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Trimipramine: Wikis


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1 : 1 mixture (racemate)
Systematic (IUPAC) name
CAS number 739-71-9
ATC code N06AA10
PubChem 5584
DrugBank APRD00498
Chemical data
Formula C20H26N2 
Mol. mass 294.434 g/mol
Pharmacokinetic data
Bioavailability 40%
Metabolism Hepatic
Half life 11-23 hours
Excretion Renal
Therapeutic considerations
Pregnancy cat. C
Legal status Prescription only
Routes Oral, IM, IV
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Trimipramine (Surmontil, Rhotrimine, Stangyl) is a tricyclic antidepressant (TCA). It has antidepressant, anxiolytic, antipsychotic, sedative, and analgesic effects.



  • Endogenous and neurotic depression with prominent agitation and anxiety
  • Depressive and non-depressive insomnia (suitable for long-term treatment)
  • Adjunctive therapy of alcohol and opioid withdrawal
  • Chronic pain of malignant and non-malignant origin


Trimipramine's mechanism of action differs from other TCAs. It is only a moderate reuptake inhibitor of norepinephrine, and a weak reuptake inhibitor of serotonin and dopamine. Its main effects are due to considerable receptor antagonism as follows:

The spectrum of effects (strong antidepressant activity, sedation and anxiolysis) and side effects (strong anticholinergic and antiadrenergic symptoms) is similar to those of doxepin. It is also a more effective sedative than amitriptyline. Trimipramine is the only effective drug against insomnia known so far that does not alter the normal sleep architecture. In particular, it does not suppress REM sleep, and dreams are said to brighten during treatment.[citation needed] However, this can occasionally go too far, as nightmares are an uncommon but possible side effect of the drug. Its relatively strong antagonistic activity at postsynaptic D2 receptors led to a clinical study trying trimipramine as atypical neuroleptic. There it exerted good antipsychotic activity with a low incidence of extrapyramidal and other side effects. But this study encompassed only 28 patients, so the use of trimipramine as a neuroleptic needs further confirmation and can currently not be recommended. Trimipramine also shows useful activity against chronic pain.



  • Tablets/capsules (10, 12.5, 25, 50, 75, 100, 150 mg)
  • Liquid concentrate (40 mg/ml)
  • Injectable concentrate (25 mg)


Whilst some standard suggested dosages are published for the treatment of depression, the proper dosage for treatment of insomnia in non-depressive patients, those on alcohol/opioid withdrawal and those with chronic pain may vary greatly and should be discussed with your physician.

Treatment should be initiated at the lowest recommended dose and increased gradually, noting carefully the clinical response and any evidence of intolerance. Days to weeks may elapse before optimal therapeutic effects of Trimipramine are seen. Increasing the dosage usually does not shorten this latent period and may increase the incidence of side effects and patient non-compliance.

In elderly or debilitated patients it may be necessary to check blood pressure and cardiac rhythm, particularly in patients who have unstable cardiovascular function.

Once a satisfactory response has been obtained, the dosage is normally adjusted to the lowest level required to maintain remission and avoid relapse. Medication should be continued for the expected duration of the depressive episode in order to minimize the possibility of relapse following clinical improvement. Afterwards, prophylactic treatment for 1 to 2 years may be indicated, but there are different opinions regarding the optimal dose and length of remission maintenance treatment.

Parenteral usage

Intramuscular injections and slow i.v.-infusions are possible, but have the disadvantage of intensified anticholinergic and antiadrenergic side effects. The advantage may be an earlier onset of action compared to oral dosage. Decreased doses are sufficient with parenteral treatment.


Trimipramine is a racemic compound with two enantiomers.[1] CYP2C19 is responsible for the demethylation of (D)- and (L)-trimipramine to (D)- (L)-desmethyltrimipramine, respectively, and CYP2D6 is responsible for the 2-hydroxylation of (D)- and (L)-desmethyltrimipramine to (D)- and (L)-2-hydroxydesmethyltrimipramine, respectively.[1] CYP2D6 also metabolizes (L)-trimipramine into (L)-2-hydroxytrimipramine.[1]



  • Concomitant treatment with monoamine oxidase inhibitors (MAOIs)
  • Known allergy or hypersensitivity to trimipramine or other TCAs
  • Acute delirum tremens
  • Untreated closed angle glaucoma
  • Hypertrophy of the prostate with urine retention
  • Paralytic ileus


  • Hypertrophy of the prostate without urine retention
  • Reduced function of the bone marrow
  • Organic brain disorders
  • Increased risk of seizures, pre-existing epilepsy
  • Pre-existing cardial damage, particular some arrhythmias (impulse conductive disorders)

Abuse & dependence

Trimipramine is not an abusable substance nor does it cause psychological dependence.

Withdrawal symptoms frequently seen when treatment with trimipramine is stopped abruptly (agitation, anxiety, insomnia, sometimes activation of mania or rebound depression) are not indicative of addiction and can be avoided by reducing the daily dose of trimipramine gradually by approximately 25% each week. If treatment has to be stopped at once due to medical reasons, the use of a benzodiazepine (e.g., lorazepam, clonazepam, or alprazolam) for a maximum of 4 weeks as needed will usually suppress withdrawal symptoms.

See also


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