A long-acting decanoateester of haloperidol is used as an injection given every four weeks to people with schizophrenia or related illnesses who have poor adherence to medication regimens (most commonly due to them forgetting to take their medication, or due to poor insight into their illness) and suffer frequent relapses of illness, or to overcome the drawbacks inherent to its orally administered counterpart.
A multiple-year study suggested this drug and other neuroleptic antipsychotic drugs commonly given to Alzheimer's patients with mild behavioural problems often make their condition worse and that its withdrawal was even beneficial for some cognitive and functional measures.
Pregnancy and lactation
Data from animal experiments indicate haloperidol is not teratogenic, but is embryotoxic in high doses. In humans, no controlled studies exist. Unconfirmed studies in pregnant women revealed possible damage to the fetus, although most of the women were exposed to multiple drugs during pregnancy. In addition, there have been reports that neonates exposed to antipsychotic drugs are at risk for extrapyramidal and/or withdrawal symptoms following delivery such as agitation, hypertonia, hypotonia, tremor, somnolence, respiratory distress, and feeding disorder. Following accepted general principles, haloperidol should be given during pregnancy only if the benefit to the mother clearly outweighs the potential fetal risk.
Haloperidol, when given to lactating women, is found in significant amounts in their milk. Breastfed children sometimes show extrapyramidal symptoms. If the use of haloperidol during lactation seems indicated, the benefit for the mother should clearly outweigh the risk for the child, or breastfeeding should be stopped.
Skeletal formula of haloperidol decanoate: The decanoate group is highlighted in blue.
During long-term treatment of chronic psychiatric disorders, the daily dose should be reduced to the lowest level needed for maintenance of remission. Sometimes, it may be indicated to terminate haloperidol treatment gradually. In addition, during long-term use, routine monitoring including measurement of BMI, blood pressure, fasting blood sugar, and lipids, is recommended due to the risk of side-effects. 
Other forms of therapy (psychotherapy, occupational therapy/ergotherapy, or social rehabilitation) should be instituted properly. PET imaging studies have suggested low doses are preferable. Clinical response was associated with at least 65% occupancy of D2 receptors, while greater than 72% was likely to cause hyperprolactinaemia and over 78% associated with extrapyramidal side effects. Doses of haloperidol greater than 5 mg increased the risk of side effects without improving efficacy. Patients responded with doses under even 2 mg in first episode psychosis. For maintenance treatment of schizophrenia, an international consensus conference recommended a reduction dosage by about 20% every 6 months until a minimal maintenance dose is established.
Depot forms are also available; these are injected deeply IM at regular intervals. The depot forms are not suitable for initial treatment, but are suitable for patients who have demonstrated inconsistency with oral dosages.
The decanoate ester of haloperidol (haloperidol decanoate, trade names Haldol decanoate, Halomonth, Neoperidole) has a much longer duration of action, so is often used in people known to be noncompliant with oral medication. A dose is given by intramuscular injection once every two to four weeks. The IUPAC name of haloperidol decanoate is 4-(4-chlorophenyl)-1-1[4-(4-fluorophenyl)-4-oxobutyl]-4 piperidinyl decanoate.
Topical formulations of haloperidol should not be used as treatment for nausea because research does not indicate that this therapy is more effective than alternatives.
Extrapyramidal side effects such as: (as haloperidol is a high potency typical antipsychotic it tends to produce significant extrapyramidal side effects. According to a recent meta-analysis of the comparative efficacy and tolerability of 15 antipsychotic drugs it was the most prone of the 15 for causing extrapyramidal side effects.)
Haloperidol has been shown to dramatically increase dopamine activity, up to 98%, in test subjects after two weeks on a "moderate to high" dose compared to chronic schizophrenics. In another study, a live survey of a patient showed the person has 90% more dopamine receptors, of the D2 subtype, than before treatment with haloperidol. The long-term effect of this is unknown, but the first study concludes this upregulation is positively associated with severe dyskinesias (more upregulation, more dyskinesia).
Some research studies have suggested effects of haloperidol on brain tissue. In a 2005 placebo-compared study of six macaques receiving haloperidol for up to 27 months, a significant brain volume change of about 10% and weight decreases were detected. In later studies (2008) of the stored samples, the previously reported changes were attributed primarily to astrocyte and oligodendrocyte loss, with the neuron loss at about 5%, which was not statistically significant. A study in 2011 of rats given haloperidol in doses comparable to clinical use for eight weeks found a reduction in brain cortex volume of 10–12%.
In other studies, the use of potent antipsychotics has been associated with cognitive decline and permanent brain damage.
Psychosis and general morbidity
Several studies have explored the possibility that psychosis and/or its pharmacological treatment with anti-psychotics such as haloperidol may enhance patients' risk of developing cancers, particularly breast cancer among women, tobacco-related cancers among men, and obesity-related cancers, as well as many other non-psychiatric disorders, among them metabolic, cardiovascular, and respiratory, some or all of which may be due to decreased access to healthcare and treatment and behaviors associated with maladjusted behavior, such as smoking, alcoholism, drug abuse, and eating disorders, rather than to specific pharmacological side effects. A link between atypical anti-psychotics, such as risperidone and quetiapine, and pituitary tumor growth has been generally reported.
Compromised liver function (as haloperidol is metabolized and eliminated mainly by the liver)
In patients with hyperthyreosis, the action of haloperidol is intensified and side effects are more likely.
IV injections: risk of hypotension or orthostatic collapse
Patients with a history of leukopenia: a complete blood count should be monitored frequently during the first few months of therapy and discontinuation of the drug should be considered at the first sign of a clinically significant decline in white blood cells.
Elderly patients with dementia-related psychosis: analysis of 17 trials showed the risk of death in this group of patients was 1.6 to 1.7 times that of placebo-treated patients. Most of the causes of death were either cardiovascular or infectious in nature. It is not clear to what extent this observation is attributed to antipsychotic drugs rather than the characteristics of the patients. The drug bears a boxed warning about this risk.
Other central depressants (alcohol, tranquilizers, narcotics): actions and side effects of these drugs (sedation, respiratory depression) are increased. In particular, the doses of concomitantly used opioids for chronic pain can be reduced by 50%.
Methyldopa: increased risk of extrapyramidal side effects and other unwanted central effects
Haloperidol has been shown to metabolize in rat and human hepatocytes via CYP-3A4 to the neurotoxic pyridinium metabolites 4-(4-chlorophenyl)-1-(4-fluorophenyl)-4-oxobutylpyridinium(HPP+)and 4-(4-chlorophenyl)-1-(4-fluorophenyl)-4-hydroxybutylpyridinium (RHPP+). HPP+ and RHPP+ are lipophilic and have elimination half lives of 67.3 hrs and 63.3 hrs, respectively. HPP+ is a structural analog of the more widely known Parkinson’s producing neurotoxin MPP+ and its precursor MPTP. Unlike MPP+, HPP+ is not dependent on MAO-B for metabolism to toxic species and does not require functional dopamine transporter protein for intracellular uptake.
Microdialysis studies were performed in the striatum, substantia nigra and cortex of conscious rats to compare the neurotoxic potential of 1-methyl-4-phenylpyridinium (MPP+) and HPP+ to dopaminergic and serotonergic neurons. HPP+ was a less potent neurotoxin than MPP+ to dopaminergic neurons and displayed equipotent serotonergic neurotoxicity. Impairment of cortico-striatal mitochondrial complex I is pathognomic of MPP+ neurotoxicity and Parkinson's cellular dysfunction. HPP+ is more potent than MPP+ at inhibiting murine mitochondrial complex I with an IC50 of 12mMol for HPP+ and 160mMol for MPP+. Prolonged, high dose (2 & 5 mg\kg) administration of haloperidol in a murine model elevates striatal nitric oxide, TNF-a, and caspase-3.
HPP+ and RHPP+ have been found in the brains of patients taking Haldol at autopsy. A short term 6 week trial failed to find statistically significant correlation between HPP+, RHPP+ and extrapyramidal symptoms. A long term retrospective study found a significant positive correlation between levels of HPP+ and severity of tardive dyskinesia.
Experimental evidence from animal studies indicates the doses needed for acute poisoning are quite high in relation to therapeutic doses. Overdoses with depot injections are uncommon, because only certified personnel are legally permitted to administer them to patients.
Symptoms are usually due to exaggerated side effects. Most often encountered are:
Treatment is merely symptomatic and involves intensive care with stabilization of vital functions. In early detected cases of oral overdose, induction of emesis, gastric lavage, and the use of activated charcoal can all be tried. Epinephrine is avoided for treatment of hypotension and shock, because its action might be reversed. In the case of a severe overdose, antidotes such as bromocryptine or ropinirole may be used to treat the extrapyramidal effects caused by haloperidol, acting as dopamine receptor agonists. ECG and vital signs should be monitored especially for QT prolongation and severe arrhythmias should be treated with anti-arrhythmic measures.
In general, the prognosis of overdose is good, and lasting damage is not known, provided the patient has survived the initial phase. An overdose of haloperidol can be fatal.
Haloperidol, 10mg oral tablet
Haloperidol is a typical butyrophenone type antipsychotic that exhibits high affinity dopamine D2 receptor antagonism and slow receptor dissociation kinetics. The drug binds preferentially to D2 and Alpha 1 receptors at low dose (ED50 = 0.13 and 0.42 mg/kg, respectively), and 5-HT2 receptors at a higher dose (ED50 = 2.6 mg/kg). Given that antagonism of D2 receptors is more beneficial on the positive symptoms of schizophrenia and 5-HT2 receptors on the negative symptoms, this characteristic underlies haloperidol's greater effect on delusions, hallucinations and other manifestations of psychosis.  Haloperidol's 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.
The bioavailability of oral haloperidol ranges from 60–70%. 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.
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. The mean T1/2 is 20.7 hours. The decanoate injectable formulation is for intramuscular administration only and is not intended to be used intravenously. The plasma concentrations of haloperidol decanoate reach a peak at about six days after the injection, falling thereafter, with an approximate half-life of three weeks.
The bioavailability is 100% in intravenous (IV) injection, and the very rapid onset of action is seen within seconds. The T1/2 is 14.1 to 26.2 hours. The apparent volume of distribution is between 9.5 to 21.7 L/kg. The duration of action is four to six hours. If haloperidol is given as a slow IV infusion, the onset of action is slowed, and the duration of action is prolonged.
Haloperidol for injection
Plasma levels of four to 25 micrograms per liter are required for therapeutic action. The determination of plasma levels can be used to calculate dose adjustments and to check compliance, particularly in long-term patients. Plasma levels in excess of the therapeutic range may lead to a higher incidence of side effects or even pose the risk of haloperidol intoxication.
The concentration of haloperidol in brain tissue is about 20-fold higher compared to blood levels. It is slowly eliminated from brain tissue, which may explain the slow disappearance of side effects when the medication is stopped.
Distribution and metabolism
Haloperidol is heavily protein bound in human plasma, with a free fraction of only 7.5 to 11.6%. It is also extensively metabolized in the liver with only about 1% of the administered dose excreted unchanged in the urine. The greatest proportion of the hepatic clearance is by glucuronidation, followed by reduction and CYP-mediated oxidation, primarily by CYP3A4. 
Coincident with civil unrest in the United States in the 1960s and 1970s, schizophrenia was racialized to match the behavior of angry/violent black men. Haldol was promoted as a way to pacify them, and was marketed to appeal to feelings of racial unease. (cf. Metzl 2010. The Protest Psychosis)
Soviet dissidents, including medical staff, have reported several times on the use of haloperidol in the Soviet Union for punitive purposes or simply to break the prisoners' will. Notable dissidents who were administered haloperidol as part of their court-ordered treatment were Sergei Kovalev and Leonid Plyushch. The accounts Plyushch gave in the West, after he was allowed to leave the Soviet Union in 1976, were instrumental in triggering Western condemnation of Soviet practices at the World Psychiatric Association's 1977 meeting. The use of haloperidol in the Soviet Union's psychiatric system was prevalent because it was one of the few psychotropic drugs produced in quantity in the USSR.
Haloperidol has been used for its sedating effects during the deportations of immigrants by the United States Immigration and Customs Enforcement (ICE). During 2002-2008, federal immigration personnel used haloperidol to sedate 356 deportees. By 2008, following court challenges over the practice, it was given to only three detainees. Following lawsuits, U.S. officials changed the procedure so the drug is administered only by the recommendation of medical personnel and under court order.
Haloperidol is sold under the tradenames Aloperidin, Bioperidolo, Brotopon, Dozic, Duraperidol (Germany), Einalon S, Eukystol, Haldol (common tradename in the US and UK), Halosten, Keselan, Linton, Peluces, Serenace and Sigaperidol.
Haloperidol is also used on many different kinds of animals. It appears to be particularly successful when given to birds, e.g., a parrot that will otherwise continuously pluck its feathers out.
^Giannini, A. James; Eighan, Michael S.; Loiselle, Robert H.; Giannini, Matthew C. (1984). "Comparison of Haloperidol and Chlorpromazine in the Treatment of Phencyclidine Psychosis". The Journal of Clinical Pharmacology24 (4): 202–4. doi:10.1002/j.1552-4604.1984.tb01831.x. PMID6725621.
^Cavanaugh, SV (1986). "Psychiatric emergencies". The Medical clinics of North America70 (5): 1185–202. PMID3736271.
^Irving, Claire B; Adams, Clive E; Lawrie, Stephen (2006). Irving, Claire B, ed. "Haloperidol versus placebo for schizophrenia". Cochrane Database of Systematic Reviews (4): CD003082. doi:10.1002/14651858.CD003082.pub2. PMID17054159.
^Allen, MH; Currier, GW; Hughes, DH; Reyes-Harde, M; Docherty, JP; Expert Consensus Panel for Behavioral Emergencies (2001). "The Expert Consensus Guideline Series. Treatment of behavioral emergencies". Postgraduate Medicine (Spec No): 1–88; quiz 89–90. PMID11500996.
^Allen, Michael H.; Currier, Glenn W.; Hughes, Douglas H.; Docherty, John P.; Carpenter, Daniel; Ross, Ruth (2003). "Treatment of Behavioral Emergencies: A Summary of the Expert Consensus Guidelines". Journal of Psychiatric Practice9 (1): 16–38. doi:10.1097/00131746-200301000-00004. PMID15985913.
^Allen, Michael H.; Currier, Glenn W.; Carpenter, Daniel; Ross, Ruth W.; Docherty, John P. (2005). "Introduction: Methods, Commentary, and Summary". Journal of Psychiatric Practice11: 5. doi:10.1097/00131746-200511001-00002.
^Oosthuizen, P.; Emsley, R. A.; Turner, J.; Keyter, N. (2001). "Determining the optimal dose of haloperidol in first-episode psychosis". Journal of Psychopharmacology15 (4): 251–5. doi:10.1177/026988110101500403. PMID11769818.
Smith, Thomas J.; Ritter, Joseph K.; Poklis, Justin L.; Fletcher, Devon; Coyne, Patrick J.; Dodson, Patricia; Parker, Gwendolyn (2012). "ABH Gel is Not Absorbed from the Skin of Normal Volunteers". Journal of Pain and Symptom Management43 (5): 961–6. doi:10.1016/j.jpainsymman.2011.05.017. PMID22560361.
^Truven Health Analytics, Inc. DrugPoint® System (Internet) [cited 2013 Sep 29]. Greenwood Village, CO: Thomsen Healthcare; 2013.
^Joint Formulary Committee. British National Formulary (BNF) 65. Pharmaceutical Pr; 2013.
^ abLeucht, Stefan; Cipriani, Andrea; Spineli, Loukia; Mavridis, Dimitris; Örey, Deniz; Richter, Franziska; Samara, Myrto; Barbui, Corrado; Engel, Rolf R; Geddes, John R; Kissling, Werner; Stapf, Marko Paul; Lässig, Bettina; Salanti, Georgia; Davis, John M (2013). "Comparative efficacy and tolerability of 15 antipsychotic drugs in schizophrenia: A multiple-treatments meta-analysis". The Lancet382 (9896): 951–62. doi:10.1016/S0140-6736(13)60733-3. PMID23810019.
^ abSilvestri, Simone; Seeman, Mary V.; Negrete, Juan-Carlos; Houle, Sylvain; Shammi, C.M.; Remington, Garry J.; Kapur, Shitij; Zipursky, Robert B.; Wilson, Alan A.; Christensen, Bruce K.; Seeman, Philip (2000). "Increased dopamine D 2 receptor binding after long-term treatment with antipsychotics in humans: A clinical PET study". Psychopharmacology152 (2): 174–80. doi:10.1007/s002130000532. PMID11057521.
^Dorph-Petersen, Karl-Anton; Pierri, Joseph N; Perel, James M; Sun, Zhuoxin; Sampson, Allan R; Lewis, David A (2005). "The Influence of Chronic Exposure to Antipsychotic Medications on Brain Size before and after Tissue Fixation: A Comparison of Haloperidol and Olanzapine in Macaque Monkeys". Neuropsychopharmacology30 (9): 1649–61. doi:10.1038/sj.npp.1300710. PMID15756305.
^Vernon, Anthony C.; Natesan, Sridhar; Modo, Mike; Kapur, Shitij (2011). "Effect of Chronic Antipsychotic Treatment on Brain Structure: A Serial Magnetic Resonance Imaging Study with Ex Vivo and Postmortem Confirmation". Biological Psychiatry69 (10): 936–44. doi:10.1016/j.biopsych.2010.11.010. PMID21195390.
^Dalton, Susanne Oksbjerg; Mellemkjaer, Lene; Thomassen, Lars; Mortensen, Preben B.; Johansen, Christoffer (2005). "Risk for cancer in a cohort of patients hospitalized for schizophrenia in Denmark, 1969–1993". Schizophrenia Research75 (2–3): 315–24. doi:10.1016/j.schres.2004.11.009. PMID15885523.
^Grinshpoon, Alexander; Barchana, Micha; Ponizovsky, Alexander; Lipshitz, Irena; Nahon, Daniella; Tal, Orna; Weizman, Abraham; Levav, Itzhak (2005). "Cancer in schizophrenia: Is the risk higher or lower?". Schizophrenia Research73 (2–3): 333–41. doi:10.1016/j.schres.2004.06.016. PMID15653279.
^Szarfman, Ana; Tonning, Joseph M; Levine, Jonathan G; Doraiswamy, P. Murali (2006). "Atypical Antipsychotics and Pituitary Tumors: A Pharmacovigilance Study". Pharmacotherapy26 (6): 748–58. doi:10.1592/phco.26.6.748. PMID16716128.
^Hippisley-Cox, Julia; Vinogradova, Y; Coupland, C; Parker, C (2007). "Risk of Malignancy in Patients with Schizophrenia or Bipolar Disorder". Archives of General Psychiatry64 (12): 1368–76. doi:10.1001/archpsyc.64.12.1368. PMID18056544.
^Levav, Itzhak; Kohn, Robert; Barchana, Micha; Lipshitz, Irena; Pugachova, Inna; Weizman, Abraham; Grinshpoon, Alexander (2009). "The risk for cancer among patients with schizoaffective disorders". Journal of Affective Disorders114 (1–3): 316–20. doi:10.1016/j.jad.2008.06.010. PMID18675461.
^Sandyk, R; Hurwitz, MD (1983). "Toxic irreversible encephalopathy induced by lithium carbonate and haloperidol. A report of 2 cases". South African medical journal64 (22): 875–6. PMID6415823.
^Bush, S. E.; Hatton, R. C.; Winterstein, A. G.; Thomson, M. R.; Woo, G. W. (2008). "Effects of concomitant amiodarone and haloperidol on Q-Tc interval prolongation". American Journal of Health-System Pharmacy65 (23): 2232–6. doi:10.2146/ajhp080039. PMID19020191.
^Igarashi, K.; Kasuya, F.; Fukui, M.; Usuki, E.; Castagnoli Jr, N. (1995). "Studies on the metabolism of haloperidol (HP): The role of CYP3A in the production of the neurotoxic pyridinium metabolite HPP+ found in rat brain following ip administration of HP". Life Sciences57 (26): 2439–46. doi:10.1016/0024-3205(95)02240-5. PMID8847965.
^Usuki, Etsuko; Pearce, Robin; Parkinson, Andrew; Castagnoli, Neal (1996). "Studies on the Conversion of Haloperidol and Its Tetrahydropyridine Dehydration Product to Potentially Neurotoxic Pyridinium Metabolites by Human Liver Microsomes". Chemical Research in Toxicology9 (4): 800–6. doi:10.1021/tx960001y. PMID8831826.
^Avent, Kathryn M.; Devoss, J. J.; Gillam, Elizabeth M. J. (2006). "Cytochrome P450-Mediated Metabolism of Haloperidol and Reduced Haloperidol to Pyridinium Metabolites". Chemical Research in Toxicology19 (7): 914–20. doi:10.1021/tx0600090. PMID16841959.
^Avent, Kathryn M.; Riker, Richard R.; Fraser, Gilles L.; Van Der Schyf, Cornelis J.; Usuki, Etsuko; Pond, Susan M. (1997). "Metabolism of haloperidol to pyridinium species in patients receiving high doses intravenously: Is HPTP an intermediate?". Life Sciences61 (24): 2383–90. doi:10.1016/S0024-3205(97)00955-7. PMID9399630.
^Kawashima, Hidekazu; Iida, Yasuhiko; Kitamura, Youji; Saji, Hideo (2004). "Binding of 4-(4-chlorophenyl)-1-[4-(4-fluorophenyl)-4-oxobutyl]pyridinium ion (HPP+), a metabolite of haloperidol, to synthetic melanin: Implications for the dopaminergic neurotoxicity of HPP+". Neurotoxicity Research6 (7–8): 535–42. doi:10.1007/BF03033449. PMID15639785.
^Bishnoi, Mahendra; Chopra, Kanwaljit; Kulkarni, Shrinivas K. (2008). "Activation of striatal inflammatory mediators and caspase-3 is central to haloperidol-induced orofacial dyskinesia". European Journal of Pharmacology590 (1–3): 241–5. doi:10.1016/j.ejphar.2008.06.033. PMID18590723.
^Eyles, Darryl W.; Avent, Kathryn M.; Stedman, Terry J.; Pond, Susan M. (1997). "Two pyridinium metabolites of haloperidol are present in the brain of patients at post-mortem". Life Sciences60 (8): 529–34. doi:10.1016/S0024-3205(96)00656-X. PMID9042387.
^Ulrich, Sven; Neuhof, Sabine; Braun, Verena; Danos, Peter; Pester, Uwe; Hoy, Ludwig (2000). "Disposition of Haloperidol Pyridinium and Reduced Haloperidol Pyridinium in Schizophrenic Patients: No Relationship with Clinical Variables During Short-Term Treatment". Journal of Clinical Psychopharmacology20 (2): 210–9. doi:10.1097/00004714-200004000-00014. PMID10770460.
^Ulrich, S.; Sandmann, U.; Genz, A. (2005). "Serum Concentrations of Haloperidol Pyridinium Metabolites and the Relationship with Tardive Dyskinesia and Parkinsonism: A Cross-Section Study in Psychiatric Patients". Pharmacopsychiatry38 (4): 171–7. doi:10.1055/s-2005-871240. PMID16025420.
^Seeman, P; Tallerico, T (1998). "Antipsychotic drugs which elicit little or no Parkinsonism bind more loosely than dopamine to brain D2 receptors, yet occupy high levels of these receptors". Molecular Psychiatry3 (2): 123–34. doi:10.1038/sj.mp.4000336. PMID9577836.
^Leysen, JE; Janssen, PM; Megens, AA; Schotte, A (1994). "Risperidone: A novel antipsychotic with balanced serotonin-dopamine antagonism, receptor occupancy profile, and pharmacologic activity". The Journal of Clinical Psychiatry55 (Suppl): 5–12. PMID7520908.
^Cobos, Enrique J.; Del Pozo, Esperanza; Baeyens, José M. (2007). "Irreversible blockade of sigma-1 receptors by haloperidol and its metabolites in guinea pig brain and SH-SY5Y human neuroblastoma cells". Journal of Neurochemistry102 (3): 812–25. doi:10.1111/j.1471-4159.2007.04533.x. PMID17419803.
^Colabufo, Nicolaantonio; Berardi, Francesco; Contino, Marialessandra; Niso, Mauro; Abate, Carmen; Perrone, Roberto; Tortorella, Vincenzo (2004). "Antiproliferative and cytotoxic effects of some σ2 agonists and σ1 antagonists in tumour cell lines". Naunyn-Schmiedeberg's Archives of Pharmacology370 (2): 106–13. doi:10.1007/s00210-004-0961-2. PMID15322732.
^ abcdefghijkKroeze, Wesley K; Hufeisen, Sandra J; Popadak, Beth A; Renock, Sean M; Steinberg, Seanna; Ernsberger, Paul; Jayathilake, Karu; Meltzer, Herbert Y; Roth, Bryan L (2003). "H1-Histamine Receptor Affinity Predicts Short-Term Weight Gain for Typical and Atypical Antipsychotic Drugs". Neuropsychopharmacology28 (3): 519–26. doi:10.1038/sj.npp.1300027. PMID12629531.
^Kornhuber, Johannes; Wiltfang, Jens; Riederer, Peter; Bleich, Stefan (2006). "Neuroleptic drugs in the human brain: Clinical impact of persistence and region-specific distribution". European Archives of Psychiatry and Clinical Neuroscience256 (5): 274–80. doi:10.1007/s00406-006-0661-7. PMID16788768.