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carbamazepine (Carbella / Carnexiv)

✓ Approved

Ligand Pharmaceuticals · SCN1A · Small Molecule

What is carbamazepine?

carbamazepine is a small molecule developed by Ligand Pharmaceuticals. It is approved for therapeutic indications via injectable (others) or intravenous (iv).

Drug Profile

Brand NamesCarbella, Carnexiv
CompanyLigand Pharmaceuticals
Drug ClassSmall Molecule
Molecular TargetSCN1A, SCN2A, SCN3A
RouteInjectable (Others), Intravenous (IV)
StatusApproved
Sources: ClinicalTrials.gov, Ligand Pharmaceuticals

Mechanism of Action

Molecular Targets

carbamazepine acts on 3 molecular targets:

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)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

carbamazepine is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Nervous system disordersGeneralised tonic-clonic seizure✓ Approved

Related Research Articles

PubMedPloS one2026-09-18

Voltage-gated sodium channel, Nav 1.8, regulates calcium dynamics in the dorsal root ganglion induced by cold nociceptive stimulus.

Dey Moushumi Rani MR, Li Baolin B, Heddleston John J, Aihara Eitaro E

Nociceptive pain responses are mediated by neurons in the dorsal root ganglion. Certain voltage-gated sodium channels, such as Nav 1.8, are necessary for action potential firing and sensing pain. Prior work has demonstrated that interfering with voltage-gated calcium channel activity can also reduce acute and chronic pain. Furthermore, it is reported that dorsal root ganglion calcium response to electric-field stimulation was inhibited by voltage-gated sodium channel blockers. Here we aim to explore the intracellular calcium dynamics in dorsal root ganglion neurons in response to cold pain via intravital confocal imaging. Genetically encoded calcium indicators, such as the GCaMP family of proteins, have been widely used to assess neuron excitability, using fluorescence due to calcium flux as a surrogate for neuron depolarization. We utilized Thy1-GCaMP6f transgenic mice to image calcium transients in live animals or freshly-isolated dorsal root ganglion neurons to identify neuron activity. Measurement of calcium transients demonstrated response to a TRPV1 agonist, capsaicin, or a voltage-gated sodium channel agonist, veratridine, and this response could be inhibited by capsazepine: a TRPV1 antagonist; carbamazepine: a pan-voltage gated sodium channel blocker; or A-803467: a Nav 1.8 inhibitor. We demonstrated through intravital imaging that the cold paw swab increases calcium transients in dorsal root ganglion neurons, and this effect was inhibited by voltage-gated calcium channel blockers. We further demonstrated by in vivo imaging that the cold-pain induced calcium transients in dorsal root ganglion neurons is blocked by A-803467. These data demonstrate that imaging can be used to visualize and measure cold pain signaling in dorsal root ganglion neurons due to L-type voltage-gated calcium channel activity triggered by Nav 1.8 activation.

PMID 42758684
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PubMedArchives of toxicology2026-09-15

Combined immune modulation reveals carbamazepine-associated CD8+ T cell-dependent skin inflammation in HLA-A*31:01 knock-in mice.

Aoki Shigeki S, Ichikawa Maho M, Masuda Yuichi Y, Komiya Kaetsu K et al.

Human leukocyte antigen (HLA) alleles are among the strongest genetic risk factors for idiosyncratic drug toxicity. HLA-A*31:01 is a risk factor for carbamazepine (CBZ)-induced delayed drug hypersensitivity, yet allele carriage alone is insufficient for disease development. CD8+ T cells are implicated in these reactions; however, their activation mechanism remains unclear. Using HLA-A*31:01 knock-in (A31-KI) mice, we investigated whether CBZ exposure elicited CD8+ T-cell responses in vivo. The mice received CBZ for 7 days by oral administration (300 mg/kg/day) and auricular application (25 mg/kg/day). CBZ alone did not induce clear CD8+ T-cell activation. Under CD4+ T-cell depletion, CBZ markedly increased programmed cell death protein 1 (PD-1) expression in CD44highCD62Llow CD8+ T cells, suggesting PD-1-mediated restraint of CBZ-responsive activation. Subsequent PD-1 blockade enhanced CD8+ T-cell activation in auricular lymph nodes and induced skin inflammation with elevated serum thymus and activation-regulated chemokine; both were attenuated by CD8+ T-cell depletion. To clarify how CBZ activated CD8+ T cells, we performed ex vivo analyses using splenocytes. CBZ (50 µM) induced proliferation of CD44highCD8+ T cells, whereas this response was absent in purified CD8+ T-cell cultures and reduced by HLA class I and costimulatory blockade, supporting an antigen-presenting cell-dependent mechanism. Collectively, CBZ can activate CD8+ T cells; however, this response is restrained and remains latent. When immune control is disrupted, particularly in an HLA-A*31:01-bearing host, the response can progress to a CD8+ T cell-dependent inflammatory phenotype. Thus, A31-KI mice provide an in vivo platform for understanding CBZ-associated idiosyncratic toxicity and pathogenesis.

PMID 42742701
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PubMedJournal of chromatography. B, Analytical technologies in the biomedical and life sciences2026-09-15

Analysis by microscale affinity chromatography of humic acid interactions with pharmaceutical micropollutants.

Suh Kyungah K, Sharmeen Sadia S, Sajeeb B K BK, Zingler Zoe Z et al.

Growing concern over the presence of pharmaceuticals in both the environment and water has led to increased interest in the effects such substances may have on human and environmental health. One factor that may affect the bioavailability, transport, and persistence of these compounds is their binding to natural and dissolved organic matter in the environment. One example of this type of substance is humic acid, a complex biomaterial that is present in water and soil and that is formed through plant and animal decay. This report uses microscale affinity chromatography with supports made by non-covalent entrapment to examine and compare the binding of humic acid with several drugs that are found as contaminants in environmental water. Leonardite humic acid is used as a model for natural humic acid and is examined for its binding with three antibiotics (i.e., ciprofloxacin, norfloxacin, and tetracycline) as well as carbamazepine, a common marker for drugs as environmental contaminants. The binding of these drugs with the entrapped Leonardite humic acid are also compared to data previously obtained with a standard commercial preparation of humic acid (i.e., Aldrich humic acid). This binding is further evaluated under various pH, ionic strength, and temperature conditions to examine the types of forces involved in these interactions. The results are used to illustrate how microscale affinity columns can be used in examining and comparing biochemical interactions with complex binding agents (e.g., Leonardite versus Aldrich humic acid). The results also provide valuable information on binding by the model drugs with humic acids, as can be used to determine how such interactions affect the bioavailability and behavior of these and related contaminants in the environment.

PMID 42743902
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PubMedWater research2026-09-15

Dual vacancy-regulated S-shaped heterojunction full spectrum photoanode in situ self-supply H2O2-driven activation: Cathode-anode cooperative photoelectrocatalysis system efficiently generates 1O2 for water purification.

Jia Lumeng L, Yu Wenchao W, Hou Xiangting X, Li Mengxue M et al.

Photoelectrocatalytic (PEC) in situ hydrogen peroxide (H2O2) production offers a green strategy for activating singlet oxygen (1O2) and degrading refractory organic pollutants. However, it suffers from low cathode yield, sluggish anode kinetics, mass-transfer losses, and low selectivity for 1O2. This study ingeniously designed an S-O double vacancy β-In2S3-Er/Yb@WO3-Ov S-type heterojunction full-spectrum photoanode, offered new perspectives on in situ oxygen reduction at the photoanode for H2O2 generation, and presented a dual-electrode cooperative PEC system. In the experiment, double vacancies at the photoanode acted as electron traps, accumulating electrons. Meanwhile, an applied bias voltage, more electrons on the surface, and weakly acidic and oxygen-permeable conditions the electrons trapped by vacancies, together with conduction band electrons, were conducive to driving the in-situ two-electron oxygen reduction reaction to H2O2 formation at the photoanode. O vacancies dominated interfacial adsorption and catalysis, while S vacancies served as electron traps for charge separation, forming a complementary synergy. Coupled with charge modulation at the S-scheme heterojunction interface, accelerating photogenerated carrier separation and preserved highly reactive holes, providing key conditions for 1O2 generation. β-In2S3-Er/Yb@WO3-Ov photoanode realized in-situ oxygen reduction reaction-induced H2O2 production and cathodic H2O2 activation simultaneously. Both routes yield ·OOH/·O2- intermediates, which were oxidized by holes to form 1O2, thereby enabling efficient carbamazepine removal (98.4%, kapp = 0.093 min-1), efficient 1O2 production (53.13 μmol/(L·min)), and low energy consumption (0.155 kWh/m3-log). This work presents an advanced PEC strategy for the synergistic synthesis of H2O2 and 1O2, offering a promising approach for high-efficiency environmental remediation.

PMID 42735543
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PubMedJournal of child psychology and psychiatry, and allied disciplines2026-09-15

Risks of neurodevelopmental disorders after prenatal exposure to antiepileptic drugs.

Lu Mong-Liang ML, Hung Tai-Hsin TH, Chen Vincent Chin-Hung VC, Chen Yi-Lung YL

To determine whether in utero exposure to antiepileptic drugs (AEDs) is associated with autism spectrum disorder (ASD), attention-deficit/hyperactivity disorder (ADHD), and intellectual disability (ID) in offspring and to test robustness to familial confounding. We conducted a nationwide population-based cohort of all live births between January 1, 2004, and December 31, 2016, with follow-up through 2021, linking birth, prescription, and health registries. Exposure was maternal dispensing of AEDs during pregnancy. We estimated hazard ratios with Cox models adjusted for parental demographics and psychiatric/medical comorbidities. To address shared familial factors, we performed sibling comparisons using stratified Cox models with mother as the stratum. We further conducted trimester-specific analyses, restricted to any neurodevelopmental disorder because of limited numbers for individual outcomes, by separately defining maternal AED dispensing during the first, second, and third trimesters to evaluate whether associations differed according to the timing of prenatal exposure. Among 2,196,156 births, 9,809 (0.45%) were exposed to AEDs during pregnancy. In adjusted population-wide analyses, carbamazepine, oxcarbazepine, valproic acid, and topiramate were associated with increased risk of any neurodevelopmental disorder, with some drug-specific associations also observed for ASD, ADHD, and ID. However, these associations were not observed in sibling comparison analyses. Trimester-specific sibling analyses showed no increased risk for first-trimester exposure, although several imprecise associations were observed for second- and third-trimester exposure. Sensitivity analyses were generally consistent with the main sibling comparison findings, except for an increased risk associated with topiramate when the exposure window was extended to 90 days before conception. Population-wide associations between prenatal AED exposure and neurodevelopmental disorders were largely attenuated in sibling comparison analyses, suggesting that shared familial factors may explain much of the observed risk. These findings support careful individualized prescribing during pregnancy while highlighting the need for further research on specific AEDs and exposure windows.

PMID 42736039
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PubMedFrontiers in chemistry2026-09-13

Synthesis and applications of bimetallic metal-organic frameworks catalyst for activating peroxymonosulfate for carbamazepine degradation.

Zhong Xin X, Huang Qi Q, Ji Meihuan M, Liao Zhao Z et al.

In this research, a series of bimetallic CuxZny-MOFs catalysts was constructed via a convenient solvothermal synthesis procedure by using the 2,3,6,7,10,11-hexaiminotriphenylene (HATP) ligand with copper and zinc metal ions. Among the series catalysts, Cu2Zn1-MOFs exhibited outstanding adsorption efficiency and degradation performance, and achieved 97.83% carbamazepine (CBZ) removal within 15 min using a catalyst dosage of 0.05 g L-1 and 0.5 mM peroxymonosulfate (PMS) concentration. The catalytic degradation rate constant of CBZ by Cu2Zn1-MOFs catalyst reached to 0.1833 min-1, which is 3.1 times higher than Cu-MOFs. In order to investigate the catalytic mechanism, density functional theory (DFT) calculations and experimental results were conducted which revealed the enhanced adsorption efficiency due to the incorporation of zinc into Cu-MOFs, thereby promoting the generation of reactive oxygen species in PMS activation. Furthermore, the CBZ degradation pathway was elucidated by detected the intermediates using LC/MS during the oxidation process. These findings highlighted the synergistic effects of bimetallic MOFs as highly efficient heterogeneous Fenton-like catalyst, which could expand the potential actual application.

PMID 42729435
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