be affected. At low doses Butabarbital has been shown clinically to induce drowsiness, depressing the sensory cortex and motor activity. In some rare cases Butabarbital has been shown to produce small bursts of excitement or euphoria prior to the sedative effects. Butabarbital is a highly potent drug however, with addictive properties, and small variations in dose can result in significant escalation of effects. Pharmacology Butabarbital is a sedative hypnotic member of the barbiturate family. It is relatively fast acting, with a short duration, producing a range of effects from mild sedation to hypnosis as a function of dosage. An overdose of butabarbital can result in deep coma or even death. Absorption, distribution and excretion Butabarbituates are rapidly distributed and absorbed in the brain, liver and kidneys. One of the more lipophilic barbiturates, butabarbital crosses the blood brain barrier with relative ease, and is slightly more potent then other less lipophilic barbiturates such as phenobarbital. Butabarbital, a weak acid, is most commonly administered orally in its sodium salt form. 3–4 hours after oral administration butabarbital sodium reaches peak plama concentrations of 203 ug/mL for sedation, or 25 ug/mL to induce sleep, absorbed via the GI tract. Once absorbed, butabarbital's effects have a duration of 6–8 hours if orally administered, or 3–6 hours following intravaneous administration. General consensus has it with a half-life of approximately 100hr, however it has also been reported in one study to have a half life of 34-42 hr. The primary way the body terminates activity is by oxidation of radicals at C5, with other biotransformations contributing to a lesser extent. Butabarbital is metabolized almost entirely by the liver, products including polar alcohols, ketones, phenols, or carboxylic acids, before it is renally excreted in the urine. Half-Life: ~100 hr Duration: 6-8 hr Onset: 45-60 min Enzymes induced: CYP1A2, CYP2C9/10, CYP3A4 Excretion: Urine Mechanism of action The mechanism of action by which barbiturates exert their effect is not yet completely understood, however they are believed to be involved in the enhancement of GABA inhibitory neurotransmitter activity in the CNS via GABAA receptors. Butabarbital, as a member of this drug class, acutely potentiates inhibitory GABAergic tone by binding with a specific site associated with a Cl− ionophore at the GABAA receptor. Butabarbital's binding causes the channel to remain open longer and thus prolongs post-synaptic inhibition by GABA. Less well characterized effects of barbiturates include direct inhibition of AMPA-type glutamate receptors,