Xanax was synthesized by Patricia Krem of the original Upjohn laboratory (Patricia Chrem). This is now part of Pfizer's conglomerate. It has patent number 2, 947, 153 and has been inaugurated since 1978. In principle, drugs were applied in the case of anxiety crisis (panic attack), later psychiatrist David Sheehan suggested that this drug is aimed at anxiety disorder.
Xanax is a triazolobenzodiazepine, its structure is attached with a triazole ring, its effect is 12 times more effective than known diazepam, but its half-life is short. It has been shown in the treatment of anxiety (anxiety), depression. Anxiety about the symptoms of disorders, depression and anxiety crisis, sometimes stroke.
Pharmacokinetics and mechanism of action
Xanax inhibits the central nervous system, mediates the effect of gamma aminobutyric acid (GABA) on the brain of the ascending retinal activation system, and also binds to the GABA A receptor blocking cortical and limbic excitement. The GABA A receptor consists of various combinations of possible 19 5 subunits and subunits. GABA receptors have different characteristics as well as different locations in the brain, and most importantly have different effects on the action of benzodiazepines.
Clinically, all benzodiazepines cause central nervous system depression, ranging from minimal change to hypnosis. Absorption: rapidly absorbed after dose, peak in serum within 1 hour and 2 hours after oral administration, administered sublingually, effect appears within about 5 minutes.
Distribution: It is widely distributed throughout the body. Approximately 70-91% of the dose binds to plasma proteins. Metabolism: Xanax is metabolized in the liver and turns into α-hydroxy alprazolam and other inactive metabolites. Elimination: The half-life of Xanax is eliminated from 9 to 14 hours. The urinary tract is the main excretion pathway and excreted as α-hydroxyalprazolam without pharmacological action and metabolite.