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Thorazine (Chlorpromazine)

Last updated on October 24th, 2023

What Is Thorazine (Chlorpromazine)?


Thorazine (Chlorpromazine) has many different applications. It is used to heal certain mental and behavioral disorders. This pill is also taken to control nausea and vomiting, nervousness before surgery, and hiccups that will not go away. It is also used to heal episodes of porphyria and in combination with other specific to remedy tetanus. This remedy may be used for other purposes; ask your doctor if you have questions.

Mechanism of Action

The therapeutic effects of antipsychotics appear to be mediated, at least in part, by interference with dopamine transmission in the brain. Chlorpromazine, thioridazine, and thioxanthene derivatives have relatively equal affinity for D1 or D2 receptors, although their metabolites tend to be more potent as D2 blockers. Butyrophenones (such as haloperidol) and diphenyl-butylpiperidines (such as pimozide) are relatively selective for D2 receptors, and the substituted benzamides (such as sulphide) are highly D2-specific. Clozapine has complex actions: it is a relatively weak inhibitor of D2 receptors but has a high affinity for some other receptors, including D1, D4, and serotonin2 (5-HT2) receptors. Other atypicals mostly share this profile of greater 5-HT2 than D2 antagonism.

The traditional hypothesis of the action of antipsychotics has been that the blockade of D2 receptors in the limbic and cortical regions is responsible for the antipsychotic effects and that adverse extrapyramidal motor effects result from the blockade of D2 receptors in the striatum (a typical motor region of the basal ganglia). Modification of prolactin secretion results from blockade of D2 receptors in the anterior pituitary. However, this hypothesis cannot satisfactorily account for the pharmacological profiles of atypical antipsychotics, and the debate concerning their mechanism of action continues.

It has been suggested that the balance between 5-HT2 and D2 antagonism is essential in determining ‘atypicality’ (but the atypical antipsychotic amisulpride lacks marked 5-HT2 antagonism) or that rapid dissociation from the D2 receptor may be the determining factor (but it is not clear that some atypicals such as risperidone meet this criterion). Other systems, such as glutamate, may play a role in modulating effectiveness against negative versus positive symptoms. It has been suggested that the calcium antagonist actions of the diphenyl-butylpiperidines may also be necessary in this respect. 

What Should I Tell My Health Care Provider Before I Take This Medicine?

They need to know if you have any of these disorders:

  • blood disorders or sickness;
  • dementia;
  • frequent alcohol use;
  • liver disorder;
  • Parkinson’s disease;
  • Reye’s syndrome;
  • uncontrollable movement disorder;
  • an unusual or allergic reaction to chlorpromazine, sulfa drugs, other drugs, foods, dyes, or preservatives;
  • pregnant or trying to get pregnant;
  • breastfeeding.

Uses and Administration

Chlorpromazine is a phenothiazine antipsychotic. It has a wide range of activity arising from its depressant actions on the CNS and its alpha-adrenergic blocking and antimuscarinic activities. Chlorpromazine is a dopamine inhibitor. The turnover of dopamine in the brain is also increased. There is some evidence that the antagonism of central dopaminergic function, especially at the D2-dopaminergic receptor, is related to therapeutic effects in mental disorders.

Chlorpromazine possesses sedative properties, but patients usually develop tolerance rapidly to sedation. It has antiemetic, serotonin-blocking, weak antihistaminic properties and slight ganglion-blocking activity. It inhibits the heat-regulating center so that the patient tends to acquire the temperature of the surroundings (poikilothermy). Chlorpromazine can relax skeletal muscle. Chlorpromazine is widely used in the management of mental disorders as well as in some non-psychotic disorders, such as:

  • acute and chronic schizophrenia in adults and children;
  • to reduce acute mania, as in bipolar disorder;
  • control of severely disturbed, agitated, or violent behavior in adults and children and sometimes other psychiatric conditions;
  • in autistic children;
  • as an adjunct for the short-term treatment of severe anxiety and to reduce pre-operative anxiety in adults and children;
  • as an antiemetic in some forms of nausea and vomiting in adults and children, it is ineffective in motion sickness;
  • in the alleviation of intractable hiccups;
  • as an adjunct in the treatment of tetanus in adults and children and to control symptoms in acute intermittent porphyria;
  • for induction of hypothermia, chlorpromazine is given orally as the hydrochloride and the embonate. For both salts, the doses are expressed as the hydrochloride chlorpromazine embonate 144 mg, which is equivalent to about 100 mg of chlorpromazine hydrochloride. Chlorpromazine is also given by injections and rectal suppositories.

Dosage varies with the individual and the purpose for which the drug is being used. In most patients with psychiatric conditions, oral treatment may be used from the start, typically commencing with a dosage of 25 mg of the hydrochloride, or its equivalent as the embonate, three times daily and increasing as necessary daily doses of 75 mg may be given as a single dose at night. In some patients, doses of 10 mg three times daily may be adequate. Maintenance doses, when required, usually range from 25 to 100 mg three times daily, although psychotic patients may require daily doses of up to 1 g or more.

For parenteral use, deep intramuscular injection is preferable. Still, diluted solutions have sometimes been given by slow intravenous infusion for indications such as tetanus, severe intractable hiccup, or nausea and vomiting associated with surgery. Subcutaneous injection is contra-indicated. After injection of chlorpromazine, patients should remain in the supine position for at least 30 minutes, and blood pressure should be monitored. The usual dose by intramuscular injection is 25 to 50 mg, repeated every 6 to 8 hours if required, although oral therapy should be substituted as soon as possible.

If the oral and parenteral routes are not suitable, chlorpromazine may be given rectally as suppositories containing 100 mg of chlorpromazine base. This is stated to have an effect comparable with 40 to 50 mg of the hydrochloride orally or 20 to 25 mg intramuscularly. The usual rectal dose is 100 mg every 6 to 8 hours. Initial oral doses of chlorpromazine of one-third to one-half the usual adult dose have been recommended for elderly or debilitated patients; doses should be increased gradually. Intramuscular doses in senior patients may need to be reduced to up to one-quarter of the usual dose.

Chlorpromazine hydrochloride may be given to children aged 1 to 12 years in a dose of 500 micrograms/kg every 4 to 6 hours orally or every 6 to 8 hours by intramuscular injection. However, for psychiatric indications, the oral dose for children over five years is usually one-third to one-half the adult dose; alternatively, the BNFC suggests a dose of 10 mg 3 times daily. Daily doses should not typically exceed 40 mg of chlorpromazine hydrochloride for children aged 1 to 5 years or 75 mg for children over five.

Chlorpromazine may be given to infants under one year old if considered life-saving. Suppositories containing 25 mg of chlorpromazine base are available in some countries for use in children. Doses of 10 to 25 mg orally every 4 to 6 hours are recommended to control nausea and vomiting. If necessary, an initial dose of 25 mg may be given by intramuscular injection, followed by 25 to 50 mg every 3 to 4 hours until vomiting stops. If an intractable hiccup does not respond to an oral dose of 25 to 50 mg three or four times daily for 2 to 3 days, then 25 to 50 mg may be given intramuscularly. If this fails, 25 to 50 mg in 500 to 1000 niL of 0.9% sodium chloride should be given by slow intravenous infusion, with the patient supine and careful blood pressure monitoring.


The classical antipsychotics are often divided into:

  • low-potency drugs (phenothiazines with an aliphatic or piperidine side-chain or thioxanthenes with an aliphatic side-chain);
  • high-potency drugs (butyrophenones, diphenylbutylpiperidines, phenothiazines, or thioxanthenes with a piperazine side-chain).

At doses with equipotent antipsychotic activity, the low-potency drugs are more prone to cause sedation and antimuscarinic or α-adrenergic-blocking effects than the high-potency drugs. However, they are associated with a lower incidence of extrapyramidal effects, except for tardive dyskinesia, likely to occur to the same extent as all classical antipsychotics.

Equivalent doses of antipsychotics quoted in the literature have varied considerably. In the UK, the following daily doses of oral antipsychotics have been suggested to have approximately equipotent antipsychotic activity for doses up to the maximum licensed doses:

  • chlorpromazine hydrochloride 100 mg;
  • clozapine 50 mg;
  • haloperidol 2 to 3 mg;
  • pimozide 2 mg;
  • risperidone 0.5 to 1 mg;
  • sulpiride 200 mg;
  • thioridazine 100 mg;
  • trifluoperazine 5 mg.

It should be noted that all patients receiving pimozide require an annual ECG, and all those receiving more than 16 mg of pimozide daily require periodic ECGs. Thioridazine also requires specialist supervision.

Suggested equipotent doses of intramuscular depot antipsychotics are:

  • flupentixol decanoate 40 mg every 2 weeks;
  • fluphenazine decanoate 25 mg every 2 weeks;
  • haloperidol (as the decanoate) 100 mg every 4 weeks;
  • pipotiazine palmitate 50 mg every 4 weeks;
  • zuclopenthixol decanoate 200 mg every 2 weeks.

It has been noted that high doses of antipsychotics (more than the equivalent of 600 mg of chlorpromazine daily) are generally not necessary for the treatment (both initial and maintenance) of psychotic disorders and may be associated with an increased risk of adverse effects as well as with a diminished clinical response. However, if high doses of antipsychotics have to be used, then doses should be increased gradually with caution and under the supervision of a specialist with facilities for emergency resuscitation available. The Royal College of Psychiatrists in the UK (which defines high-dose therapy as involving a total daily dose more than the upper limit recommended in the BNF) has issued recommendations concerning the use of high-dose antipsychotic medication. It considers:

  • current evidence does not justify the routine use of high-dose therapy with antipsychotics;
  • if high-dose therapy is used, this should only be after evidence-based strategies have failed and as a carefully monitored therapeutic trial;
  • the decision to use high-dose therapy and the expected outcome should be fully documented after an expert assessment of the patient;
  • the possible contra-indications to therapy and the risk of drug interactions should be assessed beforehand;
  • an ECG should be carried out before starting high-dose therapy and should be repeated after a few days and then every 1 to 3 months in the early stages of treatment or as clinically indicated;
  • doses should be increased in relatively small increments, with time to assess response before a further increase
  • the use of as-required antipsychotic medication and drug combinations should be carefully monitored to avoid the accidental increase of total doses above high-dose thresholds.

A therapeutic range (or therapeutic window) has not been demonstrated for most antipsychotics (with the possible exception of haloperidol), and plasma concentrations of these drugs must be interpreted cautiously. Many factors make it difficult to establish a meaningful correlation between dose, plasma concentrations, and clinical improvement. These include incomplete absorption, first-pass effect, enzyme induction, active and inactive metabolites, ethnicity, smoking, and factors occurring at the receptor level.

Administration in Children

For reference to the use of lytic cocktails containing chlorpromazine, promethazine, and pethidine and the view that alternatives should be considered in children, see below.

Bipolar Disorder

Patients with bipolar disorder suffering from acute mania with coexisting psychotic features, agitation, or disruptive behavior are usually treated with antipsychotics as they produce rapid control of symptoms. Classical antipsychotics such as chlorpromazine or haloperidol have been widely used, although the use of atypical antipsychotics, such as clozapine or olanzapine, is growing.


It has been shown that in healthy subjects, an oral dose of 25 mg of chlorpromazine hydrochloride can reduce exercise-induced breathlessness without affecting ventilation or causing sedation. Although other drugs may be preferred in patients with advanced cancer and dyspnoea, chlorpromazine may relieve air hunger unresponsive to usual measures and, if required, can sedate dying patients with unrelieved distress. It is recommended that initial doses should be small: 12.5 mg by slow intravenous injection or 25 mg by suppository may be given.





Antipsychotics such as phenothiazines, haloperidol, or pimozide are sometimes helpful in treating idiopathic dystonia in patients who have failed to respond to other drugs. However, they often act non-specifically, damping down excessive movements by causing a degree of drug-induced parkinsonism, and there is the risk of developing drug-induced extrapyramidal disorders.

Eclampsia and Pre-eclampsia

Drug combinations known as lytic cocktails have been used in many countries to manage pre-eclampsia and imminent eclampsia. The cocktail has usually consisted of a combination of chlorpromazine, pethidine, and/or promethazine. In general, however, phenothiazines are not recommended in late pregnancy, and other treatments are preferred for hypertension.


Some phenothiazines such as chlorpromazine, levomepromazine, and prochlorperazine have been used in migraine to control severe nausea and vomiting unresponsive to antiemetics such as metoclopramide and domperidone and to relieve the pain of severe migraine attacks unresponsive to parenteral dihydroergotamine or sumatriptan.


A hiccup is an involuntary spasmodic contraction of the diaphragm that causes a sudden inspiration of air, which is then checked abruptly by the closure of the glottis. Hiccups often have a simple cause, such as gastric distension, and usually resolve spontaneously or respond to simple measures. Intractable hiccups may stem from a serious underlying cause, such as brain disorders, metabolic or endocrine disturbances, CNS infections, and oesophageal or other gastrointestinal disorders. Other precipitants include anesthesia or drug therapy. Treatment of intractable hiccups should initially aim to control or remove the underlying cause, including the relief of gastric distension or oesophageal obstruction.

Measures that raise carbon dioxide pressure, such as breath holding, rebreathing, or alteration of normal respiratory rhythm, can be effective. Stimulation of the pharynx can also interrupt hiccups and may explain the action of a host of remedies such as sipping iced water, gargling, and swallowing granulated sugar. Many drugs have been tried to treat hiccups, but evidence of efficacy is mainly from anecdotal reports or uncontrolled studies. An early treatment protocol for intractable hiccups (based on a review of the literature and the author’s experience) suggested stepwise management until an effective measure was found, as follows:

  • correction of any metabolic abnormality;
  • swallowing dry granulated sugar;
  • decompressing the stomach via nasogastric tube, then irritation of the pharynx;
  • intravenous chlorpromazine 25 to 50 mg, repeated up to 3 times if necessary if parenteral therapy is effective; administer chlorpromazine orally for 10 days (licensed information recommends the use of oral therapy first);
  • metoclopramide 10 mg intravenously; if successful, administer metoclopramide orally for ten days;
  • quinidine 200 mg orally 4 times daily;
  • if this fails, consider the left phrenic nerve block and crush.

In later discussions, chlorpromazine still emerged as the most consistently effective drug treatment. Metoclopramide appeared to be an acceptable second choice and nifedipine an appropriate third choice, although haloperidol was also considered valuable. Other phenothiazines that have been used for intractable hiccups include perphenazine and promazine. It was also considered that clonazepam, carbamazepine, phenytoin, and valproic acid might be of value, especially in neuropathic hiccups.

Some beneficial results have been reported with amitriptyline and amantadine. Other drugs being tried in the treatment of hiccups include baclofen and gabapentin. The BNF recommends that in palliative care patients, a preparation combining an antacid with an antiflatulent be given for hiccups due to gastric distension. If this fails, metoclopramide (orally or by subcutaneous or intramuscular injection) should be added; baclofen, nifedipine, or chlorpromazine should be reserved for those patients in whom metoclopramide is also ineffective.

Lesch-Nyhan Syndrome

The Lesch-Nyhan syndrome is an inherited disorder caused by a complete deficiency of hypoxanthine-guanine phosphoribosyl transferase, an enzyme involved in purine metabolism. It is characterized by hyperuricemia, spasticity, choreoathetosis, self-mutilation, and mental retardation. Hyperuricemia can be controlled by drugs such as allopurinol, but there appears to be no effective treatment for the neurological deficits. It has been suggested that behavioral problems might be associated with alterations in the brain’s dopamine system. There have been rare reports of improvement in self-mutilation in patients given antipsychotics or antiepileptics such as carbamazepine and gabapentin.


See under the Headache section above.

Nausea and Vomiting

Many antipsychotics, with the notable exception of thioridazine, have antiemetic properties and have been used in the prevention and treatment of nausea and vomiting arising from a variety of causes such as radiation sickness, malignancy, and emesis caused by drugs, including antineoplastics and opioid analgesics. Reference to the risk to the fetus of therapy with phenothiazines during pregnancy can be found under Precautions.


Classical antipsychotics such as chlorpromazine, haloperidol, and thioridazine have been the traditional drug treatment of choice for patients with schizophrenia. However, atypical antipsychotics may now be preferred as first-line therapy. There is little difference in efficacy between the classical antipsychotics, but thioridazine is now restricted in treating schizophrenia because of the risk of cardiotoxicity.



Ask your doctor for advice about the use of antipsychotics for alcohol withdrawal.


In a discussion of neonatal abstinence syndrome, it was observed in 1986 that, although opioids, diazepam, and phenobarbital were widely used in the USA for the management of this condition, chlorpromazine had tended to be the preferred treatment in the UK. This was still true as late as the mid-1990s, although practice varied widely. However, a systematic review found insufficient evidence to support the use of chlorpromazine in the management of neonatal abstinence syndrome.

The following dosage schedule has been suggested: chlorpromazine is begun with a loading dose of 3 mg/kg, followed by a total oral maintenance dose of 3 mg/kg daily, divided into 4 or 6 doses. The authors suggested that this dose might be increased by 3 mg/kg daily if withdrawal symptoms were particularly severe. Once stabilized, a reduction in the dose of chlorpromazine by 2 mg/kg every third day is attempted. Complications of phenothiazine usage have been notably absent, although rarely seizures may occur.

Taste Disorders

Disturbances of the sense of taste may be broadly divided into either loss or distortion of taste. Loss of taste may be either complete (ageusia) or partial (hypogeusia). Distortion of taste (dysgeusia) may occur as aliageusia, in which stimuli such as food or drink produce an inappropriate taste, or as phantogeusia, in which an unpleasant taste is not associated with external stimuli and is sometimes referred to as a gustatory hallucination. Taste disturbances have many causes, including infections, metabolic or nutritional disturbances, radiation, CNS disorders, neoplasms, and drug therapy, or may occur due to normal aging.

Management primarily consists of the treatment of any underlying disorder. Withdrawal of offending drug therapy is commonly associated with resolution, but occasionally, effects persist and may require treatment. Zinc or vitamin therapy has been used, but there is insufficient evidence to indicate efficacy’ for taste disturbances secondary to drug therapy or medical conditions that do not involve low zinc or vitamin concentrations. Phantogeusia might be linked to excessive activity of dopaminergic receptors as it has been reported to respond to short-term treatment with small doses of antipsychotic drugs such as haloperidol or pimozide.




Do not take this pharmaceutical with any of the following

  1. Antibiotics:
  • gatifloxacin;
  • grepafloxacin;
  • sparfloxacin;
  • chloroquine;
  • cisapride;
  • clozapine;
  • droperidol;
  • ephedrine;
  • levomethadyl;
  • maprotiline.

2. Drug for mental depression.

3. Barbiturate remedies for inducing sleep or treatment seizures, like phenobarbital diuretics, local and general anesthetics, and phenytoin prescription pain-specific warfarin.

This list may not report all possible interactions. Give your doctor a list of all the specifics, herbs, non-prescription drugs, or dietary supplements you use. Also, report to them if you smoke, drink alcohol, or use illegal drugs. Some items may interact with your pharmaceutical.

Adverse Effects

Chlorpromazine generally produces less central depression than barbiturates or benzodiazepines, and tolerance to its initial sedative effects develops quickly in most patients. It has antimuscarinic properties and may cause adverse effects such as dry mouth, constipation, difficulty with micturition, blurred vision, and mydriasis. Tachycardia, ECG changes (particularly Q- and T-wave abnormalities), and, rarely, cardiac arrhythmias may occur; hypotension (usually orthostatic) is common.

Other adverse effects include delirium, agitation and, rarely, catatonic-like states, insomnia or drowsiness, nightmares, depression, miosis, EEG changes and convulsions, nasal congestion, minor abnormalities in liver function tests, inhibition of ejaculation, impotence, and priapism. Hypersensitivity reactions include urticaria, exfoliative dermatitis, erythema multiforme, and contact sensitivity. A syndrome resembling SLE has been reported. Jaundice has occurred and probably has an immuno-logical origin. Prolonged therapy may lead to pigment deposition in the skin, or the eyes’ corneal and lens opacities have occurred more frequently.

Pigmentary retinopathy has occurred only rarely with chlorpromazine. Photosensitivity reactions are more common with chlorpromazine than with other antipsychotics. Hematological disorders, including hemolytic anemia, aplastic anemia, thrombocytopenic purpura, eosinophilia, and potentially fatal agranulocytosis, have occasionally been reported they may be manifestations of a hypersensitivity reaction. Most cases of agranulocytosis have occurred within 4 to 10 weeks of starting treatment, and symptoms such as sore throat or fever should be watched for and white cell counts instituted should they appear. Mild leucopenia has been stated to occur in up to 30% of patients on prolonged high dosages.

Extrapyramidal dysfunction and resultant disorders include acute dystonia, a parkinsonism-like syndrome, and akathisia. Late effects include tardive dyskinesia and perioral tremor. The neuroleptic malignant syndrome may also occur.

Chlorpromazine alters endocrine and metabolic functions. Patients have experienced amenorrhoea, galactorrhoea, and gynaecomastia due to hyperprolactinemia, weight gain, hyperglycemia, and altered glucose tolerance. Body temperature regulation is impaired and may result in hypo- or hyperthermia, depending on the environment. There have also been reports of hypercholesterolemia.

There have been isolated reports of sudden death with chlorpromazine. Possible causes include cardiac arrhythmias or aspiration and asphyxia due to suppression of the cough and gag reflexes. Pain and irritation at the injection site may occur on injection. Nodule formation may occur after intramuscular injection.

Phenothiazines do not cause dependence of the type encountered with barbiturates or benzodiazepines. However, withdrawal symptoms have been seen as abrupt withdrawal in patients receiving prolonged and/or high-dose maintenance therapy. Although the adverse effects of other phenothiazines are broadly similar to those of chlorpromazine, their frequency, and pattern tend to fall into 3 groups.

  • Group 1 (e.g., chlorpromazine, levomepromazine, and promazine) generally has pronounced sedative effects and moderate antimuscarinic and extrapyramidal effects.
  • Group 2 (e.g., pericyazine, pipotiazine, and thioridazine) generally has moderate sedative, marked antimuscarinic, and fewer extrapyramidal effects than groups 1 or 3.
  • Group 3 (e.g., fluphenazine, perphenazine, prochlorperazine, and trifluoperazine) generally has fewer sedative and antimuscarinic effects but more pronounced extrapyramidal effects than groups 1 or 2.

Classical antipsychotics of other chemical groups tend to resemble the phenothiazines of group 3. They include butyrophenones (e.g., benperidol and haloperidol), diphenylbutylpiperidines (e.g., pimozide), thioxanthenes (flupentixol and zuclopenthixol) substituted benzamides (e.g., sulpiride) oxypertine and loxapine.


See Effects on Endocrine Function below.


Treatment with antipsychotics can result in EEG abnormalities and lowered seizure threshold.l Seizures can be induced particularly in patients with a history of epilepsy or drug-induced seizures, abnormal EEG, previous electroconvulsive therapy, or pre-existing CNS abnormalities. The risk appears to be greatest at the start of antipsychotic therapy, with high doses, abrupt dose increases, or using more than one antipsychotic. The incidence of antipsychotic-induced convulsions is, however, probably less than 1 %.

In general, the epileptic potential has been correlated with the propensity of the antipsychotic to cause sedation. Phenothiazines with marked sedative effects (Group 1), such as chlorpromazine, present a higher risk than those with strong extrapyramidal effects (Group 3). Haloperidol appears to carry a relatively low risk of seizures. The following drugs have been suggested when classical antipsychotic therapy is considered necessary in patients at risk of seizures or being treated for epilepsy: fluphenazine, haloperidol, pimozide, or trifluoperazine. Antipsychotic dosage should be increased slowly, and the possibility of interactions with antiepileptic therapy should be considered (see Interactions section).

The atypical antipsychotic clozapine appears to be associated with an exceptionally high risk of seizures. Risperidone may be preferred if an atypical antipsychotic is used in patients at risk of seizures.

Effects on the Blood

The UK CSM provided data on the reports it had received between July 1963 and January 1993 on agranulocytosis and neutropenia. Several groups of drugs were commonly implicated, among them phenothiazines, for which there were 87 reports of agranulocytosis (42 fatal) and 33 of neutropenia (22 fatal). The most frequently implicated phenothiazines were chlorpromazine, with 51 reports of agranulocytosis (26 fatal) and 12 of neutropenia (2 fatal), and thioridazine, with 20 reports of agranulocytosis (9 fatal) and 10 of neutropenia (none fatal).

Effects on Body Weight

Most antipsychotic drugs are associated with weight gain. A meta-analysis found evidence of weight gain in patients receiving both classical (chlorpromazine, fluphenazine, haloperidol, loxapine, perphenazine, thioridazine, tiotixene, or trifluoperazine) and atypical (clozapine, olanzapine, quetiapine, risperidone, sertindole, and ziprasidone) antipsychotics. Two drugs, molindone and pimozide, appeared in contrast to be associated with weight loss, although this could not be confirmed statistically in the case of pimozide. Placebo treatment was also associated with weight loss. 

Effects on the Cardiovascular System

Orthostatic hypotension is a common problem in patients taking psychotropic drugs and is particularly pronounced with low-potency antipsychotics.

Various EEG changes or frank arrhythmias have occurred in patients receiving antipsychotics. T-wave changes have been reported with low-potency antipsychotics. They are usually benign and reversible and subject to daily fluctuations. Low-potency antipsychotics, particularly thioridazine, mesoridazine, and the high-potency drug pimozide, prolong the QT interval similarly to class I antiarrhythmics such as quinidine or procainamide. Their use is, therefore, contraindicated in patients taking such antiarrhythmics.

Droperidol, another high-potency drug, has also been reported to prolong the QT interval. Thioridazine is most frequently discussed in case reports of psychotropic drug-induced torsade de pointes, which has led to restrictions on its use (see Precautions and Uses and Administration of Thioridazine). Chlorpromazine and pimozide have also been implicated. Tachycardia of the “pirouette” type has also been reported after overdosage with, or high intravenous doses of, the high-potency antipsychotic haloperidol.

There are also isolated reports of cardiac arrhythmias after attempts at rapid control with high doses of haloperidol. Melperone, a butyrophenone antipsychotic related to haloperidol, has been reported to have class III electrophysiologic and antiarrhythmic activity. In the UK, the risk of arrhythmias with antipsychotic treatment has been considered by an expert working group of the CSM. The following recommendations were made regarding ECG monitoring:

  • An ECG should be needed based on a patient’s relevant medical history, family history, and clinical examination. Seniors and those with a personal or family history of heart disease or cardiac abnormalities would benefit the most from a baseline ECG.
  • During treatment, an ECG should be performed in patients who experience palpitations or other symptoms suggestive of cardiac disease. If the QT interval is prolonged, then a dose reduction may be required; if it exceeds 500 milliseconds, treatment may need to be stopped.
  • An ECG should be considered during dose increases.
  • Potassium levels should be monitored before and during treatment, particularly during periods of acute illnesses.

Sudden, unexpected deaths have long been reported in patients receiving antipsychotics. Whether this is due to the disease being treated or to the treatment is still unclear. However, in a retrospective cohort study involving about 482 000 patients, analysis of 1487 sudden cardiac deaths indicated that patients receiving antipsychotics in doses of more than 100 mg of thioridazine or its equivalent had a 2.4-fold increase in the rate of sudden cardiac death, rising to a 3.53-fold increase in those patients with pre-existing severe cardiovascular disease. A later case-control study in 5 UK psychiatric hospitals found that sudden unexplained death in psychiatric patients was associated with hypertension, ischaemic heart disease, and current treatment with thioridazine. Although several mechanisms have been suggested for the effect, prolongation of the QT interval has been implicated in a proportion of the cases.

Results from a case-control study have suggested that classical antipsychotics may be associated with an increased risk of idiopathic venous thromboembolism. The risk was most pronounced during the first three months of treatment and was higher for low-potency than high-potency antipsychotics. This study did not examine the risk of venous thromboembolism with atypical antipsychotics.

Effects on Endocrine Function

Antipsychotics can alter the secretion of prolactin, growth hormone, and thyrotrophin from the anterior pituitary via their ability to block central dopamine-D2 receptors. Therapeutic doses of classical antipsychotics (and some atypical antipsychotics such as amisulpride and risperidone) increase serum-prolactin concentrations. This effect occurs at lower doses and after shorter latent periods than the antipsychotic effects. However, partial tolerance to the hyperprolactinaemic effect may develop on long-term use. Serum prolactin declines to average values within three weeks of stopping oral antipsychotic therapy but may remain raised for six months after an intramuscular depot injection.

The long-term consequences of gonadal hormone deficiency, secondary to raised prolactin concentrations, have caused concern. There is evidence that patients taking long-term prolactin-raising antipsychotics are at high risk of osteoporosis associated with hypogonadism. Long-term antipsychotic treatment has also been shown to increase the incidence of mammary tumors in the rat. Although early studies found little or no evidence that chronic use in humans alters the risk of breast cancer among women with schizophrenia, a later retrospective cohort study found a modest dose-related increase in the risk of breast cancer in women using antipsychotic dopamine antagonists. A similar increase was seen in women receiving antiemetic dopamine antagonists. Fears that pituitary abnormalities, including pituitary tumors, might develop in patients on long-term phenothiazine therapy have not been confirmed.

Antipsychotics can, in some circumstances, reduce both basal and stimulated growth hormone secretion, but attempts to use them to treat dysfunctions in growth hormone regulation have not been successful. Although some clinical studies show that acute dosage of antipsychotics increased basal and stimulated thyrotrophin secretion, most studies find either no change or only a small increase in thyrotrophin secretion following long-term use.

A small study has suggested that thioridazine may be more likely than other antipsychotics to decrease serum concentrations of testosterone or luteinizing hormone in men. However, concentrations were within the normal range in most patients taking antipsychotics.

Effects on the Eyes

Phenothiazines may induce pigmentary retinopathy, which depends on the dose and the duration of treatment. Those phenothiazine derivatives with piperidine side chains, such as thioridazine, have a higher risk of inducing retinal toxicity than other phenothiazine derivatives, with relatively few cases reported for those with aliphatic side chains, such as chlorpromazine. The piperazine group does not appear to exert direct ocular toxicity. The retinopathy may present either acutely (sudden loss of vision associated with retinal edema and hyperemia of the optic disc) or chronically (a fine pigment scatter appearing in the central area of the fundus, extending peripherally but sparing the macula).

Chronic paracentral and peri-central scotomas may be found. Although pigmentary disturbances may progress after withdrawal of thioridazine, they are not always paralleled by deterioration in visual function; nonetheless, some cases have led to progressive chorioretinopathy. The critical ocular toxic dose of thioridazine is reported to be 800 mg daily and UK licensed product information has recommended that a daily dose of 600 mg should not usually be exceeded. However, there is a report of pigmentary retinopathy in a patient who received long-term thioridazine in daily doses not exceeding 400 mg; the total dose was 752 g.

After using phenothiazines, pigmentation may also occur in the cornea, lens, and conjunctiva. It may be associated with pigmentary changes in the skin and is dose-related. In a study of 100 Malaysian patients, ocular pigmentation was observed in slightly more than half of those who had received a total dose of chlorpromazine of 100 to 299 g and in 13 of 15 who had received 300 to 599 g. All those who had received more than 600 g of chlorpromazine or thioridazine had ocular pigmentation. Cataract formation, mainly of an anterior polar variety, has been observed rarely, mainly in patients on chlorpromazine. It does not appear to be dose-related.

A patient who had received fortnightly injections of fluphenazine 12.5 mg for ten years (total dose 3.25 g) developed bilateral maculopathy following unprotected exposure of less than 2 minutes to a welding arc. It was postulated that accumulation of phenothiazine in the retinal epithelium sensitized the patient to photic damage. However, another patient who had received fortnightly injections of fluphenazine 25 mg for 25 years (total dose 16.25 g) developed bilateral maculopathy without exposure to any extreme photochemical sources. The authors concluded that this was due to a direct effect of fluphenazine secondary to its accumulation in the retinal epithelium.


Effects on Fluid and Electrolyte Homeostasis

There have been occasional reports of water intoxication in patients taking antipsychotics. A review of hyponatremia and the syndrome of inappropriate antidiuretic hormone secretion associated with psychotropics summarised 20 such reports for antipsychotics in the literature. The drugs implicated were thioridazine (8 reports), haloperidol (3 reports), chlorpromazine, trifluoperazine, and fluphenazine (2 reports each), and flupentixol, tiotixene, and clozapine (1 report each). Most reports did not permit clear conclusions, and, particularly in the cases of prolonged treatment, the role of the medication was unclear. However, at least 3 cases were well documented and supported the view that antipsychotics could cause hyponatremia.

A report not considered by the above review described water retention and peripheral edema associated with chlorpromazine. A small controlled study found that 5 of 10 evaluated patients receiving haloperidol decanoate had impaired fluid homeostasis.

Effects on Lipid Metabolism

Most antipsychotics are associated with hyperlipidemia. A review found evidence of a higher risk of hyperlipidemia in patients receiving low-potency classical antipsychotics, such as chlorpromazine and thioridazine, or the atypical antipsychotics, clozapine, olanzapine, and quetiapine. High-potency classical antipsychotics, such as haloperidol, and the atypical antipsychotics aripiprazole, risperidone, and ziprasidone, appeared to be associated with a lower risk of hyperlipidemia. Possible mechanisms for dyslipidemia associated with antipsychotic therapy include the development of glucose intolerance, weight gain, and dietary changes. 

Effects on the Liver

Chlorpromazine and other phenothiazines may cause hepatocanalicular cholestasis, often with hepatocyte damage suggestive of immunological liver injury. Only a few patients taking the drug are affected, and the onset is usually in the first four weeks of therapy. The drug or one of its metabolites may induce alteration in the liver-cell membrane so that it becomes antigenic. There is also good evidence for direct hepatotoxicity in producing free drug radicals. There may be an individual peculiarity in the metabolism of chlorpromazine and the production of these radicals. A study has suggested that patients with poor sulfoxidation status combined with unimpaired hydroxylation capacity may most likely develop jaundice with chlorpromazine.

A preliminary study showing a high incidence of gallstones in psychiatric inpatients in Japan found a correlation between the presence of gallstones and the duration of illness and the use of antipsychotics. It was speculated that gallstones could be a consequence of phenothiazine-induced cholestasis.

Effects on Sexual Function

The phenothiazines can cause both impotence and ejaculatory dysfunction. Thioridazine has been frequently implicated, and in an early report, 60% of 57 male patients taking the drug reported sexual dysfunction compared with 25% of 64 men taking other antipsychotics. There are also several reports of priapism with phenothiazines alpha-adrenoceptor blocking properties of these compounds may be partly responsible. Male sexual dysfunction, including priapism, has rarely been reported with other classical antipsychotics such as butyrophenones, diphenylbutylpiperidines, and thioxanthenes. Priapism has also been reported with clozapine and other atypical antipsychotics. The effects of antipsychotics on female sexual function are less well studied. Orgasmic dysfunction has been reported with thioridazine, trifluoperazine, and fluphenazine.

Effects on the Skin, Depot Injection

Of 217 patients who received a combined total of 2354 depot antipsychotic injections, 42 (19.4%) had local problems at the site of injection, 18 (8.3%) experienced chronic complications, and 30 (13.8%) had acute reactions. Acute problems reported included 31 episodes of unusual pain, 21 bleeding or hematoma, 19 clinically important drug leakage from an injection site, 11 acute inflammatory indurations, and two transient nodules. Complications were more common in patients receiving concentrated preparations, higher doses, weekly injections, haloperidol decanoate or zuclopenthixol decanoate, and injection volumes of more than 1 ml in those treated for more than five years. Chronic reactions were more common in patients aged over 50 years.


Testing in 7 subjects taking chlorpromazine revealed that photosensitivity reactions manifested primarily as immediate erythema and that sensitivity was primarily to light in the long ultraviolet (UVA) and visible wavebands. Sensitivity to UVB was normal.

The incidence of photosensitivity reactions to chlorpromazine has been given as 3%. However, a higher incidence of 16-25% has also been reported. See also Effects on the Eyes.


The pigment found in the skin of patients treated with chlorpromazine was considered a chlor-promazine-melanin polymer formed in a light-catalyzed anaerobic reaction. Hydrogen chloride liberated during the reaction could account for the skin irritation. Intracutaneous injection of a preparation of the polymer into two volunteers produced a bluish-purple discoloration, which faded in 3 days.

Extrapyramidal Disorders

Antipsychotics and some other drugs, including antiemetics such as metoclopramide and some antidepressants, can produce a range of dyskinesias or involuntary movement disorders involving the extrapyramidal motor system, including parkinsonism, akathisia, acute dystonia, and chronic tardive dyskinesia. Such reactions are a big problem in treating patients receiving antipsychotics.

Reactions of this type can occur with any antipsychotic, but (excluding tardive dyskinesia) are particularly prominent during treatment with high-potency drugs such as tricyclic piperazines and butyrophenones. Antipsychotics such as clozapine carry a low risk of extrapyramidal effects and are therefore described as atypical antipsychotics. The incidence of tardive dyskinesia does appear to be minimal with clozapine, although there is less evidence for other atypical antipsychotics.

Of 2811 patients studied in the first few months of therapy with prochlorperazine (a drug with a high propensity to cause extrapyramidal reactions), 57 reported adverse effects, 16 involving the extrapyramidal system. There were 4 dystonic-dyskinetic reactions (an incidence of 1 in 464 and 1 in 707 for patients aged under and over 30 years, respectively), 9 reports of parkinsonism (under 60 years, 1 in 1555 over 60 years, 1 in 159), and 3 reports of akathisia (1 in 562).

One explanation of extrapyramidal disorders is an imbalance between dopaminergic and cholinergic systems in the brain. However, this simple model fails to explain the co-existence of various extrapyramidal effects, and several alternative mechanisms have been proposed. Hypotheses based on interactions between different dopamine receptor types may help to explain the decreased tendency of some antipsychotic drugs to induce these reactions (see Uses and Administration section).


Akathisia is a condition of mental and motor restlessness in which there is an urge to move about constantly and an inability to sit or stand still. It is the most common motor adverse effect of treatment with antipsychotics. Acute akathisia is dose-dependent, usually develops within a few days of beginning treatment or after a rapid increase in dose, and usually improves if the drug is stopped or the dose reduced. Antimuscarinic antiparkinsonian drugs provide only limited benefit, although success may be more likely in patients with concomitant parkinsonism.

A low dose of a beta-blocker such as propranolol (although good evidence is lacking) or a benzodiazepine may be helpful. Improvement has also been reported with clonidine and amantadine, but the usefulness of these drugs may be limited by adverse effects or the development of tolerance, respectively. The tardive form, like tardive dyskinesia (see below), which appears after several months of treatment, does not respond to antimuscarinics and is challenging to treat.


Acute dystonic reactions, which mainly affect the muscles of the face, neck, and trunk and include jaw clenching (trismus), torticollis, and oculogyric crisis, are reported to occur in up to 10% of patients taking antipsychotics. Laryngeal dystonia is rare but potentially fatal. Dystonias usually occur within the first few days of treatment or after a dosage increase but may also develop on withdrawal. They are transitory and are most common in children and young adults. Dystonic reactions may be controlled by antimuscarinics such as biperiden or procyclidine or antihistamines such as diphenhydramine or promethazine. Benzodiazepines such as diazepam can also be used.

Prophylactic antimuscarinics can prevent the development of dystonias, but routine use is not recommended as not all patients require them, and tardive dyskinesia may be unmasked or worsened (see below). Such a strategy should probably be reserved for short-term use in those at high risk of developing dystonic reactions, such as young adults starting treatment with high-potency antipsychotics or in patients with a history of drug-induced dystonias. Some patients may develop tardive dystonia. A range of drugs has been tried in this condition but without consistent benefit.


Parkinsonism, often indistinguishable from idiopathic Parkinson’s disease, may develop during therapy with antipsychotics, usually after the first few weeks or months of treatment. It is generally more common in adults and older people, although a retrospective study with haloperidol found an inverse relationship between drug-induced parkinsonism and age. This parkinsonism is generally reversible on drug withdrawal or dose reduction, and may sometimes disappear gradually despite continued drug therapy. Antimuscarinic antiparkinsonian drugs are used to suppress the symptoms of parkinsonism. However, they are often minimally effective and commonly cause adverse effects. Routine use for prophylaxis is not recommended because of the risk of unmasking or exacerbating tardive dyskinesia (see below). Amantadine is an alternative to the antimuscarinics.

Tardive Dyskinesia

The central feature of tardive dyskinesia is orofacial dyskinesia, characterized by protrusion of the tongue (‘fly catching’), lip-smacking, sucking, lateral chewing, and pouting of the lips and cheeks. The trunk and limbs also become involved with choreiform movements such as repetitive ‘piano-playing’ hand movements, shoulder shrugging, foot tapping, or rocking movements. The prevalence of tardive dyskinesia among those receiving antipsychotics varies widely, but up to 60% of patients may develop symptoms. In most cases, the condition is mild, not progressive, and tends to wax and wane.

Although tardive dyskinesia usually develops after many years of antipsychotic therapy, no clear correlation has been shown between the development of the condition and the length of drug treatment or the type and class of drug. However, clozapine does not appear to be associated with the condition, and in some cases, use has improved established tardive dyskinesia. Whether other atypical antipsychotics also have a lower incidence of tardive dyskinesia remains to be established, although some data suggests that this may be the case. Symptoms of tardive dyskinesia often develop after stopping the antipsychotic or after dose reduction. Risk factors include old age, female sex, affective disorder, schizophrenia characterized by negative symptoms, and organic brain damage.

Suggested causes of tardive dyskinesia include:

  • dopaminergic overactivity;
  • the imbalance between dopaminergic and cholinergic activity;
  • supersensitivity of postsynaptic dopamine receptors;
  • pre-synaptic catecholaminergic hyperfunction;
  • alterations of the gamma-aminobutyric acid (GABA) system.

Options in the management of tardive dyskinesia include attempts at treatment while maintaining antipsychotic therapy, withdrawal of antimuscarinic therapy, and either withdrawal of the antipsychotic or reduction of the dosage to the minimum required or transfer to an atypical antipsychotic.

Although many drugs have been tried to treat tardive dyskinesia, there have been relatively few double-blind studies. Reviews of tardive dyskinesia have concluded that there appeared to be no reliable or safe treatment. Overall, classical antipsychotics appeared to be the most effective in masking symptoms of tardive dyskinesia. Still, tolerance may develop, and a worsening of the underlying pathophysiology by antipsychotics had to be assumed on theoretical grounds. Other drugs with anti-dopaminergic actions probably of comparable efficacy included reserpine, oxypertine, tetrabenazine, and metirosine.

The following most effective drugs were considered to be noradrenergic antagonists, such as clonidine. Some encouraging results had also been obtained with GABAergic drugs such as benzodiazepines, baclofen, progabide, valproate, and vigabatrin. However, systematic reviews of studies of some GABAer-gic drugs, including benzodiazepines, found the evidence inconclusive and/or unconvincing. The efficacy of cholinergic could not be confirmed. Dopaminergic and antimuscarinics mostly exacerbated symptoms, but others commented that there was no convincing evidence that long-term use of antimuscarinics increased the risk of developing the condition. Other drugs whose value is unclear include vitamin E and some calcium-channel blockers.

Withdrawal of the causative drug usually worsens the condition, although symptoms often diminish or disappear over weeks or sometimes a year or so. Success is most likely in younger patients. During withdrawal, drugs such as diazepam or clonazepam may be given to alleviate symptoms. Although classical antipsychotics are effective, their routine use to suppress symptoms is not recommended. Still, they may be required for acute distressing or life-threatening reactions or in chronic tardive dyskinesia unresponsive to other treatment.

In severe resistant cases, some have used an antipsychotic with valproate or carbamazepine or reserpine with metirosine. Because of the unsatisfactory management of tardive dyskinesia, emphasis is placed on its prevention. Antipsychotics should be prescribed only when clearly indicated, given in the minimum dose, and continued only when there is evidence of benefit. Although drug holidays have been suggested for reducing the risk of tardive dyskinesia, the limited evidence indicates that interruptions in drug treatment may increase the risk of both persistent dyskinesia and psychotic relapse. Increasing the dose of antipsychotics generally improves the condition, but only temporarily.

Neuroleptic Malignant Syndrome

Neuroleptic malignant syndrome (NMS) is a potentially fatal reaction to some drugs, including antipsychotics and other dopamine antagonists, such as metoclopramide. The clinical features of the classic syndrome are usually considered to include hyperthermia, severe extrapyramidal symptoms including muscular rigidity, autonomic dysfunction, and altered levels of consciousness. Skeletal muscle damage may occur, and the resulting myoglobinuria may lead to renal failure. However, there appear to be no universal criteria for diagnosis. Some believe the classic syndrome to be the extreme of a range of effects associated with antipsychotics and have introduced the concept of milder variants or incomplete forms.

Others consider it a rare idiosyncratic reaction and suggest that the term neuroleptic malignant syndrome should be reserved for the full-blown reaction. Consequently, incidence estimates vary greatly, and recent estimates have ranged from 0.02 to 2.5%. The mortality rate has been substantial, although it has decreased over the years with improved diagnosis and management; this may also be due to the detection and inclusion of milder or incomplete variants. Possible risk factors include dehydration, pre-existing organic brain disease, and a history of a previous episode; young males have also been reported to be particularly susceptible.

The pathogenesis of NMS is still unclear. A blockade of dopaminergic receptors in the corpus striatum is thought to cause muscular contraction and rigidity, generating heat. In contrast, the blockade of dopaminergic receptors in the hypothalamus leads to impaired heat dissipation. Peripheral mechanisms such as vasomotor paralysis may also play a role. Also, a syndrome resembling NMS has been seen after withdrawal of treatment with dopamine agonists such as levodopa. Symptoms develop rapidly over 24 to 72 hours and may occur days to months after starting antipsychotic medication or increase in dosage, but no consistent correlation with dosage or length of therapy has been found.

Symptoms may last for up to 14 days after stopping oral antipsychotics or for up to 4 weeks after stopping depot preparations. All antipsychotics can induce NMS depot preparations and may, however, be associated with prolonged recovery once it develops, and hence, a higher mortality rate. Use with lithium carbonate or antimuscarinics may increase the likelihood of developing the syndrome.

Antipsychotic medication should be withdrawn immediately once the diagnosis of the classic syndrome is made. This should be followed by symptomatic and supportive therapy, including cooling measures, correction of dehydration, and treatment of cardiovascular, respiratory, and renal complications. Whether antipsychotics should be withdrawn from patients with mild attacks and how they should be managed is a matter of debate. The efficacy of specific drug therapy remains to be proven, and justification for use is based mainly on case reports.

  • Dantrolene was first used because of its effectiveness in malignant hyperthermia. It directly affects skeletal muscle and may be particularly effective for reversing hyperthermia of muscle origin.
  • In contrast, dopaminergic agonists may resolve hyperthermia of central origin, restoring dopaminergic transmission and alleviating extrapyramidal symptoms. There have been isolated reports of success with amantadine and levodopa, but bromocriptine is generally preferred. Any underlying psychosis may, however, be aggravated by dopaminergic drugs.
  • Since dantrolene and dopaminergic act differently, combining the two might be helpful, but any advantage remains to be demonstrated.
  • Antimuscarinics are generally of little use and may aggravate the associated hyperthermia.
  • Benzodiazepines may be used for sedation in agitated patients and may be of use against concomitant catatonia. EOT may be an alternative in refractory cases of NMS or when catatonic symptoms are present.

Re-introduction of antipsychotic therapy may be possible but is not always successful, and extreme caution is advised. It has been recommended that a gap of at least 5 to 14 days should be left after resolution of the symptoms before attempting re-introduction.


Stopping treatment with an antipsychotic abruptly may produce withdrawal symptoms, the most common of which are nausea, vomiting, anorexia, diarrhea, rhinorrhoea, sweating, myalgias, paraesthesias, insomnia, restlessness, anxiety, and agitation. Patients may also experience vertigo, alternate feelings of warmth and coldness, and tremor. Symptoms generally begin within 1 to 4 days of withdrawal and decrease within 7 to 14 days. They are more severe and frequent when antimuscarinics are stopped simultaneously.

Treatment of Adverse Effects

After an overdose of chlorpromazine, patients should be managed with intensive symptomatic and supportive therapy. Activated charcoal should be given orally if a substantial amount of the phenothiazine has been taken within 1 hour of presentation, provided the airway can be protected. Emptying the stomach with gastric lavage has sometimes been recommended. Dialysis is of little or no value in poisoning by phenothiazines.

Hypotension should be corrected by raising the patient’s legs or, in severe cases, by intravascular volume expansion. An inotrope such as dopamine may be considered in refractory cases. If a vasoconstrictor is considered necessary in the management of phenothiazine-induced hypotension, the use of adrenaline or other sympathomimetics with high beta-adrenergic agonist properties should be avoided since the alpha-blocking effects of phenothiazine s may impair the usual alpha-mediated vasoconstriction of these drugs, resulting in unopposed beta-adrenergic stimulation and increased hypotension.

The treatment of neuroleptic malignant syndrome and the difficulties of treating extrapyramidal adverse effects, especially tardive dyskinesia, are discussed above.


Visit your healthcare provider for regular checks on your progress.

You may get drowsy, dizzy, or have blurred vision. Do not drive, use machinery, or do anything that needs mental alertness until you know how this medicine affects you. Refrain from standing or sitting up quickly, especially if you are an older patient. This reduces the risk of dizzy or fainting spells. Alcohol can increase possible dizziness or drowsiness. Avoid alcoholic drinks.

This drug can diminish the response of your body to heat or cold. Try not to get overheated. Avoid temperature extremes, such as saunas, hot tubs, hot or cold baths, or showers. Dress warmly in cold weather.

This pill can make you more sensitive to the sun. Store out of the sun. If you cannot avoid sun exposure, wear protective clothing and sunscreen. Do not use sun lamps or tanning beds/booths.

Your mouth may get dry. Chewing sugarless gum or sucking hard candy and drinking plenty of water may help. Contact your pediatrician if the problem does not go away or is severe.


Store out of the reach of children.
Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F). Throw away any unused pill after the expiration date.

Drug Approvals

(British Approved Name, rINN)

Synonyms: Chlorpromazinum; Clorpromazina; Klooripromatsiini; Klorpromazin

BAN: Chlorpromazine

INN: Chlorpromazine [rINN (en)]

INN: Clorpromazina [rINN (es)]

INN: Chlorpromazine [rINN (fr)]

INN: Chlorpromazinum [rINN (la)]

INN: Хлорпромазин [rINN (ru)]

Chemical name: 3-(2-Chlorophenothiazin-10-yl)propyl dimethylamine

Molecular formula: C17H19ClN2S =318.9

CAS: 50-53-3

ATC code: N05AA01

Read code: y03yl

Drug Approvals

(British Approved Name Modified, rINNM)

Synonyms: Chlorpromazine Pamoate; Clorpromazina, embonato de

BAN: Chlorpromazine Embonate [BANM]

INN: Chlorpromazine Embonate [rINNM (en)]

INN: Embonato de clorpromazina [rINNM (es)]

INN: Chlorpromazine, Embonate de [rINNM (fr)]

INN: Chlorpromazini Embonas [rINNM (la)]

INN: Хлорпромазина Ембонат [rINNM (ru)]

Molecular formula: (C17H19ClN2S)2,C23H16O6 =1026.1

ATC code: N05AA01

Drug Approvals

(British Approved Name Modified, rINNM)

Synonyms: Aminazine; Chlorpromazin hydrochlorid; Chlorpromazini Hydrochloridum; Chlorpromazino hidrochloridas; Clorpromazina, hidrocloruro de; Klórpromazin-hidroklorid; Klooripromatsiinihydrokloridi; Klorpromazinhydroklorid

BAN: Chlorpromazine Hydrochloride [BANM]

INN: Chlorpromazine Hydrochloride [rINNM (en)]

INN: Hidrocloruro de clorpromazina [rINNM (es)]

INN: Chlorpromazine, Chlorhydrate de [rINNM (fr)]

INN: Chlorpromazini Hydrochloridum [rINNM (la)]

INN: Хлорпромазина Гидрохлорид [rINNM (ru)]

Molecular formula: C17H19ClN2S,HCl =355.3

CAS: 69-09-0

ATC code: N05AA01

Read code: y0198 [Anaesthesia]; y00H5 [Nausea]; y01zj; y07ia

Pharmacopoeias. In China, EuropeInternational, Japan US.

European Pharmacopoeia, 6th ed. (Chlorpromazine Hydrochloride). A white or almost white crystalline powder. It decomposes on exposure to air and light. Very soluble in water, freely soluble in alcohol. A freshly prepared 10% solution in water has a pH of 3.5 to 4.5. Store in airtight containers. Protect from light.

The United States Pharmacopeia 31, 2008 (Chlorpromazine Hydrochloride). A white or slightly creamy-white odorless crystalline powder. It darkens on prolonged exposure to light. Soluble 1 in 1 of water, 1 in 1.5 of alcohol, and 1 in 1.5 of chloroform insoluble in ether and in benzene. Store in airtight containers. Protect from light.

Dilution. Solutions containing 2.5% chlorpromazine hydrochloride may be diluted to 100 rriL with 0.9%) sodium chloride solution provided the pH of the saline solution is such that the pH of the dilution does not exceed the critical range of pH 6.7 to 6.8.l With pH 7.0 or 7.2 saline, the final solution had a pH of 6.4.

Incompatibility. Incompatibility has been reported between chlorpromazine hydrochloride injection and several other compounds. Precipitation of chlorpromazine base from solution is particularly likely if the final pH increases. Compounds reported to be incompatible with chlorpromazine hydrochloride include aminophylline, amphotericin B, aztreonam, some barbiturates, chloramphenicol sodium succinate, chlorothiazide sodium, dimenhydrinate, heparin sodium, morphine sulfate (when preserved with chlorocresol), some penicillins, and remifentanil.

Sorption. There was a 41%> loss of chlorpromazine hydrochloride from the solution when infused for 7 hours via a plastic infusion set (cellulose propionate burette with PVC tubing) and a 79%> loss after infusion for 1 hour from a glass syringe through silastic tubing. Loss was negligible after infusion for 1 hour from a system comprising a glass syringe with polyethylene tubing.


British Pharmacopoeia 2008: Chlorpromazine Injection; Chlorpromazine Oral Solution; Chlorpromazine Suppositories; Chlorpromazine Tablets

The United States Pharmacopeia 31, 2008: Chlorpromazine Hydrochloride Injection; Chlorpromazine Hydrochloride Oral Concentrate; Chlorpromazine Hydrochloride Syrup; Chlorpromazine Hydrochloride Tablets; Chlorpromazine Suppositories.

Proprietary Preparations

Argentina: Ampliactil Conrax

Australia: Largactil

Brazil: Amplictil Clorpromaz Longactil

Canada: Chlorpromanyl Largactil

Chile: Largactil

Czech Republic: Plegomazin

Denmark: Largactil

Finland: Klorproman

France: Largactil

Germany: Propaphenin

Greece: Largactil Solidon Zuledin

Hong Kong: Largactil

Hungary: Hibernal

Indonesia: Cepezet Meprosetil Promactil

Ireland: Clonazine Largactil

Israel: Taroctyl

Italy: Largactil Prozin

Malaysia: Matcine

Mexico: Largactil

The Netherlands: Largactil

Norway: Largactil

New Zealand: Largactil

Philippines: Laractyl Psynor Thorazine

Poland: Fenactil

Portugal: Largactil Largatrex

Russia: Aminazin

South Africa: Largactil

Singapore: Largo Matcine

Spain: Largactil

Sweden: Hibernal

Switzerland: Chlorazin

Thailand: Chlormazine Chlorpromasit Chlorpromed Duncan Matcine Pogetol Prozine

Turkey: Largactil

UK: Largactil

USA: Thorazine

Venezuela: Largactil


Argentina: 6 Copin

India: Trinicalm Forte

Spain: Largatrex

Thailand: Ama

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