Loading
If this is the first time anyone has visited this substance, we may be fetching live data from TGA Product Information, PBS, and state framework sources — that can take up to a minute. Cached substances load in a second or two.
Select your state to see jurisdictional framework, reporting obligations, and authority links. Substance information above is the same in every state.
A plain-language summary of the cited sources below. Informational only — not medical advice.
Amitriptyline works by interfering with how brain cells reabsorb two chemical messengers — serotonin and norepinephrine — after they've been released. By slowing down this reabsorption process, the medication allows these messengers to remain active for longer. This mechanism is thought to be responsible for amitriptyline's antidepressant effects. The medication is formally approved in Australia for treating major depression and for bedwetting in children when physical causes have been ruled out.
Once taken, amitriptyline stays active in the body for roughly 21 hours on average, and it breaks down into another active substance called nortriptyline that lasts about 26 hours. This means the effects build up over time with regular dosing rather than wearing off quickly.
Your family member may experience some common side effects including a faster heartbeat, awareness of their heartbeat, dizziness when standing up, drowsiness, or a persistently dry mouth. More serious effects can occur and should prompt immediate medical attention: thoughts of self-harm, a severe drop in white blood cells making infections more likely, involuntary repetitive movements, severe skin reactions, or irregular heart rhythms.
Amitriptyline cannot be used in people who are allergic to it, anyone taking certain other antidepressants called monoamine oxidase inhibitors, or anyone taking cisapride. It should not be used in the weeks following a heart attack. The medication can interact with other medicines that affect how the liver processes drugs, including quinidine, cimetidine, certain heart rhythm medications, and some other antidepressants. When these interactions occur, lower doses of one or both medications may be needed.
“Amitriptyline inhibits the membrane pump mechanism responsible for uptake of noradrenaline and serotonin in adrenergic and serotonergic neurons.”
“The mean apparent elimination half-life for amitriptyline was reported by one source to be 22.4 hours; the mean half- life of its active metabolite, nortriptyline was 26 hours.”
A plain-language summary of the cited sources below. Informational only — not medical advice.
Amitriptyline is a non-selective monoamine reuptake inhibitor that blocks neuronal reuptake of serotonin and norepinephrine by inhibiting their respective membrane transporters. This potentiation of monoaminergic neurotransmission underlies its antidepressant activity. TGA-approved indications are treatment and maintenance treatment of major depression, and nocturnal enuresis where organic pathology has been excluded.
The elimination half-life is approximately 21–22 hours, with its active metabolite nortriptyline having a half-life of around 26 hours. Amitriptyline is metabolised via cytochrome P450 2D6; concomitant use with CYP2D6 inhibitors (quinidine, cimetidine) or other CYP2D6 substrates (many antidepressants, phenothiazines, Type 1C antiarrhythmics such as flecainide) may require dose adjustment of either agent. Amitriptyline is contraindicated with monoamine oxidase inhibitors (including selegiline) and with cisapride due to risk of QT prolongation and cardiac arrhythmias, and is not recommended during the acute recovery phase following myocardial infarction. Contraindication also applies in patients with prior hypersensitivity to amitriptyline.
Common adverse effects include tachycardia, palpitations, orthostatic hypotension, somnolence, and dry mouth. Serious adverse effects include suicidal thoughts or behaviour, bone marrow depression (including agranulocytosis), tardive dyskinesia, severe cutaneous adverse reactions (including DRESS), and torsades de pointes.
Working under the parallel aged-care framework? Aged-care equivalent →
Curated subset. The full adverse-effect list is in the TGA Product Information; click any citation above to open it.
“Concomitant use of tricyclic antidepressants with medicines that can inhibit cytochrome P450 2D6 (e.g. quinidine; cimetidine) and those that are substrates for P450 2D6 (many other antidepressants, phenothiazines, and the Type 1C antiarrhythmics, e.g. flecainide) may require lower doses than usually prescribed for either the tricyclic antidepressant or the other medicine.”