Mephobarbital, a barbiturate, undergoes metabolism into phenobarbital and has been employed for similar purposes, particularly in managing epilepsy; however, there exists no evidence supporting its superiority over phenobarbital. It serves to alleviate anxiety, tension, and apprehension, also functioning as an anticonvulsant for epilepsy treatment. In combination with acetaminophen or aspirin and caffeine, methylphenobarbital, a barbiturate variant, is utilized to induce sedation and relaxation in addressing tension headaches, migraines, and pain. Barbiturates exhibit nonselective depressive effects on the central nervous system, yielding a spectrum of mood alterations from stimulation to mild sedation, hypnotic states, and even profound comas under sufficiently high therapeutic dosages, including anesthesia induction. Methylphenobarbital's binding to a specific site connected to a Cl- ionopore at the GABAA receptor prolongs the opening duration of the ionopore, consequently extending GABA's inhibitory impact in the thalamus. Around 50% of an orally administered mephobarbital dose is absorbed through the gastrointestinal tract and is metabolized primarily in the liver via the hepatic microsomal enzyme system. Notably, approximately 75% of a solitary oral mephobarbital dose is transformed into phenobarbital within a 24-hour span.

Methylphenobarbital Pathway References