MONOGRAPH FOR UKPID
CHLORPROMAZINE HYDROCHLORIDE
HY Allen
ZM Everitt
AT Judd
National Poisons Information Service (Leeds Centre)
Leeds Poisons Information Centre
Leeds General Infirmary
Leeds
LS1 3EX
UK
This monograph has been produced by staff of a National Poisons
Information Service Centre in the United Kingdom. The work was
commissioned and funded by the UK Departments of Health, and was
designed as a source of detailed information for use by poisons
information centres.
Peer review group: Directors of the UK National Poisons Information
Service.
MONOGRAPH FOR UKPID
Drug name
Chlorpromazine hydrochloride
Chemical group
Phenothiazine
Origin
Synthetic
Name
UK Brand name(s)
Largactil(R), Chloractil(R)
Synonyms
Common names
Product licence number
Largactil(R) 10mg: 0012/5108R
Largactil(R) 25mg: 0012/5109R
Largactil(R) 50mg: 0012/5110R
Largactil(R) 100mg: 0012/5111R
Largactil(R) injection solution 2.5%: 0012/5308R
Largactil(R) syrup: 0012/5083R
Largactil(R) Forte Suspension: 0012/5001R
CAS number
69-09-0
Manufacturer
Rhône-Poulenc Rorer Ltd, RPR House, 50 Kings Hill Ave., Kings Hill,
West Malling, Kent, ME19 4AH.
Tel. no. 01732 584000
Fax. no. 01732 584086
Available as Largactil(R) from Rhône-Poulenc Rorer, and as generics or
branded generics from Antigen, APS, DDSA (Chloractil(R)), Hillcross,
Rosemont and Norton.
Form
Tablets
Oral liquids
Injection
Suppositories
Formulation details
Tablets of 10 mg, 25 mg, 50 mg, and 100 mg
Syrup containing 25 mg / 5 ml
Forte suspension equivalent to 100 mg/5 ml (as chlorpromazine
embonate)
Injection of 25 mg / ml.
Suppositories of 100 mg (unlicensed product)
Pack size
Largactil tabs 10 mg, 25 mg, 50 mg, and 100 mg - blister packs of 56
Largactil syrup - 100ml pack
Largactil forte suspension - 100ml pack
Largactil injection - ampoules of 1 ml and 2 ml
Pack sizes may differ for generics and branded generics.
Packaging
Largactil(R) tabs 10mg - white tablets marked LG10
Largactil(R) tabs 25mg - white tablets marked LG25
Largactil(R) tabs 50mg - white tablets marked LG50
Largactil(R) tabs 100mg - white tablets marked LG100
Chemical structure
C17H19ClN2S.HCl
Chemical name
3-(2-Chlorophenothiazin-10-yl)propyldimethylamine hydrochloride
Indication
Schizophrenia and other psychoses, (especially paranoid and
hypomania); short-term adjunctive management of anxiety, psychomotor
agitation, excitement, and violent or dangerously impulsive behaviour;
intractable hiccup; nausea and vomiting of terminal illness (where
other drugs have failed or are not available); induction of
hypothermia; childhood schizophrenia and autism.
Therapeutic dosage - adults
BY MOUTH: 75-300 mg daily in divided doses (doses up to 1 g used in
psychoses).
BY DEEP IM INJECTION: 25-50 mg every 6-8 hours.
BY RECTUM (unlicensed route): 100 mg every 6-8 hours.
For equivalent therapeutic effect:
100 mg by rectum ° 20-25 mg by IM injection ° 40-50 mg by mouth
Therapeutic dosage - children
BY MOUTH: 1-5 years: 500 micrograms/kg 4-6 hourly (maximum 40 mg
daily).
6-12 years: _ to ´ adult dose (maximum 75 mg daily).
BY DEEP IM INJECTION:
500 micrograms/kg 6-8 hourly with maximum daily dose as for
oral dose.
BY RECTUM (unlicensed route):
1-4 years: 12.5 mg 3-4 hourly.
5-12 years: 25 mg 3-4 hourly.
over 12 years: 50-100 mg 3-4 hourly.
Contra-indications
Coma caused by CNS depressants, bone marrow depression,
phaeochromocytoma.
Abuses
Epidemiology
Although the phenothiazines show similar toxic properties to the
tricyclic antidepressants, overdoses tend to be less serious, with
severe hypotension and cardiotoxicity being less common. (Ellenhorn
1997).
ADVERSE EFFECTS
There are a large number of adverse effects associated with
therapeutic use including changes in hepatic, cardiovascular,
respiratory, haematologic, ocular and endocrine functions, besides
extrapyramidal reactions and the risk of neuroleptic malignant
syndrome.
Postural hypotension commonly occurs, especially after intramuscular
administration.
INTERACTIONS
PHARMACODYNAMIC
1. Chlorpromazine enhances the central nervous system depression
produced by other CNS DEPRESSANT drugs.
2. The hypotensive effect of ANTIHYPERTENSIVE AGENTS is likely to be
enhanced, the exception being GUANETHIDINE where chlorpromazine
may antagonise its hypotensive effect (Fruncillo 1985, Janowsky
1973).
3. There is an increased risk of ventricular arrhythmias when
chlorpromazine is taken with drugs that increase the QT interval
e.g. ASTEMIZOLE, TERFENADINE, or ANTI-ARRHYTHMIC AGENTS.
4. Combination with other antidopaminergic agents such as
METOCLOPRAMIDE or PROCHLORPERAZINE increases the risk of
extrapyramidal effects.
PHARMACOKINETIC
1. The metabolism of TRICYCLIC ANTIDEPRESSANTS is impaired by
chlorpromazine, increasing the risk of toxicity (Balant-Gorgia &
Balant 1987).
OTHER
An interaction between phenothiazine drugs and 'caffeinated' beverages
has been reported. A precipitation occurs when these drugs are diluted
in tea or coffee (including decaffeinated varieties) which is
considered to be a nonspecific reaction between the
nitrogen-containing organic bases and tannic acid. The reaction is
reversible in the acid environment of the stomach (Curry et al. 1991).
ETHANOL
The administration of ethanol with chlorpromazine results in
potentiated sedative effects and impaired co-ordination (Lieber 1994,
Milner & Landauer 1971, Zirkle 1959).
MECHANISM OF ACTION
Chlorpromazine blocks post-synaptic D2 dopamine receptors. It is
considered that dopamine receptor blockade in the mesolimbic area
accounts for the antipsychotic effect, whilst blockade in the
nigrostriatal system produces the extrapyramidal effects associated
with chlorpromazine use. The anti-emetic effect results from dopamine
antagonism in the chemoreceptor trigger zone. Chlorpromazine also
possesses antimuscarinic properties. It is an antagonist at histamine
(H1), serotonin and alpha-1-adrenergic receptors (Dollery 1991).
MECHANISM OF TOXICITY
The extrapyramidal, anticholinergic, sedative, and hypotensive
features of toxicity result from the blockade of dopaminergic,
muscarinic, histaminic, and alpha adrenergic receptors respectively.
The cardiotoxic effects of phenothiazines in overdose are similar to
that of the tricyclic antidepressants. (Ellenhorn 1997). Cardiac
arrhythmia and apparent 'sudden death' have been associated with
therapeutic doses of chlorpromazine, the sudden cardiovascular
collapse being attributed to ventricular dysrhythmia (Fowler et al.
1976, Hollister & Kosec 1965).
Pharmacokinetics
ABSORPTION
Peak plasma concentrations occur on average 2-3 hours (range 1.5-8
hours) after an oral dose (Midha et al. 1989, Yeung et al. 1993).
After intramuscular injection chlorpromazine is slowly absorbed from
the injection site, with the peak plasma concentration occurring 6-24
hours after administration (Dahl & Strandjord 1977).
The oral bioavailability of chlorpromazine is about 30% that of
intramuscular doses (Dahl & Strandjord 1977) and about 10% that of
intravenous doses (Yeung et al. 1993) as a result of pre-systemic
metabolism.
DISTRIBUTION
Chlorpromazine is highly lipid soluble and is 98% bound to plasma
proteins (Dollery 1991). It is extensively distributed throughout the
body and has a mean volume of distribution of 17 L/kg (Yeung et al.
1993).
METABOLISM
Chlorpromazine is subject to significant pre-systemic metabolism
attributed to first passage through the gut wall, liver and lung
(Yeung et al. 1993).
It is extensively metabolised involving cytochrome P450 microsomal
pathways (Lieber 1994) with more than 100 metabolites being
theoretically possible (Javaid 1994). The major routes of metabolism
include hydroxylation, N-oxidation, sulphoxidation, demethylation,
deamination and conjugation (Dollery 1991). A number of the
metabolites may contribute to the pharmacological effects of
chlorpromazine including 7-hydroxychlorpromazine,
chlorpromazine-N-oxide, 3-hydroxychlorpromazine and
desmethylchlorpromazine (Chetty et al. 1994). Although the metabolite
chlorpromazine-N-oxide does not possess activity in vitro, it exerts
an indirect pharmacological effect in vivo by reverting to
chlorpromazine (Cheng & Jusko 1993). It is considered that one of the
metabolites produced (chlorpromazine-sulphoxide) may oppose the
alpha-adrenergic blocking action of chlorpromazine (Chetty et al.
1994).
There is limited evidence to suggest that following multiple doses,
the metabolism of chlorpromazine may be increased due to induction of
microsomal liver enzymes (Dahl & Strandjord 1977).
ELIMINATION
Excretion is primarily via the kidneys with less than 1% of a dose
excreted as unchanged drug in the urine, and 20-70% as conjugated or
unconjugated metabolites (Dollery 1991). 5-6% of a dose is excreted in
faeces via biliary elimination (Dollery 1991).
Some metabolites can still be detected up to 18 months after
discontinuation of long-term therapy (Dollery 1991).
HALF-LIFE
The half-life of chlorpromazine is usually within the range 8-35 hours
(Dollery 1991), although it is as short as 2 hours or as long as 60
hours in some individuals (Midha et al. 1989). The half-lives of the
primary metabolites are generally within the same range (Yeung et al.
1993).
Special populations
ELDERLY: it has been suggested that the elderly metabolise
antipsychotic drugs more slowly than do the non-elderly adult
population (Balant-Gorgia & Balant 1987).
RENAL IMPAIRMENT: the effects of renal disease on chlorpromazine
pharmacokinetics are not known, but since it is extensively
metabolised in the liver, they are not anticipated to be great.
HEPATIC IMPAIRMENT: it is considered that hepatic dysfunction will
increase the bioavailability of chlorpromazine and delay its
elimination (Dollery 1991).
GENDER:
Breast milk
Chlorpromazine has been identified in the milk of nursing mothers
receiving the drug.
In one study (Blacker et al. 1962) the peak milk concentration of
chlorpromazine (0.29 mg/L) occurred 2 hours after a single oral dose
of 1200 mg, although in this report the assay design was relatively
nonspecific and no account was taken of active metabolites.
In a later study chlorpromazine and several metabolites were
identified in the breast milk of four nursing mothers receiving the
drug (doses not specified). The milk concentrations ranged from
0.007-0.098 mg/L, with maternal serum levels ranging from 0.016-0.052
mg/L. In two of the four patients the milk concentrations of
chlorpromazine were higher than the maternal plasma concentrations.
One of the babies was reported to be drowsy and lethargic (the milk
chlorpromazine level in this case was 0.092 mg/L) (Wiles et al. 1978).
Toxicokinetics
Absorption
Distribution
Metabolism
Elimination
HALF-LIFE
HALF-LIFE - METABOLITES
Special populations
ELDERLY:
RENAL IMPAIRMENT:
HEPATIC IMPAIRMENT:
GENDER:
Breast milk
Summary
TYPE OF PRODUCT
A phenothiazine antipsychotic.
INGREDIENTS
Tablets of 10 mg, 25 mg, 50 mg, and 100 mg.
Oral liquids containing 25 mg / 5 ml, and 100 mg / 5 ml.
Injection of 25 mg / ml.
Suppositories of 100 mg (unlicensed product).
SUMMARY OF TOXICITY
Central nervous system depression is the most common feature of
toxicity and usually begins 1-2 hours after ingestion. Hypotension and
anticholinergic symptoms are also common. Acute dystonic reactions and
cardiac arrhythmias may occur. Chlorpromazine lowers the seizure
threshold (a dose-related effect) so convulsions may occur in patients
not previously known to be epileptic.
Individual response to chlorpromazine overdose is variable - an
ingestion of 20 g has been survived, whilst 2 g has proved fatal.
In children, hypotension and drowsiness can follow doses ranging from
100-375 mg, with severe central nervous system depression resulting
from higher doses. Fatalities have been reported in children, the
doses ingested ranging from 20-74 mg/kg.
In mixed drug ingestions chlorpromazine enhances the sedation produced
by other central nervous system depressants including ethanol.
FEATURES
Drowsiness, hypotension, anticholinergic symptoms (e.g. dry mouth,
dilated pupils, urinary retention, visual disturbances), acute
dystonic reactions, and cardiac arrhythmias.
UNCOMMON FEATURES
Acute pulmonary oedema, and neuroleptic malignant syndrome.
SUMMARY OF MANAGEMENT
1. Maintain a clear airway and adequate ventilation if consciousness
is impaired.
2. If within 1 hour of the ingestion and more than 500mg has been
ingested by an adult, or more than 4mg/kg by a child, give oral
activated charcoal.
3. Monitor the cardiac rhythm.
4. Manage hypotension with IV fluids.
5. Treat acute dystonic reactions with IV procyclidine or
benztropine.
Clinical Features
Features - acute
Ingestion
Hypotension, sinus tachycardia, varying degrees of CNS depression,
blurred vision, dry mouth, urinary retention, acute dystonic
reactions, akathisia, parkinsonism, ECG changes including prolonged PR
and QT intervals, ventricular tachyarrhythmias, convulsions,
hypothermia (or occasionally hyperthermia), pulmonary oedema, and
respiratory depression (Allen et al. 1980, Barry et al. 1973,
Ellenhorn 1997, Li & Gefter 1992, Reid & Harrower 1984).
Inhalation
Dermal
Contact dermatitis.
Ocular
Other routes
BY INJECTION: as for acute ingestion.
Features - chronic
Ingestion
As for acute ingestion, but with the additional risks of the
development of neuroleptic malignant syndrome (characterised by muscle
rigidity, hyperthermia, altered consciousness, and autonomic
instability), and tardive dyskinesia (involuntary movements of the
tongue, face, jaw, or mouth) (Rosenberg & Green 1989).
Inhalation
Dermal
Contact dermatitis.
Ocular
Other routes
BY INJECTION: as for chronic ingestion.
At risk groups
ELDERLY
Elderly and volume depleted subjects are particularly susceptible to
postural hypotension.
PREGNANCY
The administration of chlorpromazine near term has been associated
with unpredictable falls in maternal blood pressure which could be
dangerous to the mother and the foetus. Administration near term has
also resulted in an extrapyramidal syndrome in some infants,
characterised by tremors, increased muscle tone, and hyperactive deep
tendon reflexes persisting some months (Briggs 1994).
One psychiatric patient who ingested 8 g of chlorpromazine in the last
ten days of pregnancy, delivered a hypotonic, lethargic infant with
depressed reflexes and jaundice (Hammond & Toseland 1970).
CHILDREN
ENZYME DEFICIENCIES
ENZYME INDUCED
Occupations
Pharmacists, nurses, and other health workers should avoid direct
contact with chlorpromazine due to a risk of contact sensitisation.
Tablets should not be crushed and solutions handled with care (BNF
1998).
Others
RENAL IMPAIRMENT: renal impairment is unlikely to increase the risk of
toxicity.
HEPATIC IMPAIRMENT: increased risk of toxicity due to impaired
metabolism and hepatotoxic potential.
CARDIAC DISEASE: increased risk of cardiotoxicity due to underlying
disease.
EPILEPSY: increased risk of seizures due to lowered seizure threshold.
Management
Decontamination
If within one hour of the ingestion, and more than 500mg has been
ingested by an adult, or 100mg by a child, oral activated charcoal may
be given to reduce drug absorption.
ADULT DOSE: 50g; CHILD DOSE; 1g/kg.
If the patient is drowsy this should be administered via a nasogastric
tube, and if there is no gag reflex present, using an endotracheal
tube to protect the airway.
Supportive care
GENERAL MANAGEMENT OF THE SYMPTOMATIC PATIENT
Clear and maintain airway, and give cardiopulmonary resuscitation if
necessary.
Evaluate the patient's condition and provide support for vital
functions. The aim is to maintain vital bodily functions with minimal
intervention whilst the elimination of chlorpromazine takes place.
Particular care should be given to the prevention of hypoxia and
acidosis, and the correction of any electrolyte imbalance.
SPECIFIC MANAGEMENT OF THE SYMPTOMATIC PATIENT
1. HYPOTENSION
Hypotension should be managed by the administration of intravenous
fluids and by physical means. Where these measures fail, consideration
may be given to the use of a direct acting sympathomimetic such as
noradrenaline with appropriate haemodynamic monitoring (e.g. insertion
of Swan-Ganz catheter).
ADULT DOSE: IV infusion of noradrenaline acid tartrate 80
micrograms/ml (equivalent to noradrenaline base 40 micrograms/ml) via
a central venous catheter at an initial rate of 0.16 to 0.33 ml/minute
adjusted according to response (BNF 1998).
CHILD DOSE (unlicensed indication): IV infusion of noradrenaline
acid tartrate 0.04-0.2 microgram/kg/minute (equivalent to 0.02-0.1
microgram/kg/minute of noradrenaline base) in glucose 5% or
glucose/saline via a central venous catheter (Guy's, Lewisham & St
Thomas Paediatric Formulary, 1997).
NOTE: vasopressors with mixed alpha and beta adrenergic effects (e.g.
adrenaline, dopamine) should not be used as hypotension may be
exacerbated.
2. COMA
Good supportive care is essential.
3. CARDIOTOXICITY
In practice it is seldom necessary or advisable to use specific drug
treatment for arrhythmias. If hypoxia and acidosis are reversed, and
adequate serum potassium levels maintained, then the majority of
patients will show improvement with supportive measures. Where these
measures fail and life-threatening arrhythmias persist, intravenous
sodium bicarbonate should be given (even in the absence of acidosis)
before considering antiarrhythmic drug therapy.
Where an antiarrhythmic is considered necessary, lignocaine is the
preferred drug.
ADULT DOSE: 50-100 mg lignocaine by IV bolus given over a few
minutes, followed by an infusion of 4 mg/minute for 30 minutes, 2
mg/minute for 2 hours, then 1 mg/minute (BNF 1998).
NOTE: the use of quinidine, procainamide, flecainide, or disopyramide,
is contraindicated as these agents further depress cardiac conduction
and contractility. The use of beta-blockers and calcium channel
blockers should also be avoided as they decrease cardiac output and
exacerbate hypotension.
The ventricular arrhythmia, TORSADE DE POINTES, may prove difficult to
manage. The preferred treatment is cardiac overdrive pacing, but in
cases where cardiac pacemaker insertion is not readily available,
intravenous magnesium sulphate has been shown to be effective (Tzivoni
et al. 1988).
ADULT DOSE: 8 mmol of magnesium sulphate (4 ml of 50% solution)
by intravenous injection over 10-15 minutes, repeated once if
necessary (BNF 1998).
CHILD DOSE: clinical experience in children is lacking, but based
on the above recommendations for management in adults, doses of 0.08-
0.2 mmol/kg (0.04-0.1 ml/kg of 50% solution) may be considered
appropriate (based on Guy's, Lewisham & St Thomas Paediatric
Formulary, 1997).
Torsade de pointes has also been successfully managed in adults by the
intravenous administration of isoprenaline (infused at a starting dose
of 0.2 micrograms/minute and titrated to maintain a heart rate of 100
beats per minute) (Kemper et al. 1983). However it should be used with
caution as its beta-2-adrenergic agonist effects exacerbate
hypotension.
4. ACUTE DYSTONIC AND OTHER EXTRAPYRAMIDAL REACTIONS
Severe dystonic reactions can be controlled within a few minutes by
giving procyclidine or benztropine by the intravenous (or
intramuscular) route. Subsequent oral doses may be required for 2-3
days to prevent recurrence. Less severe extrapyramidal symptoms can be
controlled by oral doses of procyclidine, benztropine, or other
similar anticholinergic drug (Corre et al. 1984, Guy's, Lewisham & St.
Thomas Paediatric Formulary, 1997, BNF 1998).
Procyclidine IV, IM, and oral:
ADULT DOSE: 5-10 mg (use lower end of dose range in elderly),
CHILD DOSE under 2 years: 500 micrograms-2 mg (unlicensed
indication)
2-10 years: 2-5 mg (unlicensed indication).
Benztropine dose IV, IM, and oral:
ADULT DOSE: 1-2 mg (use lower end of dose range in elderly),
CHILD DOSE: 20 micrograms/kg (unlicensed indication).
5. SEIZURES/MUSCLE SPASMS
Diazepam by slow intravenous injection preferably in emulsion form,
may be given to control muscle spasms and convulsions not remitting
spontaneously.
ADULT DOSE: 10 mg repeated as required depending upon clinical
condition;
CHILD DOSE: 200 - 300 micrograms/kg.
6. TEMPERATURE DISTURBANCES
Where the patient is hypothermic the body temperature should be
allowed to recover naturally by wrapping the patient in blankets to
conserve body heat.
Conventional external cooling procedures should be used in patients
who are hyperthermic.
7. NEUROLEPTIC MALIGNANT SYNDROME
The development of neuroleptic malignant syndrome with a high central
temperature (over 39°C) is best treated by paralysing and mechanically
ventilating the patient. This usually controls the muscle spasm and
allows the temperature to fall. If the body temperature is 40°C or
over, administer intravenous dantrolene.
ADULT DOSE: 1 mg/kg body weight by rapid IV injection repeated as
required to a cumulative maximum of 10 mg/kg (BNF 1998).
8. OTHER MEASURES
Pulmonary oedema typically resolves with conventional supportive
management within 18-40 hours of ingestion (Li & Gefter 1992).
Monitoring
Monitor the heart rate and rhythm, blood pressure, arterial blood
gases, serum electrolytes, body temperature, respiratory rate and
depth, and urinary output.
Observe for a minimum of 4 hours post-ingestion where:
i) more than 4 mg/kg has been ingested by a child (or more than
the child's normal therapeutic dose, if this is greater),
ii) more than 500 mg is known to have been ingested by an adult
(or more than the patients's normal therapeutic dose, if this is
greater),
iii) the patient is symptomatic.
Where symptoms develop following overdose, they may persist for 24
hours. Complications following severe toxicity may require the patient
to be hospitalised for several days.
Antidotes
None available.
Elimination techniques
Haemodialysis and diuresis are ineffective as ways of increasing drug
elimination due to the large volume of distribution and high lipid
solubility of chlorpromazine. It is not considered that haemoperfusion
will be of benefit (Ellenhorn 1997).
Investigations
Where there is evidence of severe toxicity a chest radiograph should
be performed within 24 hours of the ingestion to exclude pulmonary
complications.
Management controversies
GASTRIC LAVAGE is not recommended as the procedure may be associated
with significant morbidity, and there is no evidence that it is of any
greater benefit than activated charcoal used alone.
If the procedure is used (i.e. in cases where activated charcoal
cannot be administered), a cuffed endotracheal tube should be used to
protect the airway if the patient is drowsy, and activated charcoal
left in the stomach following the lavage.
Case data
CASE REPORT 1
A 27 year old woman was admitted 12 hours after ingesting 8 g
chlorpromazine and 150 mg flurazepam. After 18 hours she was fully
alert and normotensive. Six hours later she sustained a cardiac arrest
and was successfully resuscitated. Subsequent ventricular tachycardia
responded to intravenous lignocaine, and a prolonged QT interval
shortened progressively to normal over the next three days (Reid &
Harrower 1984).
Analysis
Agent/toxin/metabolite
Several studies to determine the relationship between plasma
concentration and therapeutic response have been performed. The
majority of studies showed large individual variations in
chlorpromazine concentration relative to dose, and no clear
association between plasma concentration and therapeutic response has
been made (Dahl & Strandjord 1977).
As a consequence the measurement of plasma chlorpromazine
concentrations following overdose is not routinely advised.
Sample container
Storage conditions
Transport
Interpretation of data
Although no clear relationship exists between plasma concentration and
therapeutic effect,
it has been suggested that therapeutic response may be associated with
the plasma concentration range 0.05-0.30 mg/L (Rivera-Calimlim et al.
1976).
In a study of unexplained deaths in patients receiving multiple
antipsychotic therapy, five cases had concentrations of antipsychotic
drugs which were considered 'probably' toxic and were implicated in
the development of ventricular fibrillation. The plasma chlorpromazine
concentrations in these cases were in the range 0.5-7.0 mg/L (Jusic &
Lader 1994).
Conversion factors
1 mg/L = 2.817 micromoles/L
1 micromole/L = 0.355 mg/L
The molecular weight of chlorpromazine hydrochloride is 355.3
Others
Toxicological data
Carcinogenicity
Genotoxicity
Mutagenicity
Reprotoxicity
Teratogenicity
Chlorpromazine readily crosses the placenta. Although one study found
an increased incidence of malformations in first trimester
phenothiazine-exposed infants compared to non-exposed controls
(3.5%compared to 1.6%), most reports describing the use of
phenothiazines in pregnancy (during all stages of gestation) conclude
that they do not adversely affect the foetus or newborn (Briggs 1994).
Relevant animal data
Relevant in vitro data
Authors
HY Allen
ZM Everitt
AT Judd
National Poisons Information Service (Leeds Centre)
Leeds Poisons Information Centre
Leeds General Infirmary
Leeds
LS1 3EX
UK
This monograph was produced by the staff of the Leeds Centre of the
National Poisons Information Service in the United Kingdom. The work
was commissioned and funded by the UK Departments of Health, and was
designed as a source of detailed information for use by poisons
information centres.
Peer review was undertaken by the Directors of the UK National Poisons
Information Service.
Prepared November 1996
Updated May 1998
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