Lamotrigine

Class	Antiepileptic
Chemistry	Phenyltriazine compound
Routes of administration	Oral only
Absorption	Rapidly and completely absorbed; about 98% bioavailability
Solubility	pKa 5.7; moderately lipophilic
Distribution	VOD=0.9 to 1.3 L/kg, about 55% protein-bound;
Metabolism	Hepatic metabolism primarily through glucuronidation
Elimination	Minimal renal excretion - only about 10% is excreted renally unchanged
Time course of action	Half-life is 22.8 to 37.4 hours
Target receptor	Multiple molecular targets, particularly: Inhibition of voltage-gated sodium channels Inhibition of voltage-gated calcium channel Enhancement of GABA release
Mechanism of action	Multiple anticonvulsant mechanisms: lamotrigine increases the activity of GABA (mainly by enhancing its release), stabilises neuronal membranes by its activity on sodium channels, and reduces high-frequency firing of neurons by voltage-gated calcium channel blockade. Also has anti-glutamate effects, which prevents excitotoxicity
Clinical effects	Especially effective for focal partial seizures and for discrete epileptogenic foci. Also indicated for bipolar disorder as a mood stabiliser. Side effects include making the immune system very angry: for example, Stevens-Johnson Syndrome, toxic epidermal necrolysis, as well as aplastic anaemia, agranulocytosis, and DRESS syndrome.
Literature reference	Janssen & Boon, 2022
CICM details of understanding	Level 3
Mentioned around Deranged Physiology	Pharmacology of anticonvulsant drugs
Related SAQs