lamotrigine profile

Lamotrigine is an anticonvulsant medication used to treat epilepsy, bipolar disorder, and nerve pain. It was first synthesized in 1980 by scientists at Wellcome Laboratories. Lamotrigine works by reducing the release of glutamate, an excitatory neurotransmitter, in the brain. This helps to prevent seizures and reduce the symptoms of bipolar disorder. Lamotrigine is generally well-tolerated, but side effects can include dizziness, headache, and skin rash. It is important to note that lamotrigine can interact with other medications, so it is important to talk to your doctor about all the medications you are taking before starting lamotrigine. Lamotrigine is a widely studied drug due to its effectiveness in treating epilepsy and bipolar disorder. Research is ongoing to investigate the potential benefits of lamotrigine for other conditions, such as migraines and chronic pain. '

ID Source	ID
PubMed CID	3878
CHEMBL ID	741
CHEBI ID	6367
SCHEMBL ID	35439
MeSH ID	M0137818

Synonym
BIDD:GT0794
MLS001077325
6-(2,3-dichloro-phenyl)-[1,2,4]triazine-3,5-diamine
6-(2,3-dichloro-phenyl)-[1,2,4]triazine-3,5-diamine(lamotrigine)
bdbm50031299
AKOS005561147
HMS3393C10
HMS3268G17
AB00384359-16
gtpl2622
lamotrigine ,
smr000058464
lamictal
einecs 281-901-8
6-(2,3-dichlorophenyl)-1,2,4-triazine-3,5-diamine
lamictal cd
c9h7cl2n5
3,5-diamino-6-(2,3-dichlorophenyl)-as-triazine
3,5-diamino-6-(2,3-dichlorophenyl)-1,2,4-triazine
lamotrigina [spanish]
lamictal odt
bw-430c
1,2,4-triazine-3,5-diamine, 6-(2,3-dichlorophenyl)-
lamotriginum [latin]
lamictal xr
labileno
bw 430c
eur-1048
EU-0100688
lamotrigine, >=98%, powder
NCGC00015605-01
tocris-1611
NCGC00022936-02
lopac-l-3791
SMP2_000303
MLS000759486
DB00555
lamotrigine (jan/usp/inn)
lamictal (tn)
84057-84-1
D00354
MLS000069685 ,
LOPAC0_000688
NCGC00022936-04
NCGC00022936-05
NCGC00015605-02
NCGC00015605-06
HMS2051C10
L 3791 ,
HMS2093P21
AC-10298
HMS2089M08
gi 267119x; 6-(2,3-dichlorophenyl)-1,2,4-triazine-3,5-diamine
NCGC00015605-08
chebi:6367 ,
CHEMBL741 ,
nsc-759171
lamotrigina
lamotriginum
6-(2,2,4-triazine-3,5-diyldiamine
nsc-746307
nsc746307
STK628377
6-[2,3-bis(chloranyl)phenyl]-1,2,4-triazine-3,5-diamine
A840709
HMS3262I17
hsdb 7526
lamitor
bw430c
nsc 759171
nsc 746307
unii-u3h27498ks
lamotrigine [usan:usp:inn:ban]
u3h27498ks ,
nsc759171
MLS001423991
pharmakon1600-01505610
cas-84057-84-1
dtxcid203195
dtxsid2023195 ,
tox21_110179
L0241
HMS2230L04
CCG-100856
NCGC00015605-04
NCGC00015605-05
NCGC00015605-07
NCGC00015605-03
FT-0602546
NCGC00015605-10
LP00688
lamotrigine [mi]
lamotrigine [usp monograph]
lamotrigine [inn]
lamotrigine [usan]
lamotrigine [ep impurity]
lamotrigine [who-dd]
lamotrigine [usp impurity]
lamotrigine [mart.]
lamotrigine [usp-rs]
1,2,4-triazine-3,5-diamine, 6-(2,3-dichlorophenyl)
lamotrigine [ep monograph]
lamotrigine [hsdb]
lamotrigine [jan]
lamotrigine [orange book]
S3024
HMS3371O16
HY-B0495
3,5-diamino-6-(2,3,-dichlorophenyl)-1,2,4-triazine
3,5-diamino-(2,3-dichlorophenyl)-1,2,4-triazine
NC00106
SCHEMBL35439
NCGC00015605-09
tox21_110179_1
KS-1074
tox21_500688
NCGC00261373-01
ltg ,
F2173-0540
hydroxymethyl progesterone
Q-201221
6-(2,3-dichloro-phenyl)-[1,2,4]tria
zine-3,5-diamine
HB0368
AC-32483
AB00384359_18
OPERA_ID_12
AB00384359_17
mfcd00865333
lamotrigine, united states pharmacopeia (usp) reference standard
HMS3657A17
lamotrigine, pharmaceutical secondary standard; certified reference material
lamotrigine for peak identification, european pharmacopoeia (ep) reference standard
lamotrigine, european pharmacopoeia (ep) reference standard
lamotrigine for system suitability, european pharmacopoeia (ep) reference standard
lamotrigine 1.0 mg/ml in methanol
SR-01000000187-4
sr-01000000187
SR-01000000187-2
SR-01000000187-7
SR-01000000187-10
SBI-0050666.P002
HMS3715H21
lamotrigine, british pharmacopoeia (bp) reference standard
SW197486-3
FT-0670713
Q410346
FT-0670714
ltg;bw430c
BCP12156
BRD-K93460210-071-01-6
A11873
EN300-120680
SDCCGSBI-0050666.P003
HMS3885M03
NCGC00015605-23
NCGC00015605-24
AMY40805
L-205
6-(2,3-dichlorophenyl)-1,2,4-triazine-3,5-diamine.
W13018
epilepax
lamotrigine 100 microg/ml in acetonitrile
BL166799
lamotrigine- bio-x
Z1532338577
lamotrigine chewable dispersible
lamotrigine (ep impurity)
lamotrigine (usan:usp:inn:ban)
lamotrigine er
lamotirigine
n03ax09
lamotrigine extended-release
lamictalodt
lamotriginum (latin)
lamotrigine (mart.)
lamotrigine (usp impurity)
lamotrigine (ep monograph)
lamotrigine (usp monograph)
lamotriginekit
lamictalxr
subvenite
lamotrigine extended release
lamotrigine (usp-rs)
lamotrigine, 1mg/ml in ethanol

Research Excerpts

Overview

Lamotrigine is an antiepileptic drug that can be used to control many types of seizures as a single-agent or an add-on therapy in patients over 2 years of age. It was approved for use in the maintenance treatment of bipolar I disorder to delay the time to recurrence of new mood episodes.

Excerpt	Reference	Relevance
"Lamotrigine is an antiepileptic drug that was Food and Drug Administration approved in 2003 for use in the maintenance treatment of bipolar I disorder to delay the time to recurrence of new mood episodes. "	( Lamotrigine for Treating Anger in Veterans With Posttraumatic Stress Disorder. El-Saden, SM; Thompson, SI, )	3.02
"Lamotrigine (LMT) is a phenyltriazine derivative that was originally described as an antiepileptic drug."	( Lamotrigine-Associated Movement Disorder: A Literature Review. Fornari Caprara, AL; Rissardo, JP, )	3.02
"Lamotrigine (LTG) is an anticonvulsant drug used for the prevention of depressive episodes in bipolar disorder (BD) that might induce manic episodes in some cases. "	( Lamotrigine-induced mania: warning report for the identification of vulnerable populations and expert clinical recommendations for prescription. Amoretti, S; Anmella, G; Fico, G; Hidalgo-Mazzei, D; Murru, A; Pacchiarotti, I; Radua, J; Sagué-Vilavella, M; Verdolini, N; Vieta, E, 2022)	3.61
"Lamotrigine is a commonly prescribed antiepileptic drug. "	( Generic lamotrigine extended-release tablets are bioequivalent to innovator drug in fully replicated crossover bioequivalence study. Fang, L; Jiang, W; Kinjo, M; Li, Z; Lomonaco, S; Zhao, L; Zheng, N, 2023)	2.79
"Lamotrigine is an antiepileptic drug that can be used to control many types of seizures as a single-agent or an add-on therapy in patients over 2 years of age. "	( Lamotrigine induced priapism in children: case analysis and literature review. Cao, SS; Cao, XY; Ge, J; Guan, Y; Mu, F; Qiao, Y; Tang, M; Wang, JW, 2022)	3.61
"Lamotrigine. (LMT) is a triazine drug has an antiepileptic effect but with low water solubility, dissolution rate and thus therapeutic effect. "	( Formulation and characterization of lamotrigine nasal insert targeted brain for enhanced epilepsy treatment. Abdel-Hakeem, M; Abdelkader, G; Abdelmonem, R; El-Enin, HAA, 2023)	2.63
"Lamotrigine (LTG) is a second-generation antiepileptic drug that belongs to Biopharmaceutics Classification System (BCS) class II. "	( Cubosome-based thermosensitive Asfour, MH; Mohsen, AM; Salama, AAA, 2023)	2.35
"Lamotrigine is an effective antiseizure medication that can be used in the management of focal and generalized epilepsies in pediatric patients. "	( Solubility of lamotrigine in age-specific biorelevant media that simulated the fasted- and fed-conditions of the gastric and intestinal environments in pediatrics and adults: implications for traditional, re-formulated, modified, and new oral formulations Daraghmeh, A; Declèves, X; Franco, V; Qassarwi, Y; Saba'aneh, H; Shawahna, R, 2023)	2.71
"Lamotrigine is an excellent therapeutic option in the typical aura without headache."	( [Typical visual aura without headache: a case report.] Madrid Rubí, W; Sanabria Sanchinel, AA, 2019)	1.24
"Lamotrigine is a phenyltriazine medication that has been approved by the United States Food and Drug Administration as monotherapy and as an adjunctive agent for the treatment of seizure disorder. "	( Delirium Secondary to Lamotrigine Toxicity. Catalano, G; Catalano, MC; Fusick, AJ; Gunther, SR; Hernandez, MJ; Sanchez, DL; Sullivan, GA, 2020)	2.32
"Lamotrigine (LAM) is an antiepileptic agent with a relatively mild side effect spectrum, but only available in tablet form on market."	( Investigation of the Absorption of Nanosized lamotrigine Containing Nasal Powder via the Nasal Cavity. Ambrus, R; Bartos, C; Ducza, E; Gáspár, R; Gieszinger, P; Janáky, T; Kecskeméti, G; Márki, Á; Szabó-Révész, P; Sztojkov-Ivanov, A; Tömösi, F, 2020)	1.54
"Lamotrigine (LTG) is an important antiepileptic drug for the treatment of seizures in pregnant women with epilepsy. "	( Cellular uptake properties of lamotrigine in human placental cell lines: Investigation of involvement of organic cation transporters (SLC22A1-5). Furugen, A; Hasegawa, N; Iseki, K; Kobayashi, M; Koishikawa, M; Miyazawa, Y; Narumi, K; Nishimura, A; Ono, K; Umazume, T, 2020)	2.29
"Lamotrigine (LTG) is a new generation antiepileptic drug. "	( Sources of lamotrigine pharmacokinetic variability: A systematic review of population pharmacokinetic analyses. Leelakanok, N; Methaneethorn, J, 2020)	2.39
"Lamotrigine is a broad-spectrum antiepileptic drug with high interindividual variability in serum concentrations in children. "	( Dosing Recommendations for Lamotrigine in Children: Evaluation Based on Previous and New Population Pharmacokinetic Models. Aboura, R; Benaboud, S; Billette de Villemeur, T; Bouazza, N; Chenevier-Gobeaux, C; Desguerre, I; Freihuber, C; Gana, I; Hirt, D; Nabbout, R; Tauzin, M; Tréluyer, JM; Zheng, Y, 2021)	2.36
"Lamotrigine is a valid therapeutic option in the long-term prevention and stabilization of the depressive phases in patients with bipolar I disorder."	( [Lamotrigine in bipolar disorder: preventing depression to treat the disease]. Amore, M; Cuomo, A; Fagiolini, A; Vampini, C, )	1.76
"Lamotrigine is an antiepileptic medication approved as a mood stabilizer for the prevention of depressive episodes in bipolar disorder. "	( [Drug-induced mania and hypomania: analysis of a case of lamotrigine-induced mania]. Grau-López, L; Ortega-Hernández, G; Palma-Álvarez, RF; Pereira-Pinto, A; Ramos-Quiroga, JA, 2021)	2.31
"Lamotrigine is an antiepileptic drug of the phenyltriazine class that is indicated for the prevention of focal and generalized seizures in epileptic patients as well as monotherapy or adjunctive maintenance treatment for Bipolar disorder."	( Lamotrigine and Stevens-Johnson Syndrome Prevention. Crane, E; Edinoff, AN; Fitz-Gerald, MJ; Gennuso, SA; Kaye, AD; Kaye, AM; Kaye, JS; Kaye, RJ; Lewis, K; Nguyen, LH; Pierre, SS; Urits, I; Varrassi, G; Viswanath, O, 2021)	2.79
"Lamotrigine is an antiepileptic drug that has been widely used for epilepsy, as a mood stabilizer (for type 1 bipolar disorder) and in the management of neuropathic pain, it is used both in monotherapy and in complementary therapy. "	( Lamotrigine and its relationship with Stevens-Johnson syndrome and toxic epidermal necrolysis Domínguez-Cherit, J; Méndez-Flores, S; Rodríguez-Chávez, Y; Velázquez-Cárcamo, EA, 2020)	3.44
"Lamotrigine is a phenyltriazine anticonvulsant used to treat epilepsy and bipolar disorder, with species-dependent metabolic profiles. "	( UDP-glucuronosyltransferase 1A4-mediated N2-glucuronidation is the major metabolic pathway of lamotrigine in chimeric NOG-TKm30 mice with humanised-livers. Higuchi, Y; Suemizu, H; Uehara, S; Yamazaki, H; Yoneda, N, 2021)	2.28
"Lamotrigine is an anti-epileptic drug often prescribed to children and young females. "	( Lamotrigine induced lymphadenopathy: Case report and literature review. Cavanagh, JP; Ndikumana, R; Pomeroy, SJ, 2017)	3.34
"Lamotrigine is a second-generation antiepileptic drug, also used as a mood stabilizer. "	( Is it safe to use lamotrigine during pregnancy? A prospective comparative observational study. Diav-Citrin, O; Finkel-Pekarsky, V; Ornoy, A; Shechtman, S; Zvi, N, 2017)	2.23
"Lamotrigine is a novel antiepileptic drug which is also used for antiepileptogenic research."	( Effect of lamotrigine on seizure development in a rat pentylenetetrazole kindling model. Chen, Y; Fang, Z; He, X; Sun, Q; Zhou, L, 2017)	1.58
"Lamotrigine is a broad-spectrum anticonvulsant commonly used to treat seizure and bipolar mood disorders. "	( Acute lamotrigine overdose: a systematic review of published adult and pediatric cases. Alyahya, B; Friesen, M; Laliberté, M; Nauche, B, 2018)	2.4
"Lamotrigine (LTG) is a popular modern antiepileptic drug (AED), however, its mechanism of action has yet to be fully understood, as it is known to modulate many members of several ion channel families. "	( Cav2.3 (R-Type) Calcium Channels are Critical for Mediating Anticonvulsive and Neuroprotective Properties of Lamotrigine In Vivo. Alpdogan, S; Dibué-Adjei, M; Hescheler, J; Kamp, MA; Neiss, WF; Schneider, T; Tevoufouet, EE, 2017)	2.11
"Lamotrigine is an anticonvulsant drug used in the treatment of epilepsy and bipolar disorder. "	( Lamotrigine attenuates the motivation to self-administer ketamine and prevents cue- and prime-induced reinstatement of ketamine-seeking behavior in rats. Chan, MH; Chen, HH; Hsiao, YC; Lee, MY, 2019)	3.4
"Lamotrigine (LTG) is a well-established anticonvulsant that is also approved for the prevention of mood relapses in bipolar disorder. "	( Lamotrigine as a mood stabilizer: insights from the pre-clinical evidence. Miranda, AS; Teixeira, AL, 2019)	3.4
"Lamotrigine is a useful treatment in bipolar depression but requires several weeks of dose titration before its clinical effects can be assessed. "	( Changes in brain Glx in depressed bipolar patients treated with lamotrigine: A proton MRS study. Bargiotas, T; Cowen, PJ; Emir, UE; Godlewska, BR; Masaki, C, 2019)	2.2
"Lamotrigine (LTG) is a widely used anti-epileptic drug that is administered to avoid seizures and to maintain seizure-free status. "	( Determination of lamotrigine in human plasma using liquid chromatography-tandem mass spectrometry. Bito, R; Doi, M; Fukumoto, M; Itabashi, S; Kitaichi, K; Nishina, M; Soda, M; Usui, S, 2019)	2.3
"Lamotrigine is an antiepileptic drug with broad spectrum of actions, also approved for the treatment of bipolar disorder. "	( Lamotrigine abolished aggression in a patient with treatment-resistant posttraumatic stress disorder. Eterović, M; Kozarić-Kovačić, D, )	3.02
"Lamotrigine (LTG) is a popular modern antiepileptic drug (AED); however, its mechanism of action has yet to be fully understood, as it is known to modulate many members of several ion channel families. "	( Cav 2.3 (R-type) calcium channels are critical for mediating anticonvulsive and neuroprotective properties of lamotrigine in vivo. Alpdogan, S; Dibué, M; Hescheler, J; Kamp, MA; Neiss, WF; Schneider, T; Tevoufouet, EE, 2013)	2.04
"Lamotrigine is a phenyltriazine compound that inhibits voltage-gated sodium channels, decreasing release of glutamate and aspartate, and inhibits serotonin, norepinephrine and dopamine reuptake. "	( A case series of patients with lamotrigine toxicity at one center from 2003 to 2012. Burkhart, KK; Donovan, JW; Haggerty, D; Moore, PW, 2013)	2.12
"Lamotrigine is a potentially effective option for patients with SWS with migraine-like headaches."	( Lamotrigine for intractable migraine-like headaches in Sturge-Weber syndrome. Fukui, M; Nomura, S; Shimakawa, S; Tamai, H; Tanabe, T, 2014)	2.57
"Lamotrigine (LTG) is an anticonvulsant drug used in the treatment of epilepsy and bipolar disorder and it has been known that LTG targets voltage-dependent sodium channels (VGSCs). "	( Effect of lamotrigine on Na(v)1.4 voltage-gated sodium channels. Amano, T; Masuko, H; Nakatani, Y, 2013)	2.23
"Lamotrigine is an antiepileptic and mood stabilizing drug that has been detected in wastewater, groundwater, surface water and drinking water, at frequencies in surface water ranging from 47 to 97%. "	( Direct photodegradation of lamotrigine (an antiepileptic) in simulated sunlight--pH influenced rates and products. Borch, T; Chefetz, B; Desyaterik, Y; Liu, A; Young, RB, 2014)	2.14
"Lamotrigine (LTG) is a well-tolerated broad-spectrum antiepileptic drug, which is chemically unrelated to other existing antiepileptic medications. "	( Generalized myoclonus and spasticity induced by lamotrigine toxicity: a case report and literature review. Al-Rabia, MW; Aldarmahi, AA; Algahtani, HA; Almalki, WH; Bryan Young, G, )	1.83
"Lamotrigine (LTG) is a widely used antiepileptic-drug (AED) for the treatment of epilepsy. "	( Effect of comedication on lamotrigine clearance in Korean epilepsy patients. Hong, SB; Joo, EY; Kim, HJ; Kim, TE; Lee, SY; Seo, DW, 2015)	2.16
"Lamotrigine is an anticonvulsant drug used to treat partial and generalized seizure disorders. "	( Liver dysfunction induced by systemic hypersensitivity reaction to lamotrigine: case report. Cho, HJ; Im, SG; Jang, SK; Jeon, DO; Lee, SJ; Oh, MJ; Park, YM; Yoo, SH, 2015)	2.1
"Lamotrigine is a mood stabiliser recommended as combined treatment strategy in clozapine-resistant patients."	( Rapid-onset agranulocytosis in a patient treated with clozapine and lamotrigine. Cubała, WJ; Krysta, K; Landowski, J; Urban, AE; Wiglusz, MS, 2015)	1.37
"Lamotrigine (LTG) is a widely used second-generation antiepileptic drug for long-term therapy of epileptic patients. "	( Coexistence of Fetal Cardiac Malformation and Maternal Drug-Induced Lupus: Is Lamotrigine Safe? Altug, N; Alyamac Dizdar, E; Canpolat, FE; Degirmencioglu, H; Oguz, SS; Sari, FN; Say, B; Uras, N, )	1.8
"Lamotrigine is a safe anti-epileptic drug among pregnant and lactating women. "	( Lamotrigine effects on breastfed infants. Asgarzadeh, L; Dalili, H; Nayeri, F; Shariat, M, 2015)	3.3
"Lamotrigine is an anticonvulsant medication that also has utility in the treatment of bipolar disorder. "	( Lamotrigine Induced Whole Body Tics: A Case Report and Literature Review. Catalano, G; Catalano, MC; Centorino, MB, 2016)	3.32
"Lamotrigine is an effective anticonvulsant drug used in the treatment of epilepsy. "	( [Development and validation of a new HPLC method for determination of Lamotrigine and clinical application]. Charfi, R; El Jebari, H; Gaïes, E; Jebabli, N; Klouz, A; Lakhal, M; Salouage, I; Trabelsi, S, )	1.81
"Lamotrigine (LTG) is an anti-epileptic drug and mood-stabilizing agent, whose adverse effects include skin rash and dizziness. "	( Immunoglobulin A deficiency following treatment with lamotrigine. Hanaya, R; Kawano, Y; Maruyama, S; Okamoto, Y; Toyoshima, M, 2016)	2.13
"Lamotrigine is an ideal alternative drug for children who do not respond to traditional antiepileptic medication or experience significant adverse reactions; however, more high-quality RCTs with a large sample size and a long follow-up time are needed to confirm these conclusions."	( [Lamotrigine monotherapy in children with epilepsy: a systematic review]. Huang, L; Liu, YT; Zeng, LN; Zhang, LL, 2016)	2.79
"Lamotrigine (LTG) is a drug commonly used to treat epilepsy and can also be used to manage mood disorders, such as bipolar disorder. "	( Safety of Long-term Use of Lamotrigine for the Treatment of Psychiatric Disorders. Fujito, H; Inaba, T; Kawashima, T; Matsushima, J; Mizoguchi, Y; Mochinaga, S; Monji, A; Sogawa, R, )	1.87
"Lamotrigine is an anticonvulsant agent that shows clinical antidepressant properties. "	( Pharmacological evidence for the involvement of the NMDA receptor and nitric oxide pathway in the antidepressant-like effect of lamotrigine in the mouse forced swimming test. Ahangari, M; Akbarian, R; Chamanara, M; Dehpour, AR; Jazaeri, F; Nikoui, V; Norouzi-Javidan, A; Ostadhadi, S; Zolfaghari, S, 2016)	2.08
"Lamotrigine (LTG) is a broad-spectrum antiepileptic drug that is widely used in clinic. "	( Effect of lamotrigine on epilepsy-induced cognitive impairment and hippocampal neuronal apoptosis in pentylenetetrazole-kindled animal model. Dong, RF; Tian, S; Wang, WP; Zhang, B; Zhang, C; Zhang, JW, 2017)	2.3
"Lamotrigine is an anti-epileptic drug that has been approved for the maintenance treatment of bipolar disorder."	( Maternal and Fetal Outcomes After Lamotrigine Use in Pregnancy: A Retrospective Analysis from an Urban Maternal Mental Health Centre in New Zealand. Hatters-Friedman, S; Moller-Olsen, C; North, A; Prakash, C, 2016)	1.43
"Lamotrigine (LTG) is an antiepileptic drug that is metabolized via glucuronidation. "	( Hormone replacement therapy with estrogens may reduce lamotrigine serum concentrations: A matched case-control study. Reimers, A, 2017)	2.15
"Lamotrigine (LTG) is a second generation anti-epileptic drug (AED) with broad spectrum of activity, a favourable side-effect profile, simpler dosing than earlier drugs and efficacious in diverse epilepsy syndromes."	( A pharmacological overview of lamotrigine for the treatment of epilepsy. Arjunan, K; Eswaramoorthy, M; Jakki, SL; Nanjan, MJ; Senthil, V; Shanmuganathan, S; Yasam, VR, 2016)	1.44
"Lamotrigine (LTG) is an antiepileptic drug that inhibits the release of glutamate by blocking sodium channels. "	( The effect of lamotrigine on learning in mice using the passive avoidance model. Arab, F; Bijani, A; Izadpanah, F; Kazemi, S; Moghadamnia, AA; Zarghami, A, 2017)	2.26
"Lamotrigine is an antiepileptic drug used for the treatment of epilepsy, bipolar disorder and numerous off-label uses. "	( Identifying the incidence of rash, Stevens-Johnson syndrome and toxic epidermal necrolysis in patients taking lamotrigine: a systematic review of 122 randomized controlled trials. Amber, KT; Bloom, R, )	1.79
"Lamotrigine is an anticonvulsant that appears to have a mainly antidepressant effect and is indicated for the maintenance treatment of bipolar depression. "	( Lamotrigine-induced obsessional symptoms in a patient with bipolar II disorder: a case report. Caykoylu, A; Ekinci, O; Kuloglu, M; Yilmaz, E, 2009)	3.24
"Lamotrigine (LTG) is an antiepileptic drug, a glutamate release inhibitor, with action at the neuronal voltage-gated sodium channel."	( NA+, K+-ATPase activity in the brain of the rats with kainic acid-induced seizures: influence of lamotrigine. Ljubicić, D; Pelcić, JM; Simonić, A; Vitezić, D; Vitezić, M; Zupan, G, 2008)	1.28
"Lamotrigine is a commonly used agent for seizure control in epilepsy. "	( Life-threatening overdose with lamotrigine, citalopram, and chlorpheniramine. Hall, AP; O'Neil, D; Venkatraman, N, )	1.86
"Lamotrigine is an antiepileptic drug that inhibits presynaptic voltage-gated sodium channels and reduces the presynaptic release of glutamate in pathological states. "	( Ultrastructure protection and attenuation of lipid peroxidation after blockade of presynaptic release of glutamate by lamotrigine in experimental spinal cord injury. Dursun, A; Ofluoglu, E; Ozogul, C; Oztanir, N; Pasaoglu, A; Pasaoglu, H; Tufan, K; Uzum, N, 2008)	2
"Lamotrigine is an antiepileptic drug which has been used in the treatment of epilepsy and bipolar disorder. "	( Bioequivalence of generic lamotrigine 100-mg tablets in healthy Thai male volunteers: a randomized, single-dose, two-period, two-sequence crossover study. Longchoopol, C; Oo-Puthinan, S; Sayasathid, J; Srichaiya, A; Sripalakit, P; Viyoch, J, 2008)	2.09
"Lamotrigine is an established anticonvulsant agent and also an effective maintenance therapy for bipolar disorder. "	( Psychiatric symptoms related to the use of lamotrigine: a review of the literature. Bogetto, F; Frieri, T; Rocca, P; Villari, V, )	1.84
"Lamotrigine is a non-aromatic antiepileptic drug. "	( Dress syndrome and fulminant hepatic failure induced by lamotrigine. Amante, MF; Cejas, N; Filippini, AV; Imventarza, O; Lendoire, J; Parisi, C, )	1.82
"Lamotrigine is a commonly used anticonvulsant with a relatively good adverse-effects profile."	( Lamotrigine extends lifespan but compromises health span in Drosophila melanogaster. Avanesian, A; Felgner, JS; Jafari, M; Khodayari, B, 2010)	2.52
"Lamotrigine is a rarely reported and possibly underrecognized cause of aseptic meningitis. "	( Lamotrigine: an unusual etiology for aseptic meningitis. Edelson, DP; Lam, GM; Whelan, CT, 2010)	3.25
"Lamotrigine is a second generation anticonvulsant drug available in France since 1996. "	( [Therapeutic drug monitoring of lamotrigine]. Bentué-Ferrer, D; Tribut, O; Verdier, MC, )	1.86
"Lamotrigine is a newer antiepileptic drug useful as oral adjunctive therapy in refractory epilepsy. "	( Add-on lamotrigine in pediatric epilepsy in India. Jain, R; Juneja, M; Mishra, D, 2011)	2.27
"Lamotrigine (LTG) is a commonly used antiepileptic drug. "	( Hla-B alleles and lamotrigine-induced cutaneous adverse drug reactions in the Han Chinese population. Gao, MM; Liao, WP; Liu, XR; Min, FL; Shi, YW; Yu, MJ; Zan, LX, 2011)	2.15
"Lamotrigine is a sodium channel blocking agent that is widely prescribed for treatment of seizure. "	( Lipid emulsion as rescue therapy in lamotrigine overdose. Castanares-Zapatero, D; Hantson, P; Huberlant, V; Morunglav, M; Wittebole, X, 2012)	2.1
"Lamotrigine is an anti-epileptic drug used as adjunct therapy for seizures. "	( A comparison of two FDA approved lamotrigine immunoassays with ultra-high performance liquid chromatography tandem mass spectrometry. Ford, MA; Johnson-Davis, KL; Juenke, JM; McMillin, GA; Miller, KA, 2011)	2.09
"Lamotrigine is a phenyltriazine derivative used as antiepileptic drug with pharmacological profile similar to phenytoin. "	( [Massive lamotrigine poisoning--case report]. Bazylewicz, A; Kicka, M; Kłopotowski, T; Miśkiewicz, Ł; Picheta, S, 2011)	2.23
"Lamotrigine (LTG) is an anti epileptic medication (AEM) for which blood levels are helpful for optimal dosing. "	( Changed constitution without change in brand name--the risk of generics in epilepsy. Beran, RG; Cordato, DJ; Dias, M; Patel, V, 2012)	1.82
"Lamotrigine was confirmed to be a substrate and inhibitor in OCT1-transfected KCL22 cells."	( Lamotrigine is a substrate for OCT1 in brain endothelial cells. Alfirevic, A; Couraud, PO; Davies, A; Dickens, D; Giannoudis, A; Owen, A; Pirmohamed, M; Romero, IA; Weksler, B, 2012)	2.54
"Lamotrigine is an anticonvulsant and has an antiglutamatergic action, which may contribute to its antidepressant effects, since glutamate has been linked to depression. "	( Lamotrigine treatment reverses depressive-like behavior and alters BDNF levels in the brains of maternally deprived adult rats. Abelaira, HM; Cipriano, AL; Quevedo, J; Réus, GZ; Ribeiro, KF; Scaini, G; Streck, EL; Zappellini, G, 2012)	3.26
"Lamotrigine (LTG) is an antiepileptic drug (AED) that was approved in Japan in 2008. "	( Influence of concomitant antiepileptic drugs on plasma lamotrigine concentration in adult Japanese epilepsy patients. Inoue, Y; Kagawa, Y; Matsuda, K; Takahashi, Y; Yamamoto, Y, 2012)	2.07
"Lamotrigine is a sodium-channel-modulating, antiepileptic drug (AED), which was approved in the USA in 1994 for use in partial-onset seizures. "	( Lamotrigine use in pregnancy. Aggarwal, P; Moore, JL, 2012)	3.26
" Lamotrigine (LTG) is an effective clinical treatment for epilepsy associated with absence seizures. "	( Lamotrigine ameliorates seizures and psychiatric comorbidity in a rat model of spontaneous absence epilepsy. Chen, SD; Huang, HY; Lee, HW; Shaw, FZ, 2012)	2.54
"Lamotrigine is a neuroprotective agent that is used clinically for the treatment of seizures and neuropathic pain. "	( Lamotrigine increases intracellular Ca(2+) levels and Ca(2+)/calmodulin-dependent kinase II activation in mouse dorsal root ganglion neurones. Cho, YW; Han, J; Kang, D; Kim, EJ; Kim, GT; Lee, ES; Park, HJ; Ryu, JH; Tak, HM, 2013)	3.28
"Lamotrigine (LMG) is an anticonvulsant currently registered for the treatment of bipolar disorder (BP) depression. "	( Lamotrigine in binge-eating disorder associated with bipolar II depression and treatment-resistant type 2 diabetes mellitus: a case report. Hirai, A; Iyo, M; Kanahara, N; Watanabe, H; Yamamoto, T, )	3.02
"Lamotrigine is a relatively new aromatic anticonvulsant agent that is thought to act on voltage-dependent sodium channels."	( Prolonged anticonvulsant hypersensitivity syndrome related to lamotrigine in a patient with human immunodeficiency virus. Beller, TC; Boyce, JA, )	1.09
"Lamotrigine is an anti-epileptic agent with broad efficacy. "	( Review of lamotrigine and its clinical applications in epilepsy. Choi, H; Morrell, MJ, 2003)	2.16
"Lamotrigine (LTG) is an antiepileptic drug whose therapeutic effect may be due to inhibition of the excitatory transmitter glutamate release. "	( [Lamotrigine in the treatment of pharmaco-resistant epilepsy in children]. Diaconu, G; Frasin, M; Grigore, I; Moraru, D, )	2.48
"Lamotrigine is an anticonvulsant drug with good efficacy and safety in the treatment of epilepsy. "	( Lamotrigine in mood disorders. Green, B, 2003)	3.2
"Lamotrigine (LTG) is a new antiepileptic drug indicated in all kinds of partial and generalised clonic-tonic seizures, both in monotherapy and polytherapy. "	( [Lamotrigine in refractory epilepsy]. Alvarez-Saúco, M; Asensio-Asensio, M; García-Escrivà, A; López-Hernández, N; Moltó-Jordá, JM; Oliver-Navarrete, C; Palao-Sánchez, A; Pampliega-Pérez, A, )	2.48
"Lamotrigine is an antiepileptic drug for the treatment of partial and generalized seizures as well as bipolar disorder. "	( Evaluation of lamotrigine toxicity reported to poison centers. Klein-Schwartz, W; Lofton, AL, 2004)	2.13
"Lamotrigine is a broad-spectrum antiepileptic agent. "	( Determination of lamotrigine in small volumes of plasma by high-performance liquid chromatography. Cheng, CL; Chou, CH; Hu, OY, 2005)	2.11
"Lamotrigine is a useful add-on therapy in treating children with epilepsy. "	( The use of lamotrigine, vigabatrin and gabapentin as add-on therapy in intractable epilepsy of childhood. Keegan, MB; Madden, D; McDonald, DG; McMenamin, JB; Najam, Y; Whooley, M, 2005)	2.16
"Lamotrigine appears to be a safe and effective agent in the treatment of anger in women with criteria-defined BPD as defined by SCID criteria."	( Lamotrigine treatment of aggression in female borderline-patients: a randomized, double-blind, placebo-controlled study. Lahmann, C; Leiberich, PK; Loew, TH; Nickel, C; Nickel, MK; Rother, WK; Tritt, K, 2005)	2.49
"Lamotrigine is an antiepileptic agent used in a wide range of seizure disorders among the elderly. "	( [Drug hypersensitivity syndrome with lamotrigine two cases in elderly]. Bourdel-Marchasson, I; Jeandel, PY; Rainfray, M; Traissac, T, 2005)	2.04
"Lamotrigine is a relatively newer antiepileptic drug used in the treatment of partial seizures. "	( Food reduces the bioavailability of lamotrigine. Dubey, R; Kumar, H; Saha, N; Sharma, C, 2005)	2.05
"Lamotrigine is a novel anticonvulsant agent that has recently been introduced as a long-term treatment in bipolar disorder. "	( Lamotrigine in the treatment of bipolar disorder. Bhagwagar, Z; Goodwin, GM, 2005)	3.21
"Lamotrigine is an effective drug in clinical practice. "	( Effectiveness of lamotrigine in clinical practice: results of a retrospective population-based study. Deckers, CL; Egberts, AC; Hekster, YA; Keyser, A; Knoester, PD; Renier, WO, 2005)	2.11
"Lamotrigine is a broadly effective antiepileptic drug in mono- and add-on therapy for children and adolescents with focal and generalized epilepsies. "	( [Optimizing epilepsy therapy in children and adolescents with lamotrigine]. Bergmann, L; Brandl, U; Helmstädter, C; Kurlemann, G; Rating, D; Sälke-Kellermann, RA; Siemes, H; Stephani, U; Uberall, M; Wiemer-Kruel, A, )	1.81
"Lamotrigine is an antiepileptic drug that stabilizes neural membranes by blocking the activation of voltage-sensitive sodium channels and inhibiting the presynaptic release of glutamate. "	( Lamotrigine for neuropathic pain. Eisenberg, E; Krivoy, N; Shifrin, A, 2005)	3.21
"Lamotrigine is a relatively new AED which is licensed in many countries for use as an initial monotherapy."	( Lamotrigine versus carbamazepine monotherapy for epilepsy. Gamble, CL; Marson, AG; Williamson, PR, 2006)	2.5
"Lamotrigine is a relatively new anticonvulsant medication approved for seizure and psychiatric disorders."	( Lamotrigine-induced erythema multiforme mimicking contact dermatitis. Abdelmalek, M; Mahindrakar, S; Wiser, E, 2006)	2.5
"Lamotrigine (LTG) is a novel anticonvulsant drug that exerts an antiepileptic effect by decreasing glutamate release through inhibition of voltage-sensitive sodium channels. "	( Hypersexuality in two patients with epilepsy treated with lamotrigine. Grabowska-Grzyb, A; Nagańska, E; Wolańczyk, T, 2006)	2.02
"Lamotrigine (LTG) is an anti-epileptic drug that is widely used clinically in various neuropsychiatric disorders. "	( Effects of lamotrigine on field potentials, propagation, and long-term potentiation in rat prefrontal cortex in multi-electrode recording. Hsieh, YJ; Huang, CC; Huang, CW; Tsai, JJ, 2006)	2.17
"Lamotrigine is an anticonvulsant drug that exhibits a clinical antidepressant effect. "	( Dual monoamine modulation for the antidepressant-like effect of lamotrigine in the modified forced swimming test. Andreatini, R; Consoni, FT; Vital, MA, 2006)	2.02
"Lamotrigine is an anticonvulsant and a mood stabiliser that is more effective at preventing depressive relapses than most other mood stabilising drugs."	( PHARMAC and treatment of bipolar depression--the limits of utilitarianism. Ellis, P; Mulder, R; Porter, R, 2006)	1.06
"Lamotrigine is a novel anticonvulsant initially used in epilepsy treatment. "	( The relevance of monitoring lamotrigine serum concentrations in chronic pain patients. Devulder, J, 2006)	2.07
"Lamotrigine is an antiepileptic drug with a low adverse-effect profile. "	( Maternal lamotrigine treatment and elevated neonatal gamma-glutamyl transpeptidase. Dubnov-Raz, G; Merlob, P; Shapiro, R, 2006)	2.19
"Lamotrigine is an anti-epileptic drug considered as a first-line therapy in idiopathic generalised epilepsy. "	( [Exacerbation of tonicoclonic seizures in a juvenile myoclonic epileptic taking lamotrigine]. Guillon, B; Maiga, Y; Nogues, B, 2006)	2
"Lamotrigine is a broad-spectrum antiepileptic drug, initially approved in 1994 for the adjunctive treatment of partial seizures in adults and for the generalized seizures of Lennox-Gastaut syndrome in pediatric (>2 years old) and adult populations. "	( Lamotrigine and its applications in the treatment of epilepsy and other neurological and psychiatric disorders. Arif, H; Hirsch, LJ; Malik, S, 2006)	3.22
"Lamotrigine is an antiepileptic drug employed in the treatment of partial epilepsies. "	( Lamotrigine is an open-channel blocker of the nicotinic acetylcholine receptor. Barrantes, FJ; Garbus, I; Vallés, AS, 2007)	3.23
"Lamotrigine is an anticonvulsant with antidepressant properties, and reported effectiveness in bipolar depression."	( Lamotrigine in the treatment of recurrent brief depression. Ravindran, AV; Ravindran, LN, 2007)	2.5
"Lamotrigine seems to be a safe and effective option for the treatment of patients with symptoms of affective instability associated with borderline personality disorder."	( Retrospective case review of lamotrigine use for affective instability of borderline personality disorder. Jamison, KL; Weinstein, W, 2007)	2.07
"Lamotrigine is an antiepileptic agent. "	( Lamotrigine-induced seizures in a child: case report and literature review. Anderson, IB; Olson, KR; Stewart, PJ; Thundiyil, JG, 2007)	3.23
"Lamotrigine is an anticonvulsant drug that is also effective in the treatment of mood disorders, especially bipolar disorder. "	( Antidepressant-like effect of lamotrigine in the mouse forced swimming test: evidence for the involvement of the noradrenergic system. Andreatini, R; Binfaré, RW; Kaster, MP; Raupp, I; Rodrigues, AL, 2007)	2.07
"Lamotrigine (LTG) is a generally well-tolerated antiepileptic drug (AED) with broad-spectrum efficacy in several forms of partial and generalized epilepsy and is also licensed for use in bipolar disorder in several countries. "	( Development of psychosis in patients with epilepsy treated with lamotrigine: report of six cases and review of the literature. Boehme, V; Brandt, C; Fueratsch, N; Kramme, C; Pieridou, M; Pohlmann-Eden, B; Villagran, A; Woermann, F, 2007)	2.02
"Lamotrigine is an anti-epileptic drug that blocks the voltage-gated sodium channels of the presynaptic neuron and inhibits the release of glutamate."	( Neuroprotection by lamotrigine in a rat model of neonatal hypoxic-ischaemic encephalopathy. Dagklis, T; Kaiki-Astara, A; Kallaras, K; Kouvelas, D; Papazisis, G; Pourzitaki, C; Tzachanis, D, 2008)	1.4
"Lamotrigine is a clinically used drug, which inhibits Na(+) channel activity that in turn reduces glutamate release. "	( The effects of lamotrigine on alcohol seeking and relapse. Heidbreder, CA; Spanagel, R; Vengeliene, V, 2007)	2.14
"Lamotrigine is a commonly prescribed anticonvulsant medication. "	( Seizures and altered mental status after lamotrigine overdose. Geller, RJ; Schwartz, MD, 2007)	2.05
"Lamotrigine appears to be an effective and relatively safe agent in the longer-term treatment of aggression in women with BPD."	( Lamotrigine treatment of aggression in female borderline patients, Part II: an 18-month follow-up. Leiberich, P; Nickel, MK; Pedrosa Gil, F; Tritt, K, 2008)	2.51
"Lamotrigine is an anticonvulsant drug effective in the treatment of epilepsy and bipolar depression. "	( The effect of lamotrigine on platelet monoamine oxidase type B activity in patients with bipolar depression. Babic, A; Jakovljevic, M; Mihaljevic Peles, A; Muck-Seler, D; Mustapic, M; Nedic, G; Pivac, N; Sagud, M, 2008)	2.15
"Lamotrigine is a potentially very useful anti-epileptic medication in persons with complex partial seizures, but also in primary generalised epilepsy, the Lennox Gastaut syndrome and especially in those individuals who have seizures subsequent to brain damage."	( Lamotrigine: clinical experience in 93 patients with epilepsy. Buchanan, N, 1995)	2.46
"Lamotrigine is a novel antiepileptic that, although its mechanism is not completely understood, appears to affect voltage-activated sodium channels, resulting in inhibition of the presynaptic release of the excitatory neurotransmitter glutamate. "	( Lamotrigine. Burstein, AH, )	3.02
"Lamotrigine is an anticonvulsant drug soon to be introduced to the North American market. "	( Lamotrigine analysis in serum by high-performance liquid chromatography. Camfield, PR; Fraser, AD; Isner, AF; MacNeil, W, 1995)	3.18
"Lamotrigine is an antiepileptic drug which is believed to suppress seizures by inhibiting the release of excitatory neurotransmitters. "	( Lamotrigine. A review of its pharmacological properties and clinical efficacy in epilepsy. Chrisp, P; Goa, KL; Ross, SR, 1993)	3.17
"Lamotrigine appears to be a safe and effective new AED for patients with refractory partial seizures when used as an adjunctive agent. "	( Lamotrigine: an antiepileptic agent for the treatment of partial seizures. Gilman, JT, 1995)	3.18
"LTG, lamotrigine is a new antiepileptic agent chemically unrelated to any established drugs in use. "	( [Lamotrigine: first experience in Italy]. de Romanis, F; Sopranzi, N, 1995)	1.72
"Lamotrigine is an anticonvulsant chemically related to the antifolate compound pyrimidine. "	( Lamotrigine--a novel approach. Meldrum, BS, 1994)	3.17
"Lamotrigine (LTG) is a chemically novel antiepileptic drug (AED) that blocks voltage-sensitive sodium channels, leading to inhibition of neurotransmitter release, principally glutamate. "	( Lamotrigine: a review of antiepileptic efficacy. Yuen, AW, 1994)	3.17
"Lamotrigine is a new antiepileptic agent chemically unrelated to any established drugs in use. "	( Lamotrigine clinical pharmacokinetics. Rambeck, B; Wolf, P, 1993)	3.17
"Lamotrigine is a chemically novel anticonvulsant drug that has been reported to inhibit veratrine-induced neurotransmitter release from cortical slices in vitro. "	( Lamotrigine, phenytoin and carbamazepine interactions on the sodium current present in N4TG1 mouse neuroblastoma cells. Cooper, BR; Lang, DG; Wang, CM, 1993)	3.17
"Lamotrigine is an antiepileptic agent which blocks voltage-dependent sodium channels, thereby preventing excitatory neurotransmitter release. "	( Lamotrigine. An update of its pharmacology and therapeutic use in epilepsy. Fitton, A; Goa, KL, 1995)	3.18
"Lamotrigine seems to be an efficient antiepileptic drug-especially in generalized epilepsy."	( [Treatment of childhood epilepsy with lamotrigine. An evaluation of efficacy in different types of epilepsy]. Sommer, B; Uldall, PV, 1996)	1.29
"1. Lamotrigine is a new antiepileptic drug, chemically unrelated to currently used antiepileptic medication. "	( Influence of concurrent antiepileptic medication on the pharmacokinetics of lamotrigine as add-on therapy in epileptic children. Bidault, R; Cieuta, C; d'Athis, P; Dulac, O; Olive, G; Pariente-Khayat, A; Pons, G; Rey, E; Vauzelle-Kervroëdan, F, 1996)	1.14
"Lamotrigine (LTG) is a novel antiepileptic drug (AED) with a spectrum of activity in animal models of epilepsy similar to that of phenytoin and carbamazepine. "	( Lamotrigine. Messenheimer, JA, 1995)	3.18
"Lamotrigine is a useful alternative in the management of JME."	( The use of lamotrigine in juvenile myoclonic epilepsy. Buchanan, N, 1996)	1.41
"Lamotrigine (LTG) is a new antiepileptic drug (AED), chemically unrelated to the drugs in current use. "	( Serum concentrations of lamotrigine in epileptic patients: the influence of dose and comedication. Jürgens, U; May, TW; Rambeck, B, 1996)	2.04
"Lamotrigine is a very useful antiepileptic medication of a "broad spectrum' nature being effective in primary generalized epilepsy and partial seizures as add-on therapy."	( Lamotrigine: clinical experience in 200 patients with epilepsy with follow-up to four years. Buchanan, N, 1996)	2.46
"Lamotrigine (LAG) is a new antiepileptic drug which is licensed as adjunctive therapy for partial and secondary generalized seizures. "	( Presynaptic inhibition of excitatory neurotransmission by lamotrigine in the rat amygdalar neurons. Gean, PW; Hsu, KS; Huang, CC; Tsai, JJ; Wang, SJ, 1996)	1.98
"Lamotrigine (LAG) is a new anticonvulsant drug for the treatment of partial and secondarily generalized seizures. "	( Inhibition of N-type calcium currents by lamotrigine in rat amygdalar neurones. Gean, PW; Hsu, KS; Huang, CC; Tsai, JJ; Wang, SJ, 1996)	2
"Lamotrigine (LTG) is a recently marketed medication whose pharmacokinetics are significantly influenced by concomitant drugs."	( Lamotrigine pharmacokinetics in patients receiving felbamate. Gidal, BE; Kanner, A; Lensmeyer, GL; Maly, M; Rutecki, P, 1997)	2.46
"Lamotrigine is a new anticonvulsant with few side effects that may have mood-stabilizing and elevating effects."	( The anticonvulsant lamotrigine in treatment-resistant manic-depressive illness. Sachs, G; Sporn, J, 1997)	1.35
"Lamotrigine (lamictal) is a new anticonvulsant drug recently approved by the FDA for clinical use. "	( Lamotrigine analysis in plasma by gas chromatography-mass spectrometry after conversion to a tert.-butyldimethylsilyl derivative. Dasgupta, A; Hart, AP, 1997)	3.18
"Lamotrigine (lamictal) is a new anticonvulsant drug approved by the FDA for clinical use. "	( A rapid cost-effective high-performance liquid chromatographic (HPLC) assay of serum lamotrigine after liquid-liquid extraction and using HPLC conditions routinely used for analysis of barbiturates. Blackwell, W; Dasgupta, A; Hart, AP; Mazarr-Proo, S, 1997)	1.96
"Lamotrigine (LTG) is an anticonvulsant drug whose mechanism of action may involve the inhibition of glutamate release by blocking voltage-dependent sodium channels. "	( Lamotrigine protects hippocampal CA1 neurons from ischemic damage after cardiac arrest. Bergstrand, K; Cooper, AT; Cooper, BR; Crumrine, RC; Faison, WL, 1997)	3.18
"Lamotrigine is a chemically novel antiepileptic drug which has not been adequately assessed for its antineuralgic properties. "	( Lamotrigine (lamictal) in refractory trigeminal neuralgia: results from a double-blind placebo controlled crossover trial. Chaudhry, Z; Mullens, LE; Nurmikko, TJ; Patton, DW; Zakrzewska, JM, 1997)	3.18
"Lamotrigine is a phenyltriazine anticonvulsant recently approved for clinical use. "	( High-performance liquid chromatography quantitation of plasma lamotrigine concentrations: application measuring trough concentrations in patients with epilepsy. Morris, RG; Sallustio, BC, 1997)	1.98
"Lamotrigine is a phenyltriazine derivative with anticonvulsant properties that initially was tested in adults with partial seizures. "	( Adult experience with lamotrigine. Messenheimer, JA; Willmore, LJ, 1997)	2.05
"Lamotrigine is a new antiepileptic drug that may possess unique cognitive and behavioral characteristics. "	( Behavioral and cognitive effects of lamotrigine. Baker, GA; Meador, KJ, 1997)	2.01
"Lamotrigine is a sodium channel blocker that inhibits the neuronal release of glutamate. "	( Effects of intrathecally administered lamotrigine, a glutamate release inhibitor, on short- and long-term models of hyperalgesia in rats. Klamt, JG, 1998)	2.01
"Lamotrigine (LTG) is a valuable addition to the medical management of epilepsy with wide spectrum of efficacy and good outcomes for quality of life. "	( Aggressive behaviour in intellectually challenged patients with epilepsy treated with lamotrigine. Beran, RG; Gibson, RJ, 1998)	1.97
"Lamotrigine is a new antiepileptic drug that acts on amino acid neurotransmitters/neuromodulators, most prominently, glutamine, which has been reported to have potential mood-stabilizing effects."	( Lamotrigine in the treatment of resistant bipolar disorder. Kotler, M; Matar, MA, )	2.3
"Lamotrigine is a weak inducer of UGT."	( A mechanistic approach to antiepileptic drug interactions. Anderson, GD, 1998)	1.02
"Lamotrigine is a novel anticonvulsant drug which also stabilises mood in bipolar illness via an unknown mechanism. "	( Lamotrigine inhibits monoamine uptake in vitro and modulates 5-hydroxytryptamine uptake in rats. Hagan, RM; Higgins, GA; Kirkby, D; Southam, E, 1998)	3.19
"Lamotrigine is an anticonvulsant with a broad spectrum of activity that has been approved in the United States for use in adults with either partial or generalized seizures. "	( Hypersensitivity reaction in a child due to lamotrigine. Appel, JE; Brown, TS; Callen, JP; Kasteler, JS, )	1.84
"Lamotrigine monotherapy is an effective and well-tolerated treatment for bipolar depression."	( A double-blind placebo-controlled study of lamotrigine monotherapy in outpatients with bipolar I depression. Lamictal 602 Study Group. Ascher, JA; Bowden, CL; Calabrese, JR; Monaghan, E; Rudd, GD; Sachs, GS, 1999)	2.01
"Lamotrigine is a new anticonvulsant belonging to the triazine family. "	( [Lyell syndrome and Stevens-Johnson syndrome caused by lamotrigine]. Barzegar, C; Bocquet, H; Bressieux, JM; Farmer, M; Jullien, M; Revuz, J; Roujeau, JC; Soto, B, 1999)	1.99
"Lamotrigine is a relatively new agent, and this report may provide useful insights on evaluating the clinical toxicology of this agent."	( Lamotrigine overdose presenting as anticonvulsant hypersensitivity syndrome. Hollik, DA; Mylonakis, E; Rounds, S; Vittorio, CC, 1999)	2.47
"Lamotrigine is an effective add-on therapy against a range of epileptic seizure types. "	( Lamotrigine monotherapy in newly diagnosed untreated epilepsy: a double-blind comparison with phenytoin. Abbott, R; Dellaportas, CI; Findley, LJ; Gibberd, FB; Gross, M; Park, DM; Perkin, GD; Steiner, TJ, 1999)	3.19
"Lamotrigine (LTG) is an antiepileptic drug (AED) recently released in several countries. "	( Lamotrigine-associated rash: risk/benefit considerations in adults and children. Besag, FM; Brodie, MJ; Dooley, JM; Duchowny, MS; Guberman, AH; Pellock, JM; Richens, A; Stern, RS; Trevathan, E, 1999)	3.19
"Lamotrigine (LTG) is an anti-epileptic drug effective in partial seizures and generalized epilepsy. "	( Lamotrigine in typical absence epilepsy. Buoni, S; Fois, A; Grosso, S, 1999)	3.19
"Lamotrigine is a relatively new anticonvulsant. "	( Postmortem investigation of lamotrigine concentrations. Drummer, OH; King, CV; McIntyre, IM; Opeskin, K; Pricone, MG, 2000)	2.04
"Lamotrigine is a new antiepileptic drug that is effective for a broad range of seizures in adults and children. "	( Potential hepatotoxicity of lamotrigine. Choueiri, R; Fayad, M; Mikati, M, 2000)	2.04
"Lamotrigine (LTG) is a new AED, acting the sodium-channels."	( Plasma and urinary serotonin and 5-HIAA in children treated with lamotrigine for intractable epilepsy. Jović, NJ; Majkić-Singh, N; Milovanović, DD; Mirković, D, 1999)	1.26
"Lamotrigine is a novel anticonvulsant, which has proven to be effective both as add-on and monotherapy. "	( The tolerability of lamotrigine in children. Giorgi, L; Messenheimer, JA; Risner, ME, 2000)	2.07
"Lamotrigine is an antiepileptic agent that blocks use-dependent voltage-sensitive sodium channels, thereby preventing excitatory neurotransmitter release. "	( Lamotrigine. A review of its use in childhood epilepsy. Culy, CR; Goa, KL, )	3.02
"Lamotrigine is a new anticonvulsant chemically unrelated to other existing antiepileptic drugs."	( Hyponatraemia associated with lamotrigine in cranial diabetes insipidus. Aylett, S; Kirkham, F; Mewasingh, L; Stanhope, R, 2000)	1.32
"Lamotrigine is a broad-spectrum antiepileptic drug that blocks sodium channels, thereby inhibiting the pre-synaptic release of excitatory neurotransmitters. "	( Open study evaluating lamotrigine efficacy and safety in add-on treatment and consecutive monotherapy in patients with carbamazepine- or valproate-resistant epilepsy. Jozwiak, S; Terczynski, A, 2000)	2.06
"Lamotrigine (Lamictal) is a new anticonvulsant drug recently approved for use in the United States. "	( Lamotrigine distribution in two postmortem cases. Jufer, RA; Levine, B; Smialek, JE, 2000)	3.19
"Lamotrigine (LTG) is a novel antiepileptic drug effective in partial and generalized seizures. "	( Stevens-Johnson syndrome associated with concomitant use of lamotrigine and valproic acid. Karaduman, A; Yalçin, B, 2000)	1.99
"Lamotrigine is a broad-spectrum antiepileptic drug which is thought to act in part via a use-dependent blockade of voltage-sensitive sodium channels to stabilise the neuronal membrane. "	( [Open study evaluating lamotrigine efficacy and safety in add-on treatment and consecutive monotherapy in adult patients with epilepsy resistant carbamazepine and valproate]. Jóźwiak, S; Mańko, E; Niedzielska, K; Terczyński, A, )	1.88
"3. Lamotrigine is a safe and well-tolerated drug."	( [Open study evaluating lamotrigine efficacy and safety in add-on treatment and consecutive monotherapy in adult patients with epilepsy resistant carbamazepine and valproate]. Jóźwiak, S; Mańko, E; Niedzielska, K; Terczyński, A, )	0.96
"Lamotrigine (LTG) is an anticonvulsant that is currently in use for the treatment of various seizure disorders and that shows promise in the treatment of affective illness. "	( Lamotrigine treatment during amygdala-kindled seizure development fails to inhibit seizures and diminishes subsequent anticonvulsant efficacy. Krupp, E; Li, XL; Post, RM; Postma, T; Weiss, SR, 2000)	3.19
"Oral lamotrigine 200 mg daily is a well tolerated and moderately effective treatment for central poststroke pain. "	( Lamotrigine for central poststroke pain: a randomized controlled trial. Andersen, G; Gottrup, H; Jensen, TS; Kristensen, BT; Vestergaard, K, 2001)	2.27
"Lamotrigine is an antiepileptic agent that has been shown to be an effective adjunctive treatment for refractory partial and generalized seizures. "	( Lamotrigine overdose in an adult. Bateman, DN; O'Donnell, J, 2000)	3.19
"Lamotrigine (LTG) is a new antiepileptic of habitual use in monotherapy as much in partial epileptic as in generalised, which presents among other adverse effects: slight rashes and less frequently severe rashes such as Stevens-Johnson syndrome and Lyell syndrome or toxic epidermal necrolysis, above all in combination with valproate (VPA)."	( [Lyell syndrome associated with lamotrigine]. Fernández-Calvo, C; Olascoaga, J; Resano, A; Tuneu, A; Urcola, J; Zubizarreta, J, )	1.86
"Lamotrigine (LTG) is a new antiepileptic drug that it has proved to be efficacious in treating patients with partial and generalized tonic-clonic seizures in adjunctive and monotherapy. "	( [Lamotrigine in refractory partial and general epilepsies]. Espada, F; Iñiguez, C; Mauri-Llerda, JA; Morales, F; Tejero, C, )	2.48
"Lamotrigine is proving to be an effective agent in the treatment of BD and may be useful for patients who have not responded to other mood stabilizers."	( Lamotrigine: a review of clinical studies in bipolar disorders. Tabarsi, E; Zerjav-Lacombe, S, 2001)	3.2
"Lamotrigine (LAG) is an antiepileptic drug which is believed to suppress seizures by inhibiting the release of excitatory neurotransmitters. "	( Lamotrigine inhibition of glutamate release from isolated cerebrocortical nerve terminals (synaptosomes) by suppression of voltage-activated calcium channel activity. Gean, PW; Sihra, TS; Wang, SJ, 2001)	3.2
"Lamotrigine is an anticonvulsant with an efficacy profile in psychiatric disorders different from those of valproate, carbamazepine and gabapentine. "	( [Lamotrigine in the treatment of mental disorders]. Fladvad, T; Malt, UF, 2001)	2.66
"Lamotrigine is an anticonvulsant drug recently approved in Italy for clinical use. "	( New high-performance liquid chromatographic method for plasma/serum analysis of lamotrigine. Bernardi, G; Croci, D; de Grazia, U; Salmaggi, A, 2001)	1.98
"Lamotrigine (LTG) is an antiepileptic drug that is also effective in the treatment of certain psychiatric disorders. "	( Lamotrigine reduces spontaneous and evoked GABAA receptor-mediated synaptic transmission in the basolateral amygdala: implications for its effects in seizure and affective disorders. Aroniadou-Anderjaska, V; Braga, MF; Li, H; Post, RM, 2002)	3.2
"Lamotrigine is a useful and well tolerated drug for partial seizures and infantile spasms in infants <1 year of age. "	( Efficacy, tolerability, and kinetics of lamotrigine in infants. Fayad, M; Hussein, R; Kazma, A; Koleilat, M; Mikati, MA; Mounla, N; Yunis, K, 2002)	2.02
"Lamotrigine (LTG) is a new antiepileptic drug which is effective in refractory epilepsy and which has been shown to have weak antifolate properties in vitro. "	( An assessment of serum and red blood cell folate concentrations in patients with epilepsy on lamotrigine therapy. Patsalos, PN; Sander, JW, 1992)	1.95
"Lamotrigine is a novel antiepileptic drug, chemically unrelated to the major anticonvulsants in current use."	( Lamotrigine as an add-on drug in the management of Lennox-Gastaut syndrome. Richens, A; Timmings, PL, 1992)	2.45
"Lamotrigine (LTG) is a novel triazine anticonvulsant currently undergoing clinical trials. "	( Isolation and characterization of a novel quaternary ammonium-linked glucuronide of lamotrigine. Remmel, RP; Sinz, MW, )	1.8
"Lamotrigine is a low clearance drug (Cl = 2.51 +/- 0.063 ml/min/kg) with a large volume of distribution (Vss = 2.23 +/- 0.403 liter/kg)."	( A quaternary ammonium glucuronide is the major metabolite of lamotrigine in guinea pigs. In vitro and in vivo studies. Remmel, RP; Sinz, MW, )	1.09
"Lamotrigine is an investigational anticonsulvant drug undergoing clinical trials. "	( Analysis of lamotrigine and lamotrigine 2-N-glucuronide in guinea pig blood and urine by reserved-phase ion-pairing liquid chromatography. Remmel, RP; Sinz, MW, 1991)	2.1

Effects

Lamotrigine (LTG) has a broad spectrum of antiepileptic efficacy and generally benign side effects except for idiosyncratic rashes. It has a modulating effect on glutamatergic neurotransmission relevant to pathophysiology of both schizophrenia and OCD.

Lamotrigine has a favorable pharmacokinetic profile, including a long half-life, low serum protein binding, and lack of mixed-function oxidase enzyme induction. It has not been associated with an increased risk for major malformations in monotherapy in most available studies.

Excerpt	Reference	Relevance
"Lamotrigine (LTG) has a good efficacy and tolerability as initial monotherapy for patients with newly diagnosed epilepsy (NDE). "	( Depression in patients with newly diagnosed epilepsy predicts lamotrigine-induced rash: a short-term observational study. Park, SP, 2013)	2.07
"Lamotrigine has a modulating effect on glutamatergic neurotransmission relevant to pathophysiology of both schizophrenia and OCD."	( Lamotrigine augmentation in schizophrenia and schizoaffective patients with obsessive-compulsive symptoms. Glick, I; Koran, LM; Poyurovsky, M, 2010)	2.52
"Lamotrigine has a marked suppressive effect which correlates with its rather selective action on the migraine aura."	( Migraine preventive drugs differentially affect cortical spreading depression in rat. Bogdanov, VB; Bogdanova, OV; Chauvel, V; Makarchuk, MY; Multon, S; Prodanov, D; Schoenen, J, 2011)	1.09
"Lamotrigine (LTG) which has a widespread use in epilepsy treatment as an antiepileptic agent is metabolized by UDP-glucuronosyl transferase (UGT) enzymes. "	( The relationship between UGT1A4 polymorphism and serum concentration of lamotrigine in patients with epilepsy. Aker, RG; Goren, MZ; Gulcebi, MI; Onat, FY; Ozkara, C; Ozkaynakcı, A, 2011)	2.04
"Lamotrigine has a wide clinical dose range and possesses favourable pharmacokinetic properties."	( Review of lamotrigine and its clinical applications in epilepsy. Choi, H; Morrell, MJ, 2003)	1.44
"Lamotrigine has a preferable side-effect profile compared to standard agents for bipolar affective disorder such as lithium or carbamazepine."	( Lamotrigine in mood disorders. Green, B, 2003)	2.48
"Lamotrigine has a variable profile in kindling and contingent tolerance experiments and does not appear to have robust gamma-aminobutyric acid or monoaminergic actions."	( Potential mechanisms of action of lamotrigine in the treatment of bipolar disorders. Ketter, TA; Manji, HK; Post, RM, 2003)	1.32
"Lamotrigine has a side-effect profile compatible with treatment adherence and is well tolerated in combination therapy."	( Depression mood stabilisation: novel concepts and clinical management. Calabrese, JR, 2004)	1.04
"Lamotrigine has a favorable pharmacokinetic profile, including a long half-life, low serum protein binding, and lack of mixed-function oxidase enzyme induction."	( Lamotrigine: an antiepileptic agent for the treatment of partial seizures. Gilman, JT, 1995)	2.46
"Lamotrigine has a favourable pharmacokinetic profile."	( Lamotrigine--a novel approach. Meldrum, BS, 1994)	2.45
"Lamotrigine (LTG) has a broad spectrum of antiepileptic efficacy and generally benign side effects except for idiosyncratic rashes."	( Lamotrigine-induced tourettism. Lombroso, CT, 1999)	3.19
"Lamotrigine has a relatively slow penetration into both CSF and bECF compartments compared with antiepileptic drugs used in acute seizures."	( Comparison of serum, cerebrospinal fluid and brain extracellular fluid pharmacokinetics of lamotrigine. Alavijeh, MS; Patsalos, PN; Perry, H; Tong, X; Walker, MC, 2000)	1.25
"Lamotrigine has also been associated with the development of mental status changes, frequently when used concurrently with other medications that may impact the metabolism of lamotrigine."	( Delirium Secondary to Lamotrigine Toxicity. Catalano, G; Catalano, MC; Fusick, AJ; Gunther, SR; Hernandez, MJ; Sanchez, DL; Sullivan, GA, 2020)	1.59
"Lamotrigine has been used for patients with epilepsy and/or bipolar disorder, overdose of which induced the hypotension, elevation of the atrial pacing threshold, cardiac conduction delay, wide complex tachycardia, cardiac arrest and Brugada-like electrocardiographic pattern. "	( Reverse translational analysis of clinically reported, lamotrigine-induced cardiovascular adverse events using the halothane-anesthetized dogs. Goto, A; Hagiwara-Nagasawa, M; Izumi-Nakaseko, H; Kambayashi, R; Kawai, S; Matsumoto, A; Nunoi, Y; Sugiyama, A; Takei, Y, 2021)	2.31
"Lamotrigine, has shown significant efficacy in preventing or delaying the onset of depressive episodes in bipolar disease. "	( [Lamotrigine in bipolar disorder: preventing depression to treat the disease]. Amore, M; Cuomo, A; Fagiolini, A; Vampini, C, )	2.48
"Lamotrigine has acute antidepressant effects in patients with bipolar disorder. "	( Correlation between the Efficacy of Lamotrigine and the Serum Lamotrigine Level during the Remission Phase of Acute Bipolar II Depression: A Naturalistic and Unblinded Prospective Pilot Study. Aiba, T; Hiraki, K; Kikkawa, A; Kitamura, Y; Sendo, T, 2017)	2.17
"Lamotrigine has also been reported to have similar efficacy to and better tolerability than carbamazepine."	( Comparison of lamotrigine and oxcarbazepine monotherapy for pediatric focal epilepsy: An observational study. Hur, YJ, 2018)	1.56
"Lamotrigine (LTG) has been widely prescribed as an antipsychotic drug, although it causes idiosyncratic drug-induced liver injury in humans. "	( Strain and interindividual differences in lamotrigine-induced liver injury in mice. Akai, S; Oda, S; Yokoi, T, 2019)	2.22
"Lamotrigine has become the most frequently prescribed drug in the treatment of pregnant women with epilepsy. "	( A Short Communication: Lamotrigine Levels in Milk, Mothers, and Breastfed Infants During the First Postnatal Month. Brozmanova, H; Grundmann, M; Kacirova, I, 2019)	2.27
"Lamotrigine has been reported to cause DIHS in adults in China, but less in children."	( [Lamotrigine induced hypersensitivity syndrome in children: a case report]. Cui, NX; Zhu, XP, 2019)	2.15
"Lamotrigine (LTG) has a good efficacy and tolerability as initial monotherapy for patients with newly diagnosed epilepsy (NDE). "	( Depression in patients with newly diagnosed epilepsy predicts lamotrigine-induced rash: a short-term observational study. Park, SP, 2013)	2.07
"Lamotrigine (LTG) has been recognized as one of the best newer antiepileptic drugs (AEDs) used in developed countries since 1991. "	( [Effectiveness and role of lamotrigine in the paradigm shift towards new antiepileptic drugs: a therapeutic strategy proposed after an investigation of a large number of cases at a single hospital]. Enoki, H; Fujimoto, A; Kobayashi, R; Ohashi, T; Okanishi, T; Tanaka, T; Uchiyama, G; Yamamoto, T; Yamazoe, T; Yokota, T, 2014)	2.14
"Lamotrigine has been considered a safe new-generation antiepileptic drug during the perinatal period for both mothers and infants. "	( Hypotonia and poor feeding in an infant exposed to lamotrigine and valproic acid in utero. Bayhan, C; Celik, T; Takcı, S; Yiğit, S, )	1.83
"Lamotrigine (LTG) has shown benefits in animal models of cerebral ischemia, but the mechanism involved was not fully studied. "	( Lamotrigine attenuates cerebral ischemia-induced cognitive impairment and decreases β-amyloid and phosphorylated tau in the hippocampus in rats. Han, H; Qian, Q; Sun, G; Yu, Y; Zhao, D, 2015)	3.3
"Lamotrigine (LTG) has shown to confer broad-spectrum, well-tolerated control of epilepsy. "	( Efficacy and safety of lamotrigine monotherapy in children and adolescents with epilepsy. Hardison, HH; Khurana, DS; Kothare, SV; Legido, A; Marks, HG; Melvin, JJ; Piñol-Ripoll, G; Valencia, I, 2009)	2.11
"Lamotrigine has showed good efficacy and safety profile."	( Use of lamotrigine in medically intractable epilepsies in children. Catibusic, F; Cengic, A; Uzicanin, S; Zubcevic, S, 2008)	1.52
"Lamotrigine has been shown to be useful in the long-term prophylaxis of depressive episodes in BD."	( Lamotrigine-associated rash: to rechallenge or not to rechallenge? Bhagwagar, Z; Lorberg, B; Youssef, NA, 2009)	2.52
"Lamotrigine (LTG) has been used in epilepsia patients for treatment of partial seizures. "	( Unilateral radius aplasia due to lamotrigine and oxcarbazepine use in pregnancy. Cetinkaya, M; Köksal, N; Ozkan, H, 2008)	2.07
"Lamotrigine has a modulating effect on glutamatergic neurotransmission relevant to pathophysiology of both schizophrenia and OCD."	( Lamotrigine augmentation in schizophrenia and schizoaffective patients with obsessive-compulsive symptoms. Glick, I; Koran, LM; Poyurovsky, M, 2010)	2.52
"Lamotrigine treatment has been associated with multiorgan failure, DRESS syndrome, acute hepatic failure, and disseminated intravascular coagulation."	( Dress syndrome and fulminant hepatic failure induced by lamotrigine. Amante, MF; Cejas, N; Filippini, AV; Imventarza, O; Lendoire, J; Parisi, C, )	1.1
"Lamotrigine has the advantage to have an antidepressive effect and to be well tolerated in the majority of the cases. "	( Lamotrigine-trigged obstructive hypertrophic cardiomyopathy, epilepsy and metabolic myopathy. Finsterer, J; Höftberger, R; Stöllberger, C, 2011)	3.25
"Lamotrigine has the ability to cause seizures in children from acute single ingestion at a lower dose than previously described. "	( Seizures secondary to lamotrigine toxicity in a two-year-old. Banks, CJ; Close, BR, 2010)	2.12
"Lamotrigine has been widely used, mainly due to their greater tolerability and lower rate of drug interactions with other antiepileptic drugs however the newest antiepileptic drugs have high cost to patient."	( [Interchangeability among therapeutics equivalents of lamotrigine in the treatment of refractory epilepsy patients: risks and benefits]. Alexandre, V; Feletti, F; Girolineto, BM; Pereira, LR; Queiroz, RH; Sakamoto, AC, 2010)	1.33
"Lamotrigine has a marked suppressive effect which correlates with its rather selective action on the migraine aura."	( Migraine preventive drugs differentially affect cortical spreading depression in rat. Bogdanov, VB; Bogdanova, OV; Chauvel, V; Makarchuk, MY; Multon, S; Prodanov, D; Schoenen, J, 2011)	1.09
"Lamotrigine (LTG) which has a widespread use in epilepsy treatment as an antiepileptic agent is metabolized by UDP-glucuronosyl transferase (UGT) enzymes. "	( The relationship between UGT1A4 polymorphism and serum concentration of lamotrigine in patients with epilepsy. Aker, RG; Goren, MZ; Gulcebi, MI; Onat, FY; Ozkara, C; Ozkaynakcı, A, 2011)	2.04
"Lamotrigine has been postulated to be delivered to its site of action in the brain favourably despite its physicochemical properties."	( Lamotrigine is a substrate for OCT1 in brain endothelial cells. Alfirevic, A; Couraud, PO; Davies, A; Dickens, D; Giannoudis, A; Owen, A; Pirmohamed, M; Romero, IA; Weksler, B, 2012)	2.54
"Lamotrigine has gained widespread use in the USA as both an immediate and an extended-release agent."	( Lamotrigine use in pregnancy. Aggarwal, P; Moore, JL, 2012)	2.54
"Lamotrigine has been demonstrated to be effective as both an antiepileptic drug and a mood stabiliser. "	( Lamotrigine in epilepsy, pregnancy and psychiatry--a drug for all seasons? Dodd, S; Horgan, D; Vajda, FJ, 2013)	3.28
"Lamotrigine has certain advantages over carbamazepine for treatment of epilepsy as it has less side effects and higher tolerability. "	( Effectiveness and safety assessment of lamotrigine monotherapy for treatment of epilepsy. Gao, F; He, H; Jiang, W; Li, XW; Liu, YF; Ma, L; Meng, XD; Wei, D, 2012)	2.09
"Lamotrigine has benefits in bipolar disorder management principally as a component of combination treatment which includes a mood stabilizer. "	( Lamotrigine (Lamictal IR) for the treatment of bipolar disorder. Bowden, CL; Singh, V, 2012)	3.26
"Lamotrigine (LTG) has become established as an important new drug in treating a wide spectrum of seizure types, but there are no published data on whether LTG serum concentrations change when TPM is added to treatment."	( Lack of an effect of topiramate on lamotrigine serum concentrations. Berry, DJ; Besag, FM; Doose, D; Natarajan, J; Pool, F, 2002)	1.31
"Lamotrigine has been reported to be effective in relieving pain from trigeminal neuralgia refractory to other treatments, HIV neuropathy, and central post-stroke pain."	( Use of anticonvulsants for treatment of neuropathic pain. Backonja, MM, 2002)	1.04
"Lamotrigine has undergone a remarkable series of systematic studies since 1994 that now establish it as an efficacious, well-tolerated treatment in bipolar disorder. "	( Lamotrigine in the treatment of bipolar disorder. Bowden, CL, 2002)	3.2
"Lamotrigine has been found to have acute efficacy in treating episodes of bipolar depression without increasing cycling or provoking a switch into mania, as well as a long-term role in delaying relapse and recurrence of depressive episodes."	( Long-term treatment of bipolar disorder with lamotrigine. Calabrese, JR; Elhaj, O; Kimmel, SE; Rapport, DJ; Shelton, MD, 2002)	1.3
"Lamotrigine has a wide clinical dose range and possesses favourable pharmacokinetic properties."	( Review of lamotrigine and its clinical applications in epilepsy. Choi, H; Morrell, MJ, 2003)	1.44
"Lamotrigine has been shown to be an effective treatment for bipolar depression and rapid cycling in placebo-controlled clinical trials. "	( A placebo-controlled 18-month trial of lamotrigine and lithium maintenance treatment in recently manic or hypomanic patients with bipolar I disorder. Asghar, SA; Bowden, CL; Calabrese, JR; DeVeaugh-Geiss, J; Earl, N; Hompland, M; Montgomery, P; Sachs, G; Smoot, TM; Yatham, LN, 2003)	2.03
"Lamotrigine has a preferable side-effect profile compared to standard agents for bipolar affective disorder such as lithium or carbamazepine."	( Lamotrigine in mood disorders. Green, B, 2003)	2.48
"Lamotrigine has not demonstrated efficacy in the treatment of acute mania."	( Lamotrigine: a review of its use in bipolar disorder. Goldsmith, DR; Ibbotson, T; Perry, CM; Wagstaff, AJ, 2003)	2.48
"Lamotrigine has been shown to be an effective maintenance therapy for patients with bipolar I disorder, significantly delaying time to intervention for any mood episode. "	( Lamotrigine: a review of its use in bipolar disorder. Goldsmith, DR; Ibbotson, T; Perry, CM; Wagstaff, AJ, 2003)	3.2
"Lamotrigine has a variable profile in kindling and contingent tolerance experiments and does not appear to have robust gamma-aminobutyric acid or monoaminergic actions."	( Potential mechanisms of action of lamotrigine in the treatment of bipolar disorders. Ketter, TA; Manji, HK; Post, RM, 2003)	1.32
"Lamotrigine has not demonstrated efficacy in the treatment of acute mania."	( Spotlight on lamotrigine in bipolar disorder. Goldsmith, DR; Ibbotson, T; Perry, CM; Wagstaff, AJ, 2004)	1.41
"Lamotrigine has been shown to be an effective maintenance therapy for patients with bipolar I disorder, significantly delaying time to intervention for any mood episode. "	( Spotlight on lamotrigine in bipolar disorder. Goldsmith, DR; Ibbotson, T; Perry, CM; Wagstaff, AJ, 2004)	2.14
"Lamotrigine has demonstrated efficacy for the acute treatment of depression in bipolar I patients in a placebo-controlled, monotherapy study. "	( A 52-week, open-label continuation study of lamotrigine in the treatment of bipolar depression. Ascher, J; Cookson, J; Greene, P; Huffman, RF; McElroy, SL; Suppes, T; Zarate, CA, 2004)	2.03
"Lamotrigine has a side-effect profile compatible with treatment adherence and is well tolerated in combination therapy."	( Depression mood stabilisation: novel concepts and clinical management. Calabrese, JR, 2004)	1.04
"Lamotrigine has demonstrated efficacy in delaying time to depressive relapse."	( Rethinking the treatment paradigm for bipolar depression: the importance of long-term management. Baldassano, CF; Ballas, CA; O'Reardon, JP, 2004)	1.04
"Lamotrigine has also demonstrated significant efficacy in recent studies and has been approved by the FDA."	( Bipolar depression: an overview. Oral, ET; Vahip, S, 2004)	1.04
"Lamotrigine has emerged as a first line treatment for bipolar depression, which is an area of weakness for other mood stabilizers."	( Separate and concomitant use of lamotrigine, lithium, and divalproex in bipolar disorders. Goodwin, FK; Lieberman, DZ, 2004)	1.33
"Lamotrigine has been suggested as possibly effective for preventing migraine aura."	( Preventing disturbing migraine aura with lamotrigine: an open study. Caminero, AB; García-Moncó, C; Laínez, MJ; Leira, R; Mateos, V; Pascual, J; Roig, C, )	1.84
"Lamotrigine has been shown in randomized controlled studies to be efficacious in preventing bipolar depression and rapid cycling states."	( Sustained remission with lamotrigine augmentation or monotherapy in female resistant depressives with mixed cyclothymic-dysthymic temperament. Connor, PD; Cunningham, PD; Haykal, RF; Jackson, WC; Long, S; Manning, JS, 2005)	1.35
"Lamotrigine has recently been reported as an effective first line therapy."	( SUNCT syndrome: Short-lasting Unilateral Neuralgiform headache with Conjunctival injection and Tearing. Alore, PL; Jay, WM; Macken, MP, )	0.85
"Lamotrigine has benefit in bipolar depression and maintenance, but not in mania."	( Anticonvulsants in bipolar disorder. Bowden, CL; Karren, NU, 2006)	1.06
"Lamotrigine has demonstrated efficacy from published randomized clinical trials for childhood partial seizures, absence seizures, and for the generalized seizures associated with Lennox-Gastaut syndrome."	( Lamotrigine adjunctive therapy among children and adolescents with primary generalized tonic-clonic seizures. Hammer, AE; Kerls, SP; Messenheimer, JA; Trevathan, E; Vuong, A, 2006)	2.5
"If lamotrigine (LTG) has to be replaced with valproate (VPA), this exchange may be complicated by adverse events that result from the complex interaction of both drugs. "	( How to replace lamotrigine with valproate. Steinhoff, BJ, 2006)	1.31
"Lamotrigine has good absorption, minimal plasma protein binding and linear pharmacokinetics."	( Pharmacokinetics, toxicology and safety of lamotrigine in epilepsy. Biton, V, 2006)	1.32
"Lamotrigine has demonstrated particular benefit in the treatment of women and elderly patients with epilepsy."	( Lamotrigine and its applications in the treatment of epilepsy and other neurological and psychiatric disorders. Arif, H; Hirsch, LJ; Malik, S, 2006)	2.5
"Lamotrigine (LTG) has recently been shown to inhibit the cardiac rapid delayed rectifier potassium ion current (Ikr). "	( Lamotrigine in idiopathic epilepsy - increased risk of cardiac death? Aurlien, D; Gjerstad, L; Taubøll, E, 2007)	3.23
"Lamotrigine has been shown to be effective in preventing migraine aura symptoms in typical aura and in some cases of BM."	( Basilar-type migraine responsive to lamotrigine: three case reports. Bussone, G; Casucci, G; Cologno, D; d'Onofrio, F; Petretta, V, 2007)	1.34
"Lamotrigine has obtained approval in several countries for the indication of preventing bipolar depressive episodes, which raises the question of differential efficacy of other antiepileptic drugs as mood stabilizers in the prevention of either depressive or hypo-/manic episodes."	( Antiepileptic drugs and mood stability. Amann, B; Grunze, H; Trimble, M; Vieta, E, 2007)	1.06
"Lamotrigine has been reported to exacerbate seizures and myoclonic seizures in generalized epilepsy in a child with localization-related epilepsy."	( Lamotrigine intoxication provoking status epilepticus in an adult with localization-related epilepsy. Dinnerstein, E; Jobst, BC; Williamson, PD, 2007)	2.5
"Lamotrigine (LTG) has not been associated with an increased risk for major malformations in monotherapy in most available studies. "	( Teratogenicity of lamotrigine. Koren, G; Nulman, I; Shor, S, 2007)	2.12
"Lamotrigine has been found to be efficacious in the acute management of bipolar depression and long-term management of bipolar disorder, especially in delaying depressive recurrence, either as monotherapy or as adjunctive therapy. "	( Antidepressant-like effect of lamotrigine is reversed by veratrine: a possible role of sodium channels in bipolar depression. Bourin, M; Hascoet, M; Prica, C, 2008)	2.08
"Lamotrigine (LTG) has recently been approved for marketing in Australia as add-on therapy in resistant partial seizure disorders. "	( Routine use of lamotrigine, a new anti-epileptic medication, and the value of measuring its blood levels. Beran, RG; Sheehan, K; Tilley, MI, 1994)	2.08
"Lamotrigine has been licensed widely as adjunctive therapy for partial and secondary generalised seizures. "	( Double-blind comparison of lamotrigine and carbamazepine in newly diagnosed epilepsy. UK Lamotrigine/Carbamazepine Monotherapy Trial Group. Brodie, MJ; Richens, A; Yuen, AW, 1995)	2.03
"Lamotrigine has a favorable pharmacokinetic profile, including a long half-life, low serum protein binding, and lack of mixed-function oxidase enzyme induction."	( Lamotrigine: an antiepileptic agent for the treatment of partial seizures. Gilman, JT, 1995)	2.46
"Lamotrigine has a favourable pharmacokinetic profile."	( Lamotrigine--a novel approach. Meldrum, BS, 1994)	2.45
"Lamotrigine (LTG) has a broad spectrum of antiepileptic efficacy and generally benign side effects except for idiosyncratic rashes."	( Lamotrigine-induced tourettism. Lombroso, CT, 1999)	3.19
"Lamotrigine has also been shown to cause encephalopathy and thus neurotoxicity."	( Postmortem investigation of lamotrigine concentrations. Drummer, OH; King, CV; McIntyre, IM; Opeskin, K; Pricone, MG, 2000)	1.32
"Lamotrigine has a relatively slow penetration into both CSF and bECF compartments compared with antiepileptic drugs used in acute seizures."	( Comparison of serum, cerebrospinal fluid and brain extracellular fluid pharmacokinetics of lamotrigine. Alavijeh, MS; Patsalos, PN; Perry, H; Tong, X; Walker, MC, 2000)	1.25
"Lamotrigine has the most evidence in favor of its efficacy, with two double-blind studies in which it was more efficacious than placebo in the treatment of bipolar depression."	( Novel anticonvulsants: a new generation of mood stabilizers? Gaughan, S; Ghaemi, SN, )	0.85
"Lamotrigine has demonstrated efficacy in both acute bipolar depression and maintenance efficacy in rapid cycling bipolar patients, especially those patients with bipolar II disorder, which is principally manifested as depression."	( Novel treatments for bipolar disorder. Bowden, CL, 2001)	1.03
"Lamotrigine has one basic site (pK(A) 5.5) and inhibited 34% of the HVA current, with similar potency over the pH range 6.4--7.4 (IC(50) 7.5--9 microM)."	( Effects of extracellular pH on the interaction of sipatrigine and lamotrigine with high-voltage-activated (HVA) calcium channels in dissociated neurones of rat cortex. Bernardi, G; Hainsworth, AH; Lavaroni, F; Spadoni, F; Stefani, A, 2001)	1.27
"Lamotrigine has neuroprotective effect during HCA. "	( Lamotrigine plus leukocyte filtration as a neuroprotective strategy in experimental hypothermic circulatory arrest. Anttila, V; Biancari, F; Hirvonen, J; Jäntti, V; Juvonen, T; Kiviluoma, KT; Ohtonen, P; Pokela, M; Rimpiläinen, J; Romsi, P; Vainionpää, V, 2002)	3.2
"Lamotrigine has positive effects on cognitive function, but occasionally produces insomnia."	( Lamotrigine update and its use in mood disorders. Hurley, SC, 2002)	2.48

Actions

Lamotrigine does not cause significant change in the pharmacokinetics of lithium. It can cause drug-related hypersexuality by an unclear underlying mechanism.

Excerpt	Reference	Relevance
"Lamotrigine toxicity can cause coma, seizures, and intraventricular conduction disturbances, and treatment options include good supportive care. "	( Effectiveness of multiple-dose activated charcoal in lamotrigine poisoning: a case series. Haga, Y; Hanazawa, T; Hatanaka, K; Kamijo, Y; Kitamoto, T; Ochiai, H; Yoshizawa, T, 2022)	2.41
"Lamotrigine can cause pneumonitis, and this side effect should be suspected in patients who are being treated with lamotrigine and presenting with progressive dyspnoea."	( [Lamotrigine-induced pneumonitis]. Davidsen, JR; Madsen, HD, 2016)	2.07
"Lamotrigine, known to increase Ih, reversed the impact of KA on burst duration in CA1 at both time-points linking a transcriptional reduction in HCN2 function to increased burst duration."	( Excitotoxic-mediated transcriptional decreases in HCN2 channel function increase network excitability in CA1. Adams, BE; Myers, D; Ng, C; O'Brien, TJ; Phillips, AM; Powell, K; Reid, CA; Williams, DA; Zheng, T, 2009)	1.07
"Lamotrigine may cause drug-related hypersexuality by an unclear underlying mechanism."	( Hypersexuality in two patients with epilepsy treated with lamotrigine. Grabowska-Grzyb, A; Nagańska, E; Wolańczyk, T, 2006)	2.02
"Lamotrigine alone did not increase neuronal apoptosis when given in doses up to 50 mg/kg; a significant increase in cell death occurred after 100 mg/kg."	( Effects of lamotrigine alone and in combination with MK-801, phenobarbital, or phenytoin on cell death in the neonatal rat brain. Gale, K; Katz, I; Kim, J; Kondratyev, A, 2007)	1.45
"Lamotrigine does not cause significant change in the pharmacokinetics of lithium."	( The effects of lamotrigine on the pharmacokinetics of lithium. Chen, C; Veronese, L; Yin, Y, 2000)	2.1

Treatment

Lamotrigine is a useful treatment in bipolar depression but requires several weeks of dose titration before its clinical effects can be assessed. Treatment during KD is associated with a decreased efficacy of the KD.

Excerpt	Reference	Relevance
"Lamotrigine as an add-on treatment for drug-resistant focal seizures appears to be effective in reducing seizure frequency, and seems to be fairly well-tolerated. "	( Lamotrigine add-on therapy for drug-resistant focal epilepsy. Bresnahan, R; Marson, AG; Panebianco, M; Ramaratnam, S, 2020)	3.44
"Lamotrigine treatment provided significant improvement in the neurofunctional status by preventing the increase in cytokine expression, increased lipid peroxidation and oxidative stress, depletion of antioxidant enzymes activity and increased apoptosis, all of which contributing to spinal cord damage through different paths after ischemia reperfusion injury. "	( Biochemical, pathological and ultrastructural investigation of whether lamotrigine has neuroprotective efficacy against spinal cord ischemia reperfusion injury. Fesli, R; Gokce, A; Gokce, EC; Gürer, B; Kahveci, FO; Kahveci, R; Kısa, Ü; Sargon, MF; Sarı, MF, 2021)	2.3
"Lamotrigine treatment did not affect bone strength, BMD, or bone turnover."	( Effects of the antiepileptic drugs topiramate and lamotrigine on bone metabolism in rats. E Takahashi, H; Izumo, N; Kanda, J; Kobayashi, Y; Onodera, K; Shimakura, T; Wakabayashi, H; Yamamoto, N, 2017)	1.43
"Lamotrigine is a useful treatment in bipolar depression but requires several weeks of dose titration before its clinical effects can be assessed. "	( Changes in brain Glx in depressed bipolar patients treated with lamotrigine: A proton MRS study. Bargiotas, T; Cowen, PJ; Emir, UE; Godlewska, BR; Masaki, C, 2019)	2.2
"Lamotrigine treatment resulted in the rapid accumulation of immature 30S and 50S ribosomal subunits at 15 °C."	( Discovery of a small molecule that inhibits bacterial ribosome biogenesis. Brown, ED; Davis, JH; Mangat, CS; Stokes, JM; Williamson, JR, 2014)	1.12
"Lamotrigine treatment during KD is associated with a decreased efficacy of the KD."	( Concomitant lamotrigine use is associated with decreased efficacy of the ketogenic diet in childhood refractory epilepsy. Catsman-Berrevoets, CE; Desadien, R; Neuteboom, RF; van der Louw, EJ; van der Sijs, H; Vehmeijer, FO, 2015)	2.24
"Lamotrigine as an add-on treatment for partial seizures appears to be effective in reducing seizure frequency, and seems to be fairly well tolerated. "	( Lamotrigine add-on for drug-resistant partial epilepsy. Marson, AG; Panebianco, M; Ramaratnam, S, 2016)	3.32
"Lamotrigine-treated patients were more comfortable throughout the study with significantly less (p<0.05) postoperative analgesic requirement comparable to gabapentin."	( Comparative pre-emptive analgesic efficacy study of novel antiepileptic agents gabapentin, lamotrigine and topiramate in patients undergoing major surgeries at a tertiary care hospital: a randomized double blind clinical trial. Bhosale, UA; Gupta, A; Sardesai, S; Shah, P; Yegnanarayan, R, 2017)	1.4
"Lamotrigine treatment has been associated with multiorgan failure, DRESS syndrome, acute hepatic failure, and disseminated intravascular coagulation."	( Dress syndrome and fulminant hepatic failure induced by lamotrigine. Amante, MF; Cejas, N; Filippini, AV; Imventarza, O; Lendoire, J; Parisi, C, )	1.1
"Lamotrigine is the treatment of choice in the prevention of migraine aura, but is not efficacious in the treatment of headache."	( [The role of the neuromodulators in the preventive treatment of migraine]. Pascual-Gómez, J, )	0.85
"Lamotrigine treatment had no effect on oxidative stress parameters alone, while it significantly decreased oxidative stress in the pentylenetetrazole-kindled group as compared to the pentylenetetrazole-kindled carbamazepine-treated group."	( Effect of carbamazepine and lamotrigine on cognitive function and oxidative stress in brain during chemical epileptogenesis in rats. Arora, T; Banerjee, BD; Garg, GR; Mediratta, PK; Mehta, AK; Sharma, AK; Sharma, KK, 2010)	1.38
"Lamotrigine treatment also resulted in significant improvement in the severity of depressive, attention-deficit/hyperactivity disorder (ADHD), and psychotic symptoms."	( A prospective open-label trial of lamotrigine monotherapy in children and adolescents with bipolar disorder. Biederman, J; Doyle, R; Georgiopoulos, A; Hammerness, P; Joshi, G; Kotarski, M; Mick, E; Williams, C; Wozniak, J, 2010)	1.36
"Lamotrigine treatment reduced the deterioration of the timed 25-foot walk (p=0.02) but did not affect other secondary clinical outcome measures."	( Lamotrigine for neuroprotection in secondary progressive multiple sclerosis: a randomised, double-blind, placebo-controlled, parallel-group trial. Altmann, DR; Brenner, R; Chataway, J; Furby, J; Hayton, T; Hughes, RA; Kapoor, R; Miller, DH; Smith, KJ, 2010)	2.52
"Lamotrigine treatment was initiated and the patient was discharged a few days later."	( First report of lamotrigine-induced drug rash with eosinophilia and systemic symptoms syndrome with pancreatitis. Augusto, JF; Croue, A; Dib, N; Lerolle, N; Mercat, A; Peres, M; Roquin, G, 2010)	1.43
"Lamotrigine treatment was well tolerated in this sample and associated with statistically significant improvement in mood and drug cravings but not drug use. "	( Lamotrigine in patients with bipolar disorder and cocaine dependence. Bobadilla, L; Brown, ES; Nejtek, VA; Orsulak, PJ; Perantie, DC, 2003)	3.2
"Lamotrigine treatment was well tolerated, and glutamate serum levels remained stable throughout the study."	( Placebo-controlled trial of lamotrigine added to conventional and atypical antipsychotics in schizophrenia. Bar, G; Blanaru, M; Gorelik, I; Heresco-Levy, U; Javitt, DC; Kremer, I; Vass, A, 2004)	1.34
"Lamotrigine as adjunctive treatment and monotherapy may improve side effect burden and quality of life in patients requiring a change in AED therapy."	( Lamotrigine therapy in patients requiring a change in antiepileptic drug regimen. Evans, BK; Groenke, DA; Hammer, AE; Kustra, RP; Leschek-Gelman, LM; Meador, KJ; Messenheimer, JA; Nanry, KP, 2005)	3.21
"Lamotrigine in treatment-resistant schizophrenia; a randomized placebo-controlled cross over trial."	( Effects of clozapine plus lamotrigine on phencyclidine-induced hyperactivity. Dursun, SM; Robertson, H; Williams, HJ; Zamzow, CR, 2006)	1.36
"Lamotrigine treatment was associated with significant improvements in mood, drug craving, and drug use. "	( Lamotrigine for bipolar disorder and comorbid cocaine dependence: a replication and extension study. Beard, L; Brown, ES; Dhanani, N; Orsulak, P; Perantie, DC; Rush, AJ, 2006)	3.22
"Lamotrigine pretreatment prevented many of the BOLD signal changes and the symptoms."	( Glutamate and the neural basis of the subjective effects of ketamine: a pharmaco-magnetic resonance imaging study. Deakin, JF; Dursun, SM; Hallak, JE; Lees, J; McKie, S; Williams, SR, 2008)	1.07
"Lamotrigine treatment induced a decrease in total HAMD scores in bipolar depressed patients, which was not significantly correlated with reduction of platelet MAO-B activity."	( The effect of lamotrigine on platelet monoamine oxidase type B activity in patients with bipolar depression. Babic, A; Jakovljevic, M; Mihaljevic Peles, A; Muck-Seler, D; Mustapic, M; Nedic, G; Pivac, N; Sagud, M, 2008)	1.43
"Lamotrigine as add-on treatment (500 mg per day) is effective in patients with refractory epilepsy, but its high cost requires a pharmacoeconomic analysis. "	( Adjunctive lamotrigine therapy in patients with refractory seizures: a lifetime cost-utility analysis. Becagli, P; Cincotta, M; Labbate, MG; Messori, A; Trippoli, S; Zaccara, G, 1998)	2.13
"With lamotrigine treatment, the patient who had not had surgery had complete cessation of monthly episodes of status epilepticus and a dramatic reduction of generalized tonic-clonic seizures, and the other patient who received lamotrigine had a 50% reduction of her atonic seizures."	( Treatment of seizures in subcortical laminar heterotopia with corpus callosotomy and lamotrigine. Ko, TS; Lee, JK; Vossler, DG, 1999)	0.98
"Lamotrigine pretreatment altered neither the physiological responses nor the subjective ratings of cocaine's pleasurable or aversive mood effects."	( Effects of lamotrigine on behavioral and cardiovascular responses to cocaine in human subjects. Hameedi, FA; Jatlow, PI; Kosten, TR; McCance-Katz, EF; Pearsall, HR; Rosen, MI; Saleem, R; Winther, LC; Woods, SW, 2000)	1.42
"The treatment with lamotrigine increased the superoxide dismutase (SOD) and catalase activity (CAT) activities in the amygdala of stressed rats."	( Effects of lamotrigine on behavior, oxidative parameters and signaling cascades in rats exposed to the chronic mild stress model. Abelaira, HM; Dal-Pizzol, F; Mina, F; Quevedo, J; Réus, GZ; Ribeiro, KF; Romano-Silva, MA; Rosa, DV; Santana, CV; Steckert, AV, 2013)	1.1
"Treatment with lamotrigine was associated with more rashes (20% vs 5%, P value 0.03) and transient, dose-related deterioration of mobility (66% vs 34%, P value 0.001) than placebo."	( Sodium channel blockers for neuroprotection in multiple sclerosis. Hao, Z; Wen, J; Yang, C; Zeng, L; Zhang, L, 2015)	0.76
"Treatment with lamotrigine improved the patient's condition."	( [Psychogenic non-epileptic seizures: issues of comorbidity in the diagnosis and treatment]. Nikolaev, EL; Rezvy, G; SÖrlie, T, 2016)	0.77
"Pretreatment with lamotrigine significantly attenuated AMPH/CDP-induced effects, but also reduced motility when tested in the presence of CDP-alone."	( Effects of neuronal Kv7 potassium channel activators on hyperactivity in a rodent model of mania. Nielsen, AN; Redrobe, JP, 2009)	0.68
"Treatment with lamotrigine was prescribed."	( Dress syndrome and fulminant hepatic failure induced by lamotrigine. Amante, MF; Cejas, N; Filippini, AV; Imventarza, O; Lendoire, J; Parisi, C, )	0.72
"Treatment with lamotrigine was associated with statistically significant levels of improvement in mean YMRS scores (-14.9 +/- 9.7, P < 0.001) at endpoint."	( A prospective open-label trial of lamotrigine monotherapy in children and adolescents with bipolar disorder. Biederman, J; Doyle, R; Georgiopoulos, A; Hammerness, P; Joshi, G; Kotarski, M; Mick, E; Williams, C; Wozniak, J, 2010)	0.98
"Treatment with Lamotrigine and Amisulpiride achieved an excellent response, and she has remained symptom free for 7 months."	( Temporal lobe epilepsy masquerading as psychosis--a case report and literature review. Hamelijnck, J; Needham, E, 2012)	0.71
"Treatment with lamotrigine (LTG) during pregnancy is associated with a pronounced risk of seizure deterioration, because pregnancy accelerates LTG elimination. "	( Algorithm for lamotrigine dose adjustment before, during, and after pregnancy. Sabers, A, 2012)	1.09
"Treatment with lamotrigine reversed the increase in the immobility time in the deprived rats."	( Lamotrigine treatment reverses depressive-like behavior and alters BDNF levels in the brains of maternally deprived adult rats. Abelaira, HM; Cipriano, AL; Quevedo, J; Réus, GZ; Ribeiro, KF; Scaini, G; Streck, EL; Zappellini, G, 2012)	2.16
"Treatment with lamotrigine increased [Ca(2+)](i) apparently as a result of Ca(2+) release from intracellular stores and CaMKII activity."	( Lamotrigine increases intracellular Ca(2+) levels and Ca(2+)/calmodulin-dependent kinase II activation in mouse dorsal root ganglion neurones. Cho, YW; Han, J; Kang, D; Kim, EJ; Kim, GT; Lee, ES; Park, HJ; Ryu, JH; Tak, HM, 2013)	2.19
"Treatment with lamotrigine as monotherapy and as adjunctive therapy was associated with improved cognitive functioning and reduced neurocognitive side effects, regardless of index mood polarity."	( Effect of lamotrigine on cognitive complaints in patients with bipolar I disorder. Adams, BE; Asnis, GM; Davis, KH; Ginsberg, LD; Goodwin, FK; Khan, A; Krishnan, AA, 2004)	1.08
"Pretreatment with lamotrigine (5-100 mg/kg, s.c.) reversed in a dose-dependent way the withdrawal-induced increase in cerebellar Ca(2+)-dependent nitric oxide (NO) synthase activity and reduced the number of escape jumps and other motor symptoms of abstinence, at doses that did not modify locomotor activity (25-50 mg/kg)."	( Inhibition of morphine withdrawal by lamotrigine: involvement of nitric oxide. Cuéllar, B; Leza, JC; Lizasoain, I; Lorenzo, P; Moro, MA, 1996)	0.89
"The treatment with lamotrigine was successful in 9 (52%) cases, with reduction of seizures by at least 50%."	( [Comparative assessment of treatment efficacy with lamotrigine (Lamictal) together with valproate and/or carbamazepine in patients with refractory epilepsy]. Wajgt, A; Wierzba, W, )	0.7
"Treatment with lamotrigine for 1 week did not significantly alter the hypothermic or cortisol responses to ipsapirone."	( Effects of lamotrigine on the 5-HT1A receptor function in healthy human males. Lam, RW; Shiah, IS; Yatham, LN; Zis, AP, 1998)	1.04
"Pretreatment with lamotrigine (10 mg/kg or 20 mg/kg per day) or MK-801 (2 mg/kg per day) attenuated the lesions and behavioral change."	( Neuroprotective effect of lamotrigine and MK-801 on rat brain lesions induced by 3-nitropropionic acid: evaluation by magnetic resonance imaging and in vivo proton magnetic resonance spectroscopy. Chang, C; Lee, WT; Shen, YZ, 2000)	0.93

Toxicity

The overall incidence of adverse events was similar between the groups. dizziness, somnolence, fatigue, and weight increase were numerically more common in the pregabalin group than in the lamotrigine group. In our cases, DBN and truncal ataxia occurred in conjunction with toxic lamotigine serum levels.

Excerpt	Reference	Relevance
" In the pooled data from the four double-blind studies (n = 92), the incidence of adverse experiences with LTG and placebo did not differ significantly."	( Human safety of lamotrigine. Betts, T; Goodwin, G; Withers, RM; Yuen, AW, 1991)	0.63
" Finally, gabapentin is a very safe add-on medication."	( The new anticonvulsant drugs. Implications for avoidance of adverse effects. Krämer, G; Schmidt, D, 1994)	0.29
" By November 1992 about 5,800 patient-years' experience of adverse effects had been compiled."	( Safety of lamotrigine. Richens, A, 1994)	0.69
" Most adverse events were minor and resolved over time."	( Placebo-controlled study of the efficacy and safety of lamotrigine in patients with partial seizures. U.S. Lamotrigine Protocol 0.5 Clinical Trial Group. Bergen, D; Dren, AT; Faught, E; Lineberry, CG; Matsuo, F; Messenheimer, JA; Rudd, GD, 1993)	0.53
"This prospective study was designed to ascertain whether measurement of lamotrigine (LTG) concentrations in the epilepsy clinic could be used to predict the onset of complete seizure control or the emergence of adverse effects."	( Concentration--effect and concentration--toxicity relations with lamotrigine: a prospective study. Brodie, MJ; Forrest, G; Kilpatrick, ES, 1996)	0.76
" Headache, drowsiness, faintness, and diplopia, the common adverse events (AEs), were mild to moderate in intensity and occurred in 50-75% of patients in both groups (except for diplopia, occurring only with LTG)."	( Lamotrigine high-dose tolerability and safety in patients with epilepsy: a double-blind, placebo-controlled, eleven-week study. Gay, P; Lai, AA; Madsen, J; Matsuo, F; Risner, ME; Rollins, DE; Tolman, KG, 1996)	1.74
" The majority of adverse experiences were classified by the physician as being mild in intensity and only six patients (4%) withdrew from the study due to adverse experiences."	( Long-term safety and efficacy of lamotrigine (Lamictal) in paediatric patients with epilepsy. Alving, J; Besag, FM; Dulac, O; Mullens, EL, 1997)	0.58
"Standard antiepileptic drugs (AEDs) are associated with a wide variety of acute and chronic adverse events and with many interactions with each other and with non-AEDs that complicate patient management."	( Overview of the safety of newer antiepileptic drugs. Shorvon, S; Stefan, H, 1997)	0.3
" In addition, fewer than half the number of patients in monotherapy studies who were taking lamotrigine discontinued treatment because of adverse events compared to those taking carbamazepine and phenytoin."	( Safety review of adult clinical trial experience with lamotrigine. Giorgi, L; Messenheimer, J; Mullens, EL; Young, F, 1998)	0.77
"05) change in the serum concentrations of either CBZ or its epoxide metabolite when LTG was added either to the group as a whole or to the nine patients who experienced adverse CNS effects."	( Carbamazepine toxicity with lamotrigine: pharmacokinetic or pharmacodynamic interaction? Berry, DJ; Besag, FM; Newbery, JE; Pool, F; Subel, B, 1998)	0.59
" The results of these two studies suggest that LTG is acceptably safe when used for the treatment of refractory epilepsy."	( Safety of long-term lamotrigine in epilepsy. Freemantle, SN; Mackay, FJ; Mann, RD; Pearce, GL; Wilton, LV, 1997)	0.62
"Blood level monitoring helps to determine the therapeutic and toxic ranges for anticonvulsants and antidepressants."	( Lamotrigine toxicity secondary to sertraline. Gerner, R; Kaufman, KR, 1998)	1.74
" The adverse effect (AE) profile of this combination needs clarification."	( Adding lamotrigine to valproate: incidence of rash and other adverse effects. Postmarketing Antiepileptic Drug Survey (PADS) Group. Faught, E; French, J; Harden, C; Jacobson, M; Montouris, G; Morris, G; Rosenfeld, W, 1999)	0.76
" Lamotrigine is generally a safe and effective medication; however, it should be used with caution in patients on polytherapy and in those with complicated acute systemic and central nervous system conditions, such as fever, status epilepticus, epilepsia partialis, and encephalitis."	( Potential hepatotoxicity of lamotrigine. Choueiri, R; Fayad, M; Mikati, M, 2000)	1.51
" Treatment was discontinued in 7% because of adverse events."	( Open study evaluating lamotrigine efficacy and safety in add-on treatment and consecutive monotherapy in patients with carbamazepine- or valproate-resistant epilepsy. Jozwiak, S; Terczynski, A, 2000)	0.62
" However, on rare occasions, they can progress to more severe cutaneous disorders, including Stevens-Johnson syndrome and toxic epidermal necrolysis."	( Therapeutic safety monitoring: what to look for and when to look for it. Harden, CL, 2000)	0.31
" 23 patients (30%) had at least one adverse event (AE), but only 1/4 of all AEs might be reasonably regarded as an effect of the medication."	( [Open study evaluating lamotrigine efficacy and safety in add-on treatment and consecutive monotherapy in adult patients with epilepsy resistant carbamazepine and valproate]. Jóźwiak, S; Mańko, E; Niedzielska, K; Terczyński, A, )	0.44
" Lamotrigine is a safe and well-tolerated drug."	( [Open study evaluating lamotrigine efficacy and safety in add-on treatment and consecutive monotherapy in adult patients with epilepsy resistant carbamazepine and valproate]. Jóźwiak, S; Mańko, E; Niedzielska, K; Terczyński, A, )	1.35
" Serious adverse events were assessed individually."	( Adverse event monitoring in lamotrigine patients: a pharmacoepidemiologic study in the United Kingdom. Mawer, GE; Sander, JW; Wong, IC, 2001)	0.6
" The adverse events with LTG reported by this study were similar to those reported in the literature."	( Adverse event monitoring in lamotrigine patients: a pharmacoepidemiologic study in the United Kingdom. Mawer, GE; Sander, JW; Wong, IC, 2001)	0.6
" Life-threatening adverse reactions were rare."	( Adverse event monitoring in lamotrigine patients: a pharmacoepidemiologic study in the United Kingdom. Mawer, GE; Sander, JW; Wong, IC, 2001)	0.6
"Psychopharmacology research aims to expand the therapeutic ratio between efficacy, on the one hand, and adverse events and safety, on the other."	( Psychotropic drugs and adverse events in the treatment of bipolar disorders revisited. McIntyre, RS, 2002)	0.31
" Side effects were mild, but frequent; only four patients discontinued LTG because of adverse effects."	( [Lamotrigine in the adult-onset epilepsy: efficacy and long-term safety]. Alegre, M; Iriarte, J; Lázaro, D; Schlumberger, E; Urrestarazu, E; Viteri, C, 2002)	1.22
"LTG is a safe an effective drug in epilepsy."	( [Lamotrigine in the adult-onset epilepsy: efficacy and long-term safety]. Alegre, M; Iriarte, J; Lázaro, D; Schlumberger, E; Urrestarazu, E; Viteri, C, 2002)	1.22
" The goal of the study was to determine the serum levels of patients with seizure reduction of at least 50% after addition of LTG, and to assess a possible relationship between the occurrence of adverse effects due to LTG and its serum concentration."	( Prospective study on concentration-efficacy and concentration-toxicity: correlations with lamotrigine serum levels. Fröscher, W; Keller, F; Krämer, G; Vogt, H, 2002)	0.54
" The correlation between the occurrence of adverse effects and LTG serum concentration was calculated in a second group of 63 young adult, and adult patients with epilepsy (Group II)."	( Prospective study on concentration-efficacy and concentration-toxicity: correlations with lamotrigine serum levels. Fröscher, W; Keller, F; Krämer, G; Vogt, H, 2002)	0.54
" In group II patients the serum concentration associated with an adverse effect was not significantly different from the serum concentration in patients without adverse effects."	( Prospective study on concentration-efficacy and concentration-toxicity: correlations with lamotrigine serum levels. Fröscher, W; Keller, F; Krämer, G; Vogt, H, 2002)	0.54
"Clinical pharmacologists, neurologists, internists, and all health care givers must consider the efficacy, safety, and side effect profile of a given antiepileptic drug (AED) when determining which drug is best for a given patient."	( Clinical pharmacology of topiramate versus lamotrigine versus phenobarbital: comparison of efficacy and side effects using odds ratios. Claycamp, HG; Lathers, CM; Schraeder, PL, 2003)	0.58
" The most common adverse event with lamotrigine was headache."	( Safety and tolerability of lamotrigine for bipolar disorder. Asnis, GM; Bentley, B; Bowden, CL; Ginsberg, LD; Leadbetter, R; White, R, 2004)	0.9
" Veratridine (100 microM) or ouabain alone (500 microM) were not toxic to the cells."	( A novel toxicity-based assay for the identification of modulators of voltage-gated Na+ channels. Weiser, T, 2004)	0.32
"Data on single-substance exposures to lamotrigine reported to the American Association of Poison Control Centers Toxic Exposure Surveillance System in 2000 and 2001 were retrospectively analyzed."	( Evaluation of lamotrigine toxicity reported to poison centers. Klein-Schwartz, W; Lofton, AL, 2004)	0.96
"1%) exposed to lamotrigine in overdose experienced no toxic clinical effects."	( Evaluation of lamotrigine toxicity reported to poison centers. Klein-Schwartz, W; Lofton, AL, 2004)	1.04
" In our cases, DBN and truncal ataxia occurred in conjunction with toxic lamotrigine serum levels."	( Downbeat nystagmus as a result of lamotrigine toxicity. Alkawi, A; Kattah, JC; Wyman, K, 2005)	0.84
" The aim of the study was to evaluate the frequency of AED utilisation and reported adverse events, in a cohort of MS patients."	( Antiepileptic medications in multiple sclerosis: adverse effects in a three-year follow-up study. Battaglia, MA; Brichetto, G; Mancardi, GL; Messmer Uccelli, M; Solaro, C, 2005)	0.33
" The rate of patients discontinuing treatment due to adverse events or a lack of efficacy was 19% with CBZ compared to 9% with LTG (not statistically different)."	( The LAM-SAFE Study: lamotrigine versus carbamazepine or valproic acid in newly diagnosed focal and generalised epilepsies in adolescents and adults. Bergmann, L; Kurlemann, G; Schmitz, B; Siemes, H; Steinhoff, BJ; Ueberall, MA, 2005)	0.65
"5 million adverse drug reaction (ADR) reports for 8620 drugs/biologics that are listed for 1191 Coding Symbols for Thesaurus of Adverse Reaction (COSTAR) terms of adverse effects."	( Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling. Benz, RD; Contrera, JF; Kruhlak, NL; Matthews, EJ; Weaver, JL, 2004)	0.32
" Therefore, the authors summarise adverse events of greatest prevalence and/or greatest severity based on data derived predominately from studies of geriatric patients with epilepsy and/or other non-psychiatric indications."	( Safety and tolerability of mood-stabilising anticonvulsants in the elderly. Alldredge, B; Fenn, HH; Ketter, TA; Sommer, BR, 2006)	0.33
"9%) were the most frequently reported adverse events."	( Efficacy and safety of lamotrigine for adults with bipolar disorder in a private practice setting. Ginsberg, LD, 2006)	0.64
" Assessment for pain relief, overall improvement and adverse events were carried out."	( Randomized double-blind study comparing the efficacy and safety of lamotrigine and amitriptyline in painful diabetic neuropathy. Bhansali, A; Hota, D; Jose, VM; Pandhi, P, 2007)	0.58
" Of the 44 adverse events reported, 33 (75%) were with amitriptyline, sedation being the commonest [in 19 (43%) patients]."	( Randomized double-blind study comparing the efficacy and safety of lamotrigine and amitriptyline in painful diabetic neuropathy. Bhansali, A; Hota, D; Jose, VM; Pandhi, P, 2007)	0.58
"As there are few differences between the two treatments in efficacy, lamotrigine 25 mg twice daily might be the first choice as it is associated with fewer adverse effects in our population."	( Randomized double-blind study comparing the efficacy and safety of lamotrigine and amitriptyline in painful diabetic neuropathy. Bhansali, A; Hota, D; Jose, VM; Pandhi, P, 2007)	0.81
"As pharmacokinetic drug interactions frequently cause adverse events, it is important that the relevant information is given in package inserts (PIs)."	( Adverse events caused by drug interactions involving glucuronoconjugates of zidovudine, valproic acid and lamotrigine, and analysis of how such potential events are discussed in package inserts of Japan, UK and USA. Hasegawa, R; Hirata-Koizumi, M; Miyake, S; Saito, M, 2007)	0.55
"We reviewed clinical drug interactions related to glucuronoconjugates, focusing on reports of adverse events."	( Adverse events caused by drug interactions involving glucuronoconjugates of zidovudine, valproic acid and lamotrigine, and analysis of how such potential events are discussed in package inserts of Japan, UK and USA. Hasegawa, R; Hirata-Koizumi, M; Miyake, S; Saito, M, 2007)	0.55
" Of these, five combinations induced clear adverse events: (i) severe anaemia due to zidovudine and caused by interaction with valproic acid, (ii) recurrence/increased frequency of seizure or increased manic states from a reduction in therapeutic effects of valproic acid caused by panipenem, (iii) meropenem or (iv) ritonavir and (v) of lamotrigine caused by oral contraceptives."	( Adverse events caused by drug interactions involving glucuronoconjugates of zidovudine, valproic acid and lamotrigine, and analysis of how such potential events are discussed in package inserts of Japan, UK and USA. Hasegawa, R; Hirata-Koizumi, M; Miyake, S; Saito, M, 2007)	0.72
"Five combinations were identified to cause severe adverse events because of interactions related to glucuronoconjugates."	( Adverse events caused by drug interactions involving glucuronoconjugates of zidovudine, valproic acid and lamotrigine, and analysis of how such potential events are discussed in package inserts of Japan, UK and USA. Hasegawa, R; Hirata-Koizumi, M; Miyake, S; Saito, M, 2007)	0.55
" Monotherapy is preferable over polytherapy because of better compliance, fewer adverse events, less interactions, lower teratogenicity and lower cost."	( Efficacy and safety of lamotrigine monotherapy in children and adolescents with epilepsy. Hardison, HH; Khurana, DS; Kothare, SV; Legido, A; Marks, HG; Melvin, JJ; Piñol-Ripoll, G; Valencia, I, 2009)	0.66
"To determine long-term retention, percentage of patients withdrawing because of adverse events, percentage of patients achieving seizure freedom, safety profile of the new anti-epileptic drugs lamotrigine, levetiracetam and topiramate."	( The impact of side effects on long-term retention in three new antiepileptic drugs. Aldenkamp, AP; Bootsma, HP; de Krom, M; Hekster, YA; Hulsman, J; Lambrechts, D; Majoie, M; Ricker, L; Schellekens, A, 2009)	0.54
" Adverse events played a role in drug discontinuation in 154/429 patients (35."	( The impact of side effects on long-term retention in three new antiepileptic drugs. Aldenkamp, AP; Bootsma, HP; de Krom, M; Hekster, YA; Hulsman, J; Lambrechts, D; Majoie, M; Ricker, L; Schellekens, A, 2009)	0.35
"A drug that is only modestly efficacious but has a favourable safety profile may look better than a drug that is more efficacious but produces clinically meaningful adverse events."	( The impact of side effects on long-term retention in three new antiepileptic drugs. Aldenkamp, AP; Bootsma, HP; de Krom, M; Hekster, YA; Hulsman, J; Lambrechts, D; Majoie, M; Ricker, L; Schellekens, A, 2009)	0.35
"Lamotrigine was found effective and safe as add-on treatment to lithium in the acute treatment of bipolar depression."	( Efficacy and safety of lamotrigine as add-on treatment to lithium in bipolar depression: a multicenter, double-blind, placebo-controlled trial. Blom, MB; de Keyzer, HJ; Hartong, EG; Luteijn, ML; Mulder, PG; Nolen, WA; Notten, PJ; Timmermans, MA; van der Loos, ML; Vergouwen, AC; Vieta, E, 2009)	2.11
"Antiepileptic drugs (AEDs) have been widely used in patients with epilepsy but the adverse effects in adult Chinese patients have not been investigated."	( Adverse effects of carbamazepine, phenytoin, valproate and lamotrigine monotherapy in epileptic adult Chinese patients. Wang, X; Xi, Z; Yan, Y; Zeng, K, 2010)	0.6
" An adverse effect profile, as well as efficacy of monotherapy, was obtained through a face-to-face interview with the patient at each visit."	( Adverse effects of carbamazepine, phenytoin, valproate and lamotrigine monotherapy in epileptic adult Chinese patients. Wang, X; Xi, Z; Yan, Y; Zeng, K, 2010)	0.6
" Overall, 18% of patients experienced adverse effects: for CBZ (25/168; 14."	( Adverse effects of carbamazepine, phenytoin, valproate and lamotrigine monotherapy in epileptic adult Chinese patients. Wang, X; Xi, Z; Yan, Y; Zeng, K, 2010)	0.6
" No fatal adverse events occurred."	( Adverse effects of carbamazepine, phenytoin, valproate and lamotrigine monotherapy in epileptic adult Chinese patients. Wang, X; Xi, Z; Yan, Y; Zeng, K, 2010)	0.6
" There is not enough information available to establish a toxic dose or dose that requires hospital assessment."	( Seizures secondary to lamotrigine toxicity in a two-year-old. Banks, CJ; Close, BR, 2010)	0.68
" Although alopecia may not be regarded as serious from a regulatory perspective, this adverse reaction has the potential to affect compliance, resulting in decreased efficacy of the treatment regimen and detrimental effects on patient health outcomes."	( Alopecia in association with lamotrigine use: an analysis of individual case safety reports in a global database. Hill, R; Star, K; Tengstrand, M; van Puijenbroek, EP, 2010)	0.65
"Using postmarketing pharmacovigilance data collected shortly after market authorization of lamotrigine in the UK, a study was conducted to compare the adverse event (AE) profiles of children and adults taking lamotrigine, using modified signal detection methods."	( Paediatric postmarketing pharmacovigilance using prescription-event monitoring: comparison of the adverse event profiles of lamotrigine prescribed to children and adults in England. Aurich-Barrera, B; Brown, D; Shakir, S; Wilton, L, 2010)	0.79
"Data from the lamotrigine Prescription Event Monitoring (PEM) study, an observational cohort study, were stratified by age and examined using summary statistics for adverse drug reactions (ADRs), reasons for stopping treatment, deaths and follow-up information."	( Paediatric postmarketing pharmacovigilance using prescription-event monitoring: comparison of the adverse event profiles of lamotrigine prescribed to children and adults in England. Aurich-Barrera, B; Brown, D; Shakir, S; Wilton, L, 2010)	0.93
"LTG is generally an effective and safe treatment for management of TN, compared to CBZ."	( Lamotrigine for trigeminal neuralgia: efficacy and safety in comparison with carbamazepine. Abd Rahman, RB; Shaikh, S; Yaacob, HB, 2011)	1.81
"Efficacious and safe monotherapy options are needed for adult patients with newly diagnosed epilepsy."	( Efficacy and safety of pregabalin versus lamotrigine in patients with newly diagnosed partial seizures: a phase 3, double-blind, randomised, parallel-group trial. Brodie, MJ; Kälviäinen, R; Knapp, LE; Kwan, P; Weaver, J; Yurkewicz, L, 2011)	0.64
" The overall incidence of adverse events was similar between the groups and consistent with that in previous studies; dizziness (55 [17%] vs 45 [14%] patients), somnolence (29 [9%] vs 14 [4%]), fatigue (27 [8%] vs 19 [6%]), and weight increase (21 [6%] vs 7 [2%]) were numerically more common in the pregabalin group than in the lamotrigine group."	( Efficacy and safety of pregabalin versus lamotrigine in patients with newly diagnosed partial seizures: a phase 3, double-blind, randomised, parallel-group trial. Brodie, MJ; Kälviäinen, R; Knapp, LE; Kwan, P; Weaver, J; Yurkewicz, L, 2011)	0.81
"Individuals treated with combined valproate-lamotrigine rarely present late adverse effects (unrelated to introduction and titration)."	( Late adverse effects of the coadministration of valproate and lamotrigine. Moreira, B; Thome-Souza, S; Valente, KD, 2012)	0.88
" Rash was the major side effect for withdrawal."	( [Efficacy and safety of the combined therapy of valproic acid and lamotrigine for epileptics]. Hu, Q; Kang, HC; Li, X; Liu, XY; Liu, ZG; Wang, M; Xu, F; Zeng, Z; Zhu, SQ, 2012)	0.62
"The co-medication of VPA and LTG is both effective and safe for all epileptic types, especially for SPS and GS."	( [Efficacy and safety of the combined therapy of valproic acid and lamotrigine for epileptics]. Hu, Q; Kang, HC; Li, X; Liu, XY; Liu, ZG; Wang, M; Xu, F; Zeng, Z; Zhu, SQ, 2012)	0.62
" The number of patients with one or more adverse events during double-blind or open-label treatment was 455 (69 %)."	( Long-term tolerability and safety of lamotrigine extended-release: pooled analysis of three clinical trials. Biton, V; Caldwell, PT; Hammer, AE; Messenheimer, JA; Naritoku, D; Shneker, BF; Vuong, A, 2013)	0.66
"No significant changes in blood pressure, heart rate, or adverse events including rash were attributed to administration of a 50-mg dose of the intravenous LTG formulation."	( Safety of an intravenous formulation of lamotrigine. Birnbaum, AK; Conway, JM; Leppik, IE; Pennell, PB; Rarick, JO; Remmel, RP; White, JR, 2014)	0.67
" We proposed a subcortical mechanism for this complication induced by the toxic doses of LTG."	( Generalized myoclonus and spasticity induced by lamotrigine toxicity: a case report and literature review. Al-Rabia, MW; Aldarmahi, AA; Algahtani, HA; Almalki, WH; Bryan Young, G, )	0.39
"To identify adverse drug reactions associated with lamotrigine in children and compare the safety profile with other antiepileptic drugs."	( Safety of lamotrigine in paediatrics: a systematic review. Choonara, I; Egunsola, O; Sammons, HM, 2015)	1.07
" There were 2222 adverse events (AEs) reported."	( Safety of lamotrigine in paediatrics: a systematic review. Choonara, I; Egunsola, O; Sammons, HM, 2015)	0.82
" This systematic review aimed to assess the prevalence of their adverse effects (AEs) and to provide recommendations on their clinical management."	( Management of adverse effects of mood stabilizers. Hidalgo, D; León-Caballero, J; Murru, A; Pacchiarotti, I; Popovic, D; Vieta, E, 2015)	0.42
" Treatment-emergent adverse events occurred in 82% (CBZ/OXC), 76% (LTG), 73% (LEV), and 67% (VPA) of patients; most were of mild-to-moderate intensity."	( Efficacy and safety of ezogabine/retigabine as adjunctive therapy to specified single antiepileptic medications in an open-label study of adults with partial-onset seizures. Brandt, C; Daniluk, J; DeRossett, S; Edwards, S; Lerche, H; Lotay, N, 2015)	0.42
"In patients taking antiepileptic drugs (AEDs) for epilepsy, adverse effects (AEs) often lead to unfavorable quality of life, impaired adherence, and, eventually, discontinuation of pharmacological treatment."	( Specific adverse effects of antiepileptic drugs--A true-to-life monotherapy study. Fidzinski, P; Gaus, V; Holtkamp, M; Kowski, AB; Losch, F; Weissinger, F, 2016)	0.43
"All patients ≥16years of age with epilepsy for ≥12months were routinely asked to complete the Liverpool Adverse Event Profile (LAEP) just before their appointment."	( Specific adverse effects of antiepileptic drugs--A true-to-life monotherapy study. Fidzinski, P; Gaus, V; Holtkamp, M; Kowski, AB; Losch, F; Weissinger, F, 2016)	0.43
" One of the most dangerous adverse effects of LTG is skin rash, which can make early cessation necessary."	( Safety of Long-term Use of Lamotrigine for the Treatment of Psychiatric Disorders. Fujito, H; Inaba, T; Kawashima, T; Matsushima, J; Mizoguchi, Y; Mochinaga, S; Monji, A; Sogawa, R, )	0.43
" Patients were retrospectively divided into those who discontinued treatment within 6 months and those who continued for longer, and the groups were compared for adverse effects."	( Safety of Long-term Use of Lamotrigine for the Treatment of Psychiatric Disorders. Fujito, H; Inaba, T; Kawashima, T; Matsushima, J; Mizoguchi, Y; Mochinaga, S; Monji, A; Sogawa, R, )	0.43
" Of the patients who continued treatment for 6 months or longer, only 2 later discontinued treatment because of adverse effects."	( Safety of Long-term Use of Lamotrigine for the Treatment of Psychiatric Disorders. Fujito, H; Inaba, T; Kawashima, T; Matsushima, J; Mizoguchi, Y; Mochinaga, S; Monji, A; Sogawa, R, )	0.43
"Clinicians must be mindful of the adverse effects occurring early during the titration phase."	( Safety of Long-term Use of Lamotrigine for the Treatment of Psychiatric Disorders. Fujito, H; Inaba, T; Kawashima, T; Matsushima, J; Mizoguchi, Y; Mochinaga, S; Monji, A; Sogawa, R, )	0.43
" We performed a random-effects meta-analysis of depression ratings, response, remission, and adverse effects calculating standardized mean difference (SMD) and risk ratio (RR) ±95% confidence intervals (CIs)."	( Lamotrigine compared to placebo and other agents with antidepressant activity in patients with unipolar and bipolar depression: a comprehensive meta-analysis of efficacy and safety outcomes in short-term trials. Anghelescu, IG; Correll, CU; Gao, K; Normann, C; Reis, C; Schaffer, A; Solmi, M; van der Loos, ML; Veronese, N; Zaninotto, L, 2016)	1.88
" Adverse effects and all-cause/specific-cause discontinuation were similar across all comparisons."	( Lamotrigine compared to placebo and other agents with antidepressant activity in patients with unipolar and bipolar depression: a comprehensive meta-analysis of efficacy and safety outcomes in short-term trials. Anghelescu, IG; Correll, CU; Gao, K; Normann, C; Reis, C; Schaffer, A; Solmi, M; van der Loos, ML; Veronese, N; Zaninotto, L, 2016)	1.88
"Lamotrigine was superior to placebo in improving unipolar and bipolar depressive symptoms, without causing more frequent adverse effects/discontinuations."	( Lamotrigine compared to placebo and other agents with antidepressant activity in patients with unipolar and bipolar depression: a comprehensive meta-analysis of efficacy and safety outcomes in short-term trials. Anghelescu, IG; Correll, CU; Gao, K; Normann, C; Reis, C; Schaffer, A; Solmi, M; van der Loos, ML; Veronese, N; Zaninotto, L, 2016)	3.32
"Background The impact of adverse events (AEs) of antiepileptic drugs (AEDs) have an impact on compliance and dropouts."	( Antiepileptic drugs in migraine and epilepsy: Who is at increased risk of adverse events? Bedetti, C; Calabresi, P; Caproni, S; Corbelli, I; Costa, C; Cupini, LM; Eusebi, P; Romoli, M; Sarchielli, P; Siliquini, S, 2018)	0.48
" This study compared adverse event (AE) reporting rates for brand vs."	( Comparison of brand versus generic antiepileptic drug adverse event reporting rates in the U.S. Food and Drug Administration Adverse Event Reporting System (FAERS). Alatawi, Y; Berg, RL; Cheng, N; Hansen, RA; Page, D; Peissig, PL; Plotkina, AV; Qian, J; Rahman, MM, 2017)	0.46
" Food and Drug Administration Adverse Event Reporting System between January 2004 to March 2015 with lamotrigine, carbamazepine, and oxcarbazepine listed as primary or secondary suspect were classified as brand, generic, or AG based on the manufacturer."	( Comparison of brand versus generic antiepileptic drug adverse event reporting rates in the U.S. Food and Drug Administration Adverse Event Reporting System (FAERS). Alatawi, Y; Berg, RL; Cheng, N; Hansen, RA; Page, D; Peissig, PL; Plotkina, AV; Qian, J; Rahman, MM, 2017)	0.67
"Valproate alone or combined with another AED is associated with the greatest odds of adverse neurodevelopmental outcomes compared with control."	( Comparative safety of antiepileptic drugs for neurological development in children exposed during pregnancy and breast feeding: a systematic review and network meta-analysis. Cogo, E; D'Souza, J; Finkelstein, Y; Hemmelgarn, BR; Hutton, B; Kealey, R; MacDonald, H; Reynen, E; Rios, P; Soobiah, C; Straus, SE; Thavorn, K; Tricco, AC; Veroniki, AA; Yazdi, F, 2017)	0.46
" The aim of this observational cross-sectional study was to compare the A-B Neuropsychological Assessment Schedule (ABNAS), which measures cognitive side effects to the Adverse Events Profile (AEP), which looks at a broader range of side effects, and to investigate drug/dosage relationships with questionnaire scores to help determine a point at which a drug change would be indicated."	( Adverse effects of anti-epileptics in trigeminal neuralgiform pain. Cregg, R; Lee, G; O'Keeffe, AG; Reading, J; Tentolouris-Piperas, V; Zakrzewska, JM, 2018)	0.48
" Toxic range on the ABNAS was estimated to occur when scores were >43/72 (95% CI: 37."	( Adverse effects of anti-epileptics in trigeminal neuralgiform pain. Cregg, R; Lee, G; O'Keeffe, AG; Reading, J; Tentolouris-Piperas, V; Zakrzewska, JM, 2018)	0.48
" In the LTG and TPM safety populations (n=245 versus n=125), treatment-emergent adverse events (TEAEs) were reported with LTG 68."	( Efficacy, safety, and tolerability of brivaracetam with concomitant lamotrigine or concomitant topiramate in pooled Phase III randomized, double-blind trials: A post-hoc analysis. Benbadis, S; Diaz, A; Elmoufti, S; Klein, P; Schiemann, J; Whitesides, J, 2018)	0.72
" Nine volunteers reported adverse events, 2 experienced oropharyngeal pain, each receiving 25 mg and 50 mg."	( Pharmacokinetics, Safety, and Tolerability of Lamotrigine Chewable/Dispersible Tablet Following Repeat-Dose Administration in Healthy Chinese Volunteers. Hu, J; Li, H; Li, Y; Xu, Y; Zhang, F, 2018)	0.74
" Although no unexpected adverse events were observed, one Japanese patient was withdrawn from the extension phase due to mild drug-related rash developed 842 days after the start of LTG."	( Long-term efficacy and safety of lamotrigine monotherapy in Japanese and South Korean pediatric patients with newly diagnosed typical absence seizures: An open-label extension study. Kurata, A; Numachi, Y; Ohtsuka, Y; Sato, K; Shimizu, M; Yasumoto, S, 2018)	0.76
" Secondary outcomes were defined as the safety profile of the intervention, including reported discontinuation rate and adverse events."	( Lamotrigine augmentation in treatment-resistant unipolar depression: A comprehensive meta-analysis of efficacy and safety. Chen, CH; Chiu, YH; Goh, KK; Lu, ML, 2019)	1.96
" Lamotrigine augmentation is well-tolerated in terms of all-cause discontinuation rate and adverse events."	( Lamotrigine augmentation in treatment-resistant unipolar depression: A comprehensive meta-analysis of efficacy and safety. Chen, CH; Chiu, YH; Goh, KK; Lu, ML, 2019)	2.87
"According to current evidence, LTG is less effective than VPA and ESM, however, based on its relative safety, LTG might be reasonably tried as initial therapy in children and adolescents at risk of significant adverse effects from VPA and ESM, and future well-designed studies are needed to confirm our findings."	( The efficacy and safety of lamotrigine for absence seizures in children and adolescents: A systematic review and meta-analysis. Cao, J; Lin, XX; Liu, H; Ma, XM, 2020)	0.86
"Our case adds to the existing literature by demonstrating that patients may experience adverse medication effects despite lamotrigine levels that are normally considered to be in the therapeutic range, highlighting the importance of clinical correlation when obtaining medication levels."	( Delirium Secondary to Lamotrigine Toxicity. Catalano, G; Catalano, MC; Fusick, AJ; Gunther, SR; Hernandez, MJ; Sanchez, DL; Sullivan, GA, 2020)	1.08
" LEV has milder adverse events than OXC and LTG in clinical practice."	( Comparison of long-term efficacy, tolerability, and safety of oxcarbazepine, lamotrigine, and levetiracetam in patients with newly diagnosed focal epilepsy: An observational study in the real world. Li, R; Li, Y; Ou, S; Pan, S; Wang, Y; Xia, L; Zhou, Q, 2020)	0.79
" To clarify how lamotrigine induces those cardiovascular adverse events, we simultaneously assessed its cardiohemodynamic and electrophysiological effects using the halothane-anesthetized dogs (n = 4)."	( Reverse translational analysis of clinically reported, lamotrigine-induced cardiovascular adverse events using the halothane-anesthetized dogs. Goto, A; Hagiwara-Nagasawa, M; Izumi-Nakaseko, H; Kambayashi, R; Kawai, S; Matsumoto, A; Nunoi, Y; Sugiyama, A; Takei, Y, 2021)	1.21
"Our project aimed to quantify the frequency of and adoption of recommendations for lamotrigine and lithium, and their adverse effects, in a Collaborative Care program."	( Lamotrigine and lithium in primary care psychiatric consultation: adoption and adverse effects. Bale, JD; Phelps, JR; Pipitone, OR; Squires, K, 2021)	2.29
" Treatment-emergent adverse events (TEAEs; 81 % vs 73 %) and TEAEs leading to discontinuation (16 % vs 2 %) were reported more frequently in Arm 2 than Arm 1, respectively."	( Efficacy and safety of eslicarbazepine acetate as a first or later adjunctive therapy in patients with focal seizures. Blum, D; Cantu, D; Gidal, B; Grinnell, T; Hixson, J; Mehta, D; Pikalov, A; Zhang, Y, 2021)	0.62
"6 million adverse event reports made to the FDA Adverse Event Reporting System (FAERS) database between July 1, 2018 and March 31, 2020 for DILI due to ASMs commonly used in clinical practice."	( Drug-induced liver injury associated with antiseizure medications from the FDA Adverse Event Reporting System (FAERS). Catalano, C; Gupta, K; Kamitaki, BK; Minacapelli, CD; Rustgi, V; Wachuku, C; Zhang, P, 2021)	0.62
"There have been several reports that switching formulations of antiseizure medications (ASMs) has been associated with a deterioration of seizure control, seizure relapse or increased adverse effects."	( Analyzing excipient-related adverse events in antiseizure drug formulations. Ionova, Y; Peterson, T; Wilson, L, 2022)	0.72
" All the studies identified LAM as an effective and safe drug in PMDs especially, BDs."	( Efficacy and safety of lamotrigine in pediatric mood disorders: A systematic review. Ahern, K; Athreya, AP; Croarkin, PE; Garzon, J; Hassett, LC; Kumar, R; Ozger, C; Oztosun, C; Saliba, M; Singh, B; Vande Voort, JL; Yuruk, D, 2023)	1.22
"Most studies suggested that LAM was safe and effective in pediatric patients with mood disorders."	( Efficacy and safety of lamotrigine in pediatric mood disorders: A systematic review. Ahern, K; Athreya, AP; Croarkin, PE; Garzon, J; Hassett, LC; Kumar, R; Ozger, C; Oztosun, C; Saliba, M; Singh, B; Vande Voort, JL; Yuruk, D, 2023)	1.22
" 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
"All nine drugs can relieve the pain of CPSP patients to different degrees; among them pregabalin and gabapentin have the most significant effect, and gabapentin and pregabalin also have the most adverse reactions."	( Efficacy and safety of different antidepressants and anticonvulsants in central poststroke pain: A network meta-analysis and systematic review. Chen, KY; Li, RY, 2022)	0.72
" Clinical characteristics, seizure outcomes, adverse effects and patient retention rates were evaluated."	( Comparison of the retention rate, safety, and efficacy of two different titration protocols for lamotrigine in newly diagnosed epilepsy patients. Jing, W; Li, P; Li, X; Niu, C; Wang, H; Yang, D; Zhang, N, )	0.35
" There was no significant difference in seizure outcomes or adverse effects between patients treated with LTG once daily and twice daily."	( Comparison of the retention rate, safety, and efficacy of two different titration protocols for lamotrigine in newly diagnosed epilepsy patients. Jing, W; Li, P; Li, X; Niu, C; Wang, H; Yang, D; Zhang, N, )	0.35
" The changes in the depressive rating scale, remission/response rates, nervous system adverse events (NSAEs), gastrointestinal adverse events (GIAEs), metabolic parameters, and prolactin were compared between medication and placebo or among medications with the Cohen's d or number needed to treat/harm."	( Efficacy and safety profiles of mood stabilizers and antipsychotics for bipolar depression: a systematic review. Bai, Y; Cai, L; Chen, G; Yang, H, 2023)	0.91
" According to the PHARMACOM-EPI framework, plasma concentrations of lamotrigine were predicted at the time of death and patients were categorized into non-toxic and toxic groups based on the therapeutic range of lamotrigine (3-15 mg/L)."	( A novel approach for pharmacological substantiation of safety signals using plasma concentrations of medication and administrative/healthcare databases: A case study using Danish registries for an FDA warning on lamotrigine. Battini, V; Carnovale, C; Kragholm, KH; Noordam, R; Sessa, M; Soeorg, H; van Dijk, KW; van Heemst, D; Wang, W, 2023)	1.33
"This retrospective pharmacovigilance case-non-case study used disproportionality analysis to detect signals of adverse reaction of interest reported with lamotrigine to the FDA Adverse Event Reporting System (FAERS) between 1998 and 2022."	( Investigation of cardiac arrhythmia events in patients treated with lamotrigine: FDA adverse event reporing system analysis. Aboukaoud, M; Maor, E; Wilf-Yarkoni, A, 2023)	1.34
" Signals of cardiac arrest in lamotrigine could be explained by confounding factors in the psychiatric indication, such as greater concomitant use of medications with cardiac adverse events, and greater reports on overdose and suicide attempts."	( Investigation of cardiac arrhythmia events in patients treated with lamotrigine: FDA adverse event reporing system analysis. Aboukaoud, M; Maor, E; Wilf-Yarkoni, A, 2023)	1.43

Pharmacokinetics

There was no significant pharmacokinetic interaction between ESL and lamotrigine in healthy subjects. The elimination half-life of lamot rigine was approximately 25 h in subjects with normal renal function and 50 h in uraemic patients.

Excerpt	Reference	Relevance
" Pharmacokinetic parameters were calculated using 1-compartment and non-compartment models."	( Pharmacokinetics and safety of lamotrigine (Lamictal) in patients with epilepsy. Allsup, T; Chern, WH; Garnett, WR; Hubbell, J; Lai, AA; Pellock, JM; Ramsay, RE; Sanchez, RM; Valakas, AM; Wargin, WA, )	0.42
") and pharmacokinetic parameters were compared with those of a group of nine normal volunteers."	( The pharmacokinetics of lamotrigine (BW430C) in healthy subjects with unconjugated hyperbilirubinaemia (Gilbert's syndrome). Cohen, AF; Land, G; Peck, AW; Posner, J; Winton, C, 1989)	0.58
"6 microgram/ml; LTG has a favorable pharmacokinetic profile and appears to exhibit first-order linear kinetics during long-term chronic dosing; LTG shows preliminary evidence of efficacy during long-term administration; and to date, our patients represent the longest reported experience of continuous and closely monitored LTG therapy in the literature."	( Long-term tolerability, pharmacokinetic and preliminary efficacy study of lamotrigine in patients with resistant partial seizures. Ashworth, M; Keally, M; Kupferberg, H; Mikati, MA; Osborne-Shafer, P; Schachter, SC; Schomer, DL; Seaman, CA; Sheridan, PH; Valakas, A, 1989)	0.51
" All patients received a single dose of lamotrigine in the second week to determine single-dose pharmacokinetic parameters."	( Lamotrigine: single-dose pharmacokinetics and initial 1 week experience in refractory epilepsy. Hamilton, MJ; Jawad, S; Oxley, JR; Peck, AW; Richens, A; Yuen, WC, 1987)	1.98
" In a second study 10 subjects received 120 mg lamotrigine and the mean (+/- SD) of the elimination half-life (t1/2) was 24."	( Lamotrigine, a new anticonvulsant: pharmacokinetics in normal humans. Breimer, DD; Cohen, AF; Land, GS; Peck, AW; Winton, C; Yuen, WC, 1987)	1.97
" Enzyme-inducing antiepileptic drugs such as phenytoin, phenobarbital (phenobarbitone) or carbamazepine reduce the half-life of lamotrigine (to mean values of 13."	( Lamotrigine clinical pharmacokinetics. Rambeck, B; Wolf, P, 1993)	1.93
" The elimination half-life of lamotrigine was approximately 25 h in subjects with normal renal function and 50 h in uraemic patients."	( Pharmacokinetics of lamotrigine in patients with renal impairment: influence of haemodialysis. Bidault, R; Etienne, I; Fialaire, A; Fillastre, JP; Singlas, E; Taburet, AM, 1993)	0.9
" Three of the new drugs, gabapentin, topiramate and vigabatrin, are more promising on the basis of their pharmacokinetic features."	( Comparative pharmacokinetics of the newer antiepileptic drugs. Bialer, M, 1993)	0.29
" The terminal elimination half-life (t1/2z) is relatively long in neonates; it then decreases during the first postnatal month to lower values than in adults, and then progressively increases with age due to an age-dependent decrease in the metabolic rate."	( Clinical pharmacokinetics of antiepileptic drugs in paediatric patients. Part II. Phenytoin, carbamazepine, sulthiame, lamotrigine, vigabatrin, oxcarbazepine and felbamate. Avanzini, G; Battino, D; Estienne, M, 1995)	0.5
"Antiepileptic drugs (AEDs) in broad use today have a number of pharmacokinetic liabilities, including a propensity for clinically meaningful drug interactions."	( Pharmacokinetic profile of topiramate in comparison with other new antiepileptic drugs. Perucca, E, 1996)	0.29
" This study was performed to assess the pharmacokinetic profile of lamotrigine in three groups of children treated with different types of comedication: drugs known to induce, to inhibit or to have no clinically significant influence on drug metabolism, respectively."	( Influence of concurrent antiepileptic medication on the pharmacokinetics of lamotrigine as add-on therapy in epileptic children. Bidault, R; Cieuta, C; d'Athis, P; Dulac, O; Olive, G; Pariente-Khayat, A; Pons, G; Rey, E; Vauzelle-Kervroëdan, F, 1996)	0.76
" The median elimination half-life (t1/2) in patients receiving concomitant valproate (VPA) was 43."	( Pharmacokinetic interactions between lamotrigine and other antiepileptic drugs in children with intractable epilepsy. Boreus, L; Eriksson, AS; Hoppu, K; Nergårdh, A, 1996)	0.57
" All the drugs can be conveniently given as a twice daily dosage apart from gabapentin, which has a short half-life and a midday dose is needed."	( Clinical pharmacokinetics of newer antiepileptic drugs. Lamotrigine, vigabatrin, gabapentin and oxcarbazepine. Binnie, CD; Elwes, RD, 1996)	0.54
" The 90% confidence intervals of the log-transformed pharmacokinetic parameters were within the 80-125% bioequivalance limits, however."	( Effect of felbamate on the pharmacokinetics of lamotrigine. Affrime, MB; Banfield, C; Colucci, R; Glue, P; Holt, B; Lim, J; Lin, CC; Meehan, JW; Nomeir, A; Pai, S; Reidenberg, P, 1996)	0.55
"This article surveys the pharmacokinetic parameters for the new antiepileptic drugs (AEDs): felbamate, gabapentin, lamotrigine, oxcarbazepine, tiagabine, topiramate, and vigabatrin."	( Pharmacokinetics of new antiepileptic drugs. Gram, L, 1996)	0.5
"Standard antiepileptic drugs (AEDs) have a number of pharmacokinetic shortcomings, and AEDs with more favorable profiles would be preferred."	( Pharmacokinetics and interaction profile of topiramate: review and comparison with other newer antiepileptic drugs. Johannessen, SI, 1997)	0.3
" Oral clearance (CLo), apparent volume of distribution (V/F) and absorption rate constant (Ka) were the main pharmacokinetic parameters."	( Population pharmacokinetics of lamotrigine monotherapy in patients with epilepsy: retrospective analysis of routine monitoring data. Hussein, Z; Posner, J, 1997)	0.58
"01 l/kg per h, respectively), or in mean elimination half-life (33."	( Lamotrigine pharmacokinetics in patients receiving felbamate. Gidal, BE; Kanner, A; Lensmeyer, GL; Maly, M; Rutecki, P, 1997)	1.74
" The half-life of lamotrigine is between 24."	( Lamotrigine: pharmacokinetics. Garnett, WR, 1997)	2.07
"To determine whether the toxicity that occurs in some patients when lamotrigine (LTG) is added to carbamazepine (CBZ) is the result of either a pharmacokinetic or a pharmacodynamic interaction."	( Carbamazepine toxicity with lamotrigine: pharmacokinetic or pharmacodynamic interaction? Berry, DJ; Besag, FM; Newbery, JE; Pool, F; Subel, B, 1998)	0.83
" This appears to be the result of a pharmacodynamic interaction."	( Carbamazepine toxicity with lamotrigine: pharmacokinetic or pharmacodynamic interaction? Berry, DJ; Besag, FM; Newbery, JE; Pool, F; Subel, B, 1998)	0.59
"Plasma concentrations of lamotrigine, an antiepileptic drug obtained in three adult controlled clinical trials conducted in the United States were pooled and analyzed using NONMEM, a population pharmacokinetic computer program, to facilitate development of dosing guidelines."	( Population pharmacokinetics of lamotrigine adjunctive therapy in adults with epilepsy. Chen, C; Cox, E; Fiedler-Kelly, J; Grasela, TH; Risner, ME; Womble, GP, 1999)	0.89
" Pharmacokinetic parameters were calculated using noncompartmental methods."	( Pharmacokinetics of lamotrigine in children in the absence of other antiepileptic drugs. Casale, EJ; Chen, C; Culverhouse, EH; Duncan, B; Gilman, J, 1999)	0.63
" Despite methodologic limitations in the nonrandomized treatment sequence, these findings suggest that VPA and LTG exhibit a favorable pharmacodynamic interaction in patients with refractory partial epilepsy."	( The efficacy of valproate-lamotrigine comedication in refractory complex partial seizures: evidence for a pharmacodynamic interaction. Di Perri, R; Oteri, G; Perucca, E; Pisani, F; Richens, A; Russo, MF, 1999)	0.6
" None of these pharmacokinetic parameters was found to be significantly different between the two groups."	( Effects of pregnancy on the pharmacokinetics of lamotrigine in dogs. Al-Hassan, MI; Bawazir, SA; Matar, KM; Nicholls, PJ; Tekle, A, 1999)	0.56
"The apparent lack of change in the relevant pharmacokinetic parameters of LTG during pregnancy may indicate that pregnancy has little or no effect on glucuronidation; the principal pathway for the drug's elimination."	( Effects of pregnancy on the pharmacokinetics of lamotrigine in dogs. Al-Hassan, MI; Bawazir, SA; Matar, KM; Nicholls, PJ; Tekle, A, 1999)	0.56
" For all drugs that are metabolized, half-life is shortened and clearance is increased when patients receive concomitant enzyme-inducing agents such as barbiturates, phenytoin, and carbamazepine."	( The clinical pharmacokinetics of the new antiepileptic drugs. Perucca, E, 1999)	0.3
"This analysis was performed to validate a previously developed population pharmacokinetic model for lamotrigine in order to establish a basis for dosage recommendations for children."	( Validation of a population pharmacokinetic model for adjunctive lamotrigine therapy in children. Chen, C, 2000)	0.76
" Population and individual (Bayesian estimate) pharmacokinetic parameters were estimated using both the initial model, which included none of the covariates, and the final model."	( Validation of a population pharmacokinetic model for adjunctive lamotrigine therapy in children. Chen, C, 2000)	0.55
"to describe the population pharmacokinetics of lamotrigine (LTG) in developmentally disabled (DD) patients with epilepsy and (2) to determine if there is an effect of valproate (VPA) concentration on the extent of the pharmacokinetic interaction between VPA and LTG."	( Lack of an effect of valproate concentration on lamotrigine pharmacokinetics in developmentally disabled patients with epilepsy. Anderson, GD; Gidal, BE; Lanning, A; Rutecki, PR; Shaw, R, 2000)	0.82
" The mean (+/- SEM) elimination half-life of CBZ was 33."	( Effects of short-term lamotrigine treatment on pharmacokinetics of carbamazepine. Keränen, T; Kerttula, T; Malminiemi, K; Moilanen, E; Ylitalo, P, 2000)	0.62
" Pharmacokinetic parameters of LTG were not significantly different between treatments."	( Effects of steady-state bupropion on the pharmacokinetics of lamotrigine in healthy subjects. Chen, C; Odishaw, J, 2000)	0.55
" Pharmacokinetic parameters were calculated by noncompartmental analysis."	( Single-dose pharmacokinetics of lamotrigine in children: influence of age and antiepileptic comedication. Battino, D; Croci, D; Granata, T; Mamoli, D; Messina, S; Perucca, E, 2001)	0.59
" Plasma half-life mean ratios (90% confidence interval) in these two patient groups to healthy subjects were, respectively, 204% (149%, 278%) and 287% (202%, 408%)."	( Influence of cirrhosis on lamotrigine pharmacokinetics. Altman, C; Bidault, R; Boige, V; Castelnau, C; Chen, C; de Bony, F; Garret, C; Laurent-Puig, P; Mamet, JP; Marcellin, P; Rolan, P; Trinchet, JC, 2001)	0.61
" Concurrent administration of LTG with CBZ did not have any significant effect on the pharmacokinetic parameters of CBZ."	( Effect of lamotrigine on the pharmacokinetics of carbamazepine and its active metabolite in dogs. Al-Hassan, MI; Al-Khamis, KI; Bawazir, SA; Matar, KM; Nicholls, PJ, )	0.53
" Apparent clearance (CL/F) and volume of distribution (V/F) were the pharmacokinetic parameters estimated."	( Population pharmacokinetics of lamotrigine. Chan, V; Ilett, KF; Morris, RG; Tett, SE, 2001)	0.6
" In the meantime, a review of the established pharmacokinetic and pharmacodynamic activities of these agents is the first step in defining their optimal uses and limitations in the psychiatric setting."	( Pharmacokinetics of new anticonvulsants in psychiatry. Morris, HH, 1998)	0.3
"Given that administration vehicles and drug formulations can affect drug bioavailability, their influence on the pharmacokinetic profile of lamotrigine (LTG), a new-generation anti-epileptic drug, was studied in rats."	( Influence of administration vehicles and drug formulations on the pharmacokinetic profile of lamotrigine in rats. Caramona, MM; Castel-Branco, MM; Falcão, AC; Figueiredo, IV; Macedo, TR, 2002)	0.74
" This study was performed to evaluate potential pharmacokinetic interactions between both AEDs."	( Pharmacokinetic interaction between retigabine and lamotrigine in healthy subjects. Borlak, J; Hermann, R; Knebel, NG; Locher, M; Niebch, G; Richards, L, 2003)	0.57
"RGB and LTG exhibit a modest pharmacokinetic interaction on each other."	( Pharmacokinetic interaction between retigabine and lamotrigine in healthy subjects. Borlak, J; Hermann, R; Knebel, NG; Locher, M; Niebch, G; Richards, L, 2003)	0.57
" The similarity of CL/F values also was reflected by the similar exposure (AUCss), Cmax, and Cmin values of TPM in the absence, and presence of LTG."	( Topiramate and lamotrigine pharmacokinetics during repetitive monotherapy and combination therapy in epilepsy patients. Berry, DJ; Bialer, M; Brodie, MJ; Chadwick, D; Doose, DR; Oxbury, J; Schwabe, S; Wilson, EA, 2003)	0.67
"The pharmacokinetic properties of a drug are the primary deter-minant of the extent and duration of drug action, and influence susceptibility to clinically important drug interactions."	( The ideal pharmacokinetic properties of an antiepileptic drug: how close does levetiracetam come? Johannessen, SI; Perucca, E, 2003)	0.32
" Future studies of formal pharmacokinetic modeling of AEDs during pregnancy and the postpartum period could provide an important step toward achieving effective drug dosing to maintain therapeutic objectives for the mother but, at the same time, to minimize fetal drug exposure."	( Antiepileptic drug pharmacokinetics during pregnancy and lactation. Pennell, PB, 2003)	0.32
" Given the known pharmacokinetic interaction between these two drugs, clinically relevant questions that should be answered include (1) at what dose and/or concentration of VPA does this interaction begin, and (2) at what dose of VPA does maximal inhibition occur."	( Evaluation of VPA dose and concentration effects on lamotrigine pharmacokinetics: implications for conversion to lamotrigine monotherapy. Gidal, BE; Maloney, K; Parnell, J; Sale, M; Sheth, R, 2003)	0.57
" Serial blood samples were obtained over 120 h post-dose in order to calculate LTG kinetic parameters including area under the concentration-time curve, apparent oral clearance, elimination half-life and percent inhibition of LTG clearance at each dosage level of VPA."	( Evaluation of VPA dose and concentration effects on lamotrigine pharmacokinetics: implications for conversion to lamotrigine monotherapy. Gidal, BE; Maloney, K; Parnell, J; Sale, M; Sheth, R, 2003)	0.57
"LTG pharmacokinetic parameters were evaluated in adult healthy female & male volunteers."	( Evaluation of VPA dose and concentration effects on lamotrigine pharmacokinetics: implications for conversion to lamotrigine monotherapy. Gidal, BE; Maloney, K; Parnell, J; Sale, M; Sheth, R, 2003)	0.57
"The pharmacodynamic interaction between the antiepileptic drugs (AEDs) tiagabine (TGB) and lamotrigine (LTG) was characterized on basis of the anticonvulsant effect in the cortical stimulation model in the rat."	( Pharmacodynamic analysis of the anticonvulsant effects of tiagabine and lamotrigine in combination in the rat. Danhof, M; Jonker, DM; Voskuyl, RA, 2004)	0.78
" A potential pharmacokinetic interaction was accounted for by determination of total plasma concentrations of both drugs."	( Pharmacodynamic analysis of the anticonvulsant effects of tiagabine and lamotrigine in combination in the rat. Danhof, M; Jonker, DM; Voskuyl, RA, 2004)	0.56
" This analysis showed that the pharmacodynamic interaction between TGB and LTG is synergistic for the ictal signs of eye closure and head jerk."	( Pharmacodynamic analysis of the anticonvulsant effects of tiagabine and lamotrigine in combination in the rat. Danhof, M; Jonker, DM; Voskuyl, RA, 2004)	0.56
"This study demonstrates the usefulness of ictal-component analysis for studying the pharmacodynamic interaction between AEDs."	( Pharmacodynamic analysis of the anticonvulsant effects of tiagabine and lamotrigine in combination in the rat. Danhof, M; Jonker, DM; Voskuyl, RA, 2004)	0.56
" The method is suitable in pharmacokinetic investigation and monitoring lamotrigine concentration."	( Determination of lamotrigine in small volumes of plasma by high-performance liquid chromatography. Cheng, CL; Chou, CH; Hu, OY, 2005)	0.9
" However, these combinations were associated with significant pharmacokinetic interactions, in that LCZ increased brain TPM (94%), OXC (21%), FBM (46%), and LTG (8%) concentrations."	( Pharmacodynamic and pharmacokinetic interaction studies of loreclezole with felbamate, lamotrigine, topiramate, and oxcarbazepine in the mouse maximal electroshock seizure model. Czuczwar, SJ; Luszczki, JJ; Patsalos, PN; Ratnaraj, N, 2005)	0.55
" However, these conclusions are confounded by the fact that LCZ is associated with significant pharmacokinetic interactions."	( Pharmacodynamic and pharmacokinetic interaction studies of loreclezole with felbamate, lamotrigine, topiramate, and oxcarbazepine in the mouse maximal electroshock seizure model. Czuczwar, SJ; Luszczki, JJ; Patsalos, PN; Ratnaraj, N, 2005)	0.55
" Pharmacokinetic parameters were determined by noncompartmental methods."	( Lack of pharmacokinetic interaction between oxcarbazepine and lamotrigine. Ascher, J; Bullman, J; Job, S; Palmer, J; Sidhu, J; Theis, JG, 2005)	0.57
"The aim of the study was to obtain pharmacokinetic data for carbamazepine (CBZ) and its fractions not bound with proteins in bitherapy with lamotrigine (LTG), topiramate (TPM), vigabatrin (VGB) or valproic acid (VPA) in children and adolescents treated for epilepsy."	( Pharmacokinetic interactions of carbamazepine with some antiepileptic drugs during epilepsy treatment in children and adolescents. Steinborn, B, 2005)	0.53
" For pharmacokinetic calculations of total and free CBZ, one-compartment model was used according to standardized procedure."	( Pharmacokinetic interactions of carbamazepine with some antiepileptic drugs during epilepsy treatment in children and adolescents. Steinborn, B, 2005)	0.33
"No significant differences in pharmacokinetic parameters of unbound CBZ in four groups of patients on bitherapy with CBZ and LTG, TPM, VGB or VPA were found."	( Pharmacokinetic interactions of carbamazepine with some antiepileptic drugs during epilepsy treatment in children and adolescents. Steinborn, B, 2005)	0.33
" Likewise, PGB steady-state pharmacokinetic parameter values were similar among patients receiving CBZ, PHT, LTG, or VPA and, in general, were similar to those observed historically in healthy subjects receiving PGB alone."	( Pregabalin drug interaction studies: lack of effect on the pharmacokinetics of carbamazepine, phenytoin, lamotrigine, and valproate in patients with partial epilepsy. Alvey, CW; Bockbrader, HN; Brodie, MJ; Bron, NJ; Gibson, GL; Hounslow, NJ; Posvar, EL; Randinitis, EJ; Wesche, DL; Wilson, EA, 2005)	0.54
" To fit the effect-time course of lamotrigine, the PK/PD simultaneous fitting link model was used: the pharmacokinetic parameters and dosing information were used in the one-compartment first-order model to predict concentrations, which were then used to model the pharmacodynamic data with the sigmoid Emax model, in order to estimate all the parameters simultaneously."	( Lamotrigine pharmacokinetic/pharmacodynamic modelling in rats. Caramona, MM; Castel-Branco, MM; Falcão, AC; Figueiredo, IV, 2005)	2.05
"To assess the pharmacokinetic and pharmacodynamic effects of co-administration of a combined oral contraceptive (ethinyloestradiol plus levonorgestrel) and lamotrigine."	( The pharmacokinetic and pharmacodynamic consequences of the co-administration of lamotrigine and a combined oral contraceptive in healthy female subjects. Job, S; Philipson, R; Sidhu, J; Singh, S, 2006)	0.76
"Of the 22 enrolled subjects, 16 had evaluable pharmacokinetic data."	( The pharmacokinetic and pharmacodynamic consequences of the co-administration of lamotrigine and a combined oral contraceptive in healthy female subjects. Job, S; Philipson, R; Sidhu, J; Singh, S, 2006)	0.56
"A clinically relevant pharmacokinetic interaction was observed during co-administration of a combined oral contraceptive and lamotrigine."	( The pharmacokinetic and pharmacodynamic consequences of the co-administration of lamotrigine and a combined oral contraceptive in healthy female subjects. Job, S; Philipson, R; Sidhu, J; Singh, S, 2006)	0.77
"To assess the pharmacokinetic effect and tolerability of lamotrigine 200 mg day(-1) and olanzapine 15 mg day(-1) coadministration in healthy male volunteers."	( Pharmacokinetics and tolerability of lamotrigine and olanzapine coadministered to healthy subjects. Abbott, R; Ascher, J; Bullman, J; Francis, E; Job, S; Sidhu, J; Theis, JG, 2006)	0.85
" Steady state (0-24 h) pharmacokinetic profiles were determined on day 56 in each group."	( Pharmacokinetics and tolerability of lamotrigine and olanzapine coadministered to healthy subjects. Abbott, R; Ascher, J; Bullman, J; Francis, E; Job, S; Sidhu, J; Theis, JG, 2006)	0.61
"The aim of the present study was to evaluate the pharmacokinetic profile of lamotrigine (LTG) in epileptic patients submitted to video-electroencephalography (VEEG) monitoring and, in addition, to investigate the influence of concomitant antiepileptic drugs (AEDs) on the kinetics of LTG."	( Lamotrigine pharmacokinetic evaluation in epileptic patients submitted to VEEG monitoring. Almeida, AM; Baldeiras, I; Caramona, MM; Falcão, AC; Rocha, MJ; Sales, F, 2006)	2.01
" For drugs that are eliminated renally completely unchanged (gabapentin, pregabalin and vigabatrin) or mainly unchanged (levetiracetam and topiramate), the pharmacokinetic variability is less pronounced and more predictable."	( Pharmacokinetic variability of newer antiepileptic drugs: when is monitoring needed? Johannessen, SI; Tomson, T, 2006)	0.33
" The clinical impact of pharmacokinetic interactions between lamotrigine and enzyme-inducing AEDs or valproate can be minimised by adhering to recommended dose-escalation schedules with demonstrated reliability in clinical trials and clinical practice."	( Pharmacokinetics, toxicology and safety of lamotrigine in epilepsy. Biton, V, 2006)	0.84
" A reduction in the LTG Cmax was observed for LTG-XR compared to LTG-IR resulting in a decrease in the peak-to-trough fluctuation in serum LTG concentrations."	( Steady-state pharmacokinetics of lamotrigine when converting from a twice-daily immediate-release to a once-daily extended-release formulation in subjects with epilepsy (The COMPASS Study). Ali, I; Hammer, AE; Job, S; Lemme, F; Messenheimer, JA; Oliver-Willwong, R; Tompson, DJ; Vuong, A; Zhu, L, 2008)	0.63
" The goal of this study is to determine the pharmacokinetic parameters, such as clearance, and the factors that have a significant effect on these parameters to provide evidence-based information that can be used to dose elderly patients taking lamotrigine."	( Population pharmacokinetics of lamotrigine in elderly patients. Birnbaum, AK; Brundage, RC; Collins, JF; Macias, FM; Punyawudho, B; Ramsay, RE; Rowan, AJ, 2008)	0.81
" PPK model of lamotrigine was established using NONMEM, a population pharmacokinetic computer program, according to one-compartment model with first-order absorption and elimination."	( [Population pharmacokinetics of lamotrigine in Chinese children with epilepsy]. Lu, W; Wang, L; Zhang, S, 2008)	0.99
"This study develops a population pharmacokinetic model for lamotrigine (LTG) in Spanish and German patients diagnosed with epilepsy."	( Population pharmacokinetics of lamotrigine with data from therapeutic drug monitoring in German and Spanish patients with epilepsy. Buelga, DS; Domínguez-Gil, A; Elger, CE; García, MJ; Otero, MJ; Rivas, N; Santos-Borbujo, J, 2008)	0.88
" Because there is a large interindividual variability in the magnitude and time course of the pregnancy-associated pharmacokinetic changes, it is desirable to establish baseline plasma LTG concentrations in all women of childbearing potential and to monitor LTG levels at frequent intervals during pregnancy and the puerperium."	( Changes in lamotrigine pharmacokinetics during pregnancy and the puerperium. Franco, V; Gatti, G; La Neve, A; Mazzucchelli, I; Ozkaynakçi, AE; Papantonio, A; Perucca, E; Specchio, LM, 2008)	0.74
" Blood samples were collected on Days -1 and 14 for determination of lamotrigine steady-state pharmacokinetic parameters."	( A non-randomized study to investigate the effects of the atypical antipsychotic aripiprazole on the steady-state pharmacokinetics of lamotrigine in patients with bipolar I disorder. Balch, AH; Benson, J; Boulton, DW; Carlson, BX; Croop, R; Mallikaarjun, S; Schieber, FC, 2009)	0.79
"There was no significant pharmacokinetic interaction between ESL and lamotrigine in healthy subjects."	( Pharmacokinetic interaction study between eslicarbazepine acetate and lamotrigine in healthy subjects. Almeida, L; Brunet, JS; Falcão, A; Lefebvre, M; Nunes, T; Rocha, JF; Sicard, E; Soares-da-Silva, P, 2010)	0.83
" Serial pharmacokinetic sampling of atorvastatin was conducted on day 7 of atorvastatin dosing and day 70 of lamotrigine + atorvastatin dosing or day 28 of phenytoin + atorvastatin dosing."	( Effects of lamotrigine and phenytoin on the pharmacokinetics of atorvastatin in healthy volunteers. Alexander, S; Bullman, J; Fleck, R; Messenheimer, J; Miller, J; Nicholls, A; Van Landingham, K; Vuong, A, 2011)	0.97
"In the first DDI study, coadministration of ketoconazole (a CYP3A4 inhibitor) and clobazam increased clobazam's area under the concentration time curve from time zero extrapolated to infinity (AUC(0-∞) ) 54% and decreased clobazam's maximum plasma concentration (C(max) ) by 15% versus administration of clobazam alone, but the combination affected these pharmacokinetic parameters for N-CLB to a lesser degree."	( Pharmacokinetic drug interactions between clobazam and drugs metabolized by cytochrome P450 isoenzymes. Bekersky, I; Blum, RA; Tolbert, D; Walzer, M, 2012)	0.38
"The aim of this analysis was to describe the pharmacokinetics of oral lamotrigine (LTG) in Indian epileptic patients using a population pharmacokinetic (PPK) modeling approach to confirm that the PK is similar to that of the Caucasian population, and to evaluate and confirm the impact of covariates predictive of inter-individual variability using a simulation platform."	( Population pharmacokinetics of lamotrigine in Indian epileptic patients. Arumugam, K; Bathala, L; Johnson, MG; Mallaysamy, S; Rajakannan, T; Ramakrishna, D; Rao, PG; van Hasselt, JG, 2013)	0.91
" There is still insufficient documentation regarding pharmacokinetic variability of these AEDs in different patient groups."	( Pharmacokinetic variability of four newer antiepileptic drugs, lamotrigine, levetiracetam, oxcarbazepine, and topiramate: a comparison of the impact of age and comedication. Baftiu, A; Johannessen Landmark, C; Johannessen, SI; Larsson, PG; Rytter, E; Tysse, I; Valsø, B, 2012)	0.62
"The purpose of this study was to compare age and comedication as factors contributing to pharmacokinetic variability between 4 newer AEDs (lamotrigine, levetiracetam, oxcarbazepine, and topiramate) among patients with refractory epilepsy."	( Pharmacokinetic variability of four newer antiepileptic drugs, lamotrigine, levetiracetam, oxcarbazepine, and topiramate: a comparison of the impact of age and comedication. Baftiu, A; Johannessen Landmark, C; Johannessen, SI; Larsson, PG; Rytter, E; Tysse, I; Valsø, B, 2012)	0.82
" The interindividual pharmacokinetic variability was extensive, as illustrated by a 10-fold variability in serum concentration compared with dose."	( Pharmacokinetic variability of four newer antiepileptic drugs, lamotrigine, levetiracetam, oxcarbazepine, and topiramate: a comparison of the impact of age and comedication. Baftiu, A; Johannessen Landmark, C; Johannessen, SI; Larsson, PG; Rytter, E; Tysse, I; Valsø, B, 2012)	0.62
"Age and comedication are important contributors to pharmacokinetic variability."	( Pharmacokinetic variability of four newer antiepileptic drugs, lamotrigine, levetiracetam, oxcarbazepine, and topiramate: a comparison of the impact of age and comedication. Baftiu, A; Johannessen Landmark, C; Johannessen, SI; Larsson, PG; Rytter, E; Tysse, I; Valsø, B, 2012)	0.62
" This method is applicable for the pharmacokinetic studies of SMA in rats."	( A simple and sensitive HPLC-UV determination of 7-O-succinyl macrolactin A in rat plasma and urine and its application to a pharmacokinetic study. Jung, JW; Kang, HE; Kang, JS; Kim, CG; Kim, DH; Kim, JM, 2013)	0.39
" The aim of this study was to determine the pharmacokinetic parameters of lamotrigine and to investigate the effect of genetic variants of UGT1A4 and UGT2B7 and various non-genetic factors on its pharmacokinetics."	( Influence of the UGT2B7 -161C>T polymorphism on the population pharmacokinetics of lamotrigine in Thai patients. Lertkachatarn, S; Punyawudho, B; Singkham, N; Towanabut, S, 2013)	0.85
"A pharmacokinetic model was constructed for lamotrigine XR and IR formulations in the presence and absence of comedications."	( Assessing impact of real-world dosing irregularities with lamotrigine extended-release and immediate-release formulations by pharmacokinetic simulation. Chen, C; Gidal, B; Messenheimer, J; Wright, J, 2013)	0.9
" A doubled dose after a missed dose did not lead to excessive peak concentration for either treatment."	( Assessing impact of real-world dosing irregularities with lamotrigine extended-release and immediate-release formulations by pharmacokinetic simulation. Chen, C; Gidal, B; Messenheimer, J; Wright, J, 2013)	0.63
"The LTG population pharmacokinetic model developed in this study may be a reliable method for individualising the LTG dosing regimen in paediatric and young adult patients on combination therapy during therapeutic drug monitoring."	( Pharmacokinetics of lamotrigine in paediatric and young adult epileptic patients--nonlinear mixed effects modelling approach. Brzaković, B; Kovačević, SV; Martinović, Ž; Miljković, B; Pokrajac, M; Prostran, M; Vučićević, K, 2014)	0.73
"Pharmacotherapy for mood disorders during pregnancy is often complicated by pregnancy-related pharmacokinetic changes and the need for dose adjustments."	( Pharmacotherapy for mood disorders in pregnancy: a review of pharmacokinetic changes and clinical recommendations for therapeutic drug monitoring. Byatt, N; Deligiannidis, KM; Freeman, MP, 2014)	0.4
"The English-language literature indexed on MEDLINE/PubMed was searched for original observational studies (controlled and uncontrolled, prospective and retrospective), case reports, and case series that evaluated or described pharmacokinetic changes or TDM during pregnancy or the postpartum period."	( Pharmacotherapy for mood disorders in pregnancy: a review of pharmacokinetic changes and clinical recommendations for therapeutic drug monitoring. Byatt, N; Deligiannidis, KM; Freeman, MP, 2014)	0.4
"Substantial pharmacokinetic changes can occur during pregnancy in a number of commonly used antidepressants and mood stabilizers."	( Pharmacotherapy for mood disorders in pregnancy: a review of pharmacokinetic changes and clinical recommendations for therapeutic drug monitoring. Byatt, N; Deligiannidis, KM; Freeman, MP, 2014)	0.4
"The present study aimed to establish population pharmacokinetic model for phenobarbital (PB), examining and quantifying the magnitude of PB interactions with other antiepileptic drugs concomitantly used and to demonstrate its use for individualization of PB dosing regimen in adult epileptic patients."	( Nonlinear mixed effects modelling approach in investigating phenobarbital pharmacokinetic interactions in epileptic patients. Golubović, B; Jovanović, M; Kovačević, SV; Martinović, Ž; Miljković, B; Prostran, M; Vučićević, K, 2015)	0.42
" The time to peak concentration (Tmax, ss) was delayed for XR lamotrigine (3."	( Steady-state pharmacokinetics and bioavailability of immediate-release and extended-release formulations of lamotrigine in elderly epilepsy patients: Use of stable isotope methodology. Birnbaum, AK; Brundage, RC; Leppik, IE; Polepally, AR; Ramsay, RE; Rarick, JO; Remmel, RP, 2015)	0.87
"This study aimed to develop a population pharmacokinetic model for quantitative evaluation of the influence of genetic variants in metabolic enzymes and transporters on lamotrigine pharmacokinetics while taking into account the influence of various clinical, biochemical and demographic factors."	( Pharmacokinetics of lamotrigine and its metabolite N-2-glucuronide: Influence of polymorphism of UDP-glucuronosyltransferases and drug transporters. Dolžan, V; Grabnar, I; Kastelic, M; Lorber, B; Milosheska, D; Vovk, T, 2016)	0.95
" Population pharmacokinetic analysis was performed by non-linear mixed effects modelling."	( Pharmacokinetics of lamotrigine and its metabolite N-2-glucuronide: Influence of polymorphism of UDP-glucuronosyltransferases and drug transporters. Dolžan, V; Grabnar, I; Kastelic, M; Lorber, B; Milosheska, D; Vovk, T, 2016)	0.76
" The purpose of the study was to investigate 2-way pharmacokinetic interactions between ESL and other AEDs as compared to OXC and CBZ."	( The Impact of Pharmacokinetic Interactions With Eslicarbazepine Acetate Versus Oxcarbazepine and Carbamazepine in Clinical Practice. Baftiu, A; Brodtkorb, E; Burns, ML; Dinarevic, J; Johannessen Landmark, C; Johannessen, SI; Kufaas, RF; Reimers, A; Svendsen, T, 2016)	0.43
"Possible pharmacokinetic interactions have been studied for ESL as compared to OXC and CBZ."	( The Impact of Pharmacokinetic Interactions With Eslicarbazepine Acetate Versus Oxcarbazepine and Carbamazepine in Clinical Practice. Baftiu, A; Brodtkorb, E; Burns, ML; Dinarevic, J; Johannessen Landmark, C; Johannessen, SI; Kufaas, RF; Reimers, A; Svendsen, T, 2016)	0.43
" A systematic approach was developed to characterize the TI of a drug using therapeutic drug monitoring and electronic health record (EHR) data with pharmacokinetic (PK) modeling."	( Use of Therapeutic Drug Monitoring, Electronic Health Record Data, and Pharmacokinetic Modeling to Determine the Therapeutic Index of Phenytoin and Lamotrigine. Berezny, A; Cohen-Wolkowiez, M; Gonzalez, D; Greenberg, RG; Guptill, JT; Hill, KD; Hornik, CP; Jiang, W; Ku, LC; Melloni, C; Wu, H; Zheng, N, 2016)	0.63
" The objective of the study was to identify pharmacokinetic interactions of different mood stabilizers on the metabolism of risperidone (RIS) under natural conditions."	( Pharmacokinetic Drug-Drug Interactions of Mood Stabilizers and Risperidone in Patients Under Combined Treatment. Gründer, G; Haen, E; Hiemke, C; Lammertz, SE; Paulzen, M; Schoretsanitis, G; Schruers, KR; Stegmann, B, 2016)	0.43
"The data give evidence for pharmacokinetic interactions between RIS and different anticonvulsant mood stabilizers."	( Pharmacokinetic Drug-Drug Interactions of Mood Stabilizers and Risperidone in Patients Under Combined Treatment. Gründer, G; Haen, E; Hiemke, C; Lammertz, SE; Paulzen, M; Schoretsanitis, G; Schruers, KR; Stegmann, B, 2016)	0.43
" This article explores potential pharmacokinetic and pharmacodynamic drug interactions of relevance to the use of ketamine in depression."	( Ketamine for Depression, 5: Potential Pharmacokinetic and Pharmacodynamic Drug Interactions. Andrade, C, 2017)	0.46
"The aims of this study were to develop a population pharmacokinetic (PPK) model of lamotrigine (LTG) in Chinese epileptic children by using nonlinear mixed effects modeling (NONMEM) and to investigate the effects of valproic acid (VPA) and genetic polymorphisms of the major metabolizing enzymes (UGT1A4, UGT2B7) on the pharmacokinetics of LTG."	( Population pharmacokinetics of lamotrigine co-administered with valproic acid in Chinese epileptic children using nonlinear mixed effects modeling. Chen, Y; Liu, L; Liu, M; Liu, S; Lu, T; Wang, H; Xu, S; Zhao, L; Zhao, M, 2018)	0.99
"An allometrically scaled pharmacokinetic model was developed using adolescent and adult data, taking into account the effect of comedications."	( Effect of Age-Related Factors on the Pharmacokinetics of Lamotrigine and Potential Implications for Maintenance Dose Optimisation in Future Clinical Trials. Danhof, M; de Jager, NCB; Della Pasqua, O; Rauwé, WM; van Dijkman, SC, 2018)	0.73
"Population pharmacokinetic models are usually limited to a subgroup of patients, which may mask the identification of factors contributing to interindividual variability."	( Effect of Age-Related Factors on the Pharmacokinetics of Lamotrigine and Potential Implications for Maintenance Dose Optimisation in Future Clinical Trials. Danhof, M; de Jager, NCB; Della Pasqua, O; Rauwé, WM; van Dijkman, SC, 2018)	0.73
" LTG concentrations were determined at several post-dose time-points and submitted to a non-compartmental pharmacokinetic analysis."	( Effects of Paullinia cupana extract on lamotrigine pharmacokinetics in rats: A herb-drug interaction on the gastrointestinal tract with potential clinical impact. Alves, G; Falcão, A; Rodrigues, M; Ventura, S, 2018)	0.75
" Lamotrigine pharmacokinetic parameters were estimated using noncompartmental analysis."	( Pharmacokinetics, Safety, and Tolerability of Lamotrigine Chewable/Dispersible Tablet Following Repeat-Dose Administration in Healthy Chinese Volunteers. Hu, J; Li, H; Li, Y; Xu, Y; Zhang, F, 2018)	1.65
"The objectives of this study were to investigate the effect of age on pharmacokinetic parameters of lamotrigine (LTG) and estimate parameter variability."	( Lamotrigine pharmacokinetics following oral and stable-labeled intravenous administration in young and elderly adult epilepsy patients: Effect of age. Birnbaum, AK; Brundage, RC; Kistner, BM; Leppik, IE; Pennell, PB; Polepally, AR; Ramsay, RE; Remmel, RP; White, JR, 2018)	2.14
" Therefore, this study aimed to establish a population pharmacokinetic (PPK) model of LTG in Chinese children with epilepsy and to comprehensively evaluate the effects of genetic variations in drug-metabolizing enzymes, transporters, and a transcriptional regulator on LTG pharmacokinetics."	( A Population Pharmacokinetic-Pharmacogenetic Model of Lamotrigine in Chinese Children With Epilepsy. Chen, Y; Lu, T; Wang, H; Wang, Z; Xu, S; Zhao, L; Zhao, M, 2018)	0.73
" cambogia extract and lamotrigine (LTG) through two independent pharmacokinetic studies."	( Short-term effects of Garcinia cambogia extract on the pharmacokinetics of lamotrigine given as a single-dose in Wistar rats. Alves, G; Falcão, A; Rodrigues, M; Ventura, S, 2019)	1.06
"To evaluate the pharmacokinetic changes in lamotrigine (LTG) from prepregnancy to postpartum and to assess the impact of therapeutic drug monitoring (TDM) on seizure management during pregnancy in a Chinese population."	( Pharmacokinetic changes and therapeutic drug monitoring of lamotrigine during pregnancy. Ding, Y; Guo, Y; Tan, X; Zhang, S, 2019)	1.02
"The pharmacokinetic changes in LTG during pregnancy displayed marked interpatient variation."	( Pharmacokinetic changes and therapeutic drug monitoring of lamotrigine during pregnancy. Ding, Y; Guo, Y; Tan, X; Zhang, S, 2019)	0.76
"Population factors such as age, gender, ethnicity, genotype and disease state can cause inter-individual variability in pharmacokinetic (PK) profile of drugs."	( A repository of protein abundance data of drug metabolizing enzymes and transporters for applications in physiologically based pharmacokinetic (PBPK) modelling and simulation. Balhara, A; Bobe, P; Ghandikota, S; Joshi, A; Kangne, H; Ladumor, MK; Levi, D; Mishra, S; Nautiyal, V; Pammi, P; Prasad, B; Rachapally, A; Rao, VK; Sharma, S; Singh, S; Thakur, A, 2019)	0.51
"The drug concentrations in the deep cervical lymph node, superficial cervical lymph node, brain tissues and jugular vein, the pharmacokinetic parameters, and the concentrations of IL-6 in deep cervical lymph node and brain tissues were investigated following UPLC/MS, DAS3."	( Lymphatic clearance is the main drainage route of lamotrigine-loaded micelles following delivery to the brain. Chen, G; Chen, Y; Hou, D; Lin, Y; Lv, Z; Ren, J; Yan, J; Yang, F; Zhou, J; Zhu, Y, 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
"Postmarketing population pharmacokinetic (PK) and pharmacodynamic (PD) studies can be useful to capture patient characteristics affecting PK or PD in real-world settings."	( Development of a System for Postmarketing Population Pharmacokinetic and Pharmacodynamic Studies Using Real-World Data From Electronic Health Records. Abou-Khalil, BW; Beck, C; Bejan, CA; Birdwell, KA; Choi, L; Denny, JC; James, NT; McNeer, E; Niu, X; Roden, DM; Stein, CM; Van Driest, SL; Weeks, HL; Williams, ML, 2020)	0.56
"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 clinical value of therapeutic drug monitoring can be increased most significantly by integrating assay results into clinical pharmacokinetic models for optimal dosing."	( Development of a methodology to make individual estimates of the precision of liquid chromatography-tandem mass spectrometry drug assay results for use in population pharmacokinetic modeling and the optimization of dosage regimens. Jelliffe, RW; Karvaly, GB; Kovács, K; Neely, MN; Vásárhelyi, B; Vincze, I, 2020)	0.56
" This permits optimal dosages by providing the correct weighting factor of assay results in the development of population and individual pharmacokinetic models."	( Development of a methodology to make individual estimates of the precision of liquid chromatography-tandem mass spectrometry drug assay results for use in population pharmacokinetic modeling and the optimization of dosage regimens. Jelliffe, RW; Karvaly, GB; Kovács, K; Neely, MN; Vásárhelyi, B; Vincze, I, 2020)	0.56
" We aimed an observational study to develop a population pharmacokinetic model for quantitative evaluation of the factors that influence lamotrigine pharmacokinetics in Mexican adults with epilepsy."	( Dosing Recommendations Based on Population Pharmacokinetics of Lamotrigine in Mexican Adult Patients With Epilepsy. Chávez-Castillo, CE; Medellín-Garibay, SE; Milán-Segovia, RDC; Rodríguez-Leyva, I; Romano-Moreno, S, 2020)	1
" However, relatively high interindividual pharmacokinetic variability of this drug has been documented."	( Sources of lamotrigine pharmacokinetic variability: A systematic review of population pharmacokinetic analyses. Leelakanok, N; Methaneethorn, J, 2020)	0.95
"This systematic review aimed to summarize significant factors influencing LTG pharmacokinetics and their relationships with pharmacokinetic parameters as well as the magnitude of pharmacokinetic variability."	( Sources of lamotrigine pharmacokinetic variability: A systematic review of population pharmacokinetic analyses. Leelakanok, N; Methaneethorn, J, 2020)	0.95
" Population pharmacokinetic studies of LTG conducted in humans using a nonlinear-mixed effect approach were eligible for a systematic review."	( Sources of lamotrigine pharmacokinetic variability: A systematic review of population pharmacokinetic analyses. Leelakanok, N; Methaneethorn, J, 2020)	0.95
"For clinical application, LTG maintenance dose could be optimized using population pharmacokinetic models employing covariates such as concomitant antiepileptic drugs, body weight, and genetic polymorphisms."	( Sources of lamotrigine pharmacokinetic variability: A systematic review of population pharmacokinetic analyses. Leelakanok, N; Methaneethorn, J, 2020)	0.95
" The aims of this study were to evaluate the predictive performance of pediatric population pharmacokinetic (PPK) models published on lamotrigine, to build a new model with our monitoring data and to evaluate the current recommended doses."	( Dosing Recommendations for Lamotrigine in Children: Evaluation Based on Previous and New Population Pharmacokinetic Models. Aboura, R; Benaboud, S; Billette de Villemeur, T; Bouazza, N; Chenevier-Gobeaux, C; Desguerre, I; Freihuber, C; Gana, I; Hirt, D; Nabbout, R; Tauzin, M; Tréluyer, JM; Zheng, Y, 2021)	1.12
" An adult physiologically based pharmacokinetic model of lamotrigine was developed and evaluated."	( Incorporating Breastfeeding-Related Variability with Physiologically Based Pharmacokinetic Modeling to Predict Infant Exposure to Maternal Medication Through Breast Milk: a Workflow Applied to Lamotrigine. Autmizguine, J; Edginton, AN; Ito, S; Yeung, CHT, 2021)	1.06

Compound-Compound Interactions

Sodium valproate combined with lamotrigine has better clinical efficacy and higher safety in the treatment of poststroke secondary epilepsy. The drug is able to reduce the expression levels of serum inflammatory factors.

Excerpt	Reference	Relevance
"Although MSM is a valuable add-on, broad-spectrum drug when used in combination with LTG, adjustment of the LTG dose may be necessary when MSM is started or stopped, to allow for the fact that MSM lowers LTG blood levels."	( Methsuximide lowers lamotrigine blood levels: A pharmacokinetic antiepileptic drug interaction. Berry, DJ; Besag, FM; Pool, F, 2000)	0.63
" This study was designed to assess the antiepileptic activity of aspirin and to investigate the potentiation of its activity in combination with a subconvulsive dose of lamotrigine."	( Evaluation of antiepileptic activity of aspirin in combination with newer antiepileptic lamotrigine in mice. Anuradha, K; Pandhi, P; Tandon, M, 2003)	0.74
" Concerning pharmacokinetic drug interactions, we conclude that lamotrigine can be safely combined with most psychotropic drugs."	( Drug interactions between lamotrigine and psychoactive drugs: evidence from a therapeutic drug monitoring service. Reimers, A; Skogvoll, E; Spigset, O; Sund, JK, 2005)	0.87
" Felbamate administered alone or combined with lamotrigine considerably impaired exploratory and spontaneous locomotor activities of the animals tested in terms of horizontal activity."	( Effect of lamotrigine combined with felbamate on the horizontal (ambulatory) activity in mice. Andres, MM; Luszczki, JJ; Swiader, MJ, 2004)	0.98
" Patients received PGB, 600 mg/day (200 mg q8h) for 7 days, in combination with their individualized maintenance monotherapy with valproate (VPA), phenytoin (PHT), lamotrigine (LTG), or carbamazepine (CBZ)."	( Pregabalin drug interaction studies: lack of effect on the pharmacokinetics of carbamazepine, phenytoin, lamotrigine, and valproate in patients with partial epilepsy. Alvey, CW; Bockbrader, HN; Brodie, MJ; Bron, NJ; Gibson, GL; Hounslow, NJ; Posvar, EL; Randinitis, EJ; Wesche, DL; Wilson, EA, 2005)	0.74
" PGB may be added to VPA, LTG, PHT, or CBZ therapy without concern for pharmacokinetic drug-drug interactions."	( Pregabalin drug interaction studies: lack of effect on the pharmacokinetics of carbamazepine, phenytoin, lamotrigine, and valproate in patients with partial epilepsy. Alvey, CW; Bockbrader, HN; Brodie, MJ; Bron, NJ; Gibson, GL; Hounslow, NJ; Posvar, EL; Randinitis, EJ; Wesche, DL; Wilson, EA, 2005)	0.54
"To assess the efficacy of lamotrigine combined with either divalproex or lithium for the treatment of bipolar disorder."	( Lamotrigine combined with divalproex or lithium for bipolar disorder: a case series. Bowden, CL; Jamison, KL; Redmond, JR, 2006)	2.08
" This study evaluated lamotrigine alone or in combination with phenobarbital, phenytoin, or the glutamate antagonist (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine hydrogen maleate (MK-801) for a proapoptotic action in the developing rat brain."	( Effects of lamotrigine alone and in combination with MK-801, phenobarbital, or phenytoin on cell death in the neonatal rat brain. Gale, K; Katz, I; Kim, J; Kondratyev, A, 2007)	1.04
" Variables included in the analysis were age, gender, and concomitant treatment with a total of 41 drugs most often used in combination with quetiapine."	( Quetiapine and drug interactions: evidence from a routine therapeutic drug monitoring service. Castberg, I; Skogvoll, E; Spigset, O, 2007)	0.34
" On the basis of our data and pharmacokinetic considerations, the majority of drugs commonly used in psychiatry can safely be given in combination with quetiapine."	( Quetiapine and drug interactions: evidence from a routine therapeutic drug monitoring service. Castberg, I; Skogvoll, E; Spigset, O, 2007)	0.34
" Safety and tolerability results revealed no unexpected adverse events for ARI combination with LTG."	( Aripiprazole in combination with lamotrigine for the long-term treatment of patients with bipolar I disorder (manic or mixed): a randomized, multicenter, double-blind study (CN138-392). Carlson, BX; Ketter, TA; Marcus, R; McQuade, RD; Sanchez, R; Sun, W; Timko, K; Vester-Blokland, E, 2012)	0.66
"To investigate potential drug-drug interactions between clobazam and cytochrome P450 (CYP) isoenzyme substrates, inhibitors, and inducers."	( Pharmacokinetic drug interactions between clobazam and drugs metabolized by cytochrome P450 isoenzymes. Bekersky, I; Blum, RA; Tolbert, D; Walzer, M, 2012)	0.38
"Two, prospective, open-label, single-center, drug-drug interaction (DDI) studies and a population pharmacokinetics analysis of seven multicenter phase II-III trials."	( Pharmacokinetic drug interactions between clobazam and drugs metabolized by cytochrome P450 isoenzymes. Bekersky, I; Blum, RA; Tolbert, D; Walzer, M, 2012)	0.38
"Fifty-four healthy adult volunteers were enrolled in the two drug-drug interaction studies; 53 completed the studies."	( Pharmacokinetic drug interactions between clobazam and drugs metabolized by cytochrome P450 isoenzymes. Bekersky, I; Blum, RA; Tolbert, D; Walzer, M, 2012)	0.38
"In the first drug-drug interaction study, 36 participants received a single oral dose of clobazam 10 mg on day 1, followed by either ketoconazole 400 mg once/day or omeprazole 40 mg once/day on days 17-22, with a single dose of clobazam 10 mg coadministered on day 22, to study the effects of CYP3A4 or CYP2C19 inhibition, respectively, on clobazam and its active metabolite N-desmethylclobazam (N-CLB)."	( Pharmacokinetic drug interactions between clobazam and drugs metabolized by cytochrome P450 isoenzymes. Bekersky, I; Blum, RA; Tolbert, D; Walzer, M, 2012)	0.38
" In the second DDI study, no clinically significant drug-drug interactions were observed between clobazam 40 mg and the CYP probe substrates caffeine or tolbutamide."	( Pharmacokinetic drug interactions between clobazam and drugs metabolized by cytochrome P450 isoenzymes. Bekersky, I; Blum, RA; Tolbert, D; Walzer, M, 2012)	0.38
"These findings suggest no clinically meaningful drug-drug interactions between clobazam and drugs metabolized by CYP3A4, CYP2C19, CYP1A2, or CYP2C9."	( Pharmacokinetic drug interactions between clobazam and drugs metabolized by cytochrome P450 isoenzymes. Bekersky, I; Blum, RA; Tolbert, D; Walzer, M, 2012)	0.38
"The hepatic organic anion transporting polypeptides (OATPs) influence the pharmacokinetics of several drug classes and are involved in many clinical drug-drug interactions."	( Classification of inhibitors of hepatic organic anion transporting polypeptides (OATPs): influence of protein expression on drug-drug interactions. Artursson, P; Haglund, U; Karlgren, M; Kimoto, E; Lai, Y; Norinder, U; Vildhede, A; Wisniewski, JR, 2012)	0.38
"The combination of anticonvulsant mood stabilizers with antipsychotic drugs may lead to clinically relevant drug-drug interactions."	( Pharmacokinetic Drug-Drug Interactions of Mood Stabilizers and Risperidone in Patients Under Combined Treatment. Gründer, G; Haen, E; Hiemke, C; Lammertz, SE; Paulzen, M; Schoretsanitis, G; Schruers, KR; Stegmann, B, 2016)	0.43
" In another independent set of experiments, similar results of drug combination responses were also found."	( Anti-Epileptic Drug Combination Efficacy in an In Vitro Seizure Model - Phenytoin and Valproate, Lamotrigine and Valproate. French, CR; O'Brien, TJ; Taing, KD; Williams, DA, 2017)	0.67
" Therefore, in the present study, the neuroprotective effects and mechanisms of vit-D alone or in combination with lamotrigine have been evaluated in the lithium-pilocarpine model of SE in rats."	( Neuroprotective effects of vitamin D alone or in combination with lamotrigine against lithium-pilocarpine model of status epilepticus in rats. Abdel-Wahab, AF; Afify, MA; Al Ghamdi, SS; Bamagous, GA; ElSawy, NA; Ibrahim, IAA; Mahfoz, AM; Shahzad, N, 2017)	0.9
" Data from clinical trials indicate that most conventional antidepressants can probably be combined with ketamine without compromising efficacy or increasing the adverse effect burden."	( Ketamine for Depression, 5: Potential Pharmacokinetic and Pharmacodynamic Drug Interactions. Andrade, C, 2017)	0.46
"We sought to explore the effects of sodium valproate combined with lamotrigine on quality of life and serum inflammatory factors in patients with poststroke secondary epilepsy."	( Effects of Sodium Valproate Combined with Lamotrigine on Quality of Life and Serum Inflammatory Factors in Patients with Poststroke Secondary Epilepsy. Guo, D; Hao, F; Li, X; Liu, X; Sun, J; Tang, W; Tao, S, 2020)	1.06
"A total of 145 patients with post-stroke secondary epilepsy admitted to our hospital from January 2017 to June 2018 were collected: 76 treated with sodium valproate combined with lamotrigine (study group) and 69 patients treated with sodium valproate alone (control group)."	( Effects of Sodium Valproate Combined with Lamotrigine on Quality of Life and Serum Inflammatory Factors in Patients with Poststroke Secondary Epilepsy. Guo, D; Hao, F; Li, X; Liu, X; Sun, J; Tang, W; Tao, S, 2020)	1.01
"Sodium valproate combined with lamotrigine has better clinical efficacy and higher safety in the treatment of poststroke secondary epilepsy and is able to reduce the expression levels of serum inflammatory factors."	( Effects of Sodium Valproate Combined with Lamotrigine on Quality of Life and Serum Inflammatory Factors in Patients with Poststroke Secondary Epilepsy. Guo, D; Hao, F; Li, X; Liu, X; Sun, J; Tang, W; Tao, S, 2020)	1.11

Bioavailability

Lamotrigine should be taken preferably in fasting condition, as presence of food (low fat, low calorie or high fat, high calorie) decreases the bioavailability to a significant extent.

Excerpt	Reference	Relevance
" It is well absorbed after oral administration."	( Lamotrigine. Burstein, AH, )	1.57
" The bioavailability of the oral formulation is about 98%."	( Lamotrigine clinical pharmacokinetics. Rambeck, B; Wolf, P, 1993)	1.73
" Oral clearance (CLo), apparent volume of distribution (V/F) and absorption rate constant (Ka) were the main pharmacokinetic parameters."	( Population pharmacokinetics of lamotrigine monotherapy in patients with epilepsy: retrospective analysis of routine monitoring data. Hussein, Z; Posner, J, 1997)	0.58
" Lamotrigine is well absorbed with bioavailability approaching 100%."	( Lamotrigine: pharmacokinetics. Garnett, WR, 1997)	2.65
" After oral administration, absorption is rapid and relatively efficient for the new AEDs, the most notable exception being gabapentin, whose bioavailability decreases with increasing dosage."	( The clinical pharmacokinetics of the new antiepileptic drugs. Perucca, E, 1999)	0.3
"The quantitative structure-bioavailability relationship of 232 structurally diverse drugs was studied to evaluate the feasibility of constructing a predictive model for the human oral bioavailability of prospective new medicinal agents."	( QSAR model for drug human oral bioavailability. Topliss, JG; Yoshida, F, 2000)	0.31
"To determine the relative bioavailability of lamotrigine (LTG) chewable dispersible tablets after rectal administration."	( Relative bioavailability of lamotrigine chewable dispersible tablets administered rectally. Birnbaum, AK; Im, Y; Kriel, RL; Remmel, RP, 2001)	0.86
" The samples were analyzed for LTG by high-performance liquid chromatography, and the relative bioavailability was determined."	( Relative bioavailability of lamotrigine chewable dispersible tablets administered rectally. Birnbaum, AK; Im, Y; Kriel, RL; Remmel, RP, 2001)	0.6
" The bioavailability of lamotrigine is affected by food, hence the present study was done to investigate the effect of two types of food on the bioavailability of lamotrigine."	( Food reduces the bioavailability of lamotrigine. Dubey, R; Kumar, H; Saha, N; Sharma, C, 2005)	0.91
" Presence of both types of food causes decrease in mean values of C(max), AUC((0-t)), and AUC((0-alpha)) thus reducing the bioavailability of lamotrigine at significant level (P<0."	( Food reduces the bioavailability of lamotrigine. Dubey, R; Kumar, H; Saha, N; Sharma, C, 2005)	0.8
"Lamotrigine should be taken preferably in fasting condition, as presence of food (low fat, low calorie or high fat, high calorie) decreases the bioavailability to a significant extent."	( Food reduces the bioavailability of lamotrigine. Dubey, R; Kumar, H; Saha, N; Sharma, C, 2005)	2.05
" Postoperative alteration of the gastrointestinal motility and transient time leading to delayed absorption and reduced bioavailability of AED may be a major risk factor."	( Perioperative fluctuations of lamotrigine serum levels in patients undergoing epilepsy surgery. Aktas, O; Fritz, G; Lehmann, TN; Meencke, HJ; Paul, F; Veauthier, C; Zipp, F, 2007)	0.63
" The bioavailability of LTG-XR is similar to that of LTG-IR, except in patients taking enzyme-inducing AEDs in whom the bioavailability of LTG-XR is 21% lower."	( Once-daily lamotrigine extended release for epilepsy management. Rheims, S; Ryvlin, P, 2009)	0.74
" In vitro-in vivo correlation was established from the generated dissolution and bioavailability data."	( In vitro-in vivo correlation of modified release dosage form of lamotrigine. Patel, CN; Patel, DM; Shah, HJ; Subbaiah, G, 2009)	0.59
"Oral bioavailability (F) is a product of fraction absorbed (Fa), fraction escaping gut-wall elimination (Fg), and fraction escaping hepatic elimination (Fh)."	( Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination. Chang, G; El-Kattan, A; Miller, HR; Obach, RS; Rotter, C; Steyn, SJ; Troutman, MD; Varma, MV, 2010)	0.36
"OBEJCTIVE: To compare the bioavailability of two 50-mg lamotrigine dispersible tablet formulations (Epilepax®, Ivax-TEVA Argentina Laboratories, Argentina, as a test formulation, and Lamictal®, GlaxoSmithKline, UK, as a reference formulation) in 24 healthy male volunteers."	( Bioequivalence of lamotrigine 50-mg tablets in healthy male volunteers: a randomized, single-dose, 2-period, 2-sequence crossover study. de Mena, F; Olmos, L; Perez-Lloret, S; Pieczanski, P; Rodriguez Moncalvo, JJ, 2012)	0.96
" Polymorphic transporter proteins such as P-glycoprotein significantly influence pharmacokinetics and bioavailability of many structurally unrelated drugs."	( Association between lamotrigine concentrations and ABCB1 polymorphisms in patients with epilepsy. Božina, N; Božina, T; Granić, P; Hajnšek, S; Kuzman, MR; Lalić, Z; Lovrić, M; Sporiš, D, 2012)	0.7
"Brain drug bioavailability is regulated by the blood-brain barrier (BBB)."	( Expression and functional relevance of UGT1A4 in a cohort of human drug-resistant epileptic brains. Alexopolous, A; Ghosh, C; Hossain, M; Janigro, D; Marchi, N; Martinez-Gonzalez, J; Puvenna, V, 2013)	0.39
" Age was a significant factor contributing to pharmacokinetic variability in individuals using LTG, OXC, and CBZ with increasing clearance as a function of bioavailability (Cl/F) over age 18, a maximum Cl/F at 33years (CBZ) and 36 years (LTG and OXC), and a gradual decrease of Cl/F towards older age."	( The impact of age on lamotrigine and oxcarbazepine kinetics: a historical cohort study. Lindhout, D; Sander, JW; Wegner, I; Wilhelm, AJ, 2013)	0.71
" It is well absorbed from the digestive system and undergoes metabolism via glucuronidation and acetylation."	( [Retigabine - a new antiepileptic drug with a different mechanism of action]. Pietrzak, B; Zwierzyńska, E, 2013)	0.39
"A classic 2-period crossover bioavailability study was conducted to evaluate the relative and absolute bioavailability of immediate-release (IR) and extended-release (XR) lamotrigine formulations under steady-state conditions in elderly patients with epilepsy."	( Steady-state pharmacokinetics and bioavailability of immediate-release and extended-release formulations of lamotrigine in elderly epilepsy patients: Use of stable isotope methodology. Birnbaum, AK; Brundage, RC; Leppik, IE; Polepally, AR; Ramsay, RE; Rarick, JO; Remmel, RP, 2015)	0.82
" The high bioavailability achieved for intranasally administered lamotrigine (116."	( Direct nose-to-brain delivery of lamotrigine following intranasal administration to mice. Alves, G; Falcão, A; Fortuna, A; Serralheiro, A, 2015)	0.94
" Nasal powders (NPs) have better adhesion due to the additive polymers that may be, eg, gelling or good wettability agents; thus, their bioavailability is better compared to the liquid formulations."	( Preliminary study of nanonized lamotrigine containing products for nasal powder formulation. Ambrus, R; Csóka, I; Gieszinger, P; Jójárt-Laczkovich, O; Katona, G; Pallagi, E; Szabó-Révész, P, 2017)	0.74
" Bioavailability of oral LTG was approximately 74% and did not differ by age."	( Lamotrigine pharmacokinetics following oral and stable-labeled intravenous administration in young and elderly adult epilepsy patients: Effect of age. Birnbaum, AK; Brundage, RC; Kistner, BM; Leppik, IE; Pennell, PB; Polepally, AR; Ramsay, RE; Remmel, RP; White, JR, 2018)	1.92
"Although LTG bioavailability was not affected by age, LTG clearance was 27."	( Lamotrigine pharmacokinetics following oral and stable-labeled intravenous administration in young and elderly adult epilepsy patients: Effect of age. Birnbaum, AK; Brundage, RC; Kistner, BM; Leppik, IE; Pennell, PB; Polepally, AR; Ramsay, RE; Remmel, RP; White, JR, 2018)	1.92
"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
" Reducing the particle size to the nano range can affect the bioavailability of pharmaceutical products."	( Investigation of the Absorption of Nanosized lamotrigine Containing Nasal Powder via the Nasal Cavity. Ambrus, R; Bartos, C; Ducza, E; Gáspár, R; Gieszinger, P; Janáky, T; Kecskeméti, G; Márki, Á; Szabó-Révész, P; Sztojkov-Ivanov, A; Tömösi, F, 2020)	0.82
"The present study was designed to develop novel lipid microparticles in order to improve solubility, dissolution and bioavailability of a lipophilic drug of BCS class II, lamotrigine."	( Evaluation of solubility and dissolution of lamotrigine using lipid based microparticulate carriers: An in-vitro analysis. Abbas, N; Arshad, MS; Hussain, A; Inam, S; Iqbal, MS; Irfan, M; Islam, N; Khan, IU; Mohsin, NUA; Qayyum, MA; Rasul, A; Syed, HK; Zahoor, AF, 2020)	1.01
"This study aimed to prepare solid self-nanoemulsified drug delivery system (S-SNEDDS) of lamotrigine (LMG) for enhancing its dissolution and oral bioavailability (BA)."	( Development, Characterization, and in-vivo Pharmacokinetic Study of Lamotrigine Solid Self-Nanoemulsifying Drug Delivery System. Abdelmonem, R; Azer, MS; El-Nabarawi, M; Makky, A; Nada, A; Zaghloul, A, 2020)	1.02
" Systematic investigation of two mixed Poloxamer nanomicelles (P407:P403 and P407:P105) for LMN bioavailability at body temperature (37 °C) were investigated."	( Mixed Poloxamer Nanomicelles for the Anticonvulsant Lamotrigine Drug: Solubility, Micellar Characterization, and Aswal, VK; Patel, H; Ray, D; Shaikh, S; Sharma, RK, 2021)	0.87
"The SSD model serves as a good in vitro tool for assessing the effect of pH-dependent DDIs on bioavailability of weakly basic drugs with solubility/ dissolution limited absorption."	( Vitamin C Improves Dasatinib Concentrations Under Hypochlorhydric Conditions of the Simulated Stomach Duodenum Model. Aburub, A; Fadda, HM; Moghrabi, FS, 2022)	0.72
" 1-H-benzotriazole, carbamazepine, citalopram, lamotrigine, sucralose, tramadol, and venlafaxine (>80 % frequency of appearance in effluents) were assessed with respect to their bioavailability in soil as part of different scenarios of irrigation with reclaimed water following a qualitative approach."	( Multiclass target analysis of contaminants of emerging concern including transformation products, soil bioavailability assessment and retrospective screening as tools to evaluate risks associated with reclaimed water reuse. Beretsou, VG; Fatta-Kassinos, D; Lundy, L; Manoli, K; Michael, C; Nika, MC; Revitt, DM; Sui, Q; Thomaidis, NS, 2022)	0.98
" In the present work, BCRP's role as a mechanism that might contribute to drug-resistant epilepsy (DRE) in a mouse model of acute seizures was studied with further assessment of the effect of its inhibition by ko143 and metformin (MET) on lamotrigine (LTG) bioavailability and efficacy."	( Implications of BCRP modulation on PTZ-induced seizures in mice: Role of ko143 and metformin as adjuvants to lamotrigine. El-Sayed, NS; Fathelbab, MH; Harby, SA; Khalil, NA; Saleh, SR; Thabet, EH, 2023)	1.3

Dosage Studied

Lamotrigine steady-state serum concentrations stayed in a narrower range for XR-QD than for IR-BID. Seizures became diurnal and frequent, not modified by carbamazepine (CBZ) or valproate (VPA) with recommended dosage schedules for this combination.

Excerpt	Relevance	Reference
" Subjects were allocated to 1 of 2 dosing schedules according to their concomitant AEDs."	( A randomised double-blind placebo-controlled add-on trial of lamotrigine in patients with severe epilepsy. Hamilton, MJ; Oxley, JR; Patsalos, PN; Sander, JW; Yuen, WC, 1990)	0.52
" An unblinded investigator adjusted lamotrigine dosage to achieve a plasma concentration within a previously predicted therapeutic range."	( Double-blind crossover trial of lamotrigine (Lamictal) as add-on therapy in intractable epilepsy. Binnie, CD; Debets, RM; Engelsman, M; Meijer, JW; Meinardi, H; Overweg, J; Peck, AW; Van Wieringen, A; Yuen, WC, )	0.69
" Dosage was adjusted on the basis of estimated half-life."	( Seven day administration of lamotrigine in epilepsy: placebo-controlled add-on trial. Beintema, DJ; Binnie, CD; Debets, RM; Meijer, JW; Meinardi, H; Peck, AW; Van Emde Boas, W; Westendorp, AM; Yuen, WC, 1987)	0.57
" During the study, LTG was added to a stable dosage of one to three first line antiepileptic drugs (AED)."	( [Cardiac side effects and ECG changes with lamotrigine?--A clinical study]. Polatschek, B; Steinhoff, BJ; Stodieck, SR; Tiecks, FP; Wedel, R, 1994)	0.55
" Influences of valproic acid and enzyme-inducing anti-epileptics on lamotrigine eliminate necessitate dosage modification of lamotrigine."	( Lamotrigine. A review of its pharmacological properties and clinical efficacy in epilepsy. Chrisp, P; Goa, KL; Ross, SR, 1993)	1.96
" It has a favorable pharmacokinetic profile allowing for once- or twice-daily dosing and adverse effects appear mild and transient."	( Lamotrigine: an antiepileptic agent for the treatment of partial seizures. Gilman, JT, 1995)	1.73
" LTG was added to the current antiepileptic drug (AED) regimen at a daily dosage of 200-400 mg depending on the concomitant treatment."	( Long-term observations on the clinical use of lamotrigine as add-on drug in patients with epilepsy. Cocito, L; Loeb, C; Maffini, M, 1994)	0.55
" However, the rate was lower when lamotrigine dosage was increased slowly as recommended."	( Lamotrigine--a clinical overview. Wallace, SJ, 1994)	2.01
" The usual maintenance dosage of lamotrigine is 200 to 500 mg daily given in two divided doses."	( The clinical efficacy of lamotrigine as an antiepileptic drug. Pellock, JM, 1994)	0.87
" The value of measuring the concentrations of lamotrigine in helping to optimise the dosage or reduce the likelihood of adverse effects has not been established."	( Lamotrigine clinical pharmacokinetics. Rambeck, B; Wolf, P, 1993)	1.99
" For 12 patients, treatment could be reduced to monotherapy, but for those with valproate (VPA) comedication LTG dosage had to be increased; 25% of patients with VPA monotherapy exhibited skin rash, appearing 3-18 days after starting LTG."	( Lamotrigine in treatment of 120 children with epilepsy. Chavez, F; Dulac, O; Pajot, N; Palacios, L; Rey, E; Schlumberger, E, )	1.57
" ZNS daily dosage is 400-600 mg."	( Antiepileptic drugs in development: prospects for the near future. Leppik, IE, 1994)	0.29
" The risk of rash can, however, be minimised through adoption of a low, slow dosage titration schedule on initiating therapy."	( Lamotrigine. An update of its pharmacology and therapeutic use in epilepsy. Fitton, A; Goa, KL, 1995)	1.73
" In a similarly designed United States trial, LTG was significantly superior to placebo at a 500-mg/day dosage but not at a 300-mg/day dosage."	( Expanding antiepileptic drug options: clinical efficacy of new therapeutic agents. Ben-Menachem, E, 1996)	0.29
" All the drugs can be conveniently given as a twice daily dosage apart from gabapentin, which has a short half-life and a midday dose is needed."	( Clinical pharmacokinetics of newer antiepileptic drugs. Lamotrigine, vigabatrin, gabapentin and oxcarbazepine. Binnie, CD; Elwes, RD, 1996)	0.54
") dosage regimen of < or = 700 mg/day lamotrigine (LTG) and to include determination of the LTG pharmacokinetic profile at doses > or = 500 mg/day in patients receiving concomitant enzyme-inducing antiepileptic drugs (AEDs)."	( Lamotrigine high-dose tolerability and safety in patients with epilepsy: a double-blind, placebo-controlled, eleven-week study. Gay, P; Lai, AA; Madsen, J; Matsuo, F; Risner, ME; Rollins, DE; Tolman, KG, 1996)	2.01
" For 3 weeks, as outpatients they had their LTG dosage increased from 100 to 400 mg/day."	( Lamotrigine high-dose tolerability and safety in patients with epilepsy: a double-blind, placebo-controlled, eleven-week study. Gay, P; Lai, AA; Madsen, J; Matsuo, F; Risner, ME; Rollins, DE; Tolman, KG, 1996)	1.74
"To evaluate the steady-state pharmacokinetics of lamotrigine and valproate at three dosing levels of lamotrigine in normal volunteers receiving steady-state therapeutic doses of valproate."	( Bidirectional interaction of valproate and lamotrigine in healthy subjects. Anderson, GD; Dren, AT; Gidal, BE; Harris, SJ; Lai, AA; Levy, RH; Wargin, WA; Wolf, KB; Yau, MK, 1996)	0.81
" Each subject subsequently received three oral dosage regimens of lamotrigine (50, 100, or 150 mg/day) for 1 week each, with a 2-week washout period between lamotrigine treatment periods."	( Bidirectional interaction of valproate and lamotrigine in healthy subjects. Anderson, GD; Dren, AT; Gidal, BE; Harris, SJ; Lai, AA; Levy, RH; Wargin, WA; Wolf, KB; Yau, MK, 1996)	0.79
"As a consequence of the interaction between lamotrigine and sodium valproate, a dosage reduction of lamotrigine should be considered in patients taking a combination of valproate and lamotrigine."	( Bidirectional interaction of valproate and lamotrigine in healthy subjects. Anderson, GD; Dren, AT; Gidal, BE; Harris, SJ; Lai, AA; Levy, RH; Wargin, WA; Wolf, KB; Yau, MK, 1996)	0.82
" A pharmacodynamic interaction with carbamazepine necessitates a dosage reduction in some patients when LTG is introduced."	( Lamotrigine--an update. Brodie, MJ, 1996)	1.74
" Both dosage regimens of lamotrigine were well tolerated."	( A randomised open multicentre comparative trial of lamotrigine and carbamazepine as monotherapy in patients with newly diagnosed or recurrent epilepsy. Dam, M; Reunanen, M; Yuen, AW, 1996)	0.85
"These results indicate that impaired renal function will have little effect on the plasma concentrations of lamotrigine achieved for a given dosing regimen."	( Comparison of the pharmacokinetics of lamotrigine in patients with chronic renal failure and healthy volunteers. Cooper, JD; Posner, J; Rolan, PE; Sheung, CT; Soul-Lawton, J; Wootton, R, 1997)	0.78
" Specific indications and dosage schedules have been provided."	( New antiepileptic drugs. Brodie, MJ; Wilson, EA, 1996)	0.29
"In view of the wide therapeutic margin of lamotrigine and the 21% residual variability in plasma concentrations, the modest significant effects of race and auto-induction on clearance are unlikely to be clinically significant and, thus, no dosage adjustment is warranted for these effects."	( Population pharmacokinetics of lamotrigine monotherapy in patients with epilepsy: retrospective analysis of routine monitoring data. Hussein, Z; Posner, J, 1997)	0.85
"2% (mean +/- SD, n = 6) during application of 100 microM LTG, and the dose-response curve of this effect indicated an IC50 of 145 microM."	( Lamotrigine reduces voltage-gated sodium currents in rat central neurons in culture. Avoli, M; Zona, C, 1997)	1.74
" We recorded objective and subjective pain ratings and correlated them to daily dosage (400 mg maximum) and plasma levels of the drug."	( Clinical effectiveness of lamotrigine and plasma levels in essential and symptomatic trigeminal neuralgia. Albano, C; Cultrera, S; Favale, E; Fracassi, M; Leandri, M; Lunardi, G; Rubino, V, 1997)	0.6
" Thirteen patients were assessed at three or more LTG dosage levels."	( The influence of dosage, age, and comedication on steady state plasma lamotrigine concentrations in epileptic children: a prospective study with preliminary assessment of correlations with clinical response. Alessandrì, MG; Bartoli, A; Belmonte, A; Gatti, G; Guerrini, R; Perucca, E, 1997)	0.53
" Then, LTG was increased in steps to maximal dosage (200 mg or 400 mg per day) within seven weeks and maintained for three months while pre-existing antiepileptic drugs remained unchanged."	( Lamotrigine as add-on therapy in adult patients with refractory epilepsy. Kwan, SY; Lin, YY; Su, MS; Yen, DJ; Yiu, CH, 1997)	1.74
" The LTG dosage was increased step by step until clinical response or side effects were observed."	( No increase in carbamazepine-10,11-epoxide during addition of lamotrigine treatment in children. Boreus, LO; Eriksson, AS, 1997)	0.54
" A review of 52 patient specimens showed that, if patients were grouped according to coadministered anticonvulsants, a significant correlation between lamotrigine dosage and concentration was evident in those coadministered valproate (in the absence of metabolic inducers) and in those coadministered a combination of valproate and inducers, but not in patients coadministered inducers alone."	( High-performance liquid chromatography quantitation of plasma lamotrigine concentrations: application measuring trough concentrations in patients with epilepsy. Morris, RG; Sallustio, BC, 1997)	0.74
" Adverse events were infrequent but the occurrence of rash appeared to correlate with rapid ascension dosing and comedication with valproic acid."	( Adult experience with lamotrigine. Messenheimer, JA; Willmore, LJ, 1997)	0.61
" Dosing in generalized seizures is similar to that for partial seizures."	( Lamotrigine in absence and primary generalized epilepsies. Holmes, GL; Mikati, MA, 1997)	1.74
" No significant time or dosage effect or time by treatment effect was observed for YMRS."	( Lamotrigine in rapid-cycling bipolar disorder. Calabrese, JR; Fatemi, SH; Rapport, DJ; Thuras, P, 1997)	1.74
" The dosage of LTG was individualized and related to concomitant anti-epileptic drugs."	( Lamotrigine in Rett syndrome: treatment experience from a pilot study. Hagberg, B; Stenbom, Y; Tonnby, B, 1998)	1.74
" Data from clinical trials clearly point to exceeding currently recommended dosage guidelines of lamotrigine and co-administration of valproic acid (valproate sodium) as risk factors for rash."	( Safety review of adult clinical trial experience with lamotrigine. Giorgi, L; Messenheimer, J; Mullens, EL; Young, F, 1998)	0.77
" The LTG dosage was individualized in an open phase preceding the placebo/treatment phase."	( The efficacy of lamotrigine in children and adolescents with refractory generalized epilepsy: a randomized, double-blind, crossover study. Eriksson, AS; Hoppu, K; Nergårdh, A, 1998)	0.65
" In case 2, a 25 mg reduction in the total daily dose of sertraline resulted in halving of the lamotrigine blood level even though the lamotrigine dosage was increased by 33%."	( Lamotrigine toxicity secondary to sertraline. Gerner, R; Kaufman, KR, 1998)	1.96
" In an attempt to replicate and extend these preliminary open-label prospective findings, a series of multicenter, double-blind, placebo-controlled studies evaluating the efficacy and dose-response relationships of lamotrigine in the various phases of the illness, including both acute and maintenance designs in both bipolar I and II disorder, is ongoing."	( Clinical studies on the use of lamotrigine in bipolar disorder. Calabrese, JR; Kimmel, SE; Kujawa, M; Rapport, DJ; Shelton, MD, 1998)	0.77
" The median time to onset (17 days for SJS and TEN) and the median dosage at onset (50 mg vs."	( Lamotrigine-induced severe cutaneous adverse reactions. Schlienger, RG; Shapiro, LE; Shear, NH, 1998)	1.74
" These rates reflect lamotrigine dosing and concomitant AEDs used in these trials, both of which are risk factors for rash."	( Rash in adult and pediatric patients treated with lamotrigine. Messenheimer, JA, 1998)	0.87
"To review (retrospectively) the relationships between lamotrigine (LTG) dosage and plasma concentrations based on data generated in a routine therapeutic drug monitoring laboratory from a heterogeneous sample of patients with epilepsy."	( Lamotrigine and therapeutic drug monitoring: retrospective survey following the introduction of a routine service. Batty, AB; Black, AB; Harris, AL; Morris, RG; Sallustio, BC, 1998)	1.99
"All patient assays for LTG received over a 12 month period (339 requests from 149 patients) were reviewed and relationships between dosage and concentration calculated and grouped according to concomitant antiepileptic drug therapy."	( Lamotrigine and therapeutic drug monitoring: retrospective survey following the introduction of a routine service. Batty, AB; Black, AB; Harris, AL; Morris, RG; Sallustio, BC, 1998)	1.74
"Linear relationships were demonstrated between LTG dosage and concentration for the 3 treatment groups (LTG plus valproic acid (VPA), LTG plus enzyme inducing antiepileptic drugs, and LTG plus VPA and inducers), however, there were significant differences between groups (P<0."	( Lamotrigine and therapeutic drug monitoring: retrospective survey following the introduction of a routine service. Batty, AB; Black, AB; Harris, AL; Morris, RG; Sallustio, BC, 1998)	1.74
"Metabolic inhibition by VPA was shown to have a marked effect on LTG kinetics, suggesting either a significant LTG dosage reduction is required if plasma LTG concentrations are elevated, or alternatively, higher plasma LTG concentrations could be attained from lower dosages."	( Lamotrigine and therapeutic drug monitoring: retrospective survey following the introduction of a routine service. Batty, AB; Black, AB; Harris, AL; Morris, RG; Sallustio, BC, 1998)	1.74
"The dose-response effects of pretreatment with lamotrigine (a phenyltriazine derivative that inhibits neuronal glutamate release) in a porcine cerebral ischemia model during cardiopulmonary bypass were studied."	( Lamotrigine attenuates cortical glutamate release during global cerebral ischemia in pigs on cardiopulmonary bypass. Black, D; Conroy, BP; Crumrine, RC; DeWitt, DS; Jenkins, LW; Johnston, WE; Lin, CY, 1999)	2
" LTG was started with a dosage of 25 mg/day until a daily maintenance dosage of 200 mg/day was reached."	( Cortical excitability in patients after loading doses of lamotrigine: a study with magnetic brain stimulation. Bongiovanni, LG; Fiaschi, A; Manganotti, P; Turazzini, M; Zanette, G, 1999)	0.55
"Plasma concentrations of lamotrigine, an antiepileptic drug obtained in three adult controlled clinical trials conducted in the United States were pooled and analyzed using NONMEM, a population pharmacokinetic computer program, to facilitate development of dosing guidelines."	( Population pharmacokinetics of lamotrigine adjunctive therapy in adults with epilepsy. Chen, C; Cox, E; Fiedler-Kelly, J; Grasela, TH; Risner, ME; Womble, GP, 1999)	0.89
" Should similar plasma lamotrigine concentrations in adults and children be desirable, children will likely require higher weight-normalized doses at the same dosing frequency."	( Pharmacokinetics of lamotrigine in children in the absence of other antiepileptic drugs. Casale, EJ; Chen, C; Culverhouse, EH; Duncan, B; Gilman, J, 1999)	0.94
"No significant relationship was seen between dosage and serum levels, nor between serum levels and efficacy or side-effect."	( [In children with refractory epilepsy: vigabatrin or lamotrigine?]. Armijo, JA; Arteaga, R; Caviedes, BE; Herranz, JL, )	0.38
" Lamotrigine was initiated at 25 mg/day and slowly titrated every 1 to 2 weeks over 8 weeks to a maximum dosage of 500 mg/day if tolerated."	( A preliminary study of lamotrigine for the treatment of posttraumatic stress disorder. Beckham, JC; Butterfield, MI; Connor, KM; Davidson, JR; Feldman, ME; Hertzberg, MA; Sutherland, SM, 1999)	1.52
" Risk of serious rash may possibly be lessened by strict adherence to manufacturer's dosing guidelines, particularly in patients who are at higher risk: those on concurrent VPA and in the pediatric population."	( Lamotrigine-associated rash: risk/benefit considerations in adults and children. Besag, FM; Brodie, MJ; Dooley, JM; Duchowny, MS; Guberman, AH; Pellock, JM; Richens, A; Stern, RS; Trevathan, E, 1999)	1.75
" The dosage of both drugs, however, may need to be reduced to minimize the risk of intolerable side effects."	( The efficacy of valproate-lamotrigine comedication in refractory complex partial seizures: evidence for a pharmacodynamic interaction. Di Perri, R; Oteri, G; Perucca, E; Pisani, F; Richens, A; Russo, MF, 1999)	0.6
" An increase in LTG dosage to 20 mg/kg per day produced no further improvement and was followed by myoclonic status epilepticus."	( Myoclonic status epilepticus following high-dosage lamotrigine therapy. Belmonte, A; Guerrini, R; Parmeggiani, L; Perucca, E, 1999)	0.56
" Following a short titration period, the dosage was individualised for each patient while maintaining the blind over the next 24 weeks."	( Multicentre, double-blind, randomised comparison between lamotrigine and carbamazepine in elderly patients with newly diagnosed epilepsy. The UK Lamotrigine Elderly Study Group. Brodie, MJ; Giorgi, L; Overstall, PW, 1999)	0.55
" Slow dosage escalation yields good tolerability."	( Lamotrigine in the treatment of bipolar depression. Bowden, CL; Mitchell, P; Suppes, T, 1999)	1.75
" Because dosing is often modest, cost should rarely be the overriding factor in choosing a drug for a patient with newly diagnosed epilepsy in the developed world."	( Monostars: an aid to choosing an antiepileptic drug as monotherapy. Brodie, MJ, 1999)	0.3
" Lamotrigine may offer a much-needed treatment alternative for bipolar depression and could be found effective for acute mania, but the need for slow dosage adjustment and the risk of rash may limit overall clinical utility."	( Gabapentin and lamotrigine in bipolar disorder. Botts, SR; Raskind, J, 1999)	1.57
" Seizures became diurnal and frequent, not modified by carbamazepine (CBZ) or valproate (VPA) but responding to VPA and lamotrigine (LTG) with recommended dosage schedules for this combination."	( Paradoxic reaction to lamotrigine in a child with benign focal epilepsy of childhood with centrotemporal spikes. Boyd, S; Catania, S; Cross, H; de Sousa, C, 1999)	0.83
" The predominant dosage of LTG (100 to 200 mg) was similar for monotherapy and for bi-therapy in those treated with valproate, as compared with 200-400 mg in most of those in whom the associated drug was carbamazepine (24), phenobarbital (14), phenytoin (6) or other drug, with a considerable reduction in dose (of 100 mg to 250 mg) when they were treated by monotherapy instead."	( [Therapeutic benefits of monotherapy with lamotrigine]. Alarcia, R; Bertol, V; Oliveros-Cid, A; Oliveros-Juste, A; Sánchez-Marín, B, )	0.4
" After lamotrigine was added for better seizure control and the dosage of gabapentin was tapered, anorgasmia improved."	( Improved sexual function in three men taking lamotrigine for epilepsy. Carwile, ST; Husain, AM; Miller, PP; Radtke, RA, 2000)	1.02
" The mean dosage (4."	( Factors associated with behavioral and cognitive abnormalities in children receiving topiramate. Connolly, MB; Farrell, K; Gerber, PE; Hamiwka, L, 2000)	0.31
" The incidence of rash may be reduced with proper initial dosing and dose escalation."	( The tolerability of lamotrigine in children. Giorgi, L; Messenheimer, JA; Risner, ME, 2000)	0.63
" The dosage of lamotrigine was the same before and at the onset of myoclonus."	( Disabling erratic myoclonus during lamotrigine therapy with high serum level--report of two cases. Debreczeni, T; Halász, P; Janszky, J; Olajos, S; Perényi, J; Rásonyi, G; Szûcs, A, )	0.76
" We report 11 MS patients with trigeminal neuralgia (TN): 6 intolerant to a therapeutic dosage of CBZ, showing serious adverse effects and subsequently treated with a combination of low-dose CBZ and gabapentin (GBP) (group 1); 5 treated with lamotrigine (LMT), showing adverse effects and subsequently treated with GBP (group 2)."	( Low-dose gabapentin combined with either lamotrigine or carbamazepine can be useful therapies for trigeminal neuralgia in multiple sclerosis. Leandri, M; Mancardi, GL; Messmer Uccelli, M; Solaro, C; Uccelli, A, 2000)	0.75
"This analysis was performed to validate a previously developed population pharmacokinetic model for lamotrigine in order to establish a basis for dosage recommendations for children."	( Validation of a population pharmacokinetic model for adjunctive lamotrigine therapy in children. Chen, C, 2000)	0.76
" At the end of the study, 11 patients were seizure-free on LTG monotherapy, and in most other patients concomitant AED dosage could be substantially reduced."	( Efficacy of lamotrigine in idiopathic generalized epilepsy syndromes: a video-EEG-controlled, open study. de Saint-Martin, A; Gericke, CA; Hirsch, E; Marescaux, C; Picard, F; Strumia, S, 1999)	0.68
" The wide variation in dose-response and dose-toxicity relationships may reflect different neurobiologies causing refractory epilepsy and differential efficacy of AED combinations."	( Topiramate in refractory epilepsy: a prospective observational study. Brodie, MJ; Sills, GJ; Stephen, LJ, 2000)	0.31
" The present study examined the LTG metabolic inhibition dose-response relationship with valproic acid (VPA) in eight patients with epilepsy with a view to using this to benefit the patient."	( Clinical study of lamotrigine and valproic acid in patients with epilepsy: using a drug interaction to advantage? Black, AB; Lam, E; Morris, RG; Westley, IS, 2000)	0.64
" Target maintenance dosage was 200 mg/day (lamotrigine) and 20 mg/kg/day (valproic acid), with adjustment from 100 to 500 mg/day (lamotrigine) and 10 to 60 mg/kg/day (valproate) based on investigators' judgment."	( Weight change associated with valproate and lamotrigine monotherapy in patients with epilepsy. Barrett, PS; Biton, V; Hammer, AE; Mirza, W; Montouris, G; Vuong, A, 2001)	0.83
"Two-period, crossover study with a 2-week washout between dosing periods."	( Relative bioavailability of lamotrigine chewable dispersible tablets administered rectally. Birnbaum, AK; Im, Y; Kriel, RL; Remmel, RP, 2001)	0.6
"Histological damage and behavioral recovery at 7 days after MCA occlusion was not altered by LTG treatment over the dosage range used in the present study."	( Anticonvulsant lamotrigine administered on reperfusion fails to improve experimental stroke outcomes. DeVries, AC; Hurn, PD; Klaus, JA; Shaivitz, AB; Traystman, RJ, 2001)	0.66
" Similarly, valproate combined with antipsychotics provided greater improvement in mania than antipsychotic medication alone and resulted in lower dosage of the antipsychotic medication."	( Novel treatments for bipolar disorder. Bowden, CL, 2001)	0.31
" Oral dosing of lamotrigine (50-200 mg/kg) had no significant effects on behaviour but measurements of plasma concentrations of free drug showed non-linear oral absorption and lower than predicted drug levels (5-27 microM)."	( A comparison of the effects of lamotrigine on neuroma-induced action potential firing and normal behaviour in rat: implications for establishing a pre-clinical 'therapeutic index'. Butler, P; Gardiner, JC; Gupta, P; Karran, E; Loftus, JP; Pryke, JG; Roffey, SJ, 2001)	0.94
" The dosage levels studied corresponded to four times the median effective dose (ED50) in rats."	( Teratogenic effects of lamotrigine on rat fetal brain: a morphometric study. Azoubel, R; Marchi, NS; Tognola, WA, 2001)	0.62
" The median daily dosage of lamotrigine was 100 mg for monotherapy (range 75 to 500 mg) and 300 mg for add-on therapy (range 25 to 700 mg)."	( The tolerability of lamotrigine in elderly patients with epilepsy. Giorgi, L; Gomez, G; Hammer, AE; O'Neill, F; Risner, M, 2001)	0.93
"Lamotrigine, used in the currently prescribed adult dosage regimen, was well tolerated in elderly patients with epilepsy."	( The tolerability of lamotrigine in elderly patients with epilepsy. Giorgi, L; Gomez, G; Hammer, AE; O'Neill, F; Risner, M, 2001)	2.08
" This study of the population pharmacokinetics of lamotrigine in patients using the drug clinically provides useful data and should lead to better dosage individualization for lamotrigine."	( Population pharmacokinetics of lamotrigine. Chan, V; Ilett, KF; Morris, RG; Tett, SE, 2001)	0.85
" With long-term dosing and once target doses were achieved at 4 weeks, significant elevations in GABA were observed compared with baseline for all three drugs (topiramate 46%, gabapentin 25%, lamotrigine 25%)."	( Modulation of cerebral GABA by topiramate, lamotrigine, and gabapentin in healthy adults. Faught, E; Gilliam, F; Hetherington, H; Ho, S; Kuzniecky, R; Martin, R; Pan, J, 2002)	0.77
" A slow upward dose titration is recommended to reduce the incidence of serious rash, but this may delay the attainment of adequate dosage for 6 weeks."	( Lamotrigine update and its use in mood disorders. Hurley, SC, 2002)	1.76
" The classic AEDs had numerous problems, ranging from inconvenient dosing schedules to frequent side effects due to active metabolites and common drug interactions; newer agents have been developed to avoid some of these pitfalls."	( Pharmacokinetics of new anticonvulsants in psychiatry. Morris, HH, 1998)	0.3
" During 2- and 6-week titration periods, respectively, GBP dosage reached 1,800 mg/day, and LTG, 150 mg/day."	( Gabapentin versus lamotrigine monotherapy: a double-blind comparison in newly diagnosed epilepsy. Anhut, H; Brodie, MJ; Chadwick, DW; Garofalo, EA; Maton, S; Messmer, SL; Murray, G; Otte, A; Sauermann, W, 2002)	0.65
" However, it should be remembered that the proportion of persons with this side effect is much reduced when the correct dosage is used, and the sliding scale of dosage starts with sufficiently low doses."	( [Characteristics and indications of lamotrigine]. Rufo-Campos, M, 2002)	0.59
" The drug is exceptionally well-tolerated in long-term treatment, although initial dosing requires gradual dosage escalation to avoid the risk of inducing serious rashes with features within the spectrum of Stevens-Johnson syndrome."	( Lamotrigine in the treatment of bipolar disorder. Bowden, CL, 2002)	1.76
"5 mg daily until a total dosage of either 75 mg or 100 mg was obtained."	( Lamotrigine use in geriatric patients with bipolar depression. Conn, DK; Robillard, M, 2002)	1.76
" One patient did develop coarse hand tremor that improved when the lamotrigine dosage was decreased."	( Lamotrigine use in geriatric patients with bipolar depression. Conn, DK; Robillard, M, 2002)	1.99
" Its therapeutic efficacy was analyzed in relation to the form of epilepsy, the type of seizures, dosage of lamictal duration of therapy, and as patients' sex, age, and social activity."	( [Experience with lamictal in the treatment of outpatients with resistant epilepsy]. Perunova, NIu; Shershever, AS; Sorokina, EV, 2003)	0.32
" The difficulty in achieving therapeutic dosage because of side effects makes one consider whether these agents are "better" than the oldest and most side effect-prone AED, phenobarbital."	( Clinical pharmacology of topiramate versus lamotrigine versus phenobarbital: comparison of efficacy and side effects using odds ratios. Claycamp, HG; Lathers, CM; Schraeder, PL, 2003)	0.58
" Even with a low initial dosage of lamotrigine followed by a slow increase, a fatal toxic epidermal necrolysis is still possible."	( [Toxic epidermal necrolysis due to lamotrigine]. Beerhorst, K; Renier, WO, 2003)	0.87
"The exposure, or area under the plasma LTG concentration-time curve within a dosing interval at steady state (AUCss), did not change in the presence of TPM, with mean AUCss values ranging at each TPM dose level between 66 and 81 mg x h/L with concomitant LTG/TPM therapy compared with 77 mgxh/L with LTG monotherapy."	( Topiramate and lamotrigine pharmacokinetics during repetitive monotherapy and combination therapy in epilepsy patients. Berry, DJ; Bialer, M; Brodie, MJ; Chadwick, D; Doose, DR; Oxbury, J; Schwabe, S; Wilson, EA, 2003)	0.67
" Although its half-life is relatively short (6 to 8 hours), its duration of action is longer than anticipated from its pharmacokinetics in plasma, and a twice-daily dosing regimen is adequate to produce the desired response."	( The ideal pharmacokinetic properties of an antiepileptic drug: how close does levetiracetam come? Johannessen, SI; Perucca, E, 2003)	0.32
" The dosage of lamotrigine is titrated over a 6-week period to 200 mg/day to minimise the incidence of serious rash."	( Lamotrigine: a review of its use in bipolar disorder. Goldsmith, DR; Ibbotson, T; Perry, CM; Wagstaff, AJ, 2003)	2.11
" Future studies of formal pharmacokinetic modeling of AEDs during pregnancy and the postpartum period could provide an important step toward achieving effective drug dosing to maintain therapeutic objectives for the mother but, at the same time, to minimize fetal drug exposure."	( Antiepileptic drug pharmacokinetics during pregnancy and lactation. Pennell, PB, 2003)	0.32
" Different mechanisms besides the sodium-channel blockage as the main mode of action of LTG are discussed to explain the diversity of individual dose-response relationships."	( Relationship between lamotrigine oral dose, serum level and its inhibitory effect on CNS: insights from transcranial magnetic stimulation. Mercer, AJ; Nitsche, MA; Paulus, W; Somal, HS; Steinhoff, BJ; Tergau, F; Wischer, S, 2003)	0.64
" Patients were converted during an	( Lamotrigine monotherapy compared with carbamazepine, phenytoin, or valproate monotherapy in patients with epilepsy. Hammer, AE; Kaminow, L; Schimschock, JR; Vuong, A, 2003)	1.96
" The dosage of lamotrigine is titrated over a 6-week period to 200 mg/day to minimise the incidence of serious rash."	( Spotlight on lamotrigine in bipolar disorder. Goldsmith, DR; Ibbotson, T; Perry, CM; Wagstaff, AJ, 2004)	1.05
" Serial blood samples were obtained over 120 h post-dose in order to calculate LTG kinetic parameters including area under the concentration-time curve, apparent oral clearance, elimination half-life and percent inhibition of LTG clearance at each dosage level of VPA."	( Evaluation of VPA dose and concentration effects on lamotrigine pharmacokinetics: implications for conversion to lamotrigine monotherapy. Gidal, BE; Maloney, K; Parnell, J; Sale, M; Sheth, R, 2003)	0.57
" These data provide useful information to develop a dosing algorithm to facilitate conversion to LTG monotherapy."	( Evaluation of VPA dose and concentration effects on lamotrigine pharmacokinetics: implications for conversion to lamotrigine monotherapy. Gidal, BE; Maloney, K; Parnell, J; Sale, M; Sheth, R, 2003)	0.57
" Subjects were then dosed with either lamotrigine (300 mg), 4030W92 (100 mg), or placebo, followed 2 h later by capsaicin (100 microg) injected intradermally on the volar aspect of the left forearm."	( Lack of effect of two oral sodium channel antagonists, lamotrigine and 4030W92, on intradermal capsaicin-induced hyperalgesia model. Quessy, S; Schulteis, G; Wallace, MS, 2004)	0.84
" Stevens-Johnson syndrome is a concern, but the incidence of this side effect may not be as high as previously believed, if dosing is slowly titrated."	( The current understanding of lamotrigine as a mood stabilizer. Baldassano, CF; Gyulai, L; Hahn, CG; Lenox, RH, 2004)	0.61
" The severity of the cognitive side effects of TPM may be related to dosing to a certain extent, but this relationship may be disclosed only with larger sample sizes."	( Cognitive profile of topiramate as compared with lamotrigine in epilepsy patients on antiepileptic drug polytherapy: relationships to blood serum levels and comedication. Elger, CE; Helmstaedter, C; Kockelmann, E, 2004)	0.58
" A regimen was categorized as toxic if the patient experienced side effects that led to a dosage change or discontinuation of LTG."	( Correlating lamotrigine serum concentrations with tolerability in patients with epilepsy. Adams, DJ; Bazil, CW; Buchsbaum, R; Du, Y; Hager, M; Hirsch, LJ; Morrell, MJ; Resor, SR; Spencer, HT; Straka, T; Weintraub, D, 2004)	0.7
" Respondents (100% of those surveyed), (1) considered the target LTG concentration (3-14 mg/L) to be one of the primary parameters applied in individualizing LTG dosage regimens, (2) were using target concentrations above 7 mg/L in 75% of patients, and (3) reported dose-limiting toxicities in some (but not all) patients typically at concentrations above, or well above, 13 mg/L."	( Long-term follow-up using a higher target range for lamotrigine monitoring. Black, AB; Cleanthous, X; Lee, MY; Morris, RG, 2004)	0.57
"A dosing algorithm was used to guide the conversion of 77 patients with epilepsy (16 years of age) from valproate monotherapy through lamotrigine adjunctive therapy at 200mg daily to lamotrigine monotherapy at 500 mg daily in an open-label study comprising a lamotrigine escalation phase (8 weeks), a valproate withdrawal phase (6 weeks), and a lamotrigine monotherapy phase (4 weeks)."	( A dosing algorithm for converting from valproate monotherapy to lamotrigine monotherapy in patients with epilepsy. Biton, V; Blum, D; Hammer, AE; Messenheimer, JA; Natarajan, S; Sale, ME; Vuong, A, 2005)	0.77
" The dosage schedule was: 5 mg every day or every second day for 14 days, increased by 5 mg every 14th day to 25 mg a day."	( Lamotrigine-induced rash--worth a rechallenge. Dam, M; P-Codrea Tigaran, S; Sidenius, P, 2005)	1.77
" The dosage of lamotrigine was increased and the patient received clonazepam intravenously, but a new seizure quickly occurred."	( [Epileptic seizures during childbirth in a patient with idiopathic generalised epilepsy]. Bloem, BR; Renier, WO; Voermans, NC; Zwarts, MJ, 2005)	0.68
" The rate of allergic skin rashes which was very high before 1998 has decreased markedly by new dosage guidelines and is now as low as in older antiepileptic drugs."	( [Optimizing epilepsy therapy in children and adolescents with lamotrigine]. Bergmann, L; Brandl, U; Helmstädter, C; Kurlemann, G; Rating, D; Sälke-Kellermann, RA; Siemes, H; Stephani, U; Uberall, M; Wiemer-Kruel, A, )	0.37
"A simple HPLC method was developed and validated for quantitation of lamotrigine and its related substances which may coexist in solid pharmaceutical dosage forms."	( Development and validation of a new HPLC method for determination of lamotrigine and related compounds in tablet formulations. Ahmadi, F; Emami, J; Ghassami, N, 2006)	0.8
" To fit the effect-time course of lamotrigine, the PK/PD simultaneous fitting link model was used: the pharmacokinetic parameters and dosing information were used in the one-compartment first-order model to predict concentrations, which were then used to model the pharmacodynamic data with the sigmoid Emax model, in order to estimate all the parameters simultaneously."	( Lamotrigine pharmacokinetic/pharmacodynamic modelling in rats. Caramona, MM; Castel-Branco, MM; Falcão, AC; Figueiredo, IV, 2005)	2.05
" The medication dosage varied from 1 to 20 mg/kg daily."	( [The efficacy of topiramate (topamax) in the treatment of resistant epilepsy in children]. Belousova, ED; Dorofeeva, MIu; Ermakov, AIu, 2005)	0.33
" A dosage adjustment for lamotrigine may need to be considered when these agents are co-administered."	( The pharmacokinetic and pharmacodynamic consequences of the co-administration of lamotrigine and a combined oral contraceptive in healthy female subjects. Job, S; Philipson, R; Sidhu, J; Singh, S, 2006)	0.86
" Lamotrigine dosing schedules are recommended to remain unchanged when combined with olanzapine therapy."	( Pharmacokinetics and tolerability of lamotrigine and olanzapine coadministered to healthy subjects. Abbott, R; Ascher, J; Bullman, J; Francis, E; Job, S; Sidhu, J; Theis, JG, 2006)	1.52
" These drugs were maintained another 8 weeks (maintenance phase) without dosage changes."	( Cognitive effects of lamotrigine compared with topiramate in patients with epilepsy. Biton, V; Blum, D; Chung, S; Fakhoury, T; Hammer, A; Isojärvi, J; Meador, K; Mills, K; Shneker, B, 2006)	0.65
" The mean lamotrigine dosage was 211."	( Regional effects of lamotrigine on cerebral glucose metabolism in idiopathic generalized epilepsy. Hong, SB; Joo, EY; Tae, WS, 2006)	1.06
" Also discussed are findings concerning the continuation of acute treatments, including antidepressants, into the maintenance phase; dosage adjustments for maintenance treatment; the rationale for combination treatments; and implications of comorbid substance abuse and strategies for its management."	( Maintenance treatment of bipolar disorder: Applying research to clinical practice. Chou, JC; Fazzio, L, 2006)	0.33
" Lamotrigine was titrated up to a final dosage of 200 mg/day over 8 weeks, and pharmacokinetic assessments were made at baseline and during treatment weeks 6 and 10, at lamotrigine dosages of 100 and 200 mg/day respectively."	( Effect of adjunctive lamotrigine treatment on the plasma concentrations of clozapine, risperidone and olanzapine in patients with schizophrenia or bipolar disorder. D'Amico, G; D'Arrigo, C; Micò, U; Migliardi, G; Muscatello, MR; Perucca, E; Santoro, V; Spina, E, 2006)	1.56
" For these older drugs it has been common practice to adjust the dosage to achieve a serum drug concentration within a predefined 'therapeutic range', representing an interval where most patients are expected to show an optimal response."	( Pharmacokinetic variability of newer antiepileptic drugs: when is monitoring needed? Johannessen, SI; Tomson, T, 2006)	0.33
" The satisfying outcome after a sudden and complete withdrawal of LTG in both cases encouraged us to perform the switch from LTG to VPA systematically by discontinuing LTG abruptly and building up the VPA maintenance dosage very rapidly in the following five consecutive patients who required this exchange."	( How to replace lamotrigine with valproate. Steinhoff, BJ, 2006)	0.69
" Partly because of these properties, frequent dosing adjustments are generally unnecessary, and therapeutic monitoring is not required under most circumstances."	( Pharmacokinetics, toxicology and safety of lamotrigine in epilepsy. Biton, V, 2006)	0.6
"SJS was associated with lamotrigine use, despite appropriate dosing and dosage adjustment."	( Lamotrigine-induced Stevens-Johnson syndrome. Charneski, L; Hilas, O, 2007)	2.09
" We then assessed pharmacy utilization and AED dosage among LTG patients switching back to branded Lamictal compared with those staying on generic formulation."	( Compulsory generic switching of antiepileptic drugs: high switchback rates to branded compounds compared with other drug classes. Andermann, F; Duh, MS; Gosselin, A; Paradis, PE, 2007)	0.34
"To characterize possible pharmacokinetic interactions between the new antiepileptic drug carisbamate (RWJ-333369) and valproic acid (VPA) or lamotrigine (LTG) following multiple dosing in healthy subjects."	( An interaction study between the new antiepileptic and CNS drug carisbamate (RWJ-333369) and lamotrigine and valproic acid. Bialer, M; Chien, S; Doose, DR; Mertens, A; Novak, G; Solanki, B; Verhaeghe, T; Yao, C, 2007)	0.76
" The proposed methods were successfully applied for the determination of lamotrigine in bulk powder, in dosage form and in presence of its impurity."	( Development and validation of spectrophotometric, TLC and HPLC methods for the determination of lamotrigine in presence of its impurity. Taha, EA; Youssef, NF, 2007)	0.79
" The discontinuation or dosage decrease of carbamazepine or oxcarbazepine may be associated with a slow increase of lamotrigine levels over several weeks and thus increase risk of lamotrigine toxicity that may manifest as oral ulcers."	( Two case reports of oral ulcers with lamotrigine several weeks after oxcarbazepine withdrawal. de Leon, J; O'Neill, A, 2007)	0.82
" Differences in outcome compared with previous trials may be related to different dosing rates and use of a sustained-release formulation for CBZ."	( An international multicenter randomized double-blind controlled trial of lamotrigine and sustained-release carbamazepine in the treatment of newly diagnosed epilepsy in the elderly. Gjerstad, L; Isojärvi, J; Perucca, E; Saetre, E, 2007)	0.57
" Lamotrigine was given for 12 weeks, with a target dosage of 200 mg/d."	( Effect of open-label lamotrigine as monotherapy and adjunctive therapy on the self-assessed cognitive function scores of patients with bipolar I disorder. Graham, J; Kaye, NS; Nanry, K; Roberts, J; Thompson, T, 2007)	1.57
" Because of dosage changes, lamotrigine costs decreased by $29."	( The economic consequences of generic substitution for antiepileptic drugs in a public payer setting: the case of lamotrigine. Andermann, F; Crémieux, PY; Duh, MS; Manjunath, R; Paradis, PE; Weiner, J, 2007)	0.84
" We report the utility of a dosing algorithm designed to maintain stable trough lamotrigine (LTG) concentrations during conversion from valproate (VPA) to LTG monotherapy in adolescents aged 16-20 years."	( Conversion to lamotrigine monotherapy from valproate monotherapy in older adolescent patients with epilepsy. Baumann, RJ; Fakhoury, TA; Hammer, AE; Kustra, RP; Messenheimer, JA; Vuong, A, 2007)	0.93
" Lamotrigine dosing ranged from 25 mg every other day to 300 mg/day."	( Lamotrigine treatment of pathologic skin picking: an open-label study. Grant, JE; Kim, SW; Odlaug, BL, 2007)	2.69
": Two multicenter, randomized, double-blind, 12-week, parallel-group trials were conducted to compare flexibly dosed lamotrigine (100-400 mg/d) with placebo as add-on treatment in schizophrenia patients with stable, residual psychotic symptoms."	( Lamotrigine as add-on therapy in schizophrenia: results of 2 placebo-controlled trials. Citrome, L; Davy, K; Goff, DC; Keefe, R; Krystal, JH; Large, C; Thompson, TR; Volavka, J; Webster, EL, 2007)	1.99
"These novel data contribute to a rational treatment plan and dosing paradigm for lamotrigine use during pregnancy, parturition, and the postpartum period."	( Lamotrigine in pregnancy: clearance, therapeutic drug monitoring, and seizure frequency. Holley, DK; Koganti, A; Newman, M; Newport, DJ; Peng, L; Pennell, PB; Ritchie, JC; Stowe, ZN, 2008)	2.01
" The manufacturer recommends half the dosage of lamotrigine monotherapy when the patient also uses valproate."	( Lamotrigine in clinical practice: long-term experience in patients with refractory epilepsy referred to a tertiary epilepsy center. Aldenkamp, AP; Bootsma, HP; Hulsman, J; Lambrechts, D; Leenen, L; Majoie, M; Savelkoul, M; Schellekens, A; Vos, AM, 2008)	2.04
" Dosing of lamotrigine in elderly patients is based largely on studies from younger adults and not evidence-based data from elderly patients."	( Population pharmacokinetics of lamotrigine in elderly patients. Birnbaum, AK; Brundage, RC; Collins, JF; Macias, FM; Punyawudho, B; Ramsay, RE; Rowan, AJ, 2008)	1.02
"To establish a population pharmacokinetics (PPK) model of lamotrigine, an antiepileptic drug, in Chinese children with epilepsy to formulate an individualized dosage guideline."	( [Population pharmacokinetics of lamotrigine in Chinese children with epilepsy]. Lu, W; Wang, L; Zhang, S, 2008)	0.87
" The proposed model may be very useful for clinicians in establishing initial LTG dosage guidelines."	( Population pharmacokinetics of lamotrigine with data from therapeutic drug monitoring in German and Spanish patients with epilepsy. Buelga, DS; Domínguez-Gil, A; Elger, CE; García, MJ; Otero, MJ; Rivas, N; Santos-Borbujo, J, 2008)	0.63
" Patients (n = 204) received lamotrigine according to a dosing schedule that depended on prior experience with lamotrigine and concurrent antiepileptic drug therapy for up to 48 weeks or their second birthday, whichever occurred last."	( Long-term tolerability and efficacy of lamotrigine in infants 1 to 24 months old. Ayala, R; Conklin, HS; Corral, M; Elterman, RD; Messenheimer, JA; Mikati, MA; Piña-Garza, JE; Piña-Garza, MJ; Warnock, CR, 2008)	0.91
" The wide interpatient variability in LTG dosage required to attain therapeutic plasma LTG concentrations for seizure control suggests that LTG is a good candidate for therapeutic drug monitoring (TDM)."	( Seradyn quantitative microsphere system lamotrigine immunoassay on a Hitachi 911 analyzer compared with HPLC-UV. Morris, RG; Westley, IS, 2008)	0.61
" Controlled studies are necessary to identify the population at risk for obsessionality in bipolar illness following treatment with lamotrigine and to investigate a possible dose-response relationship between obsessive symptoms and lamotrigine."	( Lamotrigine-induced obsessional symptoms in a patient with bipolar II disorder: a case report. Caykoylu, A; Ekinci, O; Kuloglu, M; Yilmaz, E, 2009)	2
" The isobolographic analysis for parallel and nonparallel dose-response effects was used in the mouse maximal electroshock seizure (MES) model for evaluation of pharmacodynamic interaction."	( Isobolographic characterization of interactions of retigabine with carbamazepine, lamotrigine, and valproate in the mouse maximal electroshock-induced seizure model. Czuczwar, SJ; Luszczki, JJ; Raszewski, G; Wu, JZ, 2009)	0.58
"Rapid and sensitive spectrophotometric methods are developed for the determination of lamotrigine (LTG) in pharmaceutical dosage forms and urine samples, based on the formation of the charge-transfer (CT) complexes between LTG as an n-donor and the acceptors: bromocresol green (BCG), bromocresol purple (BCP), and chlorophenol red (CPR)."	( Spectrophotometric determination of lamotrigine in pharmaceutical preparations and urine by charge-transfer complexation. Alizadeh, N; Jabbari, A; Khakinahad, R, 2008)	0.84
" Lamotrigine was introduced at a dosage of 25 mg daily and increased to 50 mg daily 12 days later."	( Fulminant hepatitis induced by lamotrigine. Marleau, D; Ouellet, G; Tremblay, L, 2009)	1.55
" No dosage adjustment of lamotrigine is required and the combination was generally safe and well tolerated."	( A non-randomized study to investigate the effects of the atypical antipsychotic aripiprazole on the steady-state pharmacokinetics of lamotrigine in patients with bipolar I disorder. Balch, AH; Benson, J; Boulton, DW; Carlson, BX; Croop, R; Mallikaarjun, S; Schieber, FC, 2009)	0.86
" All 9 patients became hyperactive and agitated over a broad range of lamotrigine dosing (0."	( Reversible lamotrigine-induced neurobehavioral disturbances in children with epilepsy. Cardenas, JF; Ng, YT; Rho, JM, 2010)	0.98
" This was an open-label trial with a flexible dosing regimen."	( Lamotrigine versus lithium augmentation of antidepressant therapy in treatment-resistant depression: efficacy and tolerability. Cvetić, T; Damjanović, A; Ivković, M; Jasović-Gasić, M; Jovanović, A, 2009)	1.8
" Because or recurrent seizures, the lamotrigine dosage was increased from 100 mg/d to 200 mg and then to 300 mg/d."	( Lamotrigine-trigged obstructive hypertrophic cardiomyopathy, epilepsy and metabolic myopathy. Finsterer, J; Höftberger, R; Stöllberger, C, 2011)	2.09
"The derived model describes well lamotrigine clearance in terms of characteristics of Serbian patients, offering basis for rational individualization of lamotrigine dosing regimens."	( Population pharmacokinetics of lamotrigine in patients with epilepsy. Jankovic, SM; Milovanovic, JR, 2009)	0.92
" In the present study, GSH, cysteinylglycine, and N-acetyl cysteine conjugates of LTG were isolated from bile of rats orally dosed with LTG (100 mg/kg), and their structures were fully elucidated by LC/MS and NMR."	( Bioactivation of lamotrigine in vivo in rat and in vitro in human liver microsomes, hepatocytes, and epidermal keratinocytes: characterization of thioether conjugates by liquid chromatography/mass spectrometry and high field nuclear magnetic resonance spe Chen, H; Grover, S; Mutlib, A; Walker, G; Yu, L, 2010)	0.7
" If the patient is currently taking other mood stabilizers, their dosage should be optimized, and the clinician should consider adding or switching to lithium, quetiapine, or lamotrigine."	( The psychopharmacology algorithm project at the Harvard South Shore Program: an update on bipolar depression. Ansari, A; Osser, DN, )	0.32
" Geometric mean ratios (GMR) and 90% confidence intervals (90% CI) for maximum plasma concentration (C(max)) and area under the plasma concentration-time curve in the dosing interval (AUC(0-24)) were calculated for eslicarbazepine (ESL active metabolite) and lamotrigine."	( Pharmacokinetic interaction study between eslicarbazepine acetate and lamotrigine in healthy subjects. Almeida, L; Brunet, JS; Falcão, A; Lefebvre, M; Nunes, T; Rocha, JF; Sicard, E; Soares-da-Silva, P, 2010)	0.77
" Therefore, no dosage adjustment appears to be usually required in either lamotrigine or ESL when the drugs are co-administered."	( Pharmacokinetic interaction study between eslicarbazepine acetate and lamotrigine in healthy subjects. Almeida, L; Brunet, JS; Falcão, A; Lefebvre, M; Nunes, T; Rocha, JF; Sicard, E; Soares-da-Silva, P, 2010)	0.83
"The aim of this study was to characterize the anticonvulsant effects of 1-methyl-1,2,3,4-tetrahydroisoquinoline (MeTHIQ--an endogenous parkinsonism-preventing substance) in combination with four second-generation antiepileptic drugs (AEDs: lamotrigine [LTG], oxcarbazepine [OXC], pregabalin [PGB], and topiramate [TPM]) in the mouse maximal electroshock (MES)-induced seizure model by using the type I isobolographic analysis for parallel and non-parallel dose-response relationship curves (DRRCs)."	( Interactions of 1-methyl-1,2,3,4-tetrahydroisoquinoline with lamotrigine, oxcarbazepine, pregabalin, and topiramate in the mouse maximal electroshock-induced seizure model: a type I isobolographic analysis. Antkiewicz-Michaluk, L; Czuczwar, SJ; Luszczki, JJ; Raszewski, G, 2010)	0.78
" Results of our study show the positive correlation between dosage and serum concentration of CBZ."	( Carbamazepine and lamotrigine plasma concentrations in epileptic patients during optimising therapy. Bauer, S; Islami, H; Krasniqi, S; Neziri, B, 2010)	0.69
" Lamotrigine dosing ranged from 12."	( A double-blind, placebo-controlled trial of lamotrigine for pathological skin picking: treatment efficacy and neurocognitive predictors of response. Chamberlain, SR; Grant, JE; Kim, SW; Odlaug, BL, 2010)	1.53
" Eleven patients had ECT treatments with and without LMT, of which 8 were at a dosage of 200 mg/d or higher."	( Concurrent use of lamotrigine and electroconvulsive therapy. Demunter, H; Peuskens, J; Roelens, Y; Sienaert, P; Van Heeringen, C; Vansteelandt, K, 2011)	0.7
" Nicotine dose-response curves showed that in the presence of LTG, the nicotine-induced maximal current was reduced, suggesting a noncompetitive inhibition."	( The anticonvulsive drug lamotrigine blocks neuronal {alpha}4{beta}2 nicotinic acetylcholine receptors. Barrantes, FJ; Liu, Q; Lukas, RJ; Shen, J; Vallés, AS; Wang, MY; Wu, J; Yang, K; Zheng, C, 2010)	0.67
", lamotrigine [LTG], oxcarbazepine [OXC] and topiramate [TPM]) in the mouse maximal electroshock (MES)-induced seizure model by using the type I isobolographic analysis for non-parallel dose-response relationship curves (DRRCs)."	( Additive interactions of pregabalin with lamotrigine, oxcarbazepine and topiramate in the mouse maximal electroshock-induced seizure model: a type I isobolographic analysis for non-parallel dose-response relationship curves. Czuczwar, SJ; Filip, D; Luszczki, JJ, 2010)	1.35
" Newly diagnosed 52 pediatric epileptic patients were assessed standard speech test through a Computerized Speech Lab applied before the beginning of therapy with lamotrigine and 2months after dosage had been stabilized."	( Acoustic effects of lamotrigine in pediatric patients with epilepsy. Choi, YM; Eun, SH; Kim, SJ; Seol, IJ; Yun, M, 2011)	0.89
" Dosing and plasma levels of levetiracetam and concomitant antiepileptic drugs were reviewed retrospectively."	( Age and comedications influence levetiracetam pharmacokinetics in children. Dahlin, MG; Ohman, I; Wide, K, 2010)	0.36
" The differences in the starting dosage of LTG among the SJS/TEN, MPE, and LTG-tolerant control groups were not statistically significant."	( Association study of lamotrigine-induced cutaneous adverse reactions and HLA-B*1502 in a Han Chinese population. An, DM; Hu, FY; Stefan, H; Wu, XT; Yan, B; Zhou, D, 2010)	0.68
" In some cases, there was initial response to low doses, but dosage titrations were often necessary when symptoms returned several days after being managed at the same dose."	( The role of lamotrigine in the treatment of short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing syndrome. Karpinski, JP; Rosselli, JL, 2011)	0.75
" In case of breakthrough seizures or increased seizure frequency, dosage adjustment of both drugs may be required."	( Drug monitoring of lamotrigine and oxcarbazepine combination during pregnancy. de Haan, GJ; Edelbroek, P; Lindhout, D; Sander, JW; Wegner, I, 2010)	0.69
"A slow up-titration of clozapine is recommended in order to reach the optimal dosage of clozapine and diminish the risk of dose-dependent side-effects."	( Optimizing clozapine treatment. Damkier, P; Lublin, H; Nielsen, J; Taylor, D, 2011)	0.37
" Serial pharmacokinetic sampling of atorvastatin was conducted on day 7 of atorvastatin dosing and day 70 of lamotrigine + atorvastatin dosing or day 28 of phenytoin + atorvastatin dosing."	( Effects of lamotrigine and phenytoin on the pharmacokinetics of atorvastatin in healthy volunteers. Alexander, S; Bullman, J; Fleck, R; Messenheimer, J; Miller, J; Nicholls, A; Van Landingham, K; Vuong, A, 2011)	0.97
" We increased the LTG dosage every two weeks in accordance with usage recommendations."	( [Lamotrigine add-on therapy for childhood-onset refractory epilepsy: comparison of the efficacy between 3 months and 6 months after initiation]. Endoh, F; Kobayashi, K; Ohtsuka, Y; Watanabe, K; Yoshinaga, H, 2011)	1.28
" Larger placebo-controlled studies are needed to ascertain optimal timing and dosing for memantine augmentation of lamotrigine in BD-D."	( Early antidepressant effect of memantine during augmentation of lamotrigine inadequate response in bipolar depression: a double-blind, randomized, placebo-controlled trial. Anand, A; Barkay, G; Ghosh, S; Gunn, AD; Karne, HS; Mathew, SJ; Nurnberger, JI, 2012)	0.83
" Concomitant use of drugs metabolized by CYP2D6 may require dosage adjustment."	( Pharmacokinetic drug interactions between clobazam and drugs metabolized by cytochrome P450 isoenzymes. Bekersky, I; Blum, RA; Tolbert, D; Walzer, M, 2012)	0.38
"To establish a population pharmacokinetics (PPK) model for lamotrigine (LTG) in Chinese children with epilepsy in order to formulate an individualized dosage guideline."	( Population pharmacokinetics of lamotrigine in Chinese children with epilepsy. Bao, WQ; He, DK; Li, L; Liu, HT; Lu, W; Qin, J; Song, XQ; Wang, L; Zhang, JM; Zhang, S, 2012)	0.91
" The model may be very useful for establishing initial LTG dosage guidelines."	( Population pharmacokinetics of lamotrigine in Chinese children with epilepsy. Bao, WQ; He, DK; Li, L; Liu, HT; Lu, W; Qin, J; Song, XQ; Wang, L; Zhang, JM; Zhang, S, 2012)	0.66
" A significant relationship between seizure frequency per day and LTG dosage during titration and follow-up phase could be demonstrated in nine patients."	( Myoclonic astatic epilepsy (Doose syndrome) - a lamotrigine responsive epilepsy? Boor, R; Doege, C; May, TW; Siniatchkin, M; Stephani, U; von Spiczak, S, 2013)	0.65
" Mean PGB dosage was 279 mg/day."	( Effect of pregabalin add-on treatment on seizure control, quality of life, and anxiety in patients with brain tumour-related epilepsy: a pilot study. Carapella, CM; Dinapoli, L; Fabi, A; Maschio, M; Pace, A; Pompili, A; Sperati, F; Vidiri, A, 2012)	0.38
" Given the similar safety, tolerability and efficacy profiles of lamotrigine XR and lamotrigine IR, the extended-release formulation may be preferable for many patients because of its ease of use (with once-daily dosing regardless of concomitant antiepileptic drug), the potential for enhanced compliance with once-daily dosing, and the provision of more stable serum drug concentrations."	( Long-term tolerability and safety of lamotrigine extended-release: pooled analysis of three clinical trials. Biton, V; Caldwell, PT; Hammer, AE; Messenheimer, JA; Naritoku, D; Shneker, BF; Vuong, A, 2013)	0.9
"To assess the effect of common dosing irregularities on serum concentrations of antiepileptic drug (AED) lamotrigine for the extended-release (XR) formulation, which is recommended for once-daily dosing (QD), and the immediate-release (IR) formulation, which is typically dosed twice daily (BID)."	( Assessing impact of real-world dosing irregularities with lamotrigine extended-release and immediate-release formulations by pharmacokinetic simulation. Chen, C; Gidal, B; Messenheimer, J; Wright, J, 2013)	0.85
"Lamotrigine steady-state serum concentrations stayed in a narrower range for XR-QD than for IR-BID, despite the more frequent dosing of the latter."	( Assessing impact of real-world dosing irregularities with lamotrigine extended-release and immediate-release formulations by pharmacokinetic simulation. Chen, C; Gidal, B; Messenheimer, J; Wright, J, 2013)	2.08
" The approach illustrates how a model constructed on clinical trial data can be used to simulate real-world dosing scenarios and guide therapeutics."	( Assessing impact of real-world dosing irregularities with lamotrigine extended-release and immediate-release formulations by pharmacokinetic simulation. Chen, C; Gidal, B; Messenheimer, J; Wright, J, 2013)	0.63
"Little information is available on the need for dosage changes for lamotrigine in pregnant women with bipolar disorder."	( Lamotrigine dosing for pregnant patients with bipolar disorder. Clark, CT; Helsel, J; Klein, AM; Perel, JM; Wisner, KL, 2013)	2.07
"The LTG population pharmacokinetic model developed in this study may be a reliable method for individualising the LTG dosing regimen in paediatric and young adult patients on combination therapy during therapeutic drug monitoring."	( Pharmacokinetics of lamotrigine in paediatric and young adult epileptic patients--nonlinear mixed effects modelling approach. Brzaković, B; Kovačević, SV; Martinović, Ž; Miljković, B; Pokrajac, M; Prostran, M; Vučićević, K, 2014)	0.73
" The data collected included epilepsy type, seizure frequency, concomitant anti-epileptic drugs, dosage of LTG and LTG serum levels."	( [Clinical efficacy and pharmacokinetics of lamotrigine for childhood-onset intractable epilepsy]. Arakawa, C; Endo, A; Fuchigami, T; Fujita, Y; Imai, Y; Ishii, W; Kohira, R; Momoki, E; Mugishima, H, 2014)	0.67
" In addition, there was a high correlation between the LTG serum levels and the dosage of LTG in each group."	( [Clinical efficacy and pharmacokinetics of lamotrigine for childhood-onset intractable epilepsy]. Arakawa, C; Endo, A; Fuchigami, T; Fujita, Y; Imai, Y; Ishii, W; Kohira, R; Momoki, E; Mugishima, H, 2014)	0.67
"The LTG serum level is predictable based on the dosage of LTG."	( [Clinical efficacy and pharmacokinetics of lamotrigine for childhood-onset intractable epilepsy]. Arakawa, C; Endo, A; Fuchigami, T; Fujita, Y; Imai, Y; Ishii, W; Kohira, R; Momoki, E; Mugishima, H, 2014)	0.67
"Immediate release lamotrigine (LTG-IR) dosing can be limited by peak toxicity."	( Conversion from immediate-release to extended-release lamotrigine improves seizure control. Abou-Khalil, B; Osborn, M; Ramey, P, 2014)	0.98
" We collected the following parameters: age at conversion, LTG-IR dose and dosing schedule, duration on that dose, LTG-XR dose and dosing schedule, LTG serum level before and after conversion, duration of LTG-XR treatment, seizure frequency before and after conversion, and change in adverse experience profile."	( Conversion from immediate-release to extended-release lamotrigine improves seizure control. Abou-Khalil, B; Osborn, M; Ramey, P, 2014)	0.65
" Further, the poor pharmacokinetic profile due to non-selective distribution to organs other than brain reduces the efficacy of dosage regimen."	( Protein-functionalized PLGA nanoparticles of lamotrigine for neuropathic pain management. Kolate, A; Lalani, J; Lalani, R; Misra, A; Patil, S, 2015)	0.68
"The present study aimed to establish population pharmacokinetic model for phenobarbital (PB), examining and quantifying the magnitude of PB interactions with other antiepileptic drugs concomitantly used and to demonstrate its use for individualization of PB dosing regimen in adult epileptic patients."	( Nonlinear mixed effects modelling approach in investigating phenobarbital pharmacokinetic interactions in epileptic patients. Golubović, B; Jovanović, M; Kovačević, SV; Martinović, Ž; Miljković, B; Prostran, M; Vučićević, K, 2015)	0.42
"Developed population PB model may be used in estimating individual CL/F for adult epileptic patients and could be applied for individualizing dosing regimen taking into account dose-dependent effect of concomitantly given VPA."	( Nonlinear mixed effects modelling approach in investigating phenobarbital pharmacokinetic interactions in epileptic patients. Golubović, B; Jovanović, M; Kovačević, SV; Martinović, Ž; Miljković, B; Prostran, M; Vučićević, K, 2015)	0.42
" We highlighted the importance of measuring LTG blood levels, and proposed a method of adjusting the optimum dosage of LTG based on the pharmacokinetic interaction."	( [Importance of measuring blood level of lamotrigine for optimum dosing schedule]. Fukumura, S; Minagawa, K; Oyanagi, R; Watanabe, T, 2014)	0.67
"The maintenance dosage described in the PL was lower than that in our methods."	( [Importance of measuring blood level of lamotrigine for optimum dosing schedule]. Fukumura, S; Minagawa, K; Oyanagi, R; Watanabe, T, 2014)	0.67
"Measuring the LTG blood level is important to create an optimum dosing schedule."	( [Importance of measuring blood level of lamotrigine for optimum dosing schedule]. Fukumura, S; Minagawa, K; Oyanagi, R; Watanabe, T, 2014)	0.67
"The results of this study suggest that the administration of lamotrigine to patients with severe Alzheimer's disease with BPSD may be effective and may make it possible to avoid increasing the dosage of antipsychotic medications prescribed to elderly patients."	( Clinical efficacy of lamotrigine and changes in the dosages of concomitantly used psychotropic drugs in Alzheimer's disease with behavioural and psychological symptoms of dementia: a preliminary open-label trial. Gen, K; Suzuki, H, 2015)	0.98
" The patients were given ZNS as add-on treatment, and the ZNS dosing and the visit frequency were governed by the treating physician."	( Retention rate of zonisamide in intractable epilepsy. Andersen, H; Lindstrøm, P; Nakken, KO, 2015)	0.42
" After referral to the neurology clinic, he was diagnosed with generalized tonic-clonic seizure disorder, and lamotrigine was started with up-titration according to the drug's package insert to a goal dosage of 150 mg twice/day."	( Drug reaction with eosinophilia and systemic symptoms syndrome probably induced by a lamotrigine-ginseng drug interaction. Myers, AP; Strock, SB; Watson, TA, 2015)	0.85
" The median dosage at onset was 36."	( Lamotrigine-induced severe cutaneous adverse reaction: Update data from 1999-2014. Huang, XS; Lang, SY; Lv, B; Tian, CL; Wang, HF; Wang, XQ; Yu, SY; Zhang, JT; Zhang, X, 2015)	1.86
" A panel of pharmaceutical quality tests was also performed on three batches of Lamictal, three batches of Teva generic, and one batch of each of four other generics: appearance, identity, assay, impurity, uniformity of dosage units, disintegration, dissolution, friability, and loss on drying."	( Biopharmaceutic Risk Assessment of Brand and Generic Lamotrigine Tablets. Jiang, W; Kane, MA; Polli, JE; Raman, S; Ting, TY; Vaithianathan, S, 2015)	0.67
" The dose-response to DHA was obtained 15 min after intracerebroventricular (i."	( Synergistic effect of docosahexaenoic acid on anticonvulsant activity of valproic acid and lamotrigine in animal seizure models. Babapour, V; Gavzan, H; Sardari, S; Sayyah, M, 2015)	0.64
" Future studies are necessary to determine whether these SNPs can be used to provide LTG dosing guidance and influence seizure control and adverse reaction of LTG."	( Polymorphisms of ABCG2, ABCB1 and HNF4α are associated with Lamotrigine trough concentrations in epilepsy patients. Chen, Z; Huang, M; Li, H; Li, J; Wang, X; Xie, W; Zhang, J; Zhou, L; Zhou, Y, 2015)	0.66
"To assess efficacy/tolerability of ezogabine (EZG)/retigabine (RTG) in combination with specified monotherapy antiepileptic drug (AED) treatments in adults with uncontrolled partial-onset seizures using a flexible dosing regimen."	( Efficacy and safety of ezogabine/retigabine as adjunctive therapy to specified single antiepileptic medications in an open-label study of adults with partial-onset seizures. Brandt, C; Daniluk, J; DeRossett, S; Edwards, S; Lerche, H; Lotay, N, 2015)	0.42
"NCT01227902 was an open-label, uncontrolled study of flexibly dosed EZG/RTG."	( Efficacy and safety of ezogabine/retigabine as adjunctive therapy to specified single antiepileptic medications in an open-label study of adults with partial-onset seizures. Brandt, C; Daniluk, J; DeRossett, S; Edwards, S; Lerche, H; Lotay, N, 2015)	0.42
"EZG/RTG was effective as adjunctive therapy to CBZ/OXC, LTG, LEV, and VPA, using a flexible dosing regimen, in adults with partial-onset seizures; safety and tolerability were consistent with that previously observed."	( Efficacy and safety of ezogabine/retigabine as adjunctive therapy to specified single antiepileptic medications in an open-label study of adults with partial-onset seizures. Brandt, C; Daniluk, J; DeRossett, S; Edwards, S; Lerche, H; Lotay, N, 2015)	0.42
"The Equivalence among Generic Antiepileptic Drugs (EQUIGEN) chronic-dose study was a randomised, double-blind, crossover study that enrolled adults (aged ≥18 years) with epilepsy from six epilepsy centres at academic institutions across the USA who were receiving immediate-release lamotrigine dosed at 100 mg, 200 mg, 300 mg, or 400 mg twice daily."	( Generic-to-generic lamotrigine switches in people with epilepsy: the randomised controlled EQUIGEN trial. Berg, M; Diaz, FJ; Dworetzky, BA; Elder, EJ; Gidal, BE; Jiang, W; Jiang, X; Krebill, R; Pollard, JR; Privitera, MD; Szaflarski, JP; Welty, TE, 2016)	0.94
"The study was designed to evaluate the optimal dosage of lamotrigine, as monotherapy, in the treatment of adults suffering from complex partial seizures with or without secondary generalization in everyday clinical practice."	( Lamotrigine as monotherapy in clinical practice: efficacy of various dosages in epilepsy. Eilam, A; Gilad, R; Warshavsky, A, 2016)	2.12
" The dosage and efficacy of treatment were evaluated along with side effects and retention rate."	( Lamotrigine as monotherapy in clinical practice: efficacy of various dosages in epilepsy. Eilam, A; Gilad, R; Warshavsky, A, 2016)	1.88
" The mean daily dosage was 26."	( Lamotrigine monotherapy for paroxysmal kinesigenic dyskinesia in children. Hu, Y; Li, F; Li, W; Lin, ZD; Poonit, ND; Xue, CC, 2016)	1.88
"We included 100 patients with epilepsy on stable dosing with lamotrigine as mono or adjunctive therapy."	( Pharmacokinetics of lamotrigine and its metabolite N-2-glucuronide: Influence of polymorphism of UDP-glucuronosyltransferases and drug transporters. Dolžan, V; Grabnar, I; Kastelic, M; Lorber, B; Milosheska, D; Vovk, T, 2016)	1
" The correlation with dose may be a spurious finding related to the fact that physicians, in adjusting dosage according to clinical response, are more likely to use larger doses in patients with high clearance values."	( An investigation of the influence of patient-related factors and comedications on lamotrigine clearance in patients with epilepsy. Alexandre, V; Baldoni, AO; de Santi Ferreira, FI; Freitas-Lima, P; Martinez, EZ; Pereira, LR; Perucca, E; Queiroz, RH; Sakamoto, AC, 2016)	0.66
"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
" Further, CPOT of LTG based on SD proved to be successful in delivering the drug in a controlled manner ensuring the once daily dosing for the treatment of convulsive disorders."	( Development and Optimization of Controlled Porosity Osmotic Tablets of Lamotrigine Solid Dispersion. Kasarwala, M; Patel, GC, 2016)	0.67
" Lamotrigine (LTG) is a second generation anti-epileptic drug (AED) with broad spectrum of activity, a favourable side-effect profile, simpler dosing than earlier drugs and efficacious in diverse epilepsy syndromes."	( A pharmacological overview of lamotrigine for the treatment of epilepsy. Arjunan, K; Eswaramoorthy, M; Jakki, SL; Nanjan, MJ; Senthil, V; Shanmuganathan, S; Yasam, VR, 2016)	1.63
" We sought to determine whether there were regions in the dosage range of commonly used AEDs that were associated with superior efficacy in patients with refractory epilepsy."	( Association between antiepileptic drug dose and long-term response in patients with refractory epilepsy. Castagna, CE; Miller, AB; Poolos, NP; Story, TJ; Williams, S, 2017)	0.46
" The LTG PPK model developed in this study could be useful for individualizing LTG dosage regimens in pediatric patients receiving combination therapy, especially therapy that includes VPA."	( Population pharmacokinetics of lamotrigine co-administered with valproic acid in Chinese epileptic children using nonlinear mixed effects modeling. Chen, Y; Liu, L; Liu, M; Liu, S; Lu, T; Wang, H; Xu, S; Zhao, L; Zhao, M, 2018)	0.77
" In addition, simulations were performed to identify the implication of different doses and dosing regimens for each population, so as to ensure steady-state concentrations within a predefined reference range."	( Effect of Age-Related Factors on the Pharmacokinetics of Lamotrigine and Potential Implications for Maintenance Dose Optimisation in Future Clinical Trials. Danhof, M; de Jager, NCB; Della Pasqua, O; Rauwé, WM; van Dijkman, SC, 2018)	0.73
" Oxcarbazepine dosage was found to linearly correlate with AEP and ABNAS scores, better than carbamazepine dosage."	( Adverse effects of anti-epileptics in trigeminal neuralgiform pain. Cregg, R; Lee, G; O'Keeffe, AG; Reading, J; Tentolouris-Piperas, V; Zakrzewska, JM, 2018)	0.48
" Retrospectively collected data included LTG dosage and LTG plasma levels before pregnancy (T0), and LTG dosage and LTG plasma level changes in the first (T1), second (T2) and third trimester (T3), and post-partum (PP) as well as the sex of the foetus."	( UGT polymorphisms and lamotrigine clearance during pregnancy. Ekström, L; Hansen, TF; Öhman, I; Petrenaite, V; Sabers, A; Sæbye, D; Tomson, T, 2018)	0.8
"The number of patients in each of the three BRV dosage groups was small, particularly for the TPM subgroup."	( Efficacy, safety, and tolerability of brivaracetam with concomitant lamotrigine or concomitant topiramate in pooled Phase III randomized, double-blind trials: A post-hoc analysis. Benbadis, S; Diaz, A; Elmoufti, S; Klein, P; Schiemann, J; Whitesides, J, 2018)	0.72
"Despite stable LTG dosage serum concentrations on study day 20, 22, 24, 26, and 28, all were significantly lower compared to baseline (p < 0."	( Time course of reversal of valproate-mediated inhibition of lamotrigine. Gidal, BE; Leary, E; Sheth, RD, 2018)	0.72
" These data provide clinically useful information in developing a dosing algorithm for converting patients to LTG monotherapy."	( Time course of reversal of valproate-mediated inhibition of lamotrigine. Gidal, BE; Leary, E; Sheth, RD, 2018)	0.72
"The dosage and frequency of lamotrigine administration for each patient must be prescribed carefully according to the disease, age, concomitant medications, and administration period."	( A Standard Intervention Practice to Promote Appropriate Lamotrigine Therapy by Pharmacists. Itabe, H; Okada, N; Sasaki, T; Shimamura, H; Tanaka, K; Uchikura, T; Yamada, H, 2018)	1.02
"Evidence for the comparative teratogenic risk of antiepileptic drugs is insufficient, particularly in relation to the dosage used."	( Comparative risk of major congenital malformations with eight different antiepileptic drugs: a prospective cohort study of the EURAP registry. Battino, D; Bonizzoni, E; Craig, J; Lindhout, D; Perucca, E; Sabers, A; Thomas, SV; Tomson, T; Vajda, F, 2018)	0.48
"In the therapeutic drug monitoring group, clinicians had access to clinical findings and monthly serum AED levels to guide AED dosage adjustment for seizure control."	( AntiEpileptic drug Monitoring in PREgnancy (EMPiRE): a double-blind randomised trial on effectiveness and acceptability of monitoring strategies. Bagary, M; Coleman, J; D'Amico, M; Denny, E; Dodds, J; Eldridge, S; Greenhill, L; Hard, K; Kelso, A; Khan, KS; Marlin, N; McCorry, D; Middleton, L; Moss, N; Newton, S; Pirie, A; Pullen, A; Rikunenko, R; Roberts, T; Rogozińska, E; Thangaratinam, S; Weckesser, A, 2018)	0.48
" For optimal dosing in pregnancy, therapeutic drug monitoring may be required to maintain effective drug concentrations."	( Treatment of Peripartum Bipolar Disorder. Clark, CT; Wisner, KL, 2018)	0.48
" When sodium channel blockers cannot reach full dosage because of side effects, an add-on treatment with lamotrigine or baclofen should be considered."	( Current and Innovative Pharmacological Options to Treat Typical and Atypical Trigeminal Neuralgia. Cruccu, G; Di Stefano, G; Truini, A, 2018)	0.69
"The mean daily dosage of lamotrigine was 351."	( Comprehensive Measurements of Intrauterine and Postnatal Exposure to Lamotrigine. Augustin, M; Franz, C; Gründer, G; Paulzen, M; Saßmannshausen, H; Schoretsanitis, G; Stingl, JC, 2019)	1.05
" In the clinical setting, these findings can help to estimate LTG concentrations and adjust dosage and evaluate adverse drug reactions."	( The influence of concomitant antiepileptic drugs on lamotrigine serum concentrations in Northwest Chinese Han population with epilepsy. Han, X; Huang, J; Lv, J; Ma, L; Nie, X; Peng, L; Wang, J; Xia, L; Zan, X, 2019)	0.76
" The aim of this study was to establish a PPK model of MHD to investigate the effects of genetic polymorphisms in UGT2B7, UGT1A9, ABCB1, and ABCB2 in adult Chinese patients with epilepsy and to develop a new dosage guideline for OXC."	( Glomerular Filtration Rate Is a Major Predictor of Clearance of Oxcarbazepine Active Metabolite in Adult Chinese Epileptic Patients: A Population Pharmacokinetic Analysis. Jiao, Z; Lin, RF; Lin, S; Lin, WW; Lin, XH; Wang, CL; Yu, XL; Zhang, J; Zhang, WB, 2019)	0.51
" Moreover, a new dosage guideline was proposed based on the final model to individualize OXC regimens for adult patients with varying BW and renal function."	( Glomerular Filtration Rate Is a Major Predictor of Clearance of Oxcarbazepine Active Metabolite in Adult Chinese Epileptic Patients: A Population Pharmacokinetic Analysis. Jiao, Z; Lin, RF; Lin, S; Lin, WW; Lin, XH; Wang, CL; Yu, XL; Zhang, J; Zhang, WB, 2019)	0.51
" We unexpectedly discover a new class of aggregating ligands that exhibit negligible interactions with proteins but act as competitive sinks for the free inhibitor, resulting in bell-shaped dose-response curves."	( Mechanisms of Specific versus Nonspecific Interactions of Aggregation-Prone Inhibitors and Attenuators. Ahmed, R; Boulton, S; Cheng, X; Melacini, G; Selvaratnam, R; Van, K, 2019)	0.51
"Lamotrigine augmentation may serve as a possible choice for patients with treatment-resistant unipolar depression and further trials are warranted to clarify the optimal dosage of lamotrigine augmentation together with the treatment duration and safety over time."	( Lamotrigine augmentation in treatment-resistant unipolar depression: A comprehensive meta-analysis of efficacy and safety. Chen, CH; Chiu, YH; Goh, KK; Lu, ML, 2019)	3.4
"This study investigated the effect of delayed or missed doses on the pharmacokinetics (PK) of lamotrigine (LTG) in children with epilepsy and established remedial dosing recommendations for nonadherent patients."	( Remedial dosing recommendations for delayed or missed doses of lamotrigine in pediatric patients with epilepsy using Monte Carlo simulations. Ding, JJ; Jiao, Z; Wang, CY; Yu, EQ; Zhang, XH, 2019)	0.97
" C) The delayed and partial doses were coadministered immediately, the next scheduled dose was skipped, and the regular dosing was resumed at the subsequent scheduled time."	( Remedial dosing recommendations for delayed or missed doses of lamotrigine in pediatric patients with epilepsy using Monte Carlo simulations. Ding, JJ; Jiao, Z; Wang, CY; Yu, EQ; Zhang, XH, 2019)	0.75
" Remedial dosing strategies A and B were almost equivalent, whereas C showed a larger PK deviation time."	( Remedial dosing recommendations for delayed or missed doses of lamotrigine in pediatric patients with epilepsy using Monte Carlo simulations. Ding, JJ; Jiao, Z; Wang, CY; Yu, EQ; Zhang, XH, 2019)	0.75
"22) with evidence of a dose-response relationship for carbamazepine."	( Use of antiepileptic drugs and risk of skin cancer: A nationwide case-control study. Kristensen, KB; Pedersen, SA; Pottegård, A; Schmidt, SAJ, 2020)	0.56
" Daily dosage of AED was not significantly associated with psychosis."	( Increased frequency of psychosis after second-generation antiepileptic drug administration in adults with focal epilepsy. Adachi, N; Akanuma, N; Fenwick, P; Hara, K; Ishii, R; Ito, M; Kato, M; Okazaki, M; Onuma, T; Sekimoto, M, 2019)	0.51
"28), indicating a dose-response relationship."	( Pregabalin add-on for drug-resistant focal epilepsy. Bresnahan, R; Hemming, K; Marson, AG; Panebianco, M, 2019)	0.51
" Prednisolone dosage was increased to 1 mg/kg/day, and the subsequent taper was performed slowly over the course of 10 weeks."	( Drug reaction with eosinophilia and systemic symptoms syndrome in a patient taking lamotrigine. Dória, MDC; Lameiras, C; Mendes Lopes, M; Ornelas, É, 2019)	0.74
" This method was applied also for determination of lamotrigine in lamictal® tablet dosage form using the same mobile phase."	( Multiobjective optimization of microemulsion- thin layer chromatography with image processing as analytical platform for determination of drugs in plasma using desirability functions. Abou-Taleb, NH; El-Enany, NM; El-Sherbiny, DT; El-Subbagh, HI, 2020)	0.81
" Dosage changes were more frequent in patients with assays in therapeutic ranges compared to patients with plasma assays outside the therapeutic ranges (P=0."	( Clinical and biological assessment of lamotrigine and levetiracetam plasma assays at the Rennes University Hospital. Biraben, A; Degremont, A; Gicquel, T; Le Daré, B; Morel, I; Polard, E, 2020)	0.83
" 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)	0.8
" Finally, stochastic simulations were carried out to propose dosage regimens."	( Dosing Recommendations Based on Population Pharmacokinetics of Lamotrigine in Mexican Adult Patients With Epilepsy. Chávez-Castillo, CE; Medellín-Garibay, SE; Milán-Segovia, RDC; Rodríguez-Leyva, I; Romano-Moreno, S, 2020)	0.8
"The mechanical properties of powders determine the ease of manufacture and ultimately the quality of the oral solid dosage forms."	( Modulation of the powder properties of lamotrigine by crystal forms. Kavanagh, ON; Sun, CC; Walker, GM; Wang, C, 2021)	0.89
" The concomitant use of LTG and valproic acid requires a reduction of the standard final dosage of LTG to 100 mg/day in order to prevent the occurrence of adverse reactions, while an increase in the dosage of LTG (up to a maximum of 400 mg/day) is required in the case of concomitant use of enzyme inducers, such as carbamazepine."	( [Lamotrigine in bipolar disorder: preventing depression to treat the disease]. Amore, M; Cuomo, A; Fagiolini, A; Vampini, C, )	1.04
"This is a retrospective data analysis of 646 consecutive AED-naive patients aged 1-88 years treated with CBZ, LTG, or LEV between 2006 and 2012 with dosing adjustments permitted during the first 6 months."	( Effectiveness at 24 Months of Single-Source Generic Carbamazepine, Lamotrigine, or Levetiracetam in Newly Diagnosed Focal Epilepsy. Chayasirisobhon, S; Gurbani, A; Gurbani, S; Pietzsch, E; Spurgeon, B; Tovar, S, 2020)	0.79
" This study aimed to develop a refined population pharmacokinetic (PopPK) model of LTG in pregnant women with epilepsy (WWE) to identify factors explaining the variability in pharmacokinetics and to establish a model-informed individualized dosing regimen."	( Estrogen profile- and pharmacogenetics-based lamotrigine dosing regimen optimization: Recommendations for pregnant women with epilepsy. Cao, YF; Guo, Y; Sun, XY; Tao, YY; Wang, ML; Wang, ZY; Zhao, L, 2021)	0.88
" To facilitate this, manufacturers have developed a strict re-challenge dosing regimen to facilitate successful reintroduction of lamotrigine."	( Lamotrigine and Stevens-Johnson Syndrome Prevention. Crane, E; Edinoff, AN; Fitz-Gerald, MJ; Gennuso, SA; Kaye, AD; Kaye, AM; Kaye, JS; Kaye, RJ; Lewis, K; Nguyen, LH; Pierre, SS; Urits, I; Varrassi, G; Viswanath, O, 2021)	2.27
" 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)	0.89
" The time of maximal anticonvulsant effect and the dose-response relationship of the drugs were assessed."	( Effects of new antiseizure drugs on seizure activity and anxiety-like behavior in adult zebrafish. Doboszewska, U; Guz, L; Pieróg, M; Poleszak, E; Serefko, A; Socała, K; Szopa, A; Wlaź, P; Wyska, E, 2021)	0.62
" In 49% of pregnancies, ASM dosage was modified; 53% of these modifications were made in response to ASM blood levels."	( Epilepsy and Pregnancy: An Audit of Specialized Care. Li, J; Nguyen, DK; Toffa, DH, 2022)	0.72
" Lamotrigine daily dosage varied from 25 to 425 mg/d among the studies."	( Association of Optimal Lamotrigine Serum Levels and Therapeutic Efficacy in Mood Disorders: A Systematic Review. Betcher, H; Kumar, R; Nuñez, NA; Prokop, LJ; Singh, B; Veldic, M, )	1.35
"This review aims to identify the optimal therapeutic dosage of anti-epileptic drugs in terms of efficacy and safety in patients with multiple comorbidities."	( Individualizing doses of antiepileptic drugs. Burchiani, B; Di Cara, G; Liparoti, G; Mencaroni, E; Tripodi, D; Verrotti, A, 2022)	0.72
"Pharmacogenomics (PGx) is a research area aimed at identifying genetic factors that are associated with drug responses, including drug efficacy, adverse drug reactions, and the appropriate drug dosage on a case-to-case basis."	( Avoidance of cutaneous adverse drug reactions induced by antiepileptic drugs based on pharmacogenomics. Mushiroda, T, 2023)	0.91
" However, there is an increased metabolism and clearance of lamotrigine in pregnancy contributing to suboptimal drug therapy and poor disease control, prompting the need for proactive dosage adjustments."	( Dosage Optimization of Lamotrigine in Pregnancy: A Pharmacometric Approach Using Modeling and Simulation. G, SS; Kp, A; Pa, B; Thomas, G, 2022)	1.27
" LAM daily dosage varied from 12."	( Efficacy and safety of lamotrigine in pediatric mood disorders: A systematic review. Ahern, K; Athreya, AP; Croarkin, PE; Garzon, J; Hassett, LC; Kumar, R; Ozger, C; Oztosun, C; Saliba, M; Singh, B; Vande Voort, JL; Yuruk, D, 2023)	1.22
" Based on the data, there is inconsistent evidence to make conclusive recommendations on therapeutic LAM dosage for mood improvement in the pediatric population."	( Efficacy and safety of lamotrigine in pediatric mood disorders: A systematic review. Ahern, K; Athreya, AP; Croarkin, PE; Garzon, J; Hassett, LC; Kumar, R; Ozger, C; Oztosun, C; Saliba, M; Singh, B; Vande Voort, JL; Yuruk, D, 2023)	1.22
" He had taken a variety of antiepileptic drugs for a long time and developed priapism after the dosage of lamotrigine had been increased."	( Lamotrigine induced priapism in children: case analysis and literature review. Cao, SS; Cao, XY; Ge, J; Guan, Y; Mu, F; Qiao, Y; Tang, M; Wang, JW, 2022)	2.38
"This study was undertaken to determine the impact of dosage in new users of lamotrigine (LTG) and the concomitant intake of valproic acid (VPA) on epidermal necrolysis (EN)."	( Effects of dosage in new users of lamotrigine inducing epidermal necrolysis: Results of the German Registry of Severe Skin Reactions. Diederich, S; Hemmeter, U; Mockenhaupt, M; Paulmann, M, 2023)	1.42
" Evaluation of dosing regimen was restricted to cases with complete LTG dosing history (n = 74)."	( Effects of dosage in new users of lamotrigine inducing epidermal necrolysis: Results of the German Registry of Severe Skin Reactions. Diederich, S; Hemmeter, U; Mockenhaupt, M; Paulmann, M, 2023)	1.19
" In order to evaluate its use among French psychiatrists, we explored prescribing habits, therapeutic monitoring and dosage adjustment of lamotrigine through a flash survey."	( Lamotrigine in mood disorders: Flash survey on prescribing habits and blood tests practices. Bloch, V; Chouchana, M; Delage, C; Etain, B; Fontan, JE; Smati, J, 2023)	2.56
" Questions concerned the frequency of prescribing depending on the mood disorder, the frequency of plasma levels, therapeutic monitoring, dosage adjustment and the limitation represented by dermatological risk."	( Lamotrigine in mood disorders: Flash survey on prescribing habits and blood tests practices. Bloch, V; Chouchana, M; Delage, C; Etain, B; Fontan, JE; Smati, J, 2023)	2.35
" In total, 22% (n=13) always adjusted the dosage according to the result."	( Lamotrigine in mood disorders: Flash survey on prescribing habits and blood tests practices. Bloch, V; Chouchana, M; Delage, C; Etain, B; Fontan, JE; Smati, J, 2023)	2.35
"While many psychiatrists report using plasma dosage of lamotrigine, few use the plasma level result to adapt dosage and many have no opinion of the target values for plasma concentrations."	( Lamotrigine in mood disorders: Flash survey on prescribing habits and blood tests practices. Bloch, V; Chouchana, M; Delage, C; Etain, B; Fontan, JE; Smati, J, 2023)	2.6
"Our objective was to characterize the potential for particular dosing scenarios to lead to increased seizure risk or toxicity."	( Empiric dosing strategies to predict lamotrigine concentrations during pregnancy. Barry, JM; Birnbaum, AK; French, JA; Harden, CL; Karanam, A; Pennell, PB, 2023)	1.18
" Population-level simulations (N = 48,000) included six dosing scenarios and considered four preconception doses using the R package mrgsolve (Metrum Research Group)."	( Empiric dosing strategies to predict lamotrigine concentrations during pregnancy. Barry, JM; Birnbaum, AK; French, JA; Harden, CL; Karanam, A; Pennell, PB, 2023)	1.18
" While no simulated dosing regimen allowed all women in both subpopulations to maintain preconception concentrations, some regimens provided a more balanced risk profile than others."	( Empiric dosing strategies to predict lamotrigine concentrations during pregnancy. Barry, JM; Birnbaum, AK; French, JA; Harden, CL; Karanam, A; Pennell, PB, 2023)	1.18
" An arbitrary "one-size-fits-all" philosophy may not work well for lamotrigine dosing adjustments during pregnancy and reinforces the need for therapeutic drug monitoring until a patient is determined to be in the LC or HC group."	( Empiric dosing strategies to predict lamotrigine concentrations during pregnancy. Barry, JM; Birnbaum, AK; French, JA; Harden, CL; Karanam, A; Pennell, PB, 2023)	1.42
"Future studies are still needed to generate more pediatric biopharmaceutical data to help understand the performances of oral dosage forms in pediatric sub-populations."	( Solubility of lamotrigine in age-specific biorelevant media that simulated the fasted- and fed-conditions of the gastric and intestinal environments in pediatrics and adults: implications for traditional, re-formulated, modified, and new oral formulations Daraghmeh, A; Declèves, X; Franco, V; Qassarwi, Y; Saba'aneh, H; Shawahna, R, 2023)	1.27
" Data collected included: dates of lamotrigine initiation or discontinuation, lamotrigine dosing over the time of the prescription and maximum lamotrigine dose, any cardiac-related ICD-10-CM codes or a history of a cardiology appointment, EKGs with any abnormalities or changes, any concomitantly prescribed medications with known potential to cause cardiac abnormalities, any cardiac deaths."	( Lamotrigine use and potential for adverse cardiac effects: A retrospective evaluation in a Veteran population. Biehl, A; Gidal, BE; Jones, J; Kopacek, K; Kotloski, RJ; Taube, M, 2023)	2.63

[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Role	Description
anticonvulsant	A drug used to prevent seizures or reduce their severity.
antimanic drug	Antimanic drugs are agents used to treat bipolar disorders or mania associated with other affective disorders.
antidepressant	Antidepressants are mood-stimulating drugs used primarily in the treatment of affective disorders and related conditions.
non-narcotic analgesic	A drug that has principally analgesic, antipyretic and anti-inflammatory actions. Non-narcotic analgesics do not bind to opioid receptors.
calcium channel blocker	One of a class of drugs that acts by selective inhibition of calcium influx through cell membranes or on the release and binding of calcium in intracellular pools.
excitatory amino acid antagonist	Any substance which inhibits the action of receptors for excitatory amino acids.
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor	Any EC 3.4.21.* (serine endopeptidase) inhibitor that interferes with the action of prolyl oligopeptidase (EC 3.4.21.26).
environmental contaminant	Any minor or unwanted substance introduced into the environment that can have undesired effects.
xenobiotic	A xenobiotic (Greek, xenos "foreign"; bios "life") is a compound that is foreign to a living organism. Principal xenobiotics include: drugs, carcinogens and various compounds that have been introduced into the environment by artificial means.
geroprotector	Any compound that supports healthy aging, slows the biological aging process, or extends lifespan.
[role 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]

Class	Description
1,2,4-triazines	Any compound with a 1,2,4-triazine skeleton, in which nitrogen atoms replace carbon at positions 1, 2 and 4 of the core benzene ring structure.
primary arylamine	A primary amine formally derived from ammonia by replacing one hydrogen atom by an aryl group. R-NH2 where R is an aryl group.
dichlorobenzene	Any member of the class of chlorobenzenes carrying two chloro groups at unspecified positions.
[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	Taxonomy	Measurement	Average (µ)	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
Chain A, MAJOR APURINIC/APYRIMIDINIC ENDONUCLEASE	Homo sapiens (human)	Potency	0.3162	0.0032	45.4673	12,589.2998	AID2517
thioredoxin reductase	Rattus norvegicus (Norway rat)	Potency	28.4254	0.1000	20.8793	79.4328	AID488772; AID588453; AID588456
GALC protein	Homo sapiens (human)	Potency	0.7079	28.1838	28.1838	28.1838	AID1159614
EWS/FLI fusion protein	Homo sapiens (human)	Potency	34.2954	0.0013	10.1577	42.8575	AID1259252; AID1259253; AID1259255; AID1259256
cytochrome P450 2D6	Homo sapiens (human)	Potency	38.9018	0.0010	8.3798	61.1304	AID1645840
euchromatic histone-lysine N-methyltransferase 2	Homo sapiens (human)	Potency	4.2296	0.0355	20.9770	89.1251	AID504332
Bloom syndrome protein isoform 1	Homo sapiens (human)	Potency	89.1251	0.5406	17.6392	96.1227	AID2364; AID2528
cytochrome P450 2D6 isoform 1	Homo sapiens (human)	Potency	6.3096	0.0020	7.5337	39.8107	AID891
peripheral myelin protein 22 isoform 1	Homo sapiens (human)	Potency	84.9214	23.9341	23.9341	23.9341	AID1967
D(1A) dopamine receptor	Homo sapiens (human)	Potency	0.2311	0.0224	5.9449	22.3872	AID488982
nuclear factor erythroid 2-related factor 2 isoform 2	Homo sapiens (human)	Potency	29.0929	0.0041	9.9848	25.9290	AID504444
potassium voltage-gated channel subfamily H member 2 isoform d	Homo sapiens (human)	Potency	31.6228	0.0178	9.6374	44.6684	AID588834
mitogen-activated protein kinase 1	Homo sapiens (human)	Potency	35.7168	0.0398	16.7842	39.8107	AID1454; AID995
geminin	Homo sapiens (human)	Potency	1.0000	0.0046	11.3741	33.4983	AID624297
muscarinic acetylcholine receptor M1	Rattus norvegicus (Norway rat)	Potency	2.5119	0.0010	6.0009	35.4813	AID944
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Protein	Taxonomy	Measurement	Average	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
Bile salt export pump	Homo sapiens (human)	IC50 (µMol)	133.0000	0.1100	7.1903	10.0000	AID1473738
Sodium channel protein type 1 subunit alpha	Rattus norvegicus (Norway rat)	IC50 (µMol)	82.6333	0.0100	1.1405	2.9390	AID205273; AID205275
Sodium channel protein type 2 subunit alpha	Rattus norvegicus (Norway rat)	IC50 (µMol)	63.5800	0.0040	1.1485	4.7300	AID1058310; AID205273; AID205275; AID471864
Sodium channel protein type 3 subunit alpha	Rattus norvegicus (Norway rat)	IC50 (µMol)	82.6333	0.0060	0.8605	2.9390	AID205273; AID205275
Dihydrofolate reductase	Escherichia coli K-12	IC50 (µMol)	348.9000	0.0015	0.5512	6.8000	AID1255685
Dihydrofolate reductase	Escherichia coli K-12	Ki	15.2400	0.0000	0.3790	4.0200	AID1255686
Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)	IC50 (µMol)	158.4890	0.1200	4.0480	10.0000	AID1207373
Sodium channel protein type 4 subunit alpha	Homo sapiens (human)	Ki	17.0000	0.1800	0.1800	0.1800	AID205290
Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)	IC50 (µMol)	158.4890	0.1200	4.0480	10.0000	AID1207373
Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)	IC50 (µMol)	282.3930	0.0009	1.9014	10.0000	AID1207467; AID1207497; AID1207527; AID392051
Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)	IC50 (µMol)	1,421.9100	0.0003	2.2545	9.6000	AID1207283; AID1207561
Sodium channel protein type 5 subunit alpha	Homo sapiens (human)	IC50 (µMol)	67.2702	0.0003	3.6484	9.2000	AID1207313; AID1207343; AID404536
Sodium channel protein type 9 subunit alpha	Homo sapiens (human)	IC50 (µMol)	17.0000	0.0060	2.7749	9.0000	AID1233923
Sodium channel protein type 2 subunit alpha	Homo sapiens (human)	IC50 (µMol)	42.3333	0.0000	3.7401	10.0000	AID1233921; AID351546; AID404535
Sodium channel protein type 3 subunit alpha	Homo sapiens (human)	IC50 (µMol)	17.0000	0.0053	2.8085	9.0000	AID1233922
Sigma non-opioid intracellular receptor 1	Rattus norvegicus (Norway rat)	IC50 (µMol)	10.0000	0.0003	0.5570	4.2000	AID152391
Sodium channel protein type 10 subunit alpha	Homo sapiens (human)	IC50 (µMol)	97.0000	0.0080	3.1752	9.0000	AID1233920; AID404534
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Protein	Taxonomy	Measurement	Average	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Process	via Protein(s)	Taxonomy
fatty acid metabolic process	Bile salt export pump	Homo sapiens (human)
bile acid biosynthetic process	Bile salt export pump	Homo sapiens (human)
xenobiotic metabolic process	Bile salt export pump	Homo sapiens (human)
xenobiotic transmembrane transport	Bile salt export pump	Homo sapiens (human)
response to oxidative stress	Bile salt export pump	Homo sapiens (human)
bile acid metabolic process	Bile salt export pump	Homo sapiens (human)
response to organic cyclic compound	Bile salt export pump	Homo sapiens (human)
bile acid and bile salt transport	Bile salt export pump	Homo sapiens (human)
canalicular bile acid transport	Bile salt export pump	Homo sapiens (human)
protein ubiquitination	Bile salt export pump	Homo sapiens (human)
regulation of fatty acid beta-oxidation	Bile salt export pump	Homo sapiens (human)
carbohydrate transmembrane transport	Bile salt export pump	Homo sapiens (human)
bile acid signaling pathway	Bile salt export pump	Homo sapiens (human)
cholesterol homeostasis	Bile salt export pump	Homo sapiens (human)
response to estrogen	Bile salt export pump	Homo sapiens (human)
response to ethanol	Bile salt export pump	Homo sapiens (human)
xenobiotic export from cell	Bile salt export pump	Homo sapiens (human)
lipid homeostasis	Bile salt export pump	Homo sapiens (human)
phospholipid homeostasis	Bile salt export pump	Homo sapiens (human)
positive regulation of bile acid secretion	Bile salt export pump	Homo sapiens (human)
regulation of bile acid metabolic process	Bile salt export pump	Homo sapiens (human)
transmembrane transport	Bile salt export pump	Homo sapiens (human)
10-formyltetrahydrofolate biosynthetic process	Dihydrofolate reductase	Escherichia coli K-12
response to xenobiotic stimulus	Dihydrofolate reductase	Escherichia coli K-12
folic acid biosynthetic process	Dihydrofolate reductase	Escherichia coli K-12
one-carbon metabolic process	Dihydrofolate reductase	Escherichia coli K-12
response to methotrexate	Dihydrofolate reductase	Escherichia coli K-12
tetrahydrofolate biosynthetic process	Dihydrofolate reductase	Escherichia coli K-12
response to antibiotic	Dihydrofolate reductase	Escherichia coli K-12
dihydrofolate metabolic process	Dihydrofolate reductase	Escherichia coli K-12
folic acid metabolic process	Dihydrofolate reductase	Escherichia coli K-12
epithelial cell maturation	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
sensory perception of sound	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
male gonad development	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
vestibular nucleus development	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
secretory granule organization	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
regulation of ventricular cardiac muscle cell membrane repolarization	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
cellular response to cAMP	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
cellular response to acidic pH	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
cellular response to light stimulus	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
potassium ion transmembrane transport	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
cardiac muscle cell action potential involved in contraction	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
cardiac muscle cell contraction	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
ventricular cardiac muscle cell action potential	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
membrane repolarization	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
membrane repolarization during action potential	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
membrane repolarization during cardiac muscle cell action potential	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
regulation of heart rate by cardiac conduction	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
negative regulation of protein targeting to membrane	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
potassium ion export across plasma membrane	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
membrane repolarization during ventricular cardiac muscle cell action potential	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
regulation of potassium ion transmembrane transport	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
positive regulation of potassium ion transmembrane transport	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
regulation of delayed rectifier potassium channel activity	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
negative regulation of delayed rectifier potassium channel activity	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
sodium ion transport	Sodium channel protein type 4 subunit alpha	Homo sapiens (human)
muscle contraction	Sodium channel protein type 4 subunit alpha	Homo sapiens (human)
sodium ion transmembrane transport	Sodium channel protein type 4 subunit alpha	Homo sapiens (human)
regulation of skeletal muscle contraction by action potential	Sodium channel protein type 4 subunit alpha	Homo sapiens (human)
cardiac muscle cell action potential involved in contraction	Sodium channel protein type 4 subunit alpha	Homo sapiens (human)
gastrin-induced gastric acid secretion	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
glucose metabolic process	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
heart development	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
sensory perception of sound	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
rhythmic behavior	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
regulation of heart contraction	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
regulation of blood pressure	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
positive regulation of heart rate	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
iodide transport	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
erythrocyte differentiation	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
intracellular chloride ion homeostasis	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
response to insulin	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
social behavior	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
corticosterone secretion	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
inner ear morphogenesis	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
inner ear development	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
intestinal absorption	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
detection of mechanical stimulus involved in sensory perception of sound	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
potassium ion homeostasis	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
cardiac muscle contraction	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
auditory receptor cell development	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
regulation of membrane repolarization	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
regulation of ventricular cardiac muscle cell membrane repolarization	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
regulation of atrial cardiac muscle cell membrane repolarization	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
positive regulation of cardiac muscle contraction	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
regulation of gastric acid secretion	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
stomach development	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
renal absorption	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
renal sodium ion absorption	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
cellular response to cAMP	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
cellular response to xenobiotic stimulus	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
potassium ion transmembrane transport	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
cellular response to epinephrine stimulus	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
adrenergic receptor signaling pathway	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
cardiac muscle cell contraction	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
ventricular cardiac muscle cell action potential	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
membrane repolarization during action potential	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
membrane repolarization during cardiac muscle cell action potential	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
atrial cardiac muscle cell action potential	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
regulation of heart rate by cardiac conduction	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
cochlea development	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
potassium ion export across plasma membrane	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
membrane repolarization during atrial cardiac muscle cell action potential	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
membrane repolarization during ventricular cardiac muscle cell action potential	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
positive regulation of potassium ion transmembrane transport	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
non-motile cilium assembly	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
potassium ion import across plasma membrane	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
action potential	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
regulation of heart rate by cardiac conduction	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
regulation of heart rate by hormone	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
regulation of membrane potential	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
positive regulation of DNA-templated transcription	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
potassium ion homeostasis	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
cardiac muscle contraction	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
regulation of membrane repolarization	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
regulation of ventricular cardiac muscle cell membrane repolarization	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
cellular response to xenobiotic stimulus	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
potassium ion transmembrane transport	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
ventricular cardiac muscle cell action potential	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
membrane repolarization	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
membrane depolarization during action potential	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
membrane repolarization during action potential	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
membrane repolarization during cardiac muscle cell action potential	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
regulation of heart rate by cardiac conduction	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
potassium ion export across plasma membrane	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
membrane repolarization during ventricular cardiac muscle cell action potential	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
regulation of potassium ion transmembrane transport	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
negative regulation of potassium ion transmembrane transport	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
positive regulation of potassium ion transmembrane transport	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
negative regulation of potassium ion export across plasma membrane	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
potassium ion import across plasma membrane	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
immune system development	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
positive regulation of cytosolic calcium ion concentration	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
heart development	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
regulation of cardiac muscle contraction by regulation of the release of sequestered calcium ion	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
embryonic forelimb morphogenesis	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
camera-type eye development	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
positive regulation of adenylate cyclase activity	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
positive regulation of muscle contraction	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
calcium ion transport into cytosol	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
cardiac conduction	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
calcium ion transmembrane transport via high voltage-gated calcium channel	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
calcium ion transmembrane transport	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
cardiac muscle cell action potential involved in contraction	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
membrane depolarization during cardiac muscle cell action potential	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
membrane depolarization during AV node cell action potential	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
cell communication by electrical coupling involved in cardiac conduction	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
regulation of heart rate by cardiac conduction	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
regulation of ventricular cardiac muscle cell action potential	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
membrane depolarization during atrial cardiac muscle cell action potential	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
calcium ion import across plasma membrane	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
regulation of heart rate	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
cardiac conduction system development	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
cardiac ventricle development	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
brainstem development	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
sodium ion transport	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
positive regulation of sodium ion transport	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
response to denervation involved in regulation of muscle adaptation	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
telencephalon development	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
cerebellum development	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
sodium ion transmembrane transport	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
odontogenesis of dentin-containing tooth	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
positive regulation of action potential	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
positive regulation of epithelial cell proliferation	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
membrane depolarization	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
cardiac muscle contraction	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
regulation of ventricular cardiac muscle cell membrane repolarization	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
regulation of atrial cardiac muscle cell membrane depolarization	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
regulation of atrial cardiac muscle cell membrane repolarization	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
regulation of ventricular cardiac muscle cell membrane depolarization	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
cellular response to calcium ion	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
cardiac muscle cell action potential involved in contraction	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
regulation of cardiac muscle cell contraction	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
ventricular cardiac muscle cell action potential	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
membrane depolarization during action potential	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
membrane depolarization during cardiac muscle cell action potential	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
atrial cardiac muscle cell action potential	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
SA node cell action potential	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
AV node cell action potential	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
bundle of His cell action potential	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
membrane depolarization during AV node cell action potential	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
membrane depolarization during SA node cell action potential	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
membrane depolarization during Purkinje myocyte cell action potential	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
membrane depolarization during bundle of His cell action potential	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
AV node cell to bundle of His cell communication	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
regulation of heart rate by cardiac conduction	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
membrane depolarization during atrial cardiac muscle cell action potential	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
regulation of sodium ion transmembrane transport	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
sodium ion transport	Sodium channel protein type 9 subunit alpha	Homo sapiens (human)
inflammatory response	Sodium channel protein type 9 subunit alpha	Homo sapiens (human)
circadian rhythm	Sodium channel protein type 9 subunit alpha	Homo sapiens (human)
response to toxic substance	Sodium channel protein type 9 subunit alpha	Homo sapiens (human)
post-embryonic development	Sodium channel protein type 9 subunit alpha	Homo sapiens (human)
sensory perception of pain	Sodium channel protein type 9 subunit alpha	Homo sapiens (human)
sodium ion transmembrane transport	Sodium channel protein type 9 subunit alpha	Homo sapiens (human)
behavioral response to pain	Sodium channel protein type 9 subunit alpha	Homo sapiens (human)
detection of temperature stimulus involved in sensory perception of pain	Sodium channel protein type 9 subunit alpha	Homo sapiens (human)
detection of mechanical stimulus involved in sensory perception	Sodium channel protein type 9 subunit alpha	Homo sapiens (human)
cardiac muscle cell action potential involved in contraction	Sodium channel protein type 9 subunit alpha	Homo sapiens (human)
sodium ion transport	Sodium channel protein type 2 subunit alpha	Homo sapiens (human)
nervous system development	Sodium channel protein type 2 subunit alpha	Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to osmotic stress	Sodium channel protein type 2 subunit alpha	Homo sapiens (human)
neuron apoptotic process	Sodium channel protein type 2 subunit alpha	Homo sapiens (human)
memory	Sodium channel protein type 2 subunit alpha	Homo sapiens (human)
determination of adult lifespan	Sodium channel protein type 2 subunit alpha	Homo sapiens (human)
neuronal action potential	Sodium channel protein type 2 subunit alpha	Homo sapiens (human)
dentate gyrus development	Sodium channel protein type 2 subunit alpha	Homo sapiens (human)
nerve development	Sodium channel protein type 2 subunit alpha	Homo sapiens (human)
myelination	Sodium channel protein type 2 subunit alpha	Homo sapiens (human)
cellular response to hypoxia	Sodium channel protein type 2 subunit alpha	Homo sapiens (human)
cardiac muscle cell action potential involved in contraction	Sodium channel protein type 2 subunit alpha	Homo sapiens (human)
sodium ion transmembrane transport	Sodium channel protein type 2 subunit alpha	Homo sapiens (human)
sodium ion transport	Sodium channel protein type 3 subunit alpha	Homo sapiens (human)
behavioral response to pain	Sodium channel protein type 3 subunit alpha	Homo sapiens (human)
cardiac muscle cell action potential involved in contraction	Sodium channel protein type 3 subunit alpha	Homo sapiens (human)
sodium ion transmembrane transport	Sodium channel protein type 3 subunit alpha	Homo sapiens (human)
regulation of heart rate	Sodium channel protein type 10 subunit alpha	Homo sapiens (human)
sensory perception	Sodium channel protein type 10 subunit alpha	Homo sapiens (human)
regulation of monoatomic ion transmembrane transport	Sodium channel protein type 10 subunit alpha	Homo sapiens (human)
sodium ion transmembrane transport	Sodium channel protein type 10 subunit alpha	Homo sapiens (human)
odontogenesis of dentin-containing tooth	Sodium channel protein type 10 subunit alpha	Homo sapiens (human)
regulation of cardiac muscle contraction	Sodium channel protein type 10 subunit alpha	Homo sapiens (human)
regulation of atrial cardiac muscle cell membrane depolarization	Sodium channel protein type 10 subunit alpha	Homo sapiens (human)
membrane depolarization during action potential	Sodium channel protein type 10 subunit alpha	Homo sapiens (human)
AV node cell action potential	Sodium channel protein type 10 subunit alpha	Homo sapiens (human)
bundle of His cell action potential	Sodium channel protein type 10 subunit alpha	Homo sapiens (human)
regulation of presynaptic membrane potential	Sodium channel protein type 10 subunit alpha	Homo sapiens (human)
cardiac muscle cell action potential involved in contraction	Sodium channel protein type 10 subunit alpha	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Process	via Protein(s)	Taxonomy
protein binding	Bile salt export pump	Homo sapiens (human)
ATP binding	Bile salt export pump	Homo sapiens (human)
ABC-type xenobiotic transporter activity	Bile salt export pump	Homo sapiens (human)
bile acid transmembrane transporter activity	Bile salt export pump	Homo sapiens (human)
canalicular bile acid transmembrane transporter activity	Bile salt export pump	Homo sapiens (human)
carbohydrate transmembrane transporter activity	Bile salt export pump	Homo sapiens (human)
ABC-type bile acid transporter activity	Bile salt export pump	Homo sapiens (human)
ATP hydrolysis activity	Bile salt export pump	Homo sapiens (human)
dihydrofolate reductase activity	Dihydrofolate reductase	Escherichia coli K-12
protein binding	Dihydrofolate reductase	Escherichia coli K-12
folic acid binding	Dihydrofolate reductase	Escherichia coli K-12
oxidoreductase activity	Dihydrofolate reductase	Escherichia coli K-12
NADP binding	Dihydrofolate reductase	Escherichia coli K-12
methotrexate binding	Dihydrofolate reductase	Escherichia coli K-12
dihydrofolic acid binding	Dihydrofolate reductase	Escherichia coli K-12
NADP+ binding	Dihydrofolate reductase	Escherichia coli K-12
NADPH binding	Dihydrofolate reductase	Escherichia coli K-12
voltage-gated potassium channel activity	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
delayed rectifier potassium channel activity	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
voltage-gated potassium channel activity involved in cardiac muscle cell action potential repolarization	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
voltage-gated potassium channel activity involved in ventricular cardiac muscle cell action potential repolarization	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
delayed rectifier potassium channel activity	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
protein binding	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
potassium channel regulator activity	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
telethonin binding	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
protein-containing complex binding	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
transmembrane transporter binding	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
voltage-gated sodium channel activity	Sodium channel protein type 4 subunit alpha	Homo sapiens (human)
protein binding	Sodium channel protein type 4 subunit alpha	Homo sapiens (human)
voltage-gated potassium channel activity	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
delayed rectifier potassium channel activity	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
voltage-gated potassium channel activity	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
delayed rectifier potassium channel activity	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
protein binding	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
calmodulin binding	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
phosphatidylinositol-4,5-bisphosphate binding	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
protein phosphatase 1 binding	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
outward rectifier potassium channel activity	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
protein kinase A catalytic subunit binding	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
protein kinase A regulatory subunit binding	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
transmembrane transporter binding	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
voltage-gated potassium channel activity involved in cardiac muscle cell action potential repolarization	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
voltage-gated potassium channel activity involved in atrial cardiac muscle cell action potential repolarization	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
scaffold protein binding	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
voltage-gated potassium channel activity involved in ventricular cardiac muscle cell action potential repolarization	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
transcription cis-regulatory region binding	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
inward rectifier potassium channel activity	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
voltage-gated potassium channel activity	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
delayed rectifier potassium channel activity	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
protein binding	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
ubiquitin protein ligase binding	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
identical protein binding	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
protein homodimerization activity	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
C3HC4-type RING finger domain binding	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
voltage-gated potassium channel activity involved in cardiac muscle cell action potential repolarization	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
scaffold protein binding	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
voltage-gated potassium channel activity involved in ventricular cardiac muscle cell action potential repolarization	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
high voltage-gated calcium channel activity	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
voltage-gated calcium channel activity involved in cardiac muscle cell action potential	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
voltage-gated calcium channel activity	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
protein binding	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
calmodulin binding	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
high voltage-gated calcium channel activity	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
metal ion binding	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
alpha-actinin binding	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
voltage-gated calcium channel activity involved in cardiac muscle cell action potential	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
voltage-gated calcium channel activity involved in AV node cell action potential	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
voltage-gated sodium channel activity	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
protein binding	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
calmodulin binding	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
fibroblast growth factor binding	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
enzyme binding	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
protein kinase binding	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
protein domain specific binding	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
ankyrin binding	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
ubiquitin protein ligase binding	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
transmembrane transporter binding	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
nitric-oxide synthase binding	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
voltage-gated sodium channel activity involved in cardiac muscle cell action potential	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
voltage-gated sodium channel activity involved in AV node cell action potential	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
voltage-gated sodium channel activity involved in bundle of His cell action potential	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
voltage-gated sodium channel activity involved in Purkinje myocyte action potential	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
voltage-gated sodium channel activity involved in SA node cell action potential	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
scaffold protein binding	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
voltage-gated sodium channel activity	Sodium channel protein type 9 subunit alpha	Homo sapiens (human)
protein binding	Sodium channel protein type 9 subunit alpha	Homo sapiens (human)
voltage-gated sodium channel activity	Sodium channel protein type 2 subunit alpha	Homo sapiens (human)
protein binding	Sodium channel protein type 2 subunit alpha	Homo sapiens (human)
calmodulin binding	Sodium channel protein type 2 subunit alpha	Homo sapiens (human)
voltage-gated sodium channel activity	Sodium channel protein type 3 subunit alpha	Homo sapiens (human)
voltage-gated sodium channel activity	Sodium channel protein type 10 subunit alpha	Homo sapiens (human)
transmembrane transporter binding	Sodium channel protein type 10 subunit alpha	Homo sapiens (human)
voltage-gated monoatomic ion channel activity involved in regulation of presynaptic membrane potential	Sodium channel protein type 10 subunit alpha	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Process	via Protein(s)	Taxonomy
basolateral plasma membrane	Bile salt export pump	Homo sapiens (human)
Golgi membrane	Bile salt export pump	Homo sapiens (human)
endosome	Bile salt export pump	Homo sapiens (human)
plasma membrane	Bile salt export pump	Homo sapiens (human)
cell surface	Bile salt export pump	Homo sapiens (human)
apical plasma membrane	Bile salt export pump	Homo sapiens (human)
intercellular canaliculus	Bile salt export pump	Homo sapiens (human)
intracellular canaliculus	Bile salt export pump	Homo sapiens (human)
recycling endosome	Bile salt export pump	Homo sapiens (human)
recycling endosome membrane	Bile salt export pump	Homo sapiens (human)
extracellular exosome	Bile salt export pump	Homo sapiens (human)
membrane	Bile salt export pump	Homo sapiens (human)
cytosol	Dihydrofolate reductase	Escherichia coli K-12
cytosol	Dihydrofolate reductase	Escherichia coli K-12
voltage-gated potassium channel complex	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
lysosome	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
plasma membrane	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
cell surface	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
apical plasma membrane	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
Z disc	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
membrane raft	Potassium voltage-gated channel subfamily E member 1	Homo sapiens (human)
plasma membrane	Sodium channel protein type 4 subunit alpha	Homo sapiens (human)
voltage-gated sodium channel complex	Sodium channel protein type 4 subunit alpha	Homo sapiens (human)
early endosome	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
endoplasmic reticulum	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
cytoplasm	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
lysosome	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
early endosome	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
late endosome	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
endoplasmic reticulum	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
plasma membrane	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
voltage-gated potassium channel complex	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
membrane	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
basolateral plasma membrane	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
apical plasma membrane	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
transport vesicle	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
cytoplasmic vesicle membrane	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
neuron projection	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
neuronal cell body	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
membrane raft	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
ciliary base	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
lumenal side of membrane	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
basolateral part of cell	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
monoatomic ion channel complex	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
membrane	Potassium voltage-gated channel subfamily KQT member 1	Homo sapiens (human)
plasma membrane	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
cell surface	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
perinuclear region of cytoplasm	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
voltage-gated potassium channel complex	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
inward rectifier potassium channel complex	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
plasma membrane	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
cytoplasm	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
plasma membrane	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
postsynaptic density	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
membrane	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
Z disc	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
dendrite	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
perikaryon	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
postsynaptic density membrane	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
L-type voltage-gated calcium channel complex	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
voltage-gated calcium channel complex	Voltage-dependent L-type calcium channel subunit alpha-1C	Homo sapiens (human)
caveola	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
nucleoplasm	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
nucleolus	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
endoplasmic reticulum	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
plasma membrane	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
caveola	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
cell surface	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
intercalated disc	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
membrane	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
lateral plasma membrane	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
Z disc	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
T-tubule	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
sarcolemma	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
perinuclear region of cytoplasm	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
voltage-gated sodium channel complex	Sodium channel protein type 5 subunit alpha	Homo sapiens (human)
plasma membrane	Sodium channel protein type 9 subunit alpha	Homo sapiens (human)
axon	Sodium channel protein type 9 subunit alpha	Homo sapiens (human)
voltage-gated sodium channel complex	Sodium channel protein type 9 subunit alpha	Homo sapiens (human)
plasma membrane	Sodium channel protein type 2 subunit alpha	Homo sapiens (human)
plasma membrane	Sodium channel protein type 2 subunit alpha	Homo sapiens (human)
intercalated disc	Sodium channel protein type 2 subunit alpha	Homo sapiens (human)
T-tubule	Sodium channel protein type 2 subunit alpha	Homo sapiens (human)
axon	Sodium channel protein type 2 subunit alpha	Homo sapiens (human)
node of Ranvier	Sodium channel protein type 2 subunit alpha	Homo sapiens (human)
paranode region of axon	Sodium channel protein type 2 subunit alpha	Homo sapiens (human)
presynaptic membrane	Sodium channel protein type 2 subunit alpha	Homo sapiens (human)
glutamatergic synapse	Sodium channel protein type 2 subunit alpha	Homo sapiens (human)
voltage-gated sodium channel complex	Sodium channel protein type 2 subunit alpha	Homo sapiens (human)
membrane	Sodium channel protein type 2 subunit alpha	Homo sapiens (human)
sarcoplasm	Sodium channel protein type 3 subunit alpha	Homo sapiens (human)
voltage-gated sodium channel complex	Sodium channel protein type 3 subunit alpha	Homo sapiens (human)
plasma membrane	Sodium channel protein type 10 subunit alpha	Homo sapiens (human)
axon	Sodium channel protein type 10 subunit alpha	Homo sapiens (human)
presynaptic membrane	Sodium channel protein type 10 subunit alpha	Homo sapiens (human)
extracellular exosome	Sodium channel protein type 10 subunit alpha	Homo sapiens (human)
glutamatergic synapse	Sodium channel protein type 10 subunit alpha	Homo sapiens (human)
voltage-gated sodium channel complex	Sodium channel protein type 10 subunit alpha	Homo sapiens (human)
clathrin complex	Sodium channel protein type 10 subunit alpha	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Assay ID	Title	Year	Journal	Article
AID1508630	Primary qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome: Secreted ER Calcium Modulated Protein (SERCaMP) assay	2021	Cell reports, 04-27, Volume: 35, Issue:4	A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
AID1347154	Primary screen GU AMC qHTS for Zika virus inhibitors	2020	Proceedings 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.
AID1347105	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for MG 63 (6-TG R) cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1745845	Primary qHTS for Inhibitors of ATXN expression
AID1347091	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SJ-GBM2 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347407	qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Pharmaceutical Collection	2020	ACS 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.
AID1347093	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-MC cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347103	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for OHS-50 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347083	qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: Viability assay - alamar blue signal for LASV Primary Screen	2020	Antiviral research, 01, Volume: 173	A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347082	qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: LASV Primary Screen - GLuc reporter signal	2020	Antiviral research, 01, Volume: 173	A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347098	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-SH cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1296008	Cytotoxic Profiling of Annotated Libraries Using Quantitative High-Throughput Screening	2020	SLAS discovery : advancing life sciences R & D, 01, Volume: 25, Issue:1	Cytotoxic Profiling of Annotated and Diverse Chemical Libraries Using Quantitative High-Throughput Screening.
AID1347092	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for A673 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347425	Rhodamine-PBP qHTS Assay for Modulators of WT P53-Induced Phosphatase 1 (WIP1)	2019	The 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.
AID1347090	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for DAOY cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347100	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for LAN-5 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347099	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB1643 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347096	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for U-2 OS cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347102	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh18 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347089	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for TC32 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347107	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh30 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347101	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-12 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347095	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB-EBc1 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347097	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Saos-2 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347106	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for control Hh wild type fibroblast cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID651635	Viability Counterscreen for Primary qHTS for Inhibitors of ATXN expression
AID1347086	qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lymphocytic Choriomeningitis Arenaviruses (LCMV): LCMV Primary Screen - GLuc reporter signal	2020	Antiviral research, 01, Volume: 173	A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347094	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-37 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347108	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh41 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347424	RapidFire Mass Spectrometry qHTS Assay for Modulators of WT P53-Induced Phosphatase 1 (WIP1)	2019	The 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.
AID1347104	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for RD cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID588499	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set	2010	Current protocols in cytometry, Oct, Volume: Chapter 13	Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588499	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set	2006	Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5	Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588499	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set	2010	Assay and drug development technologies, Feb, Volume: 8, Issue:1	High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588497	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set	2010	Current protocols in cytometry, Oct, Volume: Chapter 13	Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588497	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set	2006	Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5	Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588497	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set	2010	Assay and drug development technologies, Feb, Volume: 8, Issue:1	High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588501	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set	2010	Current protocols in cytometry, Oct, Volume: Chapter 13	Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588501	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set	2006	Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5	Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588501	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set	2010	Assay and drug development technologies, Feb, Volume: 8, Issue:1	High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588461	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, Validation compound set	2010	Current protocols in cytometry, Oct, Volume: Chapter 13	Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588461	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, Validation compound set	2006	Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5	Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588461	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, Validation compound set	2010	Assay and drug development technologies, Feb, Volume: 8, Issue:1	High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588460	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, Validation Compound Set	2010	Current protocols in cytometry, Oct, Volume: Chapter 13	Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588460	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, Validation Compound Set	2006	Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5	Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588460	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, Validation Compound Set	2010	Assay and drug development technologies, Feb, Volume: 8, Issue:1	High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588459	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, Validation compound set	2010	Current protocols in cytometry, Oct, Volume: Chapter 13	Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588459	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, Validation compound set	2006	Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5	Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588459	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, Validation compound set	2010	Assay and drug development technologies, Feb, Volume: 8, Issue:1	High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID504810	Antagonists of the Thyroid Stimulating Hormone Receptor: HTS campaign	2010	Endocrinology, Jul, Volume: 151, Issue:7	A small molecule inverse agonist for the human thyroid-stimulating hormone receptor.
AID504812	Inverse Agonists of the Thyroid Stimulating Hormone Receptor: HTS campaign	2010	Endocrinology, Jul, Volume: 151, Issue:7	A small molecule inverse agonist for the human thyroid-stimulating hormone receptor.
AID1347411	qHTS 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) Libary	2020	ACS 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.
AID1346987	P-glycoprotein substrates identified in KB-8-5-11 adenocarcinoma cell line, qHTS therapeutic library screen	2019	Molecular pharmacology, 11, Volume: 96, Issue:5	A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1346986	P-glycoprotein substrates identified in KB-3-1 adenocarcinoma cell line, qHTS therapeutic library screen	2019	Molecular pharmacology, 11, Volume: 96, Issue:5	A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1347405	qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS LOPAC collection	2020	ACS 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.
AID1347057	CD47-SIRPalpha protein protein interaction - LANCE assay qHTS validation	2019	PloS one, , Volume: 14, Issue:7	Quantitative high-throughput screening assays for the discovery and development of SIRPα-CD47 interaction inhibitors.
AID588349	qHTS for Inhibitors of ATXN expression: Validation of Cytotoxic Assay
AID1347151	Optimization of GU AMC qHTS for Zika virus inhibitors: Unlinked NS2B-NS3 protease assay	2020	Proceedings 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.
AID1347058	CD47-SIRPalpha protein protein interaction - HTRF assay qHTS validation	2019	PloS one, , Volume: 14, Issue:7	Quantitative high-throughput screening assays for the discovery and development of SIRPα-CD47 interaction inhibitors.
AID1347410	qHTS for inhibitors of adenylyl cyclases using a fission yeast platform: a pilot screen against the NCATS LOPAC library	2019	Cellular signalling, 08, Volume: 60	A fission yeast platform for heterologous expression of mammalian adenylyl cyclases and high throughput screening.
AID1347059	CD47-SIRPalpha protein protein interaction - Alpha assay qHTS validation	2019	PloS one, , Volume: 14, Issue:7	Quantitative high-throughput screening assays for the discovery and development of SIRPα-CD47 interaction inhibitors.
AID1347049	Natriuretic polypeptide receptor (hNpr1) antagonism - Pilot screen	2019	Science translational medicine, 07-10, Volume: 11, Issue:500	Inhibition of natriuretic peptide receptor 1 reduces itch in mice.
AID1347045	Natriuretic polypeptide receptor (hNpr1) antagonism - Pilot counterscreen GloSensor control cell line	2019	Science translational medicine, 07-10, Volume: 11, Issue:500	Inhibition of natriuretic peptide receptor 1 reduces itch in mice.
AID588378	qHTS for Inhibitors of ATXN expression: Validation
AID1347050	Natriuretic polypeptide receptor (hNpr2) antagonism - Pilot subtype selectivity assay	2019	Science translational medicine, 07-10, Volume: 11, Issue:500	Inhibition of natriuretic peptide receptor 1 reduces itch in mice.
AID504836	Inducers of the Endoplasmic Reticulum Stress Response (ERSR) in human glioma: Validation	2002	The Journal of biological chemistry, Apr-19, Volume: 277, Issue:16	Sustained ER Ca2+ depletion suppresses protein synthesis and induces activation-enhanced cell death in mast cells.
AID1378415	Bactericidal activity against methicillin-resistant Staphylococcus aureus subsp. aureus Rosenbach 1884	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Topological pattern for the search of new active drugs against methicillin resistant Staphylococcus aureus.
AID190133	Toxic dose causing 50% treated mice fall from the rotarod was evaluated	1999	Bioorganic & medicinal chemistry letters, Sep-06, Volume: 9, Issue:17	Sodium channel activity and sigma binding of 2-aminopropanamide anticonvulsants.
AID404546	Ratio of drug level in brain to plasma in Sprague-Dawley rat	2008	Bioorganic & medicinal chemistry, Jun-15, Volume: 16, Issue:12	Discovery of potent furan piperazine sodium channel blockers for treatment of neuropathic pain.
AID625290	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver fatty	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079940	Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source]
AID1207403	Inhibition of slow delayed inward rectifying potassium current (Iks) in Chinese Hamster Ovary (CHO) cells transfected with KCNQ1 / Kv1.7 / KvLQT1 and KCNE1/minK measured using IonWorks automated patch clamp platform
AID1233921	Inhibition of human Nav1.2 expressed in SHSY5Y cells assessed as reduction in blue fluorescent signal by VSP-FRET assay	2015	ACS medicinal chemistry letters, Jun-11, Volume: 6, Issue:6	Discovery and Optimization of Selective Nav1.8 Modulator Series That Demonstrate Efficacy in Preclinical Models of Pain.
AID1233923	Inhibition of human Nav1.7 expressed in SHSY5Y cells assessed as reduction in blue fluorescent signal by VSP-FRET assay	2015	ACS medicinal chemistry letters, Jun-11, Volume: 6, Issue:6	Discovery and Optimization of Selective Nav1.8 Modulator Series That Demonstrate Efficacy in Preclinical Models of Pain.
AID444057	Fraction escaping hepatic elimination in human	2010	Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3	Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID471864	Inhibition of rat Nav1.2 channel expressed in chinese hamster CHL1610 cells at preconditioning pulse of -67 mV after 2 to 3 mins by whole-cell patch-clamp technique	2009	Journal of medicinal chemistry, Dec-10, Volume: 52, Issue:23	Novel, broad-spectrum anticonvulsants containing a sulfamide group: advancement of N-((benzo[b]thien-3-yl)methyl)sulfamide (JNJ-26990990) into human clinical studies.
AID633209	Blockade of voltage-gated sodium channel in mouse N1E-115 cells assessed as stimulation at 100 umol at -90 mV holding potential by whole-cell patch clamp electrophysiological assay relative to control	2011	Bioorganic & medicinal chemistry, Nov-15, Volume: 19, Issue:22	Synthesis and anticonvulsant activity of trans- and cis-2-(2,6-dimethylphenoxy)-N-(2- or 4-hydroxycyclohexyl)acetamides and their amine analogs.
AID342469	Inhibition of AQP4 expressed in rat FRT cells assessed as transepithelial osmotic water permeability at 100 uM by dye dilution method	2008	Bioorganic & medicinal chemistry, Aug-01, Volume: 16, Issue:15	Lack of aquaporin-4 water transport inhibition by antiepileptics and arylsulfonamides.
AID625281	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholelithiasis	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID444051	Total clearance in human	2010	Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3	Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID29359	Ionization constant (pKa)	2000	Journal of medicinal chemistry, Jun-29, Volume: 43, Issue:13	QSAR model for drug human oral bioavailability.
AID286877	Antihyperalgesic effects in Sprague-Dawley rat SNL model assessed as duration of paw withdrawal at 100 mg/kg, ip after 1.5 hrs, ip	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID588215	FDA HLAED, alkaline phosphatase increase	2004	Current drug discovery technologies, Dec, Volume: 1, Issue:4	Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1473738	Inhibition 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 assay	2013	Toxicological 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.
AID588217	FDA HLAED, serum glutamic pyruvic transaminase (SGPT) increase	2004	Current drug discovery technologies, Dec, Volume: 1, Issue:4	Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID678716	Inhibition of human CYP3A4 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using diethoxyfluorescein as substrate after 30 mins	2012	Chemical research in toxicology, Oct-15, Volume: 25, Issue:10	Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID352885	Inhibition of human Nav1.1 expressed in HEK293 cells assessed as change in membrane potential using MP-red voltage sensitive dye at 10 uM	2009	Journal of medicinal chemistry, May-14, Volume: 52, Issue:9	Oxadiazolylindazole sodium channel modulators are neuroprotective toward hippocampal neurones.
AID678713	Inhibition of human CYP2C9 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using 7-methoxy-4-trifluoromethylcoumarin-3-acetic acid as substrate after 30 mins	2012	Chemical research in toxicology, Oct-15, Volume: 25, Issue:10	Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID286880	Anti-dynamic allodynic effect in Sprague-Dawley rat CCI model assessed as latency to paw withdrawal after 0.5 hr	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID217929	Inhibition of veratridine-induced guanidine flux in cardiac voltage-gated sodium channel (veratridine block vs. Na release)	2001	Journal of medicinal chemistry, Jan-18, Volume: 44, Issue:2	Medicinal chemistry of neuronal voltage-gated sodium channel blockers.
AID396411	Anticonvulsant activity in ip dosed Swiss albino mouse assessed as inhibition of subcutaneous pentylenetetrazole-induced seizures administered 30 mins before PTZ challenge measured after 0.5 hrs post PTZ challenge	2008	European journal of medicinal chemistry, Dec, Volume: 43, Issue:12	Newer GABA derivatives for the treatment of epilepsy including febrile seizures: a bioisosteric approach.
AID603565	Antiallodynic activity in Wistar albino rat chronic constriction injury-induced neuropathic pain model assessed as attenuation of mechanical allodynia after 0.5 hrs at 100 mg/kg, ip	2011	European journal of medicinal chemistry, Jul, Volume: 46, Issue:7	Discovery of molecules for the treatment of neuropathic pain: synthesis, antiallodynic and antihyperalgesic activities of 5-(4-nitrophenyl)furoic-2-acid hydrazones.
AID1268923	Neurotoxicity in ip dosed CF1 albino mouse after 0.25 hrs by rotarod test	2016	Bioorganic & medicinal chemistry, Jan-15, Volume: 24, Issue:2	Chlorophenoxy aminoalkyl derivatives as histamine H(3)R ligands and antiseizure agents.
AID52790	Inhibition of chymotrypsin at 250 uM	2003	Journal of medicinal chemistry, Oct-09, Volume: 46, Issue:21	Identification and prediction of promiscuous aggregating inhibitors among known drugs.
AID1215859	Drug metabolism in human liver microsomes assessed as glucuronide formation per mg protein by mass spectrometry analysis	2013	Drug metabolism and disposition: the biological fate of chemicals, Apr, Volume: 41, Issue:4	Potential role of UGT1A4 promoter SNPs in anastrozole pharmacogenomics.
AID342468	Inhibition of AQP4 expressed in rat FRT cells assessed as osmotic water permeability at 100 uM after 60 mins by stopped-flow light scattering method	2008	Bioorganic & medicinal chemistry, Aug-01, Volume: 16, Issue:15	Lack of aquaporin-4 water transport inhibition by antiepileptics and arylsulfonamides.
AID588216	FDA HLAED, serum glutamic oxaloacetic transaminase (SGOT) increase	2004	Current drug discovery technologies, Dec, Volume: 1, Issue:4	Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1233920	Inhibition of human Nav1.8 expressed in HEK293 cells assessed as reduction in blue fluorescent signal by VSP-FRET assay	2015	ACS medicinal chemistry letters, Jun-11, Volume: 6, Issue:6	Discovery and Optimization of Selective Nav1.8 Modulator Series That Demonstrate Efficacy in Preclinical Models of Pain.
AID286882	Anti-dynamic allodynic effect in Sprague-Dawley rat CCI model assessed as latency to paw withdrawal after 1.5 hr	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID112456	Anticonvulsant potency using the maximal electroshock test in mice	1998	Journal of medicinal chemistry, Feb-12, Volume: 41, Issue:4	Synthesis and anticonvulsant activity of a new class of 2-[(arylalky)amino]alkanamide derivatives.
AID1268934	Protective index, ratio of TD50 for ip dosed CF1 albino mouse to ED50 for ip dosed CF1 albino mouse assessed as protection against maximal electroshock-induced seizure after 0.25 hrs	2016	Bioorganic & medicinal chemistry, Jan-15, Volume: 24, Issue:2	Chlorophenoxy aminoalkyl derivatives as histamine H(3)R ligands and antiseizure agents.
AID185053	Neuroprotective activity was determined in the rat middle cerebral artery occlusion (MCAO) model of focal stroke	2001	Journal of medicinal chemistry, Jan-18, Volume: 44, Issue:2	Medicinal chemistry of neuronal voltage-gated sodium channel blockers.
AID1223478	Total clearance in chimeric mouse with humanized liver at 3 mg/kg, iv by LC-MS/MS method	2012	Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 40, Issue:2	Prediction of in vivo hepatic clearance and half-life of drug candidates in human using chimeric mice with humanized liver.
AID396631	Neurotoxicity in ip dosed Swiss albino mouse assessed as inability of animal to maintain equilibrium on the rod for at least 1 min after 4 hrs by rotarod test	2008	European journal of medicinal chemistry, Dec, Volume: 43, Issue:12	Newer GABA derivatives for the treatment of epilepsy including febrile seizures: a bioisosteric approach.
AID625289	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver disease	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID588214	FDA HLAED, liver enzyme composite activity	2004	Current drug discovery technologies, Dec, Volume: 1, Issue:4	Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID625288	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for jaundice	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID249395	Ratio between Kr to Ki	2004	Journal of medicinal chemistry, Aug-12, Volume: 47, Issue:17	Phenoxyphenyl pyridines as novel state-dependent, high-potency sodium channel inhibitors.
AID114014	Effective dose for anticonvulsant activity determined in mice using MES test procedure. (Phase II)	1995	Journal of medicinal chemistry, Sep-29, Volume: 38, Issue:20	Synthesis and anticonvulsant activity of enaminones. 3. Investigations on 4'-, 3'-, and 2'-substituted and polysubstituted anilino compounds, sodium channel binding studies, and toxicity evaluations.
AID286888	Anti-cold allodynia effect in Sprague-Dawley rat CCI model assessed as duration of paw withdrawal 100 mg/kg, ip after 2 hr	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID253080	Inhibition of native TTX-R sodium currents in acutely dissociated rat dorsal root ganglion (DRG)	2004	Journal of medicinal chemistry, Aug-12, Volume: 47, Issue:17	Phenoxyphenyl pyridines as novel state-dependent, high-potency sodium channel inhibitors.
AID351546	Inhibition of human Nav1.2 channel expressed in HEK cells by patch-clamp electrophysiology method	2009	Bioorganic & medicinal chemistry, May-15, Volume: 17, Issue:10	2,4(5)-diarylimidazoles as inhibitors of hNaV1.2 sodium channels: pharmacological evaluation and structure-property relationships.
AID699539	Inhibition of human liver OATP1B1 expressed in HEK293 Flp-In cells assessed as reduction in E17-betaG uptake at 20 uM by scintillation counting	2012	Journal of medicinal chemistry, May-24, Volume: 55, Issue:10	Classification of inhibitors of hepatic organic anion transporting polypeptides (OATPs): influence of protein expression on drug-drug interactions.
AID409601	Inhibition of human aquaporin 4 M23 isoform expressed in Xenopus laevis oocytes	2009	Bioorganic & medicinal chemistry, Jan-01, Volume: 17, Issue:1	Inhibition of aquaporin 4 by antiepileptic drugs.
AID286862	Effect on spontaneous pain in Sprague-Dawley rat CCI model assessed as duration of paw withdrawal at 100 mg/kg, ip after 1.5 hrs	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID396630	Neurotoxicity in ip dosed Swiss albino mouse assessed as inability of animal to maintain equilibrium on the rod for at least 1 min after 0.5 hrs by rotarod test	2008	European journal of medicinal chemistry, Dec, Volume: 43, Issue:12	Newer GABA derivatives for the treatment of epilepsy including febrile seizures: a bioisosteric approach.
AID286895	Anti-cold allodynia effect in Sprague-Dawley rat SNL model assessed as duration of paw withdrawal 100 mg/kg, ip after 0.5 hr	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID286898	Anti-cold allodynia effect in Sprague-Dawley rat SNL model assessed as duration of paw withdrawal 100 mg/kg, ip after 2 hrs	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID603564	Antiallodynic activity in Wistar albino rat chronic constriction injury-induced neuropathic pain model assessed as reversal of spontaneous pain response up to 2 hrs at 100 mg/kg, ip	2011	European journal of medicinal chemistry, Jul, Volume: 46, Issue:7	Discovery of molecules for the treatment of neuropathic pain: synthesis, antiallodynic and antihyperalgesic activities of 5-(4-nitrophenyl)furoic-2-acid hydrazones.
AID396627	Anticonvulsant activity in Swiss albino mouse assessed as inhibition of subcutaneous picrotoxin-induced seizures at 300 mg/kg, ip administered 30 mins before PIC challenge measured after 0.5 hrs post PIC challenge	2008	European journal of medicinal chemistry, Dec, Volume: 43, Issue:12	Newer GABA derivatives for the treatment of epilepsy including febrile seizures: a bioisosteric approach.
AID286873	Effect on spontaneous pain in Sprague-Dawley rat SNL model assessed as duration of paw withdrawal at 100 mg/kg, ip after 2 hrs	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID1079949	Proposed mechanism(s) of liver damage. [column 'MEC' in source]
AID286885	Anti-cold allodynia effect in Sprague-Dawley rat CCI model assessed as duration of paw withdrawal at 100 mg/kg, ip after 0.5 hr	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID1079938	Chronic liver disease either proven histopathologically, or through a chonic elevation of serum amino-transferase activity after 6 months. Value is number of references indexed. [column 'CHRON' in source]
AID286869	Antihyperalgesic effects in Sprague-Dawley rat CCI model assessed as duration of paw withdrawal at 100 mg/kg, ip after 2.5 hrs	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID588218	FDA HLAED, lactate dehydrogenase (LDH) increase	2004	Current drug discovery technologies, Dec, Volume: 1, Issue:4	Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1079937	Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source]
AID286871	Effect on spontaneous pain in Sprague-Dawley rat SNL model assessed as duration of paw withdrawal at 100 mg/kg, ip after 1 hr	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID678712	Inhibition of human CYP1A2 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using ethoxyresorufin as substrate after 30 mins	2012	Chemical research in toxicology, Oct-15, Volume: 25, Issue:10	Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID404539	Effect on locomotor activity in po dosed Sprague-Dawley rat	2008	Bioorganic & medicinal chemistry, Jun-15, Volume: 16, Issue:12	Discovery of potent furan piperazine sodium channel blockers for treatment of neuropathic pain.
AID298032	Acid dissociation constant, pKa of the compound	2007	Journal of medicinal chemistry, Sep-20, Volume: 50, Issue:19	High-throughput screening of drug-brain tissue binding and in silico prediction for assessment of central nervous system drug delivery.
AID1079931	Moderate liver toxicity, defined via clinical-chemistry results: ALT or AST serum activity 6 times the normal upper limit (N) or alkaline phosphatase serum activity of 1.7 N. Value is number of references indexed. [column 'BIOL' in source]
AID286860	Effect on spontaneous pain in Sprague-Dawley rat CCI model assessed as duration of paw withdrawal at 100 mg/kg, ip after 0.5 hr	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID205275	Inhibition of [3H]batrachotoxin binding to rat brain sodium channel	1999	Bioorganic & medicinal chemistry letters, Sep-06, Volume: 9, Issue:17	Sodium channel activity and sigma binding of 2-aminopropanamide anticonvulsants.
AID342467	Inhibition of AQP4 expressed in rat FRT cells assessed as osmotic water permeability at 100 uM after 15 mins by stopped-flow light scattering method	2008	Bioorganic & medicinal chemistry, Aug-01, Volume: 16, Issue:15	Lack of aquaporin-4 water transport inhibition by antiepileptics and arylsulfonamides.
AID521220	Inhibition of neurosphere proliferation of mouse neural precursor cells by MTT assay	2007	Nature chemical biology, May, Volume: 3, Issue:5	Chemical genetics reveals a complex functional ground state of neural stem cells.
AID1079948	Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source]
AID404533	Blockade of Nav1.8 channel in rat dorsal root ganglion neurons assessed as inhibition of TTX-R current by whole cell patch clamp technique	2008	Bioorganic & medicinal chemistry, Jun-15, Volume: 16, Issue:12	Discovery of potent furan piperazine sodium channel blockers for treatment of neuropathic pain.
AID352892	Inhibition of human Nav1.7 expressed in HEK293 cells assessed as change in membrane potential using MP-red voltage sensitive dye at 10 uM	2009	Journal of medicinal chemistry, May-14, Volume: 52, Issue:9	Oxadiazolylindazole sodium channel modulators are neuroprotective toward hippocampal neurones.
AID286891	Anti-dynamic allodynia effect in Sprague-Dawley rat SNL model assessed as latency to paw withdrawal 100 mg/kg, ip after 1 hr	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID351544	Inhibition of human Nav1.2 channel expressed in HEK cells at 10 uM by patch-clamp electrophysiology method	2009	Bioorganic & medicinal chemistry, May-15, Volume: 17, Issue:10	2,4(5)-diarylimidazoles as inhibitors of hNaV1.2 sodium channels: pharmacological evaluation and structure-property relationships.
AID226515	Protective index (PI) is the ratio of TD50 in the rotarod test over the ED50 in the anticonvulsant test.	1999	Bioorganic & medicinal chemistry letters, Sep-06, Volume: 9, Issue:17	Sodium channel activity and sigma binding of 2-aminopropanamide anticonvulsants.
AID625285	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic necrosis	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1207433	Inhibition 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
AID1079941	Liver damage due to vascular disease: peliosis hepatitis, hepatic veno-occlusive disease, Budd-Chiari syndrome. Value is number of references indexed. [column 'VASC' in source]
AID1473740	Inhibition 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 assay	2013	Toxicological 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.
AID311933	Inhibition of ASM in rat PC12 cells assessed as residual activity at 10 uM	2008	Journal of medicinal chemistry, Jan-24, Volume: 51, Issue:2	Identification of new functional inhibitors of acid sphingomyelinase using a structure-property-activity relation model.
AID1079936	Choleostatic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is < 2 (see ACUTE). Value is number of references indexed. [column 'CHOLE' in source]
AID197266	In vivo anticonvulsant activity to prevent seizures from maximum electroshock (MES) in rat hippocampal slices	2001	Journal of medicinal chemistry, Jan-18, Volume: 44, Issue:2	Medicinal chemistry of neuronal voltage-gated sodium channel blockers.
AID286868	Antihyperalgesic effects in Sprague-Dawley rat CCI model assessed as duration of paw withdrawal at 100 mg/kg, ip after 2 hrs	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID1079935	Cytolytic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is > 5 (see ACUTE). Value is number of references indexed. [column 'CYTOL' in source]
AID1223484	Unbound fraction in po dosed human plasma	2012	Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 40, Issue:2	Prediction of in vivo hepatic clearance and half-life of drug candidates in human using chimeric mice with humanized liver.
AID244690	Dissociation constant for binding to resting state of rat brain NaIIa (rNav1.2) -B2 cell line stably expressed in HEK293 Cells	2004	Journal of medicinal chemistry, Aug-12, Volume: 47, Issue:17	Phenoxyphenyl pyridines as novel state-dependent, high-potency sodium channel inhibitors.
AID625280	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholecystitis	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID29811	Oral bioavailability in human	2000	Journal of medicinal chemistry, Jun-29, Volume: 43, Issue:13	QSAR model for drug human oral bioavailability.
AID588219	FDA HLAED, gamma-glutamyl transferase (GGT) increase	2004	Current drug discovery technologies, Dec, Volume: 1, Issue:4	Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1207561	Inhibition of long-lasting type calcium current (hICa) in Chinese Hamster Ovary (CHO) cells expressing hCav1.2 measured using IonWorks Quattro automated patch clamp platform
AID604020	Unbound drug concentration in Sprague-Dawley rat plasma administered in casettes of 2/3 drugs at 4 hr constant rate intravenous infusions using flow rate of 1 (ml/kg)/hr corresponding to dosage rate of 2 (umol/kg)/hr by LC-MS/MS method	2009	Journal of medicinal chemistry, Oct-22, Volume: 52, Issue:20	Structure-brain exposure relationships in rat and human using a novel data set of unbound drug concentrations in brain interstitial and cerebrospinal fluids.
AID1233922	Inhibition of human Nav1.3 expressed in SHSY5Y cells assessed as reduction in blue fluorescent signal by VSP-FRET assay	2015	ACS medicinal chemistry letters, Jun-11, Volume: 6, Issue:6	Discovery and Optimization of Selective Nav1.8 Modulator Series That Demonstrate Efficacy in Preclinical Models of Pain.
AID395324	Lipophilicity, log D at pH 7.4 by liquid chromatography	2009	Journal of medicinal chemistry, Mar-26, Volume: 52, Issue:6	Relationship between brain tissue partitioning and microemulsion retention factors of CNS drugs.
AID678714	Inhibition of human CYP2C19 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using 3-butyryl-7-methoxycoumarin as substrate after 30 mins	2012	Chemical research in toxicology, Oct-15, Volume: 25, Issue:10	Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID1378414	Antibacterial activity against methicillin-resistant Staphylococcus aureus subsp. aureus Rosenbach 1884	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Topological pattern for the search of new active drugs against methicillin resistant Staphylococcus aureus.
AID1079947	Comments (NB not yet translated). [column 'COMMENTAIRES' in source]
AID227700	Anticonvulsant activity	2003	Bioorganic & medicinal chemistry letters, Aug-18, Volume: 13, Issue:16	Topological virtual screening: a way to find new anticonvulsant drugs from chemical diversity.
AID1207283	Inhibition of long-lasting type calcium current (ICaL) in HEK293 cells (alpha1C/beta2a/alpha2delta1) cells measured using IonWorks Barracuda automated patch clamp platform
AID396410	Anticonvulsant activity in ip dosed Swiss albino mouse assessed as inhibition of maximal electroshock-induced seizures administered 30 mins before electroshock measured after 0.5 hrs post electroshock	2008	European journal of medicinal chemistry, Dec, Volume: 43, Issue:12	Newer GABA derivatives for the treatment of epilepsy including febrile seizures: a bioisosteric approach.
AID604023	Ratio of total drug level in brain to plasma in Sprague-Dawley rat administered in casettes of 2/3 drugs at 4 hr constant rate intravenous infusions using flow rate of 1 (ml/kg)/hr corresponding to dosage rate of 2 (umol/kg)/hr by LC-MS/MS method	2009	Journal of medicinal chemistry, Oct-22, Volume: 52, Issue:20	Structure-brain exposure relationships in rat and human using a novel data set of unbound drug concentrations in brain interstitial and cerebrospinal fluids.
AID352890	Inhibition of human Nav1.5 expressed in HEK293 cells assessed as change in membrane potential using MP-red voltage sensitive dye at 10 uM	2009	Journal of medicinal chemistry, May-14, Volume: 52, Issue:9	Oxadiazolylindazole sodium channel modulators are neuroprotective toward hippocampal neurones.
AID625292	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) combined score	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1207527	Inhibition of rapid delayed inward rectifying potassium current (IKr) measured using manual patch clamp assay
AID112461	Anticonvulsant potency using the intravenous-BIC (bicuculline) test in mice	1998	Journal of medicinal chemistry, Feb-12, Volume: 41, Issue:4	Synthesis and anticonvulsant activity of a new class of 2-[(arylalky)amino]alkanamide derivatives.
AID1495413	Neurotoxicity in ip dosed albino CF-1 mouse after 0.25 hrs by rotarod test
AID404547	Plasma clearance in Sprague-Dawley rat at 10 mg/kg	2008	Bioorganic & medicinal chemistry, Jun-15, Volume: 16, Issue:12	Discovery of potent furan piperazine sodium channel blockers for treatment of neuropathic pain.
AID1079946	Presence of at least one case with successful reintroduction. [column 'REINT' in source]
AID404549	Volume of distribution at steady state in Sprague-Dawley rat at 10 mg/kg	2008	Bioorganic & medicinal chemistry, Jun-15, Volume: 16, Issue:12	Discovery of potent furan piperazine sodium channel blockers for treatment of neuropathic pain.
AID43581	Inhibition of beta-lactamase at 100 uM	2003	Journal of medicinal chemistry, Oct-09, Volume: 46, Issue:21	Identification and prediction of promiscuous aggregating inhibitors among known drugs.
AID699541	Inhibition of human liver OATP2B1 expressed in HEK293 Flp-In cells assessed as reduction in [3H]E3S uptake at 20 uM incubated for 5 mins by scintillation counting	2012	Journal of medicinal chemistry, May-24, Volume: 55, Issue:10	Classification of inhibitors of hepatic organic anion transporting polypeptides (OATPs): influence of protein expression on drug-drug interactions.
AID190113	In vivo toxic dose in rotarod assay	2001	Journal of medicinal chemistry, Jan-18, Volume: 44, Issue:2	Medicinal chemistry of neuronal voltage-gated sodium channel blockers.
AID404548	Cmax in Sprague-Dawley rat at 10 mg/kg, po	2008	Bioorganic & medicinal chemistry, Jun-15, Volume: 16, Issue:12	Discovery of potent furan piperazine sodium channel blockers for treatment of neuropathic pain.
AID444052	Hepatic clearance in human	2010	Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3	Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID286883	Anti-dynamic allodynic effect in Sprague-Dawley rat CCI model assessed as latency to paw withdrawal after 2 hr	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID217794	Inhibition of [3H]BTX-B binding to neurotoxin site 2 of sodium channel of rat cerebral cortex synaptoneurosomes	1995	Journal of medicinal chemistry, Sep-29, Volume: 38, Issue:20	Synthesis and anticonvulsant activity of enaminones. 3. Investigations on 4'-, 3'-, and 2'-substituted and polysubstituted anilino compounds, sodium channel binding studies, and toxicity evaluations.
AID178028	Effective dose for anticonvulsant activity determined in rats using MES test procedure. (Phase VIA); not determined	1995	Journal of medicinal chemistry, Sep-29, Volume: 38, Issue:20	Synthesis and anticonvulsant activity of enaminones. 3. Investigations on 4'-, 3'-, and 2'-substituted and polysubstituted anilino compounds, sodium channel binding studies, and toxicity evaluations.
AID1473739	Inhibition 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 assay	2013	Toxicological 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.
AID1268928	Anticonvulsant activity in ip dosed CF1 albino mouse assessed as protection against subcutaneous pentetrazole-induced seizure after 0.25 hrs	2016	Bioorganic & medicinal chemistry, Jan-15, Volume: 24, Issue:2	Chlorophenoxy aminoalkyl derivatives as histamine H(3)R ligands and antiseizure agents.
AID392051	Inhibition of human ERG channel in HEK293 cells by voltage-clamp method	2008	European journal of medicinal chemistry, Nov, Volume: 43, Issue:11	Identification of "toxicophoric" features for predicting drug-induced QT interval prolongation.
AID678721	Metabolic stability in human liver microsomes assessed as GSH adduct formation at 100 uM after 90 mins by HPLC-MS analysis	2012	Chemical research in toxicology, Oct-15, Volume: 25, Issue:10	Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID114018	Effective dose for anticonvulsant activity determined in mice using subcutaneous Met test procedure. (Phase II); not determined	1995	Journal of medicinal chemistry, Sep-29, Volume: 38, Issue:20	Synthesis and anticonvulsant activity of enaminones. 3. Investigations on 4'-, 3'-, and 2'-substituted and polysubstituted anilino compounds, sodium channel binding studies, and toxicity evaluations.
AID352899	Use-dependent inhibition of human Nav1.2 expressed in HEK293 cells at 100 uM using double-pulse protocol by patch clamp technique	2009	Journal of medicinal chemistry, May-14, Volume: 52, Issue:9	Oxadiazolylindazole sodium channel modulators are neuroprotective toward hippocampal neurones.
AID217926	Inhibition of [3H]BTX binding to cardiac voltage-gated sodium channel	2001	Journal of medicinal chemistry, Jan-18, Volume: 44, Issue:2	Medicinal chemistry of neuronal voltage-gated sodium channel blockers.
AID352889	Inhibition of human Nav1.4 expressed in HEK293 cells assessed as change in membrane potential using MP-red voltage sensitive dye at 10 uM	2009	Journal of medicinal chemistry, May-14, Volume: 52, Issue:9	Oxadiazolylindazole sodium channel modulators are neuroprotective toward hippocampal neurones.
AID678722	Covalent binding affinity to human liver microsomes assessed per mg of protein at 10 uM after 60 mins presence of NADPH	2012	Chemical research in toxicology, Oct-15, Volume: 25, Issue:10	Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID396623	Anticonvulsant activity in Swiss albino mouse assessed as inhibition of subcutaneous strychnine-induced seizures at 300 mg/kg, ip administered 30 mins before STY challenge measured after 0.5 hrs post STY challenge	2008	European journal of medicinal chemistry, Dec, Volume: 43, Issue:12	Newer GABA derivatives for the treatment of epilepsy including febrile seizures: a bioisosteric approach.
AID179824	Tested for the anticonvulsant activity administered 60 min orally before MES induction	1999	Bioorganic & medicinal chemistry letters, Sep-06, Volume: 9, Issue:17	Sodium channel activity and sigma binding of 2-aminopropanamide anticonvulsants.
AID1207313	Inhibition 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
AID396629	Anticonvulsant activity in Wistar rat assessed as protection against hyperthermia-induced seizures at 100 mg/kg, ip relative to control	2008	European journal of medicinal chemistry, Dec, Volume: 43, Issue:12	Newer GABA derivatives for the treatment of epilepsy including febrile seizures: a bioisosteric approach.
AID286896	Anti-cold allodynia effect in Sprague-Dawley rat SNL model assessed as duration of paw withdrawal 100 mg/kg, ip after 1 hrs	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID342471	Inhibition of AQP4 in wild type mouse brain gilial cells assessed as reduction of osmotic equilibrium rate at 10 to 100 uM after 15 mins by calcein quenching assay relative to water permeability	2008	Bioorganic & medicinal chemistry, Aug-01, Volume: 16, Issue:15	Lack of aquaporin-4 water transport inhibition by antiepileptics and arylsulfonamides.
AID1079943	Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source]
AID286875	Antihyperalgesic effects in Sprague-Dawley rat SNL model assessed as duration of paw withdrawal at 100 mg/kg, ip after 0.5 hr, ip	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID404534	Inhibition of human recombinant Nav1.8 channel expressed in HEK293 cells by whole cell voltage clamp technique	2008	Bioorganic & medicinal chemistry, Jun-15, Volume: 16, Issue:12	Discovery of potent furan piperazine sodium channel blockers for treatment of neuropathic pain.
AID212679	Toxic dose determined in rats using MES test procedure. (Phase VIA); not determined	1995	Journal of medicinal chemistry, Sep-29, Volume: 38, Issue:20	Synthesis and anticonvulsant activity of enaminones. 3. Investigations on 4'-, 3'-, and 2'-substituted and polysubstituted anilino compounds, sodium channel binding studies, and toxicity evaluations.
AID1207373	Inhibition 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
AID1495424	Therapeutic index, ratio of ip dosed albino CF-1 mouse TD50 to ip dosed albino CF-1 mouse ED50 for MES assay
AID1255683	Binding affinity to Escherichia coli DHFR at 500 uM using spyro orange reporter dye by differential scanning fluorimetry	2015	European journal of medicinal chemistry, Oct-20, Volume: 103	Ligand binding studies, preliminary structure-activity relationship and detailed mechanistic characterization of 1-phenyl-6,6-dimethyl-1,3,5-triazine-2,4-diamine derivatives as inhibitors of Escherichia coli dihydrofolate reductase.
AID286887	Anti-cold allodynia effect in Sprague-Dawley rat CCI model assessed as duration of paw withdrawal 100 mg/kg, ip after 1.5 hr	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID604022	Fraction unbound in Sprague-Dawley rat plasma administered in casettes of 2/3 drugs at 4 hr constant rate intravenous infusions using flow rate of 1 (ml/kg)/hr corresponding to dosage rate of 2 (umol/kg)/hr by LC-MS/MS method	2009	Journal of medicinal chemistry, Oct-22, Volume: 52, Issue:20	Structure-brain exposure relationships in rat and human using a novel data set of unbound drug concentrations in brain interstitial and cerebrospinal fluids.
AID1495423	Anticonvulsant activity in ip dosed albino CF-1 mouse assessed as protection against 44 mA current-induced seizure after 0.25 hrs by 6 Hz psychomotor test
AID342470	Inhibition of AQP4 in wild type mouse brain gilial cells assessed as osmotic water permeability at 10 to 100 uM after 15 mins by calcein quenching assay	2008	Bioorganic & medicinal chemistry, Aug-01, Volume: 16, Issue:15	Lack of aquaporin-4 water transport inhibition by antiepileptics and arylsulfonamides.
AID352888	Inhibition of human Nav1.3 expressed in HEK293 cells assessed as change in membrane potential using MP-red voltage sensitive dye at 10 uM	2009	Journal of medicinal chemistry, May-14, Volume: 52, Issue:9	Oxadiazolylindazole sodium channel modulators are neuroprotective toward hippocampal neurones.
AID395325	Lipophilicity, log P by microemulsion electrokinetic chromatography	2009	Journal of medicinal chemistry, Mar-26, Volume: 52, Issue:6	Relationship between brain tissue partitioning and microemulsion retention factors of CNS drugs.
AID476929	Human intestinal absorption in po dosed human	2010	European journal of medicinal chemistry, Mar, Volume: 45, Issue:3	Neural computational prediction of oral drug absorption based on CODES 2D descriptors.
AID588213	Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in non-rodents	2010	Chemical research in toxicology, Jan, Volume: 23, Issue:1	Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID588212	Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in rodents	2010	Chemical research in toxicology, Jan, Volume: 23, Issue:1	Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID1129297	Neuroprotective activity in oxygen/glucose deprivation-induced Wistar rat hippocampal slice assessed as inhibition of cell death by measuring ATP level at 30 uM normalized to tetrodotoxin	2014	Journal of medicinal chemistry, Apr-10, Volume: 57, Issue:7	Imidazol-1-ylethylindazole voltage-gated sodium channel ligands are neuroprotective during optic neuritis in a mouse model of multiple sclerosis.
AID1209582	Unbound volume of distribution in Sprague-Dawley rat brain slices at 100 nM after 5 hrs	2011	Drug metabolism and disposition: the biological fate of chemicals, Mar, Volume: 39, Issue:3	Measurement of unbound drug exposure in brain: modeling of pH partitioning explains diverging results between the brain slice and brain homogenate methods.
AID1495416	Anticonvulsant activity in ip dosed albino CF-1 mouse assessed as protection against maximal electroshock-induced seizures after 1 hr
AID352898	Use-dependent inhibition of human Nav1.2 expressed in HEK293 cells at 30 uM using double-pulse protocol by patch clamp technique	2009	Journal of medicinal chemistry, May-14, Volume: 52, Issue:9	Oxadiazolylindazole sodium channel modulators are neuroprotective toward hippocampal neurones.
AID342466	Inhibition of AQP4 expressed in rat FRT cells assessed as osmotic water permeability at 10 uM by stopped-flow light scattering method	2008	Bioorganic & medicinal chemistry, Aug-01, Volume: 16, Issue:15	Lack of aquaporin-4 water transport inhibition by antiepileptics and arylsulfonamides.
AID1207343	Inhibition of fast sodium current (INa) in HEK293 cells transfected with human Nav1.5 measured using IonWorks Quattro automated patch clamp platform
AID396624	Anticonvulsant activity in Swiss albino mouse assessed as inhibition of subcutaneous strychnine-induced seizures at 300 mg/kg, ip administered 30 mins before STY challenge measured after 4 hrs post STY challenge	2008	European journal of medicinal chemistry, Dec, Volume: 43, Issue:12	Newer GABA derivatives for the treatment of epilepsy including febrile seizures: a bioisosteric approach.
AID27167	Delta logD (logD6.5 - logD7.4)	2000	Journal of medicinal chemistry, Jun-29, Volume: 43, Issue:13	QSAR model for drug human oral bioavailability.
AID1598719	Binding affinity to Triton-X 100 assessed as line broadening at 150 uM by 1H-NMR spectra analysis	2019	Journal of medicinal chemistry, 05-23, Volume: 62, Issue:10	Mechanisms of Specific versus Nonspecific Interactions of Aggregation-Prone Inhibitors and Attenuators.
AID444056	Fraction escaping gut-wall elimination in human	2010	Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3	Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID625282	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cirrhosis	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1598718	Binding affinity to Triton-X 100 assessed as change in chemical shift at 150 uM by 1H-NMR spectra analysis	2019	Journal of medicinal chemistry, 05-23, Volume: 62, Issue:10	Mechanisms of Specific versus Nonspecific Interactions of Aggregation-Prone Inhibitors and Attenuators.
AID1495422	Anticonvulsant activity in ip dosed albino CF-1 mouse assessed as protection against 32 mA current-induced seizure after 1 hr by 6 Hz psychomotor test
AID1223485	Ratio of drug level in blood to plasma in po dosed human	2012	Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 40, Issue:2	Prediction of in vivo hepatic clearance and half-life of drug candidates in human using chimeric mice with humanized liver.
AID624608	Specific activity of expressed human recombinant UGT1A4	2000	Annual review of pharmacology and toxicology, , Volume: 40	Human UDP-glucuronosyltransferases: metabolism, expression, and disease.
AID112455	Compound was tested for anticonvulsant potency using the 3-MPA (3-mercaptopropionic acid) test in mice upon peroral administration	1998	Journal of medicinal chemistry, Feb-12, Volume: 41, Issue:4	Synthesis and anticonvulsant activity of a new class of 2-[(arylalky)amino]alkanamide derivatives.
AID1079944	Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source]
AID205273	Concentration required to inhibit [3H]BTX binding to Sodium channel of rat brain	2004	Bioorganic & medicinal chemistry letters, Jul-05, Volume: 14, Issue:13	2-Alkyl-4-arylimidazoles: structurally novel sodium channel modulators.
AID396628	Anticonvulsant activity in Swiss albino mouse assessed as inhibition of subcutaneous picrotoxin-induced seizures at 300 mg/kg, ip administered 30 mins before PIC challenge measured after 4 hrs post PIC challenge	2008	European journal of medicinal chemistry, Dec, Volume: 43, Issue:12	Newer GABA derivatives for the treatment of epilepsy including febrile seizures: a bioisosteric approach.
AID286878	Antihyperalgesic effects in Sprague-Dawley rat SNL model assessed as duration of paw withdrawal at 100 mg/kg, ip after 2 hrs, ip	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID1079939	Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source]
AID1223480	Oral clearance in po dosed human	2012	Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 40, Issue:2	Prediction of in vivo hepatic clearance and half-life of drug candidates in human using chimeric mice with humanized liver.
AID1474166	Liver toxicity in human assessed as induction of drug-induced liver injury by measuring severity class index	2016	Drug 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.
AID352893	Inhibition of human Nav1.8 expressed in HEK293 cells assessed as change in membrane potential using MP-red voltage sensitive dye at 10 uM	2009	Journal of medicinal chemistry, May-14, Volume: 52, Issue:9	Oxadiazolylindazole sodium channel modulators are neuroprotective toward hippocampal neurones.
AID625283	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for elevated liver function tests	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079932	Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source]
AID286889	Anti-cold allodynia effect in Sprague-Dawley rat CCI model assessed as duration of paw withdrawal 100 mg/kg, ip after 2.5 hr	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID404542	Analgesic activity in po dosed Sprague-Dawley rat by edge test	2008	Bioorganic & medicinal chemistry, Jun-15, Volume: 16, Issue:12	Discovery of potent furan piperazine sodium channel blockers for treatment of neuropathic pain.
AID286890	Anti-dynamic allodynia effect in Sprague-Dawley rat SNL model assessed as latency to paw withdrawal 100 mg/kg, ip after 0.5 hr	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID286876	Antihyperalgesic effects in Sprague-Dawley rat SNL model assessed as duration of paw withdrawal at 100 mg/kg, ip after 1 hr, ip	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID1268924	Anticonvulsant activity in ip dosed CF1 albino mouse assessed as protection against maximal electroshock-induced seizure after 0.25 hrs	2016	Bioorganic & medicinal chemistry, Jan-15, Volume: 24, Issue:2	Chlorophenoxy aminoalkyl derivatives as histamine H(3)R ligands and antiseizure agents.
AID1207467	Inhibition 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
AID286866	Antihyperalgesic effects in Sprague-Dawley rat CCI model assessed as duration of paw withdrawal at 100 mg/kg, ip after 1 hr	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID286892	Anti-dynamic allodynia effect in Sprague-Dawley rat SNL model assessed as latency to paw withdrawal 100 mg/kg, ip after 1.5 hrs	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID625286	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatitis	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID286897	Anti-cold allodynia effect in Sprague-Dawley rat SNL model assessed as duration of paw withdrawal 100 mg/kg, ip after 1.5 hrs	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID1255681	Binding affinity to Escherichia coli DHFR assessed as change in melting temperature at 500 uM using spyro orange reporter dye by differential scanning fluorimetry	2015	European journal of medicinal chemistry, Oct-20, Volume: 103	Ligand binding studies, preliminary structure-activity relationship and detailed mechanistic characterization of 1-phenyl-6,6-dimethyl-1,3,5-triazine-2,4-diamine derivatives as inhibitors of Escherichia coli dihydrofolate reductase.
AID444055	Fraction absorbed in human	2010	Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3	Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID298031	Lipophilicity, log D at pH7.4	2007	Journal of medicinal chemistry, Sep-20, Volume: 50, Issue:19	High-throughput screening of drug-brain tissue binding and in silico prediction for assessment of central nervous system drug delivery.
AID352891	Inhibition of human Nav1.6 expressed in HEK293 cells assessed as change in membrane potential using MP-red voltage sensitive dye at 10 uM	2009	Journal of medicinal chemistry, May-14, Volume: 52, Issue:9	Oxadiazolylindazole sodium channel modulators are neuroprotective toward hippocampal neurones.
AID352884	Displacement of [3H]BW202W92 from voltage-gated sodium channel in Wistar rat forebrain synaptosomes by liquid scintillation counting	2009	Journal of medicinal chemistry, May-14, Volume: 52, Issue:9	Oxadiazolylindazole sodium channel modulators are neuroprotective toward hippocampal neurones.
AID286861	Effect on spontaneous pain in Sprague-Dawley rat CCI model assessed as duration of paw withdrawal at 100 mg/kg, ip after 1 hr	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID444054	Oral bioavailability in human	2010	Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3	Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID404536	Inhibition of human recombinant Nav1.5 channel expressed in HEK293 cells by whole cell voltage clamp technique	2008	Bioorganic & medicinal chemistry, Jun-15, Volume: 16, Issue:12	Discovery of potent furan piperazine sodium channel blockers for treatment of neuropathic pain.
AID244602	Dissociation constant for binding to inactivated state of rat brain NaIIa (rNav1.2) -B2 cell line stably expressed in HEK293 Cells	2004	Journal of medicinal chemistry, Aug-12, Volume: 47, Issue:17	Phenoxyphenyl pyridines as novel state-dependent, high-potency sodium channel inhibitors.
AID625291	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver function tests abnormal	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID588211	Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in humans	2010	Chemical research in toxicology, Jan, Volume: 23, Issue:1	Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID444053	Renal clearance in human	2010	Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3	Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID212346	Toxic dose determined in mice using MES test procedure. (Phase II); not determined	1995	Journal of medicinal chemistry, Sep-29, Volume: 38, Issue:20	Synthesis and anticonvulsant activity of enaminones. 3. Investigations on 4'-, 3'-, and 2'-substituted and polysubstituted anilino compounds, sodium channel binding studies, and toxicity evaluations.
AID404537	Analgesic activity in po dosed Sprague-Dawley rat assessed as attenuation of mechanical allodynia in chung model of neuropathic pain	2008	Bioorganic & medicinal chemistry, Jun-15, Volume: 16, Issue:12	Discovery of potent furan piperazine sodium channel blockers for treatment of neuropathic pain.
AID178032	Effective dose for anticonvulsant activity determined in rats using subcutaneous Met test procedure. (Phase VIA); not determined	1995	Journal of medicinal chemistry, Sep-29, Volume: 38, Issue:20	Synthesis and anticonvulsant activity of enaminones. 3. Investigations on 4'-, 3'-, and 2'-substituted and polysubstituted anilino compounds, sodium channel binding studies, and toxicity evaluations.
AID286894	Anti-dynamic allodynia effect in Sprague-Dawley rat SNL model assessed as latency to paw withdrawal 100 mg/kg, ip after 2.5 hrs	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID1223475	Elimination half life in chimeric mouse with humanized liver at 3 mg/kg, iv by LC-MS/MS method	2012	Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 40, Issue:2	Prediction of in vivo hepatic clearance and half-life of drug candidates in human using chimeric mice with humanized liver.
AID1215867	Drug metabolism in human liver microsomes assessed as retention time at 100 uM by mass spectrometry analysis	2013	Drug metabolism and disposition: the biological fate of chemicals, Apr, Volume: 41, Issue:4	Potential role of UGT1A4 promoter SNPs in anastrozole pharmacogenomics.
AID604026	Unbound CSF to plasma concentration ratio in human	2009	Journal of medicinal chemistry, Oct-22, Volume: 52, Issue:20	Structure-brain exposure relationships in rat and human using a novel data set of unbound drug concentrations in brain interstitial and cerebrospinal fluids.
AID388887	Inhibition of Nav1.2 channel in HEK cells at 100 uM by patch clamp technique	2008	Bioorganic & medicinal chemistry letters, Oct-15, Volume: 18, Issue:20	2,4(5)-Diarylimidazoles: synthesis and biological evaluation of a new class of sodium channel blockers against hNa(v)1.2.
AID205292	Affinity for resting human SkM1 sodium channel expressed in HEK293 cells	2004	Journal of medicinal chemistry, Mar-11, Volume: 47, Issue:6	3-(4-phenoxyphenyl)pyrazoles: a novel class of sodium channel blockers.
AID625287	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatomegaly	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079942	Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source]
AID1209593	Dissociation constant, pKa of the acidic compound by capillary electrophoresis-mass spectrometry analysis	2011	Drug metabolism and disposition: the biological fate of chemicals, Mar, Volume: 39, Issue:3	Measurement of unbound drug exposure in brain: modeling of pH partitioning explains diverging results between the brain slice and brain homogenate methods.
AID91481	Binding constant against human serum albumin (HSA)	2001	Journal of medicinal chemistry, Dec-06, Volume: 44, Issue:25	Cheminformatic models to predict binding affinities to human serum albumin.
AID1255686	Inhibition of Escherichia coli DHFR assessed as NADP formation by quadratic Morrison plot analysis	2015	European journal of medicinal chemistry, Oct-20, Volume: 103	Ligand binding studies, preliminary structure-activity relationship and detailed mechanistic characterization of 1-phenyl-6,6-dimethyl-1,3,5-triazine-2,4-diamine derivatives as inhibitors of Escherichia coli dihydrofolate reductase.
AID112460	Compound was tested for anticonvulsant potency using the STRY (strychnine) test in mice upon peroral administration	1998	Journal of medicinal chemistry, Feb-12, Volume: 41, Issue:4	Synthesis and anticonvulsant activity of a new class of 2-[(arylalky)amino]alkanamide derivatives.
AID286864	Effect on spontaneous pain in Sprague-Dawley rat CCI model assessed as duration of paw withdrawal at 100 mg/kg, ip after 2.5 hrs	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID286874	Effect on spontaneous pain in Sprague-Dawley rat SNL model assessed as duration of paw withdrawal at 100 mg/kg, ip after 2.5 hrs	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID678715	Inhibition of human CYP2D6 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using 4-methylaminoethyl-7-methoxycoumarin as substrate after 30 mins	2012	Chemical research in toxicology, Oct-15, Volume: 25, Issue:10	Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID232413	Relative affinity for inactivated and resting human SkM1 expressed in HEK293 cells	2004	Journal of medicinal chemistry, Mar-11, Volume: 47, Issue:6	3-(4-phenoxyphenyl)pyrazoles: a novel class of sodium channel blockers.
AID404535	Inhibition of human recombinant Nav1.2 channel expressed in HEK293 cells by whole cell voltage clamp technique	2008	Bioorganic & medicinal chemistry, Jun-15, Volume: 16, Issue:12	Discovery of potent furan piperazine sodium channel blockers for treatment of neuropathic pain.
AID539473	Solubility of the compound in Mcllvaine buffer at pH 7.4	2010	Bioorganic & medicinal chemistry letters, Dec-15, Volume: 20, Issue:24	Experimental solubility profiling of marketed CNS drugs, exploring solubility limit of CNS discovery candidate.
AID409600	Inhibition of human aquaporin 4 M23 isoform expressed in Xenopus laevis oocytes at 20 uM	2009	Bioorganic & medicinal chemistry, Jan-01, Volume: 17, Issue:1	Inhibition of aquaporin 4 by antiepileptic drugs.
AID205290	Affinity for inactive human SkM1 sodium channel expressed in HEK293 cells	2004	Journal of medicinal chemistry, Mar-11, Volume: 47, Issue:6	3-(4-phenoxyphenyl)pyrazoles: a novel class of sodium channel blockers.
AID286867	Antihyperalgesic effects in Sprague-Dawley rat CCI model assessed as duration of paw withdrawal at 100 mg/kg, ip after 1.5 hrs	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID286881	Anti-dynamic allodynic effect in Sprague-Dawley rat CCI model assessed as latency to paw withdrawal after 1 hr	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID1209581	Fraction unbound in Sprague-Dawley rat brain homogenates at 5 uM by equilibrium dialysis analysis	2011	Drug metabolism and disposition: the biological fate of chemicals, Mar, Volume: 39, Issue:3	Measurement of unbound drug exposure in brain: modeling of pH partitioning explains diverging results between the brain slice and brain homogenate methods.
AID286884	Anti-dynamic allodynic effect in Sprague-Dawley rat CCI model assessed as latency to paw withdrawal after 2.5 hr	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID395327	Dissociation constant, pKa by capillary electrophoresis	2009	Journal of medicinal chemistry, Mar-26, Volume: 52, Issue:6	Relationship between brain tissue partitioning and microemulsion retention factors of CNS drugs.
AID1079945	Animal toxicity known. [column 'TOXIC' in source]
AID604024	Unbound brain to plasma concentration ratio in Sprague-Dawley rat administered in casettes of 2/3 drugs at 4 hr constant rate intravenous infusions using flow rate of 1 (ml/kg)/hr corresponding to dosage rate of 2 (umol/kg)/hr	2009	Journal of medicinal chemistry, Oct-22, Volume: 52, Issue:20	Structure-brain exposure relationships in rat and human using a novel data set of unbound drug concentrations in brain interstitial and cerebrospinal fluids.
AID1223486	Intrinsic clearance in human hepatocytes from chimeric mouse with humanized liver assessed per 10'6 cells at 10 uM after 0.25 to 2 hrs by LC-MS/MS method	2012	Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 40, Issue:2	Prediction of in vivo hepatic clearance and half-life of drug candidates in human using chimeric mice with humanized liver.
AID1079933	Acute liver toxicity defined via clinical observations and clear clinical-chemistry results: serum ALT or AST activity > 6 N or serum alkaline phosphatases activity > 1.7 N. This category includes cytolytic, choleostatic and mixed liver toxicity. Value is
AID212211	Toxicity using neurological impairment measured by rotarod test in mice	1998	Journal of medicinal chemistry, Feb-12, Volume: 41, Issue:4	Synthesis and anticonvulsant activity of a new class of 2-[(arylalky)amino]alkanamide derivatives.
AID539464	Solubility of the compound in 0.1 M phosphate buffer at 600 uM at pH 7.4 after 24 hrs by LC/MS/MS analysis	2010	Bioorganic & medicinal chemistry letters, Dec-15, Volume: 20, Issue:24	Experimental solubility profiling of marketed CNS drugs, exploring solubility limit of CNS discovery candidate.
AID352886	Neuroprotective activity in Wistar rat hippocampal slices assessed as ATP concentration at 30 uM relative to tetrodotoxin	2009	Journal of medicinal chemistry, May-14, Volume: 52, Issue:9	Oxadiazolylindazole sodium channel modulators are neuroprotective toward hippocampal neurones.
AID286872	Effect on spontaneous pain in Sprague-Dawley rat SNL model assessed as duration of paw withdrawal at 100 mg/kg, ip after 1.5 hrs	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID352902	Inhibition of human Nav1.2 expressed in HEK293 cells assessed as change in membrane potential at 30 uM by patch clamp technique	2009	Journal of medicinal chemistry, May-14, Volume: 52, Issue:9	Oxadiazolylindazole sodium channel modulators are neuroprotective toward hippocampal neurones.
AID1255685	Inhibition of Escherichia coli DHFR assessed as NADP formation	2015	European journal of medicinal chemistry, Oct-20, Volume: 103	Ligand binding studies, preliminary structure-activity relationship and detailed mechanistic characterization of 1-phenyl-6,6-dimethyl-1,3,5-triazine-2,4-diamine derivatives as inhibitors of Escherichia coli dihydrofolate reductase.
AID1474167	Liver toxicity in human assessed as induction of drug-induced liver injury by measuring verified drug-induced liver injury concern status	2016	Drug 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.
AID404550	Oral bioavailability in Sprague-Dawley rat at 10 mg/kg	2008	Bioorganic & medicinal chemistry, Jun-15, Volume: 16, Issue:12	Discovery of potent furan piperazine sodium channel blockers for treatment of neuropathic pain.
AID106806	Inhibition of malate dehydrogenase (MDH) at 400 uM	2003	Journal of medicinal chemistry, Oct-09, Volume: 46, Issue:21	Identification and prediction of promiscuous aggregating inhibitors among known drugs.
AID352903	Inhibition of human Nav1.2 expressed in HEK293 cells assessed as change in membrane potential at 100 uM by patch clamp technique	2009	Journal of medicinal chemistry, May-14, Volume: 52, Issue:9	Oxadiazolylindazole sodium channel modulators are neuroprotective toward hippocampal neurones.
AID1058310	Inhibition of rat Nav1.2 expressed in CHL1610 cells at -67 to -107 mV after 2 to 3 mins by whole-cell patch-clamp assay	2013	Journal of medicinal chemistry, Nov-27, Volume: 56, Issue:22	Novel, broad-spectrum anticonvulsants containing a sulfamide group: pharmacological properties of (S)-N-[(6-chloro-2,3-dihydrobenzo[1,4]dioxin-2-yl)methyl]sulfamide (JNJ-26489112).
AID388886	Inhibition of Nav1.2 channel in HEK cells at 10 uM by patch clamp technique	2008	Bioorganic & medicinal chemistry letters, Oct-15, Volume: 18, Issue:20	2,4(5)-Diarylimidazoles: synthesis and biological evaluation of a new class of sodium channel blockers against hNa(v)1.2.
AID404553	Analgesic activity in po dosed Sprague-Dawley rat by rotarod test	2008	Bioorganic & medicinal chemistry, Jun-15, Volume: 16, Issue:12	Discovery of potent furan piperazine sodium channel blockers for treatment of neuropathic pain.
AID314682	Anticonvulsant activity in C57BL6J mouse assessed as prevention of shock-induced tonic-clonic seizures at 3 mg/kg, po after 30 mins	2008	Bioorganic & medicinal chemistry letters, Mar-15, Volume: 18, Issue:6	3-Amino-1,5-benzodiazepinones: potent, state-dependent sodium channel blockers with anti-epileptic activity.
AID604021	Unbound volume of distribution in Sprague-Dawley rat brain measured per gram of brain tissue administered in casettes of 2/3 drugs at 4 hr constant rate intravenous infusions using flow rate of 1 (ml/kg)/hr corresponding to dosage rate of 2 (umol/kg)/hr b	2009	Journal of medicinal chemistry, Oct-22, Volume: 52, Issue:20	Structure-brain exposure relationships in rat and human using a novel data set of unbound drug concentrations in brain interstitial and cerebrospinal fluids.
AID352877	Inhibition of voltage-gated sodium channel in Wistar rat forebrain synaptosomes assessed as inhibition of [14C]guanidium ion flux	2009	Journal of medicinal chemistry, May-14, Volume: 52, Issue:9	Oxadiazolylindazole sodium channel modulators are neuroprotective toward hippocampal neurones.
AID351545	Inhibition of human Nav1.2 channel expressed in HEK cells at 100 uM by patch-clamp electrophysiology method	2009	Bioorganic & medicinal chemistry, May-15, Volume: 17, Issue:10	2,4(5)-diarylimidazoles as inhibitors of hNaV1.2 sodium channels: pharmacological evaluation and structure-property relationships.
AID253081	Inhibition of native TTX-S sodium currents in acutely dissociated rat dorsal root ganglion (DRG)	2004	Journal of medicinal chemistry, Aug-12, Volume: 47, Issue:17	Phenoxyphenyl pyridines as novel state-dependent, high-potency sodium channel inhibitors.
AID115402	Percent inhibition of convulsions in audiogenic DBA/2 mice at dose 10 mg/kg	1998	Journal of medicinal chemistry, Jul-30, Volume: 41, Issue:16	Design, synthesis, and pharmacological evaluation of conformationally constrained analogues of N,N'-diaryl- and N-aryl-N-aralkylguanidines as potent inhibitors of neuronal Na+ channels.
AID286870	Effect on spontaneous pain in Sprague-Dawley rat SNL model assessed as duration of paw withdrawal at 100 mg/kg, ip after 0.5 hr	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID112459	Anticonvulsant potency using the PTX (picrotoxin) test in mice by peroral administration	1998	Journal of medicinal chemistry, Feb-12, Volume: 41, Issue:4	Synthesis and anticonvulsant activity of a new class of 2-[(arylalky)amino]alkanamide derivatives.
AID1473741	Inhibition 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 assay	2013	Toxicological 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.
AID699540	Inhibition of human liver OATP1B3 expressed in HEK293 Flp-In cells assessed as reduction in [3H]E17-betaG uptake at 20 uM incubated for 5 mins by scintillation counting	2012	Journal of medicinal chemistry, May-24, Volume: 55, Issue:10	Classification of inhibitors of hepatic organic anion transporting polypeptides (OATPs): influence of protein expression on drug-drug interactions.
AID604025	Unbound CSF to plasma concentration ratio in Sprague-Dawley rat administered in casettes of 2/3 drugs at 4 hr constant rate intravenous infusions using flow rate of 1 (ml/kg)/hr corresponding to dosage rate of 2 (umol/kg)/hr by LC-MS/MS method	2009	Journal of medicinal chemistry, Oct-22, Volume: 52, Issue:20	Structure-brain exposure relationships in rat and human using a novel data set of unbound drug concentrations in brain interstitial and cerebrospinal fluids.
AID286893	Anti-dynamic allodynia effect in Sprague-Dawley rat SNL model assessed as latency to paw withdrawal 100 mg/kg, ip after 2 hrs	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID286863	Effect on spontaneous pain in Sprague-Dawley rat CCI model assessed as duration of paw withdrawal at 100 mg/kg, ip after 2 hrs	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID1495419	Anticonvulsant activity in ip dosed albino CF-1 mouse assessed as protection against subcutaneous pentylenetetrazole-induced seizures measured after 1 hr
AID1079934	Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source]
AID625284	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic failure	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID205276	Inhibition of [3H]saxitoxin binding to rat brain sodium channel	1999	Bioorganic & medicinal chemistry letters, Sep-06, Volume: 9, Issue:17	Sodium channel activity and sigma binding of 2-aminopropanamide anticonvulsants.
AID152391	Inhibition of [3H]pentazocine binding to Opioid receptor sigma 1	1999	Bioorganic & medicinal chemistry letters, Sep-06, Volume: 9, Issue:17	Sodium channel activity and sigma binding of 2-aminopropanamide anticonvulsants.
AID286879	Antihyperalgesic effects in Sprague-Dawley rat SNL model assessed as duration of paw withdrawal at 100 mg/kg, ip after 2.5 hrs, ip	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID286886	Anti-cold allodynia effect in Sprague-Dawley rat CCI model assessed as duration of paw withdrawal 100 mg/kg, ip after 1 hr	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID342472	Inhibition of AQP4 in mouse erythrocytes assessed as inhibition of osmotic water permeability at 100 uM after 15 mins by stopped-flow light scattering method	2008	Bioorganic & medicinal chemistry, Aug-01, Volume: 16, Issue:15	Lack of aquaporin-4 water transport inhibition by antiepileptics and arylsulfonamides.
AID396415	Anticonvulsant activity in Swiss albino mouse assessed as inhibition of subcutaneous pentylenetetrazole-induced seizures at 300 mg/kg, ip administered 30 mins before PTZ challenge measured after 4 hrs post PTZ challenge	2008	European journal of medicinal chemistry, Dec, Volume: 43, Issue:12	Newer GABA derivatives for the treatment of epilepsy including febrile seizures: a bioisosteric approach.
AID318484	Analgesic activity in ip dosed rat chronic constriction injury model of mechanical allodynia	2007	Proceedings of the National Academy of Sciences of the United States of America, May-15, Volume: 104, Issue:20	A-803467, a potent and selective Nav1.8 sodium channel blocker, attenuates neuropathic and inflammatory pain in the rat.
AID286865	Antihyperalgesic effects in Sprague-Dawley rat CCI model assessed as duration of paw withdrawal at 100 mg/kg, ip after 0.5 hr	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID625279	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for bilirubinemia	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1207497	Inhibition of rapid delayed inward rectifying potassium current (IKr) in Chinese hamster ovary (CHO) cells stable expressing hERG measured using IonWorks Barracuda automated patch clamp platform
AID28681	Partition coefficient (logD6.5)	2000	Journal of medicinal chemistry, Jun-29, Volume: 43, Issue:13	QSAR model for drug human oral bioavailability.
AID286899	Anti-cold allodynia effect in Sprague-Dawley rat SNL model assessed as duration of paw withdrawal 100 mg/kg, ip after 2.5 hrs	2007	Journal of medicinal chemistry, May-17, Volume: 50, Issue:10	Discovery of 4-aminobutyric acid derivatives possessing anticonvulsant and antinociceptive activities: a hybrid pharmacophore approach.
AID678717	Inhibition of human CYP3A4 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using 7-benzyloxyquinoline as substrate after 30 mins	2012	Chemical research in toxicology, Oct-15, Volume: 25, Issue:10	Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID1209583	Unbound drug partitioning coefficient, Kp of the compound assessed as ratio of unbound concentration in Sprague-Dawley rat brain to unbound concentration in plasma	2011	Drug metabolism and disposition: the biological fate of chemicals, Mar, Volume: 39, Issue:3	Measurement of unbound drug exposure in brain: modeling of pH partitioning explains diverging results between the brain slice and brain homogenate methods.
AID504749	qHTS profiling for inhibitors of Plasmodium falciparum proliferation	2011	Science (New York, N.Y.), Aug-05, Volume: 333, Issue:6043	Chemical genomic profiling for antimalarial therapies, response signatures, and molecular targets.
AID1159607	Screen for inhibitors of RMI FANCM (MM2) intereaction	2016	Journal of biomolecular screening, Jul, Volume: 21, Issue:6	A High-Throughput Screening Strategy to Identify Protein-Protein Interaction Inhibitors That Block the Fanconi Anemia DNA Repair Pathway.
AID1224864	HCS microscopy assay (F508del-CFTR)	2016	PloS one, , Volume: 11, Issue:10	Increasing the Endoplasmic Reticulum Pool of the F508del Allele of the Cystic Fibrosis Transmembrane Conductance Regulator Leads to Greater Folding Correction by Small Molecule Therapeutics.
AID1794808	Fluorescence-based screening to identify small molecule inhibitors of Plasmodium falciparum apicoplast DNA polymerase (Pf-apPOL).	2014	Journal of biomolecular screening, Jul, Volume: 19, Issue:6	A High-Throughput Assay to Identify Inhibitors of the Apicoplast DNA Polymerase from Plasmodium falciparum.
AID1794808	Fluorescence-based screening to identify small molecule inhibitors of Plasmodium falciparum apicoplast DNA polymerase (Pf-apPOL).
AID1346731	Rat Nav1.2 (Voltage-gated sodium channels)	2003	Neuropharmacology, Mar, Volume: 44, Issue:3	Differential interactions of lamotrigine and related drugs with transmembrane segment IVS6 of voltage-gated sodium channels.
AID1346731	Rat Nav1.2 (Voltage-gated sodium channels)	1995	Pflugers Archiv : European journal of physiology, Jul, Volume: 430, Issue:3	Interaction of the antiepileptic drug lamotrigine with recombinant rat brain type IIA Na+ channels and with native Na+ channels in rat hippocampal neurones.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Timeframe	Studies, This Drug (%)	All Drugs %
pre-1990	9 (0.27)	18.7374
1990's	568 (16.94)	18.2507
2000's	1286 (38.35)	29.6817
2010's	1098 (32.75)	24.3611
2020's	392 (11.69)	2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Publication Type	This drug (%)	All Drugs (%)
Trials	501 (14.11%)	5.53%
Reviews	610 (17.18%)	6.00%
Case Studies	692 (19.49%)	4.05%
Observational	42 (1.18%)	0.25%
Other	1,705 (48.03%)	84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (189)

Trial Overview

Trial	Phase	Enrollment	Study Type	Start Date	Status
Monitoring of Specific Birth Defects Associated With Exposure to Lamotrigine in Pregnancy Through the EUROCAT Network [NCT01055327]		1 participants (Actual)	Observational	2009-05-31	Completed
Bariatric Surgery and Pharmacokinetics Lamotrigine: BAR-MEDS Lamotrigine [NCT03497143]		12 participants (Anticipated)	Observational	2016-11-02	Recruiting
A Multicenter, Open-label, Parallel-group Study in Study Participants With Epilepsy, to Evaluate the Effect of Oxcarbazepine on the Pharmacokinetics, Safety, and Tolerability of Padsevonil [NCT03695094]	Phase 1	31 participants (Actual)	Interventional	2018-09-18	Completed
The Efficacy of Lamotrigine in the Management of Chemotherapy-Induced Peripheral Neuropathy: A Phase III Randomized, Double Blind, Placebo-Controlled Trial [NCT00068445]	Phase 3	131 participants (Actual)	Interventional	2004-02-29	Completed
Single Dose Two-Way Crossover, Bioequivalence Study of Lamotrigine 25 mg Chewable Tablets With Lamictal 25 mg Chewable Tablets in Healthy Volunteers Under Fed Condition [NCT01131975]	Phase 1	26 participants (Actual)	Interventional	2003-01-31	Completed
Single-Dose Open-label Randomized Crossover, in Two Periods and in Two Sequences, Single-Center Comparative Bioequivalence Study of Two Formulations Lamotrigine, 100 mg Tablets (Pharmtechnology LLC, Republic of Belarus), and Lamictal®, 100 mg Tablets (Gla [NCT03898011]	Phase 1	28 participants (Actual)	Interventional	2019-03-23	Completed
An Open Label, Randomized, Cross-Over Study to Investigate the Single Dose Bioequivalence of Lamotrigine Dispersible/Chewable Tablets (5mg) Compared to Lamotrigine Compressed/Standard Tablets (25mg) in Chinese Healthy Male Subjects [NCT01357902]	Phase 1	24 participants (Actual)	Interventional	2011-04-18	Completed
A Randomized Controlled Trial of Generic Substitution of Antiepileptic Drugs [NCT02429596]	Phase 4	200 participants (Anticipated)	Interventional	2012-05-31	Recruiting
Efficacy and Tolerability of Low vs. Standard Daily Doses of Antiepileptic Drugs in Newly Diagnosed, Previously Untreated Epilepsy (STANDLOW). A Multicenter, Randomized, Single-blind, Parallel-group Trial [NCT03689114]	Phase 4	374 participants (Anticipated)	Interventional	2020-01-07	Not yet recruiting
A Pilot Study of Prophylactic Management of Lamotrigine for Bipolar Disorder in Pregnant Women [NCT03774641]		20 participants (Anticipated)	Observational	2018-12-03	Recruiting
Continuation Riluzole in the Prevention of Relapse Following Ketamine in Major Depression [NCT00419003]	Phase 4	26 participants (Actual)	Interventional	2006-12-31	Completed
An Open-label Study to Evaluate the Pharmacokinetics, Safety and Tolerability of Repeat Dosing Lamotrigine in Healthy Chinese Subjects [NCT02513654]	Phase 1	16 participants (Actual)	Interventional	2015-09-06	Completed
Randomized, 2-Way, Crossover, Bioequivalence Study of Lamotrigine 200 mg Tablets and Lamictal® 200 mg Tablets Administered as 1 x 200 mg Tablet in Healthy Subjects Under Fed Conditions [NCT00835263]	Phase 1	32 participants (Actual)	Interventional	2002-01-31	Completed
Randomized, Two-Way Crossover, Single-Dose, Fasting Bioequivalence Study of Lamotrigine 1 x 200 mg Tablet [NCT00834561]	Phase 1	32 participants (Actual)	Interventional	2002-01-31	Completed
A Phase 1, Open-label Drug Interaction Study Between Eslicarbazepine Acetate 1200mg and Lamotrigine 150mg Following Multiple Doses Administrations in Healthy Male Volunteers [NCT02283801]	Phase 1	32 participants (Actual)	Interventional	2006-11-30	Completed
Protocol Establishment for the Prevention of Lamotrigine-induced Skin Rash in Epilepsy Patients: A Pilot Study [NCT03220256]	Phase 2	30 participants (Anticipated)	Interventional	2016-08-02	Recruiting
Comparison of Oral Lamotrigine Versus Pregabalin for Control of Acute and Chronic Pain Following Modified Radical Mastectomy: Controlled Double-blind Study [NCT03419949]		0 participants	Expanded Access		Available
Lamotrigine as an Antidepressant Augmentation Agent in Treatment Refractory Unipolar Depression [NCT00901407]		138 participants (Actual)	Interventional	2003-12-31	Completed
Randomized, 2-Way Crossover, Bioequivalence Study of Lamotrigine 25 mg Chewable Dispersible Tablets and Lamictal® 25 mg Chewable Dispersible Tablets in Healthy Subjects Under Fed Conditions [NCT00838136]	Phase 1	32 participants (Actual)	Interventional	2002-02-28	Completed
A Prospective, Randomized, Double-Blind, Placebo-Controlled, Phase 2 Safety and Efficacy Study of Oral ELND005 as an Adjunctive Maintenance Treatment in Patients With Bipolar I Disorder [NCT01674010]	Phase 2	309 participants (Actual)	Interventional	2012-08-31	Terminated(stopped due to Business Decision)
Effect of Adding Lamotrigine to Sodium Valproate in Childhood Epilepsy: Clinicolabratory Study [NCT05881928]	Phase 4	50 participants (Anticipated)	Interventional	2023-07-25	Not yet recruiting
A Single-Dose, Open-Label, Randomized, Parallel-Group Study to Demonstrate the Bioequivalence of Lamotrigine Dispersible/Chewable Tablet (100mg) and Lamotrigine Compressed Tablet (100mg) in Healthy Chinese Male Subjects [NCT02064465]	Phase 1	138 participants (Actual)	Interventional	2014-03-15	Completed
Interaction Between Paracetamol and Lamotrigine: A Clinical Interaction Study. [NCT02303106]	Phase 4	12 participants (Actual)	Interventional	2014-11-30	Completed
The Effect of Lamotrigine on Cognitive Deficits Associated With Neurofibromatosis Type 1: a Phase II Randomized Controlled Multi-centre Trial (NF1-EXCEL) [NCT02256124]	Phase 2/Phase 3	41 participants (Actual)	Interventional	2014-10-31	Terminated(stopped due to Due to our experience, the small number of new inclusions, and the uncertainty regarding the COVID-19 outbreak, we have decided to discontinue the study.)
An Open-label, Two-cohort Study to Assess the Effect of Lamotrigine and Phenytoin on the Pharmacokinetics of Atorvastatin in Healthy Subjects [NCT00627575]	Phase 1	119 participants (Actual)	Interventional	2008-02-04	Completed
Drugs in Breast Milk [NCT05543122]		304 participants (Anticipated)	Observational	2022-03-09	Recruiting
Single Dose Two-Way Crossover, Bioequivalence Study of Lamotrigine 25 mg Chewable Tablets With Lamictal 25 mg Chewable Tablets in Healthy Volunteers Under Fasting Condition [NCT01131949]	Phase 1	26 participants (Actual)	Interventional	2003-01-31	Completed
Drug Use Investigation for LAMICTAL [NCT01376180]		3,000 participants (Actual)	Observational	2008-12-31	Completed
CSP #428 - Treatment of Seizures in the Elderly Population [NCT00007670]	Phase 3	720 participants	Interventional	1998-01-31	Completed
A Double-Blind Study of Lamictal in Neurotic Excoriation [NCT00513019]	Phase 2	35 participants (Actual)	Interventional	2007-08-31	Completed
A Trial to Study Acute and Delayed Effects of a Single Dose of Ketamine on Functional Brain Changes During Emotional/ Cognitive Challenges and at Rest and Their Modulation by Lamotrigine in Healthy Subjects [NCT04156035]		75 participants (Actual)	Interventional	2020-03-10	Completed
Lamotrigine in Trigeminal Neuralgia: Efficacy and Safety in Comparison With Carbamazepine [NCT00913107]	Phase 2/Phase 3	21 participants (Actual)	Interventional	2007-09-30	Completed
Special Drug Use Investigation for LAMICTAL (Long Term) [NCT01863602]		850 participants (Actual)	Observational	2009-04-30	Completed
Study of Lamotrigine Treatment of Affective Instability in Borderline Personality Disorder [NCT00634062]	Phase 4	28 participants (Actual)	Interventional	2004-12-31	Completed
A Phase III, Randomised, Double Blinded, Head-to-head, Single-site, Cross-over Trial of Lamotrigine Versus Mexiletine for Non-dystrophic Myotonias [NCT05017155]	Phase 3	60 participants (Anticipated)	Interventional	2021-08-12	Recruiting
A Randomised Controlled Trial of the Ketogenic Diet in the Treatment of Epilepsy in Children Under the Age of Two Years [NCT02205931]	Phase 4	160 participants (Anticipated)	Interventional	2015-01-31	Recruiting
Randomized, 2-Way Crossover, Bioequivalence Study of Lamotrigine 25 mg Chewable Dispersible Tablets and Lamictal® 25 mg Chewable Dispersible Tablets in Healthy Subjects Under Fasting Conditions [NCT00838279]	Phase 1	32 participants (Actual)	Interventional	2002-02-28	Completed
A Single Center, Open Label, Randomized, Single-dose, 2 Way Cross-over Study to Explore the Bioequivalence of Lamnet (Lamotrigine)100mg Tablet With the Reference Product Lamictal 100mg (Lamotrigine) Tablet Under Fasting Conditions in Healthy Male Pakistan [NCT04938856]	Phase 1	26 participants (Actual)	Interventional	2020-09-04	Completed
Inositol Hexaphosphate: A Novel Treatment Strategy for Bipolar Disorder? [NCT02081287]	Phase 1	8 participants (Actual)	Interventional	2014-05-31	Completed
Characterization of Epilepsy Patients At-risk for Adverse Outcomes Related to Switching Antiepileptic Drug Products: BEEP 2b Study [NCT02707965]	Phase 1	21 participants (Actual)	Interventional	2017-06-08	Completed
The Efficacy and Safety of First-Line Anti-Epileptic Drugs (AEDs) as Substitution Therapy in Children Who Are Resistant to Second-Line AEDs [NCT05697614]	Phase 4	100 participants (Anticipated)	Interventional	2023-03-01	Recruiting
The BrainDrugs-Epilepsy Study: A Prospective Open-label Cohort Precision Medicine Study in Epilepsy [NCT05450822]		550 participants (Anticipated)	Observational	2022-02-18	Recruiting
A Randomized, Open Label, Single Dose, Crossover, Bioequivalence Study of Lamotrigine 2 x 25 mg IR Tablets of Torrent Pharmaceuticals Pvt., Ltd., India and Lamictal ® (Lamotrigine) 2 x 25 mg Tablets of Glaxo-SmithKline, USA, in Healthy Human Adult Subject [NCT00939458]	Phase 1	0 participants	Interventional		Completed
A Randomized, Open Label, Single Dose, Crossover, Bioequivalence Study of Lamotrigine 2×25 mg IR Tablets of Torrent Pharmaceuticals Limited., India and Lamictal® (Lamotrigine) 2×25 mg Tablets of GlaxoSmithKline, USA, in Healthy Human Adult Subjects, Under [NCT00939614]	Phase 1	0 participants	Interventional		Completed
A Pilot Open Study of the Safety and Effectiveness of Lamotrigine for the Treatment of Mania in Youth Ages 6-17 With Bipolar I, Bipolar II, and Bipolar Spectrum Disorders [NCT00181844]	Phase 4	51 participants (Actual)	Interventional	2005-01-31	Completed
A Phase 1, Open-label Study to Evaluate the Effect of AG-881 on the Pharmacokinetics of a Single Dose of Lamotrigine in Healthy Adult Subjects [NCT04015687]	Phase 1	22 participants (Actual)	Interventional	2019-07-15	Completed
Comparison of Olanzapine and Lamotrigine in the Prevention of Recurrence of Depressive Episode in the Patients With Bipolar Disorders [NCT01864551]	Phase 4	60 participants (Actual)	Interventional	2008-08-31	Completed
Treatment for Bipolar Depression: Acute & Prophylactic Efficacy With Citalopram [NCT00562861]	Phase 2/Phase 3	119 participants (Actual)	Interventional	2007-11-30	Completed
Single-Dose Food In Vivo Bioequivalence Study of Lamotrigine Tablets (25 mg; Mylan) to Lamictal® Tablets (25 mg; GSK) in Healthy Volunteers [NCT00647751]	Phase 1	28 participants (Actual)	Interventional	2004-08-31	Completed
Single-Dose Fasting In Vivo Bioequivalence Study of Lamotrigine Tablets (25 mg; Mylan) to Lamictal® Tablets (25 mg; GSK) in Healthy Volunteers [NCT00650208]	Phase 1	27 participants (Actual)	Interventional	2004-07-31	Completed
An Open-Label Trial Measuring Satisfaction and Convenience of Two Formulations of Lamotrigine in Subjects With a Mood Disorder [NCT00579982]	Phase 3	97 participants (Actual)	Interventional	2008-01-31	Completed
An Open, Randomized, Multicenter Comparative Clinical Trial of Lamotrigine or Carbamazepine for Cognitive Function as Initial Monotherapy in Adult Untreated Epilepsies [NCT00896987]	Phase 4	121 participants (Actual)	Interventional	2006-05-31	Completed
Double Blind, Double-dummy, Randomised, Placebo Controlled Study to Evaluate the Effect of Single Doses of Drug A (Lamotrigine) and Drug B (Vofopitant) Alone and in Combination on Resting Motor Threshold in Healthy Subjects [NCT00907985]	Phase 1	12 participants (Actual)	Interventional	2009-05-15	Terminated(stopped due to Slow recruitment; trial unlikely to reach completion)
The Effect of Lamictal TM Augmentation of Haloperidol Decanoate in the Treatment of Resistant Schizophrenia Predominantly by Verbal Resistant Hallucinosis: Randomized, Double-blind, Placebo-controlled, Study [NCT00947375]	Phase 4	335 participants (Actual)	Interventional	2005-01-31	Terminated(stopped due to All of the mentioned aim and objectives were achieved before the February 2007)
A Multicenter, Double-blind, Randomized, Parallel-group Evaluation of LAMICTAL Extended-Release Adjunctive Therapy in Patients With Primary Generalized Tonic-Clonic Seizures [NCT00104416]	Phase 3	153 participants (Actual)	Interventional	2004-12-31	Completed
The Evaluation of Lamictal as an Add-on Treatment for Bipolar I Disorder in Children and Adolescents, 10 to 17 Years of Age [NCT00723450]	Phase 3	301 participants (Actual)	Interventional	2008-07-31	Completed
Efficacy and Safety of Antidepressant Augmentation With Lamotrigine in Patients With Treatment-Resistant Depression [NCT00652171]	Phase 3	34 participants (Actual)	Interventional	2004-01-31	Completed
A Double-Blind, Placebo-Controlled, Add-On Clinical Trial of the Safety, Pharmacokinetics and Efficacy of Lamictal in Pediatric Age Subjects (1-24 Months) [NCT00043875]	Phase 2	177 participants (Actual)	Interventional	2000-05-31	Completed
A Phase 1/2,Open-Label Study to Evaluate the Safety and Efficacy of the International Brain Research Foundation (IBRF) Disorders of Consciousness Advanced Care/MultiModal Care Protocol in Patients With Severe Disorders of Consciousness [NCT02696512]	Phase 1/Phase 2	30 participants (Anticipated)	Interventional	2016-03-31	Recruiting
Study SCA106052, a Clinical Evaluation of BW430C (Lamotrigine) in Bipolar I Disorder- Long-term Extension Study (Extension of Study SCA104779 (NCT00550407)) [NCT00566020]	Phase 3	92 participants (Actual)	Interventional	2008-05-31	Completed
Lamotrigine for Ketamine Dependence: A Randomized, Double-Blind, Placebo-Controlled Trial [NCT02556060]	Phase 2/Phase 3	30 participants (Actual)	Interventional	2015-09-30	Completed
Physiological-based Pharmacokinetics Approach to Determine the Extent of Drug Exposure of Antiseizure Medications During Pregnancy and Breastfeeding [NCT05450978]		60 participants (Anticipated)	Observational [Patient Registry]	2022-07-20	Recruiting
A Study to Investigate the Effect of Antidepressants on the Treatment for Korean Major Depressive Disorder (MDD) Patients [NCT00926835]	Phase 4	692 participants (Actual)	Interventional	2009-05-31	Terminated(stopped due to due to patient recruitment difficulties)
Lithium Versus Lamotrigine in Bipolar Disorder, Type II - a Single Blinded Randomized Controlled Trial (the LiLa-Bipolar RCT) [NCT06184581]	Phase 4	200 participants (Anticipated)	Interventional	2024-03-01	Not yet recruiting
An Open Label, Balanced, Randomized, Two-treatment, Two-period, Two-sequence, Single Dose, Crossover, Oral Bioequivalence Study in Healthy, Adult, Human Subjects Under Fasting Conditions. [NCT01888250]	Phase 1	36 participants (Actual)	Interventional	2010-08-31	Completed
Study SCA104779, an Evaluation of BW430C (Lamotrigine) Versus Placebo in the Prevention of Mood Episodes in Bipolar I Disorder Patients [NCT00550407]	Phase 3	215 participants (Actual)	Interventional	2007-11-30	Completed
Treatment of Myotonia - Lamotrigine Versus Namuscla [NCT05639257]		32 participants (Anticipated)	Interventional	2022-12-05	Recruiting
CREST-I: Resperine, Gabapentin, or Lamotrigine vs. Placebo [NCT00015106]	Phase 2	0 participants	Interventional	1997-11-30	Completed
Evaluation of Lamotrigine (Lamictal® (Registered Trademark)) Monotherapy and Gabapentin (Neurontin® (Registered Trademark)) Monotherapy in the Treatment of Mood Disorders [NCT00001482]	Phase 2	60 participants	Interventional	1995-05-31	Completed
Evaluation of Lamotrigine in Subjects With Absence Seizures [NCT00144872]	Phase 1	54 participants (Actual)	Interventional	2004-11-01	Completed
Double-Blind, Acute Depression Study Comparing Venlafaxine XR and Lamotrigine When Added to Mood Stabilizer in the Treatment of Bipolar Depression [NCT00188643]	Phase 4	40 participants	Interventional	2002-01-31	Completed
A Study for Evaluating the Efficacy and Safety of Zonisamide and Lamotrigine (Lamictal) for Subjects With Refractory Simple Partial, Complex Partial or Partial With Secondary Generalized Seizures [NCT00292461]	Phase 3	64 participants (Actual)	Interventional	2006-03-31	Completed
A Randomized, Double-blind, Placebo-controlled, Trial of Lamotrigine add-on Therapy in Outpatients With Bipolar Disorder, Depressed or Mixed Phase and Cocaine Dependence [NCT00280293]	Phase 4	112 participants (Actual)	Interventional	2006-03-31	Completed
A Randomized, Comparative, Double-Blind, Parallel-Group, Multicenter, Monotherapy, Study Of Pregabalin (Lyrica) And Lamotrigine (Lamictal) In Patients With Newly Diagnosed Partial Seizures [NCT00280059]	Phase 3	660 participants (Actual)	Interventional	2006-08-31	Completed
Clinical Evaluation of BW430C in Epilepsy [NCT00395694]	Phase 3	102 participants (Actual)	Interventional	2006-08-07	Completed
A Multicenter, Double-Blind, Randomized Conversion to Monotherapy Comparison of Two Doses of Lamotrigine for the Treatment of Partial Seizures [NCT00355082]	Phase 3	226 participants (Actual)	Interventional	2006-05-31	Completed
A Multicenter, Double-blind, Study of the Efficacy and Safety of Aripiprazole in Combination With Lamotrigine in the Long-term Maintenance Treatment of Patients With Bipolar I Disorder With a Recent Manic or Mixed Episode [NCT00277212]	Phase 4	1,169 participants (Actual)	Interventional	2005-12-31	Completed
A Single-Dose, Open-Label, Randomized, Two-Period Crossover Study to Demonstrate the Bioequivalence of Lamotrigine Dispersible/Chewable Tablets (5mg×5) and Lamotrigine Compressed Tablet (25mg) in Healthy Chinese Male Subjects. [NCT01879423]	Phase 1	24 participants (Actual)	Interventional	2013-04-28	Completed
Lamictal As Add on Treatment in Mixed States of Bipolar Disorder [NCT00223509]	Phase 4	28 participants (Actual)	Interventional	2005-08-31	Completed
An Open Label, Balanced, Randomized, Two-treatment, Two-period, Two-sequence, Single Dose, Crossover, Oral Bioequivalence Study in Healthy, Adult, Human Subjects Under Fed Conditions. [NCT01888263]	Phase 1	32 participants (Actual)	Interventional	2010-08-31	Completed
An Open Label, Balanced, Randomized, Two-treatment, Two-period, Two-sequence, Single Dose, Crossover, Oral Bioequivalence Study in Healthy, Adult, Human Subjects Under Fasting Conditions. [NCT01888731]	Phase 1	62 participants (Actual)	Interventional	2010-08-31	Completed
An Open Label, Balanced, Randomized, Two-treatment, Two-period, Two-sequence, Single Dose, Crossover, Oral Bioequivalence Study in Healthy, Adult, Human Subjects Under Fed Conditions. [NCT01888757]	Phase 1	62 participants (Actual)	Interventional	2010-09-30	Completed
A Randomized Open-Label 6 Month Acute and Maintenance Trial of Lamotrigine vs. Standard of Care Sodium Valproate Monotherapy for Treatment of Mixed Mania. [NCT00206778]	Phase 2	36 participants (Anticipated)	Interventional	2003-07-31	Completed
Lamotrigine as Treatment of Myotonia - a Phase 3 Randomized Controlled Trial Study [NCT01939561]	Phase 3	27 participants (Actual)	Interventional	2013-11-30	Completed
Second-Line Treatment Choice for Epilepsy [NCT00208520]		60 participants	Interventional	2003-07-31	Active, not recruiting
Combination Therapy in Dual Diagnosis Rapid Cycling Bipolar Disorder [NCT00221975]	Phase 3	98 participants (Actual)	Interventional	2002-07-31	Completed
A Mulitcentre, Double-blind, Randomised, Fixed-dose Evaluation of the Safety and Efficacy of Lamictal (Lamotrigine) Compared to Placebo as an add-on Therapy to Lithium or Another Mood Stabiliser in the Treatment of Bipolar Depression, Followed by Long-ter [NCT00224510]	Phase 3	120 participants (Actual)	Interventional	2002-08-31	Completed
The Use of Anticonvulsants for Treatment of Patients With Alcohol Dependence and Post Traumatic Stress Disorder [NCT00571246]	Phase 3	0 participants (Actual)	Interventional	2012-06-30	Withdrawn
A Pivotal, Single-Dose, Randomised, Parallel-Group, Open-Label Study to Demonstrate Bioequivalence of 250mg Lamotrigine XR Relative to 200mg + 50mg Lamotrigine XR and to Demonstrate Lack of Food Effect on 250mg Lamotrigine XR in Healthy Male and Female Vo [NCT00605371]	Phase 1	209 participants (Actual)	Interventional	2008-01-15	Completed
A Randomised, Double-blind Study in Healthy Volunteers to Compare the Properties and Characteristics of an Investigational Formulation of Lamotrigine With Placebo [NCT01607086]	Phase 1	24 participants (Actual)	Interventional	2008-07-11	Completed
Longitudinal Comparative Effectiveness of Bipolar Disorder Therapies [NCT02893371]		1,037,352 participants (Actual)	Observational	2016-09-30	Completed
WEUKBRE5557: IMI PROTECT (Work Package 2): Use of Antiepileptics and Risk of Suicidality [NCT01607333]		1 participants (Actual)	Observational	2011-12-31	Completed
Lamotrigine Extended-Release in Elderly Patients With Epilepsy [NCT00516139]	Phase 3	122 participants (Actual)	Interventional	2007-08-31	Completed
Liceo Study: A Prospective, Observational Study On The Effectiveness Of New Antiepileptic Drugs As First Bitherapy In The Daily Clinical Practice [NCT00855738]	Phase 4	111 participants (Actual)	Interventional	2007-05-31	Completed
The Influence of Raltegravir (MK-0518) on the Pharmacokinetics of Single-dose Lamotrigine in Healthy Male Subjects (GRANOLA) [NCT00618241]	Phase 1	24 participants (Actual)	Interventional	2008-02-29	Completed
Cognitive Effects of Treatment of Interictal Discharges [NCT00916149]		31 participants (Actual)	Interventional	2007-01-31	Completed
Proof-of-Concept Clinical Trial of Lamotrigine as a Candidate Pharmacotherapy for Adolescent Alcohol Use Disorder [NCT04770493]	Phase 2	50 participants (Anticipated)	Interventional	2022-01-24	Recruiting
Special Drug Use Investigation for LAMICTAL Bipolar [NCT01428518]		1,036 participants (Actual)	Observational	2011-11-30	Completed
Treatment of Geriatric Bipolar Mood Disorders: A Pilot Study [NCT00177567]	Phase 4	60 participants	Interventional	2001-07-31	Completed
A Multicenter, Randomized, Double-Blind, Parallel Group Study to Evaluate the Efficacy and Safety of a Flexible Dose of Lamotrigine Compared to Placebo as an Adjunctive Therapy to an Atypical Antipsychotic Agent(s) in Subjects With Schizophrenia [NCT00086593]	Phase 3	209 participants (Actual)	Interventional	2004-05-31	Completed
Lamotrigine for Ménière's Disease: a Double-blind, Placebo-controlled Pilot Study [NCT02158585]	Phase 2	15 participants (Actual)	Interventional	2014-06-30	Completed
A Multi-Center, Double-Blind, Randomized, Placebo-Controlled, Parallel-Group Evaluation of Lamotrigine Adjunctive Therapy in Subjects Wtih Primary Generalized Tonic-Clonic Seizures [NCT00043901]	Phase 4	141 participants (Actual)	Interventional	2000-12-01	Completed
Open-label, Prospective Trial of Lamotrigine for Symptoms of Geriatric Bipolar Depression [NCT00621842]	Phase 3	57 participants (Actual)	Interventional	2008-01-31	Completed
Randomized, Placebo-Controlled Phase II Monocentric Trial for the Neuroprotective Effect of Lamotrigine Plus Interferon Beta 1a 30mcg Once Weekly Intramuscular in Patients With Relapsing-Remitting Multiple Sclerosis. [NCT00917839]	Phase 2	88 participants (Anticipated)	Interventional	2009-06-30	Recruiting
Lamotrigine Pregnancy Registry (LAM05) [NCT01064297]		3,416 participants (Actual)	Observational	2001-11-30	Completed
An Open-label, Randomised, Single-dose, Parallel-group Study to Demonstrate Bioequivalence of Two Formulations and the Effect of Food and Water on One Formulation of Lamotrigine in Healthy Male and Female Volunteers [NCT00449774]	Phase 1	220 participants (Actual)	Interventional	2007-05-07	Completed
A Multi-centre, Observational Study to Evaluate the Incidence of Non-serious Rash in Korean Bipolar I Patients With Lamotrigine Therapy in Real World Setting [NCT00460226]		238 participants (Actual)	Observational	2007-03-31	Completed
Single Dose Two Way Crossover Comparative Bioavailability Study of Lamotrigine Extended-Release Tablets USP 50 mg in Healthy Male and Female Volunteers Fasting State [NCT05145608]	Phase 1	22 participants (Actual)	Interventional	2018-01-10	Completed
A Randomized, 2-Sequence, 2-Treatment, 4-Period, Open-Label, Single Dose, Fully Replicated Comparative Bioavailability Crossover Study of Two Formulations of Lamotrigine Extended Release Tablets in Healthy Subjects Under Fed Conditions [NCT02821338]	Phase 1	30 participants (Actual)	Interventional	2016-06-30	Completed
Neurobiology of Opioid Dependence: 1 [NCT00000192]	Phase 2	0 participants (Actual)	Interventional	1993-01-31	Withdrawn
A Multi-Center, Double Blind, Placebo-controlled, Randomized, Parallel Group Evaluation of the Efficacy of a Flexible Dose of Lamotrigine Versus Placebo As Add-On Therapy In Schizophrenia [NCT00071747]	Phase 3	176 participants	Interventional	2003-08-31	Completed
Phase 3: Metabolism of Lamotrigine During Treatment With Oral Contraceptives [NCT00266149]	Phase 3	10 participants	Interventional	2003-06-30	Terminated
Lamotrigine Use in Treatment Refractory Depression in Adolescents [NCT00284791]		50 participants	Interventional	2006-01-31	Terminated
Hormone Profiles in Adults Treated With Valproate vs. Lamotrigine Monotherapy for Newly Diagnosed Epilepsy: A Prospective Randomised Study [NCT00137709]	Phase 4	80 participants (Anticipated)	Interventional	2004-11-30	Recruiting
A Multicenter, Double-Blind, Randomized, Parallel-group Evaluation of LAMICTAL Extended-release Adjunctive Therapy in Subjects With Partial Seizures [NCT00113165]	Phase 3	244 participants (Actual)	Interventional	2004-10-31	Completed
Double Blind, Randomised, Placebo Controlled Study to Evaluate the Safety, Tolerability and Pharmacokinetics of Single Doses of GSK Drug and the Effect of Single Doses of GSK Drug or Lamotrigine on Resting Motor Threshold in Healthy Volunteers [NCT00488566]	Phase 1	50 participants (Actual)	Interventional	2007-05-31	Completed
Reversing Corticosteroid Induced Memory Impairment [NCT01142310]	Phase 4	54 participants (Actual)	Interventional	2010-06-30	Completed
A Randomized, Prospective, Double-Blind, Placebo-Controlled, Pilot Study to Assess the Effectiveness of a Combination of Lamotrigine and Bupropion to Treat Meniere's Disease [NCT05420350]	Phase 2	34 participants (Anticipated)	Interventional	2020-12-16	Recruiting
A Pivotal Single-dose Randomised, Parallel-group, Open-label Study to Demonstrate Bioequivalence of 300mg Lamotrigine XR Relative to 100mg + 200mg Lamotrigine XR and to Demonstrate Lack of Food Effect on 300mg Lamotrigine XR in Healthy Male and Female Vol [NCT00412191]	Phase 1	180 participants (Actual)	Interventional	2007-02-06	Completed
A Randomized, Single-Blind Comparison of Lamotrigine Add-on Versus Switch to Lamotrigine Monotherapy in the Treatment of Bipolar II Depression Unresponsive to Antidepressant Treatment [NCT00475137]	Phase 2	15 participants (Actual)	Interventional	2007-12-31	Completed
Olanzapine/Fluoxetine Combination Versus Lamotrigine in the Treatment of Bipolar I Depression [NCT00485771]	Phase 4	403 participants (Actual)	Interventional	2003-11-30	Completed
Single Dose, Two-way, Crossover, Oral Bioequivalence Study of Lamotrigine Tablets 200 mg With Lamictal® Tablets 200 mg in Healthy, Volunteers Under Fed Condition. [NCT01513681]	Phase 1	20 participants (Actual)	Interventional	2002-11-30	Completed
Single Dose, Two-way, Crossover, Oral Bioequivalence Study of Lamotrigine Tablets 200 mg With Lamictal® Tablets 200 mg in Healthy, Volunteers Under Fasting Condition. [NCT01513720]	Phase 1	20 participants (Actual)	Interventional	2002-12-31	Completed
A Randomised, Controlled Trial to Investigate the Effect of a Six Week Intensified Pharmacological Treatment for Bipolar Depression Compared to Treatment as Usual in Subjects Who Had a First-time Treatment Failure on Their First-line Treatment. [NCT05973786]	Phase 4	418 participants (Anticipated)	Interventional	2023-11-01	Not yet recruiting
Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD) [NCT00012558]		5,000 participants	Interventional	1998-09-30	Completed
An Open-Label, Uncontrolled, Long-Term Study to Assess the Safety of LAMICTAL in Pediatric Subjects Previously Enrolled in Protocol LAM20006 and In LAMICTAL-naive Subjects (1-24 Months of Age) [NCT00044278]	Phase 2	197 participants (Actual)	Interventional	2000-09-30	Completed
Acute Treatment of Bipolar II Depression [NCT00074776]	Phase 3	102 participants (Actual)	Interventional	2003-05-31	Completed
Double Blind Placebo Controlled Study of Lamictal in Acute Bipolar Depression [NCT00056277]	Phase 3	150 participants (Actual)	Interventional	2003-02-27	Completed
Lamictal for Use in Treatment of Bipolar Disorder In Adults. A Practical Clinical Assessment of Tolerability and Clinical Effectiveness. [NCT00067938]	Phase 4	1,200 participants (Actual)	Interventional	2003-08-31	Completed
Lamotrigine Therapy in the Treatment of Geriatric Bipolar Depression: An Evaluation of Markers of Cerebral Energy Metabolism [NCT00720473]		69 participants (Actual)	Interventional	2006-04-30	Completed
Randomised, Placebo Controlled, Double Blind, Parallel Group 3-Months Study of Lamotrigine Efficacy in Asthma Therapy [NCT00153244]	Phase 4	76 participants	Interventional	2002-08-31	Completed
A Multicenter, Open-Label Conversion of Valproate Monotherapy to Lamotrigine Monotherapy in Patients With Epilepsy [NCT00043914]	Phase 4	72 participants	Interventional	2002-01-14	Completed
An Open-label, Randomised, Single-dose, Parallel-group Study to Evaluate the Pharmacokinetic Characteristics, Safety and Tolerability of up to Two Formulations (With Different Taste Masking Approaches) of an Orally Disintegrating Tablet (ODT) of Lamotrigi [NCT00410371]	Phase 1	96 participants (Actual)	Interventional	2006-12-28	Completed
Lamotrigine Versus Lithium in Subjects With Bipolar Affective Disorders - a Randomised Study of Prophylactic Effect [NCT00226135]	Phase 3	150 participants	Interventional	2001-03-31	Completed
A Multicentre, Double-blind, Randomized, Phase IV Clinical Trial Comparing the Safety, Tolerability and Efficacy of Levetiracetam Versus Lamotrigine and Carbamazepine in the Oral Antiepileptic Therapy of Newly Diagnosed Elderly Patients With Focal Epileps [NCT00438451]	Phase 4	361 participants (Actual)	Interventional	2007-01-31	Completed
Comparison of Different Antiepileptic Drug Monotherapies for the Occurrence of Premenstrual Dysphoric Disorder Among Women With Epilepsy [NCT00612235]		80 participants (Actual)	Observational	2008-04-30	Completed
Determination of Bioavailability and Clearance of Lamotrigine-XR by a Stable Isotope Technique [NCT00789113]	Phase 1/Phase 2	12 participants (Actual)	Interventional	2008-11-30	Completed
An Open Label, Randomized, Multicenter Clinical Trial to Compare the Efficacy and Safety of Lamotrigine / Valproate Coadministration and Carbamazepine as Initial Pharmacotherapy in Epilepsies (Phase Ⅳ) [NCT00807989]	Phase 4	207 participants (Actual)	Interventional	2008-03-31	Completed
An Open-label, Double Conversion Study to Characterize the Pharmacokinetics of Lamotrigine When Switching Patients With Epilepsy on LAMICTAL Immediate-release to Extended-release Formulation and Vice Versa [NCT00264615]	Phase 3	45 participants	Interventional	2005-10-31	Completed
Lamotrigine Versus Levetiracetam in the Initial Monotherapy of Epilepsy: An Open, Prospective, Multicenter, Randomized Phase III Study [NCT00242606]	Phase 3	409 participants (Actual)	Interventional	2005-03-31	Completed
A Multicenter, Double-Blind, Placebo-Controlled, Fixed-Dose, 8-Week Evaluation of the Efficacy and Safety of Lamotrigine in the Treatment of Depression in Patients With Type II Bipolar Disorder [NCT00274677]	Phase 3	221 participants (Actual)	Interventional	2003-11-30	Completed
Lamotrigine in the Treatment of Binge Eating Disorder Associated With Obesity: A Single-Center, Double-Blind, Placebo-Controlled, Flexible-Dose Study in Outpatients [NCT00277641]	Phase 3	70 participants (Anticipated)	Interventional	2006-03-31	Completed
A Randomised Controlled Trial of Neuroprotection With Lamotrigine in Secondary Progressive Multiple Sclerosis: Single Centre, Phase 2 Trial [NCT00257855]	Phase 2	120 participants	Interventional	2005-11-30	Completed
Validation Of Qolie-10 For Epilepsy, Comparison Of Quality Of Life In Patients Treated With Lamotrigine Or Valproic Acid [NCT00264680]		333 participants (Actual)	Observational	2003-10-01	Completed
Lamictal in the Treatment of Post-Herpetic Neuralgia-A Safety, Efficacy,Randomized, Double Blind, Placebo Controlled, Cross-Over Study [NCT00295776]	Phase 2/Phase 3	0 participants	Interventional	2005-02-28	Terminated(stopped due to enrollment difficult due to inclusion/exclusion criteria/protocol requirements)
An Open-Label Study of Lamictal In Neurotic Excoriation [NCT00269594]	Phase 2	25 participants (Actual)	Interventional	2006-01-31	Completed
An Open Label, Randomized, Two-Period, Two-Treatment, Two-Sequence, Crossover, Balanced, Single Dose Oral Bioequivalence Study of Lamotrigine Tablets 25 mg (2 × 25 mg Tablets) and 'LAMICTAL®' (Lamotrigine) Tablets 25 mg (2 × 25 mg Tablets) in Healthy Adul [NCT01618799]	Phase 1	28 participants (Actual)	Interventional	2012-03-31	Completed
An Open Label, Randomized, Two-Period, Two-Treatment, Two-Sequence, Crossover, Balanced, Single Dose Oral Bioequivalence Study of Lamotrigine Tablets 25 mg (2 × 25 mg Tablets) and 'LAMICTAL®' (Lamotrigine) Tablets 25 mg (2 × 25 mg Tablets) in Healthy Adul [NCT01618825]	Phase 1	28 participants (Actual)	Interventional	2012-03-31	Completed
WEUSKOP6166: Prevalence of Aseptic Meningitis Among Lamotrigine Users [NCT01657864]		1 participants (Actual)	Observational	2012-05-31	Completed
Decision-Making in Bipolar Disorder [NCT01463111]		37 participants (Actual)	Interventional	2011-05-31	Completed
Equivalence Among Antiepileptic Drug Generic and Brand Products in People With Epilepsy: Chronic-Dose 4-Period Replicate Design (EQUIGEN Chronic-Dose Study) [NCT01713777]	Phase 4	35 participants (Actual)	Interventional	2013-04-30	Completed
Equivalence Among Antiepileptic Drug Generic and Brand Products in People With Epilepsy: Single-Dose 6-Period Replicate Design (EQUIGEN Single-Dose Study) [NCT01733394]	Phase 4	54 participants (Actual)	Interventional	2012-12-12	Completed
A Multi-center, Uncontrolled, Open-label, Evaluation of Lamotrigine Monotherapy on Newly Diagnosed Typical Absence Seizures in Children and Adolescents [NCT01431976]	Phase 3	20 participants (Actual)	Interventional	2011-09-30	Completed
A Randomised, Controlled Trial to Investigate the Effect of an Intensified Pharmacological Treatment for Schizophrenia, Major Depressive Disorder and Bipolar Depression in Subjects Who Had a First-time Treatment Failure on Their First-line Treatment. [NCT05603104]	Phase 3	1,254 participants (Anticipated)	Interventional	2023-08-01	Not yet recruiting
Combination Therapy in Bipolar Rapid Cycling [NCT00063362]	Phase 3	49 participants (Actual)	Interventional	2002-02-28	Terminated(stopped due to Funding Expiration)
Open Trial of Lamotrigine Monotherapy in Pediatric Bipolar Disorder [NCT00176228]	Phase 2	48 participants (Actual)	Interventional	2004-02-29	Completed
Eight-Month Maintenance Treatment of Bipolar Depression With Lamotrigine or Lamotrigine Plus Divalproex Combination [NCT00183469]	Phase 4	86 participants (Actual)	Interventional	2004-12-31	Completed
Modification of Epilepsy Screen Questionnaire and Treatment Feasibility Evaluation [NCT04939675]		40 participants (Anticipated)	Interventional	2021-07-01	Not yet recruiting
The Effect of a Single Dose of Lamotrigine on Brain Function in Healthy Volunteers [NCT04396938]		36 participants (Actual)	Interventional	2017-05-10	Completed
An Open-Label Extension Study to Assess the Safety of Lamotrigine in Subjects With Bipolar Disorder, Who Are in Remission Following a Manic/Hypomanic Index Episode or a Depressive Index Episode. [NCT00360126]	Phase 4	11 participants (Actual)	Interventional	2005-10-31	Completed
A Randomized, Placebo Controlled, Double-blind, Double-dummy Three-way Cross Over Trial to Investigate the Effect of BI 409306, BI 425809 and Lamotrigine on Ketamine-induced Cognitive Deficits in Healthy Male Subjects [NCT04602221]	Phase 1	39 participants (Actual)	Interventional	2020-12-01	Completed
Evaluation of Bioequivalence of Lamotrigine Tablets in Epileptic Patients [NCT01995825]	Phase 4	35 participants (Actual)	Interventional	2012-05-31	Completed
Melancholic Symptoms in Bipolar Depression and Responsiveness to Lamotrigine: Results From an 8-week, Multicenter, Double-blind, Placebo-controlled Trial [NCT02989727]	Phase 4	150 participants (Actual)	Interventional	2003-11-30	Completed
A Prospective, Case-control Evaluation of Ketogenic Dietary Therapy for New-onset Childhood Absence Epilepsy [NCT04274179]	Phase 3	40 participants (Anticipated)	Interventional	2020-08-10	Recruiting
The Role of Lamotrigine in Reducing Psychologic Side-Effect of Perioperative Ketamine Use [NCT03831854]	Phase 3	46 participants (Actual)	Interventional	2019-01-24	Completed
16-week Open Randomized Comparative Effectiveness Trial of Lamotrigine vs. Fluoxetine for Bipolar Depression: Pharmacogenomic and Biomarker Predictors of Response [NCT02389712]	Phase 4	2 participants (Actual)	Interventional	2015-03-31	Terminated(stopped due to Difficulties with recruitment)
Genetic Markers and Predictors of Antidepressant-induced Suicidality in Youth Depression [NCT02428439]		80 participants (Anticipated)	Observational	2015-04-30	Recruiting
The Sustained Effects of Ketamine [NCT02708849]	Phase 1	3 participants (Actual)	Interventional	2015-06-30	Terminated
Effect of Sleeve Gastroctomy on Pharmacokinetics of Paracetamol and Antiepileptic Drugs [NCT03161509]	Phase 4	2 participants (Actual)	Interventional	2017-07-01	Terminated(stopped due to publication of better study)
Pharmacovigilance in Gerontopsychiatric Patients [NCT02374567]	Phase 3	407 participants (Actual)	Interventional	2015-01-31	Terminated
[NCT00223262]	Phase 4	28 participants (Actual)	Interventional	2002-08-31	Completed
Evaluation of Lamotrigine on Neuropathic Facial Pain Using fMRI [NCT00243152]		6 participants (Actual)	Interventional	2005-10-31	Completed
Sequential Multiple Assignment Randomized Treatment (SMART) for Bipolar Disorder [NCT01588457]	Phase 4	112 participants (Actual)	Interventional	2011-06-30	Completed
A Double-Blind, Placebo-Controlled Trial of Lamotrigine In Individuals With Bipolar Disorder and Comorbid Alcohol Dependence [NCT01015586]	Phase 4	43 participants (Actual)	Interventional	2010-02-28	Completed
1H-MR Spectroscopy of Bipolar Depression Before and After Lamotrigine Treatment [NCT01042496]	Phase 3	72 participants (Actual)	Interventional	2009-12-31	Completed
Population Pharmacokinetics of Antiepileptic in Pediatrics [NCT03196466]		1,000 participants (Anticipated)	Observational	2017-06-19	Recruiting
A Multi-center, Uncontrolled, Open-label, Evaluation of Lamotrigine Monotherapy in Newly Diagnosed Epilepsy or Recurrent Epilepsy (Currently Untreated) [NCT01431963]	Phase 3	70 participants (Actual)	Interventional	2011-09-30	Completed
Pathophysiology and Treatment of Bipolar Disorder as Assessed by in Vivo Imaging [NCT01880957]		76 participants (Actual)	Interventional	2011-11-08	Completed
Childhood Absence Epilepsy Rx PK-PD-Pharmacogenetics Study [NCT00088452]	Phase 3	453 participants (Actual)	Interventional	2004-07-31	Completed
Excessive Crying in Children With Cerebral Palsy and Communication Deficits -a Fixed-sequence, Crossover Clinical Trial [NCT04523935]	Phase 4	131 participants (Actual)	Interventional	2005-12-07	Completed
Cognitive AED Outcomes in Pediatric Localization Related Epilepsy (COPE) [NCT01891890]	Phase 3	72 participants (Actual)	Interventional	2013-08-31	Terminated(stopped due to Poor recruitment)
Early Detection and Intervention for the Prevention of Psychosis Project [NCT00531518]		292 participants (Actual)	Interventional	2007-10-31	Completed
Pharmacokinetics of Lamotrigine in Pregnant and Postpartum Women With Bipolar Disorder [NCT01996293]		30 participants (Actual)	Observational	2013-09-30	Completed
Valproate Dose Reduction and Its Clinical Evaluation by Introducing Lamotrigine in Japanese Women With Epilepsy - Single Arm, Multicenter, and Open-label Study - [NCT02100644]	Phase 4	33 participants (Actual)	Interventional	2014-04-12	Completed
A Fixed-Dose Study of Lamotrigine Versus Placebo in the Long Term Prevention of Relapse and/or Recurrence of a Manic, Hypomanic, Mixed or Depressive Episode in Adult Subjects With Bipolar I Disorder [NCT01602510]	Phase 3	265 participants (Actual)	Interventional	2012-08-31	Completed
Improvement of Synaptic Plasticity and Cognitive Function in RAS Pathway Disorders [NCT03504501]	Phase 2	16 participants (Actual)	Interventional	2019-03-22	Terminated(stopped due to The study has been terminated prematurely due to recruitment difficulties. Current status: recruitment stopped and cleaning of the database is ongoing.)
Evaluation of Repeatability of Lamotrigine Pharmacokinetics in Epileptic Patients [NCT02404168]	Phase 4	4 participants (Actual)	Interventional	2015-07-07	Completed
A Double-Blind Placebo Controlled Add-on Study to Determine the Efficacy and Safety of Lamictal (Lamotrigine) in Patients With Trigeminal Neuralgia (Tic Doloureux) [NCT00203229]		20 participants (Actual)	Interventional	2003-06-30	Completed
The Efficacy and Safety of Lamotrigine Versus Carbamazepine in Focal Epilepsy: A Randomized, Open Label Clinical Trial in Dhaka Medical College Hospital [NCT05748236]	Phase 4	70 participants (Anticipated)	Interventional	2022-11-01	Enrolling by invitation
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

Trial	Outcome
NCT00063362 (1) [back to overview]	The Proportion of Patients Who Experience a Marked and Persistent Bimodal Response
NCT00068445 (10) [back to overview]	Change in Brief Pain Inventory (BPI) Worst Pain Score [Week 10 Minus Baseline]
NCT00068445 (10) [back to overview]	Change in Average Daily Pain Score as Measured Using a Pain Intensity Rating (NRS)
NCT00068445 (10) [back to overview]	Change in Average Pain Score as Measured Using the European Cooperative Oncology Group (ECOG) Neuropathy Scale (ENS)
NCT00068445 (10) [back to overview]	Change in Brief Pain Inventory (BPI) Average Pain Score [Week 10 Minus Baseline]
NCT00068445 (10) [back to overview]	Change in Brief Pain Inventory (BPI) Least Pain Score [Week 10 Minus Baseline]
NCT00068445 (10) [back to overview]	Change in Brief Pain Inventory (BPI) Pain Interference Score [Week 10 Minus Baseline]
NCT00068445 (10) [back to overview]	Change in Brief Pain Inventory (BPI) Pain Now Score [Week 10 Minus Baseline]
NCT00068445 (10) [back to overview]	Change in Brief Pain Inventory (BPI) Pain Relief Score [Week 10 Minus Baseline]
NCT00068445 (10) [back to overview]	Change in POMS Total Score [Week 10 Minus Baseline]
NCT00068445 (10) [back to overview]	The Change in Overall Quality of Life as Measured by the Uniscale QOL From Baseline to Week 10
NCT00088452 (3) [back to overview]	Number of Participants With Freedom From Treatment Failure at 16-20 Weeks of Double Blind Therapy
NCT00088452 (3) [back to overview]	Number of Participants With Freedom From Treatment Failure at 12 Months of Double Blind Therapy
NCT00088452 (3) [back to overview]	Number of Participants With Attention Deficit as Measured by the Confidence Index of the CPT-II and the K-CPT
NCT00104416 (16) [back to overview]	Number of Participants With the Indicated Time to >=50% Reduction in Seizure Frequency in the Double-Blind Treatment Phase
NCT00104416 (16) [back to overview]	Percent Change From Baseline in PGTC Seizure Frequency During the Escalation Phase, the Maintenance Phase, and During the Last 8 Weeks of the Maintenance Phase of the Double-Blind Treatment Phase
NCT00104416 (16) [back to overview]	Percent Change From Baseline in Weekly PGTC Seizure Frequency During the Entire Continuation Phase (CP), the Transition Phase, the Open-Label Phase, and the Last 8 Weeks of the Open-Label Phase
NCT00104416 (16) [back to overview]	Mean Change From Baseline in the Epworth Sleepiness Scale (ESS) 8-Item Total Score at Week 19 of the Double-Blind Treatment Phase
NCT00104416 (16) [back to overview]	Change From Baseline in Body Weight at Week 19 of the Double-Blind Treatment Phase
NCT00104416 (16) [back to overview]	Mean Change From Baseline in the Adverse Experience Profile (AEP) Total Score at Week 19 of the Double-Blind Treatment Phase
NCT00104416 (16) [back to overview]	Mean Change From Baseline in the Center for Epidemiological Studies-Depression Scale (CES-D) Total Score at Week 19 of the Double-Blind Treatment Phase
NCT00104416 (16) [back to overview]	Mean Change From Baseline in the Neurological Disorders Depression Inventory-Epilepsy (NDDI-E) 6-Item Total Score at Week 19 of the Double-Blind Treatment Phase
NCT00104416 (16) [back to overview]	Mean Change From Baseline in the Profile of Mood State (POMS) Mood Disturbance Total Score at Week 19 of the Double-Blind Treatment Phase
NCT00104416 (16) [back to overview]	Mean Change From Baseline in the Quality of Life in Epilepsy-31-P (QOLIE-31P) Overall Score at Week 19 of the Double-Blind Treatment Phase
NCT00104416 (16) [back to overview]	Mean Change From Baseline in the Seizure Severity Questionnaire (SSQ) Global Bother Score at Week 19 Double-Blind Treatment Phase
NCT00104416 (16) [back to overview]	Percent Change From Baseline in Weekly Primary Generalized Tonic-clonic (PGTC) Seizure Frequency During the Entire Double-Blind Treatment Phase
NCT00104416 (16) [back to overview]	Number of Participants With >=25%, >=50%, >=75%, or 100% Reduction in PGTC Seizure Frequency During the Entire Double-Blind (DB)Treatment Phase (TP), the Escalation Phase, the Maintenance Phase, and the Last 8 Weeks of the Maintenance Phase
NCT00104416 (16) [back to overview]	Number of Participants With >=25%, >=50%, >=75%, or 100% Reduction or >=50% Increase From Baseline in Weekly PGTC Seizure Frequency for the Entire Continuation Phase, the Transition Phase, the Open-Label (OL) Phase, and the Last 8 Weeks of the OL Phase.
NCT00104416 (16) [back to overview]	Number of Participants With Improved Clinical Status on the Investigator's Global Assessment in the Double-Blind Treatment Phase
NCT00104416 (16) [back to overview]	Number of Participants With Improved Satisfaction With Seizure Control on the Subject Satisfaction Questionnaire in the Double-Blind Treatment Phase
NCT00176228 (2) [back to overview]	Young Mania Rating Scale (YMRS),
NCT00176228 (2) [back to overview]	Child Depression Rating Scale (CDRS-R)
NCT00181844 (1) [back to overview]	Change of Mania Symptoms Assessed by Young Mania Rating Scale (YMRS)
NCT00183469 (1) [back to overview]	Mania Rating Scale
NCT00203229 (1) [back to overview]	Average Number of Pain Attacks
NCT00223262 (1) [back to overview]	Rey Auditory Verbal Learning Test (RAVLT)
NCT00243152 (2) [back to overview]	Subjective Ratings of Pain During Magnetic Resonance Scanning
NCT00243152 (2) [back to overview]	Blood Oxygenation Level-dependent (BOLD) Changes in Neural Pain Circuitry Following Treatment With Lamotrigine During Experimentally Induced Pain States
NCT00277212 (17) [back to overview]	Proportion of Participants Not Experiencing a Depressive Relapse in the Double-blind Relapse Assessment Phase (Phase 2)
NCT00277212 (17) [back to overview]	Number of Participants With Potentially Clinically Significant Electrocardiogram (ECG) Abnormalities Occurring During Double-Blind Treatment
NCT00277212 (17) [back to overview]	Adjusted Mean Change From Baseline in Body Weight, Phase 2
NCT00277212 (17) [back to overview]	Adjusted Mean Change From Baseline in Abnormal Involuntary Movement Scale (AIMS) Total Score
NCT00277212 (17) [back to overview]	Adjusted Mean Change From Baseline in Barnes Akathisia Global Clinical Assessment,
NCT00277212 (17) [back to overview]	Adjusted Mean Change From Baseline in BMI by Study Week
NCT00277212 (17) [back to overview]	Adjusted Mean Change From Baseline in Simpson-Angus Scale (SAS) Total Score
NCT00277212 (17) [back to overview]	Deaths, Treatment-Emergent Serious Adverse Events (SAEs), Adverse Events (AEs) Leading to Discontinuation of Study Medication, Treatment-Emergent AEs and Treatment-Emergent Extrapyramidal Syndrome (EPS)-Related AEs
NCT00277212 (17) [back to overview]	Number of Participants Showing Clinically Relevant Weight Gain by Study Week
NCT00277212 (17) [back to overview]	Number of Participants Showing Clinically Relevant Weight Loss by Study Week
NCT00277212 (17) [back to overview]	Number of Participants With Potentially Clinically Relevant Laboratory Abnormalities Occurring During Double-Blind Treatment (Phase 2)
NCT00277212 (17) [back to overview]	Number of Participants With Potentially Clinically Relevant Vital Sign Abnormalities Occurring During Double-Blind Treatment
NCT00277212 (17) [back to overview]	Proportion of Participants Not Experiencing Relapse (Manic, Mixed, Depressive) in the Double-blind Relapse Assessment Phase Phase 2
NCT00277212 (17) [back to overview]	Proportion of Participants Not Experiencing Relapse Through Week 52 in the Double-Blind Relapse Assessment Phase (Phase 2)
NCT00277212 (17) [back to overview]	Proportion of Participants Without Discontinuation for Any Reason in the Double-blind Relapse Assessment Phase (Phase 2)
NCT00277212 (17) [back to overview]	Summary of Concomitant Medications, Phase 1
NCT00277212 (17) [back to overview]	Summary of Concomitant Medications, Phase 2
NCT00280059 (18) [back to overview]	Percentage of Seizure-free Participants (Responders) During Efficacy Assessment Phase
NCT00280059 (18) [back to overview]	Exit for Any Reason During the Double-blind Treatment Phase (Including Dose Escalation Phase)
NCT00280059 (18) [back to overview]	Exit Due to Lack of Efficacy After 4-week Dose Escalation Phase
NCT00280059 (18) [back to overview]	Exit Due to Any Reason After 4-week Dose Escalation Phase
NCT00280059 (18) [back to overview]	Exit Due to Adverse Events During the Double-blind Treatment Phase (Including Dose Escalation Phase)
NCT00280059 (18) [back to overview]	Percentage of Participants Who Achieved at Least 6 Consecutive Months of Seizure Freedom (Responders) by Final Dosage Levels and Treatment Group
NCT00280059 (18) [back to overview]	Mean Monthy Seizure Frequency: All Seizures
NCT00280059 (18) [back to overview]	Median Monthy Seizure Frequency of Responders for the Months After Achieving 6 Consecutive Months of Seizure Freedom: All Seizures
NCT00280059 (18) [back to overview]	Change From Baseline to Week 56 in Hospital Anxiety and Depression Scale (HADS)
NCT00280059 (18) [back to overview]	Medical Outcomes Study Sleep Scale (MOS-SS): Optimal Sleep Subscale
NCT00280059 (18) [back to overview]	Median Monthy Seizure Frequency: All Seizures
NCT00280059 (18) [back to overview]	Median Monthy Seizure Frequency: All Partial Seizures
NCT00280059 (18) [back to overview]	Time to 6 Consecutive Months of Seizure-freedom After 4-week Dose Escalation Phase: All Seizures
NCT00280059 (18) [back to overview]	Median Monthy Seizure Frequency of Responders for the Months After Achieving 6 Consecutive Months of Seizure Freedom: All Partial Seizures
NCT00280059 (18) [back to overview]	Mean Monthy Seizure Frequency: All Partial Seizures
NCT00280059 (18) [back to overview]	Mean Monthy Seizure Frequency of Responders for the Months After Achieving 6 Consecutive Months of Seizure Freedom: All Seizures
NCT00280059 (18) [back to overview]	Mean Monthy Seizure Frequency of Responders for the Months After Achieving 6 Consecutive Months of Seizure Freedom: All Partial Seizures
NCT00280059 (18) [back to overview]	Time to First Seizure After the 4-Week Dose Escalation Phase
NCT00280293 (4) [back to overview]	Positive Urine Drug Screens
NCT00280293 (4) [back to overview]	Dollars Spent
NCT00280293 (4) [back to overview]	Depression Score on the Hamilton Rating Scale For Depression
NCT00280293 (4) [back to overview]	Days of Cocaine Use
NCT00292461 (4) [back to overview]	Global Assessment of Efficacy by Participants at the End of the 16-week Treatment Period
NCT00292461 (4) [back to overview]	Global Assessment of Efficacy by Physician at the End of 16-week Treatment Period
NCT00292461 (4) [back to overview]	Response Rate: Defined as the Percentage of Participants With >= 50% Reduction of Monthly Seizure Frequency at the End of 16-week Treatment From Baseline.
NCT00292461 (4) [back to overview]	The Percentage Change of Monthly Seizure Frequency at the End of the 16-week Treatment From Baseline
NCT00355082 (8) [back to overview]	Percent Change From Baseline in Weekly Seizure Frequency Between Study Visits 3 (Start of Dosing) and 9 (End of the Treatment Phase)
NCT00355082 (8) [back to overview]	Percentage of Participants Meeting Escape Criteria in the Treatment Phase
NCT00355082 (8) [back to overview]	The Percentage of Participants in the 250 mg/Day Dose Group Who Prematurely Discontinued the Study Between Study Visit 5 (Approximately Week 7) and Visit 9 (End of the Treatment Phase)
NCT00355082 (8) [back to overview]	The Percentage of Participants in the 300 mg/Day Dose Group Who Prematurely Discontinued the Study Between Study Visit 5 (Approximately Week 7) and Visit 9 (End of the Treatment Phase)
NCT00355082 (8) [back to overview]	Time to Discontinuation in the Treatment Phase
NCT00355082 (8) [back to overview]	The Number of Participants With at Least the Specified Change in Seizure Frequency, Compared to Baseline, at the End of Participation in the Continuation Phase (Maximum of 24 Weeks)
NCT00355082 (8) [back to overview]	Percent Change From Baseline in the Average Seizure Frequency Measured at the End of Participation in the Continuation Phase
NCT00355082 (8) [back to overview]	Number of Seizure-free Participants During the Last 12 Weeks of Treatment of the Treatment Phase
NCT00360126 (1) [back to overview]	Number of Participants With Serious Adverse Events (SAEs)
NCT00395694 (12) [back to overview]	Number of Drug-related and Not Related Rash Events (Including SJS and Any Other Serious Drug Eruption) up to the End of the Maintenance Phase
NCT00395694 (12) [back to overview]	Number of Rash Events Experienced (Including SJS and Any Other Serious Drug Eruption) up to the End of the Maintenance Phase
NCT00395694 (12) [back to overview]	Number of Rash Events Experienced (Including SJS and Any Other Serious Drug Eruption) During the Initial 8 Weeks of Study Treatment
NCT00395694 (12) [back to overview]	Number of Rash Events (Including SJS and Any Other Serious Drug Eruption) Adjudicated by the Rash Adjudication Committee in Participants Taking VPA
NCT00395694 (12) [back to overview]	Number of Participants With Any Rash Event (Including Stevens-Johnson Syndrome [SJS] and Any Other Serious Drug Eruption) During the Initial 8 Weeks of Study Treatment
NCT00395694 (12) [back to overview]	Percentage of Participants With Monocyte Values Outside the Normal Range (Shifted High) at Weeks 4 and 8
NCT00395694 (12) [back to overview]	Number of Drug-related and Not Related Rash Events (Including SJS and Any Other Serious Drug Eruption) During the Initial 8 Weeks of Study Treatment
NCT00395694 (12) [back to overview]	Number of Participants With Any Rash Event (Including SJS and Any Other Serious Drug Eruption) up to the End of the Maintenance Phase
NCT00395694 (12) [back to overview]	Percentage of Participants With at Least a 50 Percent Reduction in Seizure Frequency for the Indicated Types of Seizures
NCT00395694 (12) [back to overview]	Percent Change in Seizure Frequency of the Indicated Types of Seizures
NCT00395694 (12) [back to overview]	Number of Participants With the Indicated Intensity of Rash (Including SJS and Any Other Serious Drug Eruption) up to the End of the Maintenance Phase
NCT00395694 (12) [back to overview]	Number of Participants With the Indicated Intensity of Rash (Including SJS and Any Other Serious Drug Eruption) During the Initial 8 Weeks of Study Treatment
NCT00419003 (1) [back to overview]	Montgomery-Asberg Depression Rating Scale (MARDS) Score (Acute Response to IV Ketamine in Patients With Treatment Resistant Major Depression)
NCT00438451 (12) [back to overview]	QOLIE-31 (Quality Of Life In Epilepsy) Results at V6
NCT00438451 (12) [back to overview]	Portland Neurotoxicity Scale (PNS) at V6
NCT00438451 (12) [back to overview]	Time to Drop Out
NCT00438451 (12) [back to overview]	The Time (in Days) to First Break-through Seizure (From Day 1 of Treatment)
NCT00438451 (12) [back to overview]	Results of Cognitive Testing (EpiTrack© by UCB) - Score at V6
NCT00438451 (12) [back to overview]	Percentage of Patients Remaining Seizure-free at Week 30 (Visit 4)
NCT00438451 (12) [back to overview]	The Absolute Seizure Frequency During the Maintenance Phase (Weeks 7 - 58)
NCT00438451 (12) [back to overview]	Percentage of Patients Remaining Seizure Free at Week 58 (Visit 6)
NCT00438451 (12) [back to overview]	Results of Cognitive Testing (EpiTrack© by UCB) - Categories at V6
NCT00438451 (12) [back to overview]	58-week Retention Rate Measured by the Number of Drop Outs Due to Adverse Events or Seizures From Day 1 of Treatment
NCT00438451 (12) [back to overview]	Results of Cognitive Testing (EpiTrack© by UCB) - Changes to Baseline (V0) at Week 58 (V6)
NCT00438451 (12) [back to overview]	Proportion of Seizure-free Days During the Maintenance Phase for Subjects Who Enter the Maintenance Phase
NCT00513019 (1) [back to overview]	The Yale-Brown Obsessive Compulsive Scale Modified for Neurotic Excoriation (NE-YBOCS) Will be the Primary Outcome Measure
NCT00516139 (22) [back to overview]	Absorption Rate (KA) for Participants in All Concomitant AED Groups Combined: Neutral, With EIAED, and With VPA
NCT00516139 (22) [back to overview]	Apparent Clearance (CL/F) Based on the Concomitant AED Groups: Neutral, With EIAED, and With VPA
NCT00516139 (22) [back to overview]	Apparent Volume of Distribution (V/F) for Participants in All Concomitant AED Groups Combined: Neutral, With EIAED, and With VPA
NCT00516139 (22) [back to overview]	Change From Baseline in Alkaline Phosphatase (Alk P), Alanine Amino Transferase (Ala AT), and Aspartate Amino Transferase (Asp AT) at the Indicated Time Points in the Study
NCT00516139 (22) [back to overview]	Change From Baseline in Direct Bilirubin (DB), Total Bilirubin (TB), and Creatinine at the Indicated Time Points in the Study
NCT00516139 (22) [back to overview]	Number of Participants With Any Serious Adverse Event (SAE) and Any Non-serious Adverse Event
NCT00516139 (22) [back to overview]	Number of Seizure-free Participants at Baseline Who Remained Seizure-free Throughout the Entire Treatment Period
NCT00516139 (22) [back to overview]	Serum LTG Concentrations at Different LTG Doses Based on the Concomitant AED Groups: Neutral (Without Known Enzyme-inducing AED [EIAED], Valproate [VPA]) With EIAED, and With VPA
NCT00516139 (22) [back to overview]	Change From Baseline in the Weight at the Indicated Time Points in the Study
NCT00516139 (22) [back to overview]	Percent Change From Baseline in the Basophil, Eosinophil, Hemoglobin, Lymphocyte, Monocyte, Absolute Neutrophil Count, Platelet Count, and White Blood Cell Count at the Indicated Time Points in the Study
NCT00516139 (22) [back to overview]	Change From Baseline in the Height at the Indicated Time Points in the Study
NCT00516139 (22) [back to overview]	Percent Change From Baseline (BL) in Weekly Seizure (sz.) Frequency for All Partial Seizures During Each Phase of the Study
NCT00516139 (22) [back to overview]	Number of Participants With the Indicated Change From Baseline in Weekly Seizure Frequency During Each Phase of the Study
NCT00516139 (22) [back to overview]	Number of Participants With Changes From Baseline in Overall Clinical Status in the Indicated Categories, as Measured by the IGE Scale
NCT00516139 (22) [back to overview]	Change From Baseline in the Basophil, Eosinophil, Hemoglobin, Lymphocyte, Monocyte, Absolute Neutrophil Count (ANC), Platelet Count, and White Blood Cell (WBC) Count at the Indicated Time Points in the Study
NCT00516139 (22) [back to overview]	Change From Baseline in Cholesterol, High Density Lipoprotein (HDL) Cholesterol, Low Density Lipoprotein (LDL) Cholesterol, Glucose, Potassium, Sodium, Triglycerides, and Urea/Blood Urea Nitrogen (BUN) at the Indicated Time Points
NCT00516139 (22) [back to overview]	Change From Baseline in Systolic and Diastolic Blood Pressure (BP) at the Indicated Time Points in the Study
NCT00516139 (22) [back to overview]	Change From Baseline in Red Blood Cell (RBC) Count at the Indicated Time Points in the Study
NCT00516139 (22) [back to overview]	Change From Baseline in Mean Corpuscle Volume (MCV) at the Indicated Time Points in the the Study
NCT00516139 (22) [back to overview]	Change From Baseline in Mean Corpuscle Hemoglobin (MCH) at the Indicated Time Points in the Study
NCT00516139 (22) [back to overview]	Number of Participants With Changes From Baseline in Seizure Severity in the Indicated Categories, as Measured by the Investigator's Global Evaluation (IGE) Scale
NCT00516139 (22) [back to overview]	Change From Baseline in the Mean Corpuscle Hemoglobin Concentration (MCHC), Albumin, and Total Protein at the Indicated Time Points in the Study
NCT00531518 (1) [back to overview]	Psychotic Symptoms
NCT00550407 (14) [back to overview]	Change From Baseline in Hamilton Rating Scale for Depression (HAMD-17) Scores at Week 16/Withdrawal (Preliminary Phase)
NCT00550407 (14) [back to overview]	Change From Baseline in Hamilton Rating Scale for Depression (HAMD-17) Scores at Week 26/Withdrawal (Randomized Phase)
NCT00550407 (14) [back to overview]	Change From Baseline in Young Mania Rating Scale (YMRS) Total Scores at Week 16/Withdrawal (Preliminary Phase)
NCT00550407 (14) [back to overview]	Change From Baseline in Young Mania Rating Scale (YMRS) Total Scores at Week 26/Withdrawal (Randomized Phase)
NCT00550407 (14) [back to overview]	Clinical Global Impressions of Improvement (CGI-I) at Week 16/Withdrawal (Preliminary Phase)
NCT00550407 (14) [back to overview]	Clinical Global Impressions of Improvement (CGI-I) at Week 26/Withdrawal (Randomized Phase)
NCT00550407 (14) [back to overview]	Time to Withdrawal From Study
NCT00550407 (14) [back to overview]	Number of Participants With a Withdrawal Event
NCT00550407 (14) [back to overview]	Number of Participants With Intervention for a Manic, Hypomanic, or Mixed Episode
NCT00550407 (14) [back to overview]	Number of Participants With Intervention for Any Mood Episode
NCT00550407 (14) [back to overview]	Number of Participants With Intervention for Depressive Episode
NCT00550407 (14) [back to overview]	Change From Baseline in Clinical Global Impressions of Severity (CGI-S) Scores at Week 16/Withdrawal (Preliminary Phase)
NCT00550407 (14) [back to overview]	Change From Baseline in Clinical Global Impressions of Severity (CGI-S) Scores at Week 26/Withdrawal (Randomized Phase)
NCT00550407 (14) [back to overview]	Time to Intervention for Any Mood Episode (TIME)
NCT00562861 (1) [back to overview]	MADRS Rating Scale Change
NCT00566020 (22) [back to overview]	Change From Baseline in the Young Mania Rating Scale (YMRS) Total Score at Weeks 6, 16, 28, 40, and 52/EW
NCT00566020 (22) [back to overview]	Mean Body Mass Index (BMI) of All Participants at Week 0 (Baseline) and Weeks 6, 8, 12, 16, 20, 24, 28, 32,36, 40, 44, 48, and 52/EW
NCT00566020 (22) [back to overview]	Hamilton Rating Scale for Depression (HAM-D) Scale Total Score at Weeks 6, 16, 28, 40, and 52/EW
NCT00566020 (22) [back to overview]	Clinical Global Impressions of Severity (CGI-S) Total Score at Weeks 0, 2, 4, 5, 6, 8, 12, 16, 20, 24, 28, 32, 36, 40, 44, 48, and 52/EW
NCT00566020 (22) [back to overview]	Change From Baseline in the Hamilton Rating Scale for Depression (HAM-D) Scale Total Score at Weeks 6, 16, 28, 40, and 52/EW
NCT00566020 (22) [back to overview]	Mean Weight of Participants at Baseline (Week 0) and Weeks 6, 8, 12, 16, 20, 24, 28, 32, 36, 40, 44, 48, and 52/EW
NCT00566020 (22) [back to overview]	Median Serum Lamotrigine 200 mg Concentration Among Participants With Concomitant Use of Inducer and Without Inhibitor (at the Timing of Blood Sample Collection)
NCT00566020 (22) [back to overview]	Change From Baseline in the Clinical Global Impressions of Severity (CGI-S) Total Score at Weeks 2, 4, 5, 6, 8, 12, 16, 20, 24, 28, 32, 36, 40, 44, 48, and 52/EW
NCT00566020 (22) [back to overview]	Number of Participants With the Indicated Electrocardiogram (ECG) Findings at Weeks 0, 6, 28, and 52/EW
NCT00566020 (22) [back to overview]	Number of Participants With the Indicated Clinical Laboratory Test Values for Alkaline Phosphatase (ALP), Alanine Amino Transferase (ALT), Aspartate Amino Transferase (AST), Gamma Glutamyl Transferase (GGT), and Lactate Dehydrogenase (LDH)
NCT00566020 (22) [back to overview]	Number of Participants With Clinical Laboratory Test Values Out of the Normal Range and in the Normal Range for Total Protein, Hemoglobin, and Hematocrit at Weeks 0, 6, 16, 28, 40, and 52/EW
NCT00566020 (22) [back to overview]	Young Mania Rating Scale (YMRS) Total Score at Weeks 6, 16, 28, 40, and 52/EW
NCT00566020 (22) [back to overview]	Number of Participants With Clinical Laboratory Test Values Out of the Normal Range and in the Normal Range for Total Bilirubin and Creatinine at Weeks 0, 6, 16, 28, 40, and 52/EW
NCT00566020 (22) [back to overview]	Number of Participants With Clinical Laboratory Test Values Out of the Normal Range and in the Normal Range for Red Blood Cell Count at Weeks 0, 6, 16, 28, 40, and 52/EW
NCT00566020 (22) [back to overview]	Number of Participants With Clinical Laboratory Test Values Out of the Normal Range and in the Normal Range for Platelet Count and White Blood Cell Count at Weeks 0, 6, 16, 28, 40, and 52/EW
NCT00566020 (22) [back to overview]	Number of Participants With Clinical Laboratory Test Values Out of the Normal Range and in the Normal Range for Calcium, Cholesterol, Chloride, Potassium, Sodium, Triglycerides, and Urea/Blood Urea Nitrogen (BUN) at Weeks 0, 6, 16, 28, 40, and 52/EW
NCT00566020 (22) [back to overview]	Number of Participants With Any Serious Adverse Event (SAE) and Any Non Serious Adverse Event
NCT00566020 (22) [back to overview]	Number of Participants in the Indicated Category for Urine Glucose, Urine Protein, and Urine Urobilinogen at Baseline (Week 0) and Weeks 6, 16, 28, 40, and 52/EW
NCT00566020 (22) [back to overview]	Median Serum Lamotrigine 25, 100, 125, 150, 200, 225, 300, and 400 mg Concentrations Among Participants Without Concomitant Use of Inhibitor and Inducer
NCT00566020 (22) [back to overview]	Median Serum Lamotrigine 100 mg and 200 mg Concentration Among Participants With Concomitant Use of Inhibitor (at the Timing of Blood Sample Collection)
NCT00566020 (22) [back to overview]	Mean Systolic Blood Pressure and Diastolic Blood Pressure of Participants at Baseline (Week 0) and Weeks 2, 4, 5, 6, 8, 12, 16, 20, 24, 28, 32, 36, 40, 44, 48, and 52/EW
NCT00566020 (22) [back to overview]	Mean Heart Rate of Participants at Week 0 (Baseline) and Weeks 2, 4, 5, 6, 8, 12, 16, 20, 24, 28, 32, 36, 40, 44, 48, and 52/EW
NCT00579982 (16) [back to overview]	Mean Change From Baseline in the Convenience Subscale Score (CSS) Derived From the Treatment Satisfaction Questionnaire for Medication (TSQM v 1.4) Using Items 9 (Ease of Use), 10 (Ease of Planning to Use), and 11 (Convenience) at Week 3.
NCT00579982 (16) [back to overview]	Mean Change From Baseline in the Global Satisfaction Subscale Score, From the TSQM Using Items 12 (Confidence in Medicine), 13 (Certainty That Good Things About Medication Outweigh Bad Things), and 14 (Satisfaction With Medication) at Week 3
NCT00579982 (16) [back to overview]	"Number of Participants Answering the Question Compared to Standard Tablets That Need to be Swallowed With Liquid, How Convenient or Inconvenient Did You Find This Orally Disintegrating Tablet? at Week 3"
NCT00579982 (16) [back to overview]	"Number of Participants Answering the Question Compared to Standard Tablets That Need to be Swallowed With Liquid, How Easy or Difficult is it to Use This Orally Disintegrating Tablet? at Week 3"
NCT00579982 (16) [back to overview]	"Number of Participants Answering the Question Did the Tablets Dissolve Instantly (Yes or no)? at Week 3"
NCT00579982 (16) [back to overview]	"Number of Participants Answering the Question How Did the Dissolved Tablet Feel in Your Mouth? at Week 3"
NCT00579982 (16) [back to overview]	"Number of Participants Answering the Question How Satisfied Were You With the Aftertaste of the Tablet? at Week 3"
NCT00579982 (16) [back to overview]	"Number of Participants Answering the Question How Satisfied Were You With the Flavor of the Tablet? at Week 3"
NCT00579982 (16) [back to overview]	"Number of Participants Answering the Question How Would You Rate the Aftertaste of the Tablet? at Week 3."
NCT00579982 (16) [back to overview]	"Number of Participants Answering the Question How Would You Rate the Strength of the Flavor of the Tablet? at Week 3"
NCT00579982 (16) [back to overview]	Number of Companions/Caregivers Indicating Whether ODT or Standard IR Tablet is More Convenient at Week 3
NCT00579982 (16) [back to overview]	Number of Participants Indicating a Preference for ODT or the Standard IR Tablet at Week 3
NCT00579982 (16) [back to overview]	Number of Participants Indicating at Week 3 (by Answering Yes/no) That They Would be More Likely to Take the ODT Formulation
NCT00579982 (16) [back to overview]	"Number of Participants Answering the Question How Satisfied or Dissatisfied Were You With the Time it Took the Tablet to Dissolve at Week 3"
NCT00579982 (16) [back to overview]	Mean Change From Baseline in Clinical Global Impression of Illness-Severity at Week 3
NCT00579982 (16) [back to overview]	Mean Change From Baseline in the Beck Depression Inventory (BDI-II) Score at Week 3
NCT00621842 (12) [back to overview]	Change in Appearance of Extrapyramidal Symptoms From Baseline Using the Abnormal Involuntary Movement Scale (AIMS)
NCT00621842 (12) [back to overview]	Change in or Appearance of Extrapyramidal Symptoms From Baseline Using the Barnes Akathisia Scale (BAS)
NCT00621842 (12) [back to overview]	Number of Participants Who Had a Fall That Required Medical Attention
NCT00621842 (12) [back to overview]	Number of Participants Who Fell at Least Once During the Study
NCT00621842 (12) [back to overview]	Assessment of Adverse Effects With the Udvalg Fur Kliniske Undersogelser (UKU)
NCT00621842 (12) [back to overview]	Change in Manic Symptoms From Baseline Using the Young Mania Rating Scale (YMRS)
NCT00621842 (12) [back to overview]	Assessment of Change in Depressive Symptoms From Baseline on the Montgomery Asberg Depression Rating Scale (MADRS)
NCT00621842 (12) [back to overview]	Change From Baseline in Overall Clinical Diagnosis Using the CGI-BP
NCT00621842 (12) [back to overview]	Change in Body Weight From Baseline
NCT00621842 (12) [back to overview]	Change in Depressive Symptoms From Baseline Using the Hamilton Depression Rating Scale (GRID-HAM-D)
NCT00621842 (12) [back to overview]	Change in or Appearance of Extrapyramidal Symptoms From Baseline Using the Simpson Angus Scale (SAS)
NCT00621842 (12) [back to overview]	Number of Participants Who Had a Fall That Required Medical Attention and Was Related to Lamotrigine
NCT00720473 (12) [back to overview]	Associations of MADRS Changes With Glutamine to Creatine Ratio Changes From Baseline to Follow-up
NCT00720473 (12) [back to overview]	Means of MADRS Scores at 8 Weeks
NCT00720473 (12) [back to overview]	Estimated Change in Least Squares Mean in the Glutamine to Creatine Ratio Between Baseline and Follow-up
NCT00720473 (12) [back to overview]	Association of MADRS Changes With Glutamate to Creatine Ratio Changes From Baseline to Follow-up
NCT00720473 (12) [back to overview]	Associations Between Depression Symptom Severity and Glutamate to Creatine Ratio at Baseline
NCT00720473 (12) [back to overview]	Associations of MADRS Changes With NAA to Creatine Ratio Changes From Baseline to Follow-up
NCT00720473 (12) [back to overview]	Estimated Change in Least Squares Mean in Glutamate to Creatine Ratio Between Baseline and Follow-up
NCT00720473 (12) [back to overview]	Estimated Change in Least Squares Mean in the NAA to Creatine Ratio Between Baseline and Follow-up
NCT00720473 (12) [back to overview]	Mean Glutamate to Creatine Ratio by Diagnosis at Baseline
NCT00720473 (12) [back to overview]	Mean Glutamine to Creatine Ratio by Diagnosis at Baseline
NCT00720473 (12) [back to overview]	Mean Montgomery Asberg Depression Rating Scale (MADRS) Score at Baseline
NCT00720473 (12) [back to overview]	Mean N-Acetyl Aspartate (NAA) to Creatine Ratio by Diagnosis at Baseline
NCT00723450 (22) [back to overview]	Number of Participants Considered Much Improved or Very Much Improved [Defined as a Clinical Global Impression-Bipolar Version, Improvement of Illness (CGI-BP[I]), Score of 1 or 2] at Each Visit Compared to Randomization in the Randomized Phase
NCT00723450 (22) [back to overview]	Number of Participants Considered Much Improved or Very Much Improved [Defined as a Clinical Global Impression-Bipolar Version, Improvement of Illness (CGI-BP[I]), Score of 1 or 2] at Each Visit Compared to Baseline in the Open-Label Phase
NCT00723450 (22) [back to overview]	Change From Randomization in the Young Mania Rating Scale (YMRS) at Each Visit in the Randomized Phase
NCT00723450 (22) [back to overview]	Change From Baseline in the Clinical Global Impressions - Bipolar, Severity of Illness (CGI-BP[S]) at Each Visit in the Open-Label Phase
NCT00723450 (22) [back to overview]	Change From Baseline in the Conners' Global Index - Parent Version (CGI-P) at Each Visit in the Open-Label Phase
NCT00723450 (22) [back to overview]	Change From Baseline in the Parent Version of the Young Mania Rating Scale (P-YMRS) at Each Visit in the Open-Label Phase
NCT00723450 (22) [back to overview]	Change From Randomization in the Conners' Global Index - Parent Version (CGI-P) at Each Visit in the Randomized Phase.
NCT00723450 (22) [back to overview]	Change From Randomization in the Quick Inventory of Depressive Symptomatology - Self-report Adolescent Version (QIDS-A17-SR) at Each Visit in the Randomized Phase
NCT00723450 (22) [back to overview]	Change From Randomization in the Quick Inventory of Depressive Symptomatology - Clinician Interview, Semi-structured, Adolescent Version (QIDS- A17-C) at Each Visit in the Randomized Phase
NCT00723450 (22) [back to overview]	Change From Baseline in the Quick Inventory of Depressive Symptomatology - Clinician Interview, Semi-structured, Adolescent Version (QIDS- A17-C) at Each Visit in the Open-Label Phase
NCT00723450 (22) [back to overview]	Time From Randomization to Withdrawal From the Study for Any Cause (TTW)
NCT00723450 (22) [back to overview]	Change From Baseline in the Quick Inventory of Depressive Symptomatology - Self-report Adolescent Version (QIDS-A17-SR) at Each Visit in the Open-Label Phase
NCT00723450 (22) [back to overview]	Change From Baseline in the Young Mania Rating Scale (YMRS) at Each Visit in the Open-Label Phase
NCT00723450 (22) [back to overview]	Change From Randomization in the Clinical Global Impressions - Bipolar, Severity of Illness (CGI-BP[S]) at Each Visit in the Randomized Phase
NCT00723450 (22) [back to overview]	Change From Randomization in the Parent Version of the Young Mania Rating Scale (P-YMRS) at Each Visit in the Randomized Phase
NCT00723450 (22) [back to overview]	Time From Randomization to the Occurrence of a Bipolar Event (TOBE)
NCT00723450 (22) [back to overview]	Time From Randomization to Intervention for Depression (TIDep), Mania/Hypomania (TIMan), or a Mixed Episode (TIMix)
NCT00723450 (22) [back to overview]	Time From Randomization to Intervention for a Mood Episode (TIME)
NCT00723450 (22) [back to overview]	Summary of Clinical Global Impressions - Bipolar - Improvement of Illness (CGI-BP [I]) Scores During Randomized Phase
NCT00723450 (22) [back to overview]	Number of Participants Experiencing a Relapse/Recurrence Within the First 30, 90, and 180 Days in the Randomized Phase
NCT00723450 (22) [back to overview]	Number of Participants Experiencing a Relapse/Recurrence to Depression, Mania/Hypomania, or Mixed Mood State
NCT00723450 (22) [back to overview]	Summary of Clinical Global Impressions - Bipolar - Improvement of Illness (CGI-BP [I]) Scores During Open-label Phase
NCT00789113 (1) [back to overview]	Area Under the Curve (AUC) for Oral Bioavailability of Lamotrigine (LTG
NCT00807989 (3) [back to overview]	Seizure Free Rate for 24 Weeks at Initial Target Dose
NCT00807989 (3) [back to overview]	Seizure Free Rate for 52 Weeks at Initial Target Dose
NCT00807989 (3) [back to overview]	Retention Rate After 52 Weeks Maintenance Period
NCT00834561 (3) [back to overview]	Cmax - Maximum Observed Concentration
NCT00834561 (3) [back to overview]	AUC0-t - Area Under the Concentration-time Curve From Time Zero to Time of Last Non-zero Concentration (Per Participant)
NCT00834561 (3) [back to overview]	AUC0-inf - Area Under the Concentration-time Curve From Time Zero to Infinity (Extrapolated)
NCT00835263 (3) [back to overview]	Cmax - Maximum Observed Concentration
NCT00835263 (3) [back to overview]	AUC0-t - Area Under the Concentration-time Curve From Time Zero to Time of Last Non-zero Concentration (Per Participant)
NCT00835263 (3) [back to overview]	AUC0-inf - Area Under the Concentration-time Curve From Time Zero to Infinity (Extrapolated)
NCT00838136 (3) [back to overview]	Cmax - Maximum Observed Concentration
NCT00838136 (3) [back to overview]	AUC0-t - Area Under the Concentration-time Curve From Time Zero to Time of Last Non-zero Concentration (Per Participant)
NCT00838136 (3) [back to overview]	AUC0-inf - Area Under the Concentration-time Curve From Time Zero to Infinity (Extrapolated)
NCT00838279 (3) [back to overview]	Cmax - Maximum Observed Concentration
NCT00838279 (3) [back to overview]	AUC0-t - Area Under the Concentration-time Curve From Time Zero to Time of Last Non-zero Concentration (Per Participant)
NCT00838279 (3) [back to overview]	AUC0-inf - Area Under the Concentration-time Curve From Time Zero to Infinity (Extrapolated)
NCT00855738 (17) [back to overview]	Percent of Participants Who Continued on Study Medication to Month 6
NCT00855738 (17) [back to overview]	Percent of Participants Reaching Monotherapy
NCT00855738 (17) [back to overview]	Percent Change From Baseline in the Median Number of Seizures During the Last 3 Months of Treatment
NCT00855738 (17) [back to overview]	Percent of Participants Classified as Responders
NCT00855738 (17) [back to overview]	Percent of Participants Indicating Optimal Sleep on the Optimal Sleep Subscale: Medical Outcomes Study Sleep Scale (MOS-SS)
NCT00855738 (17) [back to overview]	Percent of Participants That Reduced, Maintained and Increased the Doses of the Initial Treatment Administered in Monotherapy
NCT00855738 (17) [back to overview]	Percent of Participants That Reduced, Maintained and Increased Their Doses of New Antiepileptic Drugs (AED)
NCT00855738 (17) [back to overview]	Change From Baseline to Month 6 in Total Number of Days Hospitalized Because of Epilepsy
NCT00855738 (17) [back to overview]	Percent of Participants With Cessation of Occupation, Requirement of Caregiver, or Admission to Intensive Care Unit
NCT00855738 (17) [back to overview]	Percent of Participants With Reduction in Number of Seizures >=25% and >=75% During the Last 3 Months of Treatment
NCT00855738 (17) [back to overview]	Percent of Seizure-free Participants During the Last 3 Months Before Discontinuation
NCT00855738 (17) [back to overview]	Change From Baseline to Months 3 and 6 in Health Condition: Euro Quality of Life Scale (EQ-5D) Visual Analog Scale (VAS)
NCT00855738 (17) [back to overview]	Change in Sleep Disturbances From Baseline to Month 6: Medical Outcomes Study Sleep Scale (MOS-SS)
NCT00855738 (17) [back to overview]	Change From Baseline to Month 6 in Visits to a Specialist or the Emergency Room Because of Epilepsy
NCT00855738 (17) [back to overview]	Change From Baseline to Month 6 in the Hospital Anxiety and Depression Scale (HADS)
NCT00855738 (17) [back to overview]	Change From Baseline to Month 6 in Quality of Life 10 Domains (QOLIE-10)
NCT00855738 (17) [back to overview]	Time to First Seizure
NCT00916149 (32) [back to overview]	Performance on Neuropsychological Batteries and Computerized Cognitive Testing: Grooved Pegboard
NCT00916149 (32) [back to overview]	Performance on Neuropsychological Batteries and Computerized Cognitive Testing: LNS
NCT00916149 (32) [back to overview]	Performance on Neuropsychological Batteries and Computerized Cognitive Testing: NDDIE
NCT00916149 (32) [back to overview]	Performance on Neuropsychological Batteries and Computerized Cognitive Testing: Non-verbal Working Memory Accuracy
NCT00916149 (32) [back to overview]	Performance on Neuropsychological Batteries and Computerized Cognitive Testing: Non-verbal Working Memory Reaction Time
NCT00916149 (32) [back to overview]	Performance on Neuropsychological Batteries and Computerized Cognitive Testing: QOLIE
NCT00916149 (32) [back to overview]	Performance on Neuropsychological Batteries and Computerized Cognitive Testing: Spatial Span
NCT00916149 (32) [back to overview]	Performance on Neuropsychological Batteries and Computerized Cognitive Testing: Stroop
NCT00916149 (32) [back to overview]	Performance on Neuropsychological Batteries and Computerized Cognitive Testing: Trails Test
NCT00916149 (32) [back to overview]	Performance on Neuropsychological Batteries and Computerized Cognitive Testing: Verbal Fluency
NCT00916149 (32) [back to overview]	Performance on Neuropsychological Batteries and Computerized Cognitive Testing: Verbal Recognition Accuracy
NCT00916149 (32) [back to overview]	Performance on Neuropsychological Batteries and Computerized Cognitive Testing: Verbal Recognition Reaction Time
NCT00916149 (32) [back to overview]	Performance on Neuropsychological Batteries and Computerized Cognitive Testing: Verbal Working Memory Accuracy
NCT00916149 (32) [back to overview]	Performance on Neuropsychological Batteries and Computerized Cognitive Testing: Verbal Working Memory Reaction Time
NCT00916149 (32) [back to overview]	Performance on Neuropsychological Batteries and Computerized Cognitive Testing: Digit Symbol
NCT00916149 (32) [back to overview]	Mean Change in Focal Interictal Discharges (IEDs) Per Hour, Pre to Post Treatment
NCT00916149 (32) [back to overview]	Performance on Neuropsychological Batteries and Computerized Cognitive Testing: Adverse Events Profile (AEP)
NCT00916149 (32) [back to overview]	Performance on Neuropsychological Batteries and Computerized Cognitive Testing: BVMT-R Delayed Recall
NCT00916149 (32) [back to overview]	Performance on Neuropsychological Batteries and Computerized Cognitive Testing: BVMT-R Learning
NCT00916149 (32) [back to overview]	Performance on Neuropsychological Batteries and Computerized Cognitive Testing: BVMT-R Total Learning
NCT00916149 (32) [back to overview]	Performance on Neuropsychological Batteries and Computerized Cognitive Testing: Choice Accuracy
NCT00916149 (32) [back to overview]	Performance on Neuropsychological Batteries and Computerized Cognitive Testing: Choice Reaction Time
NCT00916149 (32) [back to overview]	Performance on Neuropsychological Batteries and Computerized Cognitive Testing: CPT Accuracy
NCT00916149 (32) [back to overview]	Performance on Neuropsychological Batteries and Computerized Cognitive Testing: CPT Reaction Time (CPT RT)
NCT00916149 (32) [back to overview]	Performance on Neuropsychological Batteries and Computerized Cognitive Testing: CVLT Long Delay
NCT00916149 (32) [back to overview]	Performance on Neuropsychological Batteries and Computerized Cognitive Testing: CVLT Short Delay
NCT00916149 (32) [back to overview]	Performance on Neuropsychological Batteries and Computerized Cognitive Testing: CVLT Total Learning
NCT00916149 (32) [back to overview]	Performance on Neuropsychological Batteries and Computerized Cognitive Testing: CVLT Trial 1 Learning Score
NCT00916149 (32) [back to overview]	Performance on Neuropsychological Batteries and Computerized Cognitive Testing: Design Fluency
NCT00916149 (32) [back to overview]	Performance on Neuropsychological Batteries and Computerized Cognitive Testing: Digit Span
NCT00916149 (32) [back to overview]	Performance on Neuropsychological Batteries and Computerized Cognitive Testing: Facial Recognition Accuracy
NCT00916149 (32) [back to overview]	Performance on Neuropsychological Batteries and Computerized Cognitive Testing: Facial Recognition Reaction Time
NCT01015586 (7) [back to overview]	Montgomery-Asberg Depression Rating Scale (MADRS) Score
NCT01015586 (7) [back to overview]	Young Mania Rating Scale (YMRS) Scores
NCT01015586 (7) [back to overview]	Percent Days Abstinent From Alcohol
NCT01015586 (7) [back to overview]	Percent Heavy Drinking Days
NCT01015586 (7) [back to overview]	Neurocognitive Performance (California Verbal Learning Test)
NCT01015586 (7) [back to overview]	Biomarkers of Alcohol Use: Carbohydrate-deficient Transferrin (CDT)
NCT01015586 (7) [back to overview]	Biomarkers of Alcohol Use: Gamma-glutamyltransferase (GGT)
NCT01042496 (5) [back to overview]	N-acetylaspartic Acid (NAA) Measured in the MACC and LDLPC Using the Long TE (TE80) PRESS MRS Technique at Baseline for Both Groups, and After 12 Weeks of Lamotrigine Monotherapy for the Bipolar (BP) Group and BP Responders and Non-responders
NCT01042496 (5) [back to overview]	Glutamate+Glutamine (GLX) Measured in Mid Anterior Cingulate Cortex (MACC) & Left Dorsal Lateral Prefrontal Cortex (LDLPC) Using Long TE PRESS MRS Technique at Baseline for Both Groups; After 12 Weeks of Lamotrigine Monotherapy for the Bipolar Group
NCT01042496 (5) [back to overview]	Glutamine/Glutamate Ratio Measured in the LDLPC at Baseline Using the ProFit Magnetic Resonance Spectroscopy (MRS) Technique
NCT01042496 (5) [back to overview]	Mean Montgomery-Åsberg Depression Rating Scale (MADRS) Score at Baseline for Both Groups, and After 12 Weeks of Lamotrigine Monotherapy for the Bipolar Group
NCT01042496 (5) [back to overview]	Mean Glutamate (GLU) Measured in the MACC and LDLPC Using the ProFit MRS Technique at Baseline for Both Groups, After 12 Weeks of Lamotrigine Monotherapy for the Bipolar Group
NCT01064297 (9) [back to overview]	Birth Outcomes by Earliest Pregnancy Trimester of Exposure to Lamotrigine Monotherapy
NCT01064297 (9) [back to overview]	Number of Infants With Major Congenital Malformations by Earliest Trimester of Exposure to Lamotrigine Monotherapy
NCT01064297 (9) [back to overview]	Number of Infants With Major Congenital Malformations (MCMs) by Earliest Trimester of Exposure to Lamotrigine Polytherapy Without Valproate
NCT01064297 (9) [back to overview]	Number of Infants With Major Congenital Malformations (MCMs) by Earliest Trimester of Exposure to Lamotrigine Polytherapy With Valproate
NCT01064297 (9) [back to overview]	Number of Infants With the Indicated Major Congenital Malformations Following the First Trimester of Exposure to Lamotrigine Monotherapy According to Dose Received
NCT01064297 (9) [back to overview]	Number of Infants With the Indicated Major Congenital Malformations Following First Trimester of Exposure to Lamotrigine Polytherapy Without Valproate According to Dose of Lamotrigine Received
NCT01064297 (9) [back to overview]	Number of Infants With the Indicated Major Congenital Malformations Following First Trimester of Exposure to Lamotrigine Polytherapy With Valproate According to Dose of Lamotrigine Received
NCT01064297 (9) [back to overview]	Birth Outcomes by Earliest Pregnancy Trimester of Exposure to Lamotrigine Polytherapy Without Valproate
NCT01064297 (9) [back to overview]	Birth Outcomes by Earliest Pregnancy Trimester of Exposure to Lamotrigine Polytherapy With Valproate
NCT01142310 (1) [back to overview]	The Rey Auditory Verbal Learning Test (RAVLT)
NCT01431963 (3) [back to overview]	Time to Withdrawal/Dropout From the Study (Across Seizure Types and by Seizure Type in Past 6 Months in the Escalation and Maintenance Phases)
NCT01431963 (3) [back to overview]	Time to the First Seizure in the Maintenance Phase (Across Seizure Types and by Seizure Type)
NCT01431963 (3) [back to overview]	Number of Participants Who Were Seizure Free in the Maintenance Phase (Across Seizure Types and by Seizure Type Within 6 Months Prior to the Start of the Study)
NCT01431976 (8) [back to overview]	Number of Days With Seizure Episodes Per Week in the Extension Phase (ExP) Overall
NCT01431976 (8) [back to overview]	Number of Participants Who Were Seizure Free as Confirmed by HV-EEG at Two Consecutive Visits in the Escalation Phase (EP)
NCT01431976 (8) [back to overview]	Number of Participants Who Were Seizure Free as Confirmed by Hyperventilation (HV)-Electroencephalography (EEG) at the End of the Maintenance Phase (MP)
NCT01431976 (8) [back to overview]	Number of Days With Seizure Episodes Per Week in the Main Study Phase (Fixed Escalation Phase [FEP], Escalation Phase [EP], Maintenance Phase [MP]), and FEP+EP+MP)
NCT01431976 (8) [back to overview]	Number of Participants Who Were Seizure Free as Confirmed by HV-clinical Signs at Each Dose During the Escalation Phase
NCT01431976 (8) [back to overview]	Number of Participants Who Were Seizure Free as Confirmed by HV-clinical Signs at Each Assessment Point in the Extension Phase (ExP)
NCT01431976 (8) [back to overview]	Number of Participants Who Were Seizure Free as Confirmed by HV-clinical Signs During Week 4 and Week 8 of the Maintenance Phase
NCT01431976 (8) [back to overview]	Number of Participants Who Were Seizure Free as Confirmed by HV-EEG at Each Assessment Point in the Extension Phase (ExP)
NCT01463111 (5) [back to overview]	Change in Procrastination Assessed by the Melbourne Decision Making Questionnaire (MDMQ)
NCT01463111 (5) [back to overview]	Change in Vigilance Assessed by the Melbourne Decision Making Questionnaire (MDMQ)
NCT01463111 (5) [back to overview]	Mean Difference in Barratt Impulsiveness Scale, Version 11 (BIS-11) Score
NCT01463111 (5) [back to overview]	Change in Buckpassing Assessed by the Melbourne Decision Making Questionnaire (MDMQ)
NCT01463111 (5) [back to overview]	Change in Hypervigilance Assessed by the Melbourne Decision Making Questionnaire (MDMQ)
NCT01588457 (4) [back to overview]	Bipolar Inventory of Symptoms Scale (BISS)
NCT01588457 (4) [back to overview]	Demographic in Randomization 1 Group
NCT01588457 (4) [back to overview]	Global Assessment of Functioning
NCT01588457 (4) [back to overview]	Baseline Randomization Percentage of Bipolar Types
NCT01602510 (10) [back to overview]	Time to Intervention for Manic, Hypomanic or Mixed Episode (TIMan)
NCT01602510 (10) [back to overview]	Time to Intervention for Depressive Episode (TIDep)
NCT01602510 (10) [back to overview]	Time to Intervention for Any Mood Episode (TIME)
NCT01602510 (10) [back to overview]	Overall Survival in Study (TIME-SIS).
NCT01602510 (10) [back to overview]	Change From Baseline in Young Mania Rating Scale (YMRS) Total Score
NCT01602510 (10) [back to overview]	Change From Baseline in Hamilton Depression Rating Scale (HAMD)
NCT01602510 (10) [back to overview]	Change From Baseline in Clinical Global Impression of Severity (CGI-S)
NCT01602510 (10) [back to overview]	Change From Baseline in Clinical Global Impression of Improvements (CGI-I)
NCT01602510 (10) [back to overview]	Change From Baseline of Global Assessment Scale (GAS) Total Score
NCT01602510 (10) [back to overview]	Change From Baseline in Body Weight
NCT01674010 (1) [back to overview]	Treatment Emergent Adverse Events
NCT01880957 (5) [back to overview]	Relationship Between Change in 5-HTT or 5-HT1A Binding Potential Pre- to Post Treatment and Lithium Treatment Response
NCT01880957 (5) [back to overview]	Group Differences in 5-HT1A Binding Potential
NCT01880957 (5) [back to overview]	Group Differences in 5-HTT Binding Potential
NCT01880957 (5) [back to overview]	Prediction of Treatment Response
NCT01880957 (5) [back to overview]	Post-Lithium Treatment Hamilton Depression Rating Scale (HDRS)
NCT01891890 (11) [back to overview]	Child Behavior Checklist
NCT01891890 (11) [back to overview]	Affective Reactivity Scale
NCT01891890 (11) [back to overview]	Wechsler Intelligence Scale for Children-IV Processing Speed
NCT01891890 (11) [back to overview]	Story Memory
NCT01891890 (11) [back to overview]	Conners' Continuous Performance Test II (CPT-II) Confidence Index
NCT01891890 (11) [back to overview]	Grooved Pegboard
NCT01891890 (11) [back to overview]	The Number of Participants With a Positive Response on the Columbia-Suicide Severity Rating Scale (C-SSRS)
NCT01891890 (11) [back to overview]	Parenting Stress Inventory Short Form (PSI-4-SF)
NCT01891890 (11) [back to overview]	Pediatric Inventory for Parents
NCT01891890 (11) [back to overview]	Pediatric Neuro-QOL Score
NCT01891890 (11) [back to overview]	Symbol Digit Modalities Test
NCT01995825 (2) [back to overview]	Cmax
NCT01995825 (2) [back to overview]	AUC
NCT02100644 (7) [back to overview]	Number of Days in Total That Epileptic Seizures Occurred up to the LTG and VPA Maintenance Phase
NCT02100644 (7) [back to overview]	Percent Change in the VPA Dose
NCT02100644 (7) [back to overview]	Change From Baseline in Quality of Life in Epilepsy for Adolescents (QOLIE-AD-48) in Participants Aged 15-17 Years
NCT02100644 (7) [back to overview]	Change From Baseline in Quality of Life in Epilepsy-31-P (QOLIE-31-P) in Participants Aged 18 Years and Older
NCT02100644 (7) [back to overview]	Number of Participants With Adverse Events (AEs), AEs Leading to Discontinuation of the Investigational Product and/or Withdrawal From the Study, Drug-related AEs, Deaths and Serious Adverse Events (SAEs) Throughout the Study
NCT02100644 (7) [back to overview]	Percentage of Participants Who Completed or Discontinued From the Study
NCT02100644 (7) [back to overview]	Percentage of Participants Who Achieved Reduction in Daily VPA Dose
NCT02158585 (6) [back to overview]	Difference in Ménière's Vertigo Attacks in Three-Week Intervals Between Lamotrigine and Placebo Groups
NCT02158585 (6) [back to overview]	Improvement in Pure Tone Average in the Affected Ear
NCT02158585 (6) [back to overview]	Improvement in Symptoms Severity
NCT02158585 (6) [back to overview]	DHI Scores
NCT02158585 (6) [back to overview]	Change in Ménière's Vertigo Attack Frequency Between Lamotrigine and Placebo Group
NCT02158585 (6) [back to overview]	Change in Ménière's Vertigo Attack Frequency Within Lamotrigine Group
NCT02404168 (2) [back to overview]	AUC
NCT02404168 (2) [back to overview]	Cmax
NCT02707965 (5) [back to overview]	Number of Seizures Reported
NCT02707965 (5) [back to overview]	Mean AUC0-last_ss (Test vs. Reference)
NCT02707965 (5) [back to overview]	Mean Cmax_ss (Test vs. Reference)
NCT02707965 (5) [back to overview]	Mean Cmin_ss (Test vs. Reference)
NCT02707965 (5) [back to overview]	Number of Adverse Events
NCT02821338 (6) [back to overview]	AUC 0-Inf
NCT02821338 (6) [back to overview]	Area Under the Lamotrigine Concentration vs. Time Curve From Sample Time Point 0 Hour to Sample Time Point 144 Hour.
NCT02821338 (6) [back to overview]	Tmax
NCT02821338 (6) [back to overview]	λZ
NCT02821338 (6) [back to overview]	Thalf
NCT02821338 (6) [back to overview]	Cmax
NCT02989727 (18) [back to overview]	Montgomery-Asberg Depression Rating Scale (MADRS) Change Scores
NCT02989727 (18) [back to overview]	Hamilton Depression Rating Scale (HAMD-17) Change Scores
NCT02989727 (18) [back to overview]	Number of Participants With 50% Reduction in the Montgomery-Asberg Depression Rating Scale (MADRS)
NCT02989727 (18) [back to overview]	Number of Participants With 50% Reduction in the Hamilton Depression Rating Scale (HAMD-17)
NCT02989727 (18) [back to overview]	Number of Participants With 50% Reduction in the Montgomery-Asberg Depression Rating Scale (MADRS)
NCT02989727 (18) [back to overview]	Number of Participants With 50% Reduction in the Montgomery-Asberg Depression Rating Scale (MADRS)
NCT02989727 (18) [back to overview]	Number of Participants With 50% Reduction in the Montgomery-Asberg Depression Rating Scale (MADRS)
NCT02989727 (18) [back to overview]	Number of Participants With 50% Reduction in the Hamilton Depression Rating Scale (HAMD-17)
NCT02989727 (18) [back to overview]	Number of Participants With 50% Reduction in the Montgomery-Asberg Depression Rating Scale (MADRS)
NCT02989727 (18) [back to overview]	Number of Participants With 50% Reduction in the Montgomery-Asberg Depression Rating Scale (MADRS)
NCT02989727 (18) [back to overview]	Number of Participants With 50% Reduction in the Montgomery-Asberg Depression Rating Scale (MADRS)
NCT02989727 (18) [back to overview]	Number of Participants With 50% Reduction in the Hamilton Depression Rating Scale (HAMD-17)
NCT02989727 (18) [back to overview]	Number of Participants With 50% Reduction in the Hamilton Depression Rating Scale (HAMD-17)
NCT02989727 (18) [back to overview]	Number of Participants With 50% Reduction in the Hamilton Depression Rating Scale (HAMD-17)
NCT02989727 (18) [back to overview]	Number of Participants With 50% Reduction in the Hamilton Depression Rating Scale (HAMD-17)
NCT02989727 (18) [back to overview]	Number of Participants With 50% Reduction in the Hamilton Depression Rating Scale (HAMD-17)
NCT02989727 (18) [back to overview]	Number of Participants With 50% Reduction in the Montgomery-Asberg Depression Rating Scale (MADRS)
NCT02989727 (18) [back to overview]	Number of Participants With 50% Reduction in the Hamilton Depression Rating Scale (HAMD-17)
NCT03695094 (15) [back to overview]	The Apparent Total Plasma Clearance at Steady-state (CL/Fss) for PSL During the Study
NCT03695094 (15) [back to overview]	Trough Plasma Concentration of Mono Hydroxy Derivate (MHD) in the Inducers Group Before, During and After Dosing to Steady State With PSL
NCT03695094 (15) [back to overview]	The Time to Reach Maximum Concentration (Tmax) for UCB1447499-000 During the Study
NCT03695094 (15) [back to overview]	The Time to Reach Maximum Concentration (Tmax) for UCB1431322-000 During the Study
NCT03695094 (15) [back to overview]	The Time to Reach Maximum Concentration (Tmax) for Padsevonil During the Study
NCT03695094 (15) [back to overview]	The Ratio of PSL Metabolite UCB1431322-000 to PSL Based on the Area Under the Curve (AUCtau) During the Study
NCT03695094 (15) [back to overview]	The Maximum Observed Plasma Concentration (Cmax) of Padsevonil (PSL) During the Study
NCT03695094 (15) [back to overview]	The Maximum Observed Plasma Concentration (Cmax) for UCB1447499-000 During the Study
NCT03695094 (15) [back to overview]	The Maximum Observed Plasma Concentration (Cmax) for UCB1431322-000 During the Study
NCT03695094 (15) [back to overview]	The Area Under the Plasma Concentration Time Curve (AUCtau) Over a Dosing Interval for PSL
NCT03695094 (15) [back to overview]	The Area Under the Curve (AUCtau) Over a Dosing Interval for UCB1447499-000 During the Study
NCT03695094 (15) [back to overview]	The Area Under the Curve (AUCtau) Over a Dosing Interval for UCB1431322-000 During the Study
NCT03695094 (15) [back to overview]	The Ratio of PSL Metabolite UCB1447499-000 to PSL Based on the Area Under the Curve (AUCtau)
NCT03695094 (15) [back to overview]	Percentage of Participants With at Least One Serious Adverse Event (SAE) During the Study
NCT03695094 (15) [back to overview]	Percentage of Participants With at Least One Adverse Event (AE) During the Study
NCT03831854 (9) [back to overview]	Number of Patients With Psychologic Disturbances-
NCT03831854 (9) [back to overview]	Opioid Related Side-effects (ORSDS)-POD1
NCT03831854 (9) [back to overview]	Opioid Related Side-effects (ORSDS)-POD2
NCT03831854 (9) [back to overview]	Pain Score in PACU
NCT03831854 (9) [back to overview]	Psychologic Side-effects
NCT03831854 (9) [back to overview]	Daily Average Opioid Use During Hospital Stay
NCT03831854 (9) [back to overview]	Number of Patients Who Had PONV (Postoperative Nausea Vomiting)
NCT03831854 (9) [back to overview]	PACU Length of Stay, Hours
NCT03831854 (9) [back to overview]	Total Opioid Consumption in PACU (mg)

The Proportion of Patients Who Experience a Marked and Persistent Bimodal Response

"A marked bimodal response is defined by the following three conditions over four consecutive weeks while on triple therapy and after three weeks of ltg:~Montgomery Asberg Depression Rating Scale (MADRS) total score of <= 19~Young Mania Rating Scale (YMRS) total score of <= 12.5~Global Assessment Scale (GAS) score >= 51~The MADRS measures the severity of a subject's depression symptoms with a possible total score ranging from 0 - 60, with higher scores indicating more severe depression.~The YMRS measures the severity of a subject's manic symptoms with a possible total score ranging from 0 - 60, with higher scores indicating more severe mania.~The GAS measures a used to rate subjectively the social, occupational, and psychological functioning of a subject and ranges in score from 0-100, with a higher score indicating better social, occupational, and psychological functioning." (NCT00063362)
Timeframe: Baseline and Week 28

Intervention	participants (Number)
Lithium + Divalproex + Lamotrigine	7
Lithium + Divalproex + Placebo	8

Intervention	participants (Number)
	2 weeks	4 weeks	8 weeks	12 weeks	16 weeks
Double-Blind Phase: LTG XR	22	28	39	43	48
Double-Blind Phase: Placebo	12	12	14	20	23

Intervention	percent change (Median)
	Escalation Phase, n=72, 69	Maintenance Phase, n=70, 68	Last 8 weeks of the Maintenance Phase, n=70, 68
Double-Blind Phase: LTG XR	61.9	89.7	100.0
Double-Blind Phase: Placebo	30.6	33.3	35.4

Intervention	percent change (Median)
	Entire Continuation Phase, n=68, 66, 24	Transition Phase, n=68, 66, 20	Open-Label Phase, n=68, 64, 23	Last 8 weeks of Open-Label Phase, n=68, 63, 19
Baseline Failures	21.7	100.0	31.7	100.0
Continuation Phase: LTG/LTG	95.1	100.0	95.0	100.0
Continuation Phase: Placebo/LTG	85.2	73.1	89.2	100.0

Intervention	points on a scale (Least Squares Mean)
Double-Blind Phase: Placebo	-0.6
Double-Blind Phase: LTG XR	1.0

Intervention	kilograms (Median)
Double-Blind Phase: Placebo	1.00
Double-Blind Phase: LTG XR	0.00

Intervention	points on a scale (Least Squares Mean)
Double-Blind Phase: Placebo	-0.1
Double-Blind Phase: LTG XR	-2.4

Intervention	points on a scale (Least Squares Mean)
Double-Blind Phase: Placebo	-6.5
Double-Blind Phase: LTG XR	-8.5

Intervention	percent change (Median)
Double-Blind Phase: Placebo	32.1
Double-Blind Phase: LTG XR	75.4

Intervention	participants (Number)
	>=25% reduction, Entire DB TP, n=72, 69	>=50% reduction, Entire DB TP, n=72, 69	>=75% reduction, Entire DB TP, n=72, 69	100% reduction, Entire DB TP, n=72, 69	>=25% reduction, Escalation Phase, n=72, 69	>=50% reduction, Escalation Phase, n=72, 69	>=75% reduction, Escalation Phase, n=72, 69	100% reduction, Escalation Phase, n=72, 69	>=25% reduction, Maintenance Phase, n=70, 68	>=50% reduction, Maintenance Phase, n=70, 68	>=75% reduction, Maintenance Phase, n=70, 68	100% reduction, Maintenance Phase, n=70, 68	>=25% reduction, Last 8 Weeks of MP, n=70, 68	>=50% reduction, Last 8 Weeks of MP, n=70, 68	>=75% reduction, Last 8 Weeks of MP, n=70, 68	100% reduction, Last 8 Weeks of MP, n=70, 68
Double-Blind Phase: LTG XR	56	48	35	14	51	38	24	15	60	51	40	31	61	54	44	35
Double-Blind Phase: Placebo	43	23	14	7	39	23	14	9	46	29	14	10	47	29	18	15

Intervention	participants (Number)
	>=25% reduction, Entire CP, n=68, 66, 24	>=50% reduction, Entire CP, n=68, 66, 24	>=75% reduction, Entire CP, n=68, 66, 24	100% reduction, Entire CP, n=68, 66, 24	>=50% increase, Entire CP, n=68, 66, 24	>=25% reduction, Transition Phase, n=68, 66, 20	>=50% reduction, Transition Phase, n=68, 66, 20	>=75% reduction, Transition Phase, n=68, 66, 20	100% reduction, Transition Phase, n=68, 66, 20	>=50% increase, Transition Phase, n=68, 66, 20	>=25% reduction, Open-Label Phase, n=68, 64, 23	>=50% reduction, Open-Label Phase, n=68, 64, 23	>=75% reduction, Open-Label Phase, n=68, 64, 23	100% reduction, Open-Label Phase, n=68, 64, 23	>=50% increase, Open-Label Phase, n=68, 64, 23	>=25% reduction, Last 8 W of OL Phase,n=68, 63, 19	>=50% reduction, Last 8 W of OL Phase,n=68, 63, 19	>=75% reduction, Last 8 W of OL Phase,n=68, 63, 19	100% reduction, Last 8 W of OL Phase, n=68, 63, 19	>=50% increase, Last 8 W of OL Phase, n=68, 63, 19
Baseline Failures	11	11	8	6	10	13	12	12	12	3	12	10	8	6	10	10	10	10	10	4
Continuation Phase: LTG/LTG	63	59	49	28	1	60	56	46	41	1	61	57	49	28	1	60	53	47	41	1
Continuation Phase: Placebo/LTG	59	57	46	16	2	51	44	33	27	3	61	56	47	21	2	60	53	45	35	2

Intervention	participants (Number)
	Any improvement, score of 5-7	No change, score of 4	Any deterioration, score of 1-3
Double-Blind Phase: LTG XR	57	10	1
Double-Blind Phase: Placebo	36	33	2

Intervention	units on a scale (Mean)
	Baseline	8 week point	14 week point
Lamotrigine Effectiveness on YMRS (Mania Measure)	19.61	7.06	5.68

Intervention	units on a scale (Mean)
Double-Blind Lamotrigine and Divalproex ER	4.54
Double-Blind Lamotrigine and Placebo Divalproex ER	5.57

Intervention	scores on a pain scale (Mean)
	Heat Affected	Heat Unaffected	Cold Affected	Cold Unaffected	Brush Affected	Brush Unaffected
Lamotrigine	3.2	3	2.1	2.2	2.8	1.2
Placebo	5.5	4	2.5	1.1	3.9	.4

Intervention	Z-statistic (Number)
	Heat Affected Thalamus (10,-14,8)	Heat Affected Post-Central (-56,-12,28)	Cold Affected Post-Central (68, -8, 32)	Cold Affected Thalamus (-4, -8, 0)	Brush Affected Post-Central (66,-16,14)	Brush Affected Thalamus (-14,-22, 4)	Brush Affected Spinal Trigeminal Nucles(2,-48,-68)
Lamotrigine vs Placebo	-2.9294	-2.7323	-2.5114	-3.033	3.905	-3.791	2.9058

Intervention	Proportion of Participants (Number)
	Week 0 (n=173, n=178)	Week 2 (n=163, n=175)	Week 4 (n=151, n=160)	Week 6 (n=145, n=149)	Week 8 (n=132, n=136)	Week 12 (n=119, n=123)	Week 16 (n=102, n=113)	Week 20 (n=102, n=111)	Week 24 (n=91, n=95)	Week 28 (n=79, n=85)	Week 32 (n=74, n=82)	Week 36 (n=74, n=76)	Week 40 (n=74, n=70)	Week 44 (n=74, n=70)	Week 48 (n=74, n=70)	Week 52 (n=19, n=70)
Phase 2 Double-Blind Treatment: Lamotrigine + Aripiprazole	1.00	0.98	0.95	0.94	0.93	0.90	0.89	0.89	0.87	0.85	0.84	0.83	0.82	0.82	0.82	0.82
Phase 2 Double-Blind Treatment: Lamotrigine + Placebo	1.00	0.98	0.94	0.91	0.89	0.85	0.84	0.84	0.82	0.79	0.79	0.79	0.79	0.79	0.79	0.76

Intervention	particiapnts (Number)
	Tachycardia: ≥ 120 bpm and ↑ ≥ 15 bpm	Bradycardia: ≤ 50 bpm and ↓ 15 bpm	Sinus Tachycardia: ≥ 120 bpm and ↑ ≥ 15 bpm	Sinus Bradycardia: ≤ 50 bpm and ↓ 15 bpm	SPB: not present → present (see description)	VPB: not present → present (see description)	Supraventricular Tachycardia: not present→ present	Ventricular Tachycardia: not present → present	Atrial Fibrillation (AF): not present → present	AF With Rapid Ventricular Response	Atrial Flutter: not present → present	1st Degree A-V Block: PR ≥0.20 sec and ↑ ≥0.05 sec	2nd Degree A-V Block: not present → present	3rd Degree A-V Block: not present → present	Left Bundle Branch Block: not present → present	Right Bundle Branch Block: not present → present	Pre-excitation Syndrome: not present → present	Other Intraventricular Conduction: see description	Acute Infarction: not present → present	Subacute (recent) Infarction: not present→ present	Old Infarction: not present → present	Myocardial Ischemia: not present → present	Symmetrical T-Wave Inversions: not present→present	QTc Bazett: > 450 msec	QTc (.37): > 450 msec	QTc (.33): > 450 msec
Phase 2 Double-Blind Treatment: Lamotrigine + Aripiprazole	1	0	0	0	0	1	0	0	0	0	1	0	0	0	0	4	0	0	0	0	0	0	0	6	0	1
Phase 2 Double-Blind Treatment: Lamotrigine + Placebo	1	2	1	2	0	2	0	0	0	0	0	0	0	0	0	6	0	0	0	0	1	0	0	5	0	0

Intervention	kg (Mean)
Phase 2 Double-Blind Treatment: Lamotrigine + Placebo	-1.81
Phase 2 Double-Blind Treatment: Lamotrigine + Aripiprazole	0.43

Intervention	units on a scale (Mean)
	Baseline (n=125, 128)	Change from Baseline at Week 8 (n=124, 124)	Change from Baseline at Week 24 (n=85, 89)	Change from Baseline at Week 36 (n=54, 67)	Change from Baseline at Week 52 (n=50, 56)	Change from Baseline at Week 52 LOCF (n=153, 161)	Highest Change from Baseline (n=153, 161)
Phase 2 Double-Blind Treatment: Lamotrigine + Aripiprazole	0.14	0.06	0.04	0.13	-0.05	-0.01	0.14
Phase 2 Double-Blind Treatment: Lamotrigine + Placebo	0.21	-0.05	-0.01	-0.09	-0.11	0.05	0.10

Intervention	units on a scale (Mean)
	Baseline (n=125, 128)	Change from Baseline at Week 8 (n=125, 124)	Change from Baseline at Week 24 (n=85, 89)	Change from Baseline at Week 36 (n=54, 67)	Change from Baseline at Week 52 (n=50, 56)	Change from Baseline at Week 52 LOCF (n=153, 161)	Highest Change from Baseline (n=153, 161)
Phase 2 Double-Blind Treatment: Lamotrigine + Aripiprazole	0.27	0.04	-0.06	-0.18	-0.17	-0.05	0.15
Phase 2 Double-Blind Treatment: Lamotrigine + Placebo	0.22	-0.12	-0.09	-0.18	-0.20	-0.11	-0.02

lamotrigine

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Clinical Trials (189)

Trial Overview

Trial Outcomes

The Proportion of Patients Who Experience a Marked and Persistent Bimodal Response

Change in Brief Pain Inventory (BPI) Worst Pain Score [Week 10 Minus Baseline]

Change in Average Daily Pain Score as Measured Using a Pain Intensity Rating (NRS)

Change in Average Pain Score as Measured Using the European Cooperative Oncology Group (ECOG) Neuropathy Scale (ENS)

Change in Brief Pain Inventory (BPI) Average Pain Score [Week 10 Minus Baseline]

Change in Brief Pain Inventory (BPI) Least Pain Score [Week 10 Minus Baseline]

Change in Brief Pain Inventory (BPI) Pain Interference Score [Week 10 Minus Baseline]

Change in Brief Pain Inventory (BPI) Pain Now Score [Week 10 Minus Baseline]

Change in Brief Pain Inventory (BPI) Pain Relief Score [Week 10 Minus Baseline]

Change in POMS Total Score [Week 10 Minus Baseline]

The Change in Overall Quality of Life as Measured by the Uniscale QOL From Baseline to Week 10

Number of Participants With Freedom From Treatment Failure at 16-20 Weeks of Double Blind Therapy

Number of Participants With Freedom From Treatment Failure at 12 Months of Double Blind Therapy

Number of Participants With Attention Deficit as Measured by the Confidence Index of the CPT-II and the K-CPT

Number of Participants With the Indicated Time to >=50% Reduction in Seizure Frequency in the Double-Blind Treatment Phase

Percent Change From Baseline in PGTC Seizure Frequency During the Escalation Phase, the Maintenance Phase, and During the Last 8 Weeks of the Maintenance Phase of the Double-Blind Treatment Phase

Percent Change From Baseline in Weekly PGTC Seizure Frequency During the Entire Continuation Phase (CP), the Transition Phase, the Open-Label Phase, and the Last 8 Weeks of the Open-Label Phase

Mean Change From Baseline in the Epworth Sleepiness Scale (ESS) 8-Item Total Score at Week 19 of the Double-Blind Treatment Phase

Change From Baseline in Body Weight at Week 19 of the Double-Blind Treatment Phase

Mean Change From Baseline in the Adverse Experience Profile (AEP) Total Score at Week 19 of the Double-Blind Treatment Phase

Mean Change From Baseline in the Center for Epidemiological Studies-Depression Scale (CES-D) Total Score at Week 19 of the Double-Blind Treatment Phase

Mean Change From Baseline in the Neurological Disorders Depression Inventory-Epilepsy (NDDI-E) 6-Item Total Score at Week 19 of the Double-Blind Treatment Phase

Mean Change From Baseline in the Profile of Mood State (POMS) Mood Disturbance Total Score at Week 19 of the Double-Blind Treatment Phase

Mean Change From Baseline in the Quality of Life in Epilepsy-31-P (QOLIE-31P) Overall Score at Week 19 of the Double-Blind Treatment Phase

Mean Change From Baseline in the Seizure Severity Questionnaire (SSQ) Global Bother Score at Week 19 Double-Blind Treatment Phase

Percent Change From Baseline in Weekly Primary Generalized Tonic-clonic (PGTC) Seizure Frequency During the Entire Double-Blind Treatment Phase

Number of Participants With >=25%, >=50%, >=75%, or 100% Reduction in PGTC Seizure Frequency During the Entire Double-Blind (DB)Treatment Phase (TP), the Escalation Phase, the Maintenance Phase, and the Last 8 Weeks of the Maintenance Phase

Number of Participants With >=25%, >=50%, >=75%, or 100% Reduction or >=50% Increase From Baseline in Weekly PGTC Seizure Frequency for the Entire Continuation Phase, the Transition Phase, the Open-Label (OL) Phase, and the Last 8 Weeks of the OL Phase.

Number of Participants With Improved Clinical Status on the Investigator's Global Assessment in the Double-Blind Treatment Phase

Number of Participants With Improved Satisfaction With Seizure Control on the Subject Satisfaction Questionnaire in the Double-Blind Treatment Phase

Young Mania Rating Scale (YMRS),

Child Depression Rating Scale (CDRS-R)

Change of Mania Symptoms Assessed by Young Mania Rating Scale (YMRS)

Mania Rating Scale

Average Number of Pain Attacks

Rey Auditory Verbal Learning Test (RAVLT)

Subjective Ratings of Pain During Magnetic Resonance Scanning

Blood Oxygenation Level-dependent (BOLD) Changes in Neural Pain Circuitry Following Treatment With Lamotrigine During Experimentally Induced Pain States

Proportion of Participants Not Experiencing a Depressive Relapse in the Double-blind Relapse Assessment Phase (Phase 2)

Number of Participants With Potentially Clinically Significant Electrocardiogram (ECG) Abnormalities Occurring During Double-Blind Treatment

Adjusted Mean Change From Baseline in Body Weight, Phase 2

Adjusted Mean Change From Baseline in Abnormal Involuntary Movement Scale (AIMS) Total Score

Adjusted Mean Change From Baseline in Barnes Akathisia Global Clinical Assessment,

Adjusted Mean Change From Baseline in BMI by Study Week

Adjusted Mean Change From Baseline in Simpson-Angus Scale (SAS) Total Score

Deaths, Treatment-Emergent Serious Adverse Events (SAEs), Adverse Events (AEs) Leading to Discontinuation of Study Medication, Treatment-Emergent AEs and Treatment-Emergent Extrapyramidal Syndrome (EPS)-Related AEs

Number of Participants Showing Clinically Relevant Weight Gain by Study Week

Number of Participants Showing Clinically Relevant Weight Loss by Study Week

Number of Participants With Potentially Clinically Relevant Laboratory Abnormalities Occurring During Double-Blind Treatment (Phase 2)

Intervention	kg/m2 (Mean)
	Baseline (n=143, 150)	Change from Baseline Week 12 (n=105, 107)	Change from Baseline Week 24 (n=84, 87)	Change from Baseline Week 36 (n=54, 67)	Change from Baseline Week 52 (n=49, 56)	Change from Baseline Week 52 LOCF (n=143, 150)	Highest Change from Baseline (n=143, 150)
Phase 2 Double-Blind Treatment: Lamotrigine + Aripiprazole	30.13	-0.03	0.14	0.34	0.19	0.17	0.61
Phase 2 Double-Blind Treatment: Lamotrigine + Placebo	30.77	-0.39	-0.60	-0.63	-0.73	-0.62	-0.02

Intervention	participants (Number)
	Deaths	Treatment-Emergent SAEs	Suicide-Related SAEs	AEs Leading to Discontinuation of Study Medication	Treatment-Emergent AEs	Treatment-Emergent EPS-Related AEs
Phase 2 Double-Blind Treatment: Lamotrigine + Aripiprazole	0	5	0	14	124	28
Phase 2 Double-Blind Treatment: Lamotrigine + Placebo	0	9	0	12	111	15

Intervention	Participants (Number)
	Week 12 (n=105, 107)	Week 24 (n=84, 87)	Week 36 (n=54, 67)	Week 52 (n=49, 56)	Week 52 LOCF (n=143, 151)	At Any Time (n=147, 154)
Phase 2 Double-Blind Treatment: Lamotrigine + Aripiprazole	4	10	14	7	18	27
Phase 2 Double-Blind Treatment: Lamotrigine + Placebo	2	3	5	2	5	8

Intervention	particiapnts (Number)
	ALT ≥3 x ULN (n=151,157)	AST ≥3 x ULN (n=151, 157)	ALP ≥3 x ULN (n=151, 157)	LDH ≥3 x ULN (n=151, 158)	BUN ≥30 mg/dL (n=151, 158)	Creatine kinase (n=3, 1)	Creatinine ≥2.0 mg/dL (n=151, 157)	Uric acid (n=151, 157)	Bilirubin (total) ≥ 2.0 mg/dL (n=152, 157)	Prolactin (n=152, 158)	Cholesterol Total (n=151, 157)	Cholesterol Total (fasting) (n=126, 124)	Cholesterol Total (non-fasting) (n=68, 75)	Glucose Fasting Serum (n=126, 125)	HDL-C (n=151, 158)	HDL-C (fasting) (n=126, 125)	HDL-C (non-fasting) (n=68, 75)	LDL-C (n=151, 157)	LDL-C (fasting) (n=126, 124)	LDL-C (non-fasting) (n=68, 75)	Triglycerides (n=151, 157)	Triglycerides (fasting) (n=126, 124)	Triglycerides (non-fasting) (n=68, 75)	Sodium serum (n=152, 158)	Potassium serum (n=152, 158)	Chloride serum (n=152, 158)	Calcium (n=151, 157)	Hemoglobin ≤11.5 g/dL(m)/≤9.5 g/dL(f) (n=152, 156)	Hematocrit ≤37(m)/≤32(f) & 3 ↓from BL (n=152,156)	Leukocytes ≤2800 mm^3 or ≥16000 mm^3 (n=152, 156)	Eosinophils relative (calculated)≥10% (n=152, 156)	Neutrophils relative (calculated)≤15% (n=152, 156)	Platelets ≤75,000 mm3 or ≥700,000 mm3 (n=152,155)	Protein urine increase of ≥2 units (n=145, 152)	Glucose urine (n=149, 155)
Phase 2 Double-Blind Treatment: Lamotrigine + Aripiprazole	0	1	0	0	2	0	0	2	0	18	28	25	7	13	38	25	19	26	22	5	0	29	20	0	0	0	0	0	3	2	2	0	0	0	0
Phase 2 Double-Blind Treatment: Lamotrigine + Placebo	3	2	0	0	0	0	0	0	0	32	22	17	9	15	53	44	23	17	14	7	0	26	19	1	0	0	0	1	1	0	2	0	0	0	0

Intervention	participants (Number)
	Systolic BP, supine-Increase (n=160,168)	Systolic BP, supine-Decrease (n=160,168)	Systolic BP, standing-Increase (n=153, 157)	Systolic BP, standing-Decrease (n=153,157)	Diastolic BP, supine-Increase (n=160,168)	Diastolic BP, supine-Decrease (n=160,168)	Diastolic BP, standing-Increase (n=153,157)	Diastolic BP, standing-Decrease (n=153,157)	Heart Rate, supine-Increase (n=160,168)	Heart Rate, supine-Decrease (n=160,168)	Heart Rate, standing-Increase (n=153, 157)	Heart Rate, standing-Decrease (n=153, 157)
Phase 2 Double-Blind Treatment: Lamotrigine + Aripiprazole	1	5	0	4	0	3	1	1	0	0	2	0
Phase 2 Double-Blind Treatment: Lamotrigine + Placebo	3	7	3	2	2	0	6	0	0	3	4	1

Intervention	Proportion of Participants (Number)
	Week 0 (n=173, n=178)	Week 2 (n=163, n=175)	Week 4 (n=154, n=160)	Week 6 (n=145, n=149)	Week 8 (n=135, n=136)	Week 12 (n=121, n=123)	Week 16 (n=102, n=113)	Week 20 (n=94, n=111)	Week 24 (n=91, n=95)	Week 28 (n=78, n=85)	Week 32 (n=69, n=83)	Week 36 (n=67, n=76)	Week 40 (n=62, n=70)	Week 44 (n=62, n=70)	Week 48 (n=62, n=70)	Week 52 (n=19, n=70)
Phase 2 Double-Blind Treatment: Lamotrigine + Aripiprazole	1.00	0.95	0.91	0.88	0.84	0.82	0.80	0.80	0.78	0.77	0.75	0.74	0.73	0.73	0.73	0.73
Phase 2 Double-Blind Treatment: Lamotrigine + Placebo	1.00	0.96	0.91	0.87	0.83	0.76	0.75	0.74	0.69	0.65	0.62	0.62	0.61	0.61	0.61	0.58

Intervention	Proportion of Participants (Number)
	Week 0 (n=173, n=178)	Week 2 (n=162, n=172)	Week 4 (n=154, n=159)	Week 6 (n=142, n=147)	Week 8 (n=135, n=135)	Week 12 (n=121, n=127)	Week 16 (n=101, n=127)	Week 20 (n=94, n=127)	Week 24 (n=86, n=127)	Week 28 (n=79, n=127)	Week 32 (n=69, n=83)	Week 36 (n=67, n=83)	Week 40 (n=62, n=83)	Week 44 (n=62, n=83)	Week 48 (n=62, n=83)	Week 52 (n=62, n=83)
Phase 2 Double-Blind Treatment: Lamotrigine + Aripiprazole	1.00	0.98	0.96	0.93	0.90	0.90	0.90	0.90	0.90	0.90	0.89	0.89	0.89	0.89	0.89	0.89
Phase 2 Double-Blind Treatment: Lamotrigine + Placebo	1.00	0.98	0.97	0.95	0.93	0.89	0.88	0.88	0.84	0.81	0.78	0.78	0.77	0.77	0.77	0.77

Intervention	Proportion of Participants (Number)
	Week 0 (n=173, n=178)	Week 2 (n=164, n=175)	Week 4 (n=155, n=161)	Week 6 (n=145, n=149)	Week 8 (n=135, n=138)	Week 12 (n=122, n=124)	Week 16 (n=103, n=115)	Week 20 (n=95, n=110)	Week 24 (n=90, n=104)	Week 28 (n=78, n=89)	Week 32 (n=70, n=83)	Week 36 (n=64, n=77)	Week 40 (n=61, n=72)	Week 44 (n=57, n=69)	Week 48 (n=56, n=66)	Week 52 (n=19, n=65)
Phase 2 Double-Blind Treatment: Lamotrigine + Aripiprazole	0.99	0.91	0.84	0.78	0.70	0.65	0.62	0.59	0.51	0.47	0.44	0.41	0.39	0.38	0.37	0.37
Phase 2 Double-Blind Treatment: Lamotrigine + Placebo	0.95	0.90	0.84	0.79	0.71	0.61	0.55	0.53	0.46	0.41	0.38	0.36	0.34	0.33	0.32	0.25

Intervention	participants (Number)
	Any central nervous system Medication	Analgesic	Anesthetic, general	Anesthetic, local	Anticholinergic	Antidepressant	Antiepileptic	Antimigraine prep	Antipsychotic	Anxiolytic	Hypnotic & Sedative	Opiod	Other Analgesic & Antipyretic	Other Nervous System Drug	Psychostimulant	Any extrapyramidal syndrome Medication	Benztropine
Phase 1: Single-Blind Treatment, Lamotrigine + Aripiprazole	550	2	1	3	98	12	48	12	20	267	206	78	253	1	2	98	98

Intervention	percentage of participants (Number)
Pregabalin 150 mg/Day	70.5
Pregabalin 300 mg/Day	59.7
Pregabalin 450 mg/Day	20.4
Pregabalin 600 mg/Day	13.0
Lamotrigine 100 mg/Day	80.5
Lamotrigine 200 mg/Day	67.9
Lamotrigine 400 mg/Day	38.2
Lamotrigine 500 mg/Day	16.7