Mechanism of action 300x300pxAtipamezole is a competitive antagonist at ɑ2-adrenergic receptors that competes with dexmedetomidine, an ɑ2-adrenergic receptors agonist. It does not directly interact with dexmedetomidine; rather, their structural similarity allows<unk>  to easily compete for receptor binding sites.<unk>  reverses analgesia by blocking norepinephrine feedback inhibition on nociceptors. Pharmacokinetics Out of the three ɑ2-antagonists commonly used in veterinary medicine<unk> , yohimbine, and tolazine),<unk>  shows the highest preference for ɑ2- over ɑ1-receptors, binding to them with a ratio of 8526:1. It shows no preference for a particular ɑ2-receptor subtype.<unk>  has a rapid onset: it reverses the decreased heart rate caused by sedation within three minutes. The animal usually begins waking up within 5–10 minutes. In a study of over 100 dogs, more than half could stand up within 5 minutes, and 96% could stand up within 15.<unk>  reaches maximum serum concentration within 10 minutes of IM administration.<unk>  is distributed extensively to the tissues; at a particular time, concentrations in the brain reach two to three times the concentration in the plasma.<unk>  undergoes heavy first-pass metabolism in the liver, which includes the glucuronidation at nitrogen during. Metabolites are mostly excreted in the urine. The elimination half-life is 2.6 hours in dogs and 1.3 hours rats.
Atipamezole
Fabomotizole
Letrozole
Bisoctrizole
Dienogest
Protollin
Lapisteride
Ingenol mebutate