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Last updated on November 18th, 2021

Drug Approvals

(British Approved Name, US Adopted Name, rINN)

INNs in other languages (French, Latin, and Spanish):

Synonyms: TP-21; Thioridazin; Thioridazinum; Tioridatsiini; Tioridazin; Tioridazina; Tioridazinas
BAN: Thioridazine
USAN: Thioridazine
INN: Thioridazine [rINN (en)]
INN: Tioridazina [rINN (es)]
INN: Thioridazine [rINN (fr)]
INN: Thioridazinum [rINN (la)]
INN: Тиоридазин [rINN (ru)]
Chemical name: 10-[2-(1-Methyl-2-piperidyl)ethyl]-2-methylthiophenothiazine
Molecular formula: C21H26N2S2 =370.6
CAS: 50-52-2
ATC code: N05AC02
Read code: y03z3

Pharmacopoeias. In Europe and US.

European Pharmacopoeia, 6th ed. (Thioridazine). A white or almost white powder. Practically insoluble in water soluble in alcohol very soluble in dichloromethane freely soluble in methyl alcohol. Protect from light.

The United States Pharmacopeia 31, 2008 (Thioridazine). A white to slightly yellow crystalline or micronised powder odourless or having a faint odour. Practically insoluble in water freely soluble in dehydrated alcohol and in ether very soluble in chloroform. Protect from light.


Drug Approvals

(British Approved Name Modified, rINNM)

International Nonproprietary Names (INNs) in main languages (French, Latin, and Spanish):

Synonyms: Thioridazin hydrochlorid; Thioridazini Hydrochloridum; Tioridatsiinihydrokloridi; Tioridazina, hidrocloruro de; Tioridazinhidroklorid; Tioridazinhydroklorid; Tioridazino hidrochloridas
BAN: Thioridazine Hydrochloride [BANM]
INN: Thioridazine Hydrochloride [rINNM (en)]
INN: Hidrocloruro de tioridazina [rINNM (es)]
INN: Thioridazine, Chlorhydrate de [rINNM (fr)]
INN: Thioridazini Hydrochloridum [rINNM (la)]
INN: Тиоридазина Гидрохлорид [rINNM (ru)]
Molecular formula: C21H26N2S2,HCl =407.0
CAS: 130-61-0
ATC code: N05AC02
Read code: y021T

Pharmacopoeias. In China, Europe, Japan, and US.

European Pharmacopoeia, 6th ed. (Thioridazine Hydrochloride). A white or almost white, crystalline powder. Freely soluble in water and in methyl alcohol soluble in alcohol. A 1% solution in water has a pH of 4.2 to 5.2. Protect from light.

The United States Pharmacopeia 31, 2008 (Thiondazine Hydrochloride). A white to slightly yellow granular powder having a slight odour. Freely soluble in water, in chloroform, and in methyl alcohol insoluble in ether. pH of a 1% solution in water is between 4.2 and 5.2. Store in airtight containers. Protect from light.

Incompatibility. For a warning about incompatibility between thioridazine hydrochloride solution (Mellaril, Novartis, USA) and carbamazepine suspension (Tegretol, Novartis, USA).

Adverse Effects and Treatment

As for Chlorpromazine.

Thioridazine has been associated with a higher incidence of antimuscarinic effects, but lower incidence of extrapyramidal effects than chlorpromazine. It may also be less sedating. However, it is more likely to induce hypotension and there is an increased risk of cardiotoxicity and dose-related prolongation of the QT interval. Because of this and the consequent danger of life-threatening arrhythmias such as torsade de pointes and sudden death, its use has been restricted (see Precautions, and Uses and Administration, below). Sexual dysfunction also appears to be more frequent with thioridazine.

Pigmentary retinopathy characterised by reduced visual acuity, brownish colouring of vision, and impairment of night vision has been seen particularly in patients taking large doses.

Effects on the cardiovascular system.

Between 1964 and 2001, the UK CSM received 42 reports of suspected heart rate and rhythm disorders associated with thioridazine. There were 21 fatalities reported out of 39 cases where the outcome was known.

See also under Chlorpromazine.


Pruritus and erythematous rash on the genitals of a woman after sexual intercourse were found to be due to thioridazine present in the seminal fluid of her husband, who was taking 100 mg daily at night.


Rhabdomyolysis has been reported in a patient after overdosage with thioridazine. Twenty-four hours after taking 9.4 g of thioridazine the patient presented with difficulty in moving and speaking. On examination he had swelling and tenderness over his upper arms, thighs, and calves. Ataxia and transient dysarthria were attributed to generalised muscle weakness. Other effects were consistent with antimuscarinic effects of thioridazine. He had no signs of neuroleptic malignant syndrome but his urine contained myoglobin. The patient was treated with gastric lavage, activated charcoal, and rehydration. Serum biochemistry returned to normal over 1 week and the muscle tenderness and weakness disappeared.


As for Chlorpromazine. Thioridazine should not be used in patients with clinically significant cardiac disorders, uncorrected hypokalaemia or other electrolyte imbalance, with known or suspected QT prolongation or a family history of QT prolongation, or with a history of ventricular arrhythmias including torsade de pointes. Use is also contra-indicated in patients known to have reduced activity of the cytochrome P450 isoenzyme CYP2D6, which is responsible for thioridazine metabolism. Use with drugs liable to interfere with the metabolism of thioridazine, with other drugs known to prolong the QT interval, and with drugs likely to cause electrolyte imbalance should also be avoided (see under Interactions, below).

For all patients starting thioridazine it is recommended that a baseline ECG and electrolyte screening are performed. An ECG should also be repeated before each dose increase, 1 week after the maximum therapeutic dose has been reached, and at 6-monthly intervals in those who continue treatment. Serum electrolyte concentrations should also be monitored periodically during treatment and any imbalance corrected.


Thioridazine has been associated with acute attacks of porphyria and is considered unsafe in porphyric patients.


As for Chlorpromazine. The metabolism of thioridazine is mediated by the cytochrome P450 isoenzyme CYP2D6 thioridazine itself is also an inhibitor of CYP2D6. Therefore, there is the potential for interactions between thioridazine and other drugs that inhibit or act as a substrate for this enzyme such drugs should not be given with thioridazine. Some examples include antiarrhythmics, certain antidepressants including the SSRIs and tricyclics, certain antipsychotics, beta blockers, HIV-protease inhibitors, and opioids.

Use with other drugs known to prolong the QT interval such as class IA and class III antiarrhythmics, tricyclic antidepressants, and some other antipsychotics should also be avoided, as should use with those drugs known to cause electrolyte imbalance.


The pharmacokinetics of thioridazine appear to be generally similar to those of chlorpromazine. Thioridazine is metabolised by the cytochrome P450 isoenzyme CYP2D6. Its main active metabolite is mesoridazine (p.1007) another metabolite, sulforidazine, also has some activity. Thioridazine and its active metabolites are reported to be highly bound to plasma proteins (more than 95%). The plasma half-life of thioridazine has been estimated to be about 4 to 10 hours. It also crosses the placenta and is distributed into breast milk.


In 10 psychiatric patients stabilised on thioridazine, therapy was replaced by equipotent doses of the side-chain sulfoxide (mesoridazine) and side-chain sulfone (sulforidazine) metabolites of thioridazine. Both metabolites were shown to have an antipsychotic effect, the dose of each required being about two-thirds that of thioridazine. The serum half-lives were thioridazine 21 hours, mesoridazine 16 hours, and sulforidazine 13 hours. Apathy, depression, and restlessness gradually developed during treatment with the 2 metabolites and they could not be used for any length of time.

Extrapyramidal symptoms, hypersalivation, and drowsiness were more common with the metabolites 2 patients had epileptic seizures, and 1 receiving sulforidazine developed probable cholestatic jaundice. There is some evidence that the metabolism of thioridazine is influenced by debrisoquine hydroxylation phenotype. A single-dose study in 19 healthy male subjects demonstrated slower formation of mesoridazine, and hence higher serum-thioridazine concentrations in poor debrisoquine hydroxylators compared with extensive hydroxylators. Formation of thioridazine ringsulfoxide appeared to be compensatorily increased in slow hydroxylators.

Uses and Administration

Thioridazine is a phenothiazine with general properties similar to those of chlorpromazine. It has a piperidine side-chain and, unlike chlorpromazine, has little antiemetic activity. The use of thioridazine has been restricted to the treatment of schizophrenia in patients who fail to show an adequate response to treatment with other antipsychotics. Its use in other psychiatric disorders was abandoned after it was felt that there was an unacceptable balance of risks and benefits as a result of its cardiotoxic potential it has been withdrawn in some countries, including the UK.

For all patients starting thioridazine it is recommended that a baseline ECG and electrolyte screening are performed. An ECG should also be repeated before each dose increase, 1 week after the maximum therapeutic dose has been reached, and at 6-monthly intervals in those who continue treatment. Serum electrolyte concentrations should also be monitored periodically during treatment and any imbalance corrected. Thioridazine is given orally as the hydrochloride or the base, and doses may be expressed in terms of either. In some countries, doses of oral liquid preparations have been given in terms of the base, whereas those of the tablets have been given as the hydrochloride. In the USA, all doses are given in terms of the hydrochloride. Thioridazine 22.8 mg is equivalent to about 25 mg of thioridazine hydrochloride.

In the treatment of schizophrenia thioridazine hydrochloride should be started at the usual dose of 50 to 100 mg three times daily and slowly titrated upwards to a maximum of 800 mg daily if necessary doses should be reduced once effective control is achieved. The daily dosage range is 200 to 800 mg, which may be given in 2 to 4 divided doses. It has been recommended that increases in doses should be no more than 100 mg weekly. Thioridazine should be given in lower initial doses to patients with a low body-mass or those with hepatic or renal impairment dosage increases should also be more gradual. In those patients who require withdrawal of thioridazine, the dose should be gradually reduced over 1 to 2 weeks to avoid symptoms such as gastrointestinal disorders, dizziness, anxiety, and insomnia that are sometimes seen after abruptly stopping high-dose or long-term treatment.


The United States Pharmacopeia 31, 2008: Thioridazine Hydrochloride Oral Solution Thioridazine Hydrochloride Tablets Thioridazine Oral Suspension.

Proprietary Preparations

Argentina: Meleril

Australia: Aldazine Melleril

Austria: Melleril


Brazil: Melleril Unitidazin

Chile: Melerill Nervosan Simultan Tinsenol

Denmark: Melleril

Finland: Melleril Orsanil

France: Melleril

Germany: Melleretten Melleril

Greece: Melleril

Hong Kong: Melleril

Hungary: Melleril

India: Thioril

Indonesia: Melleril

Ireland: Melleril Melzine Thiozine

Israel: Ridazin

Italy: Melleril

Malaysia: Aldazine Melleril

Mexico: Dazithin Melleril

The Netherlands: Melleril

Norway: Melleril

New Zealand: Aldazine Melleril

Portugal: Melleril

Russia: Sonapax Thiodazine Thioril Tison

Spain: Meleril

Sweden: Mallorol

Turkey: Mellerettes Melleril

UK: Melleril Rideril

USA: Mellaril

Venezuela: Meleril

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