The clinical pharmacology of acepromazine is similar to that of other phenothiazine derived anti-psychotic agents. The primary behavioral effects are attributed to its potent antagonism of post-synaptic D2 receptors and, to a lesser degree, the other D2-like receptors. Additional effects are related to its appreciable antagonistic effects on various other receptors, including the α1-adrenergic receptors, H1 receptors, and muscarinic acetylcholine receptors. It is metabolized by the liver, oxidized to produce its primary metabolite, hydroxyethylpromazine sulfoxide, which is then excreted in the urine. Its action at the chemoreceptor trigger zone (in the area postrema) and the solitary nucleus (in the medulla oblongata) allow it to have an antiemetic effect.
