DIACOMIT® has an intrinsic anticonvulsant activity. It acts as a positive allosteric modulator of the GABAA receptor by enhancing the sensitivity of the receptor to GABA. Indeed, it increases the mean opening time of the chloride ion channels, and prolongs the duration of the inhibitory GABAergic currents. In addition, DIACOMIT® inhibits the synaptosomal re-uptake of GABA and/or its degradation in glial cells by acting on the GABA-transaminase, leading to a higher cerebral GABA concentration.

Furthermore, DIACOMIT® displays pharmacodynamic interactions with other antiepileptic drugs such as clobazam, diazepam or clonazepam. Indeed, an additive effect on GABAergic neurotransmission was observed when DIACOMIT® was combined to these benzodiazepines. There is also of fivefold of the plasma concentration of norclobazam. Their different binding sites on the GABAA receptors are likely to explain this effect.

DIACOMIT® also exhibits a pharmacokinetic effect. It inhibits the activity of hepatic enzymes (CYP450 isoenzymes: 1A2, 2C8, 2C19, 2D6 & 3A4) involved in the metabolism of some of the co-administered antiepileptic drugs.

For references, please access “About DIACOMIT” through the Bibliography part located in Resources tab.