Haloperidol stands out as a high-potency, first-generation antipsychotic from the butyrophenone class. Clinicians use it often to treat schizophrenia, acute psychosis, and delirium. The main way it works? It blocks central dopamine D₂ receptors, especially in the mesolimbic and mesocortical pathways. This blockade suppresses positive psychotic symptoms (Adams et al., 2013). But there’s a tradeoff blocking dopamine in the nigrostriatal pathway brings on extrapyramidal side effects like dystonia, akathisia, and parkinsonism. Haloperidol also binds moderately to α₁-adrenergic receptors, but it barely touches histaminergic or muscarinic receptors. That’s why it causes little sedation or anticholinergic effects (Dold et al., 2015). After you give haloperidol by mouth or injection, the body absorbs it pretty well. Still, only about 60% actually makes it into circulation because the liver breaks down a big chunk right away. Most of the drug latches onto plasma proteins in the blood. The liver does most of the heavy lifting here, mainly through the CYP3A4 and CYP2D6 enzymes, turning haloperidol into inactive forms (Kane & Correll, 2019). The drug sticks around for quite a while the elimination half-life runs anywhere from 12 up to 36 hours. That’s why you can usually get away with dosing once or twice a day. The decanoate ester version works differently: it lets the drug out slowly and keeps blood levels steady for weeks, which really helps people stick with their maintenance therapy.