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carbamazepine (Carbella / Carnexiv)

✓ Approved

Ligand Pharmaceuticals · SCN1A · 小分子

什么是 carbamazepine？

carbamazepine 是一种小分子，由Ligand Pharmaceuticals研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)、Intravenous (IV)。

药物档案

商品名Carbella, Carnexiv
公司Ligand Pharmaceuticals
药物类别小分子
分子靶点SCN1A, SCN2A, SCN3A
给药途径Injectable (Others), Intravenous (IV)
状态Approved
来源： ClinicalTrials.gov, Ligand Pharmaceuticals

作用机制

分子靶点

carbamazepine 作用于 3 个分子靶点：

SCN1Asodium voltage-gated channel alpha subunit 1 (DEE6B, FEB3)
SCN2Asodium voltage-gated channel alpha subunit 2 (Na(v)1.2, BFNIS)
SCN3Asodium voltage-gated channel alpha subunit 3 (Nav1.3, NAC3)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

carbamazepine 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Nervous system disordersGeneralised tonic-clonic seizure✓ Approved

相关研究文献

PubMedCureus2026-08-04

Initial Experience With Stereotactic Radiosurgery for Refractory Trigeminal Neuralgia Using the OXRAY System.

Mizumatsu Shinichiro S, Ryu Hiroshi H, Yoshikawa Satoshi S, Ichihara Masaya M et al.

We report our experience with frameless stereotactic radiosurgery (SRS) using a novel O-ring type linear accelerator (LINAC), the OXRAY system, for refractory trigeminal neuralgia (TN). Three elderly TN patients resistant to pharmacological therapy were included. The head was immobilized with a double-shell mask, and the target was contoured to encompass the entire diameter of the trigeminal nerve at the trigeminal impression. The treatment plan was designed to deliver a maximum dose of 90 Gy in a single fraction using 6 MV flattening filter-free (FFF), volumetric-modulated arc therapy (VMAT). During treatment, image-guided radiotherapy (IGRT) using cone-beam computed tomography (CBCT) was performed a total of five times between each arc. Case 1 was a 74-year-old woman with atypical TN of the left mandibular nerve (V3) and severe numbness, who had undergone three prior microvascular decompressions. SRS was performed with a total irradiation time of 2,492 seconds. Her pain and numbness decreased four months after SRS. At the 16-month follow-up, the Barrow Neurological Institute (BNI) pain score had improved from IV to IIIa, and the facial numbness score had improved from IV to II. The carbamazepine (CBZ) dose was reduced from 500 mg to 100 mg/day. Case 2 was a 95-year-old woman with typical right maxillary nerve (V2) TN. SRS was performed with a total irradiation time of 1,356 seconds. Her pain resolved within a week after SRS, and CBZ was tapered and discontinued over a two-month period. At the 10-month follow-up, the BNI pain score remained at I (improved from IV) without CBZ. Case 3 was an 85-year-old woman with typical right V2 and V3 TN. SRS was performed with a total irradiation time of 1,637 seconds. Her pain resolved the day after SRS, and CBZ was tapered and discontinued over a one-month period. At the five-month follow-up, the BNI pain score remained at I (improved from IV) without CBZ. In all cases, the positional displacement on CBCT was within 1 mm or 1°, and no correction was necessary. No adverse events related to SRS were observed. Frameless FFF-VMAT SRS using the OXRAY system with repeated IGRT demonstrated favorable initial pain relief. This approach may represent a feasible and effective treatment option for elderly patients with refractory TN. Long-term follow-up is necessary to evaluate the incidence of adverse events and recurrence. In the future, the addition of a continuous intrafraction motion monitoring function is expected to reduce radiation exposure, further improve accuracy, and shorten treatment time.

PMID 42549308
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PubMedThe Journal of the Association of Physicians of India2026-08-03

Navigating Bone Health in Epilepsy-A Detailed Review of Anticonvulsant-induced Osteomalacia: Its Mechanisms and Therapeutic Strategies.

Mk Sundar Sri SS, Krishnan Karthickeyan K

Anticonvulsants are the drugs given for managing epilepsy and some other types of neurological disorders; however, their long-term use is increasingly suspected of causing adverse skeletal outcomes, including osteomalacia. Osteomalacia is a condition marked by defective mineralization of bone, leading to bone softening, bone pain, muscle weakness, and predisposition to fractures. The disruption of vitamin D metabolism, impaired calcium absorption, and altered bone turnover are mechanisms attributed to several commonly used anticonvulsants, especially enzyme-inducing agents such as phenytoin, carbamazepine, and phenobarbital, in contributing to osteomalacia. Hence, this review aims to provide detailed information about the pathophysiology, clinical manifestations, diagnosis, and treatment of anticonvulsant-induced osteomalacia. The review places further emphasis on the importance of regular monitoring of bone health in individuals receiving long-term antiepileptic treatment, supplementation, lifestyle interventions, and interprofessional care. A proper understanding of this preventable complication will certainly help healthcare providers to minimize the impact in these patients and improve outcomes.

PMID 42543996
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PubMedEpilepsy & behavior : E&B2026-08-02

A network approach with motion sequencing reveals hidden patterns of repetitive behavior in a pre-clinical model of epilepsy.

Koehler Jennifer L JL, Harvey Quinn R QR, Hoffman Olivia R OR, Clemente Espina Jose Ezekiel JE et al.

Epilepsy is the 4th most prevalent neurological condition with 50 million cases worldwide. Patients with epilepsy bare a disproportionate burden of cognitive decline and psychiatric disorders which remain poorly understood and go unaddressed by current anti-epileptic treatments. Furthermore, pre-clinical work on behavioral comorbidities can be hampered by current testing frameworks which rely on well-defined, discreet tests with limited repeatability. Recent work has demonstrated a role for machine learning modalities such as Motion Sequencing (MoSeq) in assessing behavioral differences between naïve and epileptic. In this study we combined MoSeq with a novel analysis pipeline to uncover repetitive behaviors in chronically epileptic mice. These repetitive behaviors emerge alongside epilepsy specific racing behaviors which persist in epileptic mice as disease progresses. We show that epileptic mice have more fragile and dispersed behavioral networks. Finally, we test this pipeline using the FDA approved anti-seizure medication carbamazepine, showing a rescue of racing syllable and a partial rescue of behavioral network dispersion. Together, these results lay a groundwork for extracting clinically relevant phenotypes from MoSeq data throughout disease progression.

PMID 42542112
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PubMedBioorganic chemistry2026-08-02

Discovery of novel H3R antagonists with potent antiseizure activity and favorable pharmacokinetics via scaffold-hopping from pitolisant to rigid 4-phenylindoles.

Zheng Ying Y, He Guowen G, Song Mingxia M, Kang Jiuhong J et al.

In the present work, scaffold hopping starting from pitolisant furnished a novel class of 4-phenylindole histamine H₃ receptor antagonists. All twenty designed analogues were synthesized and comprehensively profiled in biological assays. Compounds 3a, 3b, 3g, 3m, and 3n showed potent H3R antagonism with IC50 values of 2.82, 3.15, 1.32, 3.37, and 1.49 μM respectively, among which 3g and 3n were the most active. In subtype selectivity assays, compounds 3g and 3m exhibited potent H2R antagonistic effects (with IC50 of 0.6970 and 0.4844 μM, respectively), and this activity was stronger than their H3R activity. Compound 3n also showed considerable H2R antagonism with IC50 values of 1.317 μM. In the mouse maximal electroshock model, compound 3n demonstrated an ED50 of 16.44 mg/kg, comparable to pitolisant (16.34 mg/kg). In the zebrafish pentylenetetrazol model, compound 3n reduced locomotor activity by 98.66% at 10 μM, superior to pitolisant (97.49%) and the classic antiseizure drug carbamazepine (58.47%). The antiseizure effect of compound 3n was confirmed to be H3R-mediated using the selective agonist RAMH, while the H2R agonist dimaprit dihydrochloride failed to reverse its activity, ruling out H2R involvement. Safety profiling revealed no neurotoxicity at therapeutic doses, a favorable hERG safety margin (IC50 = 0.9377 μM), and low cytotoxicity. Pharmacokinetic evaluation showed oral bioavailability of 60.73% for compound 3n, which was higher than that of pitolisant (31.9%), and effective blood-brain barrier penetration with brain-to-plasma ratios exceeding unity. Molecular docking revealed that compound 3n engaged H3R through a distinct hydrogen bond and π-interaction network. These results support compound 3n as a promising antiseizure candidate.

PMID 42542010
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PubMedEpilepsia2026-08-02

Acute effects of anti-seizure medications on network level dynamics: A systematic comparison using multielectrode arrays.

Marku Griselda G, Gschossmann Lena L, Hallmann Kerstin K, Beck Heinz H et al.

A multi-electrode array (MEA) is a powerful extracellular recording technique for long-term monitoring of neuronal network activity. In recent years, MEA-based assays have been applied increasingly to evaluate drug efficacy and neurotoxicity, including the assessment of anti-seizure medications (ASMs). However, systematic comparisons of ASMs with different mechanisms of action under identical experimental conditions remain limited. In this study, we evaluated the effects of 18 ASMs on neuronal network activity using MEA recordings under standardized conditions. Network activity was characterized using four components-spike, burst, network burst, and synchrony-and a total of 44 MEA-derived parameters were analyzed. Dimensionality reduction by t-distributed stochastic neighbor embedding (t-SNE) followed by hierarchical clustering classified the 18 ASMs into four distinct clusters. Cluster 1, including S-licarbazepine, oxcarbazepine, and lamotrigine, exhibited pronounced effects across all four network components. Cluster 2, comprising carbamazepine, eslicarbazepine acetate, phenytoin, phenobarbital, and stiripentol, significantly affected spike and burst duration but showed only limited effects on burst frequency, network burst frequency, or synchrony. Cluster 3 was solely diazepam, for which minimal effects were detected. The remaining ASMs were assigned to Cluster 4 and produced only minimal measurable effects in network activity. Several limitations should be considered, including the use of primary neuron cultures, incomplete maturation of certain drug targets, evaluation of only acute drug effects, and the limited spatial resolution of low-density MEA systems. Nevertheless, our results demonstrate that this MEA-based platform enables systematic evaluation of ASM effects on neuronal networks under identical experimental conditions. Furthermore, multivariate and unsupervised clustering analysis of 44 MEA parameters facilitated classification independent of drug mechanism of action. These findings suggest that MEA, combined with multidimensional data analysis, may provide a useful platform for the direct comparison of ASMs and could contribute to future pharmacological screening and drug discovery efforts.

PMID 42541378
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PubMedEpilepsia open2026-08-02

The gut microbiome and drug-resistant epilepsy: Microbiome-antiseizure medication interactions and implications for pharmacoresistance.

Zammar Khaled K, AbuAlrob Majd A MA, Ali Musab M, Lattanzi Simona S et al.

Drug-resistant epilepsy (DRE) affects approximately one-third of patients with epilepsy and represents a major unmet clinical need. While traditional hypotheses of pharmacoresistance have focused on alterations in drug targets, efflux transporter overexpression, and intrinsic disease severity, the gut microbiome has recently emerged as a potentially modifiable factor that may function as a systems-level modifier of these established mechanisms rather than a standalone pathway. The gut microbiome harbors a vast repertoire of drug-metabolizing enzymes capable of directly biotransforming orally administered antiseizure medications (ASMs)-including valproic acid, lamotrigine, carbamazepine, and oxcarbazepine-thereby altering their pharmacokinetics, bioavailability, and therapeutic efficacy. Additionally, microbial metabolites modulate host cytochrome P450 enzymes, nuclear receptors, and efflux transporters such as P-glycoprotein, while bacterial β-glucuronidases influence the enterohepatic recirculation of glucuronidated ASMs. Conversely, chronic ASM exposure reshapes the gut microbial ecosystem, creating a self-perpetuating cycle of dysbiosis and pharmacoresistance. This narrative review synthesizes current evidence on microbiome-ASM interactions in DRE, proposes a concrete experimental pipeline for characterizing ASM-specific microbial biotransformation, and outlines a framework for integrating physiologically based pharmacokinetic modeling with microbiome data. We discuss clinical implications for epileptologists-including the role of therapeutic drug monitoring in detecting microbiome-mediated pharmacokinetic variability, the concept of microbiome-neutral ASM selection, and earlier deployment of the ketogenic diet as a microbiome-targeted intervention. We highlight the translational potential of pharmacomicrobiomics-the study of how microbiome variation influences drug disposition and response-and identify critical knowledge gaps that warrant future investigation. PLAIN LANGUAGE SUMMARY: About one in three people with epilepsy continue to have seizures despite treatment. This review summarizes growing evidence that the gut microbiome-the community of bacteria living in the intestines-can influence how seizure medications work by altering their absorption, metabolism, and clearance. The medications themselves can reshape the microbiome in return, creating a cycle that may sustain treatment failure. Understanding this gut-drug relationship may open new paths to personalized epilepsy care through diet, probiotics, and microbiome-guided prescribing.

PMID 42541365
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