Pharmacodynamics +<unk>  Site Ki (nM) Action 5-HT1A 423 Antagonist 5-HT1B 14.9 Antagonist 5-HT1D 84.6 Antagonist 5-HT2A 0.17 Inverse agonist 5-HT2B 61.9 Inverse agonist 5-HT2C 12.0 Inverse agonist 5-HT5A 206 Antagonist 5-HT6 2,060 Antagonist 5-HT7 6.60 Irreversibleantagonist α1A 5.0 Antagonist α1B 9.0 Antagonist α2A 16.5 Antagonist α2B 108 Antagonist α2C 1.30 Antagonist D1 244 Antagonist D2 3.57 Antagonist D2S 4.73 Antagonist D2L 4.16 Antagonist D3 3.6 Inverse agonist D4 4.66 Antagonist D5 290 Antagonist H1 20.1 Inverse agonist H2 120 Inverse agonist >10,000 Negligible<unk>  pharmacodynamics excluding D-amino acid oxidase inhibition<unk>  has been classified as a "qualitatively atypical" antipsychotic agent with a relatively low incidence of extrapyramidal side effects (when given at low doses) that has more pronounced serotonin antagonism than dopamine antagonism.<unk>  contains the functional groups of benzisoxazole and piperidine as part of its molecular structure. Although not a butyrophenone, it was developed with the structures of benperidol and ketanserin as a basis. It has actions at several 5-HT (serotonin) receptor subtypes. These are 5-HT2C, linked to weight gain, 5-HT2A, linked to its antipsychotic action and relief of some of the extrapyramidal side effects experienced with the typical neuroleptics. It has been found that D-amino acid oxidase, the enzyme that catalyses the breakdown of D-amino acids (e.g. D-alanine and D-serine — the neurotransmitters) is inhibited by<unk> .<unk>  acts on the following receptors: Dopamine receptors: This drug is an antagonist of the D1 (D1, and D5) as well as the D2 family (D2, D3 and D4) receptors, with 70-fold selectivity for the D2 family. This drug has "tight binding" properties, which means it has a long half-life and like other antipsychotics,<unk>  blocks the mesolimbic pathway, the prefrontal cortex limbic pathway, and the tuberoinfundibular pathway in the central nervous system.<unk>  may induce extrapyramidal side effects, akathisia and tremors, associated with diminished dopaminergic activity in the striatum. It can also cause sexual side effects, galactorrhoea, infertility, gynecomastia and, with chronic use reduced bone mineral density leading to breaks, all of which are associated with increased prolactin secretion. Serotonin receptors: Its action at these receptors may be responsible for its lower extrapyramidal side effect liability (via the 5-HT2A/2C receptors) and improved negative symptom control compared to typical antipsychotics such as haloperidol for instance. Its antagonistic actions at the 5-HT2C receptor may account, in part, for its weight gain liability. Alpha α1 adrenergic receptors: This action accounts for its orthostatic hypotensive effects and perhaps some of the sedating effects of<unk> . Alpha α2 adrenergic receptors: Perhaps greater positive, negative, affective and cognitive symptom control. Histamine H1 receptors: effects on these receptors account for its sedation and reduction in vigilance. This may also lead to drowsiness and weight gain. Voltage-gated sodium channels: Because it accumulates in synaptic vesicles,<unk>  inhibits voltage-gated sodium channels at clinically used concentrations. Pharmacokinetics<unk>  undergoes hepatic metabolism and renal excretion. Lower doses are recommended for patients with severe liver and kidney disease. The active metabolite of<unk> , paliperidone, is also used as an antipsychotic.
Risperidone
Aripiprazole
Methylphenidate
Olanzapine
Ziprasidone
Sertraline
Dexmethylphenidate
Lorpiprazole