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Clinical data
Pronunciation /hæloʊpɛridɒl/
Trade names Haldol
AHFS/ Monograph
MedlinePlus a682180
 AU: C
 US: C (Risk not ruled out)

Routes of by mouth, IM, IV, depot (as

administration decanoate ester)
 N05AD01 (WHO)
ATC code

Legal status
 AU: S4 (Prescription only)
 CA: ℞-only
 UK: POM (Prescription
Legal status
 US: ℞-only

Pharmacokinetic data
Bioavailability 60–70% (Oral)[1]
Protein binding ~90%[1]
Metabolism Liver-mediated[1]
Biological half- 14–26 hours (IV), 20.7 hours
life (IM), 14–37 hours (oral)[1]
Biliary (hence in feces) and in
IUPAC name[show]
 52-86-8
CAS Number

 3559
PubChem CID

 86

 DB00502

 3438

 J6292F8L3D

 D00136

 CHEBI:5613


ECHA InfoCard 100.000.142

Chemical and physical data
Formula C21H23ClFNO2
Molar mass 375.9 g/mol
3D model  Interactive image

Haloperidol, marketed under the trade name Haldol among others, is a typical antipsychotic
medication.[3] Haloperidol is used in the treatment of schizophrenia, tics in Tourette
syndrome, mania in bipolar disorder, nausea and vomiting, delirium, agitation, acute
psychosis, and hallucinations in alcohol withdrawal.[3][4][5] It may be used by mouth, as an
injection into a muscle, or intravenously.[3] Haloperidol typically works within thirty to sixty
minutes.[3] A long-acting formulation may be used as an injection every four weeks in people
with schizophrenia or related illnesses, who either forget or refuse to take the medication by
Haloperidol may result in a movement disorder known as tardive dyskinesia which may be
permanent.[3] Neuroleptic malignant syndrome and QT interval prolongation may occur.[3] In
older people with psychosis due to dementia it results in an increased risk of death.[3] When
taken during pregnancy it may result in problems in the infant.[3][6] It should not be used in
people with Parkinson's disease.[3]

Haloperidol was discovered in 1958 by Paul Janssen.[7] It was made from pethidine
(meperidine).[8] It is on the World Health Organization's List of Essential Medicines, the most
effective and safe medicines needed in a health system.[9] It is the most commonly used
typical antipsychotic.[10] The yearly cost of the typical dose of haloperidol is about £20-800 in
the United Kingdom.[10][11] The annual cost in the United States is around $250.[12]

 1 Medical uses
o 1.1 Pregnancy and lactation
o 1.2 Other considerations
 2 Adverse effects
o 2.1 Contraindications
o 2.2 Special cautions
o 2.3 Interactions
 3 Overdose
o 3.1 Symptoms
o 3.2 Treatment
o 3.3 Prognosis
 4 Pharmacology
 5 Pharmacokinetics
o 5.1 By mouth
o 5.2 Intramuscular injections
o 5.3 Intravenous injections
o 5.4 Therapeutic concentrations
o 5.5 Distribution and metabolism
 6 History
o 6.1 Brand names
 7 Veterinary use
 8 References
 9 External links

Medical uses
Haloperidol is used in the control of the symptoms of:

 Acute psychosis, such as drug-induced psychosis caused by LSD, psilocybin,

amphetamines, ketamine,[13] and phencyclidine,[14] and psychosis associated with high
fever or metabolic disease
 Adjunctive treatment of alcohol and opioid withdrawal
 Agitation and confusion associated with cerebral sclerosis
 Alcohol-induced psychosis
 Hallucinations in alcohol withdrawal[4]
 Hyperactive delirium (to control the agitation component of delirium)
 Hyperactivity, aggression
 Otherwise uncontrollable, severe behavioral disorders in children and adolescents
 Schizophrenia[15]
 Therapeutic trial in personality disorders, such as borderline personality disorder
 Treatment of intractable hiccups[16][17]
 Treatment of neurological disorders, such as tic disorders such as Tourette syndrome,
and chorea
 Treatment of severe nausea and emesis in postoperative and palliative care, especially
for palliating adverse effects of radiation therapy and chemotherapy in oncology

Haloperidol was considered indispensable for treating psychiatric emergency situations,[18][19]

although the newer atypical drugs have gained greater role in a number of situations as
outlined in a series of consensus reviews published between 2001 and 2005.[20][21][22]

In a 2013 comparison of 15 antipsychotics in schizophrenia, haloperidol demonstrated

standard effectiveness. It was 13-16% more effective than ziprasidone, chlorpromazine, and
asenapine, approximately as effective as quetiapine and aripiprazole, and 10% less effective
than paliperidone.[23] A 2013 systematic review compared haloperidol to placebo in

Haloperidol often causes troublesome adverse effects. If there is no other antipsychotic drug,
using haloperidol to offset the consequences of untreated schizophrenia is justified. Where a
choice of drug is available, however, an alternative antipsychotic with less likelihood of
adverse effects such as parkinsonism, akathisia and acute dystonias may be more desirable.[24]
[show]Outcome Findings in words Findings in numbers Quality of evidence

Pregnancy and lactation

Data from animal experiments indicate haloperidol is not teratogenic, but is embryotoxic in
high doses. In humans, no controlled studies exist. Reports in pregnant women revealed
possible damage to the fetus, although most of the women were exposed to multiple drugs
during pregnancy. In addition, reports indicate 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.[15]

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.[citation needed]

Other considerations
Skeletal formula of haloperidol decanoate. The decanoate group is highlighted in red.

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.[25] 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.[26]

Other forms of therapy (psychotherapy, occupational therapy/ergotherapy, or social

rehabilitation) should be instituted properly.[citation needed] 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.[27] Patients responded with doses under
even 2 mg in first-episode psychosis.[28] 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.[26]

 Depot forms are also available; these are injected deeply intramuscularly at regular
intervals. The depot forms are not suitable for initial treatment, but are suitable for
patients who have demonstrated inconsistency with oral dosages.[citation needed]

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.[29] The IUPAC name of haloperidol decanoate is [4-(4-
chlorophenyl)-1-[4-(4-fluorophenyl)-4-oxobutyl]piperidin-4-yl] decanoate.

Topical formulations of haloperidol should not be used as treatment for nausea because
research does not indicate this therapy is more effective than alternatives.[30]

Adverse effects
Sources for the following lists of adverse effects[31][32][33][34]

As haloperidol is a high-potency typical antipsychotic, it tends to produce significant

extrapyramidal side effects. According to a 2013 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.[23]

With more than 6 months of use 14% percent of users gain weight.[35]

Common (>1% incidence)

 Extrapyramidal side effects including:

o Akathisia (motor restlessness)
o Dystonia (continuous spasms and muscle contractions)
o Muscle rigidity
o Parkinsonism (characteristic symptoms such as rigidity)
 Hypotension
 Anticholinergic side effects such as: (These adverse effects are more common than
with lower-potency typical antipsychotics, such as chlorpromazine and thioridazine.)
o Blurred vision
o Constipation
o Dry mouth
 Somnolence (which is not a particularly prominent side effect, as is supported by the
results of the aforementioned meta-analysis.[23])

Unknown frequency

 Anemia
 Headache
 Increased respiratory rate
 Orthostatic hypotension
 Prolonged QT interval
 Visual disturbances

Rare (<1% incidence)

 Acute hepatic failure

 Agitation
 Agranulocytosis
 Anaphylactic reaction
 Anorexia
 Bronchospasm
 Cataracts
 Cholestasis
 Confusional state
 Depression
 Dermatitis exfoliative
 Dyspnea
 Edema
 Extrasystoles
 Face edema
 Gynecomastia
 Hepatitis
 Hyperglycemia
 Hypersensitivity
 Hyperthermia
 Hypoglycemia
 Hyponatremia
 Hypothermia
 Increased sweating
 Injection site abscess
 Insomnia
 Itchiness
 Jaundice
 Laryngeal edema
 Laryngospasm
 Leukocytoclastic vasculitis
 Leukopenia
 Liver function test abnormal
 Nausea
 Neuroleptic malignant syndrome
 Neutropenia
 Pancytopenia
 Photosensitivity reaction
 Priapism
 Psychotic disorder
 Pulmonary embolism
 Rash
 Retinopathy
 Seizure
 Sudden death
 Tardive dyskinesia
 Thrombocytopenia
 Torsades de pointes
 Urinary retention
 Urticaria
 Ventricular fibrillation
 Ventricular tachycardia
 Vomiting


 Pre-existing coma, acute stroke

 Severe intoxication with alcohol or other central depressant drugs
 Known allergy against haloperidol or other butyrophenones or other drug ingredients
 Known heart disease, when combined will tend towards cardiac arrest[citation needed]

Special cautions

 A multiple-year study suggested this drug and other neuroleptic antipsychotic drugs
commonly given to people with Alzheimer's with mild behavioural problems often
make their condition worse and its withdrawal was even beneficial for some cognitive
and functional measures.[36]
 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.[15]
 Impaired liver function, as haloperidol is metabolized and eliminated mainly by the
 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 at special risk for the development of QT prolongation (hypokalemia,
concomitant use of other drugs causing QT prolongation)
 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
 Pre-existing Parkinson's disease[37] or dementia with Lewy bodies


 Amiodarone: Q-Tc interval prolongation (potentially dangerous change in heart

 Amphetamine and methylphenidate: counteracts increased action of norepinephrine
and dopamine in patients with narcolepsy or ADD/ADHD
 Epinephrine: action antagonized, paradoxical decrease in blood pressure may result
 Guanethidine: antihypertensive action antagonized
 Levodopa: decreased action of levodopa
 Lithium: rare cases of the following symptoms have been noted: encephalopathy,
early and late extrapyramidal side effects, other neurologic symptoms, and coma.[39]
 Methyldopa: increased risk of extrapyramidal side effects and other unwanted central
 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%.
 Other drugs metabolized by the CYP3A4 enzyme system: inducers such as
carbamazepine, phenobarbital, and rifampicin decrease plasma levels and inhibitors
such as quinidine, buspirone, and fluoxetine increase plasma levels[15]
 Tricyclic antidepressants: metabolism and elimination of tricyclics significantly
decreased, increased toxicity noted (anticholinergic and cardiovascular side effects,
lowering of seizure threshold)


Symptoms are usually due to side effects. Most often encountered are:

 Anticholinergic side effects (dry mouth, constipation, paralytic ileus, difficulties in

urinating, decreased perspiration)
 Coma in severe cases, accompanied by respiratory depression and massive
hypotension, shock
 Hypotension or hypertension
 Rarely, serious ventricular arrhythmia (torsades de pointes), with or without
prolonged QT-time
 Sedation
 Severe extrapyramidal side effects with muscle rigidity and tremors, akathisia, etc.


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 bromocriptine or ropinirole may be used to treat the extrapyramidal effects
caused by haloperidol, acting as dopamine receptor agonists.[citation needed] ECG and vital signs
should be monitored especially for QT prolongation and severe arrhythmias should be treated
with antiarrhythmic measures.[15]


In general, the prognosis of overdose is good, and lasting damage is not known, provided the
person has survived the initial phase. An overdose of haloperidol can be fatal.[40]


Haloperidol, 10-mg oral tablet

Haloperidol is a typical butyrophenone type antipsychotic that exhibits high affinity

dopamine D2 receptor antagonism and slow receptor dissociation kinetics.[41] It has effects
similar to the phenothiazines.[17] The drug binds preferentially to D2 and α1 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 antagonism of 5-HT2 receptors on the negative symptoms,
this characteristic underlies haloperidol's greater effect on delusions, hallucinations and other
manifestations of psychosis.[42] 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.

Haloperidol acts on these receptors: (Ki)

 D1 (silent antagonist) — Unknown efficiency[citation needed]
 D5 (silent antagonist) — Unknown efficiency[citation needed]
 D2 (inverse agonist) — 1.55 nM[43]
 D3 (inverse agonist) — 0.74 nM[44]
 D4 (inverse agonist) — 5–9 nM[45]
 σ1 (irreversible inactivation by haloperidol metabolite HPP+) – 3 nM[46]
 σ2 (agonist): 54 nM[47]
 5HT1A receptor agonist – 1927 nM[48]
 5HT2A (silent antagonist) – 53 nM[48]
 5HT2C (silent antagonist) – 10,000 nM[48]
 5HT6 (silent antagonist) – 3666 nM[48]
 5HT7 (irreversible silent antagonist) — 377.2 nM[48]
 H1 (silent antagonist) — 1,800 nM[48]
 M1 (silent antagonist) — 10,000 nM[48]
 α1A (silent antagonist) — 12 nM[48]
 α2A (silent antagonist) — 1130 nM[48]
 α2B (silent antagonist) — 480 nM[48]
 α2C (silent antagonist) — 550 nM[48]
 NR1/NR2B subunit containing NMDA receptor (antagonist; ifenprodil site): IC50 —
2,000 nM[49]

By mouth

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.[1]

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. The mean T1/2 is 20.7 hours.[1] 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.[50]

Intravenous injections

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 and 21.7 L/kg.[1] 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.[citation needed]
Haloperidol for injection

Therapeutic concentrations

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.[citation needed]

The concentration of haloperidol in brain tissue is about 20-fold higher compared to blood
levels. It is slowly eliminated from brain tissue,[51] which may explain the slow disappearance
of side effects when the medication is stopped.[51][52]

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

Haloperidol was discovered by Paul Janssen.[53] It was developed in 1958 at the Belgian
company Janssen Pharmaceutica and submitted to the first of clinical trials in Belgium later
that year.[54][55]

Haloperidol was approved by the U.S. Food and Drug Administration (FDA) on 12 April
1967; it was later marketed in the U.S. and other countries under the brand name Haldol by
McNeil Laboratories.[54]

Brand names

Haloperidol is the INN, BAN, USAN, AAN approved name.

It 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.[citation needed]

Veterinary use
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.[56]


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