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Oxcarbazepine

Oxcarbazepine: An anticonvulsant medication used to treat epilepsy and neuropathic pain.
It is structurally related to carbamazepine, but has improved tolerability and reduced drug-drug interactions.
Oxcarbazepine works by blocking sodium channels and modulating calcium influx, leading to stabilization of neuronal membranes and prevention of seizure activity.
It is commonly prescribed as a monotherapy or in combination with other antiepileptic drugs.
Researchers can optimize Oxcarbazepine research with PubCompare.ai's AI-powered protocol comparision tool, wich easily locates and evaluates protocols from literature, pre-prints, and patents to identify the most reproducible and effective methods.

Most cited protocols related to «Oxcarbazepine»

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Publication 2009
Benzodiazepines Cognition Cortex, Cerebral Drug Resistant Epilepsy Electricity Electrocorticography Epilepsy Hospitalization Medical Devices Operative Surgical Procedures Oxcarbazepine Patients Pharmaceutical Preparations phenazepam Poaceae Pulses Seizures Subdural Space Topiramate Valproic Acid Woman

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Publication 2008
A-factor (Streptomyces) Antipsychotic Agents Aripiprazole Bipolar Disorder Carbamazepine Clonazepam Clozapine Diagnosis factor A Gabapentin Lamotrigine Lithium Mood Olanzapine Oxcarbazepine Pharmaceutical Preparations Pharmacotherapy Quetiapine Risperidone Substance Abuse Topiramate Treatment Protocols Valproate
The leading symptom of VP is recurrent spontaneous attacks of vertigo. The diagnosis is generally straightforward because of the characteristic brief duration (from seconds up to one minute), the frequently recurring attacks of vertigo and the response to a treatment with carbamazepine or oxcarbazepine. There are only a few other disorders which may present with this leading symptom:

Menière’s disease: duration of the attacks from 20 min to 12 hours, low- to medium-frequency sensorineural hearing loss (>30 dB, <2000 Hz) [28 (link)].

Tumarkin’s otolithic crisis (“vestibular drop attacks”). These sudden falls are usually not accompanied by vertigo and occur most often in patients with known Menière’s disease, typically while standing, whereas in VP the attacks occur in any body positions.

Paroxysmal brainstem attacks with vertigo, dysarthria or ataxia (after stroke or in MS) may be difficult to distinguish, as they also respond to low doses of sodium-channel blockers. It was shown that they may be caused by a brainstem lesion due to MS plaques or lacunar infarctions [27 (link)], which also leads to ephaptic discharges of neighboring fibers of the brainstem paths. In such cases the use of MRI with thin brainstem slices is useful for establishing the diagnosis.

Vestibular migraine [26 (link)]: officially the duration of the attacks is 5 min to 72 hours, current or previous history of migraine, most attacks being accompanied by other migrainous symptoms. In vestibular migraine, short spells of vertigo may be induced by changes of head or body position when patients are motion sensitive during an episode of vestibular migraine.

Vertebrobasilar transient ischemic attacks: vertigo frequently occurs in isolation in this condition [33 (link)].

Panic attacks: according to DSM-5, the diagnostic criteria for a panic attack include a discrete period of intense fear or discomfort, in which four (or more) of the following symptoms develop abruptly and reach a peak within minutes: feeling dizzy, unsteady, lightheaded, or faint; nausea or abdominal distress; palpitations, and/or accelerated heart rate; sweating; trembling or shaking; sensations of shortness of breath or being smothered; feeling of choking; chest pain or discomfort; de-realization or depersonalization; fear of losing control or going insane; sense of impending death; paresthesias; chills or hot flashes. Panic attacks are often longer than typical attacks of VP. It may be helpful to ask the patient which of the symptoms come first to differentiate between the two.

Perilymph fistula: The cardinal symptoms of perilymph fistula (and superior canal dehiscence syndrome) are attacks of vertigo caused by changes in pressure, for example, by coughing, pressing, sneezing, lifting, or loud noises and accompanied by illusory movements of the environment (oscillopsia) and instability of posture and gait with or without hearing disorders. The attacks, which can last seconds to days, may also occur during changes in the position of the head (e.g., when bending over) and when experiencing significant changes in altitude (e.g., mountain tours, flights) [6 ].

Episodic ataxia type 2: the duration of the attacks varies from several minutes to hours and more than 90% of the patients have cerebellar signs, in particular gaze-evoked nystagmus and downbeat nystagmus [20, 40 (link)]. The onset of manifestations after the age of 20 is unusual. The much rarer episodic ataxia type 1 is another differential diagnosis. It is characterized by recurrent attacks of ataxia, dizziness and visual blurring, provoked by abrupt postural changes, emotion, vestibular stimulation and lasting minutes. These patients also have neuromyotonia, i.e. continuous spontaneous muscle fiber activity [19 (link)].

Epilepsy with vestibular aura: Vestibular auras can manifest with short attacks of vertigo and nystagmus. Vestibular aura with additional symptoms, so-called non-isolated vestibular aura, is much more prevalent than isolated vestibular aura, which is rare. Vestibular aura is primarily associated with temporal lobe seizures. Isolated vestibular aura spells often last only a few seconds, but longer spells are also reported [41 (link)].

Other differential diagnoses are characterized by recurrent attacks of vertigo that are induced by certain maneuvers. These differential diagnoses include BPPV, central positional vertigo/nystagmus, “rotational vertebral artery occlusion syndrome” (RVAOS), orthostatic hypotension, or rarely cysts or tumors in the cerebello-pontine angle [1, 24 (link)]. In BPPV the attacks are induced by changes of head or body position relative to gravity, and the diagnosis can be proven by the diagnostic positional maneuvers. However, if they are negative, VP remains an important differential diagnosis. In central positional/positioning nystagmus the positioning maneuvers induce a similar nystagmus in different head positions [9 (link)]. In RVAOS the attacks are induced by rotation of the head either to the right or left, and diagnosis is proven by angiography. Similar to VP the symptoms are also caused by an excitation of the peripheral vestibular system [38 (link)]. In orthostatic hypotension the symptoms occur when the patient stands up and may be associated with vertigo and downbeat nystagmus; the key to this diagnosis is measurement of supine and orthostatic blood pressure [11 (link)].
Publication 2016
Abdomen Angiography Ataxia Benign Paroxysmal Positional Vertigo Blood Pressure Brain Stem Carbamazepine Cerebellum Cerebrovascular Accident Chest Pain Chills Cyst Dental Occlusion Depersonalization Diagnosis Differential Diagnosis Drop Attack Dysarthria Dyspnea Emotions Epilepsy Epilepsy, Temporal Lobe Episodic Ataxia, Type 1 Episodic Ataxia, Type 2 Fear Fibrosis Fistula Gravity Head Hot Flashes Hypotension, Orthostatic Illusions Infarction, Lacunar Isaacs' Syndrome Migraine Disorders Movement Muscle Tissue Nausea Neoplasm Metastasis Otoconia Oxcarbazepine Panic Attacks Paresthesia Pathologic Nystagmus Patients Perilymph Pontine Tumors Positional Nystagmus Positional Vertigo Pressure Rate, Heart Senile Plaques Sensorineural Hearing Loss Sodium Channel Blockers Superior Semicircular Canal Dehiscence Syncope Transient Ischemic Attack Vertebral artery syndrome Vertigo Vestibular Labyrinth Vestibular System
The following anticonvulsants: carbamazepine (CBZ), ethosuximide (ETS), oxcarbazepine (OXC), lamotrigine (LTG), levetiracetam (LVT), zonisamide (ZSM), primidone (PMD), topiramate (TPR), and aspirin (ASP; negative control) were purchased from Sigma. Other AEDs used in this study were: diazepam (DZP; Roche), gabapentin (GBP; Fluka), tiagabine (TGB; Chemos), sodium valproate (VPA; Sanofi-Aventis), and phenytoin (PHT; Acros). All compounds were dissolved in DMSO and diluted in embryo medium to achieve a final DMSO concentration of 1% w/v. Embryo medium prepared with DMSO to a final concentration of 1% w/v served as a vehicle control (VHC). Pentylenetetrazol was also purchased from Sigma and was dissolved to 40 mM (2x stock) in embryo medium.
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Publication 2013
Anticonvulsants Aspirin Automated External Defibrillators Carbamazepine Diazepam Embryo Ethosuximide Gabapentin Lamotrigine Levetiracetam Oxcarbazepine Pentylenetetrazole Phenytoin Primidone Sodium Valproate Sulfoxide, Dimethyl Tiagabine Topiramate Zonisamide
This study was approved by the local Institutional Review Board. Assent was obtained from children ≤11 years old and consent was obtained from adolescents and parents or guardians. Subjects were compensated for their participation.
The clinical diagnoses were based on chart review. We extracted anthropometric measurements from the medical records and recorded the start and stop dates of each medication as well as changes in the dosage and formulation. This documentation, confirmed by a physician, also reflected any potential deviation from the prescribed treatments. All dosages of psychostimulants were expressed in methylphenidate (MPH) equivalents for amphetamines (×2) (Swanson et al. 2007 (link)). On the basis of the comprehensive psychiatric treatment history of each patient, we summed the duration of exposure to various psychotropics (excluding risperidone and psychostimulants), divided into those with a definite potential to induce weight gain or weight loss (following Vanina et al. 2002 (link) and the extant literature). For example, atomoxetine was considered a weight-reducing agent and olanzapine a weight-inducing one. Benzodiazepines, α-2 agonists, selective serotonin reuptake inhibitors, trazodone, venlafaxine, nortriptyline, carbamazepine, oxcarbazepine, gabapentin, lamotrigine, tiagabine, and anticholinergics were considered weight neutral.
Upon enrollment, vital signs were obtained in the sitting position, after 15 minutes of rest. Height was measured to the nearest 0.1 cm using a stadiometer (Holtain Ltd., UK) while subjects were standing erect, and weight was recorded to the nearest 0.1 kg using a digital scale (Scaletronix, Wheaton, IL) while subjects were wearing indoor clothes without shoes. Triceps and subscapular skinfold thickness was measured with a Lange skinfold caliper to the nearest 0.1 mm (Centers for Disease Control 2000 ). Waist circumference was measured, to the nearest 0.1 cm, with the measuring tape placed at the uppermost lateral border of the right iliac crest (Centers for Disease Control 2000 ). The intraclass correlation coefficient between the two dietitians who collected the waist circumference and triceps and subscapular skinfold thickness was >0.95 for each of the three variables (n = 16). The average of two measurements was used.
Pubertal stage was evaluated by a physician. Independently, the subjects, with parental help when necessary, completed a self-assessment form that included age-appropriate instructions and pictures depicting Tanner stages I through V (Marshall and Tanner 1969 (link); Marshall and Tanner 1970 (link)). Interrater agreement between the physician and self-rating was high (weighted kappa = 0.81, 95% confidence interval [CI] = 0.74−0.88, n = 74). Self-rating was used for patients (n = 18) who declined to undergo the physical exam.
During the visit, the parent was asked to compare the child's usual level of physical activity to peers using a 5-point Likert scale, and the child and the parent were asked to estimate screen time (i.e., the daily time spent watching television or playing video games).
A morning blood sample was obtained after at least a 9-hour overnight fast and before risperidone was administered, to measure TSH, glucose, total insulin, total cholesterol, HDLC, triglycerides, risperidone, and 9-hydroxyrisperidone concentrations. In 11% of the sample, the participants were not fasting and their laboratory data were excluded from the analyses. Except in 1 patient, where it was measured directly, LDL-C was calculated following the Friedewald estimation formula (Friedewald et al. 1972 (link)).
Publication 2009
Adolescent agonists Amphetamines Anticholinergic Agents Atomoxetine Benzodiazepines BLOOD Carbamazepine Child Cholesterol Diagnosis Dietitian Ethics Committees, Research Fingers Gabapentin Glucose Hypoalphalipoproteinemia, Familial Iliac Crest Insulin Lamotrigine Legal Guardians Nortriptyline Olanzapine Oxcarbazepine Paliperidone Parent Patients Pharmaceutical Preparations Physical Examination Physicians Psychotropic Drugs Puberty Reducing Agents Risperidone Selective Serotonin Reuptake Inhibitors Self-Assessment Signs, Vital Skinfold Thickness Tiagabine Trazodone Triglycerides Venlafaxine Waist Circumference

Most recents protocols related to «Oxcarbazepine»

We prospectively studied 57 consecutive patients with TN who underwent MVD surgery between January 2018 and December 2020. Written informed consent was obtained from all patients. The institutional review board approved this cohort study. The authors prepared the manuscript following the Strengthening the Reporting of Observational Studies in Epidemiology guideline.[29 (link)]
Inclusion criteria were a diagnosis of classical TN according to the International Classification of Headache Disorders 3rd edition,[9 ] age 18 years and older, demonstration of neurovascular compression on magnetic resonance imaging, and appropriate medical treatment before MVD. The patients were treated with carbamazepine at an acceptable dose. The patients allergic to carbamazepine were treated with pregabalin or gabapentin, as the regional drug administration approved oxcarbazepine for TN patients. We excluded patients who had undergone surgery for TN previously. We divided the patients into four age groups: those below 60 years, those between 60 and 69 years, those between 70 and 79 years, and those aged 80 years and older. All patients underwent MVD to mobilize the superior cerebellar artery (SCA) and other offending vessels from the trigeminal nerve root.[15 ,28 (link)] The follow-up period for recurrence and complication was 12– 48 months.
The clinical parameters were as follows: age at operation, affected side, neuralgia type, preoperative comorbidity, operative findings of offending vessels, preoperative, and postoperative Barrow Neurological Institute (BNI) pain intensity score I, no trigeminal pain, no medication; II, occasional pain, not requiring medication; III, some pain, adequately controlled with medication; IV, some pain, not adequately controlled with medication; V, severe pain/no pain relief)[24 (link)] and carbamazepine dose, postoperative complications, and recurrence of neuralgia. The offending vessels were classified into four groups: (i) SCA alone (SCA); (ii) SCA and additional vessels (SCA-plus); (iii) non-SCA arterial compressions (other arteries); and (iv) transverse pontine, pontotrigeminal, or other veins (vein).
Publication 2023
Age Groups Arteries Blood Vessel Carbamazepine Cerebellum Diagnosis Ethics Committees, Research Fifth Cranial Nerves Gabapentin Headache Disorders Neuralgia Oxcarbazepine Pain Patients Pharmaceutical Preparations Pons Postoperative Complications Pregabalin Recurrence Severity, Pain Tooth Root Veins
As the etiologically relevant exposure window, the outcome assessment window, and the covariate assessment window differ by study outcome, we created two separate study cohorts. First, cohort 1 was constructed for the analysis of congenital malformations by setting the window of interest between the last menstrual period (LMP) to LMP+90 (hereafter, first trimester), and we excluded the following: (1) pregnancies with exposure to known teratogenic drugs (e.g., antineoplastic agent, warfarin, lithium, systemic retinoids, misoprostol, thalidomide, androgens, antiepileptic medications [valproate, topiramate, carbamazepine, oxcarbazepine, phenobarbital, phenytoin]); (2) infants with chromosomal abnormalities, genetic syndromes, and malformation syndromes with known causes; (3) pregnancies with no NSAID prescription during the first trimester, but with ≥1 NSAID prescription within 3 months before the LMP (LMP-90 to LMP-1); and (4) pregnancies with only 1 NSAID prescription during the first trimester to minimize potential for misclassification of exposure. Second, cohort 2 was constructed for the analysis of nonmalformation outcomes of low birth weight, antepartum hemorrhage, and oligohydramnios, by setting a broader window to evaluate the effects of exposure prior to the outcome assessment period (LMP to 19 week of gestation [hereafter, early pregnancy]), where we excluded (1) pregnancies with no NSAID prescription during early pregnancy, but with ≥1 NSAID prescription within 3 months before the LMP, and (2) pregnancies with only 1 NSAID prescription during early pregnancy.
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Publication 2023
Androgens Anti-Inflammatory Agents, Non-Steroidal Antiepileptic Agents Antineoplastic Agents Carbamazepine Chromosome Aberrations Congenital Abnormality Hemorrhage Hereditary Diseases Infant Lithium Menstruation Misoprostol Oligohydramnios Oxcarbazepine Pharmaceutical Preparations Phenobarbital Phenytoin Pregnancy Retinoids Syndrome Teratogenesis Thalidomide Topiramate Valproate Warfarin
Serum from five patients (Pat1-5) with anti-GlyR autoantibodies was used for the experiments. Clinical data of two patients (Pat1 with SPS, Pat5 with PERM) were described previously (Rauschenberger et al., 2020 (link)). Serum from five healthy individuals served as negative control (HC), a serum from a patient with multiple sclerosis was used as disease control (DC).
Patients 2 and 3 did not have a history of cancer, SPS or PERM but another neurological disorder. Their serum and CSF samples did not exhibit antibodies directed against other neuronal surface antigens (NMDAR, AMPAR, LGI1, CASPR2, GABAAR, GABABR) but autoantibodies against the GlyR assessed by appropriate cell-based assays (Ekizoglu et al., 2014 (link)). Sera of patients 2 and 3 were included in the present study to examine general molecular mechanisms for autoantibody binding and detection.
Patient 2 was a 33-year old woman with a 16-year history of focal epilepsy of unknown cause, characterized with focal temporal seizures evolving to bilateral convulsive seizures and loss of consciousness. Her CSF and MRI examinations were normal. She favorably responded to antiepileptic medications (oxcarbazepine and topiramate) and thus immunotherapy was not considered.
Patient 3 was a 14-year old girl with a 6-year history of unclassified epileptic encephalopathy characterized with generalized tonic–clonic seizures and atypical absences. She showed mildly progressive cognitive decline with normal metabolic screening, normal CSF findings and mild cerebral atrophy on MRI. EEG showed generalized discharges and focal spikes over the right frontotemporal region. She favorable responded to IVIG treatment and anti-epileptic medications (carbamazepine and valproate).
Patient 4, a 71-year old male at blood withdrawal, developed symptoms of SPS (PERM) at age 65. He suffered from stiffness and spasms of the right arm, falls with bone fractures and a pronounced startle reaction, and was finally wheelchair bound. Extensive search for a malignoma and for other autoantibodies than GlyR antibodies was negative. Under i.v. steroid pulse therapy every 4 months and oral clonazepam at a dose of 0.25 mg in the morning and 0.375 mg in the evening he recovered the ability to walk, and his condition remained mostly stable.
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Publication 2023
anti-GlyR autoantibody Antibodies Antiepileptic Agents Atrophy Autoantibodies Biological Assay BLOOD Carbamazepine Cells Clonazepam Clonic Seizures, Tonic Encephalopathies Epilepsies, Partial Epilepsy Fracture, Bone Immunotherapy Intravenous Immunoglobulins LGI1 protein, human Males Malignant Neoplasms Mental Deterioration Multiple Sclerosis N-Methyl-D-Aspartate Receptors Nervous System Disorder Neurons Oxcarbazepine Patients Pharmaceutical Preparations Physical Examination Progressive Encephalomyelitis with Rigidity Pulse Rate Reflex, Startle Seizures, Focal Serum Spasm Steroids Surface Antigens Therapeutics Topiramate Valproate Wheelchair Woman
Prostate Cancer data Base Sweden (PCBaSe) is a nationwide population-based database that links the National Prostate Cancer Register (NPCR) of Sweden to other health care registries and demographic databases using the individually unique Swedish Personal Identity Number. PCBaSe 4.0 consists of more than 180,000 men on AEDs with comprehensive data on inpatient and outpatient care, prescription patterns, and socioeconomic factors [11 (link)]. Due to ethical considerations from the Swedish Board of Health and Welfare, age in PCBaSe is not captured more precisely than by year of birth and quarter of birth year.
All new PCa cases diagnosed between 2014 and 2016 were extracted from PCBaSe. The date of PCa diagnosis was used as the index date for cases and their respective controls. Each PCa case in this study was matched to five controls by their year of birth and residency. The five controls per case were selected from the general Swedish population and were free of PCa on the date of diagnosis for the corresponding case, lived in the same county, and had the same year of birth. Exposure was defined from filled prescription date for any AED in the Prescribed Drug Registry (within a fixed exposure window of 8.5 years) for all cases and controls. The AEDs included in the final analysis were sodium valproate (Anatomical Therapeutic Chemical (ATC) code: N03AG01), carbamazepine (ATC code: N03AF01), lamotrigine (ATC code: N03AX09), levetiracetam (ATC code: N03AX14), oxcarbazepine (ATC code: N03AF02), ethosuximide (ATC code: N03AD01), topiramate (ATC code: N03AX11), phenytoin (ATC code: N03AB02), gabapentin (ATC code: N03AX16), pregabalin (ATC code), clonazepam (ATC code: N03AX14), primidone (ATC code: N03AA03), phenobarbital (ATC code: N03AA02), lacosamide (ATC code: N03AX18), zonisamide (ATC code: N03AX15), and eslicarbazepine (ATC code: N03AF04). Sodium valproate, lamotrigine, levetiracetam, oxcarbazepine, and topiramate were AEDs with known HDACi properties.
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Publication 2023
Automated External Defibrillators Carbamazepine Care, Ambulatory Childbirth Clonazepam Contraceptive Methods Diagnosis eslicarbazepine Ethosuximide Gabapentin Inpatient Lacosamide Lamotrigine Levetiracetam Oxcarbazepine Pharmaceutical Preparations Phenobarbital Phenytoin Pregabalin Primidone Prostate Cancer Residency Sodium Valproate Therapeutics Topiramate Zonisamide
The psychotropic drugs mentioned in this study were mood stabilizers (MSs), antipsychotics (APs), antidepressants (ADs), and benzodiazepines (BZDs). Mood stabilizers were defined as valproate, lithium, lamotrigine, oxcarbazepine, or topiramate. Second-generation antipsychotics are also effective mood stabilizers, but they were classified separately in order to better classify the drugs taken and compare them with previous studies. Trazodone and mirtazapine were considered antidepressants, although they were often used to improve sleep. These included benzodiazepines, because they are commonly used in patients with BD. For each patient, the prescribed daily dose (PDD) was defined as the daily dose. The type of medication taken was defined as the daily use of any medication within the type of medication.
Polypharmacy was defined as the use of two or more psychotropic drugs. Polypharmacy might involve the same class of drugs, such as two antidepressants, or different classes of drugs, such as mood stabilizers and antipsychotics. Fifteen types of medication classes were analyzed, including four types of monotherapies, six types with two different classes of drug co-treatments, four types with three different classes of drug co-treatments, and one type with four different classes of drug co-treatment. For all patients, the numbers of drugs used were collected at baseline and at each follow-up assessment. The changes in the drug numbers were observed from the collection of these data.
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Publication 2023
Antidepressive Agents Antipsychotic Agents Benzodiazepines Lamotrigine Lithium Mirtazapine Mood Oxcarbazepine Patients Pharmaceutical Preparations Polypharmacy Psychotropic Drugs Sleep Topiramate Trazodone Valproate

Top products related to «Oxcarbazepine»

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Oxcarbazepine is a laboratory equipment product developed and manufactured by Merck Group. It is a pharmaceutical compound used in various research and analytical applications. The core function of Oxcarbazepine is to serve as a reference standard for analytical testing and quality control procedures.
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Lamotrigine is a laboratory instrument used for the detection and quantification of various molecules, compounds, or analytes in a sample. It operates on the principle of liquid chromatography-mass spectrometry (LC-MS) technology.
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Tween 80 is a non-ionic surfactant and emulsifier. It is a viscous, yellow liquid that is commonly used in laboratory settings to solubilize and stabilize various compounds and formulations.
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Topiramate is a pharmaceutical compound developed by Merck Group. It is a white crystalline powder that acts as a sodium channel blocker and gamma-aminobutyric acid (GABA) receptor agonist. Topiramate is primarily used as an active ingredient in various Merck Group's pharmaceutical products.
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DMSO is a versatile organic solvent commonly used in laboratory settings. It has a high boiling point, low viscosity, and the ability to dissolve a wide range of polar and non-polar compounds. DMSO's core function is as a solvent, allowing for the effective dissolution and handling of various chemical substances during research and experimentation.
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Levetiracetam is a pharmaceutical active ingredient manufactured by Merck Group. It is a synthetic derivative of the naturally occurring amino acid piracetam. Levetiracetam is used as a broad-spectrum antiepileptic drug.
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Trileptal is a pharmaceutical product manufactured by Novartis. It is a lab equipment used for scientific research and analysis. Trileptal's core function is to facilitate precise measurement and data collection in laboratory settings.
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Carbamazepine is a chemical compound used as a reference standard in analytical testing procedures. It is a white, crystalline powder that is commonly used to verify the accuracy and precision of analytical equipment and methods.
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Ethosuximide is a pharmaceutical compound used as an anticonvulsant medication. It is primarily utilized in the treatment of absence seizures, a type of epileptic seizure. The compound functions by suppressing the spread of seizure activity within the brain.
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Primidone is a laboratory instrument manufactured by Merck Group. It is a pharmaceutical drug that is primarily used as an anticonvulsant medication for the treatment of epilepsy. The core function of Primidone is to prevent and control seizures in individuals diagnosed with epilepsy.

More about "Oxcarbazepine"

Oxcarbazepine is an anticonvulsant medication used to treat epilepsy and neuropathic pain.
It is structurally similar to carbamazepine (Tegretol), but has improved tolerability and reduced drug-drug interactions.
Oxcarbazepine, also known by the brand name Trileptal, works by blocking sodium channels and modulating calcium influx, which helps stabilize neuronal membranes and prevent seizure activity.
This medication is commonly prescribed as a monotherapy or in combination with other antiepileptic drugs like lamotrigine (Lamictal), topiramate (Topamax), levetiracetam (Keppra), and ethosuximide (Zarontin).
Researchers can optimize their Oxcarbazepine studies by utilizing PubCompare.ai's AI-powered protocol comparison tool, which helps identify the most reproducible and effective research methods from literature, preprints, and patents.
When conducting Oxcarbazepine research, it's important to consider factors like dosage, formulation (e.g., Tween 80, DMSO), and potential interactions with other drugs.
By leveraging the insights gained from PubCompare.ai's platform, researchers can improve their study design and increase the likelihood of successful outcomes in their Oxcarbazepine-related projects.