Valproic Acid

Bruni, J.

doi:10.1001/archneur.1979.00500430023002

Cited by 120 publications

(6 citation statements)

References 49 publications

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“…VPA was the third antiepileptic drug approved by the Food and Drug Administration, and unlike most of the antiepileptic compounds, it lacks nitrogen and a ring moiety [12]. Although VPA can be employed in either generalized or partial epilepsies, it is more effective in the former, mainly to treat absence seizures [13].…”

Section: Generalities Of Valproic Acidmentioning

confidence: 99%

Exploring the Drug Repurposing Versatility of Valproic Acid as a Multifunctional Regulator of Innate and Adaptive Immune Cells

Soria-Castro

Schcolnik‐Cabrera

Rodríguez-López

et al. 2019

Journal of Immunology Research

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Valproic acid (VPA) is widely recognized for its use in the control of epilepsy and other neurological disorders in the past 50 years. Recent evidence has shown the potential of VPA in the control of certain cancers, owed in part to its role in modulating epigenetic changes through the inhibition of histone deacetylases, affecting the expression of genes involved in the cell cycle, differentiation, and apoptosis. The direct impact of VPA in cells of the immune system has only been explored recently. In this review, we discuss the effects of VPA in the suppression of some activation mechanisms in several immune cells that lead to an anti-inflammatory response. As expected, immune cells are not exempt from the effect of VPA, as it also affects the expression of genes of the cell cycle and apoptosis through epigenetic modifications. In addition to inhibiting histone deacetylases, VPA promotes RNA interference, activates histone methyltransferases, or represses the activation of transcription factors. However, during the infectious process, the effectiveness of VPA is subject to the biological nature of the pathogen and the associated immune response; this is because VPA can promote the control or the progression of the infection. Due to its various effects, VPA is a promising alternative for the control of autoimmune diseases and hypersensitivity and needs to be further explored.

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Section: Generalities Of Valproic Acidmentioning

confidence: 99%

Exploring the Drug Repurposing Versatility of Valproic Acid as a Multifunctional Regulator of Innate and Adaptive Immune Cells

Soria-Castro

Schcolnik‐Cabrera

Rodríguez-López

et al. 2019

Journal of Immunology Research

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“…All these drugs prolong the latent period and reduce the duration of tonic extensor phase of MES. [11] In PTZ-induced seizures, the percent protection of cinnarizine is 33.33% and of nifedipine is 16.66%. They also reduce the occurrence of convulsions and the number of deaths due to PTZ.…”

Section: Discussionmentioning

confidence: 99%

Role of cinnarizine and nifedipine on anticonvulsant effect of sodium valproate and carbamazepine in maximal electroshock and pentylenetetrazole model of seizures in mice

Brahmane

Wanmali

Pathak

et al. 2010

Journal of Pharmacology and Pharmacotherapeutics

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Objective:To study the effect of calcium channel blockers (CCBs) cinnarizine and nifedipine on maximal electroshock (MES)-induced and pentylenetetrazole (PTZ)-induced convulsions and also their effect in combination with conventional antiepileptic drugs (CAED).Materials and Methods:For this study, Swiss albino mice were used. Effects of cinnarizine (30 mg/kg), nifedipine (5 mg/kg), sodium valproate (300 mg/kg) and carbamazepine (8 mg/kg) alone and in combination were studied in MES and PTZ seizure models. Abolition of hind limb tonic extension was an index of anticonvulsant activity in MES, while for PTZ seizures, failure to observe even a single episode of tonic spasm for 5 s duration for 1 h was the index. With this, percentage protection was calculated and statistical analysis was carried out using Fisher’s exact test (Ovvind Langsrud software, German version).Results:In MES seizures, augmented effects were obtained when cinnarizine was combined with sodium valproate, i.e. 100%. In PTZ-induced seizures, augmented effects were obtained when nifedipine was combined with sodium valproate, i.e. 100%. Thus, cinnarizine added to sodium valproate therapy produces significant protection against MES seizures while nifedipine added to sodium valproate therapy produces significant protection against PTZ seizures.Conclusion:The results provide a lead for potential benefit of adding CCBs to sodium valproate in the treatment of epilepsy, which needs to be explored further.

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“…Venous blood samples (10 ml) were taken via an indwelling catheter from the other forearm vein at 0 , 5 , 10,15,20,30,45,60 min, 1.5,2,2. 5,3,4,5,6,8,10,12,14,16,24,30,39, and 48 h after the i.v. administration, and at 0,0.5, 1, 2, 3, 4, 5, 6, 8, 10, 12, 14, 16, 24, 30, 39, and 48 h after the oral administrations.…”

Section: Methodsmentioning

confidence: 99%

Pharmacokinetic evaluation of novel sustained‐release dosage forms of valproic acid in humans

Bialer

Friedman

Dubrovsky

et al. 1985

Biopharm & Drug Disp

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Five new sustained-release dosage forms of valproic acid (VPA) were developed. The new sustained-release formulations were administered to six healthy subjects for comparison with a standard tablet and an i.v. preparation of the drug. Three of the formulations exhibited a more prolonged and uniform absorption rate and yielded more sustained serum levels after ingestion. These three formulations maintained serum therapeutic levels of VPA for 24 h after a single oral administration of 1 g, and were bioequivalent to a marketed standard tablet of VPA. The absorption profile of the various oral formulations was analysed pharmacokinetically, using the Loo-Riegelman procedure.

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Valproic Acid

Cited by 120 publications

References 49 publications

Exploring the Drug Repurposing Versatility of Valproic Acid as a Multifunctional Regulator of Innate and Adaptive Immune Cells

Exploring the Drug Repurposing Versatility of Valproic Acid as a Multifunctional Regulator of Innate and Adaptive Immune Cells

Role of cinnarizine and nifedipine on anticonvulsant effect of sodium valproate and carbamazepine in maximal electroshock and pentylenetetrazole model of seizures in mice

Pharmacokinetic evaluation of novel sustained‐release dosage forms of valproic acid in humans

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