Thioridazine
Thioridazine is a first generation antipsychotic drug belonging to the phenothiazine drug group and was previously widely used in the treatment of schizophrenia and psychosis. The branded product was withdrawn worldwide in 2005 because it caused severe cardiac arrhythmias. However, generic versions are still available in the US.
Indications
Thioridazine was voluntarily discontinued by its manufacturer, Novartis, worldwide because it caused severe cardiac arrhythmias.Its primary use in medicine was the treatment of schizophrenia. It was also tried with some success as a treatment for various psychiatric symptoms seen in people with dementia, but chronic use of thioridazine and other anti-psychotics in people with dementia is not recommended.
Side effects
For further information see: PhenothiazineThioridazine prolongs the QTc interval in a dose-dependent manner. It produces significantly less extrapyramidal side effects than most first-generation antipsychotics. Its use, along with the use of other typical antipsychotics, has been associated with degenerative retinopathies. It has a higher propensity for causing anticholinergic side effects coupled with a lower propensity for causing extrapyramidal side effects and sedation than chlorpromazine, but also has a higher incidence of hypotension and cardiotoxicity. It is also known to possess a relatively high liability for causing orthostatic hypotension compared to other antipsychotics. Similarly to other first-generation antipsychotics it has a relatively high liability for causing prolactin elevation. It is moderate risk for causing weight gain. As with all antipsychotics thioridazine has been linked to cases of tardive dyskinesia and neuroleptic malignant syndrome. Blood dyscrasias such as agranulocytosis, leukopenia and neutropenia are possible with thioridazine treatment. Thioridazine is also associated with abnormal retinal pigmentation after many years of use.
Pharmacology
Thioridazine has the following binding profile:Biologic Protein | Binding affinity | Binding affinity of Mesoridazine | Binding affinity of Sulforidazine | Notes |
SERT | 1259 | ND | ND | |
NET | 842 | ND | ND | |
DAT | 1684 | ND | ND | |
5-HT1A | 144.35 | 500 | ND | |
5-HT1B | 109 | ND | ND | |
5-HT1D | 579 | ND | ND | |
5-HT1E | 194 | ND | ND | |
5-HT2A | 27.67 | 4.76 | ND | The ratio of 5-HT2A to D2 receptor binding is believed to dictate whether or not most antipsychotics are atypical or typical. In thioridazine's case its ratio of 5-HT2A to D2 receptor binding is below the level that's believed to be required for atypicality despite its relatively low extrapyramidal side effect liability in practice. |
5-HT2C | 53 | 157 | ND | Believed to play a role in the weight gain-promoting effects of antipsychotics. |
5-HT3 | >10000 | ND | ND | |
5-HT5A | 364 | ND | ND | |
5-HT6 | 57.05 | 380 | ND | |
5-HT7 | 99 | 73 | ND | |
α1A | 3.15 | 2 | ND | Likely the receptor responsible for the orthostatic hypotension known to occur in individuals on thioridazine. |
α1B | 2.4 | ND | ND | |
α2A | 134.15 | 1612.9 | ND | |
α2B | 341.65 | ND | ND | |
α2C | 74.9 | ND | ND | |
β1 | >10000 | ND | ND | |
β2 | >10000 | ND | ND | |
M1 | 12.8 | 10 | ND | This receptor is believed to be the chief receptor responsible for the anticholinergic side effects of thioridazine. Likely plays a role in thioridazine's low extrapyramidal side effect liability as anticholinergic drugs such as benzatropine are routinely given to treat extrapyramidal side effects resulting from antipsychotic treatment. |
M2 | 286.33 | 15 | ND | |
M3 | 29 | 90 | ND | |
M4 | 310.33 | 19 | ND | |
M5 | 12.67 | 60 | ND | |
D1 | 94.5 | ND | ND | |
D2 | 0.4 | 4.3 | 0.25 | Believed to be the receptor responsible for the therapeutic effects of antipsychotics. |
D3 | 1.5 | 2.6 | 0.7 | |
D4 | 1.5 | 9.1 | ND | |
D5 | 258 | ND | ND | |
hERG | 191 | ND | ND | Likely involved in thioridazine's cardiac effects. |
H1 | 16.5 | 1.81 | ND | Likely responsible for the sedating effects of thioridazine. |
H2 | 136 | ND | ND | Regulates the release of hydrochloric acid into the stomach. |
H4 | 2400 | ND | ND |
Note: The Binding affinities given are towards cloned human receptors unless otherwise specified
Acronyms used
HB – Human brain receptor
RC – Cloned rat receptor
ND – No data