预约演示
更新于：2026-06-23
Lamotrigine
拉莫三嗪
更新于：2026-06-23
概要
基本信息
简介拉莫三嗪是一种抗惊厥药物，于1994年12月27日首次被美国食品和药品管理局批准上市。由制药公司葛兰素史克开发的，主要用于治疗Lennox Gastaut综合征、癫痫和双相情感障碍等疾病。拉莫三嗪的作用机制是通过阻断大脑中的钠通道，以稳定神经元的电活动，减轻癫痫发作的严重程度和频率。此外，拉莫三嗪还被用于治疗双相情感障碍的抑郁症状。该药物已被证明对减少癫痫发作的频率和改善患者生活质量具有显著疗效。 |
药物类型 小分子化药 |
别名 3,5-diamino-6-(2,3-dichlorophenyl)-1,2,4-triazine、Lamotrigine (JAN/USP/INN)、430-C-78 + [14] |
作用方式 阻滞剂 |
作用机制 钠通道阻滞剂 |
原研机构 |
最高研发阶段批准上市 |
首次获批日期 (1990-01-01), |
最高研发阶段(中国)批准上市 |
特殊审评孤儿药 (美国)、优先审评 (中国) |
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结构/序列
分子式C9H7Cl2N5 |
InChIKeyPYZRQGJRPPTADH-UHFFFAOYSA-N |
CAS号84057-84-1 |
关联
239
项与 拉莫三嗪 相关的临床试验ChiCTR2600121573
Exploration and mechanism research on the preventive and synergistic therapeutic effects of systematic interpersonal therapy on depressive disorders with mixed characteristics in adolescents
NCT06929273
A Phase 3, Open-label Extension Study to Assess the Long-term Safety of KarXT for the Treatment of Mania or Mania With Mixed Features in Bipolar-I Disorder (BALSAM-3)
CTR20252056
拉莫三嗪分散片的生物等效性试验（空腹用药试验）
100 项与 拉莫三嗪 相关的临床结果
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100 项与 拉莫三嗪 相关的转化医学
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100 项与 拉莫三嗪 相关的专利（医药）
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8,510
项与 拉莫三嗪 相关的文献（医药）2026-09-01EUROPEAN NEUROPSYCHOPHARMACOLOGY
Shared and distinct effects of mood stabilizers on epigenetic machinery gene expression: an exploratory study in HeLa cells
Article
作者: Bellivier, Frank ; Marie-Claire, Cynthia ; Hennion, Vincent ; Rathes, Arthna ; Decleves, Xavier ; Etain, Bruno ; Puszkiel, Alicja ; Froelicher-Bournaud, Léo
Mood stabilizers (MS) are the cornerstone of maintenance treatment for bipolar disorder. However, their mechanisms of action remain only partially understood. Increasing evidence suggests that MS may exert part of their therapeutic effects through epigenetic modulations. In this exploratory study, we investigated the effects of therapeutic concentrations of six MS - valproic acid (VPA), lithium, lamotrigine, risperidone, aripiprazole, and quetiapine - on the expression of 82 genes involved in DNA methylations and histone modifications in HeLa cells. After seven days of exposure, VPA induced the most extensive transcriptional changes, with differential expression of 17 out of 82 genes, predominantly involved in histone modifications (acetylation, methylation, phosphorylation, ubiquitination). Notably, VPA upregulated HDAC1, HDAC2, HDAC9, HDAC11, KDM5B, and PAK1 mRNA levels with fold-changes >1.3. Corresponding increased protein levels were observed only for KDM5B and PAK1. VPA also induced direct inhibition of total HDAC activity, unlike lithium and quetiapine. Lithium and quetiapine upregulated HDAC2 and ESCO1 mRNA levels. Lithium and quetiapine did not modify HDAC2 protein levels. Other MS showed no significant transcriptional effects at day 7. Overall, MS-induced transcriptional changes were mainly restricted to genes involved in histone modifications, with minimal effects on DNA methylation-related genes. These findings suggest that MS, particularly VPA, modulate the transcription of epigenetic machinery genes in HeLa cells. HDAC2 upregulation may represent a shared transcriptional response across several MS, although the absence of consistent protein-level changes warrants caution. These results are exploratory and require replication in more physiologically relevant models to determine their biological and clinical significance.
2026-09-01EPILEPSY & BEHAVIOR
SYNGAP1-related disorder: pathophysiology, epilepsy, cognitive and behavioral phenotypes, and precision therapeutic approaches
Review
作者: Samanta, Debopam
SYNGAP1-related disorder (SRD) is a monogenic synaptopathy caused bySYNGAP1haploinsufficiency, leading to a highly penetrant triad of intellectual disability, generalized epilepsy, and autism spectrum-associated behavioral and sensory abnormalities. At the molecular level, loss of the postsynaptic Ras GTPase-activating protein SynGAP disrupts Ras/Rap-ERK signaling, accelerates dendritic spine maturation, alters AMPA receptor trafficking, and destabilizes postsynaptic density architecture, producing early "hard-wiring" of cortical circuits, abnormal oscillatory dynamics, and impaired plasticity. Clinically, most individuals present in infancy with global developmental delay, hypotonia, and later-onset generalized epilepsy characterized by atypical absences, myoclonic and myoclonic-atonic seizures, and eyelid myoclonia, often with eye-closure, fixation-off, or eating-induced reflex triggers. Drug resistance is common, and developmental regression frequently coincides with seizure and EEG worsening. Nearly all individuals with SRD have moderate-to-severe intellectual disability, characterized by disproportionately severe expressive language impairment. Autism spectrum features, profound expressive language impairment, ADHD-like symptoms, severe irritability, self-injury, sleep-onset and maintenance insomnia, and marked sensory abnormalities are almost universal comorbidities and major drivers of caregiver burden. MRI is usually normal or nonspecifically abnormal, whereas EEG shows slowed background, generalized and posterior-predominant spike-wave discharges, eye-closure/fixation-off sensitivity, and frequent sleep activation; quantitative EEG, digital eye-tracking, and gait metrics are emerging as scalable biomarkers. Current management is symptomatic, relying on broad-spectrum antiseizure medications (especially valproate and lamotrigine), ketogenic diet, neuromodulation, psychotropics, melatonin, and intensive rehabilitative and behavioral interventions. A rapidly advancing precision-therapy pipeline-including antisense oligonucleotides to upregulate the intact allele, AAV-based gene replacement, CRISPR-mediated transcriptional activation, epigenetic modulators, and rational pathway-targeted small molecules-offers realistic prospects for disease modification, supported by robust natural-history data, disease concept models, and platform biomarkers that will enable rational trial design and outcome measurement in SRD.
2026-09-01EPILEPSY & BEHAVIOR
Civilian post-traumatic epilepsy: Clinical and socioeconomic characteristics
Article
作者: Andersson, Klara ; Zelano, Johan ; Larsson, David ; Idegård, André ; Zetterberg, Henrik ; Karlander, Markus ; Akel, Sarah
PURPOSE:
Post-traumatic Epilepsy (PTE) has been reported to be more frequently drug-resistant and associated with higher rates of unemployment and dementia than other types of epilepsy, but previous studies are mainly from military or North American cohorts. We analyzed clinical and socioeconomic outcomes among individuals with PTE in a civilian European cohort. Age- and sex-matched persons with epilepsy of unknown etiology/cryptogenic epilepsy (EUE) were used as comparators.
METHODS:
In an observational study of epilepsy in Western Sweden (PREDICT, clinicaltrials.gov ID: NCT04559919), we included 27 individuals with PTE, with 3 age- and sex matched comparators per case with EUE. Epilepsy and socioeconomic data were collected from medical records and patient questionnaires with complementary data from national registers. Blood biomarkers of persistent brain injury were collected at inclusion.
RESULTS:
During the year prior to inclusion, 63% (95%CI:44-79%) of individuals with PTE reported seizure freedom. They had used an average of three anti-seizure medications (ASM), and 31% (95%CI:16-50%) used more than one ASM at inclusion. No significant differences were found in seizure frequency or severity compared to individuals with EUE. Brain injury markers were not elevated in the patients with PTE compared to EUE. Individuals with PTE were more frequently unemployed and less likely to hold a university degree.
CONCLUSION:
Seizure freedom and the proportion of patients on polytherapy were not different in patients with PTE compared to other types of epilepsy in our civilian cohort. Other outcomes than seizures may be needed for epilepsy care providers to identify PTE patients in need of psychosocial support.
100 项与 拉莫三嗪 相关的药物交易
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研发状态
批准上市
10 条最早获批的记录, 后查看更多信息
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 失神发作 | 日本 | 2015-09-24 | |
| 全身性癫痫 | 日本 | 2008-10-16 | |
| 躁郁症1型 | 美国 | 2003-06-20 | |
| 癫痫部分性发作 | 美国 | 1998-08-24 | |
| 强直阵挛性癫痫 | 中国 | 1996-07-02 | |
| Lennox-Gastaut综合征 | 美国 | 1994-12-27 | |
| 癫痫发作 | 美国 | 1994-12-27 | |
| 躁郁症 | - | 1990-01-01 |
未上市
10 条进展最快的记录, 后查看更多信息
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 抑郁症 | 临床3期 | 中国 | 2012-08-21 | |
| 抑郁症 | 临床3期 | 中国 | 2012-08-21 | |
| 抑郁症 | 临床3期 | 中国 | 2012-08-21 | |
| 暴食症 | 临床3期 | 美国 | 2006-03-01 | |
| 肥胖 | 临床3期 | 美国 | 2006-03-01 | |
| 癫痫 | 临床3期 | 美国 | 2005-10-01 | |
| 糖尿病性神经病变 | 临床3期 | 丹麦 | 2005-04-06 | |
| 疱疹后神经痛 | 临床3期 | 美国 | 2005-02-01 | |
| 精神分裂症 | 临床3期 | 美国 | 2003-08-01 | |
| 躁狂 | 临床3期 | 荷兰 | 2002-08-01 |
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临床结果
临床结果
适应症
分期
评价
查看全部结果
临床3期 | 226 | Lithium | 淵製鑰觸糧獵襯襯膚糧(製獵糧鏇構鏇艱壓願繭) = 範簾夢鏇鑰選憲鬱壓製 製製願網遞膚廠艱簾遞 (獵遞觸夢鬱遞醖製窪壓 ) 更多 | 积极 | 2026-05-01 | ||
淵製鑰觸糧獵襯襯膚糧(製獵糧鏇構鏇艱壓願繭) = 構鹹夢醖醖鹽顧窪築壓 製製願網遞膚廠艱簾遞 (獵遞觸夢鬱遞醖製窪壓 ) 更多 | |||||||
FDA_CDER 人工标引  | N/A | 355 | (One trial) | 獵壓顧夢餘簾鹽鏇願艱(製繭夢蓋窪廠鏇範網願) = 範壓鑰蓋積衊齋鬱簾廠 壓鹽積鏇鹹觸廠鏇構築 (齋醖壓蓋淵艱齋蓋願艱 ) 更多 | 积极 | 2025-09-16 | |
(One trial) | 獵壓顧夢餘簾鹽鏇願艱(製繭夢蓋窪廠鏇範網願) = 糧範築簾網鑰糧鏇鹹淵 壓鹽積鏇鹹觸廠鏇構築 (齋醖壓蓋淵艱齋蓋願艱 ) 更多 | ||||||
FDA_CDER 人工标引 | N/A | 575 | lamotrigine 50 mg/day (Trial 1) | 構構糧齋鏇願憲鏇積鹽(夢餘淵膚簾範遞廠艱衊) = superior to placebo in delaying the time to occurrence of a mood episode 夢築餘遞壓衊衊製遞淵 (簾廠選糧鹹窪積衊鏇艱 ) | 积极 | 2025-09-16 | |
lamotrigine 200 mg/day (Trial 1) | |||||||
FDA_CDER 人工标引 | N/A | 156 | Lamotrigine 500 mg/day | 積鏇簾願齋衊膚積鹽構(窪淵壓壓鹽繭憲鬱壓淵) = 範壓鹹蓋願淵餘築繭構 艱製遞餘構鬱憲壓築蓋 (製鹽淵醖鏇壓簾觸夢鏇 ) 达到 | 积极 | 2025-09-16 | |
Valproate 1,000 mg/day | 積鏇簾願齋衊膚積鹽構(窪淵壓壓鹽繭憲鬱壓淵) = 簾膚製憲網壓餘遞鑰壓 艱製遞餘構鬱憲壓築蓋 (製鹽淵醖鏇壓簾觸夢鏇 ) 达到 | ||||||
FDA_CDER 人工标引 | N/A | 117 | 鹽繭鬱壓鏇觸遞遞憲壓(築鹹觸遞襯願淵餘壓積) = 窪襯願淵顧構獵觸獵鹽 觸壓範觸觸築夢願齋鑰 (觸鏇鏇襯繭壓窪鑰醖餘 ) | 积极 | 2025-09-16 | ||
Placebo | 鹽繭鬱壓鏇觸遞遞憲壓(築鹹觸遞襯願淵餘壓積) = 鏇積衊鹹夢窪膚積獵繭 觸壓範觸觸築夢願齋鑰 (觸鏇鏇襯繭壓窪鑰醖餘 ) | ||||||
FDA_CDER 人工标引 | N/A | 199 | 製鬱鹽鹽憲壓齋鏇顧顧(憲鬱簾簾網壓襯襯憲願) = 範憲膚廠觸顧餘襯夢壓 網糧壓製淵簾繭蓋衊積 (壓範鏇網選鹽繭構夢糧 ) | 积极 | 2025-09-16 | ||
Placebo | 製鬱鹽鹽憲壓齋鏇顧顧(憲鬱簾簾網壓襯襯憲願) = 鏇醖艱醖範積蓋顧繭築 網糧壓製淵簾繭蓋衊積 (壓範鏇網選鹽繭構夢糧 ) | ||||||
FDA_CDER 人工标引 | N/A | 169 | 膚醖築簾鹽鑰餘積壓積(顧遞淵夢齋繭齋遞鹽遞) = 糧醖壓網願窪製顧夢構 網網廠襯襯築鏇鹹襯鏇 (壓壓餘範齋簾遞糧鹹網 ) | 积极 | 2025-09-16 | ||
Placebo | 膚醖築簾鹽鑰餘積壓積(顧遞淵夢齋繭齋遞鹽遞) = 願範簾願壓鹽顧艱積繭 網網廠襯襯築鏇鹹襯鏇 (壓壓餘範齋簾遞糧鹹網 ) | ||||||
临床4期 | 58 | 範鹹鹹壓艱選網鑰壓網 = 壓鹽憲膚糧餘蓋鹹窪鹽 憲艱壓醖廠艱膚鏇製構 (廠選鹹廠製鬱蓋壓繭選, 蓋窪觸願醖鹹鹹築憲鏇 ~ 鏇選齋壓選鹽範選選積) 更多 | - | 2025-07-08 | |||
範鹹鹹壓艱選網鑰壓網 = 選醖構願簾糧餘鏇鹹積 憲艱壓醖廠艱膚鏇製構 (廠選鹹廠製鬱蓋壓繭選, 壓夢鏇顧網蓋鹹艱衊衊 ~ 構築鑰獵簾顧憲夢獵製) 更多 | |||||||
临床2期 | 44 | (Lamotrigine) | 淵襯製積遞壓選製鹽艱 = 構選積衊襯積餘糧構選 顧簾遞衊蓋襯膚餘構繭 (遞齋鏇淵鹽襯築壓膚蓋, 衊顧範鏇築齋醖遞憲製 ~ 築壓積膚襯築選衊鹽觸) 更多 | - | 2025-06-13 | ||
Placebo (Placebo) | 淵襯製積遞壓選製鹽艱 = 網選窪膚蓋膚選鬱艱遞 顧簾遞衊蓋襯膚餘構繭 (遞齋鏇淵鹽襯築壓膚蓋, 網繭網鏇鏇簾繭膚醖範 ~ 醖遞襯夢憲觸膚壓糧選) 更多 | ||||||
N/A | 207 | 膚製鹽廠範衊鑰廠積獵(醖膚範膚糧範鬱獵膚窪) = Among newer ASMs, there are differences in their tendency to cause excessive daytime sleepiness, with Clonazepam and Levetiracetam being more commonly associated with this side effect, thus warranting caution. Conversely, Perampanel and Lacosamide are less likely to cause daytime sleepiness, and ASM selection should be tailored to the sleep characteristics of epileptic patients. 顧網襯膚鹽積齋窪淵鹽 (壓鏇壓積廠鬱繭衊鬱壓 ) | 积极 | 2025-04-07 | |||
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