Given that antagonism of D2 receptors is more beneficial on the positive symptoms of schizophrenia and antagonism of 5-HT2 receptors on the negative symptoms, this characteristic underlies haloperidols greater effect on delusions, hallucinations and other manifestations of psychosis. Haloperidols negligible affinity for histamine H1 receptors and muscarinic M1 acetylcholine receptors yields an antipsychotic with a lower incidence of sedation, weight gain, and orthostatic hypotension though having higher rates of treatment emergent extrapyramidal symptoms. Haloperidol acts on these receptors: (Ki)

D1 (silent antagonist) – Unknown efficiency
D5 (silent antagonist) – Unknown efficiency
D2 (inverse agonist) – 0.7 nM
D3 (inverse agonist) – 0.2 nM
D4 (inverse agonist) – 5–9 nM
σ1 (irreversible inactivation by haloperidol metabolite HPP+) –  3 nM
σ2 (agonist): 54 nM
5HT1A receptor agonist –  1927 nM
5HT2A (silent antagonist) –  53 nM
5HT2C (silent antagonist) – 10,000 nM
5HT6 (silent antagonist) – 3666 nM
5HT7 (irreversible silent antagonist) – 377.2 nM
H1 (silent antagonist) – 1,800 nM
M1 (silent antagonist) – 10,000 nM
α1A (silent antagonist) – 12 nM
α2A (silent antagonist) – 1130 nM
α2B (silent antagonist) – 480 nM
α2C (silent antagonist) – 550 nM
NR1/NR2B subunit containing NMDA receptor (antagonist; ifenprodil site): IC50 – 2,000 nM

Pharmacokinetics
By mouth
The bioavailability of oral haloperidol ranges from 60 to 70%. However, there is a wide variance in reported mean Tmax and T1/2 in different studies, ranging from 1.7 to 6.1 hours and 14.5 to 36.7 hours respectively. Intramuscular injections
The drug is well and rapidly absorbed with a high bioavailability when injected intramuscularly. The Tmax is 20 minutes in healthy individuals and 33.8 minutes in patients with schizophrenia.
Society and culture
Plerixafor has orphan drug status in the United States and European Union for the mobilization of hematopoietic stem cells. It was approved by the U.S. Food and Drug Administration (FDA) for this indication on 15 December 2008. In the European Union, the drug was approved after a positive Committee for Medicinal Products for Human Use assessment report on 29 May 2009. The drug was approved for use in Canada by Health Canada on 8 December 2011. Research
Anti-cancer properties
Plerixafor was seen to reduce metastasis in mice in several studies. It has also been shown to reduce recurrence of glioblastoma in a mouse model after radiotherapy. In this model, the cancer cells that survived radiation critically depended on bone marrow derived cells for vasculogenesis, and the recruitment of the latter was mediated by SDF-1 CXCR4 interactions, which are blocked by plerixafor. Use in stem cell research
Researchers at Imperial College have demonstrated that plerixafor in combination with vascular endothelial growth factor (VEGF) can mobilise mesenchymal stem cells and endothelial progenitor cells into the peripheral blood of mice.In double‐blind, randomized, placebo‐controlled trial, stem cell mobilization with plerixafor did not improve healing of ischemic diabetic wounds. Neurologic
Blockade of CXCR4 signalling by plerixafor has also unexpectedly been found to be effective at counteracting opioid-induced hyperalgesia produced by chronic treatment with morphine, though only animal studies have been conducted as yet. References
External links
"Plerixafor". Drug Information Portal. U.S. National Library of Medicine. MeSH JM+3100