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November 22, 2025
Brand Name :
vivactil
Synonyms :
protriptyline
Class :
Antidepressants
Dosage Forms & StrengthsÂ
TabletÂ
5mgÂ
10mgÂ
Initial dose-10mg/day and increase the dose upward every 5-7 days then,
15-60mg/day orally every 6-8 hours
Do not exceed 60mg/day
Dosage Forms & StrengthsÂ
TabletÂ
5mgÂ
10mgÂ
<12 years: Safety and efficacy not established
>12 years: 15-20mg/day orally every day
Dosage Forms & StrengthsÂ
TabletÂ
5mgÂ
10mgÂ
Initial dose: 5 mg orally every day
Maintenance dose: 5-10mg every 3-7 days when necessary
may enhance the vasopressor effect of alpha-/beta-agonists
may increase the metabolism of tricyclic antidepressants
may increase the metabolism of tricyclic antidepressants
may increase the metabolism of tricyclic antidepressants
may increase the metabolism of tricyclic antidepressants
may increase the metabolism of tricyclic antidepressants
They may increase the vasopressor effect when combined with Alpha-/Beta-Agonists
They may increase the vasopressor effect when combined with Alpha-/Beta-Agonists
They may increase the vasopressor effect when combined with Alpha-/Beta-Agonists
They may increase the vasopressor effect when combined with Alpha-/Beta-Agonists
They may increase the vasopressor effect when combined with Alpha-/Beta-Agonists
They may increase the vasopressor effect when combined with Alpha-/Beta-Agonists
They may increase the vasopressor effect when combined with Alpha-/Beta-Agonists
They may increase the vasopressor effect when combined with Alpha-/Beta-Agonists
They may increase the vasopressor effect when combined with Alpha-/Beta-Agonists
They may increase the vasopressor effect when combined with Alpha-/Beta-Agonists
may decrease the antihypertensive effect when combined with alpha2-agonists
may have an increased Effect of CNS depressant when combined with serotonergic opioids
may have an increased Effect of CNS depressant when combined with serotonergic opioids
may have an increased Effect of CNS depressant when combined with serotonergic opioids
may have an increased Effect of CNS depressant when combined with serotonergic opioids
may have an increased Effect of CNS depressant when combined with serotonergic opioids
may have an increased Effect of CNS depressant when combined with serotonergic opioids
may have an increased Effect of CNS depressant when combined with serotonergic opioids
may have an increased Effect of CNS depressant when combined with serotonergic opioids
may have an increased Effect of CNS depressant when combined with serotonergic opioids
acrivastine and pseudoephedrineÂ
may increase the vasopressor effect of alpha/beta agonists
methyldopa/hydrochlorothiazideÂ
may decrease the antihypertensive effect of alfa 2 agonist
may increase the CNS depressant effect of CNS depressants
may increase the CNS depressant effect of CNS depressants
may increase the vasopressor effect of Alpha-/Beta-Agonists
may enhance the metabolism when combined with tricyclic antidepressants
may enhance the metabolism when combined with tricyclic antidepressants
may enhance the metabolism when combined with tricyclic antidepressants
may enhance the metabolism when combined with tricyclic antidepressants
may enhance the metabolism when combined with tricyclic antidepressants
may enhance the risk of CNS depression when combined with each other
may enhance the risk of CNS depression when combined with each other
may enhance the risk of CNS depression when combined with each other
may enhance the risk of CNS depression when combined with each other
may enhance the risk of CNS depression when combined with each other
may enhance the risk of CNS depression when combined with each other
may enhance the risk of CNS depression when combined with each other
may enhance the metabolism when combined with tricyclic antidepressants
may enhance the metabolism when combined with tricyclic antidepressants
may enhance the metabolism when combined with tricyclic antidepressants
may enhance the metabolism when combined with tricyclic antidepressants
may enhance the metabolism when combined with tricyclic antidepressants
may have an increased Effect of CNS depressant when combined with serotonergic anorectic drugs
carbinoxamine: it may increase the risk of QTc prolongation agents
capsaicin: it may increase the risk of QTc prolongation agents
benzydamine: it may increase the risk of QTc prolongation agents
rosoxacin: it may increase the risk of QTc prolongation agents
may have an increased thrombogenic effect when combined with c1 inhibitors
may have an increased thrombogenic effect when combined with c1 inhibitors
bazedoxifene/conjugated estrogens
may have an increased thrombogenic effect when combined with c1 inhibitors
may have an increased thrombogenic effect when combined with c1 inhibitors
may have an increased thrombogenic effect when combined with c1 inhibitors
may decrease the therapeutic effect when combined with radiopharmaceutical iobenguane products
may decrease the therapeutic effect when combined with radiopharmaceutical iobenguane products
may decrease the therapeutic effect when combined with radiopharmaceutical iobenguane products
may decrease the therapeutic effect when combined with radiopharmaceutical iobenguane products
may decrease the therapeutic effect when combined with radiopharmaceutical iobenguane products
may have an increased serotonergic effect when combined with tricyclic antidepressants
may increase the serotonergic effect of Monoamine Oxidase Inhibitors
may increase the serotonergic effect of Monoamine Oxidase Inhibitors
amoxicillin: it may increase the risk of QTc prolongation agents
anagrelide: it may increase the risk of QTc prolongation agents
antipyrine: it may increase the risk of QTc prolongation agents
bendamustine: it may increase the risk of QTc prolongation agents
may increase the adverse/toxic effect of NSAIDs
may increase the adverse/toxic effect of NSAIDs
may increase the adverse/toxic effect of NSAIDs
may increase the adverse/toxic effect of NSAIDs
may increase the adverse/toxic effect of NSAIDs
they increase the efficacy of alpha 1-agonists
may increase the therapeutic effect
may increase the therapeutic effect
may increase the therapeutic effect
may increase the therapeutic effect
may increase the therapeutic effect
may enhance the risk of adverse effect of amphetamines
may enhance the risk of adverse effect of amphetamines
may enhance the risk of adverse effect of amphetamines
may enhance the risk of adverse effect of amphetamines
may enhance the risk of adverse effect of amphetamines
may increase the vasopressor effect
may increase the vasopressor effect
may increase the risk of adverse effects
may increase the risk of adverse effects
may increase the risk of adverse effects
may increase the risk of adverse effects
may increase the risk of adverse effects
may enhance the cholinergic blocking effect of other tricyclic antidepressants
may enhance the cholinergic blocking effect of other tricyclic antidepressants
may enhance the cholinergic blocking effect of other tricyclic antidepressants
may enhance the cholinergic blocking effect of other tricyclic antidepressants
may enhance the cholinergic blocking effect of other tricyclic antidepressants
may enhance the cholinergic blocking effect of other tricyclic antidepressants
may enhance the cholinergic blocking effect of other tricyclic antidepressants
may have an increasingly adverse effect when combined with beta2-agonists
may have an increasingly adverse effect when combined with beta2-agonists
may have an increasingly adverse effect when combined with beta2-agonists
may have an increasingly adverse effect when combined with beta2-agonists
may have an increasingly adverse effect when combined with beta2-agonists
tricyclic antidepressants: they may increase the toxic effect of Beta2-Agonists
tricyclic antidepressants: they may increase the toxic effect of Beta2-Agonists
tricyclic antidepressants: they may increase the toxic effect of Beta2-Agonists
tricyclic antidepressants: they may increase the toxic effect of Beta2-Agonists
tricyclic antidepressants: they may increase the toxic effect of Beta2-Agonists
tricyclic antidepressants: they may increase the toxic effect of Beta2-Agonists
tricyclic antidepressants: they may increase the toxic effect of Beta2-Agonists
tricyclic antidepressants: they may increase the toxic effect of Beta2-Agonists
relugolix/​estradiol/​norethindrone
androgens increase the effect of thrombogenesis of C1 inhibitors
relugolix/estradiol/norethindrone
androgens increase the effect of thrombogenesis of C1 inhibitors
androgens increase the effect of thrombogenesis of C1 inhibitors
androgens increase the effect of thrombogenesis of C1 inhibitors
androgens increase the effect of thrombogenesis of C1 inhibitors
tricyclic antidepressants: they may increase the toxic effect of Nonsteroidal Anti-Inflammatory Agents
tricyclic antidepressants: they may increase the toxic effect of Nonsteroidal Anti-Inflammatory Agents
tricyclic antidepressants: they may increase the toxic effect of Nonsteroidal Anti-Inflammatory Agents
tricyclic antidepressants: they may increase the toxic effect of Nonsteroidal Anti-Inflammatory Agents
tricyclic antidepressants: they may increase the toxic effect of Nonsteroidal Anti-Inflammatory Agents
tricyclic antidepressants: they may increase the toxic effect of Nonsteroidal Anti-Inflammatory Agents
tricyclic antidepressants: they may increase the toxic effect of Nonsteroidal Anti-Inflammatory Agents
tricyclic antidepressants: they may increase the toxic effect of Nonsteroidal Anti-Inflammatory Agents
tricyclic antidepressants: they may increase the toxic effect of Nonsteroidal Anti-Inflammatory Agents
tricyclic antidepressants: they may increase the toxic effect of Nonsteroidal Anti-Inflammatory Agents
may have an increased therapeutic effect when combined with alpha1-agonists
bunazosin (Not available in the United States)
may have an increased therapeutic effect when combined with alpha1-agonists
may have an increased therapeutic effect when combined with alpha1-agonists
may have an increased therapeutic effect when combined with alpha1-agonists
may have an increased therapeutic effect when combined with alpha1-agonists
may have an increased therapeutic effect when combined with alpha1-agonists
protriptyline: they may enhance the serum concentration of CYP2D6 Inhibitors
protriptyline: they may enhance the serum concentration of CYP2D6 Inhibitors
protriptyline: they may enhance the serum concentration of CYP2D6 Inhibitors
protriptyline: they may enhance the serum concentration of CYP2D6 Inhibitors
protriptyline: they may enhance the serum concentration of CYP2D6 Inhibitors
adverse effects of beta2 agonists are increased with tricyclic antidepressants
adverse effects of beta2 agonists are increased with tricyclic antidepressants
When bufexamac is used together with protriptyline, this leads to enhanced risk or seriousness of gastrointestinal bleeding
tricyclic antidepressants: they may enhance the serum concentration of CYP3A4 inducers
tricyclic antidepressants: they may enhance the serum concentration of CYP3A4 inducers
tricyclic antidepressants: they may enhance the serum concentration of CYP3A4 inducers
tricyclic antidepressants: they may enhance the serum concentration of CYP3A4 inducers
tricyclic antidepressants: they may enhance the serum concentration of CYP3A4 inducers
tricyclic antidepressants may become more arrhythmogenic when used with thyroid products
tricyclic antidepressants may have a more stimulatory impact when used with thyroid products
tricyclic antidepressants may become more arrhythmogenic when used with thyroid products
tricyclic antidepressants may have a more stimulatory impact when used with thyroid products
tricyclic antidepressants may become more arrhythmogenic when used with thyroid products
tricyclic antidepressants may have a more stimulatory impact when used with thyroid products
tricyclic antidepressants may become more arrhythmogenic when used with thyroid products
tricyclic antidepressants may have a more stimulatory impact when used with thyroid products
may have an increasingly adverse effect when combined with beta2-agonists
may have an increasingly adverse effect when combined with beta2-agonists
may have an increasingly adverse effect when combined with beta2-agonists
When protriptyline is used together with flunoxaprofen, this leads to enhanced risk or seriousness of gastrointestinal bleeding
may have an increased therapeutic effect when combined with alpha1-agonists
may have an increasingly adverse effect when combined with beta2-agonists
may have an increasingly adverse effect when combined with beta2-agonists
may have an increasingly adverse effect when combined with beta2-agonists
when used together, entrectinib and protriptyline both increase the QTc interval
QT-prolonging Agents may enhance the QTc-prolonging effect of haloperidol
fexinidazole may enhance the QTc-prolonging effect of QT-prolonging Agents
may increase the therapeutic effect of alfa one agonist
linezolid may enhance the serotonergic effect of tricyclic antidepressants
may enhance the adverse/toxic effect of tricyclic antidepressants
may increase the toxic effect of amphetamines
may increase the toxic effect of beta2 agonists
may increase the toxic effect of beta2 agonists
may increase the serum concentrations of CYP2D6 inhibitors
may increase the toxic effect of nonsteroidal anti-inflammatory agents
may increase the serotonergic effects
may increase the serotonergic effects
may increase the serotonergic effects
may increase the serotonergic effects
may increase the serotonergic effects
may increase the serotonergic effects
may increase the serotonergic effects
may increase the serotonergic effects
may increase the serotonergic effects
may increase the serotonergic effects
may increase the serotonergic effects
may increase the serotonergic effects
may increase the serotonergic effects
may increase the serotonergic effects
may increase the serotonergic effects
may increase the serotonergic effects
may increase the serotonergic effects
may increase the serotonergic effects
may increase the serotonergic effects
may increase the serotonergic effects
may increase the risk of adverse effects
may increase the risk of adverse effects
may increase the risk of adverse effects
may increase the risk of adverse effects
may increase the risk of adverse effects
may increase the risk of adverse effects
may enhance the arrhythmogenic effect
may enhance the arrhythmogenic effect
may enhance the arrhythmogenic effect
may enhance the arrhythmogenic effect
may enhance the arrhythmogenic effect
may enhance the arrhythmogenic effect
may enhance the arrhythmogenic effect
may enhance the arrhythmogenic effect
may enhance the cholinergic blocking effect of other tricyclic antidepressants
may enhance the cholinergic blocking effect of other tricyclic antidepressants
may enhance the cholinergic blocking effect of other tricyclic antidepressants
may enhance the cholinergic blocking effect of other tricyclic antidepressants
may enhance the cholinergic blocking effect of other tricyclic antidepressants
cyproterone and ethinyl estradiolÂ
may increase the thrombogenic effect of Estrogen Derivatives
may have an increased thrombogenic effect when combined with c1 inhibitors
may have an increased thrombogenic effect when combined with c1 inhibitors
may enhance the metabolism when combined with tricyclic antidepressants
may enhance the severity of gastrointestinal bleeding when combined
may enhance the severity of gastrointestinal bleeding when combined
may enhance the severity of gastrointestinal bleeding when combined
may enhance the severity of gastrointestinal bleeding when combined
may enhance the severity of gastrointestinal bleeding when combined
may enhance the severity of gastrointestinal bleeding when combined
may enhance the severity of gastrointestinal bleeding when combined
may enhance the severity of gastrointestinal bleeding when combined
may enhance the severity of gastrointestinal bleeding when combined
may enhance the severity of gastrointestinal bleeding when combined
cinnarizine and dimenhydrinateÂ
this combination may raise the efficacy/effects of tricyclic antidepressants
it may enhance the QTc-prolonging effect
it may enhance the QTc-prolonging effect
it may enhance the QTc-prolonging effect
it may enhance the QTc-prolonging effect
it may enhance the QTc-prolonging effect
it increases the toxicity of atropine through an unknown mechanism
tricyclic antidepressants increase the CNS depression effect of serotonergic opioids
tricyclic antidepressants increase the CNS depression effect of serotonergic opioids
tricyclic antidepressants increase the CNS depression effect of serotonergic opioids
tricyclic antidepressants increase the CNS depression effect of serotonergic opioids
Mechanism of actionÂ
It is thought to work by increasing the neurotransmitters in the brain, such as norepinephrine and serotonin. These neurotransmitters are involved in regulating mood and increasing their levels can help to alleviate symptoms of depression. Â
SpectrumÂ
It has a broad spectrum of activity, meaning they can treat a wide range of psychiatric conditions. The most common use of protriptyline is to treat depression, but it can also treat conditions such as anxiety, insomnia, and chronic pain.Â
Frequency defined:Â Â
1-10%Â
FatigueÂ
AgitationÂ
Blurred visionÂ
LethargyÂ
Dry mouthÂ
NauseaÂ
SweatingÂ
SedationÂ
HeadacheÂ
InsomniaÂ
WeaknessÂ
AnxietyÂ
VomitingÂ
Weight changeÂ
Frequency not definedÂ
TinnitusÂ
SeizureÂ
Orthostatic hypotensionÂ
TachycardiaÂ
AgranulocytosisÂ
EosinophiliaÂ
Increased LFT’sÂ
RashÂ
ConfusionÂ
DizzinessÂ
ParesthesiaÂ
SuicideÂ
ECG changesÂ
Paralytic ileusÂ
ThrombocytopeniaÂ
LeukopeniaÂ
Sexual dysfunctionÂ
Black box warningÂ
It is a tricyclic antidepressant medication. It is not approved by the FDA for use in children and adolescents under 18 because of the increased risk of suicide and suicidal thoughts associated with its use in this population. It is important to note that the medication should only be used in children and adolescents under the close supervision of a healthcare professional, and patients should be closely monitored for any signs of suicidal thoughts or behaviourÂ
ContraindicationsÂ
CautionsÂ
Pregnancy consideration: CÂ
Lactation: Excretion of the drug in human breast milk is unknownÂ
Pregnancy category:Â
Category A: well-controlled and Satisfactory studies show no risk to the fetus in the first or later trimester.  Â
Category B: there was no evidence of risk to the fetus in animal studies, and there were not enough studies on pregnant women.Â
Category C: there was evidence of risk of adverse effects in animal reproduction studies, and no adequate evidence in human studies must take care of potential risks in pregnant women.   Â
Category D: adequate data available with sufficient evidence of human fetal risk from various platforms, but despite the potential risk, and used only in emergency cases for potential benefits.   Â
Category X: Drugs listed in this category outweigh the risks over benefits. Hence these categories of drugs need to be avoided by pregnant women.   Â
Category N: There is no data available for the drug under this category.Â
PharmacologyÂ
The drugs work by inhibiting the reuptake of the neurotransmitters serotonin and norepinephrine in the central nervous system, which increases the concentration of these neurotransmitters in the brain. This mechanism of action is thought to be responsible for the therapeutic effects of these drugs in conditions such as depression and anxiety.Â
 PharmacodynamicsÂ
It is a tricyclic antidepressant (TCA) that works by increasing the levels of neurotransmitters in the brain, specifically norepinephrine and serotonin. It also has some antihistamine and anticholinergic properties. It is used to treat depression and other psychiatric conditions. It is usually taken orally, and its effects can take several weeks to become fully apparent. Some common side effects include dry mouth, drowsiness, and constipation. More severe side effects include increased heart rate, high blood pressure, and changes in blood sugar levels. Â
PharmacokineticsÂ
AbsorptionÂ
The half-life of protriptyline is 54-92 hours, meaning that it takes that amount of time for half of the drug to be eliminated from the body. The peak plasma time, or the time it takes for the drug to reach its highest concentration in the blood, is 24-30 hours.Â
DistributionÂ
It has a high protein binding of 92%, the drug is bound to proteins in the blood. It is completely absorbed when taken orally.Â
MetabolismÂ
It is metabolized in the liver through oxidation, hydroxylation, and glucuronidation. Â
Elimination/excretionÂ
It is then excreted primarily through the urine. It’s important to note that these values may vary depending on individual factors such as age, weight, and other medications being taken.Â
AdministrationÂ
protriptyline is typically administered orally in tablet form. The usual starting dose is 10 mg per day, which can be increased by 10 mg every 3-7 days until the desired therapeutic effect is achieved. The maximum recommended dose is 40 mg per day. It is typically taken once a day at bedtime to minimize the risk of side effects such as drowsiness.
It’s also important to note that treatment with protriptyline should be started under the close supervision of a healthcare professional, and the patient should be monitored regularly for side effects and therapeutic efficacy. It may take several weeks to realize the full therapeutic effects of protriptyline. It’s also important to note that protriptyline should not be used in children and with caution in elderly patients and patients with a history of cardiovascular disease.Â
Patient information leafletÂ
Generic Name: protriptylineÂ
Pronounced: [ proe-TRIP-ti-leen ]Â
Why do we use protriptyline?Â
It is primarily used as an antidepressant to treat major depressive disorder and other psychiatric conditions such as attention deficit hyperactivity disorder (ADHD) and chronic pain. It increases neurotransmitters, specifically norepinephrine and serotonin, in the brain.Â
It is also sometimes used as a secondary treatment for other conditions, such as enuresis (bedwetting) in children and chronic headaches. Â