ALPRAZOLAM

Pharmacodynamics:
Alprazolam is a benzodiazepine-derived agent with anxiolytic activity. Although its exact mechanism of action is unknown, it is postulated that its depressant effects on the central nervous system (CNS) are mediated by the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). Experimental evidence suggests that alprazolam binds to benzodiazepine-specific recognition sites coupled to the postsynaptic GABA receptor (GABA-A subtype), thereby increasing the neurotransmitter’s affinity for this structure. When GABA interacts with its receptor (GABA-A), chloride ions enter the neuron, causing hyperpolarization and a consequent reduction in excitability. The resulting central depression (due to increased GABA activity) can vary, depending on the alprazolam dose used, from mild sedation to hypnosis or deep coma. The drug does not act on the other subtypes of the GABA receptor (GABA-B or GABA-C).

Pharmacokinetics:
Following oral administration, alprazolam is efficiently absorbed from the gastrointestinal tract, reaching peak serum levels within 1-2 hours. When administered in extended-release formulations, absorption is slower, resulting in sustained concentrations for 5 to 11 hours. Food slows the absorption process but does not affect the extent of absorption. Alprazolam is approximately 80% bound to plasma proteins and widely distributed throughout the body (Vd: 0.8-1.4 L/kg). It crosses the blood-brain barrier, the placenta, and is excreted in breast milk. It is extensively metabolized in the liver (via CYP3A4), producing inactive products that are excreted, along with intact alprazolam, primarily in the urine. The elimination half-life of immediate-release formulations is 11-12 hours, while extended-release formulations range from 10 to 16 hours. These values ​​are increased in patients with hepatic impairment and in the elderly.