Retigabine (ezogabine), withdrawn from many markets but still examined for its unique mechanism, exerts its anticonvulsant effect by:

• A Opening KCNQ (Kv7) potassium channels, stabilising the resting membrane potential ✓
• B Blocking T-type calcium channels in thalamic neurons
• C Antagonism of the glycine site of the NMDA receptor
• D Enhancing slow inactivation of voltage-gated sodium channels

Explanation

Retigabine is the only antiepileptic that acts as a positive allosteric opener of KCNQ (Kv7) potassium channels, the channels underlying the M-current. Enhancing this potassium leak hyperpolarises neurons and reduces excitability. Ethosuximide blocks T-type calcium channels, lacosamide promotes slow sodium channel inactivation, and no antiepileptic targets the glycine site of NMDA receptors. Skin discolouration limited its clinical use.

Reference: Goodman and Gilman's The Pharmacological Basis of Therapeutics, 14th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.