chemistry, Apr-26, Volume: 39, Issue:9
Synthesis and anticonvulsant activities of N-Benzyl-2-acetamidopropionamide derivatives.
AID480278Anticonvulsant activity in ip dosed albino mouse assessed as inhibition of maximal electroshock-induced seizures after 0.5 hrs2010Journal of medicinal chemistry, May-13, Volume: 53, Issue:9
Merging the structural motifs of functionalized amino acids and alpha-aminoamides: compounds with significant anticonvulsant activities.
AID189456Protective index between TD50/MES ED50 when administered orally to rat1996Journal of medicinal chemistry, Apr-26, Volume: 39, Issue:9
Synthesis and anticonvulsant activities of N-Benzyl-2-acetamidopropionamide derivatives.
AID226538Protective index as the ratio of TD50 value to that of ED50 value in mice.2002Journal of medicinal chemistry, Oct-10, Volume: 45, Issue:21
Design and evaluation of affinity labels of functionalized amino acid anticonvulsants.
AID178377Effective dose against maximal electroshock seizure in rat after oral administration1996Journal of medicinal chemistry, Apr-26, Volume: 39, Issue:9
Synthesis and anticonvulsant activities of N-Benzyl-2-acetamidopropionamide derivatives.
AID687774Neurotoxicity in ip dosed NMRI mouse assessed as minimal motor impairment after 30 mins2011Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13
Primary amino acid derivatives: compounds with anticonvulsant and neuropathic pain protection activities.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (706)

TimeframeStudies, This Drug (%)All Drugs %
pre-19900 (0.00)18.7374
1990's2 (0.28)18.2507
2000's47 (6.66)29.6817
2010's467 (66.15)24.3611
2020's190 (26.91)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 104.88

According to the monthly volume, diversity, and competition of internet searches for this compound, as well the volume and growth of publications, there is estimated to be very strong demand-to-supply ratio for research on this compound.

MetricThis Compound (vs All)
Research Demand Index104.88 (24.57)
Research Supply Index6.71 (2.92)
Research Growth Index6.65 (4.65)
Search Engine Demand Index188.94 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (104.88)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials90 (12.38%)5.53%
Trials0 (0.00%)5.53%
Reviews107 (14.72%)6.00%
Reviews0 (0.00%)6.00%
Case Studies115 (15.82%)4.05%
Case Studies0 (0.00%)4.05%
Observational32 (4.40%)0.25%
Observational0 (0.00%)0.25%
Other383 (52.68%)84.16%
Other6 (100.00%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (97)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
Lacosamide Effects on Alcohol Self Administration and Craving in Heavy Drinkers [NCT03271528]Phase 166 participants (Actual)Interventional2018-04-15Completed
Phase IV Study of Cognitive and Behavioral Effects of Lacosamide as Adjunctive Therapy in Patients With Partial Epilepsy [NCT01175954]Phase 432 participants (Actual)Interventional2010-05-31Completed
COMPARISON OF EFFICACY OF DICLOFENAC VERSUS DICLOFENAC PLUS CODEINE AND DICLOFENAC PLUS LACOSAMIDE IN ACUTE SCIATICA [NCT05626140]Phase 3120 participants (Actual)Interventional2021-09-28Completed
A Multi-Centre, Randomized, Double-Blind, Placebo Controlled Pilot Trial to Assess the Efficacy, Safety, and Tolerability of SPM 927 in Subjects With Postherpetic Neuralgia (PHN). [NCT00861068]Phase 244 participants (Actual)Interventional2002-02-28Completed
A Multicenter, Double-blind, Double-dummy, Randomized Trial to Investigate the Safety, Tolerability and Pharmacokinetics of Intravenous SPM 927 as Replacement for Oral SPM 927 in Subjects With Partial Seizures With or Without Secondary Generalization [NCT00800215]Phase 260 participants (Actual)Interventional2004-03-04Completed
A Multi-Center, Open-Label, Follow-On Trial to Assess the Long Term Safety and Efficacy of SPM 927 in Subjects With Painful Distal Diabetic Neuropathy [NCT00235443]Phase 2/Phase 3451 participants (Actual)Interventional2004-09-30Completed
Open-label Clinical Trial: Safety of Lacosamide in Patients With Amyotrophic Lateral Sclerosis [NCT03186040]Phase 1/Phase 27 participants (Actual)Interventional2017-07-13Completed
Combined Effect of Pregabalin and Oxycodone, and Lacosamide and Oxycodone, on Breathing: an Exploratory Study in Healthy Volunteers (The Polo Study) [NCT05598905]Phase 424 participants (Anticipated)Interventional2022-10-10Recruiting
An Open-label, Multicenter Extension Study to Evaluate the Long-term Safety and Efficacy of Lacosamide as Adjunctive Therapy for Uncontrolled Primary Generalized Tonic-Clonic Seizures in Subjects With Idiopathic Generalized Epilepsy [NCT02408549]Phase 3239 participants (Actual)Interventional2015-08-03Completed
Open Label Trial of Add on Lacosamide Versus High Dose Monotherapy in Patients With a Seizure Disorder [NCT01345058]Phase 356 participants (Actual)Interventional2011-08-01Completed
A Phase I, Randomized Double-blind, Placebo-controlled, Single-center, Single-dose, Three-way Cross-over Study to Evaluate the Safety, Tolerability, and Pharmacokinetics of Lacosamide Tablets in Healthy Male Chinese and Japanese Subjects [NCT01375387]Phase 133 participants (Actual)Interventional2011-03-31Completed
Phase II Trial of Seizure Prophylaxis in Brain Tumor Patients Undergoing Neurosurgical Procedure [NCT03436433]Phase 24 participants (Actual)Interventional2019-01-31Terminated(stopped due to Did not enroll as planned)
Pharmacokinetics of Antiepileptic Drugs in Critically Ill Patients Undergoing Continuous Renal Replacement Therapy [NCT03632915]18 participants (Actual)Observational2017-11-20Completed
[NCT01382017]18 participants (Actual)Interventional2011-06-30Completed
A Multicenter, Open-label, Follow-up Study to Assess the Long-term Use of Lacosamide (Flexible Dose From 200 to 600 mg/Day) Used as Monotherapy in Subjects Who Completed SP0994 and Received Lacosamide Monotherapy Treatment [NCT02582866]Phase 3106 participants (Actual)Interventional2016-01-31Completed
Efficacy and Safety of Rapid Titration Protocols of Lacosamide: An Exploratory Study [NCT03607851]Phase 475 participants (Actual)Interventional2018-08-03Completed
Effect of Antiseizure Medication in Seizure Networks at Early Stages of Acute Brain Injury. The Rs-fMRI, Open-label Pilot Trial [NCT06081283]Phase 454 participants (Anticipated)Interventional2023-11-20Recruiting
Safety and Efficacy of Lacosamide Versus Propranolol in Migraine [NCT05851781]Phase 3600 participants (Actual)Interventional2022-06-01Completed
Drugs in Breast Milk [NCT05543122]304 participants (Anticipated)Observational2022-03-09Recruiting
A Multicenter, Open-Label, Randomized, Active Comparator Study to Evaluate the Efficacy, Safety, and Pharmacokinetics of Lacosamide in Neonates With Repeated Electroencephalographic Neonatal Seizures [NCT04519645]Phase 232 participants (Anticipated)Interventional2021-03-31Recruiting
A Multicenter, Open-label Extension Trial to Assess the Long-term Safety and Tolerability of Lacosamide as Adjunctive Therapy in Subjects With Partial-onset Seizures [NCT00655486]Phase 397 participants (Actual)Interventional2008-04-30Completed
An Open-Label Study To Determine Safety, Tolerability And Efficacy Of Long -Term Oral Lacosamide (LCM) As Adjunctive Therapy In Children With Epilepsy [NCT00938912]Phase 2366 participants (Actual)Interventional2009-12-09Completed
A Multicenter, Open Label Study to Evaluate the Tolerability, Safety and Efficacy of Lacosamide (200mg - 400mg/Day) as add-on Therapy for Patients With Partial Onset Epilepsy Using a Flexible Dose-escalation Schedule and Individualized Maintenance Doses [NCT01235403]Phase 4100 participants (Actual)Interventional2010-06-30Completed
An Open-label Extension Trial to Determine Safety and Efficacy of Long-term Oral SPM 927 in Patients With Partial Seizures [NCT00522275]Phase 3308 participants (Actual)Interventional2004-10-31Completed
A Randomized, Double-Blind Placebo Controlled Trial to Investigate Safety and Efficacy of SPM927 in Painful Diabetic Neuropathy [NCT00861445]Phase 2119 participants (Actual)Interventional2001-06-30Completed
SUPER-refractory Status Epilepticus After Cardiac Arrest: a Multicenter, Retrospective, Cohort Study of Dual Anti-glutamate Therapy With Ketamine and Perampanel [NCT05756621]80 participants (Anticipated)Observational2022-01-15Recruiting
A Non-interventional, Observational Study Evaluating Changes in Drug Load and Seizure Frequency Using Vimpat (Lacosamide) in Daily Clinical Practice in Combination Therapy With Sodium Channel Blocking Anti-epileptic Drugs (AEDs) or Non Sodium Channel Bloc [NCT01673282]315 participants (Actual)Observational2012-07-31Completed
Compassionate Use Program With Lacosamide in Patients With Partial-onset or Generalized Tonic-clonic Seizures ≥16 Years of Age Coming From the SP0994 Study [NCT03559673]0 participants Expanded AccessNo longer available
A Clinical Study Exploring Lacosamide and Levetiracetam in Improving Cognitive in Patients With Alzheimer's Disease and Epilepsy [NCT05969054]Phase 4140 participants (Anticipated)Interventional2023-07-05Recruiting
An International Open-label Extension Trial to Determine Safety and Efficacy of Long-term Oral Lacosamide (SPM 927) in Patients With Partial Seizures [NCT00515619]Phase 3376 participants (Actual)Interventional2004-12-31Completed
A Multicenter, Randomized, Double-blind, Placebo-controlled Trial to Assess the Efficacy and Safety of 100mg/Day and 300mg/Day Lacosamide for Migraine Prophylaxis. [NCT00440518]Phase 2218 participants (Actual)Interventional2007-02-28Completed
A Parallel, Randomized, Double-Blind, Placebo-Controlled, Multicenter Proof of Concept Trial to Assess the Efficacy and Safety of 400 mg/Day Lacosamide Tablets in Subjects With Signs and Symptoms Associated With Fibromyalgia Syndrome [NCT00401830]Phase 2159 participants (Actual)Interventional2006-10-31Completed
An Open-label Continuation Trial to Assess the Continued Efficacy and Safety of Ascending Doses of Lacosamide in Subjects With Chronic Refractory Neuropathic Pain [NCT00237458]Phase 27 participants (Actual)Interventional2001-05-31Completed
An Open Label, Balanced, Randomized, Two-Treatment, Two-Period, Two-Sequence, Two-way Crossover, Oralcomparative Pharmacokinetic(PK)Study of Lacosamide Extended-Release Tablets , Adult, Human Subjects Under Fasting Conditions. [NCT05788159]Phase 116 participants (Anticipated)Interventional2023-04-01Not yet recruiting
Post-Authorization Safety Study to Evaluate the Long-Term Safety and Tolerability of Vimpat® (Lacosamide) as Add-On Therapy in Epilepsy Patients With Partial-Onset Seizures Who Are Uncontrolled on Current Therapy [NCT00771927]1,005 participants (Actual)Observational2008-10-31Completed
A Multicenter, Randomized, Double-blind, Placebo-controlled Trial to Assess the Efficacy and Safety of 400mg/Day Lacosamide in Subjects With Osteoarthritis of the Knee [NCT00485472]Phase 2194 participants (Actual)Interventional2007-03-31Terminated(stopped due to Based on the outcome of the planned first interim analysis, it was decided not to continue the trial. No safety concerns were identified.)
A Multicenter, Open-label Trial to Assess the Long-term Safety and Efficacy of Lacosamide in Subjects With Painful Diabetic Neuropathy [NCT00220337]Phase 3371 participants (Actual)Interventional2004-12-21Completed
A Multicenter, Open-Label, Follow-Up Study to Assess the Long-Term Use of Oral Lacosamide in Study Participants Who Completed EP0034 or SP848 and Received Lacosamide Treatment [NCT04627285]Phase 348 participants (Actual)Interventional2020-12-28Active, not recruiting
A Multicenter, Open-Label Study to Investigate the Safety and Tolerability of Intravenous Lacosamide in Children (>= 1 Month to < 17 Years of Age) With Epilepsy [NCT02710890]Phase 2/Phase 3103 participants (Actual)Interventional2017-05-30Completed
A Pilot Placebo-controlled Human Laboratory Feasibility Study of Lacosamide Effects in Alcohol Use Disorder [NCT03897348]Phase 24 participants (Actual)Interventional2018-09-17Completed
IV Lacosamide: The Safety of Intravenous Lacosamide [NCT00832884]Phase 440 participants (Actual)Interventional2010-03-31Completed
A Single Center Open-label, Randomized, Single-dose, 3-way Crossover Study to Compare the Safety, Tolerability, and Pharmacokinetics of Lacosamide Administered as Oral Tablet or Intravenous Infusion in Healthy Japanese Subjects [NCT01986608]Phase 126 participants (Actual)Interventional2013-11-30Completed
An Open-label follow-on Trial to Assess the Long-term Safety and Efficacy of Oral SPM 927 in Subjects With Diabetic Neuropathy [NCT00861042]Phase 269 participants (Actual)Interventional2002-04-30Completed
A Multicenter, Open-label Extension Trial to Assess the Long-term Use of Lacosamide Monotherapy and Safety of Lacosamide Monotherapy and Adjunctive Therapy in Subjects With Partial-onset Seizures [NCT00530855]Phase 3322 participants (Actual)Interventional2008-02-29Completed
Efficacy, Safety and Tolerability of Lacosamide in Patients With Gain-of-function Nav1.7 Mutations Related Small Fiber Neuropathy: a Randomized, Double-blind, Placebo Controlled, Crossover Trial [NCT01911975]Phase 325 participants (Actual)Interventional2014-09-30Completed
IV Lacosamide: The Safety of Intravenous Lacosamide [NCT01981447]Phase 340 participants (Actual)Interventional2010-04-30Completed
A Multicenter, Open-Label Study To Investigate The Safety, Tolerability, And Pharmacokinetics Of Lacosamide (LCM) Oral Solution (Syrup) As Adjunctive Therapy In Children With Partial-Onset Seizures [NCT00938431]Phase 247 participants (Actual)Interventional2009-11-30Completed
An Open-Label Extension Study to Assess the Safety and Seizure Frequency Associated With Long-Term Oral Lacosamide for Uncontrolled Primary Generalized Tonic-Clonic Seizures in Subjects With Idiopathic Generalized Epilepsy [NCT01118962]Phase 239 participants (Actual)Interventional2010-08-31Completed
A Multi-center, Open-label, follow-on Trial to Assess the Long-term Safety and Efficacy of Lacosamide in Subjects With Painful Distal Diabetic Neuropathy Including a Double-blind, Randomized Time Point Withdrawal Subtrial. [NCT00546351]Phase 3621 participants (Actual)Interventional2004-05-31Completed
A Multicenter, Open-label Trial to Assess the Safety and Tolerability of a Single Intravenous Loading Dose of Lacosamide Followed by Oral Lacosamide Maintenance as Adjunctive Therapy in Subjects With Partial-onset Seizures [NCT00655551]Phase 3100 participants (Actual)Interventional2008-04-30Completed
Evaluation of Efficacy and Safety of Levetiracetam, Lacosamide and Ketamine as Adjunctive Treatment of Refractory Status Epilepticus [NCT02726867]Phase 30 participants (Actual)Interventional2014-02-28Withdrawn(stopped due to No participants enrolled)
A Historical-controlled, Multicenter, Double-blind, Randomized Trial to Assess the Efficacy and Safety of Conversion to Lacosamide 400 mg/Day Monotherapy in Subjects With Partial-onset Seizures [NCT00520741]Phase 3426 participants (Actual)Interventional2007-08-31Completed
An Open-Label Pilot Study to Assess the Safety of Oral Lacosamide as Adjunctive Therapy for Uncontrolled Primary Generalized Tonic-Clonic Seizures in Subjects With Idiopathic Generalized Epilepsy [NCT01118949]Phase 249 participants (Actual)Interventional2010-05-31Completed
"Searching for Sleep Friendly Therapies for a Sleepy Population: A Double-Blind, Placebo-Controlled, Randomized Trial to Assess the Effects of Lacosamide on Sleep and Wake in Adults With Focal Epilepsy" [NCT01190098]Phase 459 participants (Actual)Interventional2010-08-31Completed
A Single-Center, Open-Label, Randomized, Single-Oral Dose, 2-Way Cross-Over Study to Investigate the Bioequivalence Between Lacosamide Tablet and Dry Syrup in Healthy Male Japanese Subjects [NCT02972125]Phase 124 participants (Actual)Interventional2016-11-30Completed
Observational Retrospective Study of Effectivity and Tolerability in Patients With Lacosamide Medication [NCT01858870]860 participants (Actual)Observational2012-04-30Completed
Multi-center, Observational, Drug-utilization Study in Belgium to Evaluate the Use of VIMPAT® in Clinical Practice as Adjunctive Treatment of Partial Onset Epilepsy in Subjects Aged 16 and Older. [NCT01236001]192 participants (Actual)Observational2010-09-30Completed
A Multicenter, Double-blind, Double-dummy, Randomized, Positive- Controlled Study Comparing the Efficacy and Safety of Lacosamide (200 to 600 mg/Day) to Controlled Release Carbamazepine (400 to 1200 mg/Day), Used as Monotherapy in Subjects (≥ 16 Years) Ne [NCT01243177]Phase 3888 participants (Actual)Interventional2011-04-30Completed
An Open-Label, Multicenter, Multinational Study of Lacosamide as First Add-On Anti-epileptic Drug (AED) Treatment in Subjects With Partial-Onset Seizures [NCT00955357]Phase 4461 participants (Actual)Interventional2009-08-31Completed
STTEPP: Safety, Tolerability and Dose Limiting Toxicity of Lacosamide in Patients With Painful Chronic Pancreatitis [NCT05603702]Phase 124 participants (Anticipated)Interventional2023-03-17Recruiting
Single-center, Open-label, Randomized 2-way Crossover Study of the Effect of Lacosamide 200 mg Twice Daily on the Single-dose Pharmacokinetics and Pharmacodynamics of Warfarin (25 mg) in Healthy Male Volunteers [NCT01526083]Phase 116 participants (Actual)Interventional2012-01-31Completed
A Multicenter, Randomized, Double-blind, Double-dummy, 2-period Crossover Study of Neuropsychological Effects of Lacosamide and Carbamazepine Immediate Release in Healthy Subjects [NCT01530022]Phase 160 participants (Actual)Interventional2012-05-31Completed
A Multicenter, Open-label Study to Determine the Effects of Lacosamide on Sleep in Healthy Subjects [NCT01530386]Phase 125 participants (Actual)Interventional2012-01-31Completed
The Effect of Lacosamide in Peripheral Neuropathic Pain: a Randomized, Double-blind, Placebo Controlled, Phenotype-stratified Study [NCT03777956]Phase 263 participants (Actual)Interventional2019-01-15Terminated(stopped due to COVID 19 and recruitment problems)
A Multicenter Clinical Study of Acute Sympotomatic Seizure Secondary to Autoimmune Encephalitis and Autoimmune-associated Epilepsy [NCT05422664]500 participants (Anticipated)Observational2018-01-01Enrolling by invitation
Efficacy of Lacosamide in Neonatal Status Epilepticus: A Randomized Controlled Study [NCT05291455]Phase 360 participants (Anticipated)Interventional2022-03-01Recruiting
Effects of Lacosamide on Post-operative Opioid Requirements After a Total Hip Arthroplasty: A Randomized Double -Blinded, Placebo-controlled Pilot Study. [NCT02342977]Phase 20 participants (Actual)Interventional2014-11-30Withdrawn(stopped due to We were unable to enroll any patients into the study.)
Multicenter, Open-label, Single-arm Study to Evaluate Hormone and Lipid Levels in Male Subjects With Partial-onset Seizures After a Switch of Treatment From Carbamazepine as Adjunctive Treatment to Levetiracetam to Lacosamide as Adjunctive Treatment to Le [NCT01375374]Phase 311 participants (Actual)Interventional2011-07-31Terminated(stopped due to Slow progress despite recruitment boosting efforts e.g., expert advice obtained from leading study center Investigators; decision thus made to terminate.)
A Multicenter, Open-label Study to Evaluate the Safety and Tolerability of Intravenous Lacosamide as Replacement for Oral Lacosamide in Japanese Adults With Partial-onset Seizures With or Without Secondary Generalization [NCT02192814]Phase 39 participants (Actual)Interventional2014-06-30Completed
Comparative Clinical Study Evaluating the Possible Efficacy of Duloxetine, Gabapentin and Lacosamide on Oxaliplatin-Induced Peripheral Neuropathy in Cancer Patients [NCT05510856]Phase 490 participants (Anticipated)Interventional2022-09-01Recruiting
Lacosamid-i.v.-Register [NCT01620840]130 participants (Actual)Observational2011-06-30Completed
A Multicenter, Double-blind, Randomized, Placebo-controlled, Parallel-group Study to Evaluate the Efficacy and Safety of Lacosamide as Adjunctive Therapy in Japanese and Chinese Adults With Uncontrolled Partial-Onset Seizures With or Without Secondary Gen [NCT01710657]Phase 3548 participants (Actual)Interventional2012-09-30Completed
An Open-label Extension Trial to Determine Tolerability and Efficacy of Long-term Oral SPM 927 as Adjunctive Therapy in Patients With Partial Seizures [NCT00552305]Phase 2370 participants (Actual)Interventional2001-08-31Completed
A Multi-center,Open-label Real-world Study to Evaluate the Efficacy and Pharmaco-economics of Lacosamide as First Add-on Therapy for Adults and Children With Focal Onset Seizures [NCT04737837]200 participants (Anticipated)Observational [Patient Registry]2021-01-31Not yet recruiting
Utility of Intravenous Lacosamide Compared With Fosphenytoin in the Treatment of Patients With Frequent Nonconvulsive Seizures [NCT01458522]Phase 274 participants (Actual)Interventional2012-05-31Completed
International Multicenter, Double-blind, Randomized, Placebo-controlled Evaluation of the Efficacy and Safety of Lacosamide in the Treatment of Pediatric Patients With Focal Refractory Epilepsy. [NCT04144218]Phase 4300 participants (Anticipated)Interventional2019-11-08Recruiting
A Pilot Study of NSICU Assessment of Seizure Prophylaxis With Lacosamide [NCT01110187]11 participants (Actual)Interventional2010-05-31Terminated(stopped due to Lack of enrollement)
Single-site, Randomized, Double-blind, Placebo-controlled, Parallel-group, Single/Repeated Dose Trial to Evaluate the Pharmacokinetics and Safety/Tolerability of Lacosamide in 3 Dosages in Healthy Male Korean Subjects [NCT01450111]Phase 151 participants (Actual)Interventional2008-11-30Completed
Systematic Review: Retigabine for Adjunctive Therapy in Partial Epilepsy [NCT01587339]6,498 participants (Actual)Observational2010-09-30Completed
A Randomized, Open-Label, Single-Dose, 2-Period Crossover Study to Investigate the Bioequivalence of Lacosamide Tablet (200mg) and Syrup (10mg/ml) in Healthy Chinese Male Subjects [NCT03086382]Phase 124 participants (Actual)Interventional2017-02-27Completed
A Multicenter, Double-Blind, Randomized, Placebo-Controlled, Parallel-Group Study to Investigate the Efficacy and Safety of Lacosamide as Adjunctive Therapy in Subjects With Epilepsy >=1 Month to <4 Years of Age With Partial-Onset Seizures [NCT02477839]Phase 3255 participants (Actual)Interventional2015-06-05Completed
A Multi-center, Open-label, Uncontrolled, Long-term, Extension Study to Evaluate the Safety and Efficacy of Lacosamide as Adjunctive Therapy in Japanese and Chinese Adults With Partial-onset Seizures With or Without Secondary Generalization [NCT01832038]Phase 3473 participants (Actual)Interventional2013-03-26Completed
a Randomized Pilot Study of Lacosamide's Effect on Calcitonin Gene-related Peptide in Migraine Patients [NCT05632133]Phase 3200 participants (Anticipated)Interventional2022-06-01Recruiting
A Double-blind, Randomized, Placebo-controlled, Parallel-Group, Multicenter Study to Evaluate the Efficacy and Safety of Lacosamide as Adjunctive Therapy for Uncontrolled Primary Generalized Tonic-Clonic Seizures in Subjects With Idiopathic Generalized Ep [NCT02408523]Phase 3242 participants (Actual)Interventional2015-04-30Completed
Open-label, Single Arm, Study Evaluating Tolerability and Efficacy of Lacosamide When Added to Levetiracetam With Withdrawal of Concomitant Sodium Channel Blocking Antiepileptic Drug in Subjects With Uncontrolled Partial-onset Seizures [NCT01484977]Phase 3120 participants (Actual)Interventional2011-12-31Completed
A Multicenter, Double-blind, Double-dummy, Follow up Study Evaluating the Long-term Safety of Lacosamide in Comparison With Controlled-release Carbamazepine Used as Monotherapy in Subjects With Partial-onset or Generalized Tonic-clonic Seizures ≥16 Years [NCT01465997]Phase 3551 participants (Actual)Interventional2012-05-31Completed
Multicenter, Open-Label, Long-Term Study to Investigate the Safety of Conversion to Lacosamide at Doses up to 600 mg/Day as Monotherapy in Japanese Adults With Partial-Onset Seizures With or Without Secondary Generalization [NCT02124564]Phase 319 participants (Actual)Interventional2014-04-30Completed
Prospective, Randomized, Single-blinded Comparative Trial of IV Lacosamide Versus Phenytoin for Seizure Management [NCT02409433]Phase 43 participants (Actual)Interventional2014-08-31Terminated(stopped due to due to slow recruitment and budgetary restraints study was prematurely terminated)
A Multicenter, Open-label, Long-term Extension Study to Investigate the Efficacy and Safety of Lacosamide as Adjunctive Therapy in Pediatric Subjects With Epilepsy With Partial-Onset Seizures [NCT01964560]Phase 3540 participants (Actual)Interventional2014-08-13Completed
Pharmacovigilance in Gerontopsychiatric Patients [NCT02374567]Phase 3407 participants (Actual)Interventional2015-01-31Terminated
Randomized, Double-Blind, Placebo-Controlled Trial of Lacosamide for Seizure Prophylaxis in Patients With High-Grade Gliomas [NCT01432171]37 participants (Actual)Interventional2012-07-25Terminated
Lacosamide IV and EEG/EKG (LIVE) Study [NCT01724918]Phase 272 participants (Actual)Interventional2013-05-31Terminated(stopped due to Time limitation for recruitment exceeded. 72 of 90 estimated sample recruited.)
Population Pharmacokinetics of Antiepileptic in Pediatrics [NCT03196466]1,000 participants (Anticipated)Observational2017-06-19Recruiting
Open, Non-randomized, Sequential Group Comparison to Investigate the Pharmacokinetics, Safety, and Tolerability of 100 mg SPM 927 in Male and Female Subjects With Renal Impairment Including Subjects Requiring Dialysis Compared With Male and Female Healthy [NCT01796938]Phase 140 participants (Actual)Interventional2004-06-30Completed
A Multicenter, Double Blind, Randomized, Placebo Controlled, Parallel Group Study to Investigate the Efficacy and Safety of Lacosamide as Adjunctive Therapy in Subjects With Epilepsy ≥4 Years to <17 Years of Age With Partial Onset Seizures [NCT01921205]Phase 3404 participants (Actual)Interventional2013-08-29Completed
A MULTI-CENTER, OPEN-LABEL, EXPLORATORY STUDY TO INVESTIGATE THE SAFETY AND EFFICACY OF LACOSAMIDE AS ADJUNCTIVE THERAPY IN SUBJECTS ≥1 MONTH TO <18 YEARS WITH EPILEPSY SYNDROMES ASSOCIATED WITH GENERALIZED SEIZURES. [NCT01969851]Phase 255 participants (Actual)Interventional2014-02-13Completed
A Randomized, Open-Label, Single-Dose, 2-Way Crossover Study to Investigate the Bioequivalence of Lacosamide 200mg Administered as Intravenous Solution and Oral Tablet in Healthy Chinese Male Subjects [NCT03204474]Phase 130 participants (Actual)Interventional2017-06-08Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT00220337 (113) [back to overview]Percentage of Subjects With Marked Abnormalities in Physical Examination Findings After Start of Treatment.
NCT00220337 (113) [back to overview]Change in Different Symptoms of Neuropathic Pain From Visit 2 (Baseline) to Visit 9.1
NCT00220337 (113) [back to overview]Change in Different Symptoms of Neuropathic Pain From Visit 2 (Baseline) to Visit 9.0
NCT00220337 (113) [back to overview]Change in Different Symptoms of Neuropathic Pain From Visit 2 (Baseline) to Visit 6
NCT00220337 (113) [back to overview]Change in Different Symptoms of Neuropathic Pain From Visit 2 (Baseline) to Visit 4
NCT00220337 (113) [back to overview]Change in Different Symptoms of Neuropathic Pain From Visit 2 (Baseline) to Termination Visit
NCT00220337 (113) [back to overview]Change in Current Pain From Visit 2 (Baseline) to Each Subsequent Visit as Measured by a 100 mm Visual Analogue Scale (VAS)
NCT00220337 (113) [back to overview]Change in Average Pain Interference With Sleep From the Baseline Week to the 7 Days Prior to Each Visit
NCT00220337 (113) [back to overview]Change in Average Pain Interference With General Activity From the Baseline Week to the 7 Days Prior to Each Visit
NCT00220337 (113) [back to overview]Percentage of Subjects With Adverse Events (AE) Reported Spontaneously by the Subject or Observed by the Investigator
NCT00220337 (113) [back to overview]Percentage of Subjects Who Withdrew Due to Adverse Events (AEs)
NCT00220337 (113) [back to overview]Number of Subjects With Urine White Blood Cell Count 'Negative' at Baseline, Categorized by Urine White Blood Cell Count at Last Visit
NCT00220337 (113) [back to overview]Number of Subjects With Urine Urobilinogen Value 66 µmol/l at Baseline, Categorized by Urine Urobilinogen Value at Last Visit
NCT00220337 (113) [back to overview]Number of Subjects With Urine Urobilinogen Value 3 µmol/l at Baseline, Categorized by Urine Urobilinogen Value at Last Visit
NCT00220337 (113) [back to overview]Number of Subjects With Urine Urobilinogen Value 16 µmol/l at Baseline, Categorized by Urine Urobilinogen Value at Last Visit
NCT00220337 (113) [back to overview]Number of Subjects With Urine Protein Status 'Trace' at Baseline, Categorized by Urine Protein Status at Last Visit
NCT00220337 (113) [back to overview]Number of Subjects With Urine Protein Status 'Positive +++' at Baseline, Categorized by Urine Protein Status at Last Visit
NCT00220337 (113) [back to overview]Number of Subjects With Urine Protein Status 'Positive ++' at Baseline, Categorized by Urine Protein Status at Last Visit
NCT00220337 (113) [back to overview]Number of Subjects With Urine Protein Status 'Positive +' at Baseline, Categorized by Urine Protein Status at Last Visit
NCT00220337 (113) [back to overview]Number of Subjects With Urine Protein Status 'Negative' at Baseline, Categorized by Urine Protein Status at Last Visit
NCT00220337 (113) [back to overview]Number of Subjects With Urine pH= 8.0 at Baseline, Categorized by Urine pH at Last Visit
NCT00220337 (113) [back to overview]Change in Quality of Life From Visit 2 (Baseline) to Visit 9.6
NCT00220337 (113) [back to overview]Number of Subjects With Urine White Blood Cell Count 'Trace' at Baseline, Categorized by Urine White Blood Cell Count at Last Visit
NCT00220337 (113) [back to overview]Change in Quality of Life From Visit 2 (Baseline) to Visit 9.5
NCT00220337 (113) [back to overview]Number of Subjects With Urine White Blood Cell Count 'Positive ++' at Baseline, Categorized by Urine White Blood Cell Count at Last Visit
NCT00220337 (113) [back to overview]Change in Quality of Life From Visit 2 (Baseline) to Visit 9.4
NCT00220337 (113) [back to overview]Change in Quality of Life From Visit 2 (Baseline) to Visit 9.3
NCT00220337 (113) [back to overview]Change in Quality of Life From Visit 2 (Baseline) to Visit 9.2
NCT00220337 (113) [back to overview]Change in Quality of Life From Visit 2 (Baseline) to Visit 9.0
NCT00220337 (113) [back to overview]Change in Quality of Life From Visit 2 (Baseline) to Visit 6
NCT00220337 (113) [back to overview]Change in Quality of Life From Visit 2 (Baseline) to Visit 4
NCT00220337 (113) [back to overview]Change in Quality of Life From Visit 2 (Baseline) to Termination Visit
NCT00220337 (113) [back to overview]Change in Different Symptoms of Neuropathic Pain From Visit 2 (Baseline) to Visit 9.8
NCT00220337 (113) [back to overview]Change in Different Symptoms of Neuropathic Pain From Visit 2 (Baseline) to Visit 9.7
NCT00220337 (113) [back to overview]Change in Different Symptoms of Neuropathic Pain From Visit 2 (Baseline) to Visit 9.6
NCT00220337 (113) [back to overview]Change in Different Symptoms of Neuropathic Pain From Visit 2 (Baseline) to Visit 9.5
NCT00220337 (113) [back to overview]Change in Different Symptoms of Neuropathic Pain From Visit 2 (Baseline) to Visit 9.4
NCT00220337 (113) [back to overview]Change in Different Symptoms of Neuropathic Pain From Visit 2 (Baseline) to Visit 9.3
NCT00220337 (113) [back to overview]Change in Different Symptoms of Neuropathic Pain From Visit 2 (Baseline) to Visit 9.2
NCT00220337 (113) [back to overview]Number of Subjects With Urine pH= 7.5 at Baseline, Categorized by Urine pH at Last Visit
NCT00220337 (113) [back to overview]Number of Subjects With Urine pH= 7.0 at Baseline, Categorized by Urine pH at Last Visit
NCT00220337 (113) [back to overview]Number of Subjects With Urine pH= 6.5 at Baseline, Categorized by Urine pH at Last Visit
NCT00220337 (113) [back to overview]Number of Subjects With Urine pH= 6.0 at Baseline, Categorized by Urine pH at Last Visit
NCT00220337 (113) [back to overview]Number of Subjects With Urine pH= 5.0 at Baseline, Categorized by Urine pH at Last Visit
NCT00220337 (113) [back to overview]Number of Subjects With Urine Nitrite Status 'Positive' at Baseline, Categorized by Urine Nitrite Status at Last Visit
NCT00220337 (113) [back to overview]Number of Subjects With Urine Nitrite Status 'Negative' at Baseline, Categorized by Urine Nitrite Status at Last Visit
NCT00220337 (113) [back to overview]Percentage of Subjects With Presence of Spontaneous Pain Categorized by Duration of Pain at Visit 9.8
NCT00220337 (113) [back to overview]Percentage of Subjects With Presence of Spontaneous Pain Categorized by Duration of Pain at Visit 9.7
NCT00220337 (113) [back to overview]Percentage of Subjects With Presence of Spontaneous Pain Categorized by Duration of Pain at Visit 9.6
NCT00220337 (113) [back to overview]Percentage of Subjects With Presence of Spontaneous Pain Categorized by Duration of Pain at Visit 9.5
NCT00220337 (113) [back to overview]Percentage of Subjects With Presence of Spontaneous Pain Categorized by Duration of Pain at Visit 9.4
NCT00220337 (113) [back to overview]Percentage of Subjects With Presence of Spontaneous Pain Categorized by Duration of Pain at Visit 9.3
NCT00220337 (113) [back to overview]Percentage of Subjects With Presence of Spontaneous Pain Categorized by Duration of Pain at Visit 9.2
NCT00220337 (113) [back to overview]Percentage of Subjects With Presence of Spontaneous Pain Categorized by Duration of Pain at Visit 9.1
NCT00220337 (113) [back to overview]Percentage of Subjects With Presence of Spontaneous Pain Categorized by Duration of Pain at Visit 9.0
NCT00220337 (113) [back to overview]Percentage of Subjects With Presence of Spontaneous Pain Categorized by Duration of Pain at Visit 6
NCT00220337 (113) [back to overview]Percentage of Subjects With Presence of Spontaneous Pain Categorized by Duration of Pain at Visit 4
NCT00220337 (113) [back to overview]Number of Subjects With Urine White Blood Cell Count 'Positive +' at Baseline, Categorized by Urine White Blood Cell Count at Last Visit
NCT00220337 (113) [back to overview]Percentage of Subjects With Presence of Spontaneous Pain Categorized by Duration of Pain at Visit 2 (Baseline)
NCT00220337 (113) [back to overview]Percentage of Subjects With Presence of Spontaneous Pain Categorized by Duration of Pain at Termination Visit
NCT00220337 (113) [back to overview]Percentage of Subjects With Pain Attacks in Last the 24 Hours Categorized by Number of Pain Attacks at Visit 9.8
NCT00220337 (113) [back to overview]Percentage of Subjects With Pain Attacks in Last the 24 Hours Categorized by Number of Pain Attacks at Visit 9.7
NCT00220337 (113) [back to overview]Percentage of Subjects With Pain Attacks in Last the 24 Hours Categorized by Number of Pain Attacks at Visit 9.6
NCT00220337 (113) [back to overview]Percentage of Subjects With Pain Attacks in Last the 24 Hours Categorized by Number of Pain Attacks at Visit 9.5
NCT00220337 (113) [back to overview]Percentage of Subjects With Pain Attacks in Last the 24 Hours Categorized by Number of Pain Attacks at Visit 9.4
NCT00220337 (113) [back to overview]Percentage of Subjects With Pain Attacks in Last the 24 Hours Categorized by Number of Pain Attacks at Visit 9.3
NCT00220337 (113) [back to overview]Percentage of Subjects With Pain Attacks in Last the 24 Hours Categorized by Number of Pain Attacks at Visit 9.2
NCT00220337 (113) [back to overview]Percentage of Subjects With Pain Attacks in Last the 24 Hours Categorized by Number of Pain Attacks at Visit 9.1
NCT00220337 (113) [back to overview]Percentage of Subjects With Pain Attacks in Last the 24 Hours Categorized by Number of Pain Attacks at Visit 9.0
NCT00220337 (113) [back to overview]Percentage of Subjects With Pain Attacks in Last the 24 Hours Categorized by Number of Pain Attacks at Visit 6
NCT00220337 (113) [back to overview]Percentage of Subjects With Pain Attacks in Last the 24 Hours Categorized by Number of Pain Attacks at Visit 4
NCT00220337 (113) [back to overview]Percentage of Subjects With Pain Attacks in Last the 24 Hours Categorized by Number of Pain Attacks at Visit 2 (Baseline)
NCT00220337 (113) [back to overview]Percentage of Subjects With Pain Attacks in Last the 24 Hours Categorized by Number of Pain Attacks at Termination Visit
NCT00220337 (113) [back to overview]Percentage of Subjects With Marked Abnormalities in Vital Signs After Start of Treatment
NCT00220337 (113) [back to overview]Number of Subjects With Urine Ketone Status 'Trace' at Baseline, Categorized by Urine Ketone Status at Last Visit
NCT00220337 (113) [back to overview]Percentage of Subjects With Marked Abnormalities in Neurological Examination Findings After Start of Treatment
NCT00220337 (113) [back to overview]Percentage of Subjects With Marked Abnormalities in Hematology Parameters After Start of Treatment During the Titration Period
NCT00220337 (113) [back to overview]Percentage of Subjects With Marked Abnormalities in Hematology Parameters After Start of Treatment During the Maintenance Period
NCT00220337 (113) [back to overview]Percentage of Subjects With Marked Abnormalities Clinical Chemistry Parameters After Start of Treatment During the Titration Period
NCT00220337 (113) [back to overview]Percentage of Subjects With Marked Abnormalities Clinical Chemistry Parameters After Start of Treatment During the Maintenance Period
NCT00220337 (113) [back to overview]Percentage of Subjects With Abnormal Electrocardiogram (ECG) Findings
NCT00220337 (113) [back to overview]Percentage of Patients With Categorized Patient's Global Impression of Change in Pain (PGIC) at Visit 9.8
NCT00220337 (113) [back to overview]Percentage of Patients With Categorized Patient's Global Impression of Change in Pain (PGIC) at Visit 9.7
NCT00220337 (113) [back to overview]Percentage of Patients With Categorized Patient's Global Impression of Change in Pain (PGIC) at Visit 9.6
NCT00220337 (113) [back to overview]Percentage of Patients With Categorized Patient's Global Impression of Change in Pain (PGIC) at Visit 9.5
NCT00220337 (113) [back to overview]Percentage of Patients With Categorized Patient's Global Impression of Change in Pain (PGIC) at Visit 9.4
NCT00220337 (113) [back to overview]Percentage of Patients With Categorized Patient's Global Impression of Change in Pain (PGIC) at Visit 9.3
NCT00220337 (113) [back to overview]Percentage of Patients With Categorized Patient's Global Impression of Change in Pain (PGIC) at Visit 9.2
NCT00220337 (113) [back to overview]Number of Subjects With Urine Ketone Status 'Small' at Baseline, Categorized by Urine Ketone Status at Last Visit
NCT00220337 (113) [back to overview]Number of Subjects With Urine Ketone Status 'Negative' at Baseline, Categorized by Urine Ketone Status at Last Visit
NCT00220337 (113) [back to overview]Number of Subjects With Urine Ketone Status 'Moderate' at Baseline, Categorized by Urine Ketone Status at Last Visit
NCT00220337 (113) [back to overview]Number of Subjects With Urine Glucose Value 55 mmol/l at Baseline, Categorized by Urine Glucose Value at Last Visit
NCT00220337 (113) [back to overview]Number of Subjects With Urine Glucose Value 5.5 mmol/l at Baseline, Categorized by Urine Glucose Value at Last Visit
NCT00220337 (113) [back to overview]Percentage of Patients With Categorized Patient's Global Impression of Change in Pain (PGIC) at Visit 9.1
NCT00220337 (113) [back to overview]Percentage of Patients With Categorized Patient's Global Impression of Change in Pain (PGIC) at Visit 9.0
NCT00220337 (113) [back to overview]Percentage of Patients With Categorized Patient's Global Impression of Change in Pain (PGIC) at Visit 6
NCT00220337 (113) [back to overview]Percentage of Patients With Categorized Patient's Global Impression of Change in Pain (PGIC) at Visit 4
NCT00220337 (113) [back to overview]Percentage of Patients With Categorized Patient's Global Impression of Change in Pain (PGIC) at Termination Visit
NCT00220337 (113) [back to overview]Number of Subjects With Urine Glucose Value 28 mmol/l at Baseline, Categorized by Urine Glucose Value at Last Visit
NCT00220337 (113) [back to overview]Number of Subjects With Urine Glucose Value 14 mmol/l at Baseline, Categorized by Urine Glucose Value at Last Visit
NCT00220337 (113) [back to overview]Number of Subjects With Urine Glucose Value >=111 mmol/l at Baseline, Categorized by Urine Glucose Value at Last Visit
NCT00220337 (113) [back to overview]Number of Subjects With Urine Glucose Value 'Negative' at Baseline, Categorized by Urine Glucose Value at Last Visit
NCT00220337 (113) [back to overview]Number of Subjects With Urine Blood Status 'Trace (N)' at Baseline, Categorized by Urine Blood Status at Last Visit
NCT00220337 (113) [back to overview]Number of Subjects With Urine Blood Status 'Trace (H)' at Baseline, Categorized by Urine Blood Status at Last Visit
NCT00220337 (113) [back to overview]Number of Subjects With Urine Blood Status 'Positive ++' at Baseline, Categorized by Urine Blood Status at Last Visit
NCT00220337 (113) [back to overview]Number of Subjects With Urine Blood Status 'Positive +' at Baseline, Categorized by Urine Blood Status at Last Visit
NCT00220337 (113) [back to overview]Number of Subjects With Urine Blood Status 'Negative' at Baseline, Categorized by Urine Blood Status at Last Visit
NCT00220337 (113) [back to overview]Number of Subjects With Urine Bilirubin Status 'Positive ++' at Baseline, Categorized by Urine Bilirubin Status at Last Visit
NCT00220337 (113) [back to overview]Number of Subjects With Urine Bilirubin Status 'Positive +' at Baseline, Categorized by Urine Bilirubin Status at Last Visit
NCT00220337 (113) [back to overview]Number of Subjects With Urine Bilirubin Status 'Negative' at Baseline, Categorized by Urine Bilirubin Status at Last Visit
NCT00220337 (113) [back to overview]Change in Quality of Life From Visit 2 (Baseline) to Visit 9.8
NCT00220337 (113) [back to overview]Change in Quality of Life From Visit 2 (Baseline) to Visit 9.7
NCT00220337 (113) [back to overview]Change in Quality of Life From Visit 2 (Baseline) to Visit 9.1
NCT00235443 (18) [back to overview]Change From Baseline in Average Daily Pain Score Using an 11-point Likert Scale (0-10).
NCT00235443 (18) [back to overview]Change From Baseline in Average Pain Interference With Activity (11-point Likert Scale)
NCT00235443 (18) [back to overview]Change From Baseline in Average Pain Interference With Sleep (11-point Likert Scale)
NCT00235443 (18) [back to overview]Change From Baseline in Average Pain Score as Measured by a 100mm Visual Analogue Scale (VAS).
NCT00235443 (18) [back to overview]Change From Baseline in Quality of Life Using the SF-36 Health Survey - Mental Component Summary (MCS)
NCT00235443 (18) [back to overview]Change From Baseline in Quality of Life Using the SF-36 Health Survey - Physical Component Summary (PCS)
NCT00235443 (18) [back to overview]Number of Subjects With Adverse Events (AEs) Reported Spontaneously by the Subject or Observed by the Investigator.
NCT00235443 (18) [back to overview]Within-subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Cold
NCT00235443 (18) [back to overview]Within-subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Deep Pain
NCT00235443 (18) [back to overview]Within-subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Dullness
NCT00235443 (18) [back to overview]Within-subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Heat
NCT00235443 (18) [back to overview]Within-subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Intensity.
NCT00235443 (18) [back to overview]Within-subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Itchiness
NCT00235443 (18) [back to overview]Within-subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Sensitivity
NCT00235443 (18) [back to overview]Within-subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Sharpness
NCT00235443 (18) [back to overview]Within-subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Surface Pain
NCT00235443 (18) [back to overview]Within-subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Unpleasantness
NCT00235443 (18) [back to overview]Patient's Global Impression of Change (PGIC) From Baseline in Pain.
NCT00237458 (13) [back to overview]Number of Subjects Reporting At Least 1 Treatment-Emergent Adverse Event (TEAE) During The Treatment Period.
NCT00237458 (13) [back to overview]Number of Subjects Withdrawing From Study Due To A Treatment-Emergent Adverse Event (TEAE) During The Treatment Period.
NCT00237458 (13) [back to overview]Within-Subject Change In Average Daily Pain Score During the Treatment Period.
NCT00237458 (13) [back to overview]Within-Subject Change In The Perception Of Each Of The Individual Cardinal Symptoms of Pain During The Treatment Period - Allodynia.
NCT00237458 (13) [back to overview]Within-Subject Change In The Perception Of Each Of The Individual Cardinal Symptoms of Pain During The Treatment Period - Burning.
NCT00237458 (13) [back to overview]Within-Subject Change In The Perception Of Each Of The Individual Cardinal Symptoms of Pain During The Treatment Period - Numbness.
NCT00237458 (13) [back to overview]Within-Subject Change In The Perception Of Each Of The Individual Cardinal Symptoms of Pain During The Treatment Period - Paraesthesiae.
NCT00237458 (13) [back to overview]Within-Subject Change In The Perception Of Each Of The Individual Cardinal Symptoms of Pain During The Treatment Period - Shooting.
NCT00237458 (13) [back to overview]Investigator's Global Impression of Change In Pain During The Treatment Period.
NCT00237458 (13) [back to overview]Subject's Global Impression of Change In Pain During The Treatment Period.
NCT00237458 (13) [back to overview]"Percentage of Days With Concomitant Pain (Rescue) Medications Taken During Baseline Phase."
NCT00237458 (13) [back to overview]"Percentage of Days With Concomitant Pain (Rescue) Medications Taken During Titration and Treatment Phases."
NCT00237458 (13) [back to overview]"Percentage of Days With Concomitant Pain (Rescue) Medications Taken During Titration Phase."
NCT00401830 (14) [back to overview]Change From Baseline in Fibromyalgia Impact Questionnaire (FIQ) Total Score to the Last Assessment in the 12-week Treatment Phase
NCT00401830 (14) [back to overview]Change From Baseline in Morning Pain Score to the Last 2 Weeks of the 12-week Treatment Phase
NCT00401830 (14) [back to overview]Change From Baseline in Total Myalgic Score to the Last Assessment in the 12-week Treatment Phase
NCT00401830 (14) [back to overview]Lacosamide Plasma Concentration at the End of the Maintenance Phase/ Week 12
NCT00401830 (14) [back to overview]Percentage of Patients Using Alcohol for Pain During the 12-week Treatment Phase
NCT00401830 (14) [back to overview]Percentage of Patients Using Rescue Medication During the 12-week Treatment Phase
NCT00401830 (14) [back to overview]Change From Baseline in Fibromyalgia Symptom Scores to the Last Assessment in the 12-week Treatment Phase
NCT00401830 (14) [back to overview]Change From Baseline in Hospital Anxiety and Depression Scale (HADS) Scores to the Last Assessment in the 12-week Treatment Phase
NCT00401830 (14) [back to overview]Patient Global Impression of Change (PGIC) Assessment From Baseline to the Last Assessment in the 12-week Treatment Phase
NCT00401830 (14) [back to overview]Change From Baseline in Evening Pain Score to the Last 2 Weeks of the 12-week Treatment Phase
NCT00401830 (14) [back to overview]Change From Baseline in Daily Interference With General Activity to the Last 2 Weeks of the 12-week Treatment Phase
NCT00401830 (14) [back to overview]Change From Baseline in Average Daily Pain Score to the Last 2 Weeks of the 12-week Treatment Phase (Based on the Per Protocol Set)
NCT00401830 (14) [back to overview]Change From Baseline in Average Daily Pain Score to the Last 2 Weeks of the 12-week Treatment Phase (Based on the Full Analysis Set)
NCT00401830 (14) [back to overview]Change From Baseline in Average Daily Interference With Sleep to the Last 2 Weeks of the 12-week Treatment Phase
NCT00440518 (5) [back to overview]Change From Baseline in Mean Migraine Headache Rates During the Last 4 Weeks of the Maintenance Period
NCT00440518 (5) [back to overview]Change From Baseline in Mean Migraine Headache Rates During the Entire 14-week Maintenance Period
NCT00440518 (5) [back to overview]Number of Subjects Who Experience a 50 Percent or Greater Reduction From Baseline in Migraine Frequency During the Last 4 Weeks of the Maintenance Period.
NCT00440518 (5) [back to overview]Number of Subjects Who Experience a 50 Percent or Greater Reduction From Baseline in Migraine Frequency During the Entire 14-week Maintenance Period.
NCT00440518 (5) [back to overview]Changes From Baseline in Improvement of Function and Reduction of Disability Using the Headache Impact Test (HIT-6)
NCT00485472 (9) [back to overview]Patient's Global Impression of Change From Baseline at the End of 8 Week Maintenance Period.
NCT00485472 (9) [back to overview]Response at the End of 8 Week Maintenance Period Versus Baseline Based on the (Slightly Modified)Criteria of the Osteoarthritis Research Society International (OARSI) and the Outcome Measures in Rheumatology Initiative (OMERACT).
NCT00485472 (9) [back to overview]Amount of Rescue Medication Use During 8 Week Maintenance Period.
NCT00485472 (9) [back to overview]Change From Baseline to End of 8 Week Maintenance Period in Perception of Pain Interference With Subject's Sleep.
NCT00485472 (9) [back to overview]Change From Baseline to End of 8 Week Maintenance Period in Profile of Mood States (Total Mood Disturbance Score).
NCT00485472 (9) [back to overview]Change From Baseline to End of 8 Week Maintenance Period in Total WOMAC Score.
NCT00485472 (9) [back to overview]Change From Baseline to End of 8 Week Maintenance Period in WOMAC Physical Function Subscale Score.
NCT00485472 (9) [back to overview]Change From Baseline to End of 8 Week Maintenance Period in WOMAC Stiffness Subscale Score.
NCT00485472 (9) [back to overview]Change of the Western Ontario and McMaster Universities (WOMAC) Pain Subscale Score (Visual Analogue Scale Version) From Baseline to the End of the 8 Week Maintenance Period
NCT00515619 (5) [back to overview]Number of Subjects Reporting at Least 1 Treatment-emergent Adverse Event (TEAE) During the Treatment Period (up to 5.5 Years)
NCT00515619 (5) [back to overview]Percentage of at Least 50% Responders During the Treatment Period (up to 5.5 Years)
NCT00515619 (5) [back to overview]Number of Subjects Prematurely Discontinuing Due to a Treatment-emergent Adverse Event (TEAE) During the Treatment Period (up to 5.5 Years)
NCT00515619 (5) [back to overview]Median Percentage Change From Baseline in 28-day Seizure Frequency During the Treatment Period (up to 5.5 Years)
NCT00515619 (5) [back to overview]Number of Subjects Reporting at Least 1 Serious Adverse Event (SAE) During the Treatment Period (up to 5.5 Years)
NCT00520741 (6) [back to overview]Duration of Monotherapy Treatment During the Monotherapy Phase of The Maintenance Period (Visit 9 - Visit 12)
NCT00520741 (6) [back to overview]Percentage of Subjects (Using Kaplan-Meier) Who Are Identified As Meeting At Least 1 Pre-defined Exit Criteria By Day 112 Relative To The Start of Withdrawal of Background Antiepileptic Drug(s)
NCT00520741 (6) [back to overview]Percentage of Subjects (Using Kaplan-Meier) Who Are Identified as Meeting at Least 1 Pre-defined Exit Criteria by Day 112, Withdrew Due to Adverse Event (AE) or Withdrew Due to Lack of Efficacy During The Maintenance Period
NCT00520741 (6) [back to overview]Time to First Occurrence of Any Exit Event During The Maintenance Period
NCT00520741 (6) [back to overview]Clinical Global Impression of Change (CGIC) From Baseline To Last Visit
NCT00520741 (6) [back to overview]Patient's Global Impression of Change (PGIC) From Baseline To Last Visit
NCT00522275 (5) [back to overview]Number of Subjects Reporting at Least 1 Serious Adverse Event (SAE) During the Treatment Period (Maximum 6 Years)
NCT00522275 (5) [back to overview]Median Percentage Change From Baseline in 28-day Seizure Frequency During the Treatment Period (Maximum 6 Years)
NCT00522275 (5) [back to overview]Number of Subjects Reporting at Least 1 Treatment-Emergent Adverse Event (TEAE) During the Treatment Period (Maximum 6 Years)
NCT00522275 (5) [back to overview]Number of Subjects Prematurely Discontinuing Due to a Treatment-Emergent Adverse Event (TEAE) During the Treatment Period (Maximum 6 Years)
NCT00522275 (5) [back to overview]Percentage of at Least 50 % Responders During the Treatment Period (Maximum 6 Years)
NCT00530855 (4) [back to overview]Duration of Lacosamide (LCM) Monotherapy Treatment From Visit 1 to End of Study
NCT00530855 (4) [back to overview]Occurrence of At Least One Treatment-Emergent Adverse Event (TEAE) From Visit 1 to End of Study
NCT00530855 (4) [back to overview]Occurrence of Treatment-Emergent Adverse Events (TEAE) Leading to Subject Withdrawal From Visit 1 to End of Study
NCT00530855 (4) [back to overview]Percentage of Subjects on Lacosamide (LCM) Monotherapy at Any Time Between Visit 1 and End of Study
NCT00546351 (25) [back to overview]Average Pain Score as Measured by a 100 mm Visual Analogue Scale (VAS) at Last Visit.
NCT00546351 (25) [back to overview]Average Pain Score as Measured by a 100 mm Visual Analog Scale (VAS) at Baseline.
NCT00546351 (25) [back to overview]Average Pain Interference With Sleep (11-point Likert Scale) at Last Visit.
NCT00546351 (25) [back to overview]Average Quality of Life Using the SF-36 Health Survey - Mental Component Summary (MCS) at Baseline.
NCT00546351 (25) [back to overview]Patient's Global Impression of Change (PGIC) at Last Visit.
NCT00546351 (25) [back to overview]Within-Subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Unpleasantness at Final Visit.
NCT00546351 (25) [back to overview]Within-Subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Surface Pain at Last Visit.
NCT00546351 (25) [back to overview]Within-Subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Sharpness at Last Visit.
NCT00546351 (25) [back to overview]Within-Subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Itchiness at Final Visit.
NCT00546351 (25) [back to overview]Within-Subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Intensity at Last Visit.
NCT00546351 (25) [back to overview]Within-Subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Heat at Last Visit.
NCT00546351 (25) [back to overview]Within-Subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Dullness at Last Visit.
NCT00546351 (25) [back to overview]Within-Subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Deep Pain at Last Visit.
NCT00546351 (25) [back to overview]Within-Subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Sensitivity at Last Visit.
NCT00546351 (25) [back to overview]Within-Subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Cold at Last Visit.
NCT00546351 (25) [back to overview]Average Quality of Life Using the SF-36 Health Survey - Mental Component Summary (MCS) at Last Visit.
NCT00546351 (25) [back to overview]Average Quality of Life Using the SF-36 Health Survey - Physical Component Summary (PCS) at Baseline.
NCT00546351 (25) [back to overview]Number of Participants Experiencing the Occurrence of at Least One Treatment-emergent Adverse Event (TEAE) During the Evaluation Period From Entry Visit 1 Through End of Treatment (Approximately 6.5 Years).
NCT00546351 (25) [back to overview]Number of Participants Experiencing the Occurrence of at Least One Serious Adverse Event (SAE) During the Evaluation Period From Entry Visit 1 Through End of Treatment (Approximately 6.5 Years).
NCT00546351 (25) [back to overview]Average Quality of Life Using the SF-36 Health Survey - Physical Component Summary (PCS) at Last Visit.
NCT00546351 (25) [back to overview]Average Daily Pain Score Using an 11-point Likert Scale (0-10) at Baseline Visit.
NCT00546351 (25) [back to overview]Average Daily Pain Score Using an 11-point Likert Scale (0-10) at Last Visit.
NCT00546351 (25) [back to overview]Average Pain Interference With Activity (11-point Likert Scale) at Baseline.
NCT00546351 (25) [back to overview]Average Pain Interference With Activity (11-point Likert Scale) at Last Visit.
NCT00546351 (25) [back to overview]Average Pain Interference With Sleep (11-point Likert Scale) at Baseline.
NCT00552305 (5) [back to overview]Percentage of at Least 50% Responders During the Treatment Period (up to 8 Years)
NCT00552305 (5) [back to overview]Median Percentage Change From Baseline in 28-day Seizure Frequency During the Treatment Period (up to 8 Years)
NCT00552305 (5) [back to overview]Number of Subjects Prematurely Discontinuing Due to a Treatment-Emergent Adverse Event (TEAE) During the Treatment Period (up to 8 Years)
NCT00552305 (5) [back to overview]Number of Subjects Reporting at Least 1 Serious Adverse Event (SAE) During the Treatment Period (up to 8 Years)
NCT00552305 (5) [back to overview]Number of Subjects Reporting at Least 1 Treat-Emergent Adverse Event (TEAE) During the Treatment Period (up to 8 Years)
NCT00655486 (2) [back to overview]Number of Subjects Who Withdrew From the Study Due to an Adverse Event (Maximum Study Duration 2 Years)
NCT00655486 (2) [back to overview]Number of Subjects With at Least One Adverse Event During This Open-label Extension Study (Maximum Study Duration 2 Years)
NCT00655551 (3) [back to overview]Number of Subjects With at Least One Adverse Event During the Treatment Period (up to 7 Days)
NCT00655551 (3) [back to overview]Number of Subjects With at Least One Adverse Event With an Onset Within 4 Hours of Start of Infusion
NCT00655551 (3) [back to overview]Number of Subjects Who Withdrew From the Trial Due to an Adverse Event
NCT00771927 (2) [back to overview]The Incidence of Predefined Cardiovascular Treatment-Emergent Adverse Events (TEAEs) in Epilepsy Patients With Partial-onset Seizures While on Vimpat or Any Other add-on Antiepileptic Drug (AED) Treatment During the Study
NCT00771927 (2) [back to overview]The Incidence of Predefined Psychiatric Treatment-Emergent Adverse Events (TEAEs) in Epilepsy Patients With Partial-onset Seizures While on Vimpat or Any Other add-on Antiepileptic Drug (AED) Treatment During the Study
NCT00938431 (12) [back to overview]Number of Subjects That Report at Least One Treatment-emergent Adverse Event During the Study (Approximately 13 Weeks)
NCT00938431 (12) [back to overview]Plasma Ctrough Values for Lacosamide at Day 28
NCT00938431 (12) [back to overview]Plasma Ctrough Values for Lacosamide at Day 35
NCT00938431 (12) [back to overview]Plasma Ctrough Values for Lacosamide at Day 42
NCT00938431 (12) [back to overview]Plasma Ctrough Values for Lacosamide at Day 7
NCT00938431 (12) [back to overview]Plasma Ctrough Values for SPM 12809 at Day 28
NCT00938431 (12) [back to overview]Plasma Ctrough Values for SPM 12809 at Day 35
NCT00938431 (12) [back to overview]Plasma Ctrough Values for SPM 12809 at Day 42
NCT00938431 (12) [back to overview]Plasma Ctrough Values for SPM 12809 at Day 7
NCT00938431 (12) [back to overview]Caregiver Global Impression of Change Score at Visit 5 (Day 27/28) or Early Termination
NCT00938431 (12) [back to overview]Clinical Global Impression of Change Score at Visit 5 (Day 27/28) or Early Termination
NCT00938431 (12) [back to overview]Change in Seizure Frequency From Baseline to End of Treatment
NCT00938912 (8) [back to overview]Number of Seizure Days Per 28 Days for Participants With Generalized Seizures
NCT00938912 (8) [back to overview]Percentage of Participants With ≥75% Reduction in 28-day Partial-onset Seizure Frequency
NCT00938912 (8) [back to overview]Percentage of Participants With ≥50% Reduction in 28-day Partial-onset Seizure Frequency
NCT00938912 (8) [back to overview]Percentage of Participants Who Achieved a Seizure-free Status
NCT00938912 (8) [back to overview]Number of Participants That Withdraw Due to a Treatment-Emergent Adverse Event
NCT00938912 (8) [back to overview]Number of Participants With Serious Adverse Events (SAEs)
NCT00938912 (8) [back to overview]Percent Change From Baseline in 28 Day Partial-onset Seizure Frequency to the End of the Treatment Period
NCT00938912 (8) [back to overview]Number of Participants With At Least One Treatment-Emergent Adverse Event (TEAE)
NCT00955357 (1) [back to overview]"The Proportion of Subjects Who Achieved Seizure-free Status During the First 12 Weeks of the Maintenance Phase"
NCT01110187 (2) [back to overview]Number of Adverse Events
NCT01110187 (2) [back to overview]Number of Participants With Seizures
NCT01118949 (6) [back to overview]Change in the Number of Seizure Days With Myoclonic Seizures From the Baseline Phase to the Maintenance Phase
NCT01118949 (6) [back to overview]Change in the Number of Seizure Days With Absence Seizures From the Baseline Phase to the Maintenance Phase
NCT01118949 (6) [back to overview]Changes in Count of 3 Hertz (Hz) Spike-wave Discharges (During Waking Hours) on 24-hour Ambulatory Electroencephalogram (EEG) From Visit 2 (Baseline Phase) to Visit 6 (Maintenance Phase)
NCT01118949 (6) [back to overview]Changes in Count of Generalized Spike-wave Discharges on 24-hour Ambulatory Electroencephalogram (EEG) From Visit 2 (Baseline Phase) to Visit 6 (Maintenance Phase)
NCT01118949 (6) [back to overview]Number of Subjects With Treatment Emergent Adverse Events (TEAEs) During the 10-week Treatment Period
NCT01118949 (6) [back to overview]Number of Subjects Withdrawn From the Study Due to Treatment Emergent Adverse Events (TEAEs) During the 10-week Treatment Period
NCT01118962 (2) [back to overview]Number of Participants Withdrawn From the Study Due to Treatment-emergent Adverse Events (TEAEs) From Visit 1 to the End of Study (Approximately 61 Weeks)
NCT01118962 (2) [back to overview]Number of Participants With Treatment-emergent Adverse Events (TEAEs) From Visit 1 to the End of Study (Approximately 61 Weeks)
NCT01190098 (8) [back to overview]Change in Adverse Event Profile (AEP) From Baseline to Visit 4.
NCT01190098 (8) [back to overview]Change in Daily Seizure Frequency From Baseline to Visit 4
NCT01190098 (8) [back to overview]Change in Epworth Sleepiness Scale Score From Baseline to Visit 4
NCT01190098 (8) [back to overview]Change in Functional Outcomes of Sleep Questionnaire (FOSQ) From Baseline to Visit 4.
NCT01190098 (8) [back to overview]Change in Patient Health Questionnaire-9 (PHQ-9) From Baseline to Visit 4.
NCT01190098 (8) [back to overview]Change in Pittsburgh Sleep Quality Inventory (PSQI) From Baseline to Visit 4
NCT01190098 (8) [back to overview]Change in Quality of Life in Epilepsy (QOLIE-31) From Baseline to Visit 4
NCT01190098 (8) [back to overview]Change in the Fatigue Severity Scale From Baseline to Visit 4.
NCT01235403 (3) [back to overview]Number of Subjects Prematurely Discontinuing Due to a TEAE During the Study
NCT01235403 (3) [back to overview]Number of Subjects Reporting at Least 1 Treatment-Emergent Adverse Event (TEAE) During the Study
NCT01235403 (3) [back to overview]Percentage of Subjects Retained on Vimpat Through the End of the 24-week Treatment Period
NCT01236001 (11) [back to overview]Percentage of Subjects Who Received Concomitant Antiepileptic Drug Treatment
NCT01236001 (11) [back to overview]Treatment Persistence of VIMPAT® After 6 Months
NCT01236001 (11) [back to overview]Galenic Formulation Repartition in Subjects Treated by VIMPAT® at 3 Months
NCT01236001 (11) [back to overview]Galenic Formulation Repartition in Subjects Treated by VIMPAT® at 6 Months
NCT01236001 (11) [back to overview]Galenic Formulation Repartition in Subjects Treated by VIMPAT® at Baseline
NCT01236001 (11) [back to overview]Percentage of Subjects by Category of Clinical Evolution of Seizure Control at 3 Months
NCT01236001 (11) [back to overview]Percentage of Subjects by Category of Clinical Evolution of Seizure Control at 6 Months
NCT01236001 (11) [back to overview]Percentage of Subjects by Category of Clinical Evolution of Seizure Control at Baseline
NCT01236001 (11) [back to overview]Mean Total Daily Dose of VIMPAT® (mg) at 3 Months
NCT01236001 (11) [back to overview]Mean Total Daily Dose of VIMPAT® (mg) at 6 Months
NCT01236001 (11) [back to overview]Mean Total Daily Dose of VIMPAT® (mg) at Baseline
NCT01243177 (6) [back to overview]Proportion of Subjects in the Full Analysis Set (FAS) Remaining Seizure Free for 6 Consecutive Months (26 Consecutive Weeks) of Treatment Following Stabilization at the Last Evaluated Dose for Each Subject
NCT01243177 (6) [back to overview]Proportion of Subjects Remaining Seizure Free for 12 Consecutive Months (52 Consecutive Weeks) Following Stabilization at the Last Evaluated Dose for Each Subject
NCT01243177 (6) [back to overview]Proportion of Subjects in the Per Protocol Set (PPS) Remaining Seizure Free for 6 Consecutive Months (26 Consecutive Weeks) of Treatment Following Stabilization at the Last Evaluated Dose for Each Subject
NCT01243177 (6) [back to overview]Number of Subjects Who Withdraw From the Study Due to a Treatment-emergent Adverse Event (AE) During the Treatment Phase (up to 113 Weeks)
NCT01243177 (6) [back to overview]Number of Subjects With at Least One Treatment-emergent Adverse Event (AE) During the Treatment Phase (up to 113 Weeks)
NCT01243177 (6) [back to overview]Number of Subjects With at Least One Treatment-emergent Serious Adverse Event (SAE) During the Treatment Phase (up to 113 Weeks)
NCT01345058 (5) [back to overview]Number of Seizure-Free Days
NCT01345058 (5) [back to overview]Time to First Seizure After Therapeutic Dose is Reached
NCT01345058 (5) [back to overview]Retention Rate
NCT01345058 (5) [back to overview]Percentage of Participants Achieving Six Month Seizure Freedom
NCT01345058 (5) [back to overview]Number of Participants With Treatment-Emergent Adverse Events (TEAE)
NCT01375374 (4) [back to overview]Change in Serum Sex Hormone Binding Globulin (SHBG) From Baseline to Treatment Period End (Comprised of a 4-week Titration Period and an 8-week Maintenance Period)
NCT01375374 (4) [back to overview]Change in Serum Thyroid Hormone Free Thyroxine Level From Baseline to Treatment Period End (Comprised of a 4-week Titration Period and an 8-week Maintenance Period)
NCT01375374 (4) [back to overview]Change in Sex Hormone Calculated Free Androgen Index Levels From Baseline to Treatment Period End (Comprised of a 4-week Titration Period and an 8-week Maintenance Period)
NCT01375374 (4) [back to overview]Change in Total Cholesterol Level From Baseline to Treatment Period End (Comprised of a 4-week Titration Period and an 8-week Maintenance Period)
NCT01432171 (1) [back to overview]Number of Participants With Seizures
NCT01458522 (11) [back to overview]Percentage of Subjects in Whom Study Drug is Withdrawn Early After Treatment With Treatment Arm 1
NCT01458522 (11) [back to overview]Percentage of Subjects Who Experience no Nonconvulsive Seizures (NCS) for 24 Hours Following Treatment With LCM vs. fPHT, as Measured by Continuous Electroencephalography (cEEG) Monitoring.
NCT01458522 (11) [back to overview]Percentage of Subjects Who Require a Rebolus of the Initial Antiepileptic Drugs (AED) to Control Nonconvulsive Seizures (NCS) in the LCM vs fPHT Arms.
NCT01458522 (11) [back to overview]Seizure Burden Change From Baseline to End of Crossover, Excluding Initial Treatment Arm
NCT01458522 (11) [back to overview]Seizure Burden Change From Baseline to End of Initial Treatment
NCT01458522 (11) [back to overview]Change in Functional Status as Measured by the Functional Disability Scale at Day 7 to 9 Postrandomization and Day 30 Post-randomization in the LCM vs fPHT Arms.
NCT01458522 (11) [back to overview]Days in the Intensive Care Unit/Hospital
NCT01458522 (11) [back to overview]Time of First Bolus to End of Seizures After Initial Treatment Arm, Time From Crossover to End of Seizures in Crossover Treatment Arm
NCT01458522 (11) [back to overview]Percentage of All Subjects Who Have Had a Seizure, Are on Antiepileptic Drug (AED) Therapy, and Are Alive/Dead at Day 30
NCT01458522 (11) [back to overview]Number of Predefined Adverse Events (AE) After Treatment Arm 1 Administration
NCT01458522 (11) [back to overview]Number of Subjects Who Required a Second Antiepileptic Drug (AED) to Control Nonconvulsive Seizures (NCS)
NCT01465997 (3) [back to overview]Number of Subjects Who Withdrew From the Study Due to a Treatment-emergent Adverse Event (AE) During the Treatment Phase (Maximum 3.5 Years)
NCT01465997 (3) [back to overview]Number of Subjects With at Least One Treatment-emergent Serious Adverse Event (SAE) During the Treatment Phase (Maximum of 3.5 Years)
NCT01465997 (3) [back to overview]Number of Subjects With at Least One Treatment-emergent Adverse Event (AE) During the Treatment Phase (Maximum of 3.5 Years)
NCT01484977 (1) [back to overview]Retention at the End of the 21-week Treatment Period
NCT01673282 (1) [back to overview]The Percent Change in Ratio of Dose and Defined Daily Dose (DDD) for the Drug Load of Concomitant Anti-Epileptic Drugs (AEDs) From Baseline to the End of Observation Period (Day 0 to 6 Months)
NCT01710657 (4) [back to overview]Change in Partial-Onset Seizure Frequency Per 28 Days From Baseline to the Treatment Period (i.e., Titration + Maintenance Period)
NCT01710657 (4) [back to overview]Change in Partial-Onset Seizure Frequency Per 28 Days From Baseline to the Maintenance Period
NCT01710657 (4) [back to overview]The Proportion of Individual Patients Who Experience a 50 % or Greater Reduction in Seizure Frequency From Baseline to the Maintenance Period (50 % Responder Rate)
NCT01710657 (4) [back to overview]Percent Change in Partial-Onset Seizure Frequency Per 28 Days From Baseline to the Maintenance Period
NCT01832038 (4) [back to overview]Number of Participants With at Least One Adverse Event Reported Spontaneously by the Subject or Observed by the Investigator From Baseline Until the End of Study Visit
NCT01832038 (4) [back to overview]Number of Participants That Withdrew Due to Adverse Events From Baseline Until the End of Study Visit
NCT01832038 (4) [back to overview]Percentage of Participants With 50 % Response Rate in Partial-onset Seizure Frequency Per 28 Days From Baseline of Study EP0008 [NCT01710657] Until the End of Study Visit in Study EP0009
NCT01832038 (4) [back to overview]Percent Change in Partial-onset Seizure Frequency Per 28 Days From Baseline of Study EP0008 [NCT01710657] Until the End of Study Visit in Study EP0009
NCT01921205 (12) [back to overview]Proportion of Subjects Experiencing no Change in Partial Onset Seizure Frequency (Between <25 % Reduction and <25 % Increase) Per 28 Days From Baseline to the Entire Treatment (ie, Titration+Maintenance Periods)
NCT01921205 (12) [back to overview]Proportion of Subjects Experiencing a >=25 % to <50 %, 50 % to 75 %, or >75 % Reduction in Partial Onset Seizure Frequency Per 28 Days From Baseline to the Entire Treatment (ie, Titration+Maintenance Periods)
NCT01921205 (12) [back to overview]Proportion of Subjects Experiencing a >=25 % to <50 %, 50 % to 75 %, or >75 % Reduction in Partial Onset Seizure Frequency Per 28 Days From Baseline to the End of Maintenance Period
NCT01921205 (12) [back to overview]"Proportion of Subjects Who Achieved Seizure Free Status (Yes/no) for Subjects Who Completed the Maintenance Period"
NCT01921205 (12) [back to overview]Change in Partial Onset Seizure (POS) Frequency Per 28 Days From Baseline to the Maintenance Period
NCT01921205 (12) [back to overview]Change in Partial Onset Seizure Frequency Per 28 Days From Baseline to the Entire Treatment (ie, Titration+Maintenance Periods)
NCT01921205 (12) [back to overview]Change in Partial Onset Seizure Frequency Per 28 Days From Baseline to the Entire Treatment (ie, Titration+Maintenance Periods) for Complex Partial Seizures
NCT01921205 (12) [back to overview]Change in Partial Onset Seizure Frequency Per 28 Days From Baseline to the Entire Treatment (ie, Titration+Maintenance Periods) for Secondary Generalized Seizures
NCT01921205 (12) [back to overview]Change in Partial Onset Seizure Frequency Per 28 Days From Baseline to the Entire Treatment (ie, Titration+Maintenance Periods) for Simple Partial Seizures
NCT01921205 (12) [back to overview]Proportion of Responders Where a Responder is Defined as a Participant With >= 50% Reduction in Partial Onset Seizure Frequency Per 28 Days From Baseline to the Maintenance Period
NCT01921205 (12) [back to overview]Proportion of Seizure Free Days During the Maintenance Period for Subjects Who Completed the Maintenance Period
NCT01921205 (12) [back to overview]Proportion of Subjects Experiencing an Increase in Partial Onset Seizure Frequency Per 28 Days of >=25 % From Baseline to the Entire Treatment (ie, Titration+Maintenance Periods)
NCT01964560 (4) [back to overview]Percentage of Seizure-free Days During the Study
NCT01964560 (4) [back to overview]Percentage of Participants With Serious TEAEs
NCT01964560 (4) [back to overview]Percentage of Participants With TEAEs Leading to Study Discontinuation
NCT01964560 (4) [back to overview]Percentage of Participants With Treatment-emergent Adverse Events (TEAEs)
NCT01969851 (5) [back to overview]Number of Subjects Experiencing at Least 1 Treatment-emergent Adverse Event From Baseline to End of Study (Approximately 32 Weeks)
NCT01969851 (5) [back to overview]Mean Change in Days With Any Generalized Seizures (Absence, Myoclonic, Clonic, Tonic, Tonic-clonic, Atonic, Partial Evolving to Secondarily Generalized) Per 28 Days From the Baseline Period to the Maintenance Period (Approximately 24 Weeks)
NCT01969851 (5) [back to overview]Mean Changes in Count of 3 Hz Spike-wave Discharges (During Waking Hours) on 24-hour Ambulatory EEG From Visit 2 to Visit 6
NCT01969851 (5) [back to overview]Mean Changes in Count of Generalized Spike-wave Discharges on 24-hour Ambulatory Electroencephalogram (EEG) From Visit 2 to Visit 6
NCT01969851 (5) [back to overview]Number of Subject Withdrawals Due to Adverse Events From Baseline to End of Study (Approximately 32 Weeks)
NCT02124564 (7) [back to overview]Number of Subjects Remaining Seizure Free for 6 Consecutive Months During the Monotherapy Period
NCT02124564 (7) [back to overview]Number of Subjects Remaining Seizure Free for 12 Consecutive Months During the Monotherapy Period
NCT02124564 (7) [back to overview]Number of Subjects With at Least One Incidence of Serious Adverse Events (SAEs) During the Study
NCT02124564 (7) [back to overview]Number of Subjects With at Least One Incidence of Treatment-Emergent Adverse Events (TEAEs) During the Study
NCT02124564 (7) [back to overview]Percentage of Participants in the Monotherapy Period Without Discontinuation Due to Adverse Events (AE) or Lack of Efficacy (LOE)
NCT02124564 (7) [back to overview]Plasma Concentrations of Lacosamide Versus Time Postdose
NCT02124564 (7) [back to overview]Number of Subjects Who Withdraw Due to Adverse Events (AEs) During the Study
NCT02192814 (8) [back to overview]Maximum Plasma Concentration (Cmax) for Lacosamide (LCM) (End of Infusion) on Day 1
NCT02192814 (8) [back to overview]Maximum Plasma Concentration (Cmax) for Lacosamide (LCM) (End of Infusion) on Day 2
NCT02192814 (8) [back to overview]Maximum Plasma Concentration (Cmax) for Lacosamide (LCM) (End of Infusion) on Day 5
NCT02192814 (8) [back to overview]Plasma Trough Concentration (Ctrough) for Lacosamide (LCM) on Day 1
NCT02192814 (8) [back to overview]Plasma Trough Concentration (Ctrough) for Lacosamide (LCM) on Day 2
NCT02192814 (8) [back to overview]Plasma Trough Concentration (Ctrough) for Lacosamide (LCM) on Day 5
NCT02192814 (8) [back to overview]The Total Number of Subject Withdrawal Due to Adverse Events During the Study
NCT02192814 (8) [back to overview]The Total Number of Subjects Experiencing at Least One Adverse Event During the Study
NCT02408523 (5) [back to overview]Plasma Concentrations of Lacosamide
NCT02408523 (5) [back to overview]Time to the Second Primary Generalized Tonic Clonic (PGTC) Seizure During the 24-week Treatment Period From Visit 2 (Week 0) to Visit 10 (Week 24)
NCT02408523 (5) [back to overview]Time to the First Primary Generalized Tonic Clonic (PGTC) Seizure During the Treatment Period From Visit 2 (Week 0) to Visit 10 (Week 24)
NCT02408523 (5) [back to overview]Percentage of Participants With at Least One Adverse Event (AE) as Reported Spontaneously by the Subject and/or Caregiver or Observed by the Investigator
NCT02408523 (5) [back to overview]Percentage of Participants With Seizure Freedom for Primary Generalized Tonic Clonic (PGTC) Seizures During the 24-week Treatment Period From Visit 2 (Week 0) to Visit 10 (Week 24)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Serum Chemistry Parameters (Creatinine)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Serum Chemistry Parameters (Calcium)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Serum Chemistry Parameters (Alkaline Phosphatase)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Serum Chemistry Parameters (Albumin)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Hematology Parameters (Monocytes Absolute )
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Hematology Parameters (Leukocytes)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Hematology Parameters (Erythrocytes)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Hematology Parameters (Basophils Absolute)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Chemistry Parameters (Total Bilirubin)
NCT02408549 (49) [back to overview]Percentage of Study Participants With at Least 50% Worsening in Days With Myoclonic Seizures
NCT02408549 (49) [back to overview]Percentage of Study Participants With at Least 50% Worsening in Days With Absence Seizures
NCT02408549 (49) [back to overview]Percent Change in Primary Generalized Tonic-clonic Seizure (PGTCS) Frequency Per 28 Days From Combined Baseline
NCT02408549 (49) [back to overview]Number of Study Participants Withdrawn Due to TEAEs
NCT02408549 (49) [back to overview]Number of Study Participants With Treatment-emergent Adverse Events (TEAEs) Over the Duration of the Treatment Period
NCT02408549 (49) [back to overview]Number of Study Participants With an Increase of up to 25% in Days With Myoclonic Seizures Per 28 Days During the Treatment Period as Compared to the Prospective Baseline (of Study SP0982)
NCT02408549 (49) [back to overview]Number of Study Participants With an Increase of up to 25% in Days With Absence Seizures Per 28 Days During the Treatment Period as Compared to the Prospective Baseline (of Study SP0982)
NCT02408549 (49) [back to overview]Number of Study Participants With an Increase of Greater Than (>)25% to 50% in Days With Absence Seizures Per 28 Days During the Treatment Period as Compared to the Prospective Baseline (of Study SP0982)
NCT02408549 (49) [back to overview]Number of Study Participants With an Increase of >75% in Days With Myoclonic Seizures Per 28 Days During the Treatment Period as Compared to the Prospective Baseline (of Study SP0982)
NCT02408549 (49) [back to overview]Number of Study Participants With an Increase of >75% in Days With Absence Seizures Per 28 Days During the Treatment Period as Compared to the Prospective Baseline (of Study SP0982)
NCT02408549 (49) [back to overview]Number of Study Participants With an Increase of >50% to 75% in Days With Myoclonic Seizures Per 28 Days During the Treatment Period as Compared to the Prospective Baseline (of Study SP0982)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Serum Chemistry Parameters (Potassium)
NCT02408549 (49) [back to overview]Number of Study Participants With an Increase of >50% to 75% in Days With Absence Seizures Per 28 Days During the Treatment Period as Compared to the Prospective Baseline (of Study SP0982)
NCT02408549 (49) [back to overview]Number of Study Participants With an Increase of >25% to 50% in Days With Myoclonic Seizures Per 28 Days During the Treatment Period as Compared to the Prospective Baseline (of Study SP0982)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Hematology Parameters (Platelets)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Serum Chemistry Parameters (Chloride)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Vital Sign Measurements (Systolic Blood Pressure)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Vital Sign Measurements (Pulse Rate)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Vital Sign Measurements (Diastolic Blood Pressure)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Vital Sign Measurements (Body Weight)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Serum Chemistry Parameters (Phosphate)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Serum Chemistry Parameters (Glucose)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Serum Chemistry Parameters (Gamma Glutamyl Transferase)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Serum Chemistry Parameters (Bicarbonate)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Serum Chemistry Parameters (Aspartate Aminotransferase)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Serum Chemistry Parameters (Alanine Aminotransferase)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Hematology Parameters (Neutrophils Absolute)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Hematology Parameters (Lymphocytes Absolute)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Hematology Parameters (Hemoglobin)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Hematology Parameters (Hematocrit)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Hematology Parameters (Eosinophils Absolute)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in 12-lead Electrocardiogram (ECG) Parameter (QT Interval)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in 12-lead ECG Parameter (QTc(F) Interval)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in 12-lead ECG Parameter (QTc(B) Interval)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in 12-lead ECG Parameter (QRS Interval)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in 12-lead ECG Parameter (PR Interval)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in 12-lead ECG Parameter (Heart Rate Interval)
NCT02408549 (49) [back to overview]Number of Study Participants With New Appearance of Absence and/or Myoclonic Seizures During the Treatment Period
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Serum Chemistry Parameters (Total Protein)
NCT02408549 (49) [back to overview]Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Serum Chemistry Parameters (Sodium)
NCT02477839 (12) [back to overview]Percentage of Participants Experiencing no Change in Average Daily Frequency (ADF) of Electrographic Partial-onset Seizures (Between <25% Reduction and <25% Increase) From EOB Period Video-EEG to EOM Period Video-EEG
NCT02477839 (12) [back to overview]Percentage of Participants Who Achieved 'Seizure-free' Status From All Seizure Types During the End-of-Maintenance (EOM) Period Video-EEG
NCT02477839 (12) [back to overview]Percentage of Participants Who Achieved 'Seizure-free' Status From Partial-onset Seizure Types Only During the End-of-Maintenance (EOM) Period Video-EEG
NCT02477839 (12) [back to overview]Percentage of Participants With Adverse Events Reported Spontaneously by the Participant's Parent(s) and/or Legal Representative(s)/Caregiver(s) (in Accordance With Local Regulation) or Observed by the Investigator
NCT02477839 (12) [back to overview]Percentage of Participants Experiencing a >=25% to <50% Reduction in Average Daily Frequency (ADF) of Electrographic Partial-onset Seizures From End-of-Baseline (EOB) Period Video-EEG to End-of-Maintenance (EOM) Period Video-EEG
NCT02477839 (12) [back to overview]Percentage of Participants Experiencing an Increase in Average Daily Frequency (ADF) of Electrographic Partial-onset Seizures of >=25% From End-of-Baseline (EOB) Period Video-EEG to End-of-Maintenance (EOM) Period Video-EEG
NCT02477839 (12) [back to overview]Percent Change in Average Daily Frequency (ADF) of Electrographic Partial-onset Seizures From End-of-Baseline (EOB) Period Video-EEG to End-of-Maintenance (EOM) Period Video-EEG
NCT02477839 (12) [back to overview]Participant Withdrawals Due to Adverse Events (AEs) During the Study
NCT02477839 (12) [back to overview]Change in Average Daily Frequency (ADF) of Electrographic Partial-onset Seizures From End-of-Baseline (EOB) Period Video-EEG to End-of-Maintenance (EOM) Period Video-EEG
NCT02477839 (12) [back to overview]Absolute Change in Average Daily Frequency (ADF) of Electrographic Partial-onset Seizures From End-of-Baseline (EOB) Period Video-EEG to End-of-Maintenance (EOM) Period Video-EEG
NCT02477839 (12) [back to overview]Percentage of Participants Experiencing a >75% Reduction in Average Daily Frequency (ADF) of Electrographic Partial-onset Seizures From End-of-Baseline (EOB) Period Video-EEG to End-of-Maintenance (EOM) Period Video-EEG
NCT02477839 (12) [back to overview]Percentage of Participants Experiencing a 50% to 75% Reduction in Average Daily Frequency (ADF) of Electrographic Partial-onset Seizures From End-of-Baseline (EOB) Period Video-EEG to End-of-Maintenance (EOM) Period Video-EEG
NCT02582866 (3) [back to overview]Percentage of Participants Experiencing Any Adverse Events (AEs) Reported Spontaneously by the Subject and/or Caregiver or Observed by Investigator
NCT02582866 (3) [back to overview]Percentage of Participants Experiencing Any Serious Adverse Events (SAEs) Reported Spontaneously by the Subject and/or Caregiver or Observed by Investigator
NCT02582866 (3) [back to overview]Percentage of Participants That Withdrew Due to Adverse Events (AEs)
NCT02710890 (2) [back to overview]Percentage of Participants With at Least One Adverse Event Reported Spontaneously by the Participant/or Caregiver (Including Parent/Legal Guardian) or Observed by the Investigator During the Study
NCT02710890 (2) [back to overview]Percentage of Participants That Withdrew Due to Adverse Events During the Study
NCT03271528 (21) [back to overview]Alcohol Craving: Alcohol Urge Questionnaire (AUQ) Self-Administration Blocks 1 and 2, Minute 120
NCT03271528 (21) [back to overview]Alcohol Craving: Alcohol Urge Questionnaire (AUQ) Self-Administration Blocks 1 and 2, Minute 30
NCT03271528 (21) [back to overview]Alcohol Craving: Alcohol Urge Questionnaire (AUQ) Self-Administration Blocks 1 and 2, Minute 60
NCT03271528 (21) [back to overview]Verbal Fluency: Controlled Word Association (COWAT)
NCT03271528 (21) [back to overview]Cognitive Function: Spatial Span Forward
NCT03271528 (21) [back to overview]Cognitive Function: Spatial Span Backward
NCT03271528 (21) [back to overview]Cognitive Function: Digit Span Sequencing
NCT03271528 (21) [back to overview]Cognitive Function: Digit Span Forward
NCT03271528 (21) [back to overview]Cognitive Function: Digit Span Backward
NCT03271528 (21) [back to overview]Alcohol Craving: Visual Analog Scale (VAS) Self-Administration Blocks 1 and 2, Minute 90
NCT03271528 (21) [back to overview]Alcohol Craving: Visual Analog Scale (VAS) Observation Period, Minute 30
NCT03271528 (21) [back to overview]Alcohol Craving: Obsessive-Compulsive Drinking Scale (OCDS) Pretrial
NCT03271528 (21) [back to overview]Alcohol Craving: Visual Analog Scale (VAS) Self-Administration Blocks 1 and 2, Minute 60
NCT03271528 (21) [back to overview]Alcohol Craving: Visual Analog Scale (VAS) Self-Administration Blocks 1 and 2, Minute 30
NCT03271528 (21) [back to overview]Alcohol Craving: Visual Analog Scale (VAS) Self-Administration Blocks 1 and 2, Minute 120
NCT03271528 (21) [back to overview]Alcohol Craving: Visual Analog Scale (VAS) Pretrial
NCT03271528 (21) [back to overview]Alcohol Craving: Visual Analog Scale (VAS) Observation Period, Minute 40
NCT03271528 (21) [back to overview]Alcohol Craving: Visual Analog Scale (VAS) Observation Period, Minute 20
NCT03271528 (21) [back to overview]Alcohol Craving: Visual Analog Scale (VAS) Observation Period, Minute 10
NCT03271528 (21) [back to overview]Alcohol Craving: Alcohol Urge Questionnaire (AUQ) Self-Administration Blocks 1 and 2, Minute 90
NCT03271528 (21) [back to overview]Alcohol Consumption in Alcohol Self-Administration Trials
NCT03436433 (2) [back to overview]Number of Participants With an Adverse Event Within First 30 Days After Craniotomy
NCT03436433 (2) [back to overview]Percentage of Patients With an ED Visit/Hospital Readmission Within 30 Days of Craniotomy
NCT03897348 (6) [back to overview]Alcohol Craving
NCT03897348 (6) [back to overview]Alcohol Consumption (Number of Standard Drinks Consumed)
NCT03897348 (6) [back to overview]Retention Feasibility (Proportion of Participants Completing the Alcohol Drinking Paradigm (ADP) Sessions)
NCT03897348 (6) [back to overview]Tolerability (Number of Participants With Mild, Moderate, or Severe Adverse Events)
NCT03897348 (6) [back to overview]Subjective Effects of Alcohol Consumption
NCT03897348 (6) [back to overview]Recruitment Feasibility (Time, in Months,) Required to Recruit, Screen and Conduct the Study Procedures

Percentage of Subjects With Marked Abnormalities in Physical Examination Findings After Start of Treatment.

Changes in physical examination findings is reported as percentage of subjects with marked abnormalities in following categories: - Ears, Eyes, Nose, Mouth, Throat - Cardiovascular - Peripheral vascular - Pulmonary - Musculoskeletal - Hepato- / Gastrointestinal - Renal / Genitourological - Neurological - Metabolic / Endocrine - Psychiatric - Hematological / Lymphatic Nodes - Dermatological - Other The percentages are based on the number of subjects with examinations done at each visit for each body system. (NCT00220337)
Timeframe: Last Visit (up to 140 weeks)

Interventionpercentage of participants (Number)
Ears, Eyes, Nose, Mouth, ThroatCardiovascularPeripheral vascularPulmonaryMusculoskeletalHepato- / GastrointestinalRenal / GenitourologicalNeurologicalMetabolic / EndocrinePsychiatricHematological / Lymphatic NodesDermatologicalOther
Lacosamide12.215.214.22.113.35.21.349.519.51.50.616.793.3

[back to top]

Change in Different Symptoms of Neuropathic Pain From Visit 2 (Baseline) to Visit 9.1

Subjects were asked to assess different symptoms of neuropathic pain with respect to severity using the NPSI at different visits. It comprised of 10 descriptive symptom questions (pain feels like burning, squeezing, pressure electric shocks, stabbing, pins/needles, tingling, provoked or increased by brushing, pressure or contact with something cold), which were rated on an 11-point scale from 0 (absence of pain) to 10 (maximum intensity of pain), and are reported in categories below and 2 temporal questions (duration of pain, number of pain attacks). This assessment was done only in subjects from countries in which a validated version of the NPSI was available. Total NPSI scale ranged from 0 (no pain) to 100 (maximum pain). Higher scores indicate a greater intensity of pain. A negative value indicates improvement in symptoms from Baseline. (NCT00220337)
Timeframe: Baseline, Visit 9.1

Interventionunits on a scale (Mean)
BurningSqueezingPressureElectric shocksStabbingBrushingIncreased by pressureContact with coldPins and needlesTingling
Lacosamide-3.1-2.1-2.8-3.1-2.9-1.0-2.3-1.4-3.1-2.9

[back to top]

Change in Different Symptoms of Neuropathic Pain From Visit 2 (Baseline) to Visit 9.0

Subjects were asked to assess different symptoms of neuropathic pain with respect to severity using the NPSI at different visits. It comprised of 10 descriptive symptom questions (pain feels like burning, squeezing, pressure electric shocks, stabbing, pins/needles, tingling, provoked or increased by brushing, pressure or contact with something cold), and 2 temporal questions (duration of pain, number of pain attacks). The NPSI scores of the descriptive questions are reported in categories below, which were rated on an 11-point scale from 0 (absence of pain) to 10 (maximum intensity of pain). Higher scores indicate a greater intensity of pain. A negative value indicates improvement in symptoms from Baseline. This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Baseline, Visit 9.0

Interventionunits on a scale (Mean)
BurningSqueezingPressureElectric shocksStabbingBrushingIncreased by pressureContact with coldPins and needlesTingling
Lacosamide-3.0-2.2-2.7-2.9-2.9-1.0-2.4-1.2-3.2-2.9

[back to top]

Change in Different Symptoms of Neuropathic Pain From Visit 2 (Baseline) to Visit 6

Subjects were asked to assess different symptoms of neuropathic pain with respect to severity using the NPSI at different visits. It comprised of 10 descriptive symptom questions (pain feels like burning, squeezing, pressure electric shocks, stabbing, pins/needles, tingling, provoked or increased by brushing, pressure or contact with something cold), and 2 temporal questions (duration of pain, number of pain attacks). The NPSI scores of the descriptive questions are reported in categories below, which were rated on an 11-point scale from 0 (absence of pain) to 10 (maximum intensity of pain). Higher scores indicate a greater intensity of pain. A negative value indicates improvement in symptoms from Baseline. This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Baseline, Visit 6

Interventionunits on a scale (Mean)
BurningSqueezingPressureElectric shocksStabbingBrushingIncreased by pressureContact with coldPins and needlesTingling
Lacosamide-2.9-1.7-2.5-2.5-2.6-1.2-1.8-1.2-3.3-2.9

[back to top]

Change in Different Symptoms of Neuropathic Pain From Visit 2 (Baseline) to Visit 4

Subjects were asked to assess different symptoms of neuropathic pain with respect to severity using the Neuropathic Pain Symptoms Inventory (NPSI) at different visits. It comprised of 10 descriptive symptom questions (pain feels like burning, squeezing, pressure electric shocks, stabbing, pins/needles, tingling, provoked or increased by brushing, pressure or contact with something cold), and 2 temporal questions (duration of pain, number of pain attacks). The NPSI scores of the descriptive questions are reported in categories below, which were rated on an 11-point scale from 0 (absence of pain) to 10 (maximum intensity of pain). Higher scores indicate a greater intensity of pain. A negative value indicates improvement in symptoms from Baseline. This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Baseline, Visit 4

Interventionunits on a scale (Mean)
BurningSqueezingPressureElectric shocksStabbingBrushingIncreased by pressureContact with coldPins and needlesTingling
Lacosamide-3.1-1.5-2.6-2.3-2.6-1.0-1.9-1.4-2.7-2.3

[back to top]

Change in Different Symptoms of Neuropathic Pain From Visit 2 (Baseline) to Termination Visit

Subjects were asked to assess different symptoms of neuropathic pain with respect to severity using the NPSI at different visits. It comprised of 10 descriptive symptom questions (pain feels like burning, squeezing, pressure electric shocks, stabbing, pins/needles, tingling, provoked or increased by brushing, pressure or contact with something cold), and 2 temporal questions (duration of pain, number of pain attacks). The NPSI scores of the descriptive questions are reported in categories below, which were rated on an 11-point scale from 0 (absence of pain) to 10 (maximum intensity of pain). Higher scores indicate a greater intensity of pain. A negative value indicates improvement in symptoms from Baseline. This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Baseline, Termination Visit (last treatment visit)

Interventionunits on a scale (Mean)
BurningSqueezingPressureElectric shocksStabbingBrushingIncreased by pressureContact with coldPins and needlesTingling
Lacosamide-2.6-1.5-2.0-2.1-2.3-1.0-1.8-0.7-2.7-2.5

[back to top]

Change in Current Pain From Visit 2 (Baseline) to Each Subsequent Visit as Measured by a 100 mm Visual Analogue Scale (VAS)

A 100 mm visual analogue scale (VAS) was used to assess the subject's current pain. The subject rated their current pain from 0 (no pain) to 100 (worst possible pain). A negative value indicates improvement in symptoms. (NCT00220337)
Timeframe: Baseline, Visit 2.1, Visit 2.2, Visit 2.4, Visit 2.5, Visit 3, Visit 4, Visit 5, Visit 6, Visit 7, Visit 8, Visit 9.0, Visit 9.1, Visit 9.2, Visit 9.3, Visit 9.4, Visit 9.5, Visit 9.6, Visit 9.7, Visit 9.8, Visit 9.9

Interventionunits on a scale (Mean)
Visit 2.1Visit 2.2Visit 2.3Visit 2.4Visit 2.5Visit 3Visit 4Visit 5Visit 6Visit 7Visit 8Visit 9.0Visit 9.1Visit 9.2Visit 9.3Visit 9.4Visit 9.5Visit 9.6Visit 9.7Visit 9.8Visit 9.9
Lacosamide-12.32-20.79-27.87-14.80-20.33-35.23-37.01-37.91-37.71-40.06-40.25-40.24-41.47-40.08-41.56-41.00-41.45-40.88-41.69-41.83-43.63

[back to top]

Change in Average Pain Interference With Sleep From the Baseline Week to the 7 Days Prior to Each Visit

Pain interference scores at each visit (sleep and activity respectively) were defined as the average of the respective daily interference scores during the 7 last available days prior to the corresponding visit. An 11-point Likert scale was used to assess the subject's sleep. The subject rated how the pain had interfered with sleep over the past 12 hours, from 0 (no interference) to 10 (complete interference). A negative value indicates improvement in symptoms from Baseline. Subjects rated pain interference over the past 12 hours for 7 days prior to each visit and an average value was calculated for each subject. (NCT00220337)
Timeframe: Baseline, Visit 2.1, Visit 2.2, Visit 2.4, Visit 2.5, Visit 3, Visit 4, Visit 5, Visit 6, Visit 7, Visit 8, Visit 9.0, Visit 9.1, Visit 9.2, Visit 9.3, Visit 9.4, Visit 9.5, Visit 9.6, Visit 9.7, Visit 9.8, Visit 9.9

Interventionunits on a scale (Mean)
Visit 2.1Visit 2.2Visit 2.3Visit 2.4Visit 2.5Visit 3Visit 4Visit 5Visit 6Visit 7Visit 8Visit 9.0Visit 9.1Visit 9.2Visit 9.3Visit 9.4Visit 9.5Visit 9.6Visit 9.7Visit 9.8Visit 9.9
Lacosamide-0.99-1.35-1.77-1.25-1.38-2.62-3.05-3.29-3.27-3.37-3.45-3.51-3.44-3.45-3.65-3.56-3.60-3.47-3.54-3.62-3.35

[back to top]

Change in Average Pain Interference With General Activity From the Baseline Week to the 7 Days Prior to Each Visit

Pain interference scores at each visit (sleep and activity respectively) were defined as the average of the respective daily interference scores during the 7 last available days prior to the corresponding visit. An 11-point Likert scale was used to assess the subject's sleep. The subject rated how the pain had interfered with sleep over the past 12 hours, from 0 (no interference) to 10 (complete interference). A negative value indicates improvement in symptoms from Baseline. Subjects rated pain interference over the past 12 hours for 7 days prior to each visit and an average value was calculated for each subject. (NCT00220337)
Timeframe: Baseline, Visit 2.1, Visit 2.2, Visit 2.4, Visit 2.5, Visit 3, Visit 4, Visit 5, Visit 6, Visit 7, Visit 8, Visit 9.0, Visit 9.1, Visit 9.2, Visit 9.3, Visit 9.4, Visit 9.5, Visit 9.6, Visit 9.7, Visit 9.8, Visit 9.9

Interventionunits on a scale (Mean)
Visit 2.1Visit 2.2Visit 2.3Visit 2.4Visit 2.5Visit 3Visit 4Visit 5Visit 6Visit 7Visit 8Visit 9.0Visit 9.1Visit 9.2Visit 9.3Visit 9.4Visit 9.5Visit 9.6Visit 9.7Visit 9.8Visit 9.9
Lacosamide-0.99-1.38-1.66-1.21-1.62-2.56-2.97-3.14-3.17-3.27-3.32-3.45-3.52-3.50-3.62-3.60-3.65-3.50-3.53-3.66-3.56

[back to top]

Percentage of Subjects With Adverse Events (AE) Reported Spontaneously by the Subject or Observed by the Investigator

An AE is any untoward medical occurrence in a patient or clinical investigation subject administered a pharmaceutical product that does not necessarily have a causal relationship with this treatment. (NCT00220337)
Timeframe: From Screening until Safety Follow up Visit (up to 140 weeks)

Interventionpercentage of participants (Number)
Lacosamide80.9

[back to top]

Percentage of Subjects Who Withdrew Due to Adverse Events (AEs)

An AE is any untoward medical occurrence in a patient or clinical investigation subject administered a pharmaceutical product that does not necessarily have a causal relationship with this treatment. (NCT00220337)
Timeframe: During the study period (up to 140 weeks)

Interventionpercentage of participants (Number)
Lacosamide16.4

[back to top]

Number of Subjects With Urine White Blood Cell Count 'Negative' at Baseline, Categorized by Urine White Blood Cell Count at Last Visit

Urinalysis was performed locally at all visits using a urine dipstick test. Categories are as following: negative, trace, positive +, positive ++, positive +++, not done (data not available). Positive categories (+,++,+++) indicate worsening from Baseline. (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
negativetracepositive +positive ++positive +++not done
Lacosamide32173517

[back to top]

Number of Subjects With Urine Urobilinogen Value 66 µmol/l at Baseline, Categorized by Urine Urobilinogen Value at Last Visit

Categories are as following: 3 µmol/l, 16 µmol/l, 33 µmol/l, 66 µmol/l, not done (data not available). (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
3 µmol/l16 µmol/l33 µmol/l66 µmol/lNot done
Lacosamide10000

[back to top]

Number of Subjects With Urine Urobilinogen Value 3 µmol/l at Baseline, Categorized by Urine Urobilinogen Value at Last Visit

Categories are as following: 3 µmol/l, 16 µmol/l, 33 µmol/l, 66 µmol/l, not done (data not available). (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
3 µmol/l16 µmol/l33 µmol/l66 µmol/lNot done
Lacosamide3513007

[back to top]

Number of Subjects With Urine Urobilinogen Value 16 µmol/l at Baseline, Categorized by Urine Urobilinogen Value at Last Visit

Categories are as following: 3 µmol/l, 16 µmol/l, 33 µmol/l, 66 µmol/l, not done (data not available). (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
3 µmol/l16 µmol/l33 µmol/l66 µmol/lNot done
Lacosamide71100

[back to top]

Number of Subjects With Urine Protein Status 'Trace' at Baseline, Categorized by Urine Protein Status at Last Visit

Urinalysis was performed locally at all visits using a urine dipstick test. Categories are as following: negative, trace, positive +, positive ++, positive +++, not done (data not available). Positive category (+, ++, +++) indicate worsening from Baseline. (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
NegativeTracePositive +Positive ++Positive +++Not done
Lacosamide2774001

[back to top]

Number of Subjects With Urine Protein Status 'Positive +++' at Baseline, Categorized by Urine Protein Status at Last Visit

Urinalysis was performed locally at all visits using a urine dipstick test. Categories are as following: negative, trace, positive +, positive ++, positive +++, not done (data not available). Positive category (+, ++, +++) indicate worsening from Baseline. (NCT00220337)
Timeframe: Last Visit (up to 140 weeks)

InterventionParticipants (Number)
NegativeTracePositive +Positive ++Positive +++Not done
Lacosamide000110

[back to top]

Number of Subjects With Urine Protein Status 'Positive ++' at Baseline, Categorized by Urine Protein Status at Last Visit

Urinalysis was performed locally at all visits using a urine dipstick test. Categories are as following: negative, trace, positive +, positive ++, positive +++, not done (data not available). Positive category (+, ++, +++) indicate worsening from Baseline. (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
NegativeTracePositive +Positive ++Positive +++Not done
Lacosamide203010

[back to top]

Number of Subjects With Urine Protein Status 'Positive +' at Baseline, Categorized by Urine Protein Status at Last Visit

Urinalysis was performed locally at all visits using a urine dipstick test. Categories are as following: negative, trace, positive +, positive ++, positive +++, not done (data not available). Positive category (+, ++, +++) indicate worsening from Baseline. (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
NegativeTracePositive +Positive ++Positive +++Not done
Lacosamide311200

[back to top]

Number of Subjects With Urine Protein Status 'Negative' at Baseline, Categorized by Urine Protein Status at Last Visit

Urinalysis was performed locally at all visits using a urine dipstick test. Categories are as following: negative, trace, positive +, positive ++, positive +++, not done (data not available). Positive categories (+,++,+++) indicate worsening from Baseline. (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
NegativeTracePositive +Positive ++Positive +++Not done
Lacosamide292133126

[back to top]

Number of Subjects With Urine pH= 8.0 at Baseline, Categorized by Urine pH at Last Visit

Urinalysis was performed locally at all visits using a urine dipstick test. Categories are as following: pH= 5.0, pH= 6.0, pH= 6.5, pH= 7.0, pH= 7.5, pH= 8.0, pH= 8.5, not done (data not available). Baseline value taken at Visit 2 or at screening for parameters not collected at Visit 2. Last visit is the last post-baseline visit observed under exposure of trial medication, including unscheduled visits. (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
pH= 5.0pH= 6.0pH= 6.5pH= 7.0pH= 7.5pH= 8.0pH= 8.5not done
Lacosamide00100000

[back to top]

Change in Quality of Life From Visit 2 (Baseline) to Visit 9.6

Quality of life was analyzed using the SF-36 Health Survey quality of life questionnaire. The SF-36 is a participant self-rated questionnaire which consists of 8 sub-scores ranging from 0-100 with higher scores indicating a better health state. The sub-scores are: 1. Physical Functioning, 2. Role-Physical, 3. Bodily Pain, 4. General Health, 5. Vitality, 6. Social Functioning, 7. Role-Emotional, 8. Mental Health. Items 1-4 primarily contribute to the PCS score of the SF-36. Items 5-8 primarily contribute to the MCS score of the SF-36. The PCS and MCS were based on the standardized values of the 8 domains. The maximum and minimum possible values for PCS and MCS is 0-100, where higher scores indicate good condition. A positive value indicates improvement from baseline in quality of life. (NCT00220337)
Timeframe: Baseline, Visit 9.6

Interventionunits on a scale (Mean)
Physical FunctioningRole-PhysicalBodily PainGeneral healthVitalitySocial FunctioningRole-EmotionalMental HealthPCSMCS
Lacosamide8.618.424.87.07.98.812.74.96.52.3

[back to top]

Number of Subjects With Urine White Blood Cell Count 'Trace' at Baseline, Categorized by Urine White Blood Cell Count at Last Visit

Urinalysis was performed locally at all visits using a urine dipstick test. Categories are as following: negative, trace, positive +, positive ++, positive +++, not done (data not available). Positive categories (+,++,+++) indicate worsening from Baseline. (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
negativetracepositive +positive ++positive +++not done
Lacosamide1310010

[back to top]

Change in Quality of Life From Visit 2 (Baseline) to Visit 9.5

Quality of life was analyzed using the SF-36 Health Survey quality of life questionnaire. The SF-36 is a participant self-rated questionnaire which consists of 8 sub-scores ranging from 0-100 with higher scores indicating a better health state. The sub-scores are: 1. Physical Functioning, 2. Role-Physical, 3. Bodily Pain, 4. General Health, 5. Vitality, 6. Social Functioning, 7. Role-Emotional, 8. Mental Health. Items 1-4 primarily contribute to the PCS score of the SF-36. Items 5-8 primarily contribute to the MCS score of the SF-36. The PCS and MCS were based on the standardized values of the 8 domains. The maximum and minimum possible values for PCS and MCS is 0-100, where higher scores indicate good condition. A positive value indicates improvement from baseline in quality of life. (NCT00220337)
Timeframe: Baseline, Visit 9.5

Interventionpercentage of participants (Mean)
Physical FunctioningRole-PhysicalBodily PainGeneral healthVitalitySocial FunctioningRole-EmotionalMental HealthPCSMCS
Lacosamide8.619.125.97.97.58.29.93.77.01.4

[back to top]

Number of Subjects With Urine White Blood Cell Count 'Positive ++' at Baseline, Categorized by Urine White Blood Cell Count at Last Visit

Urinalysis was performed locally at all visits using a urine dipstick test. Categories are as following: negative, trace, positive +, positive ++, positive +++, not done (data not available). Positive categories (+,++,+++) indicate worsening from Baseline. (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
negativetracepositive +positive ++positive +++not done
Lacosamide302100

[back to top]

Change in Quality of Life From Visit 2 (Baseline) to Visit 9.4

Quality of life was analyzed using the SF-36 Health Survey quality of life questionnaire. The SF-36 is a participant self-rated questionnaire which consists of 8 sub-scores ranging from 0-100 with higher scores indicating a better health state. The sub-scores are: 1. Physical Functioning, 2. Role-Physical, 3. Bodily Pain, 4. General Health, 5. Vitality, 6. Social Functioning, 7. Role-Emotional, 8. Mental Health. Items 1-4 primarily contribute to the PCS score of the SF-36. Items 5-8 primarily contribute to the MCS score of the SF-36. The PCS and MCS were based on the standardized values of the 8 domains. The maximum and minimum possible values for PCS and MCS is 0-100, where higher scores indicate good condition. A positive value indicates improvement from baseline in quality of life. (NCT00220337)
Timeframe: Baseline, Visit 9.4

Interventionunits on a scale (Mean)
Physical FunctioningRole-PhysicalBodily PainGeneral healthVitalitySocial FunctioningRole-EmotionalMental HealthPCSMCS
Lacosamide9.317.324.16.88.79.012.15.06.42.4

[back to top]

Change in Quality of Life From Visit 2 (Baseline) to Visit 9.3

Quality of life was analyzed using the SF-36 Health Survey quality of life questionnaire. The SF-36 is a participant self-rated questionnaire which consists of 8 sub-scores ranging from 0-100 with higher scores indicating a better health state. The sub-scores are: 1. Physical Functioning, 2. Role-Physical, 3. Bodily Pain, 4. General Health, 5. Vitality, 6. Social Functioning, 7. Role-Emotional, 8. Mental Health. Items 1-4 primarily contribute to the PCS score of the SF-36. Items 5-8 primarily contribute to the MCS score of the SF-36. The PCS and MCS were based on the standardized values of the 8 domains. The maximum and minimum possible values for PCS and MCS is 0-100, where higher scores indicate good condition. A positive value indicates improvement from baseline in quality of life. (NCT00220337)
Timeframe: Baseline, Visit 9.3

Interventionunits on a scale (Mean)
Physical FunctioningRole-PhysicalBodily PainGeneral healthVitalitySocial FunctioningRole-EmotionalMental HealthPCSMCS
Lacosamide10.320.226.38.39.99.814.85.17.22.7

[back to top]

Change in Quality of Life From Visit 2 (Baseline) to Visit 9.2

Quality of life was analyzed using the SF-36 Health Survey quality of life questionnaire. The SF-36 is a participant self-rated questionnaire which consists of 8 sub-scores ranging from 0-100 with higher scores indicating a better health state. The sub-scores are: 1. Physical Functioning, 2. Role-Physical, 3. Bodily Pain, 4. General Health, 5. Vitality, 6. Social Functioning, 7. Role-Emotional, 8. Mental Health. Items 1-4 primarily contribute to the PCS score of the SF-36. Items 5-8 primarily contribute to the MCS score of the SF-36. The PCS and MCS were based on the standardized values of the 8 domains. The maximum and minimum possible values for PCS and MCS is 0-100, where higher scores indicate good condition. A positive value indicates improvement from baseline in quality of life. (NCT00220337)
Timeframe: Baseline, Visit 9.2

Interventionunits on a scale (Mean)
Physical FunctioningRole-PhysicalBodily PainGeneral healthVitalitySocial FunctioningRole-EmotionalMental HealthPCSMCS
Lacosamide9.619.223.86.79.79.913.96.76.33.3

[back to top]

Change in Quality of Life From Visit 2 (Baseline) to Visit 9.0

Quality of life was analyzed using the SF-36 Health Survey quality of life questionnaire. The SF-36 is a participant self-rated questionnaire which consists of 8 sub-scores ranging from 0-100 with higher scores indicating a better health state. The sub-scores are: 1. Physical Functioning, 2. Role-Physical, 3. Bodily Pain, 4. General Health, 5. Vitality, 6. Social Functioning, 7. Role-Emotional, 8. Mental Health. Items 1-4 primarily contribute to the PCS score of the SF-36. Items 5-8 primarily contribute to the MCS score of the SF-36. The PCS and MCS were based on the standardized values of the 8 domains. The maximum and minimum possible values for PCS and MCS is 0-100, where higher scores indicate good condition. A positive value indicates improvement from baseline in quality of life. (NCT00220337)
Timeframe: Baseline, Visit 9.0

Interventionunits on a scale (Mean)
Physical FunctioningRole-PhysicalBodily PainGeneral healthVitalitySocial FunctioningRole-EmotionalMental HealthPCSMCS
Lacosamide10.417.525.38.810.510.312.15.07.12.6

[back to top]

Change in Quality of Life From Visit 2 (Baseline) to Visit 6

Quality of life was analyzed using the SF-36 Health Survey quality of life questionnaire. The SF-36 is a participant self-rated questionnaire which consists of 8 sub-scores ranging from 0-100 with higher scores indicating a better health state. The sub-scores are: 1. Physical Functioning, 2. Role-Physical, 3. Bodily Pain, 4. General Health, 5. Vitality, 6. Social Functioning, 7. Role-Emotional, 8. Mental Health. Items 1-4 primarily contribute to the PCS score of the SF-36. Items 5-8 primarily contribute to the MCS score of the SF-36. The PCS and MCS were based on the standardized values of the 8 domains. The maximum and minimum possible values for PCS and MCS is 0-100, where higher scores indicate good condition. A positive value indicates improvement from baseline in quality of life. (NCT00220337)
Timeframe: Baseline, Visit 6

Interventionunits on a scale (Mean)
Physical FunctioningRole-PhysicalBodily PainGeneral healthVitalitySocial FunctioningRole-EmotionalMental HealthPCSMCS
Lacosamide8.012.122.47.28.48.48.25.05.72.2

[back to top]

Change in Quality of Life From Visit 2 (Baseline) to Visit 4

Quality of life was analyzed using the Short Form-36 (SF-36) Health Survey quality of life questionnaire. The SF-36 is a participant self-rated questionnaire which consists of 8 sub-scores ranging from 0-100 with higher scores indicating a better health state. The sub-scores are: 1. Physical Functioning, 2. Role-Physical, 3. Bodily Pain, 4. General Health, 5. Vitality, 6. Social Functioning, 7. Role-Emotional, 8. Mental Health. Items 1-4 primarily contribute to the physical component Summary (PCS) score of the SF-36. Items 5-8 primarily contribute to the mental component summary (MCS) score of the SF-36. The PCS and MCS were based on the standardized values of the 8 domains. The maximum and minimum possible values for PCS and MCS is 0-100, where higher scores indicate good condition. A positive value indicates improvement from baseline in quality of life. (NCT00220337)
Timeframe: Baseline, Visit 4

Interventionunits on a scale (Mean)
Physical FunctioningRole-PhysicalBodily PainGeneral healthVitalitySocial FunctioningRole-EmotionalMental HealthPCSMCS
Lacosamide7.413.120.86.18.58.27.15.65.32.2

[back to top]

Change in Quality of Life From Visit 2 (Baseline) to Termination Visit

Quality of life was analyzed using the SF-36 Health Survey quality of life questionnaire. The SF-36 is a participant self-rated questionnaire which consists of 8 sub-scores ranging from 0-100 with higher scores indicating a better health state. The sub-scores are: 1. Physical Functioning, 2. Role-Physical, 3. Bodily Pain, 4. General Health, 5. Vitality, 6. Social Functioning, 7. Role-Emotional, 8. Mental Health. Items 1-4 primarily contribute to the PCS score of the SF-36. Items 5-8 primarily contribute to the MCS score of the SF-36. The PCS and MCS were based on the standardized values of the 8 domains. The maximum and minimum possible values for PCS and MCS is 0-100, where higher scores indicate good condition. A positive value indicates improvement from baseline in quality of life. (NCT00220337)
Timeframe: Baseline, Termination Visit (last treatment visit)

Interventionunits on a scale (Mean)
Physical FunctioningRole-PhysicalBodily PainGeneral HealthVitalitySocial FunctioningRole-EmotionalMental HealthPCSMCS
Lacosamide5.07.819.34.14.54.22.51.24.70.1

[back to top]

Change in Different Symptoms of Neuropathic Pain From Visit 2 (Baseline) to Visit 9.8

Subjects were asked to assess different symptoms of neuropathic pain with respect to severity using the NPSI at different visits. It comprised of 10 descriptive symptom questions (pain feels like burning, squeezing, pressure electric shocks, stabbing, pins/needles, tingling, provoked or increased by brushing, pressure or contact with something cold), and 2 temporal questions (duration of pain, number of pain attacks). The NPSI scores of the descriptive questions are reported in categories below, which were rated on an 11-point scale from 0 (absence of pain) to 10 (maximum intensity of pain). Higher scores indicate a greater intensity of pain. A negative value indicates improvement in symptoms from Baseline. This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Baseline, Visit 9.8

Interventionunits on a scale (Mean)
BurningSqueezingPressureElectric shocksStabbingBrushingIncreased by pressureContact with coldPins and needlesTingling
Lacosamide-2.3-2.0-1.7-3.0-2.5-0.4-1.6-1.4-3.0-3.2

[back to top]

Change in Different Symptoms of Neuropathic Pain From Visit 2 (Baseline) to Visit 9.7

Subjects were asked to assess different symptoms of neuropathic pain with respect to severity using the NPSI at different visits. It comprised of 10 descriptive symptom questions (pain feels like burning, squeezing, pressure electric shocks, stabbing, pins/needles, tingling, provoked or increased by brushing, pressure or contact with something cold), and 2 temporal questions (duration of pain, number of pain attacks). The NPSI scores of the descriptive questions are reported in categories below, which were rated on an 11-point scale from 0 (absence of pain) to 10 (maximum intensity of pain). Higher scores indicate a greater intensity of pain. A negative value indicates improvement in symptoms from Baseline. This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Baseline, Visit 9.7

Interventionunits on a scale (Mean)
BurningSqueezingPressureElectric shocksStabbingBrushingIncreased by pressureContact with coldPins and needlesTingling
Lacosamide-3.2-2.1-2.2-2.9-2.5-1.0-2.5-1.2-3.2-3.3

[back to top]

Change in Different Symptoms of Neuropathic Pain From Visit 2 (Baseline) to Visit 9.6

Subjects were asked to assess different symptoms of neuropathic pain with respect to severity using the NPSI at different visits. It comprised of 10 descriptive symptom questions (pain feels like burning, squeezing, pressure electric shocks, stabbing, pins/needles, tingling, provoked or increased by brushing, pressure or contact with something cold), and 2 temporal questions (duration of pain, number of pain attacks). The NPSI scores of the descriptive questions are reported in categories below, which were rated on an 11-point scale from 0 (absence of pain) to 10 (maximum intensity of pain). Higher scores indicate a greater intensity of pain. A negative value indicates improvement in symptoms from Baseline. This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Baseline, Visit 9.6

Interventionunits on a scale (Mean)
BurningSqueezingPressureElectric shocksStabbingBrushingIncreased by pressureContact with coldPins and needlesTingling
Lacosamide-3.0-2.0-2.8-3.1-2.8-0.8-2.7-1.4-3.1-3.5

[back to top]

Change in Different Symptoms of Neuropathic Pain From Visit 2 (Baseline) to Visit 9.5

Subjects were asked to assess different symptoms of neuropathic pain with respect to severity using the NPSI at different visits. It comprised of 10 descriptive symptom questions (pain feels like burning, squeezing, pressure electric shocks, stabbing, pins/needles, tingling, provoked or increased by brushing, pressure or contact with something cold), and 2 temporal questions (duration of pain, number of pain attacks). The NPSI scores of the descriptive questions are reported in categories below, which were rated on an 11-point scale from 0 (absence of pain) to 10 (maximum intensity of pain). Higher scores indicate a greater intensity of pain. A negative value indicates improvement in symptoms from Baseline. This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Baseline, Visit 9.5

Interventionunits on a scale (Mean)
BurningSqueezingPressureElectric shocksStabbingBrushingIncreased by pressureContact with coldPins and needlesTingling
Lacosamide-3.1-2.0-2.4-2.8-2.8-1.0-2.3-1.6-3.0-3.1

[back to top]

Change in Different Symptoms of Neuropathic Pain From Visit 2 (Baseline) to Visit 9.4

Subjects were asked to assess different symptoms of neuropathic pain with respect to severity using the NPSI at different visits. It comprised of 10 descriptive symptom questions (pain feels like burning, squeezing, pressure electric shocks, stabbing, pins/needles, tingling, provoked or increased by brushing, pressure or contact with something cold), and 2 temporal questions (duration of pain, number of pain attacks). The NPSI scores of the descriptive questions are reported in categories below, which were rated on an 11-point scale from 0 (absence of pain) to 10 (maximum intensity of pain). Higher scores indicate a greater intensity of pain. A negative value indicates improvement in symptoms from Baseline. This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Baseline, Visit 9.4

Interventionunits on a scale (Mean)
BurningSqueezingPressureElectric shocksStabbingBrushingIncreased by pressureContact with coldPins and needlesTingling
Lacosamide-2.8-1.5-2.3-2.3-2.8-0.9-2.2-1.4-2.8-3.1

[back to top]

Change in Different Symptoms of Neuropathic Pain From Visit 2 (Baseline) to Visit 9.3

Subjects were asked to assess different symptoms of neuropathic pain with respect to severity using the NPSI at different visits. It comprised of 10 descriptive symptom questions (pain feels like burning, squeezing, pressure electric shocks, stabbing, pins/needles, tingling, provoked or increased by brushing, pressure or contact with something cold), and 2 temporal questions (duration of pain, number of pain attacks). The NPSI scores of the descriptive questions are reported in categories below, which were rated on an 11-point scale from 0 (absence of pain) to 10 (maximum intensity of pain). Higher scores indicate a greater intensity of pain. A negative value indicates improvement in symptoms from Baseline. This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Baseline, Visit 9.3

Interventionunits on a scale (Mean)
BurningSqueezingPressureElectric shocksStabbingBrushingIncreased by pressureContact with coldPins and needlesTingling
Lacosamide-3.1-1.9-2.6-3.0-2.8-0.8-2.5-1.5-2.9-3.3

[back to top]

Change in Different Symptoms of Neuropathic Pain From Visit 2 (Baseline) to Visit 9.2

Subjects were asked to assess different symptoms of neuropathic pain with respect to severity using the NPSI at different visits. It comprised of 10 descriptive symptom questions (pain feels like burning, squeezing, pressure electric shocks, stabbing, pins/needles, tingling, provoked or increased by brushing, pressure or contact with something cold), and 2 temporal questions (duration of pain, number of pain attacks). The NPSI scores of the descriptive questions are reported in categories below, which were rated on an 11-point scale from 0 (absence of pain) to 10 (maximum intensity of pain). Higher scores indicate a greater intensity of pain. A negative value indicates improvement in symptoms from Baseline. This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Baseline, Visit 9.2

Interventionunits on a scale (Mean)
BurningSqueezingPressureElectric shocksStabbingBrushingIncreased by pressureContact with coldPins and needlesTingling
Lacosamide-3.2-2.4-2.7-2.8-3.0-1.0-2.3-1.7-3.2-3.0

[back to top]

Number of Subjects With Urine pH= 7.5 at Baseline, Categorized by Urine pH at Last Visit

Urinalysis was performed locally at all visits using a urine dipstick test. Categories are as following: pH= 5.0, pH= 6.0, pH= 6.5, pH= 7.0, pH= 7.5, pH= 8.0, pH= 8.5, not done (data not available). Baseline value taken at Visit 2 or at screening for parameters not collected at Visit 2. Last visit is the last post-baseline visit observed under exposure of trial medication, including unscheduled visits. (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
pH= 5.0pH= 6.0pH= 6.5pH= 7.0pH= 7.5pH= 8.0pH= 8.5not done
Lacosamide30300000

[back to top]

Number of Subjects With Urine pH= 7.0 at Baseline, Categorized by Urine pH at Last Visit

Urinalysis was performed locally at all visits using a urine dipstick test. Categories are as following: pH= 5.0, pH= 6.0, pH= 6.5, pH= 7.0, pH= 7.5, pH= 8.0, pH= 8.5, not done (data not available). Baseline value taken at Visit 2 or at screening for parameters not collected at Visit 2. Last visit is the last post-baseline visit observed under exposure of trial medication, including unscheduled visits. (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
pH= 5.0pH= 6.0pH= 6.5pH= 7.0pH= 7.5pH= 8.0pH= 8.5not done
Lacosamide43100000

[back to top]

Number of Subjects With Urine pH= 6.5 at Baseline, Categorized by Urine pH at Last Visit

Urinalysis was performed locally at all visits using a urine dipstick test. Categories are as following: pH= 5.0, pH= 6.0, pH= 6.5, pH= 7.0, pH= 7.5, pH= 8.0, pH= 8.5, not done (data not available). Baseline value taken at Visit 2 or at screening for parameters not collected at Visit 2. Last visit is the last post-baseline visit observed under exposure of trial medication, including unscheduled visits. (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
pH= 5.0pH= 6.0pH= 6.5pH= 7.0pH= 7.5pH= 8.0pH= 8.5not done
Lacosamide107500101

[back to top]

Number of Subjects With Urine pH= 6.0 at Baseline, Categorized by Urine pH at Last Visit

Urinalysis was performed locally at all visits using a urine dipstick test. Categories are as following: pH= 5.0, pH= 6.0, pH= 6.5, pH= 7.0, pH= 7.5, pH= 8.0, pH= 8.5, not done (data not available). Baseline value taken at Visit 2 or at screening for parameters not collected at Visit 2. Last visit is the last post-baseline visit observed under exposure of trial medication, including unscheduled visits. (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
pH= 5.0pH= 6.0pH= 6.5pH= 7.0pH= 7.5pH= 8.0pH= 8.5not done
Lacosamide5231421102

[back to top]

Number of Subjects With Urine pH= 5.0 at Baseline, Categorized by Urine pH at Last Visit

Urinalysis was performed locally at all visits using a urine dipstick test. Categories are as following: pH= 5.0, pH= 6.0, pH= 6.5, pH= 7.0, pH= 7.5, pH= 8.0, pH= 8.5, not done (data not available). Baseline value taken at Visit 2 or at screening for parameters not collected at Visit 2. Last visit is the last post-baseline visit observed under exposure of trial medication, including unscheduled visits. (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
pH= 5.0pH= 6.0pH= 6.5pH= 7.0pH= 7.5pH= 8.0pH= 8.5not done
Lacosamide19435231004

[back to top]

Number of Subjects With Urine Nitrite Status 'Positive' at Baseline, Categorized by Urine Nitrite Status at Last Visit

Urinalysis was performed locally at all visits using a urine dipstick test. Categories are as following: negative, positive, not done (data not available). Positive category indicate worsening from Baseline. (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
negativepositivenot done
Lacosamide330

[back to top]

Number of Subjects With Urine Nitrite Status 'Negative' at Baseline, Categorized by Urine Nitrite Status at Last Visit

Urinalysis was performed locally at all visits using a urine dipstick test. Categories are as following: negative, positive, not done (data not available). Positive category indicate worsening from Baseline. (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
negativepositivenot done
Lacosamide35357

[back to top]

Percentage of Subjects With Presence of Spontaneous Pain Categorized by Duration of Pain at Visit 9.8

Presence of spontaneous pain was analyzed using the Neuropathic Pain Symptom Inventory (NPSI). This questionnaire comprises 10 descriptive questions, which are rated on 0 to 10 point scales, and 2 temporal questions. Categories of duration of pain are as following: permanently, between 8 and 12 h, between 4 and 7 h, between 1 and 3 h, Less than 1 h. This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Visit 9.8

Interventionpercentage of participants (Number)
PermanentlyBetween 8 and 12 hBetween 4 and 7 hBetween 1 and 3 hLess than 1 h
Lacosamide010.526.326.336.8

[back to top]

Percentage of Subjects With Presence of Spontaneous Pain Categorized by Duration of Pain at Visit 9.7

Presence of spontaneous pain was analyzed using the Neuropathic Pain Symptom Inventory (NPSI). This questionnaire comprises 10 descriptive questions, which are rated on 0 to 10 point scales, and 2 temporal questions. Categories of duration of pain are as following: permanently, between 8 and 12 h, between 4 and 7 h, between 1 and 3 h, Less than 1 h. This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Visit 9.7

Interventionpercentage of participants (Number)
PermanentlyBetween 8 and 12 hBetween 4 and 7 hBetween 1 and 3 hLess than 1 h
Lacosamide7.47.414.816.753.7

[back to top]

Percentage of Subjects With Presence of Spontaneous Pain Categorized by Duration of Pain at Visit 9.6

Presence of spontaneous pain was analyzed using the Neuropathic Pain Symptom Inventory (NPSI). This questionnaire comprises 10 descriptive questions, which are rated on 0 to 10 point scales, and 2 temporal questions. Categories of duration of pain are as following: permanently, between 8 and 12 h, between 4 and 7 h, between 1 and 3 h, Less than 1 h. This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Visit 9.6

Interventionpercentage of participants (Number)
PermanentlyBetween 8 and 12 hBetween 4 and 7 hBetween 1 and 3 hLess than 1 h
Lacosamide3.610.723.217.944.6

[back to top]

Percentage of Subjects With Presence of Spontaneous Pain Categorized by Duration of Pain at Visit 9.5

Presence of spontaneous pain was analyzed using the Neuropathic Pain Symptom Inventory (NPSI). This questionnaire comprises 10 descriptive questions, which are rated on 0 to 10 point scales, and 2 temporal questions. Categories of duration of pain are as following: permanently, between 8 and 12 h, between 4 and 7 h, between 1 and 3 h, Less than 1 h. This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Visit 9.5

Interventionpercentage of participants (Number)
PermanentlyBetween 8 and 12 hBetween 4 and 7 hBetween 1 and 3 hLess than 1 h
Lacosamide8.36.715.021.748.3

[back to top]

Percentage of Subjects With Presence of Spontaneous Pain Categorized by Duration of Pain at Visit 9.4

Presence of spontaneous pain was analyzed using the Neuropathic Pain Symptom Inventory (NPSI). This questionnaire comprises 10 descriptive questions, which are rated on 0 to 10 point scales, and 2 temporal questions. Categories of duration of pain are as following: permanently, between 8 and 12 h, between 4 and 7 h, between 1 and 3 h, Less than 1 h. This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Visit 9.4

Interventionpercentage of participants (Number)
PermanentlyBetween 8 and 12 hBetween 4 and 7 hBetween 1 and 3 hLess than 1 h
Lacosamide6.311.115.922.244.4

[back to top]

Percentage of Subjects With Presence of Spontaneous Pain Categorized by Duration of Pain at Visit 9.3

Presence of spontaneous pain was analyzed using the Neuropathic Pain Symptom Inventory (NPSI). This questionnaire comprises 10 descriptive questions, which are rated on 0 to 10 point scales, and 2 temporal questions. Categories of duration of pain are as following: permanently, between 8 and 12 h, between 4 and 7 h, between 1 and 3 h, Less than 1 h. This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Visit 9.3

Interventionpercentage of participants (Number)
PermanentlyBetween 8 and 12 hBetween 4 and 7 hBetween 1 and 3 hLess than 1 h
Lacosamide3.13.115.628.150.0

[back to top]

Percentage of Subjects With Presence of Spontaneous Pain Categorized by Duration of Pain at Visit 9.2

Presence of spontaneous pain was analyzed using the Neuropathic Pain Symptom Inventory (NPSI). This questionnaire comprises 10 descriptive questions, which are rated on 0 to 10 point scales, and 2 temporal questions. Categories of duration of pain are as following: permanently, between 8 and 12 h, between 4 and 7 h, between 1 and 3 h, Less than 1 h. This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Visit 9.2

Interventionpercentage of participants (Number)
PermanentlyBetween 8 and 12 hBetween 4 and 7 hBetween 1 and 3 hLess than 1 h
Lacosamide5.69.78.322.254.2

[back to top]

Percentage of Subjects With Presence of Spontaneous Pain Categorized by Duration of Pain at Visit 9.1

Presence of spontaneous pain was analyzed using the Neuropathic Pain Symptom Inventory (NPSI). This questionnaire comprises 10 descriptive questions, which are rated on 0 to 10 point scales, and 2 temporal questions. Categories of duration of pain are as following: permanently, between 8 and 12 h, between 4 and 7 h, between 1 and 3 h, Less than 1 h. This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Visit 9.1

Interventionpercentage of participants (Number)
PermanentlyBetween 8 and 12 hBetween 4 and 7 hBetween 1 and 3 hLess than 1 hNot done
Lacosamide9.38.115.126.739.51.2

[back to top]

Percentage of Subjects With Presence of Spontaneous Pain Categorized by Duration of Pain at Visit 9.0

Presence of spontaneous pain was analyzed using the Neuropathic Pain Symptom Inventory (NPSI). This questionnaire comprises 10 descriptive questions, which are rated on 0 to 10 point scales, and 2 temporal questions. Categories of duration of pain are as following: permanently, between 8 and 12 h, between 4 and 7 h, between 1 and 3 h, Less than 1 h. This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Visit 9.0

Interventionpercentage of participants (Number)
PermanentlyBetween 8 and 12 hBetween 4 and 7 hBetween 1 and 3 hLess than 1 h
Lacosamide11.18.910.022.247.8

[back to top]

Percentage of Subjects With Presence of Spontaneous Pain Categorized by Duration of Pain at Visit 6

Presence of spontaneous pain was analyzed using the Neuropathic Pain Symptom Inventory (NPSI). This questionnaire comprises 10 descriptive questions, which are rated on 0 to 10 point scales, and 2 temporal questions. Categories of duration of pain are as following: permanently, between 8 and 12 h, between 4 and 7 h, between 1 and 3 h, Less than 1 h. This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Visit 6

Interventionpercentage of participants (Number)
PermanentlyBetween 8 and 12 hBetween 4 and 7 hBetween 1 and 3 hLess than 1 h
Lacosamide12.67.811.724.343.7

[back to top]

Percentage of Subjects With Presence of Spontaneous Pain Categorized by Duration of Pain at Visit 4

Presence of spontaneous pain was analyzed using the Neuropathic Pain Symptom Inventory (NPSI). This questionnaire comprises 10 descriptive questions, which are rated on 0 to 10 point scales, and 2 temporal questions. Categories of duration of pain are as following: permanently, between 8 and 12 h, between 4 and 7 h, between 1 and 3 h, Less than 1 h. This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Visit 4

Interventionpercentage of participants (Number)
PermanentlyBetween 8 and 12 hBetween 4 and 7 hBetween 1 and 3 hLess than 1 h
Lacosamide10.913.617.320.937.3

[back to top]

Number of Subjects With Urine White Blood Cell Count 'Positive +' at Baseline, Categorized by Urine White Blood Cell Count at Last Visit

Urinalysis was performed locally at all visits using a urine dipstick test. Categories are as following: negative, trace, positive +, positive ++, positive +++, not done (data not available). Positive categories (+,++,+++) indicate worsening from Baseline. (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
negativetracepositive +positive ++positive +++not done
Lacosamide320100

[back to top]

Percentage of Subjects With Presence of Spontaneous Pain Categorized by Duration of Pain at Visit 2 (Baseline)

Presence of spontaneous pain was analyzed using the Neuropathic Pain Symptom Inventory (NPSI). This questionnaire comprises 10 descriptive questions, which are rated on 0 to 10 point scales, and 2 temporal questions. Categories of duration of pain are as following: permanently, between 8 and 12 h, between 4 and 7 h, between 1 and 3 h, Less than 1 h. This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Visit 2 (Baseline)

Interventionpercentage of participants (Number)
PermanentlyBetween 8 and 12 hBetween 4 and 7 hBetween 1 and 3 hLess than 1 h
Lacosamide37.621.319.114.27.8

[back to top]

Percentage of Subjects With Presence of Spontaneous Pain Categorized by Duration of Pain at Termination Visit

Presence of spontaneous pain was analyzed using the Neuropathic Pain Symptom Inventory (NPSI). This questionnaire comprises 10 descriptive questions, which are rated on 0 to 10 point scales, and 2 temporal questions. Categories of duration of pain are as following: permanently, between 8 and 12 h, between 4 and 7 h, between 1 and 3 h, Less than 1 h. This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Termination Visit (last treatment visit)

Interventionpercentage of participants (Number)
PermanentlyBetween 8 and 12 hBetween 4 and 7 hBetween 1 and 3 hLess than 1 h
Lacosamide16.113.616.918.634.7

[back to top]

Percentage of Subjects With Pain Attacks in Last the 24 Hours Categorized by Number of Pain Attacks at Visit 9.8

Pain attacks were analyzed using the Neuropathic Pain Symptom Inventory (NPSI). This questionnaire comprises 10 descriptive questions, which are rated on 0 to 10 point scales, and 2 temporal questions. Categories of number of pain attacks are as following: no pain attack, between 1 and 5, between 6 and 10, between 11 and 20, more than 20, not done (data not available). This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Visit 9.8

Interventionpercentage of participants (Number)
No pain attackBetween 1 and 5Between 6 and 10Between 11 and 20More than 20Not done
Lacosamide26.352.615.805.30

[back to top]

Percentage of Subjects With Pain Attacks in Last the 24 Hours Categorized by Number of Pain Attacks at Visit 9.7

Pain attacks were analyzed using the Neuropathic Pain Symptom Inventory (NPSI). This questionnaire comprises 10 descriptive questions, which are rated on 0 to 10 point scales, and 2 temporal questions. Categories of number of pain attacks are as following: no pain attack, between 1 and 5, between 6 and 10, between 11 and 20, more than 20, not done (data not available). This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Visit 9.7

Interventionpercentage of participants (Number)
No pain attackBetween 1 and 5Between 6 and 10Between 11 and 20More than 20Not done
Lacosamide33.337.016.75.67.40

[back to top]

Percentage of Subjects With Pain Attacks in Last the 24 Hours Categorized by Number of Pain Attacks at Visit 9.6

Pain attacks were analyzed using the Neuropathic Pain Symptom Inventory (NPSI). This questionnaire comprises 10 descriptive questions, which are rated on 0 to 10 point scales, and 2 temporal questions. Categories of number of pain attacks are as following: no pain attack, between 1 and 5, between 6 and 10, between 11 and 20, more than 20, not done (data not available). This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Visit 9.6

Interventionpercentage of participants (Number)
No pain attackBetween 1 and 5Between 6 and 10Between 11 and 20More than 20Not done
Lacosamide30.444.614.35.45.40

[back to top]

Percentage of Subjects With Pain Attacks in Last the 24 Hours Categorized by Number of Pain Attacks at Visit 9.5

Pain attacks were analyzed using the Neuropathic Pain Symptom Inventory (NPSI). This questionnaire comprises 10 descriptive questions, which are rated on 0 to 10 point scales, and 2 temporal questions. Categories of number of pain attacks are as following: no pain attack, between 1 and 5, between 6 and 10, between 11 and 20, more than 20, not done (data not available). This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Visit 9.5

Interventionpercentage of participants (Number)
No pain attackBetween 1 and 5Between 6 and 10Between 11 and 20More than 20Not done
Lacosamide35.035.021.73.35.00

[back to top]

Percentage of Subjects With Pain Attacks in Last the 24 Hours Categorized by Number of Pain Attacks at Visit 9.4

Pain attacks were analyzed using the Neuropathic Pain Symptom Inventory (NPSI). This questionnaire comprises 10 descriptive questions, which are rated on 0 to 10 point scales, and 2 temporal questions. Categories of number of pain attacks are as following: no pain attack, between 1 and 5, between 6 and 10, between 11 and 20, more than 20, not done (data not available). This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Visit 9.4

Interventionpercentage of participants (Number)
No pain attackBetween 1 and 5Between 6 and 10Between 11 and 20More than 20Not done
Lacosamide31.733.319.011.14.80

[back to top]

Percentage of Subjects With Pain Attacks in Last the 24 Hours Categorized by Number of Pain Attacks at Visit 9.3

Pain attacks were analyzed using the Neuropathic Pain Symptom Inventory (NPSI). This questionnaire comprises 10 descriptive questions, which are rated on 0 to 10 point scales, and 2 temporal questions. Categories of number of pain attacks are as following: no pain attack, between 1 and 5, between 6 and 10, between 11 and 20, more than 20, not done (data not available). This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Visit 9.3

Interventionpercentage of participants (Number)
No pain attackBetween 1 and 5Between 6 and 10Between 11 and 20More than 20Not done
Lacosamide27.044.420.63.24.80

[back to top]

Percentage of Subjects With Pain Attacks in Last the 24 Hours Categorized by Number of Pain Attacks at Visit 9.2

Pain attacks were analyzed using the Neuropathic Pain Symptom Inventory (NPSI). This questionnaire comprises 10 descriptive questions, which are rated on 0 to 10 point scales, and 2 temporal questions. Categories of number of pain attacks are as following: no pain attack, between 1 and 5, between 6 and 10, between 11 and 20, more than 20, not done (data not available). This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Visit 9.2

Interventionpercentage of participants (Number)
No pain attackBetween 1 and 5Between 6 and 10Between 11 and 20More than 20Not done
Lacosamide27.449.39.69.64.10

[back to top]

Percentage of Subjects With Pain Attacks in Last the 24 Hours Categorized by Number of Pain Attacks at Visit 9.1

Pain attacks were analyzed using the Neuropathic Pain Symptom Inventory (NPSI). This questionnaire comprises 10 descriptive questions, which are rated on 0 to 10 point scales, and 2 temporal questions. Categories of number of pain attacks are as following: no pain attack, between 1 and 5, between 6 and 10, between 11 and 20, more than 20, not done (data not available). This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Visit 9.1

Interventionpercentage of participants (Number)
No pain attackBetween 1 and 5Between 6 and 10Between 11 and 20More than 20Not done
Lacosamide28.734.520.74.610.31.1

[back to top]

Percentage of Subjects With Pain Attacks in Last the 24 Hours Categorized by Number of Pain Attacks at Visit 9.0

Pain attacks were analyzed using the Neuropathic Pain Symptom Inventory (NPSI). This questionnaire comprises 10 descriptive questions, which are rated on 0 to 10 point scales, and 2 temporal questions. Categories of number of pain attacks are as following: no pain attack, between 1 and 5, between 6 and 10, between 11 and 20, more than 20, not done (data not available). This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Visit 9.0

Interventionpercentage of participants (Number)
No pain attackBetween 1 and 5Between 6 and 10Between 11 and 20More than 20Not done
Lacosamide36.735.620.05.62.20

[back to top]

Percentage of Subjects With Pain Attacks in Last the 24 Hours Categorized by Number of Pain Attacks at Visit 6

Pain attacks were analyzed using the Neuropathic Pain Symptom Inventory (NPSI). This questionnaire comprises 10 descriptive questions, which are rated on 0 to 10 point scales, and 2 temporal questions. Categories of number of pain attacks are as following: no pain attack, between 1 and 5, between 6 and 10, between 11 and 20, more than 20, not done (data not available). This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Visit 6

Interventionpercentage of participants (Number)
No pain attackBetween 1 and 5Between 6 and 10Between 11 and 20More than 20Not done
Lacosamide26.942.320.27.72.90

[back to top]

Percentage of Subjects With Pain Attacks in Last the 24 Hours Categorized by Number of Pain Attacks at Visit 4

Pain attacks were analyzed using the Neuropathic Pain Symptom Inventory (NPSI). This questionnaire comprises 10 descriptive questions, which are rated on 0 to 10 point scales, and 2 temporal questions. Categories of number of pain attacks are as following: no pain attack, between 1 and 5, between 6 and 10, between 11 and 20, more than 20, not done (data not available). This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Visit 4

Interventionpercentage of participants (Number)
No pain attackBetween 1 and 5Between 6 and 10Between 11 and 20More than 20Not done
Lacosamide29.139.120.95.55.50

[back to top]

Percentage of Subjects With Pain Attacks in Last the 24 Hours Categorized by Number of Pain Attacks at Visit 2 (Baseline)

Pain attacks were analyzed using the Neuropathic Pain Symptom Inventory (NPSI). This questionnaire comprises 10 descriptive questions, which are rated on 0 to 10 point scales, and 2 temporal questions. Categories of number of pain attacks are as following: no pain attack, between 1 and 5, between 6 and 10, between 11 and 20, more than 20, not done (data not available). This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Visit 2 (Baseline)

Interventionpercentage of participants (Number)
No pain attackBetween 1 and 5Between 6 and 10Between 11 and 20More than 20Not done
Lacosamide6.433.320.620.619.10

[back to top]

Percentage of Subjects With Pain Attacks in Last the 24 Hours Categorized by Number of Pain Attacks at Termination Visit

Pain attacks were analyzed using the Neuropathic Pain Symptom Inventory (NPSI). This questionnaire comprises 10 descriptive questions, which are rated on 0 to 10 point scales, and 2 temporal questions. Categories of number of pain attacks are as following: no pain attack, between 1 and 5, between 6 and 10, between 11 and 20, more than 20, not done (data not available). This assessment was done only in subjects from countries in which a validated version of the NPSI was available. (NCT00220337)
Timeframe: Termination Visit (last treatment visit)

Interventionpercentage of participants (Number)
No pain attackBetween 1 and 5Between 6 and 10Between 11 and 20More than 20Not done
Lacosamide28.835.615.311.09.30

[back to top]

Percentage of Subjects With Marked Abnormalities in Vital Signs After Start of Treatment

Changes in vital signs examination findings is reported as percentage of subjects with marked abnormalities in - Systolic Blood Pressure (SBP) >=180 mmHg and increase of >=20 mmHg - Systolic Blood Pressure >=90 mmHg and decrease of >=20 mmHg - Diastolic Blood Pressure (DBP) >=105 mmHg and increase of >=15 mmHg - Diastolic Blood Pressure >=50 mmHg and decrease of >=15 mmHg - Pulse Rate (PR) >=120 beats/min and increase of >=15 beats/min - Pulse Rate >=50 beats/min and decrease of >=15 beats/min (NCT00220337)
Timeframe: During study period (up to 140 weeks)

Interventionpercentage of participants (Number)
SBP >=180 and increase of >=20 mmHgSBP <=90 and decrease of >=20 mmHgDBP >=105 and increase of >=15 mmHgDBP <=50 and decrease of >=15 mmHgPR >=120 and increase of >=15 beats/minPR <=50 and decrease of >=15 beats/min
Lacosamide7.50.33.50.80.30.8

[back to top]

Number of Subjects With Urine Ketone Status 'Trace' at Baseline, Categorized by Urine Ketone Status at Last Visit

Urinalysis was performed locally at all visits using a urine dipstick test. Categories are as following: negative, trace (N), trace, small, moderate, not done (data not available). (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
NegativeTraceSmallModerateNot Done
Lacosamide190200

[back to top]

Percentage of Subjects With Marked Abnormalities in Neurological Examination Findings After Start of Treatment

Changes in neurological examination findings is reported as percentage of subjects with marked abnormalities in following categories: - General - Cranial Nerves - Reflexes - Muscle Strength and Tone - Coordination and Cerebellar Function - Motor System - Sensation: Upper Extremities - Sensation: Lower Extremities The percentages are based on the number of subjects with examinations done at last visit for each category or parameter. (NCT00220337)
Timeframe: Last Visit (up to 140 weeks)

Interventionpercentage of participants (Number)
GeneralCranial NervesReflexesMuscle Strength and ToneCoordination and Cerebellar FunctionMotor SystemSensation: Upper ExtremitiesSensation: Lower Extremities
Lacosamide3.613.469.913.47.03.721.187.5

[back to top]

Percentage of Subjects With Marked Abnormalities in Hematology Parameters After Start of Treatment During the Titration Period

Changes in hematology parameters is reported as incidence of marked abnormalities in - Hematocrit (<=.85x Lower Limit Normal [LLN] or >= 1.15x Upper Limit Normal [ULN] - Hemoglobin (<=.85x LLN or >=1.15x ULN) - White Blood Cell (WBC) Count (<=3.0 or >=16.0 G/l) - Basophils (>=5.0%) - Eosinophils (>=10%) - Monocytes (>=20%) - Platelet Count (<=100 or >=600 G/l) (NCT00220337)
Timeframe: During the titration period (up to Week 8)

Interventionpercentage of participants (Number)
HematocritHemoglobinWhite Blood CellBasophilsEosinophilsMonocytesPlatelet Count
Lacosamide0.80.51.41.1001.1

[back to top]

Percentage of Subjects With Marked Abnormalities in Hematology Parameters After Start of Treatment During the Maintenance Period

Changes in hematology parameters is reported as incidence of marked abnormalities in - Hematocrit (<=.85x Lower Limit Normal [LLN] or >= 1.15x Upper Limit Normal [ULN] - Hemoglobin (<=.85x LLN or >=1.15x ULN) - White Blood Cell (WBC) Count (<=3.0 or >=16.0 G/l) - Basophils (>=5.0%) - Eosinophils (>=10%) - Monocytes (>=20%) - Platelet Count (<=100 or >=600 G/l) (NCT00220337)
Timeframe: During the maintenance period (up to 136 weeks)

Interventionpercentage of participants (Number)
HematocritHemoglobinWBC CountBasophilsEosinophilsMonocytesPlatelet Count
Lacosamide6.25.52.82.82.80.34.4

[back to top]

Percentage of Subjects With Marked Abnormalities Clinical Chemistry Parameters After Start of Treatment During the Titration Period

Changes in clinical chemistry parameters is reported as incidence of marked abnormalities in - Alanine aminotransferase ([ALT] 3x ULN) - Alanine aminotransferase ([ALT] 5x ULN) - Alanine aminotransferase [(ALT] 10x ULN) - Aspartate aminotransferase ([AST] 3x ULN) - Aspartate aminotransferase ([AST] 5x ULN) - Aspartate aminotransferase ([AST] 10x ULN) - Alkaline Phosphatase (3x ULN) - Gamma-glutamyltransferase ([GGT] 3x ULN) - Total Bilirubin (2x ULN) - Albumin (<26 g/l) - Blood Urea Nitrogen (>=14.28 mmol/l) - Creatinine (>=2.0 mg/dl) - Calcium (<=7.6 or >=11.0 mg/dl) - Chloride (<=90 or >=112 mmol/l) - Phosphorus (<=2.0 or >=6.0 mg/dl) - Potassium (<=3.0 or >=6.0 mmol/l) - Sodium (<127 or >151 mmol/l) - Glucose (<50 or >=200 mg/dl) - Total Cholesterol (>6.5 mmol/l) - Uric Acid (>565.06 umol/l) (NCT00220337)
Timeframe: During the titration period (up to Week 8)

Interventionpercentage of participants (Number)
ALT 3xULNALT 5xULNALT 10xULNAST 3xULNAST 5xULNAST 10xULNAlkaline PhosphataseGGT 3xULNTotal BilirubinAlbuminBlood Urea NitrogenCreatinineCalciumChloridePhosphorusPotassiumSodiumGlucoseTotal CholesterolUric Acid
Lacosamide0.50000000.60.500.801.70.31.40.3040.63.21.1

[back to top]

Percentage of Subjects With Marked Abnormalities Clinical Chemistry Parameters After Start of Treatment During the Maintenance Period

Changes in clinical chemistry parameters is reported as incidence of marked abnormalities in - Alanine aminotransferase ([ALT] 3x ULN) - Alanine aminotransferase ([ALT] 5x ULN) - Alanine aminotransferase [(ALT] 10x ULN) - Aspartate aminotransferase ([AST] 3x ULN) - Aspartate aminotransferase ([AST] 5x ULN) - Aspartate aminotransferase ([AST] 10x ULN) - Alkaline Phosphatase (3x ULN) - Gamma-glutamyltransferase ([GGT] 3x ULN) - Total Bilirubin (2x ULN) - Albumin (<26 g/l) - Blood Urea Nitrogen (>=14.28 mmol/l) - Creatinine (>=2.0 mg/dl) - Calcium (<=7.6 or >=11.0 mg/dl) - Chloride (<=90 or >=112 mmol/l) - Phosphorus (<=2.0 or >=6.0 mg/dl) - Potassium (<=3.0 or >=6.0 mmol/l) - Sodium (<127 or >151 mmol/l) - Glucose (<50 or >=200 mg/dl) - Total Cholesterol (>6.5 mmol/l) - Uric Acid (>565.06 umol/l) (NCT00220337)
Timeframe: During the maintenance period (up to 136 weeks)

Interventionpercentage of participants (Number)
ALT 3xULNALT 5xULNALT 10xULNAST 3xULNAST 5xULNAST 10xULNAlkaline PhosphataseGGT 3xULNTotal BilirubinAlbuminBlood Urea NitrogenCreatinineCalciumChloridePhosphorusPotassiumSodiumGlucoseTotal CholesterolUric Acid
Lacosamide0.60.300000.34.70.30.32.10.62.53.43.42.8066.80.71.5

[back to top]

Percentage of Subjects With Abnormal Electrocardiogram (ECG) Findings

Changes in 12-lead ECGs is reported as percentage of subjects with abnormal ECG findings categorized in 'Abnormal, possibly insignificant' and 'Abnormal, possibly significant' based on the alert criterion by the ECG vendor and not on the investigator's assessment. (NCT00220337)
Timeframe: Last Visit (up to 140 weeks)

Interventionpercentage of participants (Number)
Abnormal, possibly insignificantAbnormal, possibly significant
Lacosamide4.718.0

[back to top]

Percentage of Patients With Categorized Patient's Global Impression of Change in Pain (PGIC) at Visit 9.8

The PGIC is a 7-point categorical rating scale in which the subject rates the change in his/her pain since starting trial medication. Categories are as following: much worse, moderately worse, mildly worse, no change, mildly better, moderately better, much better. (NCT00220337)
Timeframe: Visit 9.8

Interventionpercentage of participants (Number)
Much WorseModerately WorseMildly WorseNo ChangeMildly BetterModerately BetterMuch Better
Lacosamide02.04.18.210.236.738.8

[back to top]

Percentage of Patients With Categorized Patient's Global Impression of Change in Pain (PGIC) at Visit 9.7

The PGIC is a 7-point categorical rating scale in which the subject rates the change in his/her pain since starting trial medication. Categories are as following: much worse, moderately worse, mildly worse, no change, mildly better, moderately better, much better. (NCT00220337)
Timeframe: Visit 9.7

Interventionpercentage of participants (Number)
Much WorseModerately WorseMildly WorseNo ChangeMildly BetterModerately BetterMuch Better
Lacosamide0.52.23.86.020.131.535.9

[back to top]

Percentage of Patients With Categorized Patient's Global Impression of Change in Pain (PGIC) at Visit 9.6

The PGIC is a 7-point categorical rating scale in which the subject rates the change in his/her pain since starting trial medication. Categories are as following: much worse, moderately worse, mildly worse, no change, mildly better, moderately better, much better. (NCT00220337)
Timeframe: Visit 9.6

Interventionpercentage of participants (Number)
Much WorseModerately WorseMildly WorseNo ChangeMildly BetterModerately BetterMuch Better
Lacosamide03.01.57.919.331.237.1

[back to top]

Percentage of Patients With Categorized Patient's Global Impression of Change in Pain (PGIC) at Visit 9.5

The PGIC is a 7-point categorical rating scale in which the subject rates the change in his/her pain since starting trial medication. Categories are as following: much worse, moderately worse, mildly worse, no change, mildly better, moderately better, much better. (NCT00220337)
Timeframe: Visit 9.5

Interventionpercentage of participants (Number)
Much WorseModerately WorseMildly WorseNo ChangeMildly BetterModerately BetterMuch Better
Lacosamide01.93.36.618.434.435.4

[back to top]

Percentage of Patients With Categorized Patient's Global Impression of Change in Pain (PGIC) at Visit 9.4

The PGIC is a 7-point categorical rating scale in which the subject rates the change in his/her pain since starting trial medication. Categories are as following: much worse, moderately worse, mildly worse, no change, mildly better, moderately better, much better. (NCT00220337)
Timeframe: Visit 9.4

Interventionpercentage of participants (Number)
Much WorseModerately WorseMildly WorseNo ChangeMildly BetterModerately BetterMuch Better
Lacosamide00.94.45.818.635.035.4

[back to top]

Percentage of Patients With Categorized Patient's Global Impression of Change in Pain (PGIC) at Visit 9.3

The PGIC is a 7-point categorical rating scale in which the subject rates the change in his/her pain since starting trial medication. Categories are as following: much worse, moderately worse, mildly worse, no change, mildly better, moderately better, much better. (NCT00220337)
Timeframe: Visit 9.3

Interventionpercentage of participants (Number)
Much WorseModerately WorseMildly WorseNo ChangeMildly BetterModerately BetterMuch Better
Lacosamide01.33.04.220.734.636.3

[back to top]

Percentage of Patients With Categorized Patient's Global Impression of Change in Pain (PGIC) at Visit 9.2

The PGIC is a 7-point categorical rating scale in which the subject rates the change in his/her pain since starting trial medication. Categories are as following: much worse, moderately worse, mildly worse, no change, mildly better, moderately better, much better. (NCT00220337)
Timeframe: Visit 9.2

Interventionpercentage of participants (Number)
Much WorseModerately WorseMildly WorseNo ChangeMildly BetterModerately BetterMuch Better
Lacosamide0.40.84.04.417.334.538.6

[back to top]

Number of Subjects With Urine Ketone Status 'Small' at Baseline, Categorized by Urine Ketone Status at Last Visit

Urinalysis was performed locally at all visits using a urine dipstick test. Categories are as following: negative, trace (N), trace, small, moderate, not done (data not available). (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
NegativeTraceSmallModerateNot Done
Lacosamide22000

[back to top]

Number of Subjects With Urine Ketone Status 'Negative' at Baseline, Categorized by Urine Ketone Status at Last Visit

Urinalysis was performed locally at all visits using a urine dipstick test. Categories are as following: negative, trace (N), trace, small, moderate, not done (data not available). (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
NegativeTraceSmallModerateNot done
Lacosamide3288107

[back to top]

Number of Subjects With Urine Ketone Status 'Moderate' at Baseline, Categorized by Urine Ketone Status at Last Visit

Urinalysis was performed locally at all visits using a urine dipstick test. Categories are as following: negative, trace (N), trace, small, moderate, not done (data not available). (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
NegativeTraceSmallModerateNot Done
Lacosamide20000

[back to top]

Number of Subjects With Urine Glucose Value 55 mmol/l at Baseline, Categorized by Urine Glucose Value at Last Visit

Categories are as following: negative, 5.5 mmol/l, 14 mmol/l, 28 mmol/l, 55 mmol/l, >= 111 mmol/l, not done (data not available). (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
Negative5.5 mmol/l14 mmol/l28 mmol/l55 mmol/l>=111 mmolNot Done
Lacosamide5513140

[back to top]

Number of Subjects With Urine Glucose Value 5.5 mmol/l at Baseline, Categorized by Urine Glucose Value at Last Visit

Categories are as following: negative, 5.5 mmol/l, 14 mmol/l, 28 mmol/l, 55 mmol/l, >= 111 mmol/l, not done (data not available). (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
Negative5.5 mmol/l14 mmol/l28 mmol/l55 mmol/l>=111 mmolNot Done
Lacosamide181521001

[back to top]

Percentage of Patients With Categorized Patient's Global Impression of Change in Pain (PGIC) at Visit 9.1

The PGIC is a 7-point categorical rating scale in which the subject rates the change in his/her pain since starting trial medication. Categories are as following: much worse, moderately worse, mildly worse, no change, mildly better, moderately better, much better. (NCT00220337)
Timeframe: Visit 9.1

Interventionpercentage of participants (Number)
Much WorseModerately WorseMildly WorseNo ChangeMildly BetterModerately BetterMuch Better
Lacosamide0.70.42.65.618.237.235.3

[back to top]

Percentage of Patients With Categorized Patient's Global Impression of Change in Pain (PGIC) at Visit 9.0

The PGIC is a 7-point categorical rating scale in which the subject rates the change in his/her pain since starting trial medication. Categories are as following: much worse, moderately worse, mildly worse, no change, mildly better, moderately better, much better. (NCT00220337)
Timeframe: Visit 9.0

Interventionpercentage of participants (Number)
Much WorseModerately WorseMildly WorseNo ChangeMildly BetterModerately BetterMuch Better
Lacosamide00.71.46.118.835.737.2

[back to top]

Percentage of Patients With Categorized Patient's Global Impression of Change in Pain (PGIC) at Visit 6

The PGIC is a 7-point categorical rating scale in which the subject rates the change in his/her pain since starting trial medication. Categories are as following: much worse, moderately worse, mildly worse, no change, mildly better, moderately better, much better. (NCT00220337)
Timeframe: Visit 6

Interventionpercentage of participants (Number)
Much WorseModerately WorseMildly WorseNo ChangeMildly BetterModerately BetterMuch Better
Lacosamide0028.423.734.831.1

[back to top]

Percentage of Patients With Categorized Patient's Global Impression of Change in Pain (PGIC) at Visit 4

The PGIC is a 7-point categorical rating scale in which the subject rates the change in his/her pain since starting trial medication. Categories are as following: much worse, moderately worse, mildly worse, no change, mildly better, moderately better, much better. (NCT00220337)
Timeframe: Visit 4

Interventionpercentage of participants (Number)
Much WorseModerately WorseMildly WorseNo ChangeMildly BetterModerately BetterMuch Better
Lacosamide000.96.027.132.533.4

[back to top]

Percentage of Patients With Categorized Patient's Global Impression of Change in Pain (PGIC) at Termination Visit

The PGIC is a 7-point categorical rating scale in which the subject rates the change in his/her pain since starting trial medication. Categories are as following: much worse, moderately worse, mildly worse, no change, mildly better, moderately better, much better. (NCT00220337)
Timeframe: Termination Visit (last treatment visit)

Interventionpercentage of participants (Number)
Much WorseModerately WorseMildly WorseNo ChangeMildly BetterModerately BetterMuch Better
Lacosamide0.92.43.613.420.428.630.7

[back to top]

Number of Subjects With Urine Glucose Value 28 mmol/l at Baseline, Categorized by Urine Glucose Value at Last Visit

Categories are as following: negative, 5.5 mmol/l, 14 mmol/l, 28 mmol/l, 55 mmol/l, >= 111 mmol/l, not done (data not available). (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
Negative5.5 mmol/l14 mmol/l28 mmol/l55 mmol/l>=111 mmolNot Done
Lacosamide10333010

[back to top]

Number of Subjects With Urine Glucose Value 14 mmol/l at Baseline, Categorized by Urine Glucose Value at Last Visit

Categories are as following: negative, 5.5 mmol/l, 14 mmol/l, 28 mmol/l, 55 mmol/l, >= 111 mmol/l, not done (data not available). (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
Negative5.5 mmol/l14 mmol/l28 mmol/l55 mmol/l>=111 mmolNot Done
Lacosamide6801201

[back to top]

Number of Subjects With Urine Glucose Value >=111 mmol/l at Baseline, Categorized by Urine Glucose Value at Last Visit

Categories are as following: negative, 5.5 mmol/l, 14 mmol/l, 28 mmol/l, 55 mmol/l, >= 111 mmol/l, not done (data not available). (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
Negative5.5 mmol/l14 mmol/l28 mmol/l55 mmol/l>=111 mmolNot Done
Lacosamide3202211

[back to top]

Number of Subjects With Urine Glucose Value 'Negative' at Baseline, Categorized by Urine Glucose Value at Last Visit

Categories are as following: negative, 5.5 mmol/l, 14 mmol/l, 28 mmol/l, 55 mmol/l, >= 111 mmol/l, not done (data not available). (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
Negative5.5 mmol/l14 mmol/l28 mmol/l55 mmol/l>=111 mmolNot Done
Lacosamide194301612464

[back to top]

Number of Subjects With Urine Blood Status 'Trace (N)' at Baseline, Categorized by Urine Blood Status at Last Visit

Urinalysis was performed locally at all visits using a urine dipstick test. Categories are as following: negative, trace (N), trace (H), positive +, positive ++, positive +++, not done (data not available). Positive category (+, ++, +++) indicate worsening from Baseline. (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
NegativeTrace (N)Trace (H)Positive +Positive ++Positive +++Not done
Lacosamide14201000

[back to top]

Number of Subjects With Urine Blood Status 'Trace (H)' at Baseline, Categorized by Urine Blood Status at Last Visit

Urinalysis was performed locally at all visits using a urine dipstick test. Categories are as following: negative, trace (N), trace (H), positive +, positive ++, positive +++, not done (data not available). Positive category (+, ++, +++) indicate worsening from Baseline. (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
NegativeTrace (N)Trace (H)Positive +Positive ++Positive +++Not done
Lacosamide4200000

[back to top]

Number of Subjects With Urine Blood Status 'Positive ++' at Baseline, Categorized by Urine Blood Status at Last Visit

Urinalysis was performed locally at all visits using a urine dipstick test. Categories are as following: negative, trace (N), trace (H), positive +, positive ++, positive +++, not done (data not available). Positive category (+, ++, +++) indicate worsening from Baseline. (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
NegativeTrace (N)Trace (H)Positive +Positive ++Positive +++Not done
Lacosamide1100000

[back to top]

Number of Subjects With Urine Blood Status 'Positive +' at Baseline, Categorized by Urine Blood Status at Last Visit

Urinalysis was performed locally at all visits using a urine dipstick test. Categories are as following: negative, trace (N), trace (H), positive +, positive ++, positive +++, not done (data not available). Positive category (+, ++, +++) indicate worsening from Baseline. (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
NegativeTrace (N)Trace (H)Positive +Positive ++Positive +++Not done
Lacosamide1000000

[back to top]

Number of Subjects With Urine Blood Status 'Negative' at Baseline, Categorized by Urine Blood Status at Last Visit

Urinalysis was performed locally at all visits using a urine dipstick test. Categories are as following: negative, trace (N), trace (H), positive +, positive ++, positive +++, not done (data not available). Positive category (+, ++, +++) indicate worsening from Baseline. (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
NegativeTrace (N)Trace (H)Positive +Positive ++Positive +++Not done
Lacosamide319713447

[back to top]

Number of Subjects With Urine Bilirubin Status 'Positive ++' at Baseline, Categorized by Urine Bilirubin Status at Last Visit

Urinalysis was performed locally at all visits using a urine dipstick test. Categories are as following: negative, positive +, positive ++, not done (data not available). Positive category (+, ++) indicate worsening from Baseline. (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
NegativePositive +Positive ++Not done
Lacosamide3000

[back to top]

Number of Subjects With Urine Bilirubin Status 'Positive +' at Baseline, Categorized by Urine Bilirubin Status at Last Visit

Urinalysis was performed locally at all visits using a urine dipstick test. Categories are as following: negative, positive +, positive ++, not done (data not available). Positive category (+, ++) indicate worsening from Baseline. (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
NegativePositive +Positive ++Not done
Lacosamide8000

[back to top]

Number of Subjects With Urine Bilirubin Status 'Negative' at Baseline, Categorized by Urine Bilirubin Status at Last Visit

Urinalysis was performed locally at all visits using a urine dipstick test. Categories are as following: negative, positive +, positive ++, not done (data not available). Positive category (+, ++) indicate worsening from Baseline. (NCT00220337)
Timeframe: Baseline, Last Visit (up to 140 weeks)

InterventionParticipants (Number)
NegativePositive +Positive ++Not done
Lacosamide351207

[back to top]

Change in Quality of Life From Visit 2 (Baseline) to Visit 9.8

Quality of life was analyzed using the SF-36 Health Survey quality of life questionnaire. The SF-36 is a participant self-rated questionnaire which consists of 8 sub-scores ranging from 0-100 with higher scores indicating a better health state. The sub-scores are: 1. Physical Functioning, 2. Role-Physical, 3. Bodily Pain, 4. General Health, 5. Vitality, 6. Social Functioning, 7. Role-Emotional, 8. Mental Health. Items 1-4 primarily contribute to the PCS score of the SF-36. Items 5-8 primarily contribute to the MCS score of the SF-36. The PCS and MCS were based on the standardized values of the 8 domains. The maximum and minimum possible values for PCS and MCS is 0-100, where higher scores indicate good condition. A positive value indicates improvement from baseline in quality of life. (NCT00220337)
Timeframe: Baseline, Visit 9.8

Interventionunits on a scale (Mean)
Physical FunctioningRole-PhysicalBodily PainGeneral healthVitalitySocial FunctioningRole-EmotionalMental HealthPCSMCS
Lacosamide6.92.022.20.23.24.3-7.53.34.6-0.9

[back to top]

Change in Quality of Life From Visit 2 (Baseline) to Visit 9.7

Quality of life was analyzed using the SF-36 Health Survey quality of life questionnaire. The SF-36 is a participant self-rated questionnaire which consists of 8 sub-scores ranging from 0-100 with higher scores indicating a better health state. The sub-scores are: 1. Physical Functioning, 2. Role-Physical, 3. Bodily Pain, 4. General Health, 5. Vitality, 6. Social Functioning, 7. Role-Emotional, 8. Mental Health. Items 1-4 primarily contribute to the PCS score of the SF-36. Items 5-8 primarily contribute to the MCS score of the SF-36. The PCS and MCS were based on the standardized values of the 8 domains. The maximum and minimum possible values for PCS and MCS is 0-100, where higher scores indicate good condition. A positive value indicates improvement from baseline in quality of life. (NCT00220337)
Timeframe: Baseline, Visit 9.7

Interventionunits on a scale (Mean)
Physical FunctioningRole-PhysicalBodily PainGeneral HealthVitalitySocial FunctioningRole-EmotionalMental HealthPCSMCS
Lacosamide9.418.625.37.17.48.78.24.37.01.4

[back to top]

Change in Quality of Life From Visit 2 (Baseline) to Visit 9.1

Quality of life was analyzed using the SF-36 Health Survey quality of life questionnaire. The SF-36 is a participant self-rated questionnaire which consists of 8 sub-scores ranging from 0-100 with higher scores indicating a better health state. The sub-scores are: 1. Physical Functioning, 2. Role-Physical, 3. Bodily Pain, 4. General Health, 5. Vitality, 6. Social Functioning, 7. Role-Emotional, 8. Mental Health. Items 1-4 primarily contribute to the PCS score of the SF-36. Items 5-8 primarily contribute to the MCS score of the SF-36. The PCS and MCS were based on the standardized values of the 8 domains. The maximum and minimum possible values for PCS and MCS is 0-100, where higher scores indicate good condition. A positive value indicates improvement from baseline in quality of life. (NCT00220337)
Timeframe: Baseline, Visit 9.1

Interventionunits on a scale (Mean)
Physical FunctioningRole-PhysicalBodily PainGeneral healthVitalitySocial FunctioningRole-EmotionalMental HealthPCSMCS
Lacosamide10.618.424.67.39.610.614.75.66.73.0

[back to top]

Change From Baseline in Average Daily Pain Score Using an 11-point Likert Scale (0-10).

Change from Baseline in average daily pain score using an 11-point Likert scale (0-10). On Likert scale, 0=no pain and 10=worst possible pain. (NCT00235443)
Timeframe: Baseline to end of entire treatment phase (maximum study period of 2.8 years).

InterventionUnits on a scale (Mean)
Lacosamide 100mg/Day-5.15
Lacosamide 200mg/Day-4.30
Lacosamide 300mg/Day-3.70
Lacosamide 400mg/Day-3.29
Lacosamide 500mg/Day-3.54
Lacosamide 600mg/Day-2.73
Total-3.49

[back to top]

Change From Baseline in Average Pain Interference With Activity (11-point Likert Scale)

Change from Baseline in average pain interference with activity (11-point Likert scale) where 0=no interfence with activity and 10=worst possible interference with activity. (NCT00235443)
Timeframe: Baseline to end of entire treatment phase visit

InterventionUnits on a scale (Mean)
Lacosamide 100mg/Day-4.82
Lacosamide 200mg/Day-3.82
Lacosamide 300mg/Day-3.36
Lacosamide 400mg/Day-3.00
Lacosamide 500mg/Day-3.30
Lacosamide 600mg/Day-2.54
Total-3.18

[back to top]

Change From Baseline in Average Pain Interference With Sleep (11-point Likert Scale)

Change from Baseline in average pain interference with sleep (11-point Likert scale) where 0=no interference with sleep and 10=worst possible interference with sleep. (NCT00235443)
Timeframe: Baseline to end of entire treatment phase visit

InterventionUnits on a scale (Mean)
Lacosamide 100mg/Day-4.62
Lacosamide 200mg/Day-3.86
Lacosamide 300mg/Day-3.32
Lacosamide 400mg/Day-3.15
Lacosamide 500mg/Day-3.34
Lacosamide 600mg/Day-2.85
Total-3.29

[back to top]

Change From Baseline in Average Pain Score as Measured by a 100mm Visual Analogue Scale (VAS).

Change from Baseline in average pain score as measured by a 100mm Visual Analogue Scale (VAS). On VAS 0mm=no pain and 100mm=worst possible pain. (NCT00235443)
Timeframe: Baseline to end of entire treatment phase (maximum study period of 2.8 years).

InterventionUnits on a scale (Mean)
Lacosamide 100mg/Day-47.83
Lacosamide 200mg/Day-43.06
Lacosamide 300mg/Day-35.24
Lacosamide 400mg/Day-30.06
Lacosamide 500mg/Day-36.73
Lacosamide 600mg/Day-27.70
Total-33.39

[back to top]

Change From Baseline in Quality of Life Using the SF-36 Health Survey - Mental Component Summary (MCS)

Change from Baseline in quality of life using the SF-36 Health Survey - Mental Component Summary (MCS). Values range from 0 to 100 with high values indicating a good condition. Positive change in baseline values indicate improvement in quality of life. (NCT00235443)
Timeframe: Baseline to Termination Visit

InterventionUnits on a scale (Mean)
Lacosamide 100mg/Day-3.4
Lacosamide 200mg/Day-0.1
Lacosamide 300mg/Day0.7
Lacosamide 400mg/Day-1.1
Lacosamide 500mg/Day-3.7
Lacosamide 600mg/Day-0.4
Total-0.9

[back to top]

Change From Baseline in Quality of Life Using the SF-36 Health Survey - Physical Component Summary (PCS)

Change from Baseline in quality of life using the SF-36 Health Survey - Physical Component Summary (PCS). Values range from 0 to 100 with high values indicating a good condition. Positive change in baseline values indicate improvement in quality of life. (NCT00235443)
Timeframe: Baseline to Termination Visit

InterventionUnits on a scale (Mean)
Lacosamide 100mg/Day3.3
Lacosamide 200mg/Day5.5
Lacosamide 300mg/Day5.1
Lacosamide 400mg/Day3.7
Lacosamide 500mg/Day3.5
Lacosamide 600mg/Day2.1
Total4.0

[back to top]

Number of Subjects With Adverse Events (AEs) Reported Spontaneously by the Subject or Observed by the Investigator.

Number of subjects with adverse events (AEs) reported spontaneously by the subject or observed by the investigator (serious and non-serious). (NCT00235443)
Timeframe: Throughout the study up to a maximum study period of 2.8 years

InterventionParticipants (Number)
Lacosamide 100mg/Day11
Lacosamide 200mg/Day52
Lacosamide 300mg/Day74
Lacosamide 400mg/Day196
Lacosamide 500mg/Day33
Lacosamide 600mg/Day50
Total416

[back to top]

Within-subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Cold

"Within-subject change in neuropathic pain using the Neuropathic Pain Scale (NPS) with cold sensation where 0=not cold and 10=most cold sensation imaginable (freezing)." (NCT00235443)
Timeframe: Baseline to Termination Visit

InterventionUnits on a scale (Mean)
Lacosamide 100mg/Day-1.6
Lacosamide 200mg/Day-1.9
Lacosamide 300mg/Day-1.2
Lacosamide 400mg/Day-1.7
Lacosamide 500mg/Day-2.2
Lacosamide 600mg/Day-0.5
Total-1.5

[back to top]

Within-subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Deep Pain

Within-subject change in neuropathic pain using the Neuropathic Pain Scale (NPS) with deep pain where 0=no deep pain and 10=most intense deep pain sensation imaginable. (NCT00235443)
Timeframe: Baseline to Termination Visit

InterventionUnits on a scale (Mean)
Lacosamide 100mg/Day-4.5
Lacosamide 200mg/Day-3.3
Lacosamide 300mg/Day-3.2
Lacosamide 400mg/Day-2.7
Lacosamide 500mg/Day-3.3
Lacosamide 600mg/Day-1.5
Total-2.8

[back to top]

Within-subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Dullness

Within-subject change in neuropathic pain using the Neuropathic Pain Scale (NPS) with dullness of pain where 0=not dull and 10=most dull sensation imaginable. (NCT00235443)
Timeframe: Baseline to Termination Visit

InterventionUnits on a scale (Mean)
Lacosamide 100mg/Day-3.4
Lacosamide 200mg/Day-2.6
Lacosamide 300mg/Day-2.6
Lacosamide 400mg/Day-2.4
Lacosamide 500mg/Day-2.4
Lacosamide 600mg/Day-1.8
Total-2.4

[back to top]

Within-subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Heat

"Within-subject change in neuropathic pain using the Neuropathic Pain Scale (NPS) with heat sensation where 0=not hot and 10=the most hot sensation imaginable (on fire)." (NCT00235443)
Timeframe: Baseline to Termination Visit

InterventionUnits on a scale (Mean)
Lacosamide 100mg/Day-5.3
Lacosamide 200mg/Day-3.0
Lacosamide 300mg/Day-3.1
Lacosamide 400mg/Day-2.6
Lacosamide 500mg/Day-2.8
Lacosamide 600mg/Day-1.2
Total-2.7

[back to top]

Within-subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Intensity.

Within-subject change in neuropathic pain using the Neuropathic Pain Scale (NPS) for intensity of pain where 0=no pain and 10=most intense pain sensation imaginable. (NCT00235443)
Timeframe: Baseline to Termination Visit

InterventionUnits on a scale (Mean)
Lacosamide 100mg/Day-4.6
Lacosamide 200mg/Day-4.4
Lacosamide 300mg/Day-3.1
Lacosamide 400mg/Day-2.7
Lacosamide 500mg/Day-3.5
Lacosamide 600mg/Day-2.0
Total-3.0

[back to top]

Within-subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Itchiness

"Within-subject change in neuropathic pain using the Neuropathic Pain Scale (NPS) with itchiness where 0=not itchy and 10=most itchy sensation imaginable (like poison oak)." (NCT00235443)
Timeframe: Baseline to Termination Visit

InterventionUnits on a scale (Mean)
Lacosamide 100mg/Day-2.2
Lacosamide 200mg/Day-2.0
Lacosamide 300mg/Day-1.4
Lacosamide 400mg/Day-1.1
Lacosamide 500mg/Day-2.1
Lacosamide 600mg/Day-0.5
Total-1.3

[back to top]

Within-subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Sensitivity

"Within-subject change in neuropathic pain using the Neuropathic Pain Scale (NPS) with sensitivity of pain where 0=not sensitive and 10=most sensitive sensation imaginable (raw skin)." (NCT00235443)
Timeframe: Baseline to Termination Visit

InterventionUnits on a scale (Mean)
Lacosamide 100mg/Day-2.8
Lacosamide 200mg/Day-3.4
Lacosamide 300mg/Day-1.8
Lacosamide 400mg/Day-2.1
Lacosamide 500mg/Day-2.7
Lacosamide 600mg/Day-1.4
Total-2.2

[back to top]

Within-subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Sharpness

"Within-subject change in neuropathic pain using the Neuropathic Pain Scale (NPS) for sharpness of pain where 0=not sharp and 10=most sharp sensation imaginable (like a knife)." (NCT00235443)
Timeframe: Baseline to Termination Visit

InterventionUnits on a scale (Mean)
Lacosamide 100mg/Day-4.5
Lacosamide 200mg/Day-4.2
Lacosamide 300mg/Day-3.3
Lacosamide 400mg/Day-2.8
Lacosamide 500mg/Day-3.9
Lacosamide 600mg/Day-1.9
Total-3.1

[back to top]

Within-subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Surface Pain

Within-subject change in neuropathic pain using the Neuropathic Pain Scale (NPS) with surface pain where 0=no surface pain and 10=most intense surface pain imaginable. (NCT00235443)
Timeframe: Baseline to Termination Visit

InterventionUnits on a scale (Mean)
Lacosamide 100mg/Day-3.5
Lacosamide 200mg/Day-3.3
Lacosamide 300mg/Day-3.3
Lacosamide 400mg/Day-2.6
Lacosamide 500mg/Day-2.7
Lacosamide 600mg/Day-1.5
Total-2.7

[back to top]

Within-subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Unpleasantness

"Within-subject change in neuropathic pain using the Neuropathic Pain Scale (NPS) with unpleasantness where 0=not pleasant and 10=most unpleasant sensation imaginable (intolerable)." (NCT00235443)
Timeframe: Baseline to Termination Visit

InterventionUnits on a scale (Mean)
Lacosamide 100mg/Day-5.0
Lacosamide 200mg/Day-4.0
Lacosamide 300mg/Day-3.3
Lacosamide 400mg/Day-2.9
Lacosamide 500mg/Day-3.3
Lacosamide 600mg/Day-1.5
Total-3.0

[back to top]

Patient's Global Impression of Change (PGIC) From Baseline in Pain.

Patient's Global Impression of Change (PGIC) from Baseline in Pain. Original categorical responses are much worse, moderately worse, mildly worst, no change, mildly better, moderately better, and much better. Reported results are presented as Better (sum of mildly, moderately, or much better), No Change, or Worse (sum of mildly, moderately, or much worse). (NCT00235443)
Timeframe: Baseline to Termination Visit

,,,,,,
InterventionParticipants (Number)
BetterNo ChangeWorse
Lacosamide 100mg/Day1001
Lacosamide 200mg/Day4230
Lacosamide 300mg/Day50102
Lacosamide 400mg/Day1471520
Lacosamide 500mg/Day2604
Lacosamide 600mg/Day3417
Total3092934

[back to top]

Number of Subjects Reporting At Least 1 Treatment-Emergent Adverse Event (TEAE) During The Treatment Period.

(NCT00237458)
Timeframe: From Baseline Visit to Final Week of Treatment (approximately 10 years)

Interventionparticipants (Number)
Lacosamide7

[back to top]

Number of Subjects Withdrawing From Study Due To A Treatment-Emergent Adverse Event (TEAE) During The Treatment Period.

(NCT00237458)
Timeframe: From Baseline Visit to Final Week of Treatment (approximately 10 years)

Interventionparticipants (Number)
Lacosamide2

[back to top]

Within-Subject Change In Average Daily Pain Score During the Treatment Period.

The Average Daily Pain Score is calculated using an 11-point Likert scale, ranging from 0 (no pain) to 10 (worst pain ever experienced). (NCT00237458)
Timeframe: From Baseline Visit to Final Week of Treatment (approximately 9 years)

Interventionunits on a scale (Mean)
Lacosamide-2.9

[back to top]

Within-Subject Change In The Perception Of Each Of The Individual Cardinal Symptoms of Pain During The Treatment Period - Allodynia.

"Each individual cardinal symptom of pain is calculated using an 11-point Likert scale, ranging from 0 (no pain) to 10 (worst possible pain).~Allodynia is defined as neuropathic pain caused by normally innocuous stimuli becoming painful." (NCT00237458)
Timeframe: From Baseline Visit to Final Week of Treatment (approximately 9 years)

Interventionunits on a scale (Mean)
Lacosamide0.6

[back to top]

Within-Subject Change In The Perception Of Each Of The Individual Cardinal Symptoms of Pain During The Treatment Period - Burning.

Each individual cardinal symptom of pain is calculated using an 11-point Likert scale, ranging from 0 (no pain) to 10 (worst possible pain). (NCT00237458)
Timeframe: From Baseline Visit to Final Week of Treatment (approximately 9 years)

Interventionunits on a scale (Mean)
Lacosamide0.4

[back to top]

Within-Subject Change In The Perception Of Each Of The Individual Cardinal Symptoms of Pain During The Treatment Period - Numbness.

Each individual cardinal symptom of pain is calculated using an 11-point Likert scale, ranging from 0 (no pain) to 10 (worst possible pain). (NCT00237458)
Timeframe: From Baseline Visit to Final Week of Treatment (approximately 9 years)

Interventionunits on a scale (Mean)
Lacosamide-2.4

[back to top]

Within-Subject Change In The Perception Of Each Of The Individual Cardinal Symptoms of Pain During The Treatment Period - Paraesthesiae.

Each individual cardinal symptom of pain is calculated using an 11-point Likert scale, ranging from 0 (no pain) to 10 (worst possible pain). (NCT00237458)
Timeframe: From Baseline Visit to Final Week of Treatment (approximately 9 years)

Interventionunits on a scale (Mean)
Lacosamide-2.1

[back to top]

Within-Subject Change In The Perception Of Each Of The Individual Cardinal Symptoms of Pain During The Treatment Period - Shooting.

Each individual cardinal symptom of pain is calculated using an 11-point Likert scale, ranging from 0 (no pain) to 10 (worst possible pain). (NCT00237458)
Timeframe: From Baseline Visit to Final Week of Treatment (approximately 9 years)

Interventionunits on a scale (Mean)
Lacosamide-2.3

[back to top]

Investigator's Global Impression of Change In Pain During The Treatment Period.

"The Investigator's Global Impression of Change is a physician's assessment of the patient's overall change in relief of neuropathic pain since the beginning of the study rated on a 7-point scale ranging from:~Much better~Moderately better~Mildly better~No change~Mildly worse~Moderately worse~Much worse" (NCT00237458)
Timeframe: From Baseline Visit to Final Week of Treatment (approximately 9 years)

Interventionpercentage of participants (Number)
BetterNo ChangeWorse
Lacosamide85.714.30

[back to top]

Subject's Global Impression of Change In Pain During The Treatment Period.

"The Subject's Global Impression of Change is a self-evaluation by the subject of their overall change in relief of neuropathic pain since the beginning of the study rated on a 7-point scale ranging from:~Much better~Moderately better~Mildly better~No change~Mildly worse~Moderately worse~Much worse" (NCT00237458)
Timeframe: From Baseline Visit to Final Week of Treatment (approximately 9 years)

Interventionpercentage of participants (Number)
BetterNo ChangeWorse
Lacosamide85.714.30

[back to top]

"Percentage of Days With Concomitant Pain (Rescue) Medications Taken During Baseline Phase."

"The percentage of days where rescue medication was taken is summarized by visit and by Treatment Phase (Baseline, Titration, and Titration + Treatment).~The percentage of days of rescue medication use is defined as the number of days observed within the visit/study phase with rescue medication divided by the number of days in the visit/study phase times 100 for subjects who had taken the rescue medication.~Summary statistics include mean and standard deviation." (NCT00237458)
Timeframe: Baseline Period (approximately 1 week)

Interventionpercentage of days (Mean)
Lacosamide100

[back to top]

"Percentage of Days With Concomitant Pain (Rescue) Medications Taken During Titration and Treatment Phases."

"The percentage of days where rescue medication was taken is summarized by visit and by Treatment Phase (Baseline, Titration, and Titration + Treatment).~The percentage of days of rescue medication use is defined as the number of days observed within the visit/study phase with rescue medication divided by the number of days in the visit/study phase times 100 for subjects who had taken the rescue medication.~Summary statistics include mean and standard deviation." (NCT00237458)
Timeframe: From Titration Phase through Treatment Phase (approximately 9 years)

Interventionpercentage of days (Mean)
Lacosamide12.3

[back to top]

"Percentage of Days With Concomitant Pain (Rescue) Medications Taken During Titration Phase."

"The percentage of days where rescue medication was taken is summarized by visit and by Treatment Phase (Baseline, Titration, and Titration + Treatment).~The percentage of days of rescue medication use is defined as the number of days observed within the visit/study phase with rescue medication divided by the number of days in the visit/study phase times 100 for subjects who had taken the rescue medication.~Summary statistics include mean and standard deviation." (NCT00237458)
Timeframe: Titration Period (approximately 6 weeks)

Interventionpercentage of days (Mean)
Lacosamide51.3

[back to top]

Change From Baseline in Fibromyalgia Impact Questionnaire (FIQ) Total Score to the Last Assessment in the 12-week Treatment Phase

The Fibromyalgia Impact Questionnaire (FIQ) Total Score ranges from 0 to 100 with higher scores corresponding to a greater impact of fibromyalgia (NCT00401830)
Timeframe: Baseline, Last assessment in the 12-week Treatment Phase

InterventionScore on a scale (Mean)
Placebo-14.7
Lacosamide-17.5

[back to top]

Change From Baseline in Morning Pain Score to the Last 2 Weeks of the 12-week Treatment Phase

An 11-point Likert scale was used for subjects to assess pain, from 0 (no pain) to 10 (worst pain ever experienced). (NCT00401830)
Timeframe: Baseline, Last 2 weeks of the 12 week Treatment Phase

InterventionScore on a scale (Mean)
Placebo-1.29
Lacosamide-1.77

[back to top]

Change From Baseline in Total Myalgic Score to the Last Assessment in the 12-week Treatment Phase

Total Myalgic Score ranges from 0 to 54 with higher scores corresponding to a greater level of pain. (NCT00401830)
Timeframe: Baseline, Last assessment in the 12-week Treatment Phase

InterventionScore on a scale (Mean)
Placebo-6.7
Lacosamide-9.7

[back to top]

Lacosamide Plasma Concentration at the End of the Maintenance Phase/ Week 12

(NCT00401830)
Timeframe: End of the Maintenance Phase/Week 12

Interventionug/ML (Mean)
Lacosamide9.44

[back to top]

Percentage of Patients Using Alcohol for Pain During the 12-week Treatment Phase

Use of alcohol to treat pain in the past 24 hours was recorded (Yes/No response). (NCT00401830)
Timeframe: 12-week Treatment Phase

InterventionPercentage of patients (Number)
Placebo17.5
Lacosamide15.4

[back to top]

Percentage of Patients Using Rescue Medication During the 12-week Treatment Phase

Subjects recorded use of rescue medication for pain in the diary daily in the evening with a Yes/No response. (NCT00401830)
Timeframe: 12-week Treatment Phase

InterventionPercentage of patients (Number)
Placebo83.8
Lacosamide83.3

[back to top]

Change From Baseline in Fibromyalgia Symptom Scores to the Last Assessment in the 12-week Treatment Phase

All scores range from 0 to 10 with higher scores corresponding to a greater level of symptom severity. (NCT00401830)
Timeframe: Baseline, Last assessment in the 12-week Treatment Phase

,
InterventionScore on a scale (Mean)
Muscular PainFatigueInsomniaJoint painsHeadachesRestless legsParesthesiasImpaired memoryLeg crampsImpaired concentrationAbdominal pain, alternating diarrhea/constipation
Lacosamide-2.4-1.9-2.4-1.9-1.2-1.2-1.30.0-1.4-0.5-1.2
Placebo-1.9-1.7-1.9-1.9-0.7-1.5-1.6-1.3-1.5-1.2-1.7

[back to top]

Change From Baseline in Hospital Anxiety and Depression Scale (HADS) Scores to the Last Assessment in the 12-week Treatment Phase

The Hospital Anxiety and Depression Scale (HADS) is a self-administered instrument for detecting anxiety and depression in medical outpatients. Scores range from 0 to 21 for each subscale with higher scores reflecting a greater level of anxiety or depression. (NCT00401830)
Timeframe: Baseline, Last assessment in the 12-week Treatment Phase

,
InterventionScore on a scale (Mean)
Depression score (Placebo n=67, Lacosamide n=67)Anxiety Score (Placebo n=67, Lacosamide n=66)
Lacosamide-0.8-1.2
Placebo-1.1-1.2

[back to top]

Patient Global Impression of Change (PGIC) Assessment From Baseline to the Last Assessment in the 12-week Treatment Phase

The PGIC is a 7-point self-administered categorical rating scale in which the subject rated the change in pain since starting trial medication (from much worse [score of 1] to much better [score of 7]). (NCT00401830)
Timeframe: Baseline, Last assessment in the 12-week Treatment Phase

,
InterventionPatients (Number)
Much betterModerately betterMildly betterNo changeMildly worseModerately worseMuch worse
Lacosamide17121313363
Placebo8141817523

[back to top]

Change From Baseline in Evening Pain Score to the Last 2 Weeks of the 12-week Treatment Phase

An 11-point Likert scale was used for subjects to assess pain, from 0 (no pain) to 10 (worst pain ever experienced). (NCT00401830)
Timeframe: Baseline, Last 2 weeks of the 12 week Treatment Phase

InterventionScore on a scale (Mean)
Placebo-1.32
Lacosamide-1.84

[back to top]

Change From Baseline in Daily Interference With General Activity to the Last 2 Weeks of the 12-week Treatment Phase

General activity scale - the subject rated how the pain had interfered with general activity, from 0 (did not interfere) to 10 (completely interfered) (NCT00401830)
Timeframe: Baseline, Last 2 weeks of the 12-week Treatment Phase

InterventionScore on a scale (Mean)
Placebo-1.27
Lacosamide-1.44

[back to top]

Change From Baseline in Average Daily Pain Score to the Last 2 Weeks of the 12-week Treatment Phase (Based on the Per Protocol Set)

The average daily pain score is calculated using an 11-point Likert scale, ranging from 0 (no pain) to 10 (worst pain ever experienced). (NCT00401830)
Timeframe: Baseline, Last 2 weeks of the 12-week Treatment Phase

InterventionScore on a scale (Mean)
Placebo-2.11
Lacosamide-2.40

[back to top]

Change From Baseline in Average Daily Pain Score to the Last 2 Weeks of the 12-week Treatment Phase (Based on the Full Analysis Set)

The average daily pain score is calculated using an 11-point Likert scale, ranging from 0 (no pain) to 10 (worst pain ever experienced). (NCT00401830)
Timeframe: Baseline, Last 2 weeks of the 12-week Treatment Phase

InterventionScore on a scale (Mean)
Placebo-1.30
Lacosamide-1.80

[back to top]

Change From Baseline in Average Daily Interference With Sleep to the Last 2 Weeks of the 12-week Treatment Phase

Sleep scale - the subject rated quality of sleep, from 0 (very good sleep) to 10 (very poor sleep) (NCT00401830)
Timeframe: Baseline, Last 2 weeks of the 12-week Treatment Phase

InterventionScore on a scale (Mean)
Placebo-1.24
Lacosamide-1.64

[back to top]

Change From Baseline in Mean Migraine Headache Rates During the Last 4 Weeks of the Maintenance Period

(NCT00440518)
Timeframe: Baseline, last 4 weeks of the 14-week Maintenance Period

InterventionNumber of migraine headaches (Mean)
Placebo-1.3
Lacosamide 100mg-1.3
Lacosamide 300mg-1.7

[back to top]

Change From Baseline in Mean Migraine Headache Rates During the Entire 14-week Maintenance Period

(NCT00440518)
Timeframe: Baseline, Entire 14-week Maintenance Period

InterventionNumber of migraine headaches (Mean)
Placebo-1.4
Lacosamide 100mg-1.4
Lacosamide 300mg-1.6

[back to top]

Number of Subjects Who Experience a 50 Percent or Greater Reduction From Baseline in Migraine Frequency During the Last 4 Weeks of the Maintenance Period.

(NCT00440518)
Timeframe: Baseline, last 4 weeks of the 14-week Maintenance Period

InterventionParticipants (Number)
Placebo27
Lacosamide 100mg27
Lacosamide 300mg33

[back to top]

Number of Subjects Who Experience a 50 Percent or Greater Reduction From Baseline in Migraine Frequency During the Entire 14-week Maintenance Period.

(NCT00440518)
Timeframe: Baseline, Entire 14-week Maintenance Period

InterventionParticipants (Number)
Placebo26
Lacosamide 100mg32
Lacosamide 300mg29

[back to top]

Changes From Baseline in Improvement of Function and Reduction of Disability Using the Headache Impact Test (HIT-6)

Headache Impact Test (HIT-6™) consists of 6 items designed to measure the impact headaches have on a person's ability to function. Scores from the 6 questions will be added to create a total score. Range of the total score is 36 to 78. Higher scores indicate a greater impact on the subject's quality of life. (NCT00440518)
Timeframe: Baseline, last visit in the 17-week Trial Period

InterventionScores on a scale (Mean)
Placebo-3.8
Lacosamide 100mg-4.3
Lacosamide 300mg-3.5

[back to top]

Patient's Global Impression of Change From Baseline at the End of 8 Week Maintenance Period.

Patient's global impression of change from baseline is a score that ranges from 'very much worse' to 'very much improved'. (NCT00485472)
Timeframe: at the end of 8 week Maintenance Period

,
InterventionParticipants (Number)
Very much worseMuch worseWorseNo changeMildly improvedMuch improvedVery much improvedMuch + very much improvedMuch + very much + mildly improved
Lacosamide411018121582335
Placebo151010301331646

[back to top]

Response at the End of 8 Week Maintenance Period Versus Baseline Based on the (Slightly Modified)Criteria of the Osteoarthritis Research Society International (OARSI) and the Outcome Measures in Rheumatology Initiative (OMERACT).

Improvement = reduction of >= 20% and >= 10 mm in both WOMAC pain and physical function subscale. Those who met the criteria in either of the subscales had improved if response to Patient's Global Impression of change from baseline was at least 'mildly improved'. High improvement = reduction of >= 50% and >= 20 mm in either of the subscales. Response = either high improvement or improvement. (NCT00485472)
Timeframe: Baseline, end of 8 week Maintenance Period

,
Interventionparticipants (Number)
High improvementImprovementResponse
Lacosamide333838
Placebo325252

[back to top]

Amount of Rescue Medication Use During 8 Week Maintenance Period.

Use of rescue medication is expressed in number of tablets equivalent to 500 mg Paracetamol per day. (NCT00485472)
Timeframe: during 8 week Maintenance Period

Interventiontablets/day (Mean)
Lacosamide0.48
Placebo0.70

[back to top]

Change From Baseline to End of 8 Week Maintenance Period in Perception of Pain Interference With Subject's Sleep.

Pain interference with sleep refers to patient's last evening prior to the visit and was assessed using a 100mm visual analog scale (VAS). The VAS ranges from 0 (did not interfere) to 100 (completely interfered). (NCT00485472)
Timeframe: Baseline, end of 8 week Maintenance Period

InterventionUnit on a scale (Mean)
Lacosamide-19.8
Placebo-21.6

[back to top]

Change From Baseline to End of 8 Week Maintenance Period in Profile of Mood States (Total Mood Disturbance Score).

Total Mood Disturbance score sums up over the domain scores regarding Tension-anxiety, Depression-ejection, Anger-hostility, Vigor-activity (was subtracted), Fatigue-inertia, Confusion-bewilderment. Domain scores were derived as sum of the respective items and range from 0 to 20. With exception of Vigor-activity high values describe bad mood. (NCT00485472)
Timeframe: Baseline, end of 8 week Maintenance Period

InterventionUnit on a scale (Mean)
Lacosamide0.9
Placebo-4.5

[back to top]

Change From Baseline to End of 8 Week Maintenance Period in Total WOMAC Score.

The WOMAC total score is the sum of the normalized subscale scores for pain, stiffness, and physical function and ranges from 0 to 300, high values describe high grade of impact. (NCT00485472)
Timeframe: Baseline, end of 8 week Maintenance Period

InterventionUnit on a scale (Mean)
Lacosamide-60.85
Placebo-75.24

[back to top]

Change From Baseline to End of 8 Week Maintenance Period in WOMAC Physical Function Subscale Score.

The WOMAC physical function subscale score (Visual Analogue Scale version) ranges from 0 to 100, high values describe high grade of difficulty in performing daily activities. (NCT00485472)
Timeframe: Baseline, end of 8 week Maintenance Period

InterventionUnit on a scale (Mean)
Lacosamide-17.09
Placebo-23.31

[back to top]

Change From Baseline to End of 8 Week Maintenance Period in WOMAC Stiffness Subscale Score.

The WOMAC stiffness subscale score (Visual Analogue Scale version) ranges from 0 to 100, high values describe high grade of stiffness. (NCT00485472)
Timeframe: Baseline, end of 8 week Maintenance Period

InterventionUnit on a scale (Mean)
Lacosamide-18.92
Placebo-23.43

[back to top]

Change of the Western Ontario and McMaster Universities (WOMAC) Pain Subscale Score (Visual Analogue Scale Version) From Baseline to the End of the 8 Week Maintenance Period

The Visual Analogue Scale (VAS) version of the WOMAC pain subscale ranges from 0 to 100, high values describe high grade of pain. (NCT00485472)
Timeframe: Baseline, end of 8 week Maintenance Period

InterventionUnit on a scale (Mean)
Lacosamide-24.85
Placebo-28.49

[back to top]

Number of Subjects Reporting at Least 1 Treatment-emergent Adverse Event (TEAE) During the Treatment Period (up to 5.5 Years)

Adverse events are any untoward medical occurrences in a subject administered study treatment, whether or not these events are related to treatment. (NCT00515619)
Timeframe: During the Treatment Period (up to 5.5 years)

InterventionSubjects (Number)
Lacosamide311

[back to top]

Percentage of at Least 50% Responders During the Treatment Period (up to 5.5 Years)

At least 50 percent response is based on the percentage reduction in 28-day seizure frequency during the Treatment Period of the open-label extension relative to the Baseline Phase of the prior study. This endpoint reflects the percentage of subjects with at least 50% reduction (ie, at least 50% change) in 28-day partial onset seizure frequency (NCT00515619)
Timeframe: Treatment Period (up to 5.5 years)

InterventionPercentage of subjects (Number)
Lacosamide50.0

[back to top]

Number of Subjects Prematurely Discontinuing Due to a Treatment-emergent Adverse Event (TEAE) During the Treatment Period (up to 5.5 Years)

Adverse events are any untoward medical occurrences in a subject administered study treatment, whether or not these events are related to treatment. (NCT00515619)
Timeframe: During the Treatment Period (up to 5.5 years)

InterventionSubjects (Number)
Lacosamide33

[back to top]

Median Percentage Change From Baseline in 28-day Seizure Frequency During the Treatment Period (up to 5.5 Years)

"Median percentage change is the median value with respect to the percent change from Baseline across the population of subjects. Percentage change is calculated as 100 times the difference of the seizure frequency for the treatment period and the Baseline seizure frequency divided by the baseline seizure frequency.~Negative changes from Baseline indicate an improvement (i.e., a reduction) in 28-day seizure frequency." (NCT00515619)
Timeframe: Baseline, Treatment Period (up to 5.5 years)

InterventionPercentage change (Median)
Lacosamide-49.9

[back to top]

Number of Subjects Reporting at Least 1 Serious Adverse Event (SAE) During the Treatment Period (up to 5.5 Years)

A serious adverse event is any untoward medical occurrences in a subject administered study treatment, whether or not the event is related to treatment, with at least one of the follow outcomes: death, life-threatening, initial inpatient hospitalization or prolongation of hospitalization, significant or persistent disability/incapacity, congenital anomaly/birth defect, or an important medical event that may jeopardize the subject and require a medical/surgical intervention. (NCT00515619)
Timeframe: During the Treatment Period (up to 5.5 years)

InterventionSubjects (Number)
Lacosamide87

[back to top]

Duration of Monotherapy Treatment During the Monotherapy Phase of The Maintenance Period (Visit 9 - Visit 12)

Days on Monotherapy Treatment were defined as the number of days during the Monotherapy Phase when the subject took Lacosamide (LCM) only (ie, the total number of days exposed to LCM during the Monotherapy Phase minus any days where a concomitant or rescue Anti-epileptic Drug (AED) was taken by the subject). The days on Monotherapy Treatment did not need to be consecutive. (NCT00520741)
Timeframe: Visit 9 - Visit 12 (approximately 10 weeks)

Interventiondays (Median)
Lacosamide 300 mg/Day71
Lacosamide 400 mg/Day71

[back to top]

Percentage of Subjects (Using Kaplan-Meier) Who Are Identified As Meeting At Least 1 Pre-defined Exit Criteria By Day 112 Relative To The Start of Withdrawal of Background Antiepileptic Drug(s)

"Pre-defined exit criteria:~A 2-fold or greater increase in average monthly (28-day) partial seizure frequency (motor and non-motor) compared to average monthly partial seizure frequency (motor and non-motor) during the Baseline Phase~A 2-fold or greater increase in consecutive 2-day partial seizure frequency (motor and non-motor) versus the highest consecutive 2-day partial seizure frequency (motor and non-motor) that occurred during the Baseline Phase.~Note: if the highest consecutive 2-day partial seizure frequency during the Baseline Phase is 1, a 2-day partial seizure frequency of ≥3 is required to meet this exit criterion~Occurrence of a single generalized tonic-clonic seizure if none had occurred in the 6 months prior to randomization~A prolongation or worsening of overall seizure duration, frequency, type or pattern considered by the investigator as serious enough to warrant trial discontinuation~Status epilepticus, or new onset of serial/cluster seizures" (NCT00520741)
Timeframe: 16 Weeks Maintenance Period (approximately 112 days)

Interventionpercentage of subjects (Number)
Lacosamide 400 mg/Day30.0

[back to top]

Percentage of Subjects (Using Kaplan-Meier) Who Are Identified as Meeting at Least 1 Pre-defined Exit Criteria by Day 112, Withdrew Due to Adverse Event (AE) or Withdrew Due to Lack of Efficacy During The Maintenance Period

"Subjects were classified as having an exit event if they experienced at least 1 of the following events during the Maintenance Phase as of Day 112:~Met at least 1 exit criterion based on the calculations applied for the Primary Efficacy Analysis~Withdrawal due to AE with onset during the Maintenance Phase~Withdrew prematurely due to lack of efficacy during the Maintenance Phase~The date the subject experienced the event was set to the earliest date the subject met an exit criterion or the date of the last Maintenance Phase dose for subjects not meeting an exit criterion but withdrawing due to an AE or lack of efficacy.~The secondary analysis is only conducted on the Lacosamide 400 mg/day group." (NCT00520741)
Timeframe: 16 Weeks Maintenance Period (approximately 112 days)

Interventionpercentage of subjects (Number)
Lacosamide 400 mg/Day32.3

[back to top]

Time to First Occurrence of Any Exit Event During The Maintenance Period

The time to first occurrence (days) of any exit event was estimated using Kaplan-Meier methods and was based on the time from the start of the Maintenance Phase to the earliest date a subject met an exit criterion. Subjects who discontinued during the Maintenance Phase due to non-exit criteria reasons or who completed the Maintenance Phase before 112 days and did not meet an exit criterion were censored as of the last Maintenance Phase dose date. Subjects completing 112 days in the Maintenance Phase were censored as of Day 112. (NCT00520741)
Timeframe: 16 Weeks Maintenance Period (approximately 112 days)

Interventiondays (Median)
Lacosamide 300 mg/Day39
Lacosamide 400 mg/Day45.0

[back to top]

Clinical Global Impression of Change (CGIC) From Baseline To Last Visit

"For the assessment of the Clinical Global Impression of Change (CGIC), the investigator should provide his/her assessment of the subject's clinical status, compared to Baseline, including an evaluation of seizure frequency and intensity, the occurrence of AEs, and subject's functional status. He was asked the following:Please check the number that best describes the subject's condition over the past 4 weeks compared to Baseline:~Very much improved~Much improved~Minimally improved~No change~Minimally worse~Much worse~Very much worse" (NCT00520741)
Timeframe: Baseline; Last Visit (approximately 27 weeks)

,
Interventionparticipants (Number)
Very much improvedMuch improvedMinimally improvedNo changeMinimally worseMuch worseVery much worseNot done
Lacosamide 300 mg/Day21331886814
Lacosamide 400 mg/Day5611642181623112

[back to top]

Patient's Global Impression of Change (PGIC) From Baseline To Last Visit

"For the assessment of the Patient's Global Impression of Change, the subject should provide his/her assessment of his/her own clinical status, compared to Baseline, including an evaluation of seizure frequency and intensity, the occurrence of AEs, and subject's functional status.The subject was asked to answer the following:~Over the past 4 weeks, how have you felt compared to before you entered this clinical trial? (Please check the number that best describes your condition.)~Very much improved~Much improved~Minimally improved~No change~Minimally worse~Much worse~Very much worse" (NCT00520741)
Timeframe: Baseline; Last Visit (approximately 27 weeks)

,
Interventionparticipants (Number)
Very much improvedMuch improvedMinimally improvedNo changeMinimally worseMuch worseVery much worseNot done
Lacosamide 300 mg/Day243315103734
Lacosamide 400 mg/Day819337151922314

[back to top]

Number of Subjects Reporting at Least 1 Serious Adverse Event (SAE) During the Treatment Period (Maximum 6 Years)

Serious adverse events are any untoward serious medical occurrences in a subject administered study treatment, whether or not these events are related to treatment. (NCT00522275)
Timeframe: During the Treatment Period (Maximum 6 years)

Interventionsubjects (Number)
Lacosamide71

[back to top]

Median Percentage Change From Baseline in 28-day Seizure Frequency During the Treatment Period (Maximum 6 Years)

Negative changes from Baseline indicate an improvement (i.e., a reduction) in 28-day seizure frequency. (NCT00522275)
Timeframe: Baseline (8-week Baseline Period from the parent study SP0754 [NCT00136019]), Treatment Period (Maximum 6 years)

Interventionpercentage change (Median)
Lacosamide-48.5

[back to top]

Number of Subjects Reporting at Least 1 Treatment-Emergent Adverse Event (TEAE) During the Treatment Period (Maximum 6 Years)

Adverse events are any untoward medical occurrences in a subject administered study treatment, whether or not these events are related to treatment. (NCT00522275)
Timeframe: During the Treatment Period (Maximum 6 years)

Interventionsubjects (Number)
Lacosamide288

[back to top]

Number of Subjects Prematurely Discontinuing Due to a Treatment-Emergent Adverse Event (TEAE) During the Treatment Period (Maximum 6 Years)

Adverse events are any untoward medical occurrences in a subject administered study treatment, whether or not these events are related to treatment. (NCT00522275)
Timeframe: During the Treatment Period (Maximum 6 years)

Interventionsubjects (Number)
Lacosamide33

[back to top]

Percentage of at Least 50 % Responders During the Treatment Period (Maximum 6 Years)

At least 50 percent response is based on the percentage reduction in 28-day seizure frequency during the Treatment Period of the open-label extension relative to the Baseline Phase of the prior study. (NCT00522275)
Timeframe: Treatment Period (Maximum 6 years)

Interventionpercentage of subjects (Number)
Lacosamide48.2

[back to top]

Duration of Lacosamide (LCM) Monotherapy Treatment From Visit 1 to End of Study

Duration of total Lacosamide Monotherapy From Visit 1 to End of Study. (NCT00530855)
Timeframe: From Visit 1 to End of Study (approximately 2 years)

Interventiondays (Mean)
Lacosamide479.1

[back to top]

Occurrence of At Least One Treatment-Emergent Adverse Event (TEAE) From Visit 1 to End of Study

"A TEAE is defined as any untoward medical occurrence (eg, noxious or pathological changes) in a subject or clinical investigation subject compared with pre-existing conditions, that occurs during any phase of a clinical trial including Pretreatment, Run-In, Wash-Out, or Follow-Up Phases.~An TEAE is defined as being independent of assumption of any causality (eg, to trial or concomitant medication, primary or concomitant disease, or trial design)." (NCT00530855)
Timeframe: From Visit 1 to End of Study (approximately 2 years)

InterventionParticipants (Number)
Lacosamide296

[back to top]

Occurrence of Treatment-Emergent Adverse Events (TEAE) Leading to Subject Withdrawal From Visit 1 to End of Study

(NCT00530855)
Timeframe: From Visit 1 to End of Study (approximately 2 years)

InterventionParticipants (Number)
Lacosamide22

[back to top]

Percentage of Subjects on Lacosamide (LCM) Monotherapy at Any Time Between Visit 1 and End of Study

Percentage of Subjects on Lacosamide (LCM) Monotherapy at any time between Visit 1 and End of Study. (NCT00530855)
Timeframe: From Visit 1 to End of Study (approximately 2 years)

InterventionParticipants (Number)
Lacosamide292

[back to top]

Average Pain Score as Measured by a 100 mm Visual Analogue Scale (VAS) at Last Visit.

On VAS 0 mm = no pain and 100 mm = worst possible pain. (NCT00546351)
Timeframe: Last Visit (approximately 2 years)

Interventionunits on a scale (Mean)
Lacosamide30.47

[back to top]

Average Pain Score as Measured by a 100 mm Visual Analog Scale (VAS) at Baseline.

Visual Analog Scale (VAS) 0 mm = no pain and 100 mm = worst possible pain. (NCT00546351)
Timeframe: Baseline

Interventionunits on a scale (Mean)
Lacosamide65.83

[back to top]

Average Pain Interference With Sleep (11-point Likert Scale) at Last Visit.

0 = no interference with sleep and 10 = worst possible interference with sleep. (NCT00546351)
Timeframe: Last Visit

Interventionunits on a scale (Mean)
Lacosamide2.73

[back to top]

Average Quality of Life Using the SF-36 Health Survey - Mental Component Summary (MCS) at Baseline.

The SF-36 Health Survey measures health-related quality of life across multiple disease states. It has 36 questions with 8 subscale scores and 2 summary scores: PCS = physical functioning, role-physical, bodily pain, and general health; MCS = vitality, social functioning, role-emotional, and mental health. Scoring is done for both subscores and summary scores. For both, 0 = worst score (or quality of life) and 100 = best score. (NCT00546351)
Timeframe: Baseline

Interventionunits on a scale (Mean)
Lacosamide42.8

[back to top]

Patient's Global Impression of Change (PGIC) at Last Visit.

"The PGIC is a 7-point self-administered categorical rating scale in which the subject rated the change in pain since starting trial medication (from much worse [score of 1] to much better [score of 7]).~Reported results are presented as Better (sum of mildly, moderately, or much better), No Change, or Worse (sum of mildly, moderately, or much worse)." (NCT00546351)
Timeframe: Last Visit (approximately 2 years)

Interventionpercentage of participants (Number)
BetterNo ChangeWorse
Lacosamide82.611.46.0

[back to top]

Within-Subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Unpleasantness at Final Visit.

0 = not unpleasant and 10 = most unpleasant sensation imaginable. (NCT00546351)
Timeframe: Baseline Visit; Last Visit (approximately 2 years)

Interventionunits on a scale (Mean)
Lacosamide3.8

[back to top]

Within-Subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Surface Pain at Last Visit.

0 = no surface pain and 10 = most intense surface pain imaginable. (NCT00546351)
Timeframe: Baseline Visit; Last Visit (approximately 2 years)

Interventionunits on a scale (Mean)
Lacosamide3.2

[back to top]

Within-Subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Sharpness at Last Visit.

0 = not sharp and 10 = most sharp sensation imaginable. (NCT00546351)
Timeframe: Baseline Visit; Last Visit (approximately 2 years)

Interventionunits on a scale (Mean)
Lacosamide3.0

[back to top]

Within-Subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Itchiness at Final Visit.

0 = not itchy and 10 = most itchy sensation imaginable. (NCT00546351)
Timeframe: Baseline Visit; Last Visit (approximately 2 years)

Interventionunits on a scale (Mean)
Lacosamide2.0

[back to top]

Within-Subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Intensity at Last Visit.

0 = no pain and 10 = most intense pain sensation imaginable. (NCT00546351)
Timeframe: Baseline Visit; Last Visit (approximately 2 years)

Interventionunits on a scale (Mean)
Lacosamide-3.2

[back to top]

Within-Subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Heat at Last Visit.

0 = not hot and 10 = the most hot sensation imaginable. (NCT00546351)
Timeframe: Baseline Visit; Last Visit (approximately 2 years)

Interventionunits on a scale (Mean)
Lacosamide2.9

[back to top]

Within-Subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Dullness at Last Visit.

0 = not dull and 10 = most dull sensation imaginable. (NCT00546351)
Timeframe: Baseline Visit; Last Visit (approximately 2 years)

Interventionunits on a scale (Mean)
Lacosamide2.9

[back to top]

Within-Subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Deep Pain at Last Visit.

0 = no deep pain and 10 = most intense deep pain imaginable. (NCT00546351)
Timeframe: Baseline Visit; Last Visit (approximately 2 years)

Interventionunits on a scale (Mean)
Lacosamide3.4

[back to top]

Within-Subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Sensitivity at Last Visit.

0 = not sensitive and 10 = most sensitive sensation imaginable. (NCT00546351)
Timeframe: Baseline Visit; Last Visit (approximately 2 years)

Interventionunits on a scale (Mean)
Lacosamide2.9

[back to top]

Within-Subject Change in Neuropathic Pain Using the Neuropathic Pain Scale (NPS) - Cold at Last Visit.

0 = not cold and 10 = the coldest sensation imaginable. (NCT00546351)
Timeframe: Baseline Visit; Last Visit (approximately 2 years)

Interventionunits on a scale (Mean)
Lacosamide2.1

[back to top]

Average Quality of Life Using the SF-36 Health Survey - Mental Component Summary (MCS) at Last Visit.

The SF-36 Health Survey measures health-related quality of life across multiple disease states. It has 36 questions with 8 subscale scores and 2 summary scores: PCS = physical functioning, role-physical, bodily pain, and general health; MCS = vitality, social functioning, role-emotional, and mental health. Scoring is done for both subscores and summary scores. For both, 0 = worst score (or quality of life) and 100 = best score. (NCT00546351)
Timeframe: Last Visit

Interventionunits on a scale (Mean)
Lacosamide44.5

[back to top]

Average Quality of Life Using the SF-36 Health Survey - Physical Component Summary (PCS) at Baseline.

The SF-36 Health Survey measures health-related quality of life across multiple disease states. It has 36 questions with 8 subscale scores and 2 summary scores: PCS = physical functioning, role-physical, bodily pain, and general health; MCS = vitality, social functioning, role-emotional, and mental health. Scoring is done for both subscores and summary scores. For both, 0 = worst score (or quality of life) and 100 = best score. (NCT00546351)
Timeframe: Baseline

Interventionunits on a scale (Mean)
Lacosamide32.8

[back to top]

Number of Participants Experiencing the Occurrence of at Least One Treatment-emergent Adverse Event (TEAE) During the Evaluation Period From Entry Visit 1 Through End of Treatment (Approximately 6.5 Years).

Adverse events are any untoward medical occurrences in a subject administered study treatment, whether or not these events are related to treatment. (NCT00546351)
Timeframe: From entry Visit 1 through end of treatment (approximately 6.5 years)

Interventionparticipants (Number)
Lacosamide416

[back to top]

Number of Participants Experiencing the Occurrence of at Least One Serious Adverse Event (SAE) During the Evaluation Period From Entry Visit 1 Through End of Treatment (Approximately 6.5 Years).

"A Serious Adverse Event (SAE) is any untoward medical occurrence that at any dose:~Is fatal~Is life-threatening~Results in persistent or significant disability/incapacity~Requires inpatient hospitalization~Prolongs existing inpatient hospitalization~Is a congenital anomaly/birth defect~Is considered to be an important medical event. Such an event may not be immediately life threatening or result in death or hospitalization but may jeopardize the subject or may require intervention to prevent one of the other outcomes listed in the definitions above" (NCT00546351)
Timeframe: From entry Visit 1 through end of treatment (approximately 6.5 years)

Interventionparticipants (Number)
Lacosamide132

[back to top]

Average Quality of Life Using the SF-36 Health Survey - Physical Component Summary (PCS) at Last Visit.

The SF-36 Health Survey measures health-related quality of life across multiple disease states. It has 36 questions with 8 subscale scores and 2 summary scores: PCS = physical functioning, role-physical, bodily pain, and general health; MCS = vitality, social functioning, role-emotional, and mental health. Scoring is done for both subscores and summary scores. For both, 0 = worst score (or quality of life) and 100 = best score. (NCT00546351)
Timeframe: Last Visit

Interventionunits on a scale (Mean)
Lacosamide38.4

[back to top]

Average Daily Pain Score Using an 11-point Likert Scale (0-10) at Baseline Visit.

On the Likert Scale, 0 = no pain and 10 = worst possible pain. (NCT00546351)
Timeframe: Baseline

Interventionunits on a scale (Mean)
Lacosamide6.45

[back to top]

Average Daily Pain Score Using an 11-point Likert Scale (0-10) at Last Visit.

On the Likert Scale, 0 = no pain and 10 = worst possible pain. (NCT00546351)
Timeframe: Last Visit (approximately 2 years)

Interventionunits on a scale (Mean)
Lacosamide3.01

[back to top]

Average Pain Interference With Activity (11-point Likert Scale) at Baseline.

0 = no interference with activity and 10 = worst possible interference with activity. (NCT00546351)
Timeframe: Baseline

Interventionunits on a scale (Mean)
Lacosamide6.11

[back to top]

Average Pain Interference With Activity (11-point Likert Scale) at Last Visit.

0 = no interference with activity and 10 = worst possible interference with activity. (NCT00546351)
Timeframe: Last Visit

Interventionunits on a scale (Mean)
Lacosamide2.89

[back to top]

Average Pain Interference With Sleep (11-point Likert Scale) at Baseline.

0 = no interference with sleep and 10 = worst possible interference with sleep. (NCT00546351)
Timeframe: Baseline

Interventionunits on a scale (Mean)
Lacosamide5.98

[back to top]

Percentage of at Least 50% Responders During the Treatment Period (up to 8 Years)

At least 50 percent response is based on the percentage reduction in 28-day seizure frequency during the Treatment Period of the open-label extension relative to the Baseline Phase of the prior study. This endpoint reflects the percentage of subjects with at least 50% reduction (ie, at least 50% change) in 28-day partial onset seizure frequency (NCT00552305)
Timeframe: Treatment Period (up to 8 years)

Interventionpercentage of subjects (Number)
Lacosamide51.2

[back to top]

Median Percentage Change From Baseline in 28-day Seizure Frequency During the Treatment Period (up to 8 Years)

"Median percentage change is the median value with respect to the percent change from Baseline across the population of subjects. Percentage change is calculated as 100 times the difference of the seizure frequency for the treatment period and the Baseline seizure frequency divided by the baseline seizure frequency.~Negative changes from Baseline indicate an improvement (i.e., a reduction) in 28-day seizure frequency." (NCT00552305)
Timeframe: Baseline, End of Treatment Period (up to 8 years)

Interventionpercentage change (Median)
Lacosamide-50.8

[back to top]

Number of Subjects Prematurely Discontinuing Due to a Treatment-Emergent Adverse Event (TEAE) During the Treatment Period (up to 8 Years)

Adverse events are any untoward medical occurrences in a subject administered study treatment, whether or not these events are related to treatment. (NCT00552305)
Timeframe: During the Treatment Period (up to 8 years)

Interventionsubjects (Number)
Lacosamide47

[back to top]

Number of Subjects Reporting at Least 1 Serious Adverse Event (SAE) During the Treatment Period (up to 8 Years)

A serious adverse event is any untoward medical occurrences in a subject administered study treatment, whether or not the event is related to treatment, with at least one of the follow outcomes: death, life-threatening, initial inpatient hospitalization or prolongation of hospitalization, significant or persistent disability/incapacity, congenital anomaly/birth defect, or an important medical event that may jeopardize the subject and require a medical/surgical intervention. (NCT00552305)
Timeframe: During the Treatment Period (up to 8 years)

Interventionsubjects (Number)
Lacosamide125

[back to top]

Number of Subjects Reporting at Least 1 Treat-Emergent Adverse Event (TEAE) During the Treatment Period (up to 8 Years)

Adverse events are any untoward medical occurrences in a subject administered study treatment, whether or not these events are related to treatment. (NCT00552305)
Timeframe: During the Treatment Period (up to 8 years)

Interventionsubjects (Number)
Lacosamide343

[back to top]

Number of Subjects Who Withdrew From the Study Due to an Adverse Event (Maximum Study Duration 2 Years)

An Adverse Event (AE) is any untoward medical occurrence (eg, noxious or pathological changes) in a subject or clinical investigation subject compared with pre-existing conditions, that occurs during any period of a clinical trial including Pre-treatment, Run-In, Wash-Out, or Follow-Up Periods. An AE is defined as being independent of assumption of any causality (eg, to study or concomitant medication, primary or concomitant disease, or study design). (NCT00655486)
Timeframe: 2 years

Interventionsubjects (Number)
Lacosamide10

[back to top]

Number of Subjects With at Least One Adverse Event During This Open-label Extension Study (Maximum Study Duration 2 Years)

An Adverse Event (AE) is any untoward medical occurrence (eg, noxious or pathological changes) in a subject or clinical investigation subject compared with pre-existing conditions, that occurs during any period of a clinical trial including Pre-treatment, Run-In, Wash-Out, or Follow-Up Periods. An AE is defined as being independent of assumption of any causality (eg, to study or concomitant medication, primary or concomitant disease, or study design). (NCT00655486)
Timeframe: 2 years

Interventionsubjects (Number)
Lacosamide93

[back to top]

Number of Subjects With at Least One Adverse Event During the Treatment Period (up to 7 Days)

An Adverse Event (AE) is any untoward medical occurrence (eg, noxious or pathological changes) in a subject or clinical investigation subject compared with pre-existing conditions, that occurs during any period of a clinical trial including Pre-treatment, Run-In, Wash-Out, or Follow-Up Periods. An AE is defined as being independent of assumption of any causality (eg, to study or concomitant medication, primary or concomitant disease, or study design). (NCT00655551)
Timeframe: Treatment period (up to 7 days)

Interventionsubjects (Number)
Lacosamide (200 mg)17
Lacosamide (300 mg)42
Lacosamide (400 mg)20

[back to top]

Number of Subjects With at Least One Adverse Event With an Onset Within 4 Hours of Start of Infusion

An Adverse Event (AE) is any untoward medical occurrence (eg, noxious or pathological changes) in a subject or clinical investigation subject compared with pre-existing conditions, that occurs during any period of a clinical trial including Pre-treatment, Run-In, Wash-Out, or Follow-Up Periods. An AE is defined as being independent of assumption of any causality (eg, to study or concomitant medication, primary or concomitant disease, or study design). (NCT00655551)
Timeframe: 0-4 hours post start of the infusion

Interventionsubjects (Number)
Lacosamide (200 mg)5
Lacosamide (300 mg)24
Lacosamide (400 mg)16

[back to top]

Number of Subjects Who Withdrew From the Trial Due to an Adverse Event

An Adverse Event (AE) is any untoward medical occurrence (eg, noxious or pathological changes) in a subject or clinical investigation subject compared with pre-existing conditions, that occurs during any period of a clinical trial including Pre-treatment, Run-In, Wash-Out, or Follow-Up Periods. An AE is defined as being independent of assumption of any causality (eg, to study or concomitant medication, primary or concomitant disease, or study design). (NCT00655551)
Timeframe: Entire trial period (up to 6 weeks), screening through safety follow-up period (2 weeks post last medication)

Interventionsubjects (Number)
Lacosamide (200 mg)0
Lacosamide (300 mg)3
Lacosamide (400 mg)4

[back to top]

The Incidence of Predefined Cardiovascular Treatment-Emergent Adverse Events (TEAEs) in Epilepsy Patients With Partial-onset Seizures While on Vimpat or Any Other add-on Antiepileptic Drug (AED) Treatment During the Study

"Predefined cardiovascular-related Adverse Events (AEs), ie, Atrioventricular (AV) block, syncope, bradycardia, and PR prolongation, were identified as AEs coded to one of the following MedDRA Preferred Terms: Adams-Stokes syndrome, Atrioventricular block, Atrioventricular block complete, Atrioventricular block first degree, Atrioventricular block second degree, Syncope, Bradycardia, Bradyarrhythmia, Sinus bradycardia, or Electrocardiogram PR prolongation.~Treatment-emergent Adverse Events (TEAEs) are those that start on or after the day of first intake of the add-on AED treatment and up to 30 days after the day of last add-on AED treatment intake." (NCT00771927)
Timeframe: From Baseline up to 12 months

InterventionTreatment-Emergent Adverse Events (Number)
Lacosamide4
Other AED3

[back to top]

The Incidence of Predefined Psychiatric Treatment-Emergent Adverse Events (TEAEs) in Epilepsy Patients With Partial-onset Seizures While on Vimpat or Any Other add-on Antiepileptic Drug (AED) Treatment During the Study

"Predefined psychiatric-related AEs, ie, depression, suicide/self-injury, drug abuse, drug dependence, substance abuse, and intentional drug misuse were predefined as AEs coded to one of the following MedDRA Preferred Terms: Depression, Major depression, Depressed mood, Depression suicidal, Completed suicide, Suicidal behavior, Suicidal ideation, Suicide attempt, Intentional self-injury, Self-injurious behavior, Self-injurious ideation, Poisoning deliberate, Drug abuse, Drug abuser, Drug dependence, Substance abuse, Substance abuser, Polysubstance dependence, Intentional drug misuse, Intentional overdose, or Multiple drug overdose intentional.~Treatment-emergent Adverse Events (TEAEs) are those that start on or after the day of first intake of the add-on AED treatment and up to 30 days after the day of last add-on AED treatment intake." (NCT00771927)
Timeframe: From Baseline up to 12 months

InterventionTreatment-Emergent Adverse Events (Number)
Lacosamide22
Other AED31

[back to top]

Number of Subjects That Report at Least One Treatment-emergent Adverse Event During the Study (Approximately 13 Weeks)

(NCT00938431)
Timeframe: 13 weeks

Interventionparticipants (Number)
>=1 Month to <4 Years (Safety Set)14
>=4 Years to <12 Years (Safety Set)19
>=12 Years to <=17 Years (Safety Set)9

[back to top]

Plasma Ctrough Values for Lacosamide at Day 28

"During SP0847, the time points for collection of blood samples for plasma concentration analysis varied per enrollment cohort. To provide a standard summary of this information, we present the mean plasma trough concentrations (Ctrough). Ctrough levels represent the lowest level of LCM that was present in the subject with measurement taken pre-dose before the next scheduled dose of LCM.~The blood sample for plasma concentration schedule varied per enrollment cohort and with protocol amendments. A PK sample was not required for a subject to be in the included in the SS although all subjects did have at least one PK sample taken during SP0847. Therefore the number of subjects presented for the PK assessments is based on the subjects in the SS who attended the respective visits and had PK concentration data at the respective time point." (NCT00938431)
Timeframe: Day 28

Interventionμg/mL (Geometric Mean)
All Subjects (Safety Set)3886.0

[back to top]

Plasma Ctrough Values for Lacosamide at Day 35

"During SP0847, the time points for collection of blood samples for plasma concentration analysis varied per enrollment cohort. To provide a standard summary of this information, we present the mean plasma trough concentrations (Ctrough). Ctrough levels represent the lowest level of LCM that was present in the subject with measurement taken pre-dose before the next scheduled dose of LCM.~The blood sample for plasma concentration schedule varied per enrollment cohort and with protocol amendments. A PK sample was not required for a subject to be in the included in the SS although all subjects did have at least one PK sample taken during SP0847. Therefore the number of subjects presented for the PK assessments is based on the subjects in the SS who attended the respective visits and had PK concentration data at the respective time point." (NCT00938431)
Timeframe: Day 35

Interventionμg/mL (Geometric Mean)
All Subjects (Safety Set)4033.8

[back to top]

Plasma Ctrough Values for Lacosamide at Day 42

"During SP0847, the time points for collection of blood samples for plasma concentration analysis varied per enrollment cohort. To provide a standard summary of this information, we present the mean plasma trough concentrations (Ctrough). Ctrough levels represent the lowest level of LCM that was present in the subject with measurement taken pre-dose before the next scheduled dose of LCM.~The blood sample for plasma concentration schedule varied per enrollment cohort and with protocol amendments. A PK sample was not required for a subject to be in the included in the SS although all subjects did have at least one PK sample taken during SP0847. Therefore the number of subjects presented for the PK assessments is based on the subjects in the SS who attended the respective visits and had PK concentration data at the respective time point." (NCT00938431)
Timeframe: Day 42

Interventionμg/mL (Geometric Mean)
All Subjects (Safety Set)4169.5

[back to top]

Plasma Ctrough Values for Lacosamide at Day 7

"During SP0847, the time points for collection of blood samples for plasma concentration analysis varied per enrollment cohort. To provide a standard summary of this information, we present the mean plasma trough concentrations (Ctrough). Ctrough levels represent the lowest level of LCM that was present in the subject with measurement taken pre-dose before the next scheduled dose of LCM.~The blood sample for plasma concentration schedule varied per enrollment cohort and with protocol amendments. A PK sample was not required for a subject to be in the included in the SS although all subjects did have at least one PK sample taken during SP0847. Therefore the number of subjects presented for the PK assessments is based on the subjects in the SS who attended the respective visits and had PK concentration data at the respective time point." (NCT00938431)
Timeframe: Day 7

Interventionμg/mL (Geometric Mean)
All Subjects (Safety Set)839.9

[back to top]

Plasma Ctrough Values for SPM 12809 at Day 28

"SPM 12809 is major metabolite of LCM and is known as O-desmethyl-lacosamide. During SP0847, the time points for collection of blood samples for plasma concentration analysis varied per enrollment cohort. To provide a standard summary of this information, we present the mean plasma trough concentrations (Ctrough). Ctrough levels represent the lowest level of LCM that was present in the subject with measurement taken pre-dose before the next scheduled dose of LCM.~The blood sample for plasma concentration schedule varied per enrollment cohort and with protocol amendments. A PK sample was not required for a subject to be in the included in the SS although all subjects did have at least one PK sample taken during SP0847. Therefore the number of subjects presented for the PK assessments is based on the subjects in the SS who attended the respective visits and had PK concentration data at the respective time point." (NCT00938431)
Timeframe: Day 28

Interventionμg/mL (Geometric Mean)
All Subjects (Safety Set)754.9

[back to top]

Plasma Ctrough Values for SPM 12809 at Day 35

"SPM 12809 is major metabolite of LCM and is known as O-desmethyl-lacosamide. During SP0847, the time points for collection of blood samples for plasma concentration analysis varied per enrollment cohort. To provide a standard summary of this information, we present the mean plasma trough concentrations (Ctrough). Ctrough levels represent the lowest level of LCM that was present in the subject with measurement taken pre-dose before the next scheduled dose of LCM.~The blood sample for plasma concentration schedule varied per enrollment cohort and with protocol amendments. A PK sample was not required for a subject to be in the included in the SS although all subjects did have at least one PK sample taken during SP0847. Therefore the number of subjects presented for the PK assessments is based on the subjects in the SS who attended the respective visits and had PK concentration data at the respective time point." (NCT00938431)
Timeframe: Day 35

Interventionμg/mL (Geometric Mean)
All Subjects (Safety Set)955.1

[back to top]

Plasma Ctrough Values for SPM 12809 at Day 42

"SPM 12809 is major metabolite of LCM and is known as O-desmethyl-lacosamide. During SP0847, the time points for collection of blood samples for plasma concentration analysis varied per enrollment cohort. To provide a standard summary of this information, we present the mean plasma trough concentrations (Ctrough). Ctrough levels represent the lowest level of LCM that was present in the subject with measurement taken pre-dose before the next scheduled dose of LCM.~The blood sample for plasma concentration schedule varied per enrollment cohort and with protocol amendments. A PK sample was not required for a subject to be in the included in the SS although all subjects did have at least one PK sample taken during SP0847. Therefore the number of subjects presented for the PK assessments is based on the subjects in the SS who attended the respective visits and had PK concentration data at the respective time point." (NCT00938431)
Timeframe: Day 42

Interventionμg/mL (Geometric Mean)
All Subjects (Safety Set)1725.8

[back to top]

Plasma Ctrough Values for SPM 12809 at Day 7

"SPM 12809 is major metabolite of LCM and is known as O-desmethyl-lacosamide. During SP0847, the time points for collection of blood samples for plasma concentration analysis varied per enrollment cohort. To provide a standard summary of this information, we present the mean plasma trough concentrations (Ctrough). Ctrough levels represent the lowest level of LCM that was present in the subject with measurement taken pre-dose before the next scheduled dose of LCM.~The blood sample for plasma concentration schedule varied per enrollment cohort and with protocol amendments. A PK sample was not required for a subject to be in the included in the SS although all subjects did have at least one PK sample taken during SP0847. Therefore the number of subjects presented for the PK assessments is based on the subjects in the SS who attended the respective visits and had PK concentration data at the respective time point." (NCT00938431)
Timeframe: Day 7

Interventionμg/mL (Geometric Mean)
All Subjects (Safety Set)258.4

[back to top]

Caregiver Global Impression of Change Score at Visit 5 (Day 27/28) or Early Termination

"For the assessment of the Caregiver Global Impression of Change, the caregiver (including parent/legal guardian) provided his/her assessment of the subject's clinical status, compared to Baseline (Visit 1), including an evaluation of seizure frequency and intensity, the occurrence of Adverse Events (AEs), and subject's functional status.~The caregiver will be asked to check the number that best describes the subject's condition over the past 4 weeks compared to Baseline:~Very much improved~Much improved~Minimally improved~No change~Minimally worse~Much worse~Very much worse" (NCT00938431)
Timeframe: Visit 5 (Day 27/28) or Early Termination

,,
InterventionParticipants (Number)
Very Much ImprovedMuch ImprovedMinimally ImprovedNo ChangeMiniamally WorseMuch WorseNo data available
>=1 Month to <4 Years (Full Analysis Set)3730001
>=12 Years to <=17 Years (Full Analysis Set)0431001
>=4 Years to <12 Years (Full Analysis Set)2882120

[back to top]

Clinical Global Impression of Change Score at Visit 5 (Day 27/28) or Early Termination

"For assessment of the Clinical Global Impression of Change, the investigator provided his/her assessment of the subject's clinical status, compared to Baseline (Visit 1), including an evaluation of seizure frequency and intensity, the occurrence of AEs, and subject's functional status.~The investigator will be asked to check the number that best describes the subject's condition over the past 4 weeks compared to Baseline:~Very much improved~Much improved~Minimally improved~No Change~Minimally worse~Much worse~Very much worse" (NCT00938431)
Timeframe: Visit 5 (Day 27/28) or Early Termination

,,
InterventionParticipants (Number)
Very Much ImprovedMuch ImprovedMinimally ImprovedNo ChangeMinimally WorseMuch WorseNo data available
>=1 Month to <4 Years (Full Analysis Set)2641010
>=12 Years to <=17 Years (Full Analysis Set)0710001
>=4 Years to <12 Years (Full Analysis Set)2792300

[back to top]

Change in Seizure Frequency From Baseline to End of Treatment

(NCT00938431)
Timeframe: From Baseline to End of Treatment (approximately 13 weeks)

Interventionpercentage change (Mean)
>=1 Month to <4 Years (Full Analysis Set)18.94
>=4 Years to <12 Years (Full Analysis Set)18.38
>=12 Years to <=17 Years (Full Analysis Set)34.59

[back to top]

Number of Seizure Days Per 28 Days for Participants With Generalized Seizures

"A seizure day was defined as a day where any type of seizure was reported in the seizure diary and seizures were assessed. Days in the seizure diary which were marked as not done on the CRF/eCRF were not counted as seizure-free days." (NCT00938912)
Timeframe: Weeks 4, 8, 12, 20, 28, 36, 44, 52, 60, 72, 84 and 96

Interventionseizure days per 28 days (Mean)
Week 4Week 8Week 12Week 20Week 28Week 36Week 44Week 52Week 60Week 72Week 84Week 96
Lacosamide (All Participants) (FAS)14.5914.8313.6812.5713.1011.439.2410.4810.3111.1511.8710.73

[back to top]

Percentage of Participants With ≥75% Reduction in 28-day Partial-onset Seizure Frequency

A 75% responder is a participant experiencing a ≥75% reduction in partial-onset seizure frequency per 28 days from Baseline to end of the specified time interval, otherwise a participant is a non-responder. For rollover participants, the Baseline values from the previous pediatric studies were designated as Baseline values in SP848. The Baseline value for seizure counts for directly enrolled participants were taken from the historical seizure count CRF/eCRF module in combination with the seizure diary data collected from the date of the Screening Visit to the day prior to the date of first dose of LCM. Participants from EP0060 RxL enrollment group had no baseline data due to taking oral LCM prior to EP0060. (NCT00938912)
Timeframe: From Baseline to End of Treatment Period (up to 4.2 years)

Interventionpercentage of participants (Number)
Lacosamide (All Participants) (FAS)40.3

[back to top]

Percentage of Participants With ≥50% Reduction in 28-day Partial-onset Seizure Frequency

A 50% responder is a participant experiencing a ≥50% reduction in partial-onset seizure frequency per 28 days from Baseline to end of the specified time interval, otherwise a participant is a non-responder. For rollover participants, the Baseline values from the previous pediatric studies were designated as Baseline values in SP848. The Baseline value for seizure counts for directly enrolled participants were taken from the historical seizure count CRF/eCRF module in combination with the seizure diary data collected from the date of the Screening Visit to the day prior to the date of first dose of LCM. Participants from EP0060 RxL enrollment group had no baseline data due to taking oral LCM prior to EP0060. (NCT00938912)
Timeframe: From Baseline to End of Treatment Period (up to 4.2 years)

Interventionpercentage of participants (Number)
Lacosamide (All Participants) (FAS)53.6

[back to top]

Percentage of Participants Who Achieved a Seizure-free Status

"Study participants were considered seizure-free for a given period if they completed the period, reported zero seizures during the period, and had no more than 10% of days in the period for which seizure data were not available (ie, not done was noted on the Seizure Frequency CRF/eCRF module)." (NCT00938912)
Timeframe: From Baseline to End of Treatment Period (up to 4.2 years)

Interventionpercentage of participants (Number)
Lacosamide (All Participants) (FAS)7.4

[back to top]

Number of Participants That Withdraw Due to a Treatment-Emergent Adverse Event

TEAEs were defined as those events which started on or after the date of first SP848 LCM administration and occurred within 30 days after last dose of LCM, or whose severity worsened on or after the date of first SP848 LCM administration. (NCT00938912)
Timeframe: From Baseline to End of Safety Follow-Up (up to 4.3 years)

InterventionParticipants (Count of Participants)
Lacosamide (All Participants) (SS)27

[back to top]

Number of Participants With Serious Adverse Events (SAEs)

SAE was any untoward medical occurrence that at any dose resulted in death, is life-threatening, required in participant hospitalization or prolongation of existing hospitalization, is a congenital anomaly or birth defect, is an infection that requires treatment with parenteral antibiotics, other important medical events which based on medical or scientific judgement may jeopardize the participants, or may require medical or surgical intervention to prevent any of the above. (NCT00938912)
Timeframe: From Baseline to End of Safety Follow-Up (up to 4.3 years)

InterventionParticipants (Count of Participants)
Lacosamide (All Participants) (SS)82

[back to top]

Percent Change From Baseline in 28 Day Partial-onset Seizure Frequency to the End of the Treatment Period

Percent change in seizure frequency per 28 days (PCH) from the Baseline value (B) to Treatment Period interval (T) was defined as:PCH = [(SFT - SFB)/SFB] x 100 where, SFT corresponded to seizure frequency during Treatment Period for relative interval in open-label study and SFB corresponded to Baseline seizure frequency. For both periods, the frequency was standardized to the number of seizures per 28 days. For rollover participants, the Baseline values from the previous pediatric studies were designated as Baseline values in SP848. The Baseline value for seizure counts for directly enrolled participants were taken from the historical seizure count case report form/electronic case report form (CRF/eCRF) module in combination with the seizure diary data collected from the date of the Screening Visit to the day prior to the date of first dose of LCM. Participants from EP0060 RxL enrollment group had no baseline data due to taking oral LCM prior to EP0060. (NCT00938912)
Timeframe: From Baseline to End of Treatment Period (up to 4.2 years)

Interventionpercent change (Mean)
Lacosamide (All Participants) (FAS)-24.13

[back to top]

Number of Participants With At Least One Treatment-Emergent Adverse Event (TEAE)

An AE is any untoward medical occurrence in a participant or clinical investigation study participant administered a pharmaceutical product, which does not necessarily have a causal relationship with this treatment. TEAEs were defined as those events which started on or after the date of first SP848 LCM administration and occurred within 30 days after last dose of LCM, or whose severity worsened on or after the date of first SP848 LCM administration. (NCT00938912)
Timeframe: From Baseline to End of Safety Follow-Up (up to 4.3 years)

InterventionParticipants (Count of Participants)
Lacosamide (All Participants) (SS)336

[back to top]

"The Proportion of Subjects Who Achieved Seizure-free Status During the First 12 Weeks of the Maintenance Phase"

"A subject will be considered seizure-free if the subject completes the first 12 weeks of the Maintenance Phase, reports zero seizures, and has no seizure data missing for any day during the period of time.~This study was intended to assess the efficacy outcomes in the First Add-On Group and the Later Add-On Group individually relative to historical data. Comparisons between the 2 groups should not be attempted and conclusions should not be drawn." (NCT00955357)
Timeframe: From Week 7 (end of Week 6) to end of Week 18

Interventionpercentage of subjects (Number)
First Add-on37.5
Later Add-on14.9

[back to top]

Number of Adverse Events

The primary outcome measure is the incidence of clinical adverse events. These will be followed by daily clinical observations during the hospital stay. Subjects will be evaluated for e.g., seizures, fever, neurological changes, cardiovascular, hematologic and dermatologic abnormalities, liver failure, renal failure, and death; EKGs will be requested as per ICU routines through day 7. (NCT01110187)
Timeframe: baseline to 7 days

Interventionnumber of events experienced (Number)
IV LCM12
IV fPHT21

[back to top]

Number of Participants With Seizures

Number of seizures in the first 72 hours based on EEG recording (NCT01110187)
Timeframe: baseline to 72 hours

Interventionnumber of participants with seizures (Number)
IV LCM0
IV fPHT0

[back to top]

Change in the Number of Seizure Days With Myoclonic Seizures From the Baseline Phase to the Maintenance Phase

"During the study subjects kept a diary to record daily seizure activity from Visit 1 until the end of study participation. The following information has been recorded:~Seizure type~Seizure frequency~A negative value in change of seizure days with myoclonic seizures shows a decrease in seizure days with myoclonic seizures." (NCT01118949)
Timeframe: From Baseline Phase (Weeks 0 to 4) to Maintenance Phase (Weeks 8 to 13)

Interventionnumber of seizure days (Mean)
Lacosamide-2.19

[back to top]

Change in the Number of Seizure Days With Absence Seizures From the Baseline Phase to the Maintenance Phase

"During the study subjects kept a diary to record daily seizure activity from Visit 1 until the end of study participation. The following information has been recorded:~Seizure type~Seizure frequency~A negative value in change of seizure days with absence seizures shows a decrease in seizure days with absence seizures." (NCT01118949)
Timeframe: From Baseline Phase (Weeks 0 to 4) to Maintenance Phase (Weeks 8 to 13)

Interventionnumber of seizure days (Mean)
Lacosamide-0.37

[back to top]

Changes in Count of 3 Hertz (Hz) Spike-wave Discharges (During Waking Hours) on 24-hour Ambulatory Electroencephalogram (EEG) From Visit 2 (Baseline Phase) to Visit 6 (Maintenance Phase)

Subjects were asked to return to the clinic on the morning of the day prior to Visit 2 and Visit 6 to begin 24-hour ambulatory EEG recordings for evaluation of spike-wave discharges. Only subjects with an evaluable EEG measurement with > 19 interpretable hours at Visit 2 and Visit 6 are included in this analysis. The 3 Hertz (Hz) spike-wave discharges are calculated per awake hours. (NCT01118949)
Timeframe: From Visit 2 (Week 4) to Visit 6 (Week 8)

Intervention1/hour (Mean)
Lacosamide0.13

[back to top]

Changes in Count of Generalized Spike-wave Discharges on 24-hour Ambulatory Electroencephalogram (EEG) From Visit 2 (Baseline Phase) to Visit 6 (Maintenance Phase)

Subjects were asked to return to the clinic on the morning of the day prior to Visit 2 and Visit 6 to begin 24-hour ambulatory EEG recordings for evaluation of spike-wave discharges. Only subjects with an evaluable EEG measurement with > 19 interpretable hours at Visit 2 and Visit 6 are included in this analysis. The general spike-wave discharges are calculated per interpretable hours. (NCT01118949)
Timeframe: From Visit 2 (Week 4) to Visit 6 (Week 8)

Intervention1/hour (Mean)
Lacosamide-3.47

[back to top]

Number of Subjects With Treatment Emergent Adverse Events (TEAEs) During the 10-week Treatment Period

An Adverse Event (AE) is any untoward medical occurrence in a patient or clinical investigation subject administered a pharmaceutical product, which does not necessarily have a causal relationship with this treatment. (NCT01118949)
Timeframe: From Visit 2 (Week 4) to Visit 7 (Week 13)

Interventionparticipants (Number)
Lacosamide43

[back to top]

Number of Subjects Withdrawn From the Study Due to Treatment Emergent Adverse Events (TEAEs) During the 10-week Treatment Period

An Adverse Event (AE) is any untoward medical occurrence in a patient or clinical investigation subject administered a pharmaceutical product, which does not necessarily have a causal relationship with this treatment. (NCT01118949)
Timeframe: From Visit 2 (Week 4) to Visit 7 (Week 13)

Interventionparticipants (Number)
Lacosamide5

[back to top]

Number of Participants Withdrawn From the Study Due to Treatment-emergent Adverse Events (TEAEs) From Visit 1 to the End of Study (Approximately 61 Weeks)

(NCT01118962)
Timeframe: From Visit 1 to the end of study (Approximately 61 weeks)

Interventionparticipants (Number)
Lacosamide2

[back to top]

Number of Participants With Treatment-emergent Adverse Events (TEAEs) From Visit 1 to the End of Study (Approximately 61 Weeks)

(NCT01118962)
Timeframe: From Visit 1 to the end of study (Approximately 61 weeks)

Interventionparticipants (Number)
Lacosamide37

[back to top]

Change in Adverse Event Profile (AEP) From Baseline to Visit 4.

Range 19-76, where higher scores indicate more severe impairment (in terms of 19 common antiepileptic drug side effects. (NCT01190098)
Timeframe: Baseline to visit 4 (approximately 1 - 2 months)

Interventionunits on a scale (Mean)
Lacosamide-1.2
Sugar Pill-6.0

[back to top]

Change in Daily Seizure Frequency From Baseline to Visit 4

Number of seizures per day. (NCT01190098)
Timeframe: Baseline to visit 4 (approximately 1 - 2 months)

Interventionnumber of seizures per day (Median)
Lacosamide0.0
Sugar Pill0.0

[back to top]

Change in Epworth Sleepiness Scale Score From Baseline to Visit 4

Scale 0 - 24 Higher scores indicate more severe symptoms (NCT01190098)
Timeframe: Baseline and Visit 4 (approximately 1 - 2 months)

InterventionUnits on a scale (Mean)
Lacosamide-1.2
Sugar Pill-1.1

[back to top]

Change in Functional Outcomes of Sleep Questionnaire (FOSQ) From Baseline to Visit 4.

Range 0-20 where lower scores indicate more impairment (sleep related QOL). (NCT01190098)
Timeframe: Baseline to visit 4 (approximately 1 - 2 months)

Interventionunits on a scale (Mean)
Lacosamide0.3
Sugar Pill1.1

[back to top]

Change in Patient Health Questionnaire-9 (PHQ-9) From Baseline to Visit 4.

Range 0-27, where higher scores indicate more impairment (depressive symptoms) (NCT01190098)
Timeframe: Baseline to visit 4 (approximately 1 - 2 months)

Interventionunits on a scale (Mean)
Lacosamide-1.1
Sugar Pill-1.2

[back to top]

Change in Pittsburgh Sleep Quality Inventory (PSQI) From Baseline to Visit 4

Range 0-21, where higher scores more impairment (in terms of sleep quality). (NCT01190098)
Timeframe: Baseline to Visit 4 (approximately 1 - 2 months)

Interventionunits on a scale (Mean)
Lacosamide-1.6
Sugar Pill-1.3

[back to top]

Change in Quality of Life in Epilepsy (QOLIE-31) From Baseline to Visit 4

Range 0 -10 where higher scores reflect better quality of life. (NCT01190098)
Timeframe: Baseline to visit 4 (approximately 1 - 2 months)

Interventionunits on a scale (Mean)
Lacosamide4.0
Sugar Pill4.2

[back to top]

Change in the Fatigue Severity Scale From Baseline to Visit 4.

Fatigue Severity Scale (FSS): Range 7- 63 where higher scores indicate more severe fatigue. (NCT01190098)
Timeframe: Baseline to Visit 4 (approximately 1 - 2 months)

Interventionunits on a scale (Mean)
Lacosamide0.30
Sugar Pill-5.4

[back to top]

Number of Subjects Prematurely Discontinuing Due to a TEAE During the Study

Number of subjects prematurely discontinuing due to a TEAE during the study. The study is comprised of a 12-week Titration Phase, a 12 -week Maintenance Phase, and a 3 to 4 week Taper Phase if needed. (NCT01235403)
Timeframe: During the study (up to 24 - 28 weeks)

Interventionsubjects (Number)
Lacosamide14

[back to top]

Number of Subjects Reporting at Least 1 Treatment-Emergent Adverse Event (TEAE) During the Study

Number of subjects reporting at least 1 Treatment-Emergent Adverse Event (TEAE) during the study. The study is comprised of a 12-week Titration Phase, a 12 -week Maintenance Phase, and a 3 to 4 week Taper Phase if needed. (NCT01235403)
Timeframe: During the study ( up to 24 - 28 weeks)

Interventionsubjects (Number)
Lacosamide64

[back to top]

Percentage of Subjects Retained on Vimpat Through the End of the 24-week Treatment Period

"The number of subjects continuing on Vimpat up to and including Visit 4 (Week 24) divided by the number of patients who took at least 1 dose of Vimpat multiplied by 100.~The overall Treatment Period comprises of a 12-week Titration Phase and 12-week Maintenance Phase." (NCT01235403)
Timeframe: End of Treatment Period (24-week)

Interventionpercentage of subjects (Number)
Lacosamide73

[back to top]

Percentage of Subjects Who Received Concomitant Antiepileptic Drug Treatment

Concomitant antiepileptic drug (AED) treatments are defined as treatments which started after or at the date of the first administration of VIMPAT®. (NCT01236001)
Timeframe: From baseline to study termination (6 months)

Interventionpercentage of patients (Number)
Patients Treated With VIMPAT® Prior to Enrollment98.1
Patients Who Started VIMPAT® Treatment on/After Enrollment96.6
Total Population97.4

[back to top]

Treatment Persistence of VIMPAT® After 6 Months

Treatment persistence is defined as the percentage of subjects being treated under VIMPAT® after a given duration (>=6 months). (NCT01236001)
Timeframe: >=6 months

Interventionpercentage of participants (Number)
Patients Treated With VIMPAT® Prior to Enrollment95.2
Patients Who Started VIMPAT® Treatment on/After Enrollment56.3
Total Population77.6

[back to top]

Galenic Formulation Repartition in Subjects Treated by VIMPAT® at 3 Months

VIMPAT is available as tablet and oral solution formulation in Belgium. The use of each galenic formulation will be presented with number of subjects by formulation. (NCT01236001)
Timeframe: 3 months

,,
Interventionparticipants (Number)
TabletOral Solution
Patients Treated With VIMPAT® Prior to Enrollment740
Patients Who Started VIMPAT® Treatment on/After Enrollment630
Total Population1370

[back to top]

Galenic Formulation Repartition in Subjects Treated by VIMPAT® at 6 Months

VIMPAT is available as tablet and oral solution formulation in Belgium. The use of each galenic formulation will be presented with number of subjects by formulation. (NCT01236001)
Timeframe: 6 months

,,
Interventionparticipants (Number)
TabletOral Solution
Patients Treated With VIMPAT® Prior to Enrollment870
Patients Who Started VIMPAT® Treatment on/After Enrollment670
Total Population1540

[back to top]

Galenic Formulation Repartition in Subjects Treated by VIMPAT® at Baseline

"This outcome will be only provided for subjects who were already treated by VIMPAT® at Baseline.~VIMPAT is available as tablet and oral solution formulation in Belgium. The use of each galenic formulation will be presented with number of subjects by formulation." (NCT01236001)
Timeframe: Baseline

Interventionparticipants (Number)
TabletOral Solution
Patients Treated With VIMPAT® Prior to Enrollment1041

[back to top]

Percentage of Subjects by Category of Clinical Evolution of Seizure Control at 3 Months

Clinical evolution of seizures following administration of VIMPAT compared to baseline before start of VIMPAT. The evolution of seizure control is subjectively assessed by the investigator on a four categorical scale, with options being 1=worsened, 2=stable, 3=improved, 4=much improved. If seizure control is worse, the investigator will try to document the reason. (NCT01236001)
Timeframe: 3 months

,,
Interventionpercentage of participants (Number)
Much improvedImprovedStableWorsenedUnknown
Patients Treated With VIMPAT® Prior to Enrollment16.743.634.65.10
Patients Who Started VIMPAT® Treatment on/After Enrollment16.233.835.19.55.4
Total Population16.438.834.97.22.7

[back to top]

Percentage of Subjects by Category of Clinical Evolution of Seizure Control at 6 Months

Clinical evolution of seizures following administration of VIMPAT compared to baseline before start of VIMPAT. The evolution of seizure control is subjectively assessed by the investigator on a four categorical scale, with options being 1=worsened, 2=stable, 3=improved, 4=much improved. If seizure control is worse, the investigator will try to document the reason (NCT01236001)
Timeframe: 6 months

,,
Interventionpercentage of participants (Number)
Much improvedImprovedStableWorsened
Patients Treated With VIMPAT® Prior to Enrollment18.935.840.05.3
Patients Who Started VIMPAT® Treatment on/After Enrollment19.238.434.28.2
Total Population19.036.937.56.5

[back to top]

Percentage of Subjects by Category of Clinical Evolution of Seizure Control at Baseline

"This outcome will be only provided for subjects who were already treated by VIMPAT® at Baseline.~Clinical evolution of seizures following administration of VIMPAT compared to baseline before start of VIMPAT. The evolution of seizure control is subjectively assessed by the investigator on a four categorical scale, with options being 1=worsened, 2=stable, 3=improved, 4=much improved. If seizure control is worse, the investigator will try to document the reason." (NCT01236001)
Timeframe: Baseline

Interventionpercentage of participants (Number)
Much ImprovedImprovedStableWorsenedUnknown
Patients Treated With VIMPAT® Prior to Enrollment16.239.030.52.911.4

[back to top]

Mean Total Daily Dose of VIMPAT® (mg) at 3 Months

(NCT01236001)
Timeframe: 3 months

Interventionmg/day of Vimpat (Mean)
Patients Treated With VIMPAT® Prior to Enrollment316.2
Patients Who Started VIMPAT® Treatment on/After Enrollment211.1
Total Population267.9

[back to top]

Mean Total Daily Dose of VIMPAT® (mg) at 6 Months

(NCT01236001)
Timeframe: 6 months

Interventionmg/day of Vimpat (Mean)
Patients Treated With VIMPAT® Prior to Enrollment329.9
Patients Who Started VIMPAT® Treatment on/After Enrollment262.7
Total Population300.6

[back to top]

Mean Total Daily Dose of VIMPAT® (mg) at Baseline

Mean total daily dose at baseline will be only provided for subjects who were already treated by VIMPAT® at Baseline. (NCT01236001)
Timeframe: Baseline

Interventionmg/day of Vimpat (Mean)
Patients Treated With VIMPAT® Prior to Enrollment272.1

[back to top]

Proportion of Subjects in the Full Analysis Set (FAS) Remaining Seizure Free for 6 Consecutive Months (26 Consecutive Weeks) of Treatment Following Stabilization at the Last Evaluated Dose for Each Subject

The proportion of subjects remaining seizure free for 6 months (26 weeks) was estimated using Kaplan-Meier methods. (NCT01243177)
Timeframe: 6 consecutive months (26 consecutive weeks) of treatment following stabilization at the last evaluated dose for each subject

Interventionpercentage of subjects (Number)
Lacosamide89.8
Carbamazepine-Controlled Release (CBZ-CR)91.1

[back to top]

Proportion of Subjects Remaining Seizure Free for 12 Consecutive Months (52 Consecutive Weeks) Following Stabilization at the Last Evaluated Dose for Each Subject

The proportion of subjects remaining seizure free for 12 months (52 weeks) was estimated using Kaplan-Meier methods. (NCT01243177)
Timeframe: 12 consecutive months of treatment following stabilization at the last evaluated dose for each subject

Interventionpercentage of subjects (Number)
Lacosamide77.8
Carbamazepine-Controlled Release (CBZ-CR)82.7

[back to top]

Proportion of Subjects in the Per Protocol Set (PPS) Remaining Seizure Free for 6 Consecutive Months (26 Consecutive Weeks) of Treatment Following Stabilization at the Last Evaluated Dose for Each Subject

The proportion of subjects remaining seizure free for 6 months (26 weeks) was estimated using Kaplan-Meier methods. (NCT01243177)
Timeframe: 6 consecutive months (26 consecutive weeks) of treatment

Interventionpercentage of subjects (Number)
Lacosamide91.4
Carbamazepine-Controlled Release (CBZ-CR)92.8

[back to top]

Number of Subjects Who Withdraw From the Study Due to a Treatment-emergent Adverse Event (AE) During the Treatment Phase (up to 113 Weeks)

An Adverse Event is any untoward medical occurrence in a patient or clinical investigation subject administered a pharmaceutical product which does not necessarily have a causal relationship with this treatment. An AE can therefore be any unfavorable and unintended sign, symptom, or disease temporally associated with the use of a medicinal (investigational) product, whether or not related to the medicinal (investigational) product. Treatment-emergent AEs were defined as AEs that started on or after the date of first dose of study medication and within 30 days following the date of final study medication administration, or AEs whose intensity worsened on or after the date of first dose of study medication and within 30 days following the date of last dose. (NCT01243177)
Timeframe: Duration of the Treatment Phase (up to 113 weeks)

InterventionParticipants (Number)
Lacosamide47
Carbamazepine-Controlled Release (CBZ-CR)69

[back to top]

Number of Subjects With at Least One Treatment-emergent Adverse Event (AE) During the Treatment Phase (up to 113 Weeks)

An Adverse Event is any untoward medical occurrence in a patient or clinical investigation subject administered a pharmaceutical product which does not necessarily have a causal relationship with this treatment. An AE can therefore be any unfavorable and unintended sign, symptom, or disease temporally associated with the use of a medicinal (investigational) product, whether or not related to the medicinal (investigational) product. Treatment-emergent AEs were defined as AEs that started on or after the date of first dose of study medication and within 30 days following the date of final study medication administration, or AEs whose intensity worsened on or after the date of first dose of study medication and within 30 days following the date of last dose. (NCT01243177)
Timeframe: Duration of the Treatment Phase (up to 113 weeks)

InterventionParticipants (Number)
Lacosamide328
Carbamazepine-Controlled Release (CBZ-CR)332

[back to top]

Number of Subjects With at Least One Treatment-emergent Serious Adverse Event (SAE) During the Treatment Phase (up to 113 Weeks)

"An Adverse Event is any untoward medical occurrence in a patient or clinical investigation subject administered a pharmaceutical product which does not necessarily have a causal relationship with this treatment. An AE can therefore be any unfavorable and unintended sign, symptom, or disease temporally associated with the use of a medicinal (investigational) product, whether or not related to the medicinal (investigational) product.~A Serious Adverse Event must meet 1 or more predefined criteria like death, life-threatening, etc. Treatment-emergent AEs were defined as AEs that started on or after the date of first dose of study medication and within 30 days following the date of final study medication administration, or AEs whose intensity worsened on or after the date of first dose of study medication and within 30 days following the date of last dose." (NCT01243177)
Timeframe: Duration of the Treatment Phase (up to 113 weeks)

InterventionParticipants (Number)
Lacosamide32
Carbamazepine-Controlled Release (CBZ-CR)43

[back to top]

Number of Seizure-Free Days

(NCT01345058)
Timeframe: 6 Months

Interventiondays (Mean)
Lacosamide + Low-Dose Levetiracetam118.11
Control Group (High-Dose Levetiracetam)114.0

[back to top]

Time to First Seizure After Therapeutic Dose is Reached

Time in days until the first seizure after the therapeutic dose is reached occurs. (NCT01345058)
Timeframe: 6 Months

Interventiondays (Median)
Lacosamide + Low-Dose Levetiracetam162.0
Control Group (High-Dose Levetiracetam)116.5

[back to top]

Retention Rate

Retention rate is defined as the percentage of participants who remained on the study drug after study completion. (NCT01345058)
Timeframe: 6 Months

Interventionpercentage of participants (Number)
Lacosamide + Low-Dose Levetiracetam89
Control Group (High-Dose Levetiracetam)80

[back to top]

Percentage of Participants Achieving Six Month Seizure Freedom

Seizure freedom is defined as having no seizures and was evaluated in the 6 month period after receiving the drug. (NCT01345058)
Timeframe: 6 Months

Interventionpercentage of participants (Number)
Lacosamide + Low-Dose Levetiracetam47.4
Control Group (High-Dose Levetiracetam)41.7

[back to top]

Number of Participants With Treatment-Emergent Adverse Events (TEAE)

An Adverse Event (AE) is defined as any untoward medical occurrence (side effect) in a clinical investigation participant administered a drug; it does not necessarily have to have a causal relationship with this treatment. A TEAE is defined as an adverse event that occurs after receiving the drug. (NCT01345058)
Timeframe: 6 Months

InterventionParticipants (Count of Participants)
Lacosamide + Low-Dose Levetiracetam11
Control Group (High-Dose Levetiracetam)26

[back to top]

Change in Serum Sex Hormone Binding Globulin (SHBG) From Baseline to Treatment Period End (Comprised of a 4-week Titration Period and an 8-week Maintenance Period)

Due to premature termination of enrollment prior to achieving the planned sample size (a total of 28 subjects), this primary safety variable was assessed for descriptive purposes only. A negative value indicates an improvement. (NCT01375374)
Timeframe: From Day 1 (Baseline) to Day 84 (Treatment Period End)

Interventionnmol/L (Median)
Lacosamide-12.80

[back to top]

Change in Serum Thyroid Hormone Free Thyroxine Level From Baseline to Treatment Period End (Comprised of a 4-week Titration Period and an 8-week Maintenance Period)

The change in the serum thyroid hormone free thyroxine level from Baseline to the end of the Maintenance Period was summarized descriptively by visit. (NCT01375374)
Timeframe: From Day 1 (Baseline) to Day 84 (Treatment Period End)

Interventionpmol/L (Median)
Lacosamide2.70

[back to top]

Change in Sex Hormone Calculated Free Androgen Index Levels From Baseline to Treatment Period End (Comprised of a 4-week Titration Period and an 8-week Maintenance Period)

The change in sex hormone calculated free androgen index (100 x Testosterone/sex hormone binding globulin) levels from Baseline to the end of Maintenance Period was summarized descriptively by visit. A negative value indicates an improvement. (NCT01375374)
Timeframe: From Day 1 (Baseline) to Day 84 (Treatment Period End)

InterventionFree Androgen Index (Median)
Lacosamide9.493

[back to top]

Change in Total Cholesterol Level From Baseline to Treatment Period End (Comprised of a 4-week Titration Period and an 8-week Maintenance Period)

The change in total cholesterol levels from Baseline to the end of the Maintenance Period was summarized descriptively by visit. A negative value indicates an improvement. (NCT01375374)
Timeframe: From Day 1 (Baseline) to Day 84 (Treatment Period End)

Interventionmmol/L (Median)
Lacosamide-0.540

[back to top]

Number of Participants With Seizures

Number of Participants that had seizure in a randomized, two-arm, parallel groups of post-operative participants with newly-diagnosed high-grade glioma (HGG) (NCT01432171)
Timeframe: 12 months or first seizure

InterventionParticipants (Count of Participants)
Lacosamide0
Placebo1

[back to top]

Percentage of Subjects in Whom Study Drug is Withdrawn Early After Treatment With Treatment Arm 1

Percentage of subjects in whom study drug is withdrawn early after treatment with treatment arm 1 (NCT01458522)
Timeframe: baseline to end of treatment arm 1

InterventionParticipants (Count of Participants)
LCM Treatment2
fPHT Treatment3

[back to top]

Percentage of Subjects Who Experience no Nonconvulsive Seizures (NCS) for 24 Hours Following Treatment With LCM vs. fPHT, as Measured by Continuous Electroencephalography (cEEG) Monitoring.

Percentage of subjects who experience no nonconvulsive seizures (NCS) for 24 hours (after the 2-hour observation-only period) following treatment with LCM vs. fPHT, as measured by continuous electroencephalography (cEEG) monitoring with blinded review. (NCT01458522)
Timeframe: 24 hours

InterventionParticipants (Count of Participants)
LCM 400mg19
fPHT 20mg PE/kg22

[back to top]

Percentage of Subjects Who Require a Rebolus of the Initial Antiepileptic Drugs (AED) to Control Nonconvulsive Seizures (NCS) in the LCM vs fPHT Arms.

The percentage of subjects who require a rebolus of the initial antiepileptic drug (AED) to control nonconvulsive seizures (NCS) in the LCM vs fPHT arms. (NCT01458522)
Timeframe: 24 hours

InterventionParticipants (Count of Participants)
LCM 400mg16
fPHT 20mg PE/kg13

[back to top]

Seizure Burden Change From Baseline to End of Crossover, Excluding Initial Treatment Arm

Absolute change defined as the number of minutes of ESz activity per hour before treatment and at the end of the second treatment arm. This measure does not evaluate seizure activity in the first treatment arm. If less than 1 hour of recording time is available, seizure time will be extrapolated to 1 hour. (NCT01458522)
Timeframe: baseline, 26-68 hours

Interventionmin/hour (Mean)
LCM First, Then fPHT-0.78
fPHT First, Then LCM-0.83

[back to top]

Seizure Burden Change From Baseline to End of Initial Treatment

Absolute change in seizure time (defined as the number of minutes of electrographic seizure (ESz) activity per hour) before treatment and at the end of the first treatment arm. If less than 1 hour of recording time is available, seizure time will be extrapolated to 1 hour. The maximum amount of time that can be used to determine baseline seizure time is 6 hours. (NCT01458522)
Timeframe: Baseline, 24 hours

Interventionmin/hour (Mean)
LCM 400mg-0.58
fPHT 20mg PE/kg-0.54

[back to top]

Change in Functional Status as Measured by the Functional Disability Scale at Day 7 to 9 Postrandomization and Day 30 Post-randomization in the LCM vs fPHT Arms.

Change in functional status as measured by the Functional Disability Scale, using a 0-29 rating (0=w/o disability; 29=extreme vegetative state) at Day 7 to 9 postrandomization and Day 30 post-randomization in the LCM first, then fPHT versus fPHT first, then LCM arms. Data was analyzed in a manner consistent with determining if one treatment arm resulted in a greater change in functional status than the other. (NCT01458522)
Timeframe: Baseline to day 7-9, baseline to day 30

,
Interventionunits on a scale (Mean)
Change from baseline to day 7-9Change from baseline to day 30
fPHT First, Then LCM0.3-3.7
LCM First, Then fPHT-4.1-8.5

[back to top]

Days in the Intensive Care Unit/Hospital

Data was acquired in a manner consistent with determining if one treatment arm (LCM first, then fPHT versus fPHT first, then LCM) resulted in more days of hospitalization than the other over the course of the study. (NCT01458522)
Timeframe: initial bolus to end of study

,
Interventiondays (Mean)
Days in ICUDays in hospital
fPHT First, Then LCM6.512.5
LCM First, Then fPHT7.412.7

[back to top]

Time of First Bolus to End of Seizures After Initial Treatment Arm, Time From Crossover to End of Seizures in Crossover Treatment Arm

Time of first bolus to end of seizures after initial treatment arm, time from crossover to end of seizures in crossover treatment arm (NCT01458522)
Timeframe: time of first bolus to end of seizures after initial treatment arm, time from crossover to end of seizures in crossover treatment arm

,
Interventionhours (Mean)
Initial TreatmentCrossover Treatment
fPHT First, Then LCM9.81.7
LCM First, Then fPHT8.48.2

[back to top]

Percentage of All Subjects Who Have Had a Seizure, Are on Antiepileptic Drug (AED) Therapy, and Are Alive/Dead at Day 30

Percentage of all subjects who have had a seizure, are on antiepileptic drug (AED) therapy, and are alive and dead at day 30. Data was acquired in a manner consistent with determining if one treatment arm (LCM first, then fPHT versus fPHT first, then LCM) resulted in a greater effect on seizures, antiepileptic drug (AED) use, and survival at day 30 after the acute treatment period. The acute treatment period could range from 6 to 30 hours. (NCT01458522)
Timeframe: both acute treatment periods to 30 days

,
Interventionpercentage of participants (Number)
any seizure within 30 days after acute tx periodAED use within 30 days after acute tx periodDied within 30 days after randomization
fPHT First, Then LCM38.974.016.0
LCM First, Then fPHT27.482.215.5

[back to top]

Number of Predefined Adverse Events (AE) After Treatment Arm 1 Administration

Number of predefined adverse events (AE) after treatment arm 1 administration. These predefined adverse events include Patients with at least one AE of interest, Cardiac disorders, investigations, suspected hypersensitivity reactions, vascular disorders, and hypotension. (NCT01458522)
Timeframe: 24 hours

InterventionNumber of predefined AEs (Number)
LCM 400mg4
fPHT 20mg PE/kg5

[back to top]

Number of Subjects Who Required a Second Antiepileptic Drug (AED) to Control Nonconvulsive Seizures (NCS)

Number of subjects who required a second antiepileptic drug (AED) to control nonconvulsive seizures (NCS) (NCT01458522)
Timeframe: 24-26 hours

InterventionParticipants (Count of Participants)
LCM First, Then fPHT15
fPHT First, Then LCM10

[back to top]

Number of Subjects Who Withdrew From the Study Due to a Treatment-emergent Adverse Event (AE) During the Treatment Phase (Maximum 3.5 Years)

Treatment-emergent AEs were defined as those events which started on or after the date of first dose of SP0994 study medication, or events in which severity worsened on or after the date of first dose of SP0994 study medication. AEs which occurred within 30 days after last dose of study medication were considered treatment emergent. (NCT01465997)
Timeframe: Up to 3.5 Years (Duration of the Treatment Phase)

InterventionParticipants (Count of Participants)
Lacosamide12
Carbamazepine-Controlled Release (CBZ-CR)21

[back to top]

Number of Subjects With at Least One Treatment-emergent Serious Adverse Event (SAE) During the Treatment Phase (Maximum of 3.5 Years)

A Serious Adverse Event is any untoward medical occurrence that at any dose results in death, is life threatening, requires in-patient hospitalization or prolongation of existing hospitalization, results in persistent or significant disability/incapacity is a congenital anomaly/birth defect. (NCT01465997)
Timeframe: Up to 3.5 Years (Duration of the Treatment Phase)

InterventionParticipants (Count of Participants)
Lacosamide32
Carbamazepine-Controlled Release (CBZ-CR)22

[back to top]

Number of Subjects With at Least One Treatment-emergent Adverse Event (AE) During the Treatment Phase (Maximum of 3.5 Years)

Treatment-emergent AEs were defined as those events which started on or after the date of first dose of SP0994 study medication, or events in which severity worsened on or after the date of first dose of SP0994 study medication. AEs which occurred within 30 days after last dose of study medication were considered treatment emergent. (NCT01465997)
Timeframe: Up to 3.5 Years (Duration of the Treatment Phase)

InterventionParticipants (Count of Participants)
Lacosamide (SS)181
Carbamazepine-Controlled Release (CBZ-CR) (SS)182

[back to top]

Retention at the End of the 21-week Treatment Period

Retention is a summary measure that integrates both the patient's and clinician's assessment of efficacy and tolerability in epilepsy clinical studies to provide a measure of effectiveness. (NCT01484977)
Timeframe: Duration of the Treatment Period (21 Weeks)

Interventionpercentage of participants (Number)
Lacosamide73.3

[back to top]

The Percent Change in Ratio of Dose and Defined Daily Dose (DDD) for the Drug Load of Concomitant Anti-Epileptic Drugs (AEDs) From Baseline to the End of Observation Period (Day 0 to 6 Months)

Drug load is defined as the sum of the ratios of the actual doses divided by the defined daily dose for all concomitant AEDs. (NCT01673282)
Timeframe: From Baseline (Day 0) to 6 months

Interventionpercent change of ratio in dose (Mean)
Vimpat + Na Channel Blocking AED-15.0
Vimpat + Non-Na Channel Blocking AED-4.4

[back to top]

Change in Partial-Onset Seizure Frequency Per 28 Days From Baseline to the Treatment Period (i.e., Titration + Maintenance Period)

"Partial-onset seizure (POS) frequency per 28 days was calculated as:~POS frequency = (Number of POS over the specified time interval) / (Number of days in the interval with available diary data) x 28.~A negative value in Change in Partial-onset seizure frequency indicates a reduction of Partial-onset seizure frequency from Baseline to the Treatment Period." (NCT01710657)
Timeframe: 8-week Baseline Period (Visit 1 to 3) to the 16-week Treatment Period (Visit 3 to 8)

InterventionSeizures per 28 days (Median)
Placebo-1.10
Lacosamide 200 mg/Day-3.39
Lacosamide 400 mg/Day-4.00

[back to top]

Change in Partial-Onset Seizure Frequency Per 28 Days From Baseline to the Maintenance Period

"Partial-onset seizure (POS) frequency per 28 days was calculated as:~POS frequency = (Number of POS over the specified time interval) / (Number of days in the interval with available diary data) x 28.~A negative value in Change in Partial-onset seizure frequency indicates a reduction of Partial-onset seizure frequency from Baseline to the Maintenance Period." (NCT01710657)
Timeframe: 8-week Baseline Period (Visit 1 to 3) and 12-week Maintenance Period (Visit 5 to 8)

InterventionSeizures per 28 days (Median)
Placebo-1.22
Lacosamide 200 mg/Day-3.33
Lacosamide 400 mg/Day-4.50

[back to top]

The Proportion of Individual Patients Who Experience a 50 % or Greater Reduction in Seizure Frequency From Baseline to the Maintenance Period (50 % Responder Rate)

(NCT01710657)
Timeframe: 8-week Baseline Period (Visit 1 to 3) to the 12-week Maintenance Period (Visit 5 to 8)

Interventionparticipants (Number)
Placebo36
Lacosamide 200 mg/Day70
Lacosamide 400 mg/Day88

[back to top]

Percent Change in Partial-Onset Seizure Frequency Per 28 Days From Baseline to the Maintenance Period

Calculates as 28-day seizure frequency during the Maintenance Period - 28-day seizure frequency during the Baseline Period, divided by the 28-day seizure frequency during the Baseline Period with this quantity multiplied by 100. A negative value in percent change from Baseline indicates a decrease in Partial-Onset Seizure frequency from Baseline to the Maintenance Period. (NCT01710657)
Timeframe: 8-week Baseline Period (Visit 1 to 3) to the 12-week Maintenance Period (Visit 5 to 8)

Interventionpercentage change (Median)
Placebo-10.10
Lacosamide 200 mg/Day-36.75
Lacosamide 400 mg/Day-48.78

[back to top]

Number of Participants With at Least One Adverse Event Reported Spontaneously by the Subject or Observed by the Investigator From Baseline Until the End of Study Visit

An Adverse Event (AE) is any untoward medical occurrence in a patient or clinical investigation participant administered a pharmaceutical product, which does not necessarily have a causal relationship with this treatment. An AE could therefore be any unfavorable and unintended sign, symptom, or disease temporally associated with the use of a medicinal (investigational) product, whether or not related to the medicinal (investigational) product. (NCT01832038)
Timeframe: From Visit 1 (Week 0) up to approximately Week 323

InterventionParticipants (Count of Participants)
Lacosamide (SS)410

[back to top]

Number of Participants That Withdrew Due to Adverse Events From Baseline Until the End of Study Visit

An Adverse Event (AE) is any untoward medical occurrence in a patient or clinical investigation participant administered a pharmaceutical product, which does not necessarily have a causal relationship with this treatment and led to the withdrawal of the participants from the study. An AE could therefore be any unfavorable and unintended sign, symptom, or disease temporally associated with the use of a medicinal (investigational) product, whether or not related to the medicinal (investigational) product. (NCT01832038)
Timeframe: From Visit 1 (Week 0) up to approximately Week 323

InterventionParticipants (Count of Participants)
Lacosamide (SS)51

[back to top]

Percentage of Participants With 50 % Response Rate in Partial-onset Seizure Frequency Per 28 Days From Baseline of Study EP0008 [NCT01710657] Until the End of Study Visit in Study EP0009

A responder is a subject experiencing a greater than or equal to (≥) 50 % reduction in partial-onset seizure frequency per 28 days from baseline. Baseline was defined as the Baseline Period of study EP0008 [NCT01710657]. (NCT01832038)
Timeframe: From Visit 1 in study EP0008 [NCT01710657] up to approximately Week 323 in study EP0009

Interventionpercentage of participants (Number)
Lacosamide (FAS)57.1

[back to top]

Percent Change in Partial-onset Seizure Frequency Per 28 Days From Baseline of Study EP0008 [NCT01710657] Until the End of Study Visit in Study EP0009

The percent change from Baseline to the Treatment Period was calculated as {[(Seizure frequency per 28 days during the Treatment Period) minus (Seizure frequency per 28 days during Baseline Period)] divided by (Seizure frequency per 28 days during Baseline Period)} multiplied by 100. Baseline was defined as the Baseline Period of study EP0008 [NCT01710657]. (NCT01832038)
Timeframe: From Visit 1 in study EP0008 [NCT01710657] up to approximately Week 323 in study EP0009

InterventionPercent change (Mean)
Lacosamide (FAS)-44.47

[back to top]

Proportion of Subjects Experiencing no Change in Partial Onset Seizure Frequency (Between <25 % Reduction and <25 % Increase) Per 28 Days From Baseline to the Entire Treatment (ie, Titration+Maintenance Periods)

Proportion of subjects is presented as percentage of participants. No change is defined as between <25% reduction and <25% increase in POS frequency per 28 days from Baseline to the entire Treatment Period, otherwise not between <25% reduction and <25% increase is defined as a change. (NCT01921205)
Timeframe: Baseline to Week 16 (or last value on treatment)

Interventionpercentage of participants (Number)
Placebo (FAS)32.0
Lacosamide (FAS)20.6

[back to top]

Proportion of Subjects Experiencing a >=25 % to <50 %, 50 % to 75 %, or >75 % Reduction in Partial Onset Seizure Frequency Per 28 Days From Baseline to the Entire Treatment (ie, Titration+Maintenance Periods)

Proportion of subjects is presented as percentage of participants. A >=25%-<50% response in the Treatment Period is defined as >=25% to <50% reduction in POS frequency per 28 days from Baseline to end of Treatment Period. A >=50%-<=75% response in the Treatment Period is defined as >=50% to <=75% reduction in POS frequency per 28 days from Baseline to end of Treatment Period. A 75% response in the Treatment Period is defined as >75% reduction in POS frequency per 28 days from Baseline to end of Treatment Period. (NCT01921205)
Timeframe: Baseline to Week 16 (or last value on treatment)

,
Interventionpercentage of participants (Number)
>=25% - <50%>=50% - <=75%>75%
Lacosamide (FAS)16.520.623.5
Placebo (FAS)15.320.68.8

[back to top]

Proportion of Subjects Experiencing a >=25 % to <50 %, 50 % to 75 %, or >75 % Reduction in Partial Onset Seizure Frequency Per 28 Days From Baseline to the End of Maintenance Period

Proportion of subjects is presented as percentage of participants. A >=25%-<50% response in the Maintenance Period is defined as >=25% to <50% reduction in POS frequency per 28 days from Baseline to end of Maintenance Period. A >=50%-<=75% response in the Maintenance Period is defined as >=50% to <=75% reduction in POS frequency per 28 days from Baseline to end of Maintenance Period. A 75% response in the Maintenance Period is defined as >75% reduction in POS frequency per 28 days from Baseline to end of Maintenance Period. (NCT01921205)
Timeframe: Baseline to Week 16 (or last value on treatment)

,
Interventionpercentage of participants (Number)
>=25% - <50%>=50% - <=75%>75%
Lacosamide (FAS)11.821.831.2
Placebo (FAS)14.717.115.9

[back to top]

"Proportion of Subjects Who Achieved Seizure Free Status (Yes/no) for Subjects Who Completed the Maintenance Period"

The proportion of seizure free days is calculated as (days with number of seizures = 0) divided by (days with recorded data in the subject diary), where 'days with recorded data in the subject diary' excludes any days where 'Not Done' is recorded. (NCT01921205)
Timeframe: Week 7 to Week 16

Interventionpercentage of participants (Number)
Placebo (FAS)9.7
Lacosamide (FAS)15.1

[back to top]

Change in Partial Onset Seizure (POS) Frequency Per 28 Days From Baseline to the Maintenance Period

The POS frequency is standardized to a 28-day duration. Negative values indicate improvement from Baseline. (NCT01921205)
Timeframe: Baseline to Week 16 (or last value on treatment)

InterventionSeizures per 28 days (Median)
Placebo (FAS)-1.55
Lacosamide (FAS)-3.05

[back to top]

Change in Partial Onset Seizure Frequency Per 28 Days From Baseline to the Entire Treatment (ie, Titration+Maintenance Periods)

The POS frequency is standardized to a 28-day duration. Negative values indicate improvement from Baseline. (NCT01921205)
Timeframe: Baseline to Week 16 (or last value on treatment)

InterventionSeizures per 28 days (Median)
Placebo (FAS)-1.22
Lacosamide (FAS)-2.46

[back to top]

Change in Partial Onset Seizure Frequency Per 28 Days From Baseline to the Entire Treatment (ie, Titration+Maintenance Periods) for Complex Partial Seizures

The POS frequency is standardized to a 28-day duration. Negative values indicate improvement from Baseline. (NCT01921205)
Timeframe: Baseline to Week 16 (or last value on treatment)

InterventionSeizures per 28 days (Median)
Placebo (FAS)-0.98
Lacosamide (FAS)-2.06

[back to top]

Change in Partial Onset Seizure Frequency Per 28 Days From Baseline to the Entire Treatment (ie, Titration+Maintenance Periods) for Secondary Generalized Seizures

The POS frequency is standardized to a 28-day duration. Negative values indicate improvement from Baseline. (NCT01921205)
Timeframe: Baseline to Week 16 (or last value on treatment)

InterventionSeizures per 28 days (Median)
Placebo (FAS)-1.0
Lacosamide (FAS)-2.81

[back to top]

Change in Partial Onset Seizure Frequency Per 28 Days From Baseline to the Entire Treatment (ie, Titration+Maintenance Periods) for Simple Partial Seizures

The POS frequency is standardized to a 28-day duration. Negative values indicate improvement from Baseline. (NCT01921205)
Timeframe: Baseline to Week 16 (or last value on treatment)

InterventionSeizures per 28 days (Median)
Placebo (FAS)-1.14
Lacosamide (FAS)-1.25

[back to top]

Proportion of Responders Where a Responder is Defined as a Participant With >= 50% Reduction in Partial Onset Seizure Frequency Per 28 Days From Baseline to the Maintenance Period

Proportion of responders is presented as percentage of participants. A responder is a subject experiencing a 50 % or greater reduction in partial onset seizure frequency per 28 days from Baseline to the Maintenance Period. (NCT01921205)
Timeframe: Baseline to Week 16 (or last value on treatment)

Interventionpercentage of participants (Number)
Placebo (FAS)33.3
Lacosamide (FAS)52.9

[back to top]

Proportion of Seizure Free Days During the Maintenance Period for Subjects Who Completed the Maintenance Period

The proportion of seizure free days is calculated as (days with number of seizures = 0) divided by (days with recorded data in the subject diary), where 'days with recorded data in the subject diary' excludes any days where 'Not Done' is recorded. (NCT01921205)
Timeframe: Week 7 to Week 16

Interventiondays (Mean)
Placebo (FAS)0.65
Lacosamide (FAS)0.71

[back to top]

Proportion of Subjects Experiencing an Increase in Partial Onset Seizure Frequency Per 28 Days of >=25 % From Baseline to the Entire Treatment (ie, Titration+Maintenance Periods)

Proportion of subjects is presented as percentage of participants. An increase is defined as a >=25% increase in POS frequency per 28 days from Baseline to the entire Treatment Period, otherwise <25% increase is defined as no increase. (NCT01921205)
Timeframe: Baseline to Week 16 (or last value on treatment)

Interventionpercentage of participants (Number)
Placebo (FAS)23.1
Lacosamide (FAS)18.8

[back to top]

Percentage of Seizure-free Days During the Study

The number of seizure-free days was the total number of days within an interval for which daily diary data were available and no seizures were reported. The percentage of seizure-free days was computed as 100 times the number of seizure-free days in the interval divided by the number of days in the interval for which daily diary data were available. Percentage of seizure-free days was measured using data obtained from participant diaries from EP0034 and is presented for the overall Treatment only. (NCT01964560)
Timeframe: From Week 0 to End of Treatment (up to Week 96)

Interventionpercentage of seizure free days (Mean)
Lacosamide (All Subjects)66.96

[back to top]

Percentage of Participants With Serious TEAEs

A serious adverse event (SAE) must meet 1 or more of the following criteria: • Death, • Life-threatening (Life-threatening does not include a reaction that might have caused death had it occurred in a more severe form.), • Significant or persistent disability/incapacity, • Congenital anomaly/birth defect (including that occurring in a fetus), • Important medical event that, based upon appropriate medical judgment, may jeopardize the patient or participant and may require medical or surgical intervention to prevent 1 of the other outcomes listed in the definition of serious., • Initial inpatient hospitalization or prolongation of hospitalization. Treatment-emergent is defined as starting on or after the date of first dose of LCM in EP0034, and within 30 days of last dose. (NCT01964560)
Timeframe: From Week 0 to the End of Safety Follow-Up (up to Week 104)

Interventionpercentage of participants (Number)
Lacosamide (All Subjects)20.6

[back to top]

Percentage of Participants With TEAEs Leading to Study Discontinuation

An adverse event (AE) is any untoward medical occurrence in a patient or clinical investigation participant administered a pharmaceutical product, which does not necessarily have a causal relationship with this treatment. AEs leading to study discontinuation. Treatment-emergent is defined as starting on or after the date of first dose of LCM in EP0034, and within 30 days of last dose. (NCT01964560)
Timeframe: From Week 0 to the End of Safety Follow-Up (up to Week 104)

Interventionpercentage of participants (Number)
Lacosamide (All Subjects)4.1

[back to top]

Percentage of Participants With Treatment-emergent Adverse Events (TEAEs)

An adverse event (AE) is any untoward medical occurrence in a patient or clinical investigation participant administered a pharmaceutical product that does not necessarily have a causal relationship with this treatment. An AE can therefore be any unfavorable and unintended sign (including an abnormal laboratory finding), symptom, or disease temporally associated with the use of a medicinal (investigational) product, whether or not related to the medicinal (investigational) product. Treatment-emergent is defined as starting on or after the date of first dose of LCM in EP0034, and within 30 days of last dose. (NCT01964560)
Timeframe: From Week 0 to the End of Safety Follow-Up (up to Week 104)

Interventionpercentage of participants (Number)
Lacosamide (All Subjects)77.2

[back to top]

Number of Subjects Experiencing at Least 1 Treatment-emergent Adverse Event From Baseline to End of Study (Approximately 32 Weeks)

An Adverse Event (AE) is any untoward medical occurrence in a patient or clinical investigation subject administered a pharmaceutical product that does not necessarily have a causal relationship with this treatment. (NCT01969851)
Timeframe: From Baseline to End of Study (approximately 32 weeks)

InterventionParticipants (Count of Participants)
Lacosamide 1 Month - <4 Years SS10
Lacosamide 4 Years - <2 Years SS21
Lacosamide 12 Years - <18 Years SS18

[back to top]

Mean Change in Days With Any Generalized Seizures (Absence, Myoclonic, Clonic, Tonic, Tonic-clonic, Atonic, Partial Evolving to Secondarily Generalized) Per 28 Days From the Baseline Period to the Maintenance Period (Approximately 24 Weeks)

The mean change in the count of days with generalized seizures was presented. (NCT01969851)
Timeframe: Baseline Period to the Maintenance Period (approximately 24 weeks)

Interventiondays (Mean)
Lacosamide 1 Month - <4 Years SS0.50
Lacosamide 4 Years - <2 Years SS-1.90
Lacosamide 12 Years - <18 Years SS-3.38

[back to top]

Mean Changes in Count of 3 Hz Spike-wave Discharges (During Waking Hours) on 24-hour Ambulatory EEG From Visit 2 to Visit 6

The mean change in the count of 3 Hertz (Hz) spike-wave discharges was presented. Visit 6 (Week 6) was the End of the Titration Period. (NCT01969851)
Timeframe: From Baseline (Day 1) to Visit 6 (Week 6)

Interventioncount of discharges (Mean)
Lacosamide 1 Month - <4 Years SS-0.14
Lacosamide 4 Years - <2 Years SS-1.60
Lacosamide 12 Years - <18 Years SS0.00

[back to top]

Mean Changes in Count of Generalized Spike-wave Discharges on 24-hour Ambulatory Electroencephalogram (EEG) From Visit 2 to Visit 6

The mean change in the count of generalized spike-wave discharges was presented. Visit 6 (Week 6) was the End of the Titration Period. (NCT01969851)
Timeframe: From Baseline (Day 1) to Visit 6 (Week 6)

Interventiondischarges (Mean)
Lacosamide 1 Month - <4 Years SS-4.55
Lacosamide 4 Years - <2 Years SS-166.22
Lacosamide 12 Years - <18 Years SS-203.12

[back to top]

Number of Subject Withdrawals Due to Adverse Events From Baseline to End of Study (Approximately 32 Weeks)

An Adverse Event (AE) is any untoward medical occurrence in a patient or clinical investigation subject administered a pharmaceutical product that does not necessarily have a causal relationship with this treatment. (NCT01969851)
Timeframe: From Baseline to End of Study (approximately 32 weeks)

InterventionParticipants (Count of Participants)
Lacosamide 1 Month - <4 Years SS0
Lacosamide 4 Years - <2 Years SS0
Lacosamide 12 Years - <18 Years SS3

[back to top]

Number of Subjects Remaining Seizure Free for 6 Consecutive Months During the Monotherapy Period

"Subjects were considered seizure free if their seizure counts for every day over the entire Treatment Period was zero and if they completed the Treatment Period.~A subject was considered seizure free, if no seizure occurred during the 6 consecutive months in the Evaluation Period. If one of the following occurred, the subject was not considered seizure free:~A documented seizure during 6 consecutive months of the Evaluation Analysis Period~Subject discontinued the study prematurely during the Evaluation Analysis Period~Missing Seizure Count Case Report Forms (CRFs) prior to completing the Evaluation Analysis Period" (NCT02124564)
Timeframe: From the beginning of the Monotherapy Period to the end of the Follow-Up Period (up to 3.1 years until the time of approval granted)

InterventionParticipants (Count of Participants)
Lacosamide (FAS)6

[back to top]

Number of Subjects Remaining Seizure Free for 12 Consecutive Months During the Monotherapy Period

"Subjects were considered seizure free if their seizure counts for every day over the entire Treatment Period was zero and if they completed the Treatment Period.~A subject was considered seizure free, if no seizure occurred during the 12 consecutive months in the Evaluation Period. If one of the following occurred, the subject was not considered seizure free:~A documented seizure during 6 consecutive months of the Evaluation Analysis Period~Subject discontinued the study prematurely during the Evaluation Analysis Period~Missing Seizure Count Case Report Forms (CRFs) prior to completing the Evaluation Analysis Period.~Subjects who discontinued before the end date of 6 consecutive months were included in this analysis." (NCT02124564)
Timeframe: From the beginning of the Monotherapy Period to the end of the Follow-Up Period (up to 3.1 years until the time of approval granted)

InterventionParticipants (Count of Participants)
Lacosamide (FAS)6

[back to top]

Number of Subjects With at Least One Incidence of Serious Adverse Events (SAEs) During the Study

"A Serious Adverse Event (SAE) is any untoward medical occurrence that at any dose:~Results in death~Is life-threatening~Requires in patient hospitalization or prolongation of existing hospitalization~Is a congenital anomaly or birth defect~Is as infection that requires treatment parenteral antibiotics~Other important medical events which based on medical or scientific judgement may jeopardize the patients, or may require medical or surgical intervention to prevent any of the above" (NCT02124564)
Timeframe: From the Titration Period (investigational product is taken) to the End of Study Visit (up to 3.5 years)

InterventionParticipants (Count of Participants)
Lacosamide (Safety Set)2

[back to top]

Number of Subjects With at Least One Incidence of Treatment-Emergent Adverse Events (TEAEs) During the Study

An Adverse Event (AE) is any untoward medical occurrence in a patient or clinical investigation subject administered a pharmaceutical product, which does not necessarily have a causal relationship with this treatment. An AE could therefore be any unfavorable and unintended sign, symptom, or disease temporally associated with the use of a medicinal (investigational) product, whether or not related to the medicinal (investigational) product. (NCT02124564)
Timeframe: From the Titration Period (investigational product is taken) to the End of Study Visit (up to 3.5 years)

InterventionParticipants (Count of Participants)
Lacosamide (Safety Set)19

[back to top]

Percentage of Participants in the Monotherapy Period Without Discontinuation Due to Adverse Events (AE) or Lack of Efficacy (LOE)

For Time to discontinuation (event), Retention rate and 95% CI was calculated using the Kaplan-Meier method. Retention rate is indicated in Percent and 95% confidence intervals (CI) with respect to the Time to discontinuation. (NCT02124564)
Timeframe: From the beginning of the Monotherapy Period to the end of the Follow-Up Period (up to 3.1 years until the time of approval granted)

InterventionPercentage of participant (Median)
Retention Rate after 6-monthsRetention Rate after 12-monthsRetention Rate after 18-monthsRetention Rate after 24-months
Lacosamide (FAS)81.381.381.381.3

[back to top]

Plasma Concentrations of Lacosamide Versus Time Postdose

Dose-normalized lacosamide Plasma Concentration (µg/mL) by Visit and Dose during the Evaluation Period. (NCT02124564)
Timeframe: From Titration Period up to Week 94

Interventionµg/mL (Mean)
Concentration at First VisitConcentration at Last Visit
Lacosamide (Safety Set)0.0280.034

[back to top]

Number of Subjects Who Withdraw Due to Adverse Events (AEs) During the Study

An Adverse Event (AE) is any untoward medical occurrence in a patient or clinical investigation subject administered a pharmaceutical product, which does not necessarily have a causal relationship with this treatment. An AE could therefore be any unfavorable and unintended sign, symptom, or disease temporally associated with the use of a medicinal (investigational) product, whether or not related to the medicinal (investigational) product. (NCT02124564)
Timeframe: From the Titration Period (investigational product is taken) to the End of Study Visit (up to 3.5 years)

InterventionParticipants (Count of Participants)
Lacosamide (Safety Set)2

[back to top]

Maximum Plasma Concentration (Cmax) for Lacosamide (LCM) (End of Infusion) on Day 1

(NCT02192814)
Timeframe: 20 minutes prior infusion at Day 1

Interventionµg/mL (Geometric Mean)
Lacosamide (LCM)10.838

[back to top]

Maximum Plasma Concentration (Cmax) for Lacosamide (LCM) (End of Infusion) on Day 2

(NCT02192814)
Timeframe: 20 minutes prior infusion at Day 2

Interventionµg/mL (Geometric Mean)
Lacosamide (LCM)10.330

[back to top]

Maximum Plasma Concentration (Cmax) for Lacosamide (LCM) (End of Infusion) on Day 5

(NCT02192814)
Timeframe: 20 minutes prior infusion at Day 5

Interventionµg/mL (Geometric Mean)
Lacosamide (LCM)9.621

[back to top]

Plasma Trough Concentration (Ctrough) for Lacosamide (LCM) on Day 1

(NCT02192814)
Timeframe: 20 minutes prior infusion at Day 1

Interventionµg/mL (Geometric Mean)
Lacosamide (LCM)4.738

[back to top]

Plasma Trough Concentration (Ctrough) for Lacosamide (LCM) on Day 2

(NCT02192814)
Timeframe: 20 minutes prior infusion at Day 2

Interventionµg/mL (Geometric Mean)
Lacosamide (LCM)4.004

[back to top]

Plasma Trough Concentration (Ctrough) for Lacosamide (LCM) on Day 5

(NCT02192814)
Timeframe: 20 minutes prior infusion at Day 5

Interventionµg/mL (Geometric Mean)
Lacosamide (LCM)3.615

[back to top]

The Total Number of Subject Withdrawal Due to Adverse Events During the Study

An Adverse Event (AE) is any untoward medical occurrence in a patient or clinical investigation subject administered a pharmaceutical product that does not necessarily have a causal relationship with this treatment. An AE can therefore be any unfavorable and unintended sign (including an abnormal laboratory finding), symptom, or disease temporally associated with the use of a medicinal (investigational) product, whether or not related to the medicinal (investigational) product. (NCT02192814)
Timeframe: During the study (Screening through End of Study (Day -1 through Day 6))

Interventionparticipants (Number)
Lacosamide (LCM)0

[back to top]

The Total Number of Subjects Experiencing at Least One Adverse Event During the Study

An Adverse Event (AE) is any untoward medical occurrence in a patient or clinical investigation subject administered a pharmaceutical product that does not necessarily have a causal relationship with this treatment. An AE can therefore be any unfavorable and unintended sign (including an abnormal laboratory finding), symptom, or disease temporally associated with the use of a medicinal (investigational) product, whether or not related to the medicinal (investigational) product. (NCT02192814)
Timeframe: During the study (Screening through End of Study (Day -1 through Day 6))

Interventionparticipants (Number)
Lacosamide (LCM)4

[back to top]

Plasma Concentrations of Lacosamide

"Lacosamide plasma concentration was expressed in micrograms per milliliter (μg/mL).~Means and standard deviation (SD) were only calculated if at least 2/3 of the concentrations were quantified at the respective timepoint. Values Below Limit of Quantification (BLQ) were replaced by value of 0 in calculations of means and SDs." (NCT02408523)
Timeframe: During the Treatment Period from Visit 2 (Week 0) to Visit 10 (Week 24)

Interventionug/mL (Mean)
Visit 5, Week 6 (Titration)Visit 10, Week 24 (Maintenance)Early Termination Visit
Lacosamide (SS)8.6109618.0744278.138085

[back to top]

Time to the Second Primary Generalized Tonic Clonic (PGTC) Seizure During the 24-week Treatment Period From Visit 2 (Week 0) to Visit 10 (Week 24)

"The primary efficacy variable was the time to the second primary generalized tonic clonic seizure (PGTCS) during the 24-week Treatment Period. Relative difference between groups (Lacosamide vs Placebo) was expressed as Hazard Ratio.~The indicated measured values are the observed number of events of second PGTCS in the treatment period which form the basis of the statistical analysis of the time to event analysis.~The hazard ratio compares 2 treatment groups for the times to a specified number of events (125) for the combined treatment groups, and so both the number of events and the times until those events pertain to the computation of the hazard ratio.~A Hazard Ratio below 1 indicates time to second PGTCS was improved for LCM compared to Placebo." (NCT02408523)
Timeframe: During the Treatment Period from Visit 2 (Week 0) to Visit 10 (Week 24)

Interventionevents (Number)
Placebo (FAS)76
Lacosamide (FAS)49

[back to top]

Time to the First Primary Generalized Tonic Clonic (PGTC) Seizure During the Treatment Period From Visit 2 (Week 0) to Visit 10 (Week 24)

"The secondary efficacy variable was the time to the first primary generalized tonic clonic seizure (PGTCS) during the 24-week Treatment Period. Relative difference between groups (Lacosamide vs Placebo) was expressed as Hazard Ratio.~The indicated measured values are the observed number of events of first PGTCS in the treatment period which form the basis of the statistical analysis of the time to event analysis.~The hazard ratio compares 2 treatment groups for the times to the number of events for the combined treatment groups, and so both the number of events and the times until those events pertain to the computation of the hazard ratio.~A Hazard Ratio below 1 indicates time to second PGTCS was improved for LCM compared to Placebo." (NCT02408523)
Timeframe: During the Treatment Period from Visit 2 (Week 0) to Visit 10 (Week 24)

Interventionevents (Number)
Placebo (FAS)97
Lacosamide (FAS)79

[back to top]

Percentage of Participants With at Least One Adverse Event (AE) as Reported Spontaneously by the Subject and/or Caregiver or Observed by the Investigator

An AE was any untoward medical occurrence in a patient or clinical investigation study participant administered a pharmaceutical product that did not necessarily have a causal relationship with this treatment. An AE could therefore have been any unfavorable and unintended sign (including an abnormal laboratory finding), symptom, or disease temporally associated with the use of an investigational medicinal product (IMP), whether or not related to the IMP. (NCT02408523)
Timeframe: From Visit 1 (Week -4) to End of Study Period (up to Week 36)

Interventionpercentage of participants (Number)
Placebo (SS)81.8
Lacosamide (SS)82.6

[back to top]

Percentage of Participants With Seizure Freedom for Primary Generalized Tonic Clonic (PGTC) Seizures During the 24-week Treatment Period From Visit 2 (Week 0) to Visit 10 (Week 24)

A seizure-free day from primary generalized tonic clonic seizures (PGTCS) was defined as a day where no PGTCS were reported in the seizure diary and PGTCS were assessed, which was estimated using Kaplan-Meier (KM) methods. (NCT02408523)
Timeframe: During the Treatment Period from Visit 2 (Week 0) to Visit 10 (Week 24)

Interventionpercentage of participants (Number)
Placebo (FAS)17.3
Lacosamide (FAS)31.0

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Serum Chemistry Parameters (Creatinine)

TEMA values are defined in the SAP as significant deviations from the expected range of age-appropriate values. TEMA laboratory results of Creatinine were those that were observed post- BL during the Treatment Period but not present at Baseline. For the age range, '1-<10 years', the abnormality criteria were '>106.8' micromole per litre (umol/L), for '10-<16 years', the abnormality criteria were '>159.12' umol/L and for '>=16 years', the abnormality criteria was '>=176.8' umol/L for serum Creatinine. (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
All Participants (Lacosamide)0

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Serum Chemistry Parameters (Calcium)

TEMA values are defined in the SAP as significant deviations from the expected range of age-appropriate values. TEMA laboratory results of Calcium were those that were observed post- BL during the Treatment Period but not present at Baseline. For the age range, '1 year -<17 years', the abnormality criteria were '<=1.85' millimoles per litre (mmol/L) and '>=2.95' mmol/L. For age range, '>=17 years', the abnormality criteria was '<=1.9 mmol/L' and '>=2.75 mmol/L' of serum Calcium. (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
All Participants (Lacosamide)0

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Serum Chemistry Parameters (Alkaline Phosphatase)

TEMA values are defined in the SAP as significant deviations from the expected range of age-appropriate values. TEMA laboratory results of Alkaline Phosphatase were those that were observed post- BL during the Treatment Period but not present at Baseline. For the age range, '4 years -<10 years', the abnormality criteria was '>=834 U/L', for '10 years -<17 years', the abnormality criteria was '>=1761 U/L' and for '>=17 years', the abnormality criteria was '>=3.0 U/L x ULN' of serum alkaline phosphatase. (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
All Participants (Lacosamide)0

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Serum Chemistry Parameters (Albumin)

TEMA values are defined in the SAP as significant deviations from the expected range of age-appropriate values. TEMA laboratory results of Albumin were those that were observed post- BL during the Treatment Period but not present at Baseline. For the age range, '>=1 year to <17 years', the abnormality criteria were '<24' g/L and '>84' g/L and for age range, '>=17 years', the abnormality criteria was '<26' g/L of serum albumin. (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
All Participants (Lacosamide)0

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Hematology Parameters (Monocytes Absolute )

TEMA values are defined in the SAP as significant deviations from the expected range of age-appropriate values. TEMA laboratory results of Monocytes Absolute were those that are observed post-BL during the Treatment Period but not present at BL. For the age range, '>1 month', the abnormality criteria was '>=2.0' 10^9/L of Monocytes in blood. (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
All Participants (Lacosamide)0

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Hematology Parameters (Leukocytes)

TEMA values are defined in the SAP as significant deviations from the expected range of age-appropriate values. TEMA laboratory results of Leukocytes were those that were observed post-BL during the Treatment Period but not present at BL. For all age ranges, the abnormality criteria were '<=3.0' 10^9/L (Low) and '>= 16.0' 10^9/L (High) of Leukocytes values in blood. (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
All Participants (Lacosamide)0.5

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Hematology Parameters (Erythrocytes)

TEMA values are defined in the SAP as significant deviations from the expected range of age-appropriate values. TEMA laboratory results of Erythrocytes parameter were those that were observed post-BL during the Treatment Period but not present at BL. For the age range, '>=2years', the abnormality criteria were '<3.5' 10^12/L of Erythrocytes value in blood. Early Termination Visit (TV) was last visit in the study (up to approximately 5 years). (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
All Participants (Lacosamide)1.7

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Hematology Parameters (Basophils Absolute)

TEMA values are defined in the SAP as significant deviations from the expected range of age-appropriate values. TEMA laboratory results of Basophils Absolute were those that were observed post-BL during the Treatment Period but not present at BL. For the age range, '>1 month', the abnormality criteria were '>=0.4' 10^9/L of Basophils in blood. (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
All Participants (Lacosamide)0.4

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Chemistry Parameters (Total Bilirubin)

TEMA values are defined in the SAP as significant deviations from the expected range of age-appropriate values. TEMA laboratory results of Total Bilirubin were those that were observed post- BL during the Treatment Period but not present at Baseline. For the age range, '>1 month', the abnormality criteria was '≥34.208' umol/L of serum Bilirubin. (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
All Participants (Lacosamide)0.5

[back to top]

Percentage of Study Participants With at Least 50% Worsening in Days With Myoclonic Seizures

Seizure worsening was defined as a participant experiencing >=50% increase in the number of days with myoclonic seizures per 28 days from Prospective Baseline. Percentages for seizure worsening were based on those participants who have reported a history of or an occurrence of myoclonic seizures in Prospective Baseline or the Treatment Period. (NCT02408549)
Timeframe: From Visit 1 (Week 0) to End of Treatment Period (up to approximately 5 years)

Interventionpercentage of participants (Number)
All Participants (Lacosamide)3.2

[back to top]

Percentage of Study Participants With at Least 50% Worsening in Days With Absence Seizures

Seizure worsening was defined as a participant experiencing >=50% increase in the number of days with absence seizures per 28 days from Prospective Baseline. Percentages for seizure worsening were based on those participants who have reported a history of or an occurrence of absence seizures in Prospective Baseline or the Treatment Period. (NCT02408549)
Timeframe: From Visit 1 (Week 0) to End of Treatment Period (up to approximately 5 years)

Interventionpercentage of participants (Number)
All Participants (Lacosamide)0

[back to top]

Percent Change in Primary Generalized Tonic-clonic Seizure (PGTCS) Frequency Per 28 Days From Combined Baseline

The 28-day PGTCS frequency during the relative period was subtracted from the 28-day Combined Baseline PGTCS frequency and the result was divided by 28-day Combined Baseline PGTCS frequency and the result was then multiplied by 100 to get percent change in PGTCS frequency per 28 days from Combined Baseline Period (CB) to the appropriate analysis Period. The CB was defined as the combined 12-week Historical Baseline and 4-week Prospective Baseline periods immediately prior to randomization in the study SP0982 or prior to Visit 1 (first dose) if direct enrollers in EP0012. (NCT02408549)
Timeframe: From Combined Baseline until end of Treatment Period (up to approximately 5 years)

Interventionpercent change (Median)
All Participants (Lacosamide)-88.58

[back to top]

Number of Study Participants Withdrawn Due to TEAEs

AEs were considered treatment-emergent if event had onset on or after date of first study medication dose in EP0012 and within 30 days following last study medication dose or events whose intensity worsened on or after date of first study medication dose and within 30 days following date of last study medication administration. Adverse Events were reported spontaneously by the participant and/or caregiver or observed by the investigator. (NCT02408549)
Timeframe: From Visit 1 (Week 0) to End of Treatment Period (up to approximately 5 years)

InterventionParticipants (Count of Participants)
All Participants (Lacosamide)19

[back to top]

Number of Study Participants With Treatment-emergent Adverse Events (TEAEs) Over the Duration of the Treatment Period

AEs were considered treatment-emergent if event had onset on or after date of first study medication dose in EP0012 and within 30 days following last study medication dose or events whose intensity worsened on or after date of first study medication dose and within 30 days following date of last study medication administration. Adverse Events were reported spontaneously by the participant and/or caregiver or observed by the investigator. (NCT02408549)
Timeframe: From Visit 1 (Week 0) to End of Treatment Period (up to approximately 5 years)

InterventionParticipants (Count of Participants)
All Participants (Lacosamide)222

[back to top]

Number of Study Participants With an Increase of up to 25% in Days With Myoclonic Seizures Per 28 Days During the Treatment Period as Compared to the Prospective Baseline (of Study SP0982)

The number of participants experiencing an increase of up to 25% in the number of days with myoclonic seizures per 28 days during the Treatment Period compared to the Prospective Baseline Period (for those participants with myoclonic seizure data reported in the 4-week Prospective Baseline Period in SP0982) were reported. This period started on the day of Visit 1 of SP0982 and ended the day before Visit 2 of SP0982. For the direct enrollers into EP0012, Prospective Baseline ended the day before Visit 1 (or prior to first dose) of EP0012. (NCT02408549)
Timeframe: From Visit 1 (Week 0) to End of Treatment Period (up to approximately 5 years), compared to the Prospective SP0982 Baseline Period

InterventionParticipants (Count of Participants)
All Participants (Lacosamide)4

[back to top]

Number of Study Participants With an Increase of up to 25% in Days With Absence Seizures Per 28 Days During the Treatment Period as Compared to the Prospective Baseline (of Study SP0982)

The number of participants experiencing an increase of up to 25% in the number of days with absence seizures per 28 days during the Treatment Period compared to the Prospective Baseline Period (for those participants with absence seizure data reported in the 4-week Prospective Baseline Period in SP0982) were reported. This period started on the day of Visit 1 of SP0982 and ended the day before Visit 2 of SP0982. For the direct enrollers into EP0012, Prospective Baseline ended the day before Visit 1 (or prior to first dose) of EP0012. (NCT02408549)
Timeframe: From Visit 1 (Week 0) to End of Treatment Period (up to approximately 5 years), compared to the Prospective SP0982 Baseline Period

InterventionParticipants (Count of Participants)
All Participants (Lacosamide)5

[back to top]

Number of Study Participants With an Increase of Greater Than (>)25% to 50% in Days With Absence Seizures Per 28 Days During the Treatment Period as Compared to the Prospective Baseline (of Study SP0982)

The number of participants experiencing an increase of >25% to 50% in the number of days with absence seizures per 28 days during the Treatment Period compared to the Prospective Baseline Period (for those participants with absence seizure data reported in the 4-week Prospective Baseline Period in SP0982) were reported. This period started on the day of Visit 1 of SP0982 and ended the day before Visit 2 of SP0982. For the direct enrollers into EP0012, Prospective Baseline ended the day before Visit 1 (or prior to first dose) of EP0012. (NCT02408549)
Timeframe: From Visit 1 (Week 0) to End of Treatment Period (up to approximately 5 years), compared to the Prospective SP0982 Baseline Period

InterventionParticipants (Count of Participants)
All Participants (Lacosamide)1

[back to top]

Number of Study Participants With an Increase of >75% in Days With Myoclonic Seizures Per 28 Days During the Treatment Period as Compared to the Prospective Baseline (of Study SP0982)

The number of participants experiencing an increase of >75% in the number of days with myoclonic seizures per 28 days during the Treatment Period compared to the Prospective Baseline Period (for those participants with myoclonic seizure data reported in the 4-week Prospective Baseline Period in SP0982) were reported. This period started on the day of Visit 1 of SP0982 and ended the day before Visit 2 of SP0982. For the direct enrollers into EP0012, Prospective Baseline ended the day before Visit 1 (or prior to first dose) of EP0012. (NCT02408549)
Timeframe: From Visit 1 (Week 0) to End of Treatment Period (up to approximately 5 years), compared to the Prospective SP0982 Baseline Period

InterventionParticipants (Count of Participants)
All Participants (Lacosamide)2

[back to top]

Number of Study Participants With an Increase of >75% in Days With Absence Seizures Per 28 Days During the Treatment Period as Compared to the Prospective Baseline (of Study SP0982)

The number of participants experiencing an increase of >75% in the number of days with absence seizures per 28 days during the Treatment Period compared to the Prospective Baseline Period (for those participants with absence seizure data reported in the 4-week Prospective Baseline Period in SP0982) were reported. This period started on the day of Visit 1 of SP0982 and ended the day before Visit 2 of SP0982. For the direct enrollers into EP0012, Prospective Baseline ended the day before Visit 1 (or prior to first dose) of EP0012. (NCT02408549)
Timeframe: From Visit 1 (Week 0) to End of Treatment Period (up to approximately 5 years), compared to the Prospective SP0982 Baseline Period

InterventionParticipants (Count of Participants)
All Participants (Lacosamide)0

[back to top]

Number of Study Participants With an Increase of >50% to 75% in Days With Myoclonic Seizures Per 28 Days During the Treatment Period as Compared to the Prospective Baseline (of Study SP0982)

The number of participants experiencing an increase of >50% to 75% in the number of days with myoclonic seizures per 28 days during the Treatment Period compared to the Prospective Baseline Period (for those participants with myoclonic seizure data reported in the 4-week Prospective Baseline Period in SP0982) were reported. This period started on the day of Visit 1 of SP0982 and ended the day before Visit 2 of SP0982. For the direct enrollers into EP0012, Prospective Baseline ended the day before Visit 1 (or prior to first dose) of EP0012. (NCT02408549)
Timeframe: From Visit 1 (Week 0) to End of Treatment Period (up to approximately 5 years), compared to the Prospective SP0982 Baseline Period

InterventionParticipants (Count of Participants)
All Participants (Lacosamide)1

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Serum Chemistry Parameters (Potassium)

TEMA values are defined in the SAP as significant deviations from the expected range of age-appropriate values. TEMA laboratory results of Potassium were those that were observed post- BL during the Treatment Period but not present at Baseline. For the age range, '>=1 year', the abnormality criteria were '<= 3.0' mmol/L (Low) and '>= 6.0' mmol/L (High) of serum Potassium. (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
All Participants (Lacosamide)0.4

[back to top]

Number of Study Participants With an Increase of >50% to 75% in Days With Absence Seizures Per 28 Days During the Treatment Period as Compared to the Prospective Baseline (of Study SP0982)

The number of participants experiencing an increase of >50% to 75% in the number of days with absence seizures per 28 days during the Treatment Period compared to the Prospective Baseline Period (for those participants with absence seizure data reported in the 4-week Prospective Baseline Period in SP0982) were reported. This period started on the day of Visit 1 of SP0982 and ended the day before Visit 2 of SP0982. For the direct enrollers into EP0012, Prospective Baseline ended the day before Visit 1 (or prior to first dose) of EP0012. (NCT02408549)
Timeframe: From Visit 1 (Week 0) to End of Treatment Period (up to approximately 5 years), compared to the Prospective SP0982 Baseline Period

InterventionParticipants (Count of Participants)
All Participants (Lacosamide)0

[back to top]

Number of Study Participants With an Increase of >25% to 50% in Days With Myoclonic Seizures Per 28 Days During the Treatment Period as Compared to the Prospective Baseline (of Study SP0982)

The number of participants experiencing an increase of >25% to 50% in the number of days with myoclonic seizures per 28 days during the Treatment Period compared to the Prospective Baseline Period (for those participants with myoclonic seizure data reported in the 4-week Prospective Baseline Period in SP0982) were reported. This period started on the day of Visit 1 of SP0982 and ended the day before Visit 2 of SP0982. For the direct enrollers into EP0012, Prospective Baseline ended the day before Visit 1 (or prior to first dose) of EP0012. (NCT02408549)
Timeframe: From Visit 1 (Week 0) to End of Treatment Period (up to approximately 5 years), compared to the Prospective SP0982 Baseline Period

InterventionParticipants (Count of Participants)
All Participants (Lacosamide)1

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Hematology Parameters (Platelets)

TEMA values are defined in the SAP as significant deviations from the expected range of age-appropriate values. TEMA laboratory results of Platelet count were those that were observed post-BL during the Treatment Period but not present at BL. For the age range of '>1 month', the abnormality criteria were '<=100' 10^9/L and '>=600' 10^9/L of Platelets count value. (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
All Participants (Lacosamide)0

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Serum Chemistry Parameters (Chloride)

TEMA values are defined in the SAP as significant deviations from the expected range of age-appropriate values. TEMA laboratory results of Chloride were those that were observed post- BL during the Treatment Period but not present at Baseline. For the age range, '>1 month', the abnormality criteria were '<=90' mmol/L (Low) and '>=112' mmol/L (High) of serum Chloride. (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
High: Wk 2 (>1 m)High: Wk 22 (>1 m)High: Wk 46 (>1 m)High: Wk 62 (>1 m)High: Wk 78 (>1 m)High: Wk 94 (>1 m)High: Wk 118 (>1 m)High: Wk 214 (>1 m)High: TV (>1 m)
All Participants (Lacosamide)1.32.32.51.53.11.23.42.31.4

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Vital Sign Measurements (Systolic Blood Pressure)

TEMA values of Systolic Blood Pressure (BP) results were those that were observed post- BL during the Treatment Period but not present at Baseline. For the age range, '3 years -<12 years', the abnormality criteria were '<80 millimeters of mercury (mmHg)' (Low) and '>140 mmHg' (High). For the age range, '>=12 years - <17 years', the abnormality criteria were '<90 mmHg' (Low) and '>160 mmHg' (High). For the age range, '>=17 years', the abnormality criteria were '<=90 mmHg and decrease from Baseline of >=20 mmHg' (Low A), '>=180 mmHg and increase from Baseline of >=20' mmHg (High A), '<90 mmHg' (Low B), '>140 mmHg (High B), and '>160 mmHg' (High C). Systolic BP were reported as per positions such as 'Sup 3 min', 'Std 1 min, and 'Std 3 min'. (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
High B: Wk 2 (>=17 y)- Sup 3 minLow B: Wk 2 (>=17 y)- Std 1 minHigh B: Wk 2 (>=17 y)- Std 1 minHigh B: Wk 2 (>=17 y)- Std 3 minHigh B: Wk 6 (>=17 y)- Sup 3 minHigh B: Wk 6 (>=17 y)- Std 1 minLow B: Wk 6 (>=17 y)- Std 3 minHigh B: Wk 6 (>=17 y)- Std 3 minLow B: Wk 14 (>=17 y)- Sup 3 minHigh B: Wk 14 (>=17 y)- Sup 3 minHigh B: Wk 14 (>=17 y)- Std 1 minHigh B: Wk 14 (>=17 y)- Std 3 minHigh B: Wk 22 (>=17 y)- Sup 3 minHigh B: Wk 22 (>=17 y)- Std 1 minHigh B: Wk 22 (>=17 y)- Std 3 minLow B: Wk 30 (>=17 y)- Sup 3 minHigh B: Wk 30 (>=17 y)- Sup 3 minHigh B: Wk 30 (>=17 y)- Std 1 minHigh B: Wk 30 (>=17 y)- Std 3 minLow B: Wk 38 (>=17 y)- Sup 3 minHigh B: Wk 38 (>=17 y)- Sup 3 minLow B: Wk 38 (>=17 y)- Std 1 minHigh B: Wk 38 (>=17 y)- Std 1 minHigh B: Wk 38 (>=17 y)- Std 3 minLow: Wk 46 (>=12 y-<17 y)- Sup 3 minHigh B: Wk 46 (>=17 y)- Sup 3 minLow: Wk 46 (>=12 y-<17 y)- Std 1 minHigh B: Wk 46 (>=17 y)- Std 1 minLow: Wk 46 (>=12 y-<17 y)- Std 3 minHigh B: Wk 46 (>=17 y)- Std 3 minHigh C: Wk 46 (>=17 y)- Std 3 minLow B: Wk 62 (>=17 y)- Sup 3 minHigh B: Wk 62 (>=17 y)- Sup 3 minLow: Wk 62 (>=12 y-<17 y)- Std 1 minLow A: Wk 62 (>=17 y)- Std 1 minLow B: Wk 62 (>=17 y)- Std 1 minHigh B: Wk 62 (>=17 y)- Std 1 minLow A: Wk 62 (>=17 y)- Std 3 minLow B: Wk 62 (>=17 y)- Std 3 minHigh B: Wk 62 (>=17 y)- Std 3 minLow A: Wk 78 (>=17 y)- Sup 3 minHigh B: Wk 78 (>=17 y)- Sup 3 minHigh B: Wk 78 (>=17 y)- Std 1 minHigh B: Wk 78 (>=17 y)- Std 3 minHigh B: Wk 94 (>=17 y)- Sup 3 minHigh B: Wk 94 (>=17 y)- Std 1 minHigh B: Wk 94 (>=17 y)- Std 3 minHigh B: Wk 118 (>=17 y)- Sup 3 minHigh C: Wk 118 (>=17 y)- Sup 3 minHigh B: Wk 118 (>=17 y)- Std 1 minHigh C: Wk 118 (>=17 y)- Std 1 minHigh B: Wk 118 (>=17 y)- Std 3 minHigh C: Wk 118 (>=17 y)- Std 3 minHigh B: Wk 142 (>=17 y)- Sup 3 minHigh B: Wk 142 (>=17 y)- Std 1 minHigh B: Wk 142 (>=17 y)- Std 3 minHigh B: Wk 166 (>=17 y)- Sup 3 minHigh B: Wk 166 (>=17 y)- Std 1 minHigh B: Wk 166 (>=17 y)- Std 3 minHigh B: Wk 190 (>=17 y)- Sup 3 minHigh B: Wk 214 (>=17 y)- Std 1 minHigh C: Wk 214 (>=17 y)- Std 1 minHigh B: Wk 214 (>=17 y)- Std 3 minHigh B: Wk 262 (>=17 y)- Std 3 minHigh B: Early TV (>=17 y)- Sup 3 minHigh B: Early TV (>=17 y)- Std 1 minHigh B: TV (>=17 y)- Std 1 minHigh B: TV (>=17 y)- Std 3 min
All Participants (Lacosamide)3.51.02.53.63.12.00.53.60.53.13.63.64.24.23.70.85.92.55.00.92.80.92.83.76.32.96.32.36.33.40.60.63.56.30.60.62.30.61.71.21.71.71.71.74.14.14.15.41.15.51.16.61.16.36.36.33.87.87.82.95.95.95.91001.81.84.02.0

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Vital Sign Measurements (Pulse Rate)

TEMA values are defined in the SAP as significant deviations from the expected range of age-appropriate values. TEMA vital signs results of Pulse rate were those that were observed post- BL during the Treatment Period but not present at Baseline. For the age range, '3 years -<12 years', the abnormality criteria were '<60 bpm' (Low) and '>130 bpm' (High). For the age range, '12 years - <17 years', the abnormality criteria were '<=50 bpm' (Low) and '>=120 bpm' (High). For the age range, '>=17 years', the abnormality criteria were '<=50 bpm and a decrease from Baseline of >=15 bpm' (Low A), '>=120 bpm and an increase from Baseline of >=15 bpm' (High A), '<60 bpm' (Low B) and '>100 bpm' (High B). The Pulse rate was reported as per positions such as 'Supine 3 minute (Sup 3 min)', 'Standing 1 minute' (Std 1 min), and 'Standing 3 minute' (Std 3 min). (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
Low B: Wk 2 (>=17 y)-Sup 3 minHigh B: Wk 2 (>=17 y)- Sup 3 minHigh: Wk 2 (>=12 y-<17 y)-Std 1 minLow B: Wk 2 (>=17 y)-Std 1 minHigh B: Wk 2 (>=17 y)-Std 1 minLow B: Wk 2 (>=17 y)-Std 3 minHigh B: Wk 2 (>=17 y)-Std 3 minLow A: Wk 6 (>=17 y)-Sup 3 minLow B: Wk 6 (>=17 y)-Sup 3 minHigh B: Wk 6 (>=17 y)-Sup 3 minHigh: Wk 6 (>=12 y-<17 y)- Std 1 minLow B: Wk 6 (>=17 y)- Std 1 minHigh B: Wk 6 (>=17 y)- Std 1 minLow A: Wk 6 (>=17 y)- Std 3 minLow B: Wk 6 (>=17 y)- Std 3 minHigh B: Wk 6 (>=17 y)- Std 3 minLow B: Wk 14 (>=17 y)- Sup 3 minHigh B: Wk 14 (>=17 y)- Sup 3 minHigh: Wk 14 (>=12 y-<17 y)- Std 1 minLow B: Wk 14 (>=17 y)- Std 1 minHigh B: Wk 14 (>=17 y)- Std 1 minLow B: Wk 14 (>=17 y)- Std 3 minHigh B: Wk 14 (>=17 y)- Std 3 minLow B: Wk 22 (>=17 y)- Sup 3 minHigh B: Wk 22 (>=17 y)- Sup 3 minHigh A: Wk 22 (>=17 y)- Std 1 minLow B: Wk 22 (>=17 y)- Std 1 minHigh B: Wk 22 (>=17 y)- Std 1 minLow B: Wk 22 (>=17 y)- Std 3 minHigh B: Wk 22 (>=17 y)- Std 3 minLow B: Wk 30 (>=17 y)- Sup 3 minLow B: Wk 30 (>=17 y)- Std 1 minHigh B: Wk 30 (>=17 y)- Std 1 minLow B: Wk 30 (>=17 y)- Std 3 minHigh B: Wk 30 (>=17 y)- Std 3 minLow B: Wk 38 (>=17 y)- Sup 3 minLow B: Wk 38 (>=17 y)- Std 1 minHigh B: Wk 38 (>=17 y)- Std 1 minLow B: Wk 38 (>=17 y)- Std 3 minHigh B: Wk 38 (>=17 y)- Std 3 minLow B: Wk 46 (>=17 y)- Sup 3 minHigh B: Wk 46 (>=17 y)- Sup 3 minLow A: Wk 46 (>=17 y)- Std 1 minHigh A: Wk 46 (>=17 y)- Std 1 minLow B: Wk 46 (>=17 y)- Std 1 minHigh B: Wk 46 (>=17 y)- Std 1 minLow B: Wk 46 (>=17 y)- Std 3 minHigh B: Wk 46 (>=17 y)- Std 3 minLow B: Wk 62 (>=17 y)- Sup 3 minHigh B: Wk 62 (>=17 y)- Sup 3 minLow: Wk 62 (>=12 y-<17 y)- Std 1 minHigh A: Wk 62 (>=17 y)- Std 1 minLow B: Wk 62 (>=17 y)- Std 1 minHigh B: Wk 62 (>=17 y)- Std 1 minHigh A: Wk 62 (>=17 y)- Std 3 minLow B: Wk 62 (>=17 y)- Std 3 minHigh B: Wk 62 (>=17 y)- Std 3 minLow B: Wk 78 (>=17 y)- Sup 3 minHigh B: Wk 78 (>=17 y)- Sup 3 minLow B: Wk 78 (>=17 y)- Std 1 minHigh B: Wk 78 (>=17 y)- Std 1 minLow B: Wk 78 (>=17 y)- Std 3 minHigh B: Wk 78 (>=17 y)- Std 3 minLow B: Wk 94 (>=17 y)- Sup 3 minHigh B: Wk 94 (>=17 y)- Sup 3 minLow B: Wk 94 (>=17 y)- Std 1 minHigh B: Wk 94 (>=17 y)- Std 1 minLow B: Wk 94 (>=17 y)- Std 3 minHigh B: Wk 94 (>=17 y)- Std 3 minLow B: Wk 118 (>=17 y)- Sup 3 minHigh B: Wk 118 (>=17 y)- Sup 3 minLow B: Wk 118 (>=17 y)- Std 1 minHigh B: Wk 118 (>=17 y)- Std 1 minLow B: Wk 118 (>=17 y)- Std 3 minHigh B: Wk 118 (>=17 y)- Std 3 minHigh A: Wk 142 (>=17 y)- Sup 3 minLow B: Wk 142 (>=17 y)- Sup 3 minHigh B: Wk 142 (>=17 y)- Sup 3 minHigh A: Wk 142 (>=17 y)- Std 1 minHigh B: Wk 142 (>=17 y)- Std 1 minHigh A: Wk 142 (>=17 y)- Std 3 minLow B: Wk 142 (>=17 y)- Std 3 minHigh B: Wk 142 (>=17 y)- Std 3 minLow B: Wk 166 (>=17 y)- Sup 3 minHigh B: Wk 166 (>=17 y)- Sup 3 minLow B: Wk 166 (>=17 y)- Std 1 minHigh B: Wk 166 (>=17 y)- Std 1 minHigh B: Wk 166 (>=17 y)- Std 3 minLow B: Wk 190 (>=17 y)- Sup 3 minHigh B: Wk 190 (>=17 y)- Sup 3 minHigh B: Wk 190 (>=17 y)- Std 1 minHigh B: Wk 190 (>=17 y)- Std 3 minHigh B: Wk 214 (>=17 y)- Sup 3 minHigh B: Wk 214 (>=17 y)- Std 1 minHigh B: Wk 214 (>=17 y)- Std 3 minLow B: Early TV (>=17 y)- Sup 3 minHigh B: Early TV (>=17 y)- Sup 3 minHigh: Early TV (>=12 y-<17 y)- Std 1 minLow B: Early TV (>=17 y)- Std 1 minHigh B: Early TV (>=17 y)- Std 1 minLow A: TV (>=17 years)- Sup 3 minLow B: TV (>=17 years)- Sup 3 minHigh B: TV (>=17 years)- Sup 3 minLow B: TV (>=17 years)- Std 1 minHigh B: TV (>=17 years)- Std 1 minLow B: TV (>=17 years)- Std 3 minHigh B: TV (>=17 years)- Std 3 min
All Participants (Lacosamide)4.50.55.02.53.01.52.60.54.62.04.81.53.10.51.02.64.11.05.63.12.60.54.13.20.50.51.64.22.13.71.75.03.42.51.73.72.85.60.92.85.71.70.61.14.05.22.94.65.22.36.30.64.64.00.62.32.96.71.76.76.76.75.06.10.72.74.11.42.72.22.22.23.32.24.41.66.34.83.27.91.63.27.93.81.92.05.95.92.98.811.817.65.95.95.93.61.833.33.65.52.04.02.02.04.02.02.0

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Vital Sign Measurements (Diastolic Blood Pressure)

TEMA values of Diastolic BP results were those that are observed post- BL during the Treatment Period but not present at Baseline. For the age range, '3 years -<12 years', the abnormality criteria were '<50 mmHg' (Low) and '>80 mmHg' (High), '>=12 years - <17 years', the abnormality criteria were '<=50 mmHg' (Low) and '>=105 mmHg' (High), and '>=17 years', the abnormality criteria were '<=50 mmHg and decrease from Baseline of >=15 mmHg' (Low A), '>=105 mmHg and increase from Baseline of >=15' mmHg (High A), '<50 mmHg' (Low B), '>90 mmHg' (High B), and '>100 mmHg' (High C). Diastolic BP were reported as per positions such as 'Sup 3 min', 'Std 1 min, and 'Std 3 min'. (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
Low: Wk 2 (3 y-<12 y)- Sup 3 minLow B: Wk 2 (>=17 y)- Sup 3 minHigh B: Wk 2 (>=17 y)- Sup 3 minLow: Wk 2 (3 y-<12 y)- Std 1 minHigh: Wk 2 (3 y-<12 y)- Std 1 minHigh B: Wk 2 (>=17 y)- Std 1 minHigh C: Wk 2 (>=17 y)- Std 1 minLow: Wk 2 (3 y-<12 y)- Std 3 minHigh: Wk 2 (3 y-<12 y)- Std 3 minHigh B: Wk 2 (>=17 y)- Std 3 minHigh C: Wk 2 (>=17 y)- Std 3 minLow A: Wk 6 (>=17 y)- Sup 3 minHigh B: Wk 6 (>=17 y)- Sup 3 minHigh C: Wk 6 (>=17 y)- Sup 3 minLow A: Wk 6 (>=17 y)- Std 1 minHigh A: Wk 6 (>=17 y)- Std 1 minHigh B: Wk 6 (>=17 y)- Std 1 minHigh C: Wk 6 (>=17 y)- Std 1 minHigh: Wk 6 (3 y-<12 y)- Std 3 minLow A: Wk 6 (>=17 y)- Std 3 minLow B: Wk 6 (>=17 y)- Std 3 minHigh B: Wk 6 (>=17 y)- Std 3 minHigh C: Wk 6 (>=17 y)- Std 3 minHigh: Wk 14 (3 y-<12 y)- Sup 3 minHigh B: Wk 14 (>=17 y)- Sup 3 minHigh C: Wk 14 (>=17 y)- Sup 3 minHigh A: Wk 14 (>=17 y)- Std 1 minHigh B: Wk 14 (>=17 y)- Std 1 minHigh C: Wk 14 (>=17 y)- Std 1 minHigh: Wk 14 (3 y-<12 y)- Std 3 minHigh B: Wk 14 (>=17 y)- Std 3 minHigh C: Wk 14 (>=17 y)- Std 3 minHigh: Wk 22 (3 y-<12 y)- Sup 3 minLow: Wk 22 (>=12 y-<17 y)- Sup 3 minHigh B: Wk 22 (>=17 y)- Sup 3 minHigh C: Wk 22 (>=17 y)- Sup 3 minHigh: Wk 22 (3 y-<12 y)- Std 1 minLow A: Wk 22 (>=17 y)- Std 1 minLow B: Wk 22 (>=17 y)- Std 1 minHigh B: Wk 22 (>=17 y)- Std 1 minHigh C: Wk 22 (>=17 y)- Std 1 minHigh: Wk 22 (3 y-<12 y)- Std 3 minLow A: Wk 22 (>=17 y)- Std 3 minHigh B: Wk 22 (>=17 y)- Std 3 minHigh C: Wk 22 (>=17 y)- Std 3 minHigh B: Wk 30 (>=17 y)- Sup 3 minHigh C: Wk 30 (>=17 y)- Sup 3 minHigh: Wk 30 (3 y-<12 y)- Std 1 minHigh A: Wk 30 (>=17 y)- Std 1 minHigh B: Wk 30 (>=17 y)- Std 1 minHigh C: Wk 30 (>=17 y)- Std 1 minHigh B: Wk 30 (>=17 y)- Std 3 minHigh B: Wk 38 (>=17 y)- Sup 3 minHigh: Wk 38 (3 y-<12 y)- Std 1 minHigh B: Wk 38 (>=17 y)- Std 1 minHigh C: Wk 38 (>=17 y)- Std 1 minHigh B: Wk 38 (>=17 y)- Std 3 minLow A: Wk 46 (>=17 y)- Sup 3 minHigh B: Wk 46 (>=17 y)- Sup 3 minLow: Wk 46 (>=12 y-<17 y)- Std 1 minHigh B: Wk 46 (>=17 y)- Std 1 minHigh C: Wk 46 (>=17 y)- Std 1 minHigh B: Wk 46 (>=17 y)- Std 3 minHigh C: Wk 46 (>=17 y)- Std 3 minHigh A: Wk 62 (>=17 y)- Sup 3 minHigh B: Wk 62 (>=17 y)- Sup 3 minHigh C: Wk 62 (>=17 y)- Sup 3 minHigh: Wk 62 (3 y-<12 y)- Std 1 minLow: Wk 62 (>=12 y-<17 y)- Std 1 minHigh A: Wk 62 (>=17 y)- Std 1 minHigh B: Wk 62 (>=17 y)- Std 1 minHigh C: Wk 62 (>=17 y)- Std 1 minLow B: Wk 62 (>=17 y)- Std 3 minHigh B: Wk 62 (>=17 y)- Std 3 minHigh C: Wk 62 (>=17 y)- Std 3 minLow: Wk 78 (>=12 y-<17 y)- Sup 3 minHigh B: Wk 78 (>=17 y)- Sup 3 minHigh B: Wk 78 (>=17 y)- Std 1 minHigh B: Wk 78 (>=17 y)- Std 3 minHigh C: Wk 78 (>=17 y)- Std 3 minHigh B: Wk 94 (>=17 y)- Sup 3 minHigh B: Wk 94 (>=17 y)- Std 1 minHigh: Wk 94 (3 y-<12 y)- Std 3 minHigh A: Wk 94 (>=17 y)- Std 3 minHigh B: Wk 94 (>=17 y)- Std 3 minHigh C: Wk 94 (>=17 y)- Std 3 minLow A: Wk 118 (>=17 y)- Sup 3 minHigh A: Wk 118 (>=17 y)- Sup 3 minLow B: Wk 118 (>=17 y)- Sup 3 minHigh B: Wk 118 (>=17 y)- Sup 3 minHigh C: Wk 118 (>=17 y)- Sup 3 minLow A: Wk 118 (>=17 y)- Std 1 minLow B: Wk 118 (>=17 y)- Std 1 minHigh B: Wk 118 (>=17 y)- Std 1 minHigh B: Wk 118 (>=17 y)- Std 3 minHigh B: Wk 142 (>=17 y)- Sup 3 minHigh B: Wk 142 (>=17 y)- Std 1 minHigh B: Wk 142 (>=17 y)- Std 3 minHigh B: Wk 166 (>=17 y)- Sup 3 minHigh B: Wk 166 (>=17 y)- Std 1 minHigh A: Wk 166 (>=17 y)- Std 3 minHigh B: Wk 166 (>=17 y)- Std 3 minHigh C: Wk 166 (>=17 y)- Std 3 minHigh B: Wk 190 (>=17 y)- Std 3 minHigh B: Wk 214 (>=17 y)- Sup 3 minHigh A: Wk 214 (>=17 y)- Std 1 minHigh B: Wk 214 (>=17 y)- Std 1 minHigh C: Wk 214 (>=17 y)- Std 1 minHigh A: Wk 214 (>=17 y)- Std 3 minHigh B: Wk 214 (>=17 y)- Std 3 minHigh C: Wk 214 (>=17 y)- Std 3 minHigh B: Early TV (>=17 y)- Sup 3 minHigh C: Early TV (>=17 y)- Sup 3 minHigh B: Early TV (>=17 y)- Std 1 minHigh C: Early TV (>=17 y)- Std 1 minHigh A: Early TV (>=17 y)- Std 3 minHigh B: Early TV (>=17 y)- Std 3 minHigh C: Early TV (>=17 y)- Std 3 minHigh: TV (3 y-<12 y)- Sup 3 minHigh B: TV (>=17 y)- Sup 3 minHigh B: TV (>=17 y)- Std 1 minHigh B: TV (>=17 y)- Std 3 minHigh C: TV (>=17 y)- Std 3 min
All Participants (Lacosamide)6.30.52.56.36.35.10.56.312.56.10.50.54.60.50.50.54.10.57.10.50.56.60.57.72.00.50.53.11.08.34.60.515.46.31.60.515.41.10.57.90.57.70.56.31.13.40.814.30.85.90.84.22.820.05.60.99.30.64.06.38.00.69.81.10.65.21.220.06.30.65.81.20.65.80.616.71.73.33.31.71.44.114.30.74.70.71.11.11.12.21.11.11.14.47.76.37.97.93.85.92.011.82.02.95.95.95.95.95.95.95.93.61.89.11.81.810.93.616.74.02.04.02.0

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Vital Sign Measurements (Body Weight)

TEMA values are defined in the SAP as significant deviations from the expected range of age-appropriate values. TEMA vital signs parameter results were those that are observed post- BL during the Treatment Period but not present at Baseline. For the age range, '1 month - <17 years', the abnormality criteria were '<3% of normal body weight' in Kilograms (kg) or '>97% of normal body weight' in kgs. Here, '<3% of normal' is presented as 'Low' and '>97% of normal' is presented as 'High'. For the age range '>=17 years', the abnormality criteria were 'Increase/decrease of >=10%' body weight in kgs (presented as Inc/Dec A) or 'Increase/decrease of >=7%' body weight in kgs (presented as Inc/Dec B). (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
High- Wk 14 (1 m - <17 y)Inc/Dec A- Wk 14 (>=17 y)Inc/Dec B- Wk 14 (>=17 y)High- Wk 30 (1 m - <17 y)Inc/Dec A- Wk 30 (>=17 y)Inc/Dec B- Wk 30 (>=17 y)High- Wk 46 (1 m - <17 y)Inc/Dec A- Wk 46 (>=17 y)Inc/Dec B- Wk 46 (>=17 y)High- Wk 62 (1 m - <17 y)Inc/Dec A- Wk 62 (>=17 y)Inc/Dec B- Wk 62 (>=17 y)Inc/Dec A- Wk 78 (>=17 y)Inc/Dec B- Wk 78 (>=17 y)High- Wk 94 (1 m - <17 y)Inc/Dec A- Wk 94 (>=17 y)Inc/Dec B- Wk 94 (>=17 y)Low- Wk 118 (1 m - <17 y)High- Wk 118 (1 m - <17 y)Inc/Dec A- Wk 118 (>=17 y)Inc/Dec B- Wk 118 (>=17 y)Low- Wk 142 (1 m - <17 y)High- Wk 142 (1 m - <17 y)Inc/Dec A- Wk 142 (>=17 y)Inc/Dec B- Wk 142 (>=17 y)High- Wk 166 (1 m - <17 y)Inc/Dec A- Wk 166 (>=17 y)Inc/Dec B- Wk 166 (>=17 y)Low- Wk 190 (1 m - <17 y)Inc/Dec A- Wk 190 (>=17 y)Inc/Dec B- Wk 190 (>=17 y)Low- Wk 214 (1 m - <17 y)Inc/Dec A- Wk 214 (>=17 y)Inc/Dec B- Wk 214 (>=17 y)Inc/Dec A- Wk 238 (>=17 y)Inc/Dec B- Wk 238 (>=17 y)Inc/Dec A- Wk 262 (>=17 y)Inc/Dec B- Wk 262 (>=17 y)Inc/Dec A- Early TV (>=17 y)Inc/Dec B- Early TV (>=17 y)High- TV (1 m - <17 y)Inc/Dec A- TV (>=17 y)Inc/Dec B- TV (>=17 y)
All Participants (Lacosamide)9.75.616.410.55.919.37.112.422.67.714.921.819.030.213.016.430.95.310.521.633.07.77.719.532.510.025.045.016.726.150.050.031.854.516.750.033.333.326.333.321.434.552.7

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Serum Chemistry Parameters (Phosphate)

TEMA values are defined in the SAP as significant deviations from the expected range of age-appropriate values. TEMA laboratory results of Phosphate were those that are observed post- BL during the Treatment Period but not present at Baseline. For the age range, '1 year-<17 years', the abnormality criteria were from '<0.5814' mmol/L (Low) and '>2.3902' mmol/L (High). For age range, '>=17 years', the abnormality Criteria were '<=0.646' mmol/L (Low) and '>=1.938' mmol/L (High) of serum phosphate. (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
Low: Wk 94 (>=17 y)Low: Wk 118 (>=17 y)
All Participants (Lacosamide)0.70.8

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Serum Chemistry Parameters (Glucose)

TEMA values are defined in the SAP as significant deviations from the expected range of age-appropriate values. TEMA laboratory results of Glucose were those that were observed post- BL during the Treatment Period but not present at Baseline. For the age range, '>1 month-<17 years', the abnormality criteria were from '<2.775' mmol/L (Low) and '>=9.99' mmol/L (High). For age range, '>=17 years', the abnormality criteria were '<2.775' mmol/L (Low) and '>=11.1' mmol/L (High) of serum Glucose. (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
Low: Wk 2 (>=17 y)Low: Wk 62 (>=17 y)Low: Wk 94 (>=17 y)Low: Wk 118 (>=17 y)High: Wk 2 (>=17 y)High: Wk 22 (>=17 y)High: Wk 46 (>=17 y)High: Wk 62 (>=17 y)High: Wk 78 (>=17 y)High: Wk 94 (>=17 y)High: Wk 118 (>=17 y)High: Early TV (>=17 y)
All Participants (Lacosamide)0.50.60.70.81.01.11.21.83.40.70.81.9

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Serum Chemistry Parameters (Gamma Glutamyl Transferase)

TEMA values are defined in the SAP as significant deviations from the expected range of age-appropriate values. TEMA laboratory results of Gamma Glutamyl Transferase (GGT) were those that were observed post- BL during the Treatment Period but not present at Baseline. For the age range, '1 year-<13 years', the abnormality criteria was '>=66' U/L (High A), for '13 years-<17 years', the abnormality criteria was '>=126' U/L (High B) and for '>=17 years', the abnormality criteria was '>=3.0 U/L x ULN' (High C) of serum GGT. (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
High A: TV (1-<13 y)High C: Wk 2 (>=17 y)High C: Wk 22 (>=17 y)High C: Wk 62 (>=17 y)High C: Wk 78 (>=17 y)High C: Wk 118 (>=17 y)High C: Wk 166 (>=17 y)High C:TV (>=17 y)
All Participants (Lacosamide)16.71.00.51.83.40.81.10.8

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Serum Chemistry Parameters (Bicarbonate)

TEMA values are defined in the SAP as significant deviations from the expected range of age-appropriate values. TEMA laboratory results of Bicarbonate were those that were observed post- BL during the Treatment Period but not present at Baseline. For the age range, '>1 month-<17 years', the abnormality criteria were '<15' mmol/L (Low) and '>38' mmol/L (High). For age range, '>=17 years', the abnormality criteria were '<18' mmol/L (Low) and '>38' mmol/L (High) of serum Bicarbonate. (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
Low: Wk 2 (>=17 y)Low: Wk 46 (>=17 y)Low: Wk 62 (>=17 y)Low: Wk 94 (>=17 y)
All Participants (Lacosamide)1.11.21.30.7

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Serum Chemistry Parameters (Aspartate Aminotransferase)

TEMA values are defined in the SAP as significant deviations from the expected range of age-appropriate values. TEMA laboratory results of Aspartate Aminotransferase (AST) were those that were observed post- BL during the Treatment Period but not present at Baseline. For all ages, the abnormality criteria were specified as '≥3.0 units per litre (U/L) x ULN' (High A), '≥5.0 U/L x ULN' (High B), and '≥10.0 U/L x ULN' (High C) of serum AST. (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
High A: All ages (Early TV)High A: All ages (TV)High B: All ages (TV)High C: All ages (TV)
All Participants (Lacosamide)1.70.70.70.7

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Serum Chemistry Parameters (Alanine Aminotransferase)

TEMA values are defined in the SAP as significant deviations from the expected range of age-appropriate values. TEMA laboratory results of Alanine Aminotransferase (ALT) were those that were observed post- BL during the Treatment Period but not present at Baseline. For all ages, the abnormality criteria were specified as '≥3.0 U/L x ULN' (High A), '≥5.0 U/L x ULN' (High B), and '≥10.0 U/L x ULN' (High C) of serum ALT. (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
High A: All ages (Wk 2)High A: All ages (Wk 46)High A: All ages (Wk 62)High A: All ages (Wk 118)High A: All ages (TV)High B: All ages (Wk 2)
All Participants (Lacosamide)0.40.50.50.70.70.4

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Hematology Parameters (Neutrophils Absolute)

TEMA values are defined in the SAP as significant deviations from the expected range of age-appropriate values. TEMA laboratory results of Neutrophils Absolute were those that were observed post-BL during the Treatment Period but not present at BL. For the age range, '>1 month', the abnormality criteria was '<1.5' 10^9/L of Neutrophils in blood. (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
<1.5: Wk 2 (>1 m)<1.5: Wk 22 (>1 m)<1.5: Wk 46 (>1 m)<1.5: Wk 62 (>1 m)<1.5: Wk 94 (>1 m)<1.5: Wk 214 (>1 m)
All Participants (Lacosamide)0.90.50.50.50.62.4

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Hematology Parameters (Lymphocytes Absolute)

TEMA values are defined in the SAP as significant deviations from the expected range of age-appropriate values. TEMA laboratory results of Lymphocytes Absolute were those that were observed post-Baseline (BL) during the Treatment Period but not present at Baseline. For the age range, '2 years - <6 years', the abnormality criteria were '<0.7' 10^9/L (Low) and '>6.9' 10^9/L (High). For age range, '>=6 years', the abnormality criteria were '<0.6' 10^9/L (Low) and '>5.0' 10^9/L (High) for Lymphocytes Absolute in the blood. (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
High: Wk 2 (>=6 y)High: Wk 78 (>=6 y)High: Wk 118 (>=6 y)
All Participants (Lacosamide)0.43.20.7

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Hematology Parameters (Hemoglobin)

TEMA values are defined in the Statistical Analysis Plan (SAP) as significant deviations from the expected range of age-appropriate values. TEMA laboratory results of Hematology parameter, Hemoglobin were those that were observed post-Baseline (BL) during the Treatment Period but not present at Baseline. For the age range, '2 years (y) to <17 years', the abnormality criteria were '<=95' grams/deciliter (g/dL) (Low) and '>160' g/dL (High). For age range, '>=17 years', the abnormality Criteria were '<=85% of lower limit of normal (LLN)' value (Low) and '>=115% of upper limit of normal (ULN)' value (High) of Hemoglobin in blood. (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
Low: Week (Wk) 78 (2-<17 y)Low: Wk 0 (>=17 y)Low: Wk 2 (>=17 y)Low: Wk 118 (>=17 y)Low: Wk 166 (>=17 y)Low: Wk 214 (>=17 y)Low: Termination Visit (TV) (>=17 y)
All Participants (Lacosamide)14.33.70.50.81.22.51.6

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Hematology Parameters (Hematocrit)

TEMA values are defined in the SAP as significant deviations from the expected range of age-appropriate values. TEMA laboratory results of Hematocrit were those that were observed post-BL during the Treatment Period but not present at BL. For the age range, '2 years to <17 years', the abnormality criteria were '<=29%' (Low) and '>47%' (High) hematocrit values. For age range, '>=17 years', the abnormality criteria were '<=85% of LLN' (Low) and '>=115% of ULN' (High) of Hematocrit values in blood. (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
High: Wk 22 (2-<17 y)High: Wk 46 (2-<17 y)Low: Wk 46 (>=17 y)Low: Wk 118 (>=17 y)Low: Wk 166 (>=17 y)Low: TV (>=17 y)
All Participants (Lacosamide)6.93.71.21.61.20.8

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Hematology Parameters (Eosinophils Absolute)

TEMA values are defined in the SAP as significant deviations from the expected range of age-appropriate values. TEMA laboratory results of Eosinophils Absolute were those that were observed post-BL during the Treatment Period but not present at BL. For the age range, '>1 month', the abnormality criteria were '>=1.0' 10^9/L of Eosinophils in the blood. (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
>=1.0: Wk 2 (>1 month)>=1.0: Wk 22 (>1 month)>=1.0: TV (>1 month)
All Participants (Lacosamide)0.90.51.5

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in 12-lead Electrocardiogram (ECG) Parameter (QT Interval)

TEMA values are defined in the SAP as significant deviations from the expected range of age-appropriate values. TEMA ECG results of QT interval parameter were those that were observed post- BL during the Treatment Period but not present at Baseline. For the age range, '1 month (m)-<12 years', the abnormality criteria were '>=500 milliseconds (ms)' (Abnormal (Abn) A). For age range, '>=12 years', the abnormality criteria were '>=500 ms' (Abn B) or '>=60 ms increase from Baseline' (Abn C). The abnormality in QT interval was observed at Week 0 as the participant was rolled over from SP0982 study and was constantly having abnormal ECG parameters while in SP0982 and EP0012. (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
Abn C: Wk 0 (>=12 years)Abn C: Wk 2 (>=12 years)Abn C: Wk 14 (>=12 years)Abn C: Wk 30 (>=12 years)Abn B: Wk 46 (>=12 years)Abn C: Wk 46 (>=12 years)Abn C: Wk 62 (>=12 years)Abn C: Wk 78 (>=12 years)Abn C: Wk 94 (>=12 years)Abn C: Wk 118 (>=12 years)Abn C: Wk 142 (>=12 years)Abn C: Wk 190 (>=12 years)Abn C: Early TV (>=12 years)Abn C: TV (>=12 years)
All Participants (Lacosamide)33.30.53.30.80.52.72.21.62.513.06.93.23.82.3

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in 12-lead ECG Parameter (QTc(F) Interval)

TEMA values are defined in the SAP as significant deviations from the expected range of age-appropriate values. TEMA ECG results of QTc(F) interval were those that are observed post- BL during the Treatment Period but not present at Baseline. For the age range '3 years -<12 years' and '>=12 years- <17 years', the abnormality criteria were from '>440 ms' (Abn A) and '>15% increase from Baseline' value (Abn B). For age range, '>=17 years', the abnormality Criteria were '>450 ms' (Abn C), '>480 ms' (Abn D), '>500 ms' (Abn E) or '>=60 ms increase from Baseline' value (Abn F). The abnormality in QTc(F) interval was observed at Week 0 as the participant was rolled over from SP0982 study and was constantly having abnormal ECG parameters while in SP0982 and EP0012. (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
Abn C: Wk 0 (>=17 y)Abn D: Wk 0 (>=17 y)Abn F: Wk 0 (>=17 y)Abn C: Wk 2 (>=17 y)Abn F: Wk 2 (>=17 y)Abn A: Wk 14 (>=12 y-<17 y)Abn C: Wk 14 (>=17 y)Abn D: Wk 14 (>=17 y)Abn E: Wk 14 (>=17 y)Abn F: Wk 14 (>=17 y)Abn F: Wk 30 (>=17 y)Abn C: Wk 46 (>=17 y)Abn D: Wk 46 (>=17 y)Abn E: Wk 46 (>=17 y)Abn F: Wk 46 (>=17 y)Abn A: Wk 62 (>=12 y-<17 y)Abn B: Wk 62 (>=12 y-<17 y)Abn C: Wk 62 (>=17 y)Abn D: Wk 62 (>=17 y)Abn F: Wk 62 (>=17 y)Abn F: Wk 78 (>=17 y)Abn C: Wk 94 (>=17 y)Abn D: Wk 94 (>=17 y)Abn E: Wk 94 (>=17 y)Abn F: Wk 94 (>=17 y)Abn C: Wk 118 (>=17 y)Abn F: Wk 118 (>=17 y)Abn C: Wk 142 (>=17 y)Abn F: Wk 142 (>=17 y)Abn C: Early TV (>=17 y)Abn D: Early TV (>=17 y)Abn E: Early TV (>=17 y)Abn F: Early TV (>=17 y)Abn C: TV (>=17 y)Abn F: TV (>=17 y)
All Participants (Lacosamide)33.333.333.31.51.05.62.11.00.53.71.75.21.71.22.36.36.32.40.61.81.82.72.02.03.49.54.82.12.16.12.02.04.12.85.6

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in 12-lead ECG Parameter (QTc(B) Interval)

TEMA values are defined in the SAP as significant deviations from the expected range of age-appropriate values. TEMA ECG results of QTc(B) interval were those that are observed post- BL during the Treatment Period but not present at Baseline. For the age range '3 years -<12 years' and '>=12 years- <17 years', the abnormality criteria were '>450 ms' (Abn A) and '>15% increase from Baseline' value (Abn B). For age range, '>=17 years', the abnormality criteria were '>450 ms' (Abn C), '>480 ms' (Abn D), '>500 ms' (Abn E) or '>=60 ms increase from Baseline' value (Abn F). The abnormality in QTc(B) interval was observed at Week 0 as the participant was rolled over from SP0982 study and was constantly having abnormal ECG parameters while in SP0982 and EP0012. (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
Abn C: Wk 0 (>=17 y)Abn D: Wk 0 (>=17 y)Abn E: Wk 0 (>=17 y)Abn F: Wk 0 (>=17 y)Abn C: Wk 2 (>=17 y)Abn F: Wk 2 (>=17 y)Abn A: Wk 14 (>=12 y-<17 y)Abn C: Wk 14 (>=17 y)Abn D: Wk 14 (>=17 y)Abn E: Wk 14 (>=17 y)Abn F: Wk 14 (>=17 y)Abn C: Wk 30 (>=17 y)Abn F: Wk 30 (>=17 y)Abn C: Wk 46 (>=17 y)Abn D: Wk 46 (>=17 y)Abn E: Wk 46 (>=17 y)Abn F: Wk 46 (>=17 y)Abn A: Wk 62 (>=12 y-<17 y)Abn B: Wk 62 (>=12 y-<17 y)Abn C: Wk 62 (>=17 y)Abn D: Wk 62 (>=17 y)Abn E: Wk 62 (>=17 y)Abn F: Wk 62 (>=17 y)Abn C: Wk 78 (>=17 y)Abn F: Wk 78 (>=17 y)Abn C: Wk 94 (>=17 y)Abn D: Wk 94 (>=17 y)Abn E: Wk 94 (>=17 y)Abn F: Wk 94 (>=17 y)Abn A: Wk 118 (>=12 y-<17 y)Abn C: Wk 118 (>=17 y)Abn D: Wk 118 (>=17 y)Abn E: Wk 118 (>=17 y)Abn F: Wk 118 (>=17 y)Abn A: Wk 142 (>=12 y-<17 y)Abn C: Wk 142 (>=17 y)Abn F: Wk 142 (>=17 y)Abn F: Wk 166 (>=17 y)Abn C: Wk 190 (>=17 y)Abn F: Wk 190 (>=17 y)Abn C: Early TV (>=17 y)Abn D: Early TV (>=17 y)Abn E: Early TV (>=17 y)Abn F: Early TV (>=17 y)Abn C: TV (>=17 y)Abn D: TV (>=17 y)Abn F: TV (>=17 y)
All Participants (Lacosamide)33.333.333.333.33.62.05.65.81.61.03.72.51.77.02.91.23.56.36.32.40.60.63.55.41.85.42.02.03.450.014.34.84.89.59.18.54.333.37.73.86.12.02.06.12.82.85.6

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in 12-lead ECG Parameter (QRS Interval)

TEMA values are defined in the SAP as significant deviations from the expected range of age-appropriate values. TEMA ECG results of QRS interval were those that were observed post- BL during the Treatment Period but not present at Baseline. For the age range, '3 years -<12 years', the abnormality criteria were '>100 ms' (Abn A) and '>25% increase from Baseline' value (Abn B). For the age range, '>=12 years - <17 years', the abnormality criteria were '>110 ms' (Abn C) and '>25% increase from Baseline' (Abn D). For age range, '>=17 years', the abnormality criteria were treatment-emergent values above '>100 ms' (Abn E), '>120 ms' (Abn F), or '>140 ms' (Abn G). (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
Abn E: Wk 2 (>=17 y)Abn D: Wk 14 (>=12 y-<17 y)Abn E: Wk 14 (>=17 y)Abn F: Wk 14 (>=17 y)Abn E: Wk 30 (>=17 y)Abn A: Wk 46 (3 y-<12 y)Abn D: Wk 46 (>=12 y-<17 y)Abn E: Wk 46 (>=17 y)Abn D: Wk 62 (>=12 y-<17 y)Abn E: Wk 62 (>=17 y)Abn F: Wk 62 (>=17 y)Abn E: Wk 78 (>=17 y)Abn F: Wk 78 (>=17 y)Abn C: Wk 94 (>=12 y-<17 y)Abn D: Wk 94 (>=12 y-<17 y)Abn E: Wk 94 (>=17 y)Abn F: Wk 94 (>=17 y)Abn E: Wk 118 (>=17 y)Abn E: Wk 142 (>=17 y)Abn E: Early TV (>=17 y)Abn E: TV (>=17 y)Abn F: TV (>=17 y)
All Participants (Lacosamide)5.15.69.90.57.68.36.37.66.310.61.88.91.87.17.16.10.714.310.610.25.65.6

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in 12-lead ECG Parameter (PR Interval)

TEMA values are defined in the SAP as significant deviations from the expected range of age-appropriate values. TEMA ECG results of PR interval were those that were observed post- BL during the Treatment Period but not present at Baseline. For the age range, '3 years -<12 years', the abnormality criteria were '>180 ms' (Abn A) and '>25% increase from Baseline' value (Abn B). For the age range, '>=12 years - <17 years', the abnormality criteria were '>200 ms' (Abn C) and '>25% increase from Baseline' value (Abn D). For age range, '>=17 years', the abnormality criteria were treatment-emergent values above '>200 ms' (Abn E), '>220 ms' (Abn F), or '>250 ms' (Abn G). (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
Abn B: Wk 2 (3 y-<12 y)Abn D: Wk 2 (>=12 y-<17 y)Abn E: Wk 2 (>=17 y)Abn F: Wk 2 (>=17 y)Abn E: Wk 14 (>=17 y)Abn E: Wk 30 (>=17 y)Abn F: Wk 30 (>=17 y)Abn C: Wk 46 (>=12 y-<17 y)Abn E: Wk 46 (>=17 y)Abn B: Wk 62 (3 y-<12 y)Abn C: Wk 62 (>=12 y-<17 y)Abn E: Wk 62 (>=17 y)Abn F: Wk 62 (>=17 y)Abn E: Wk 78 (>=17 y)Abn F: Wk 78 (>=17 y)Abn G: Wk 78 (>=17 y)Abn B: Wk 94 (3 y-<12 y)Abn C: Wk 94 (>=12 y-<17 y)Abn E: Wk 94 (>=17 y)Abn F: Wk 94 (>=17 y)Abn G: Wk 94 (>=17 y)Abn D: Wk 118 (>=12 y-<17 y)Abn E: Wk 142 (>=17 y)Abn F: Wk 142 (>=17 y)Abn E: Early TV (>=17 y)Abn F: Early TV (>=17 y)
All Participants (Lacosamide)6.35.01.50.51.01.70.96.31.220.06.32.90.65.41.81.828.67.12.70.70.750.08.72.22.02.0

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in 12-lead ECG Parameter (Heart Rate Interval)

TEMA values are defined in the SAP as significant deviations from the expected range of age-appropriate values. TEMA ECG results of Heart rate interval were those that were observed post- BL during the Treatment Period but not present at Baseline. For the age range, '3 years -<12 years', the abnormality criteria were '<60 beats per minute (bpm)' (Abn A) and '>130 bpm' (Abn B). For the age range, '>=12 years', the abnormality criteria were '<50 bpm' (Abn C) and '>120 bpm' (Abn D). (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
Abn C: Wk 2 (>=12 y)Abn C: Wk 14 (>=12 y)Abn C: Wk 30 (>=12 y)Abn C: Wk 46 (>=12 y)Abn D: Wk 46 (>=12 y)Abn C: Wk 62 (>=12 y)Abn D: Wk 62 (>=12 y)Abn C: Wk 78 (>=12 y)Abn C: Wk 94 (>=12 y)Abn C: Wk 118 (>=12 y)Abn D: Wk 214 (>=12 y)Abn D: TV (>=12 y)
All Participants (Lacosamide)1.42.41.50.50.53.20.53.31.24.31002.3

[back to top]

Number of Study Participants With New Appearance of Absence and/or Myoclonic Seizures During the Treatment Period

The number of study participants with appearance of new absence and/or myoclonic seizure types experienced during the Treatment Period but who did not experience in Combined Baseline Period or in seizure classification history, before taking LCM were reported. To determine appearance of new seizure type, the Combined Baseline Period was used. Thus, the participants who directly enrolled into EP0012, the Baseline absence, and/or myoclonic seizure data from SP0982's 4-week Prospective Baseline Period were combined with any reported Baseline absence, and myoclonic seizure information in the daily seizure diary from EP0012 (reported before first dose in EP0012) to recalculate the study participant's Baseline variables such as days with absence, and/or myoclonic seizures per 28 days. (NCT02408549)
Timeframe: From Visit 1 (Week 0) to End of Treatment Period (up to approximately 5 years)

InterventionParticipants (Count of Participants)
Absence seizuresMyoclonic seizures
All Participants (Lacosamide)35

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Serum Chemistry Parameters (Total Protein)

TEMA values are defined in the SAP as significant deviations from the expected range of age-appropriate values. TEMA laboratory results of Total Protein were those that were observed post- BL during the Treatment Period but not present at Baseline. For the age range, '1 year to <17 years', the abnormality criteria were '<43' g/L and '>120' g/L. For age range, '>=17 years', the abnormality criteria were '<43' g/L and '>130' g/L of serum protein. (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
All Participants (Lacosamide)0

[back to top]

Percentage of Study Participants With Treatment-emergent Marked Abnormalities (TEMAs) in Serum Chemistry Parameters (Sodium)

TEMA values are defined in the SAP as significant deviations from the expected range of age-appropriate values. TEMA laboratory results of Sodium were those that were observed post- BL during the Treatment Period but not present at Baseline. For the age range, '>1 month', the abnormality criteria were '<127' mmol/L (Low) and '>151' mmol/L (High) of serum Sodium. (NCT02408549)
Timeframe: During the study (up to approximately 5 years)

Interventionpercentage of participants (Number)
All Participants (Lacosamide)0

[back to top]

Percentage of Participants Experiencing no Change in Average Daily Frequency (ADF) of Electrographic Partial-onset Seizures (Between <25% Reduction and <25% Increase) From EOB Period Video-EEG to EOM Period Video-EEG

No change was defined as between <25% reduction and <25% increase in ADF of electrographic partial-onset seizures (POS) from the End-of-Baseline (EOB) video-EEG to the End-of-Maintenance (EOM) video-EEG. (NCT02477839)
Timeframe: End-of-Baseline Period (Day -3 to Day 1) to End-of-Maintenance Period (Day 24 to Day 27)

Interventionpercentage of participants (Number)
Placebo (FAS)28.3
Lacosamide (FAS)27.6

[back to top]

Percentage of Participants Who Achieved 'Seizure-free' Status From All Seizure Types During the End-of-Maintenance (EOM) Period Video-EEG

A study participant was considered seizure-free from all seizures if the End-of-Maintenance (EOM) Period video-EEG had zero seizures reported from all seizure types (not just partial-onset seizures (POS)). (NCT02477839)
Timeframe: During the End-of-Maintenance Period (Day 24 to Day 27)

Interventionpercentage of participants (Number)
Placebo (FAS)15.8
Lacosamide (FAS)17.1

[back to top]

Percentage of Participants Who Achieved 'Seizure-free' Status From Partial-onset Seizure Types Only During the End-of-Maintenance (EOM) Period Video-EEG

A study participant was considered seizure free from partial-onset seizures (POS) if the End-of-Maintenance (EOM) Period video-EEG had zero POS reported. (NCT02477839)
Timeframe: During the End-of-Maintenance Period (Day 24 to Day 27)

Interventionpercentage of participants (Number)
Placebo (FAS)16.7
Lacosamide (FAS)18.8

[back to top] [back to top]

Percentage of Participants Experiencing a >=25% to <50% Reduction in Average Daily Frequency (ADF) of Electrographic Partial-onset Seizures From End-of-Baseline (EOB) Period Video-EEG to End-of-Maintenance (EOM) Period Video-EEG

A ≥25% to <50% response was defined as ≥25% to <50% reduction in ADF of electrographic partial-onset seizures (POS) from the End-of-Baseline (EOB) video-EEG to the End-of-Maintenance (EOM) video-EEG. (NCT02477839)
Timeframe: End-of-Baseline Period (Day -3 to Day 1) to End-of-Maintenance Period (Day 24 to Day 27)

Interventionpercentage of participants (Number)
Placebo (FAS)18.3
Lacosamide (FAS)18.1

[back to top]

Percentage of Participants Experiencing an Increase in Average Daily Frequency (ADF) of Electrographic Partial-onset Seizures of >=25% From End-of-Baseline (EOB) Period Video-EEG to End-of-Maintenance (EOM) Period Video-EEG

An increase was defined as ≥25% increase in ADF of electrographic partial-onset seizures (POS) from the End-of-Baseline (EOB) video-EEG to the End-of-Maintenance (EOM) video-EEG. (NCT02477839)
Timeframe: End-of-Baseline Period (Day -3 to Day 1) to End-of-Maintenance Period (Day 24 to Day 27)

Interventionpercentage of participants (Number)
Placebo (FAS)15.0
Lacosamide (FAS)12.9

[back to top]

Percent Change in Average Daily Frequency (ADF) of Electrographic Partial-onset Seizures From End-of-Baseline (EOB) Period Video-EEG to End-of-Maintenance (EOM) Period Video-EEG

The percent change in ADF of electrographic partial-onset seizures as measured on the End-of-Maintenance Period video-EEG compared to the End-of-Baseline Period video-EEG. (NCT02477839)
Timeframe: End-of-Baseline Period (Day -3 to Day 1) to End-of-Maintenance Period (Day 24 to Day 27)

Interventionpercent change (Mean)
Placebo (FAS)-26.7927
Lacosamide (FAS)-32.3564

[back to top]

Participant Withdrawals Due to Adverse Events (AEs) During the Study

An adverse event (AE) is any untoward medical occurrence in a patient or clinical study participant, temporally associated with the use of study medication, whether or not considered related to the study medication. An AE could, therefore, be any unfavorable and unintended sign (including an abnormal laboratory finding), symptom, or disease (new or exacerbated) temporally associated with the use of study medication. (NCT02477839)
Timeframe: From the Baseline Period (Day -7) to the End of Study Visit (up to 93 days)

Interventionpercentage of participants (Number)
Placebo (SS)0
Lacosamide (SS)1.6

[back to top]

Change in Average Daily Frequency (ADF) of Electrographic Partial-onset Seizures From End-of-Baseline (EOB) Period Video-EEG to End-of-Maintenance (EOM) Period Video-EEG

"The change in ADF of electrographic partial-onset seizures as measured on the End-of-Maintenance Period video-electroencephalogram (EEG) compared to the End-of-Baseline Period video-EEG.~Seizure frequency was analyzed using an analysis of covariance (ANCOVA) with terms for treatment, pooled randomized age stratum, pooled center, and Baseline seizure ADF. Seizure ADF was log transformed using the transformation of ln(X+1), where X is the seizure ADF. Baseline seizure ADF was log transformed.~Least squares means were based on log-transformed data of the full ANCOVA model." (NCT02477839)
Timeframe: End-of-Baseline Period (Day -3 to Day 1) to End-of-Maintenance Period (Day 24 to Day 27)

Interventionpercent change (Least Squares Mean)
Placebo (FAS)1.44
Lacosamide (FAS)1.40

[back to top]

Absolute Change in Average Daily Frequency (ADF) of Electrographic Partial-onset Seizures From End-of-Baseline (EOB) Period Video-EEG to End-of-Maintenance (EOM) Period Video-EEG

The absolute change in ADF of electrographic partial-onset seizures as measured on the End-of-Maintenance Period video-EEG compared to the End-of-Baseline Period video-EEG. (NCT02477839)
Timeframe: End-of-Baseline Period (Day -3 to Day 1) to End-of-Maintenance Period (Day 24 to Day 27)

Interventionseizures per day (Mean)
Placebo (FAS)-4.7650
Lacosamide (FAS)-2.9427

[back to top]

Percentage of Participants Experiencing a >75% Reduction in Average Daily Frequency (ADF) of Electrographic Partial-onset Seizures From End-of-Baseline (EOB) Period Video-EEG to End-of-Maintenance (EOM) Period Video-EEG

A >75% response was defined as >75% reduction in ADF of electrographic partial-onset seizures (POS) from the End-of-Baseline (EOB) video-EEG to the End-of-Maintenance (EOM) video-EEG. (NCT02477839)
Timeframe: End-of-Baseline Period (Day -3 to Day 1) to End-of-Maintenance Period (Day 24 to Day 27)

Interventionpercentage of participants (Number)
Placebo (FAS)20.0
Lacosamide (FAS)31.0

[back to top]

Percentage of Participants Experiencing a 50% to 75% Reduction in Average Daily Frequency (ADF) of Electrographic Partial-onset Seizures From End-of-Baseline (EOB) Period Video-EEG to End-of-Maintenance (EOM) Period Video-EEG

A ≥50% to ≤75% response was defined as ≥50% to ≤75% reduction in ADF of electrographic partial-onset seizures (POS) from the End-of-Baseline (EOB) video-EEG to the End-of-Maintenance (EOM) video-EEG. (NCT02477839)
Timeframe: End-of-Baseline Period (Day -3 to Day 1) to End-of-Maintenance Period (Day 24 to Day 27)

Interventionpercentage of participants (Number)
Placebo (FAS)17.5
Lacosamide (FAS)10.3

[back to top]

Percentage of Participants Experiencing Any Adverse Events (AEs) Reported Spontaneously by the Subject and/or Caregiver or Observed by Investigator

An Adverse Event (AE) is any untoward medical occurrence in a patient or clinical study participant, temporally associated with the use of study medication, whether or not considered related to the study medication. An AE could, therefore, be any unfavorable and unintended sign (including an abnormal laboratory finding), symptom, or disease (new or exacerbated) temporally associated with the use of study medication. (NCT02582866)
Timeframe: From Visit 1 (Week 0) to Final Visit (up to Week 158)

Interventionpercentage of participants (Number)
Lacosamide (SS)59.4

[back to top]

Percentage of Participants Experiencing Any Serious Adverse Events (SAEs) Reported Spontaneously by the Subject and/or Caregiver or Observed by Investigator

"A Serious Adverse Event (SAE) is any untoward medical occurrence that at any dose:~Results in death~Is life-threatening~Requires in patient hospitalization or prolongation of existing hospitalization~Is a congenital anomaly or birth defect~Is an infection that requires treatment parenteral antibiotics~Other important medical events which based on medical or scientific judgement may jeopardize the study participants, or may require medical or surgical intervention to prevent any of the above." (NCT02582866)
Timeframe: From Visit 1 (Week 0) to Final Visit (up to Week 158)

Interventionpercentage of participants (Number)
Lacosamide (SS)14.2

[back to top]

Percentage of Participants That Withdrew Due to Adverse Events (AEs)

An Adverse Event (AE) is any untoward medical occurrence in a patient or clinical study participant, temporally associated with the use of study medication, whether or not considered related to the study medication. An AE could, therefore, be any unfavorable and unintended sign (including an abnormal laboratory finding), symptom, or disease (new or exacerbated) temporally associated with the use of study medication. (NCT02582866)
Timeframe: From Visit 1 (Week 0) to Final Visit (up to Week 158)

Interventionpercentage of participants (Number)
Lacosamide (SS)0.9

[back to top]

Percentage of Participants With at Least One Adverse Event Reported Spontaneously by the Participant/or Caregiver (Including Parent/Legal Guardian) or Observed by the Investigator During the Study

"An Adverse Event (AE) is any untoward medical occurrence in a patient or clinical investigation participant administered a pharmaceutical product, which does not necessarily have a causal relationship with this treatment. An AE could therefore be any unfavorable and unintended sign, symptom, or disease temporally associated with the use of a medicinal (investigational) product, whether or not related to the medicinal (investigational) product.~26 adverse events are reported splitting into at least 19 occurrences of individual pre-treatment emergent adverse events and 7 treatment emergent adverse events (TEAEs)." (NCT02710890)
Timeframe: From Screening Period (Day -7 to Day -1) up to the End-of-Study Period (up to Day 37)

Interventionpercentage of participants (Number)
Lacosamide Age Cohort ≥ 1 Month - < 8 Years (SS-iv)12.5
Lacosamide Age Cohort ≥ 8 - < 17 Years (SS-iv)14.5

[back to top]

Percentage of Participants That Withdrew Due to Adverse Events During the Study

An Adverse Event (AE) is any untoward medical occurrence in a patient or clinical investigation participant administered a pharmaceutical product, which does not necessarily have a causal relationship with this treatment and led to the withdrawal of the participants from the study. An AE could therefore be any unfavorable and unintended sign, symptom, or disease temporally associated with the use of a medicinal (investigational) product, whether or not related to the medicinal (investigational) product. (NCT02710890)
Timeframe: From Screening Period (Day -7 to Day -1) up to the End-of-Study Period (up to Day 37)

Interventionpercentage of participants (Number)
Lacosamide Age Cohort ≥ 1 Month - < 8 Years (SS-iv)0
Lacosamide Age Cohort ≥ 8 - < 17 Years (SS-iv)0

[back to top]

Alcohol Craving: Alcohol Urge Questionnaire (AUQ) Self-Administration Blocks 1 and 2, Minute 120

The Alcohol Urge Questionnaire (AUQ) is an 8-item self report that measures the participant's urge for an alcoholic drink at the time the questionnaire is completed. Questions are in the form of a 7-point Likert scale (from strongly disagree to strongly agree) and the participant selects the extent to which they disagree or agree with the 8 statements relating to desire to drink, expectation of a desired outcome from drinking, and inability to avoid drinking if alcohol was available. Each of the 8 items is scored 1-7. The total score is calculated by adding the scores for each of the items. The total score range is 8-56. Lower scores indicate less urge for alcohol and higher scores indicate more urge for alcohol. (NCT03271528)
Timeframe: 1 minute

Interventionscore on a scale (Mean)
Lacosamide24.94
Placebo Oral Capsule25.44

[back to top]

Alcohol Craving: Alcohol Urge Questionnaire (AUQ) Self-Administration Blocks 1 and 2, Minute 30

The Alcohol Urge Questionnaire (AUQ) is an 8-item self report that measures the participant's urge for an alcoholic drink at the time the questionnaire is completed. Questions are in the form of a 7-point Likert scale (from strongly disagree to strongly agree) and the participant selects the extent to which they disagree or agree with the 8 statements relating to desire to drink, expectation of a desired outcome from drinking, and inability to avoid drinking if alcohol was available. Each of the 8 items is scored 1-7. The total score is calculated by adding the scores for each of the items. The total score range is 8-56. Lower scores indicate less urge for alcohol and higher scores indicate more urge for alcohol. (NCT03271528)
Timeframe: 1 minute

Interventionscore on a scale (Mean)
Lacosamide24.00
Placebo Oral Capsule23.94

[back to top]

Alcohol Craving: Alcohol Urge Questionnaire (AUQ) Self-Administration Blocks 1 and 2, Minute 60

The Alcohol Urge Questionnaire (AUQ) is an 8-item self report that measures the participant's urge for an alcoholic drink at the time the questionnaire is completed. Questions are in the form of a 7-point Likert scale (from strongly disagree to strongly agree) and the participant selects the extent to which they disagree or agree with the 8 statements relating to desire to drink, expectation of a desired outcome from drinking, and inability to avoid drinking if alcohol was available. Each of the 8 items is scored 1-7. The total score is calculated by adding the scores for each of the items. The total score range is 8-56. Lower scores indicate less urge for alcohol and higher scores indicate more urge for alcohol. (NCT03271528)
Timeframe: 1 minute

Interventionscore on a scale (Mean)
Lacosamide24.88
Placebo Oral Capsule26.25

[back to top]

Verbal Fluency: Controlled Word Association (COWAT)

The Controlled Word Association (COWAT) is a verbal fluency test that measures the spontaneous production of words beginning with some designated letter. The participant is asked to name words beginning with a given letter, excluding proper nouns, for one minute and this procedure is repeated three times with a different letter each time. A different set of letters was used in each of the two alcohol self-administration trials: C-F-L and P-R-W. The examiner writes down the words provided by the participant on a piece of paper. This test is scored by counting the number of words generated by the subject for each letter, then adding the scores for each of the three letters to calculate a total test score. The lowest possible score is 0 and there is no upper limit to the score range. A higher score is indicative of better outcomes (I.e. better verbal fluency). (NCT03271528)
Timeframe: 3 minutes

Interventionscore on a scale (Mean)
Lacosamide38.19
Placebo Oral Capsule42.25

[back to top]

Cognitive Function: Spatial Span Forward

The Wechsler Memory Scale (WMS-III) Spatial Span test will be used to assess subjects' working memory. Subjects will be shown a sequence of block tapping and asked to repeat back an increasing number of tapped blocks in the same order. Each of the 16 items on this test is scored 0 (incorrect answer) or 1 (correct answer). The total score is calculated by adding the scores for each of the 16 items. The total score range is 0-16. Higher scores are indicative of higher levels of working memory (better outcome) and lower scores are indicative of lesser working memory function (worse outcome). (NCT03271528)
Timeframe: 10 minutes

Interventioncorrect items (Mean)
Lacosamide8.44
Placebo Oral Capsule7.75

[back to top]

Cognitive Function: Spatial Span Backward

The Wechsler Memory Scale (WMS-III) Spatial Span test will be used to assess subjects' working memory. Subjects will be shown a sequence of block tapping and asked to repeat back an increasing number of tapped blocks in the opposite order. Each of the 16 items on this test is scored 0 (incorrect answer) or 1 (correct answer). The total score is calculated by adding the scores for each of the 16 items. The total score range is 0-16. Higher scores are indicative of higher levels of working memory (better outcome) and lower scores are indicative of lesser working memory function (worse outcome). (NCT03271528)
Timeframe: 10 minutes

Interventionscore on a scale (Mean)
Lacosamide7.19
Placebo Oral Capsule7.62

[back to top]

Cognitive Function: Digit Span Sequencing

The Wechsler Adult Intelligence Scale (WAIS-IV) Digit Span test will be used to assess subjects' working memory. Subjects will be read and asked to repeat back an increasing number of digits in ascending order. Each of the 16 items on this test is scored 0 (incorrect answer) or 1 (correct answer). The total score is calculated by adding the scores for each of the 16 items. The total score range is 0-16. Higher scores are indicative of higher levels of working memory (better outcome) and lower scores are indicative of lesser working memory function (worse outcome). (NCT03271528)
Timeframe: 10 minutes

Interventionscore on a scale (Mean)
Lacosamide8.12
Placebo Oral Capsule7.62

[back to top]

Cognitive Function: Digit Span Forward

The Wechsler Adult Intelligence Scale (WAIS-IV) Digit Span test will be used to assess subjects' working memory. Subjects will be read and asked to repeat back an increasing number of digits in the same order. Each of the 16 items on this test is scored 0 (incorrect answer) or 1 (correct answer). The total score is calculated by adding the scores for each of the 16 items. The total score range is 0-16. Higher scores are indicative of higher levels of working memory (better outcome) and lower scores are indicative of lesser working memory function (worse outcome). (NCT03271528)
Timeframe: 10 minutes

Interventionscore on a scale (Mean)
Lacosamide10.81
Placebo Oral Capsule10.81

[back to top]

Cognitive Function: Digit Span Backward

The Wechsler Adult Intelligence Scale (WAIS-IV) Digit Span test will be used to assess subjects' working memory. Subjects will be read and asked to repeat back an increasing number of digits in the opposite order. Each of the 16 items on this test is scored 0 (incorrect answer) or 1 (correct answer). The total score is calculated by adding the scores for each of the 16 items. The total score range is 0-16. Higher scores are indicative of higher levels of working memory (better outcome) and lower scores are indicative of lesser working memory function (worse outcome). (NCT03271528)
Timeframe: 10 minutes

Interventionscore on a scale (Mean)
Lacosamide8.06
Placebo Oral Capsule7.62

[back to top]

Alcohol Craving: Visual Analog Scale (VAS) Self-Administration Blocks 1 and 2, Minute 90

Alcohol craving was measured by self report with the Visual Analog Scale (VAS). The VAS is a straight horizontal line with one end indicating no alcohol craving and the other end indicating intense alcohol craving. The participant marks a point on the line that matches their present amount of alcohol craving. Location of the point on the line is measured for a score range of 0-100. A lower score indicates less craving for alcohol and a higher score indicated more craving for alcohol. (NCT03271528)
Timeframe: 1 minute

Interventionscore on a scale (Mean)
Lacosamide21.62
Placebo Oral Capsule27.81

[back to top]

Alcohol Craving: Visual Analog Scale (VAS) Observation Period, Minute 30

Alcohol craving was measured by self report with the Visual Analog Scale (VAS). The VAS is a straight horizontal line with one end indicating no alcohol craving and the other end indicating intense alcohol craving. The participant marks a point on the line that matches their present amount of alcohol craving. Location of the point on the line is measured for a score range of 0-100. A lower score indicates less craving for alcohol and a higher score indicated more craving for alcohol. (NCT03271528)
Timeframe: 1 minute

Interventionscore on a scale (Mean)
Lacosamide35.19
Placebo Oral Capsule37.81

[back to top]

Alcohol Craving: Obsessive-Compulsive Drinking Scale (OCDS) Pretrial

The Obsessive-Compulsive Drinking Scale (OCDS) is a quick and reliable 14-item self-rating instrument that provides a total score that measures some cognitive aspects of alcohol craving (obsessive and compulsive drinking). Each of the 14 items is scored from 0 to 4. The total score is calculated by adding the scores for each of the 14 items. The total score range is 0-56. Higher scores are indicative of more obsessive or compulsive drinking and lower scores are indicative of less obsessive or compulsive drinking. (NCT03271528)
Timeframe: 5 minutes

Interventionscores on a scale (Mean)
Lacosamide10.19
Placebo Oral Capsule12.25

[back to top]

Alcohol Craving: Visual Analog Scale (VAS) Self-Administration Blocks 1 and 2, Minute 60

Alcohol craving was measured by self report with the Visual Analog Scale (VAS). The VAS is a straight horizontal line with one end indicating no alcohol craving and the other end indicating intense alcohol craving. The participant marks a point on the line that matches their present amount of alcohol craving. Location of the point on the line is measured for a score range of 0-100. A lower score indicates less craving for alcohol and a higher score indicated more craving for alcohol. (NCT03271528)
Timeframe: 1 minute

Interventionscore on a scale (Mean)
Lacosamide24.94
Placebo Oral Capsule30.37

[back to top]

Alcohol Craving: Visual Analog Scale (VAS) Self-Administration Blocks 1 and 2, Minute 30

Alcohol craving was measured by self report with the Visual Analog Scale (VAS). The VAS is a straight horizontal line with one end indicating no alcohol craving and the other end indicating intense alcohol craving. The participant marks a point on the line that matches their present amount of alcohol craving. Location of the point on the line is measured for a score range of 0-100. A lower score indicates less craving for alcohol and a higher score indicated more craving for alcohol. (NCT03271528)
Timeframe: 1 minute

Interventionscore on a scale (Mean)
Lacosamide28.00
Placebo Oral Capsule31.87

[back to top]

Alcohol Craving: Visual Analog Scale (VAS) Self-Administration Blocks 1 and 2, Minute 120

Alcohol craving was measured by self report with the Visual Analog Scale (VAS). The VAS is a straight horizontal line with one end indicating no alcohol craving and the other end indicating intense alcohol craving. The participant marks a point on the line that matches their present amount of alcohol craving. Location of the point on the line is measured for a score range of 0-100. A lower score indicates less craving for alcohol and a higher score indicated more craving for alcohol. (NCT03271528)
Timeframe: 1 minute

Interventionscore on a scale (Mean)
Lacosamide23.62
Placebo Oral Capsule29.00

[back to top]

Alcohol Craving: Visual Analog Scale (VAS) Pretrial

Alcohol craving was measured by self report with the Visual Analog Scale (VAS). The VAS is a straight horizontal line with one end indicating no alcohol craving and the other end indicating intense alcohol craving. The participant marks a point on the line that matches their present amount of alcohol craving. Location of the point on the line is measured for a score range of 0-100. A lower score indicates less craving for alcohol and a higher score indicated more craving for alcohol. (NCT03271528)
Timeframe: 1 minute

Interventionscores on a scale (Mean)
Lacosamide30.25
Placebo Oral Capsule31.60

[back to top]

Alcohol Craving: Visual Analog Scale (VAS) Observation Period, Minute 40

Alcohol craving was measured by self report with the Visual Analog Scale (VAS). The VAS is a straight horizontal line with one end indicating no alcohol craving and the other end indicating intense alcohol craving. The participant marks a point on the line that matches their present amount of alcohol craving. Location of the point on the line is measured for a score range of 0-100. A lower score indicates less craving for alcohol and a higher score indicated more craving for alcohol. (NCT03271528)
Timeframe: 1 minute

Interventionscore on a scale (Mean)
Lacosamide36.87
Placebo Oral Capsule36.69

[back to top]

Alcohol Craving: Visual Analog Scale (VAS) Observation Period, Minute 20

Alcohol craving was measured by self report with the Visual Analog Scale (VAS). The VAS is a straight horizontal line with one end indicating no alcohol craving and the other end indicating intense alcohol craving. The participant marks a point on the line that matches their present amount of alcohol craving. Location of the point on the line is measured for a score range of 0-100. A lower score indicates less craving for alcohol and a higher score indicated more craving for alcohol. (NCT03271528)
Timeframe: 1 minute

Interventionscores on a scale (Mean)
Lacosamide35.31
Placebo Oral Capsule39.75

[back to top]

Alcohol Craving: Visual Analog Scale (VAS) Observation Period, Minute 10

Alcohol craving was measured by self report with the Visual Analog Scale (VAS). The VAS is a straight horizontal line with one end indicating no alcohol craving and the other end indicating intense alcohol craving. The participant marks a point on the line that matches their present amount of alcohol craving. Location of the point on the line is measured for a score range of 0-100. A lower score indicates less craving for alcohol and a higher score indicated more craving for alcohol. (NCT03271528)
Timeframe: 1 minute

Interventionscores on a scale (Mean)
Lacosamide26.75
Placebo Oral Capsule41.87

[back to top]

Alcohol Craving: Alcohol Urge Questionnaire (AUQ) Self-Administration Blocks 1 and 2, Minute 90

The Alcohol Urge Questionnaire (AUQ) is an 8-item self report that measures the participant's urge for an alcoholic drink at the time the questionnaire is completed. Questions are in the form of a 7-point Likert scale (from strongly disagree to strongly agree) and the participant selects the extent to which they disagree or agree with the 8 statements relating to desire to drink, expectation of a desired outcome from drinking, and inability to avoid drinking if alcohol was available. Each of the 8 items is scored 1-7. The total score is calculated by adding the scores for each of the items. The total score range is 8-56. Lower scores indicate less urge for alcohol and higher scores indicate more urge for alcohol. (NCT03271528)
Timeframe: 1 minute

Interventionscore on a scale (Mean)
Lacosamide22.94
Placebo Oral Capsule22.00

[back to top]

Alcohol Consumption in Alcohol Self-Administration Trials

Alcohol consumption will be measured by using a graduated cylinder to determine the amount of alcohol given to the subject that was consumed. This outcome will be measured as standard drink units. A standard drink contains approximately 0.6 fluid ounces of pure alcohol. (NCT03271528)
Timeframe: 2 hours

InterventionStandard Drink Units (SDU) (Mean)
Lacosamide3.02
Placebo Oral Capsule2.35

[back to top]

Number of Participants With an Adverse Event Within First 30 Days After Craniotomy

Adverse events related to LCM, LEV, and no drug within first 30 days after craniotomy. (NCT03436433)
Timeframe: 30 days following surgery

,,
InterventionParticipants (Count of Participants)
DizzinessSomnolenceCognitive disturbanceNauseaVomitingAtaxiaSuicide thoughtSuicide attemptAnxietyDepressionIrritabilityPsychosisPersonality change
Lacosamide1111110010100
Levetiracetam1201000010100
No Anti-epileptic1110000000000

[back to top]

Percentage of Patients With an ED Visit/Hospital Readmission Within 30 Days of Craniotomy

The primary objective of this study is to assess the impact of LCM, LEV or, no AED in patients undergoing craniotomy for suspected new, recurrent or transformed glioma (WHO Gr I-IV) or brain metastasis on ED visits and readmissions within 30 days of craniotomy. (NCT03436433)
Timeframe: 30 days following surgery

InterventionParticipants (Count of Participants)
Lacosamide0
Levetiracetam0
No Anti-epileptic1

[back to top]

Alcohol Craving

Alcohol craving will be measured during Alcohol Drinking Paradigm (ADP) sessions 1, 2 and 3 using the total score of the Alcohol Urge Questionnaire (AUQ). The AUQ has 8 items. Each item is scored on a 1 to 7 scale (Strongly Disagree = 1 and Strongly Agree = 7; items 2 and 7 are reverse scored). Higher scores reflect greater craving. Total score range is from a minimum of 8 to a maximum of 56. The AUQ is administered before study medication and at various times after study medication. The AUQ score reported here is the highest AUQ score following administration of study medication. (NCT03897348)
Timeframe: 3 days (1 day each for ADP Session 1, 2, and 3. Each ADP Session included 1 dose of the drug intervention, either Placebo, Lacosamide 100 mg, or Lacosamide 200 mg).

Interventionscore on a scale (Mean)
Placebo34.7
Lacosamide 100 mg36
Lacosamide 200 mg37.8

[back to top]

Alcohol Consumption (Number of Standard Drinks Consumed)

Alcohol consumption is measured during each of the Alcohol Drinking Paradigm (ADP) sessions, 1, 2 and 3. In each session participants received one of the 3 drug interventions, Placebo, Lacosamide 100 mg, or Lacosamide 200 mg. Consumption was measured using the number of alcoholic standard drinks consumed during the ADP sessions. A standard drink per NIAAA definition is 14 grams of pure alcohol. (NCT03897348)
Timeframe: 3 days (1 day each for ADP Session 1, 2, and 3. Each ADP Session included 1 dose of the drug intervention, either Placebo, Lacosamide 100 mg, or Lacosamide 200 mg).

Interventionstandard drinks (Mean)
Placebo3.44
Lacosamide 100 mg2.84
Lacosamide 200 mg4.46

[back to top]

Retention Feasibility (Proportion of Participants Completing the Alcohol Drinking Paradigm (ADP) Sessions)

Retention feasibility will be measured by the proportion of participants completing the Alcohol Drinking Paradigm (ADP) Sessions 1, 2 and 3. (NCT03897348)
Timeframe: 6.5 weeks

InterventionParticipants (Count of Participants)
Total3

[back to top]

Tolerability (Number of Participants With Mild, Moderate, or Severe Adverse Events)

Tolerability will be measured by the number of participants with mild, moderate, and severe adverse events for each of the 3 drug interventions (100 mg lacosamide, 200 mg lacosamide and placebo). (NCT03897348)
Timeframe: 3 days (1 day each for ADP Session 1, 2, and 3)

,,
InterventionParticipants (Count of Participants)
mild adverse eventsmoderate adverse eventssevere adverse events
Lacosamide 100 mg310
Lacosamide 200 mg311
Placebo110

[back to top]

Subjective Effects of Alcohol Consumption

Subjective effects of alcohol consumption are measured during the Alcohol Drinking Paradigm (ADP) sessions 1, 2 and 3 using the Biphasic Alcohol Effects Scale (BAES), which has 2 subscales; the Stimulation Subscale range is 0 - 70, where 0 is the least and 70 is the greatest stimulation; the Sedation Subscale range is 0 - 70, where 0 is the least and 70 is the greatest sedation. The BAES was administered both before and at various timepoints after study medication administration in each of the ADP sessions. The BAES scores reported here are the peak Stimulation scores after medication administration and peak Sedation scores after medication administration for each of ADP sessions 1, 2 and 3. (NCT03897348)
Timeframe: 3 days (1 day each for ADP Session 1, 2, and 3. Each ADP Session included 1 dose of the drug intervention, either Placebo, Lacosamide 100 mg, or Lacosamide 200 mg).

,,
Interventionscore on a scale (Mean)
Stimulation subscaleSedative subscale
Lacosamide 100 mg44.326.7
Lacosamide 200 mg45.230.5
Placebo31.327.3

[back to top]

Recruitment Feasibility (Time, in Months,) Required to Recruit, Screen and Conduct the Study Procedures

Recruitment feasibility will be measured as the time (in months) required to recruit, screen and conduct the study procedures for a total of 4 participants. (NCT03897348)
Timeframe: 7 months

Interventionmonths (Number)
Total7.0

[back to top]