Pharmacodynamics +<unk>  (and metabolite) Site Action Ref >10,000 927 Blocker >10,000 58 Blocker >10,000 >10,000 5-HT1A 320–432 45 Partial agonist 5-HT1B 1,109–2,050 1,117 5-HT1D >10,000 249 5-HT1E 1,250–2,402 97 5-HT1F 2,240 5-HT2A 96–101 48 Antagonist 5-HT2B 14 Antagonist 5-HT2C 2,502 107 Antagonist 5-HT3 >10,000 394 Antagonist 5-HT4 5-HT5A 3,120 768 5-HT6 1,865 503 Antagonist 5-HT7 307 76 Antagonist α1A 22 144 Antagonist α1B 39 95 Antagonist α2A 2,230–3,630 237 Antagonist α2B 90–747 378 Antagonist α2C 28.7–350 736 Antagonist β1 >10,000 >10,000 β2 >10,000 >10,000 D1 712 214 Antagonist D2 245 196 Antagonist D2L 700 Antagonist D2S 390 Antagonist D3 340–483 567 Antagonist D4 1,202 1,297 Antagonist D4.2 1,600 Antagonist D5 1,738 1,419 Antagonist H1 2.2–11 3.5 Antagonist H2 >10,000 298 Antagonist H3 >10,000 >10,000 H4 >10,000 1,660 M1 858 39 Antagonist M2 1,339 453 M3 >10,000 23 Antagonist M4 542 110 M5 1,942 23 Antagonist σ1 220–3,651 >10,000 σ2 1,344 1,050 () >10,000 Antagonist >10,000 >10,000() Values are Ki (nM), unless otherwise noted. The smaller the value, the more strongly the drug binds to the site. All data are for human cloned proteins, except σ1 (guinea pig), σ2 (rat), and (rat).<unk>  has the following pharmacological actions: * Dopamine D1, D2, D3, D4, and D5 receptor antagonist * Serotonin 5-HT1A receptor partial agonist, 5-HT2A, 5-HT2B, 5-HT2C, 5-HT3, 5-HT6, and 5-HT7 receptor antagonist, and 5-HT1B, 5-HT1D, 5-HT1E, and 5-HT1F receptor ligand * α1- and α2-adrenergic receptor antagonist * Histamine H1 receptor antagonist * Muscarinic acetylcholine receptor antagonist This means<unk>  is a dopamine, serotonin, and adrenergic antagonist, and a potent antihistamine with some anticholinergic properties.<unk>  binds strongly to serotonin receptors; the drug acts as partial agonist at 5-HT1A receptors. Serial PET scans evaluating the D2 receptor occupancy of<unk>  have demonstrated that<unk>  very rapidly disassociates from the D2 receptor. Theoretically, this allows for normal physiological surges of dopamine to elicit normal effects in areas such as the nigrostriatal and tuberoinfundibular pathways, thus minimizing the risk of side-effects such as pseudo-parkinsonism as well as elevations in prolactin. Some of the antagonized receptors (serotonin, norepinephrine) are actually autoreceptors whose blockade tends to increase the release of neurotransmitters. At very low doses,<unk>  acts primarily as a histamine receptor blocker (antihistamine) and α1-adrenergic blocker. When the dose is increased,<unk>  activates the adrenergic system and binds strongly to serotonin receptors and autoreceptors. At high doses,<unk>  starts blocking significant amounts of dopamine receptors. Off-label prescriptions, e.g. for chronic insomnia, of low-dose<unk>  is not recommended due to the harmful side-effects. When treating schizophrenia, antagonism of D2 receptor by<unk>  in the mesolimbic pathway relieves positive symptoms and antagonism of the 5HT2A receptor in the frontal cortex of the brain relieves negative symptoms.<unk>  has fewer extrapyramidal side effects and is less likely to cause hyperprolactinemia when compared to other drugs used to treat schizophrenia, so is used as a first line treatment. Pharmacokinetics Peak levels of<unk>  occur 1.5 hours after a dose. The plasma protein binding of<unk>  is 83%. The major active metabolite of<unk>  is norquetiapine (N-desalkylquetiapine).<unk>  has an elimination half-life of 6 or 7 hours. Its metabolite, norquetiapine, has a half-life of 9 to 12 hours.<unk>  is excreted primarily via the kidneys (73%) and in feces (20%) after hepatic metabolism, the remainder (1%) is excreted as the drug in its unmetabolized form. Skeletal formula of norquetiapine
Quetiapine
Sertraline
Mirtazapine
Fluparoxan
Asenapine
Aripiprazole
Citalopram
Loxapine