Amoxapine - a tricyclic antidepressant with antipsychotic effects

Amoxapine increases the synaptic concentration of serotonin and norepinephrine in the central nervous system by inhibiting their reuptake by the presynaptic neuronal membrane pump.

It is used to treat patients with unipolar major depression that may include depression with psychotic features.

 

Adult dose :

Major Unipolar depressive disorder:

    • 25 - 50 mg orally 1 - 3 times a day
    • The dose may be increased over 1 -2 weeks to the usual dose of 200 - 300 mg/day in 2 - 3 divided doses if tolerated.
    • The maximum daily dose for outpatients use is 400 mg per day and for hospitalized patients is 600 mg/day.
    • Higher doses should be used with caution in patients with refractory depression with no history of seizures.
    • Doses greater than 300 mg per day should be given in divided doses.
  • Discontinuation of therapy:

    • Discontinuation of therapy should be gradual over 2 - 4 weeks to minimize the incidence of withdrawal symptoms.
    • Patients who develop intolerable withdrawal symptoms should resume the previously prescribed dose and then titrate the drug more gradually.
    • Patients with a history of discontinuation syndrome may benefit from a more gradual tapering regimen over at least 3 months.
  • Switching antidepressants:

    • Although data regarding switching strategies from one antidepressant to another antidepressant is limited, some of the important points are listed here:
      • Cross-titration: This method is usually followed especially when amoxapine or another antidepressant has been used for more than 2 – 4 weeks. One drug is gradually tapered while the dose of the other drug is increased gradually at the same time.
      • Direct switch: Direct switch is the abrupt discontinuation of one drug and initiating the other drug at an equivalent dose. This method may be appropriate in cases where the drug has been used for less than 1 – 2 weeks or when the drug is discontinued because of the adverse effects.
  • Switching to or from an MAOI:

    • At least a 14 days drug-free interval should be allowed when switching from an MAOI to amoxapine and vice versa.
    • Cross titration is contraindicated when switching from an MAOI to an SSRI and vice versa.

Dose in children :

 Not recommended

 

Pregnancy Risk Factor C

 

 

 

Amoxapine use during breastfeeding:

 

 

  • It can be excreted in breast milk so it should not be used by breastfeeding mothers.

 

Renal Dose :

Adjustment in the dose has not been recommended. It should be avoided in severe renal impairment. 

Dose in Liver disease :

Adjustment in the dose has not been recommended. It should be avoided in severe hepatic impairment. 

 

Common Side Effects of Amoxapine Include:

  • Central nervous system:
    • Drowsiness
  • Gastrointestinal:
    • Xerostomia
    • Constipation

Less Common Side Effects of Amoxapine Include:

  • Cardiovascular:
    • Edema
    • Palpitations
  • Central nervous system:
    • Anxiety,
    • Ataxia,
    • Confusion,
    • Dizziness,
    • EEG pattern changes,
    • Excitement,
    • Fatigue,
    • Headache,
    • Insomnia,
    • Nervousness,
    • Nightmares,
    • Restlessness
  • Dermatologic:
    • Diaphoresis,
    • Skin rash
  • Endocrine & metabolic:
    • Increased serum prolactin
  • Gastrointestinal:
    • Increased appetite,
    • Nausea
  • Neuromuscular & skeletal:
    • Tremor,
    • Weakness
  • Ophthalmic:
    • Blurred vision

 

Contraindication to Amoxapine Include:

 

 

  • Allergy reactions to amoxapine or dibenzoxazepine compound, or any component of the formulation
  • Within 14 days of MAOIs, coadministration
  • Acute recovery phase following myocardial infarction

Warnings and Precautions

    • Suicidal thoughts/behavior [US Boxed Warning]
      • AmoxapineThis product is not FDA-approved for use in children.
      • Antidepressants increase the risk of suicidal thinking and behavior in children, adolescents, and young adults (18 to 24 years of age) with major depressive disorder (MDD) and other psychiatric disorders.
      • Families and caregivers should be informed to report any changes in behavior and watch for the following behaviors:
        • Anxiety
        • Agitation
        • Panic attacks
        • insomnia,
        • irritability,
        • Hostility
        • Impulsivity
        • Akathisia
        • Hypomania is a condition that causes depression.
        • mania.
      • For any clinical changes, behavior changes, or suicidality, the patient should be closely monitored during the first 1 - 2 month.
      • Stopping the medication should be done if you have suicidal thoughts or are experiencing worsening depression.
    • Anticholinergic effects
      • You should use it with caution when treating the following patients:
        • Reduced gastrointestinal motility
        • Increased intraocular pressure
        • Narrow-angle glaucoma
        • Paralytic ileus
        • Urinary retention
        • Benign prostatic hyperplasia
        • xerostomia
        • Visual problems
      • It has a higher degree of anticholinergic effect than other antidepressants.
    • CNS depression:
      • CNS depression can result in mental or physical impairments from Amitriptyline. It is important to warn patients about tasks that require mental alertness.
      • It is mildly sedative compared to antidepressants.
    • Extrapyramidal symptoms:
      • Extrapyramidal symptoms may occur, which could include the following:
        • Pseudoparkinsonism
        • Acute dystonic reactions
        • Akathisia
        • Tardive dyskinesia
      • Extrapyramidal symptoms are most likely to occur if you use high doses and frequent doses.
      • Tardive dyskinesia can be irreversible. Treatment must be stopped immediately.
      • The clinical signs of tardive dyskinesia may be masking by antipsychotics.
    • Fractures
      • Undiagnosed bone pain, swelling, bruise, or tenderness after taking amitriptyline should prompt a physician to investigate for bone fractures.
      • TCAs have been linked to fragility fractures in the long-term.
    • Neuroleptic malignant syndrome (NMS):
      • Its use could be linked to the neuroleptic malignant disorder.
      • Monitor the patient for changes in mental state, muscle rigidity, fever, or autonomic instability.
    • Ocular effects
      • Because of pupillary dilation, it may worsen angle-closure glaucoma.
    • Orthostatic hypotension
      • Patients with hypovolemia, cerebrovascular disease, and cardiovascular disease should be cautious.
    • Cardiovascular disease
    • Diabetes:
      • It can alter glucose regulation. Patients with diabetes should use it with caution.
    • Hepatic impairment
      • Patients with liver disease should be cautious.
    • Hypomania and mania:
      • For the treatment of bipolar disorder, it is not FDA approved. It is important to screen patients for signs of hypomania or mania, and then treat them accordingly.
    • Renal impairment
      • Patients suffering from kidney disease should be cautious.
    • Seizure disorder:
      • Patients at high risk for seizures such as those with seizures due to head trauma, brain damage or alcoholism should be cautious.

 

Amoxapine: Drug Interaction

Note: Drug Interaction Categories:

  • Risk Factor C: Monitor When Using Combination
  • Risk Factor D: Consider Treatment Modification
  • Risk Factor X: Avoid Concomitant Use
    •  

    Risk Factor C (Monitor therapy).

    Acetylcholinesterase inhibitors Anticholinergic Agents may have a decreased therapeutic effect. Anticholinergic Agents can decrease the therapeutic effects of Acetylcholinesterase inhibitors.
    Ajmaline High risk of Inhibitors increasing serum concentrations of CYP2D6 Substrates
    Alcohol (Ethyl) CNS Depressants can increase the CNS depressant effects of Alcohol (Ethyl).
    Alizapride CNS Depressants may increase the CNS depressant effects.
    Alpha1-Agonists Tricyclic Antidepressants could decrease the therapeutic effects of Alpha1Agonists. Tricyclic Antidepressants could decrease the vasopressor effects of Alpha1Agonists. Tricyclic Antidepressants could enhance Alpha1-Agonists' therapeutic effects. Tricyclic Antidepressants could enhance Alpha1-Agonists' vasopressor effects.
    Alpha2-Agonists (Ophthalmic). Tricyclic Antidepressants could decrease the therapeutic effects of Alpha2-Agonists.
    Altretamine May increase the orthostatic hypotensive effects of Tricyclic Antidepressants.
    Amantadine Anticholinergic Agents may have an enhanced anticholinergic effect.
    Amezinium Might increase the toxic/adverse effects of Tricyclic Antidepressants.
    Amifampridine Agents with Seizure Threshold Lower Potential can enhance the neuroexcitatory or seizure-potentiating effects of Amifampridine.
    Amphetamines Tricyclic Antidepressants can enhance Amphetamines' stimulatory effects. Tricyclic Antidepressants can also increase the cardiovascular effects of Amphetamines.
    Anticholinergic Agents Other Anticholinergic Agents may have an adverse/toxic effect.
    Antiemetics (5HT3 Antagonists) This may increase the serotonergic effects of Serotonin Activators. This could lead to serotonin syndrome.
    Antipsychotic Agents Antipsychotic Agents may have a greater adverse/toxic effect if they are regulated with serotonin modulators. Serotonin modulators can increase dopamine blockade and, therefore, may increase the risk of developing neuroleptic malignant syndrome. Serotonin modulators may have a serotonergic effect that is enhanced by antipsychotic agents. This could lead to serotonin syndrome.
    Beta2-Agonists Tricyclic Antidepressants can increase the toxic/adverse effect of Beta2Agonists.
    Botulinum Toxin-Containing Products Anticholinergic Agents may have an enhanced anticholinergic effect.
    Brexanolone CNS Depressants can increase the CNS depressant effects of Brexanolone.
    Brimonidine (Topical) CNS Depressants may increase the CNS depressant effects.
    Cannabidiol CNS Depressants may increase the CNS depressant effects.
    Cannabis CNS Depressants may increase the CNS depressant effects.
    CarBAMazepine Might decrease serum Tricyclic Antidepressants.
    Chloral Betaine Anticholinergic Agents may have an adverse/toxic effect.
    Chlorphenesin Carbamate CNS Depressants may have an adverse/toxic effect that can be exacerbated by them.
    Cimetidine May reduce the metabolism of Tricyclic Antdepressants.
    CloBAZam High risk of Inhibitors increasing serum concentrations of CYP2D6 Substrates
    CNS Depressants Can increase the toxic/adverse effects of CNS Depressants.
    Cobicistat High risk of Inhibitors increasing serum concentrations of CYP2D6 Substrates
    Moderate CYP2D6 inhibitors Might decrease metabolism of CYP2D6 substrates (High Risk with Inhibitors).
    Darunavir High risk of Inhibitors increasing serum concentrations of CYP2D6 Substrates
    Desmopressin Tricyclic Antidepressants can increase the toxic/adverse effects of Desmopressin.
    Dexmethylphenidate Might increase the toxic/adverse effects of Tricyclic Antidepressants. The serum concentrations of Tricyclic Antidepressants may be increased by Dexmethylphenidate.
    Dimethindene (Topical). CNS Depressants may increase the CNS depressant effects.
    Doxylamine CNS Depressants may have a greater depressant effect on the brain. Management: The manufacturer of Diclegis (doxylamine/pyridoxine), intended for use in pregnancy, specifically states that use with other CNS depressants is not recommended.
    Dronabinol CNS Depressants may increase the CNS depressant effects.
    DULoxetine This may increase the serotonergic effects of Tricyclic Antidepressants. This could lead to serotonin syndrome. DULoxetine could decrease the metabolism Tricyclic Antidepressants.
    Esketamine CNS Depressants may increase the CNS depressant effects.
    Gastrointestinal Agents (Prokinetic) Anticholinergic Agents can reduce the therapeutic effects of Gastrointestinal Agents (Prokinetic).
    Glucagon Anticholinergic agents may increase the toxic/adverse effects of Glucagon. Particularly, there may be an increase in the likelihood of gastrointestinal adverse reactions.
    Guanethidine Tricyclic Antidepressants can reduce the therapeutic effects of Guanethidine.
    HydrOXYzine CNS Depressants may increase the CNS depressant effects.
    Imatinib High risk of Inhibitors increasing serum concentrations of CYP2D6 Substrates
    Ioflupane I 123 Amoxapine can decrease the diagnostic effectiveness of Ioflupane I123.
    Itopride Itopride's therapeutic effects may be diminished by anticholinergic agents.
    Kava Kava CNS Depressants may have an adverse/toxic effect that can be exacerbated by them.
    Lumefantrine High risk of Inhibitors increasing serum concentrations of CYP2D6 Substrates
    Magnesium Sulfate CNS Depressants may increase the CNS depressant effects.
    Metaxalone This may increase the serotonergic effects of Serotonin Activators. This could lead to serotonin syndrome.
    Methylphenidate May increase the toxic/adverse effects of Tricyclic Antidepressants. The serum concentrations of Tricyclic Antidepressants may be increased by Methylphenidate.
    Methylphenidate Can increase the toxic/adverse effects of Serotonin-Modulators. In particular, there may be an increase in the risk of serotonin syndrome and serotonin toxicities.
    MetyroSINE MetyroSINE may have a sedative effect that can be enhanced by CNS depressants.
    MetyroSINE Might increase the toxic/adverse effects of Tricyclic Antidepressants.
    Mianserin Anticholinergic Agents may have an enhanced anticholinergic effect.
    Minocycline CNS Depressants may increase the CNS depressant effects.
    Mirabegron Anticholinergic agents may increase the toxic/adverse effects of Mirabegron.
    Mirtazapine CNS Depressants can increase the CNS depressant effects of Mirtazapine.
    Nabilone CNS Depressants may increase the CNS depressant effects.
    Nicorandil Tricyclic Antidepressants can increase the hypotensive effects of Nicorandil.
    Nitroglycerin The absorption of Nitroglycerin may be decreased by anticholinergic agents. Anticholinergic Agents may reduce the dissolution sublingual nitroglycerin tablet, which could impair or slow down nitroglycerin absorbtion.
    Panobinostat High risk of Inhibitors increasing serum concentrations of CYP2D6 Substrates
    Peginterferon Alfa-2b High risk with inhibitors. May lower serum concentration of CYP2D6 substrates. Peginterferon Alf-2b could increase serum concentrations of CYP2D6 Substrates.
    Perhexiline Perhexiline may be increased by CYP2D6 Substrates. Perhexiline can increase serum concentrations of CYP2D6 substrates (High Risk with Inhibitors).
    Piribedil CNS Depressants could increase the CNS depressant effects of Piribedil.
    Pitolisant Tricyclic Antidepressants can reduce the therapeutic effects of Pitolisant.
    Pramipexole Pramipexole may have a greater sedative effect if it is combined with CNS depressants.
    Protease inhibitors May increase serum Tricyclic Antidepressants.
    QuiNINE High risk of Inhibitors increasing serum concentrations of CYP2D6 Substrates
    Ramosetron Ramosetron's constipating effects may be enhanced by anticholinergic agents.
    ROPINIRole CNS Depressants can increase the sedative effects of ROPINIRole.
    Rotigotine CNS Depressants can increase the sedative effects of Rotigotine.
    Rufinamide CNS Depressants may have an adverse/toxic effect that can be exacerbated by this. Particularly, dizziness and sleepiness may be increased.
    Selective Serotonin Reuptake inhibitors CNS Depressants can increase the toxic/adverse effects of Selective Serotonin Resuptake Inhibitors. Particularly, psychomotor impairment could be increased.
    Serotonin Modulators This may increase the toxic/adverse effects of other Serotonin Activators. Serotonin syndrome can develop. Exceptions: Nicergoline; Tedizolid.
    Sodium Phosphates Tricyclic Antidepressants can increase the toxic/adverse effects of Sodium Phosphates. Patients with severe sodium phosphate-induced fluid/electrolyte abnormalities may have a higher risk of losing consciousness and seizure.
    Sulfonylureas Cyclic Antidepressants can increase the hypoglycemic effects of Sulfonylureas.
    Tedizolid This may increase the serotonergic effects of Serotonin Activators. This could lead to serotonin syndrome.
    Tetrahydrocannabinol CNS Depressants may increase the CNS depressant effects.
    Tetrahydrocannabinol, and Cannabidiol CNS Depressants may increase the CNS depressant effects.
    Thiazide and Thiazide -Like Diuretics Anticholinergic Agents can increase serum Thiazide or Thiazide-Like Diuretics.
    Thyroid Products May increase the arrhythmogenic effects of Tricyclic Antidepressants. Thyroid Products can increase the stimulatory effects of Tricyclic Antidepressants.
    Topiramate Topiramate's toxic/adverse effects may be exacerbated by anticholinergic agents.
    Trimeprazine CNS Depressants may increase the CNS depressant effects.
    Valproate Products May increase serum Tricyclic Antidepressants.
    Vitamin K antagonists (eg warfarin) Tricyclic Antidepressants can increase the anticoagulant effects of Vitamin K Antagonists.
    Yohimbine Tricyclic Antidepressants can increase Yohimbine's serum concentration.

    Risk Factor D (Consider therapy modifications)

     
    Abiraterone Acetate High risk of Inhibitors causing an increase in serum concentrations of CYP2D6 substrates. When possible, avoid concurrent use of abiraterone and CYP2D6 Substrates with a narrow therapeutic index. If concurrent use cannot be avoided, closely monitor patients for signs/symptoms and treatment.
    Direct-Acting Alpha-/Beta Agonists Tricyclic Antidepressants can increase the vasopressor effects of Alpha/Beta-Agonists (Direct Acting). Patients on tricyclic antidepressants should avoid direct-acting alpha/beta-agonists. Monitor for increased pressure effects when combined and reduce the initial doses of alpha/beta-agonists.
    Alpha2-Agonists Tricyclic Antidepressants can reduce the antihypertensive effects of Alpha2Agonists. Management: Avoid this combination. Monitor for decreased alpha2-agonist effects if the combination is used. If you are discontinuing the use of an alpha2-agonist for a patient who is on a TCA, be careful. Lofexidine, Brimonidine (Ophthalmic), Apraclonidine are exceptions.
    Asunaprevir High risk of Inhibitors increasing serum concentrations of CYP2D6 Substrates
    Barbiturates May increase metabolism of Tricyclic Antdepressants.
    Blonanserin CNS Depressants can increase the CNS depressant effects of Blonanserin.
    Buprenorphine CNS Depressants can increase the CNS depressant effects of buprenorphine. Management: Consider reduced doses of other CNS depressants, and avoiding such drugs in patients at high risk of buprenorphine overuse/self-injection. Buprenorphine patches (Butrans) should be initiated at 5 mg/hr for adults when taken with other CNS depression drugs.
    Chlormethiazole CNS Depressants may increase the CNS depressant effects. Monitoring: Look out for signs of CNS depression. If a combination of chlormethiazole and other drugs is required, a reduced dose should be used.
    Cinacalcet It may increase serum levels of Tricyclic Antidepressants. Management: Look for alternatives whenever possible. These combinations should be monitored closely to ensure that there are no increased effects/toxicity or elevated serum levels (if testing is possible) of the tricyclic-antidepressant.
    Citalopram Tricyclic Antidepressants can increase the toxic/adverse effects of Citalopram. Tricyclic Antidepressants can increase Citalopram's serum concentration. Citalopram could increase serum levels of Tricyclic Depressants. Management: If possible, consider alternatives to this combination. When citalopram is used with a TCA, monitor for any adverse effects such as serotonin syndrome or QT-interval prolongation.
    Strong CYP2D6 inhibitors Might decrease metabolism of CYP2D6 substrates (High Risk with Inhibitors).
    Dacomitinib High risk of Inhibitors causing an increase in serum concentrations of CYP2D6 substrates. Management: Do not use dacomitinib concurrently with CYP2D6 Substrates that have a narrow therapeutic Index.
    Droperidol CNS Depressants may increase the CNS depressant effects. Management: Droperidol and other CNS agents, such as opioids, may be reduced or used in combination with droperidol. Separate drug interaction monographs provide more detail on exceptions to this monograph.
    Escitalopram Tricyclic Antidepressants can increase the toxic/adverse effects of Escitalopram. The serum concentrations of Tricyclic Antidepressants may be increased by Escitalopram. Management: If possible, consider alternatives to this combination. When a TCA is used with escitalopram, monitor for any adverse effects such as serotonin syndrome or QT-interval prolongation.
    Flunitrazepam CNS Depressants can increase the CNS depressant effects of Flunitrazepam.
    FLUoxetine Might increase the toxic/adverse effects of Tricyclic Antidepressants. FLUoxetine can increase serum levels of Tricyclic Antepressants. Management: If possible, consider alternatives to this combination. When fluoxetine is used with a TCA, monitor for any adverse effects such as serotonin syndrome or QT-interval prolongation.
    FluvoxaMINE Could increase the toxic/adverse effects of Tricyclic Antidepressants. FluvoxaMINE could increase serum levels of Tricyclic Antepressants. Management: If possible, consider alternatives to this combination. When a TCA is used with fluvoxamine, monitor for any adverse effects such as serotonin syndrome or QT-interval prolongation.
    HYDROcodone CNS Depressants can increase the CNS depressant effects of HYDROcodone. When possible, avoid concomitant use with hydrocodone, benzodiazepines, or other CNS depressionants. Combining these agents is not recommended unless there are other options. Limit the amount and duration of each drug when combined.
    Iohexol Agents with Seizure Threshold Lowering Potential can increase the toxic/adverse effects of Iohexol. The risk of seizures could be elevated. Management: Stop using agents that lower the seizure threshold 48 hrs before you start intrathecal iohexol. To resume these agents, wait at least 24 hours following the procedure. Consider using prophylactic anticonvulsants in non-elective procedures.
    Iomeprol Agents with Seizure Threshold Lowering Potential can increase the toxic/adverse effects of Iomeprol. The risk of seizures could be elevated. Management: Stop using agents that lower the seizure threshold 48 hrs before you start intrathecal iomeprol. To resume these agents, wait at least 24 hours following the procedure. Consider using prophylactic anticonvulsants in non-elective procedures.
    Iopamidol Agents with Seizure Threshold Lowering Potential can increase the toxic/adverse effects of Iopamidol. The risk of seizures could be elevated. Management: Stop using agents that lower the seizure threshold 48 hrs before you start intrathecal iopamidol. To resume these agents, wait at least 24 hours following the procedure. Consider using prophylactic anticonvulsants in non-elective procedures.
    Linezolid This may increase the serotonergic effects of Tricyclic Antidepressants. This could lead to serotonin syndrome. Management: If possible, consider other combinations. Linezolid should be initiated only if it is clinically approved.
    Linezolid This may increase the serotonergic effects of Serotonin Activators. This could lead to serotonin syndrome. Management: Serotonin syndrome/serotonin toxicemia can occur if serotonin modulators are stopped 2 weeks before linezolid is administered. Stop using serotonin modators immediately if you need to initiate linezolid immediately.
    Lithium May increase the neurotoxic effects of tricyclic antidepressants. You should exercise caution when using this combination. If combined treatment is clinically recommended, be sure to monitor for signs of serotonin toxicities/serotonin syndrome.
    Lofexidine Tricyclic Antidepressants can reduce the therapeutic effects of Lofexidine. This combination should be avoided. Monitor for any decreased alpha2-agonist effects if the combination is used. If you are discontinuing the use of an alpha2-agonist for a patient who is receiving a TCA, be careful.
    Methotrimeprazine Methotrimeprazine may have a higher CNS depressant activity than CNS Depressants. Methotrimeprazine can increase the CNS depressant effects of CNS Depressants. Management: Lower the adult dose of CNS Depressants by 50% and start concomitant methotrimeprazine treatment. After clinically proven efficacy of methotrimeprazine, further CNS depressant dose adjustments should only be made.
    Metoclopramide This may increase the toxic/adverse effects of Tricyclic Antidepressants. Management: If possible, seek alternatives to this combination. Patients receiving metoclopramide and tricyclic antidepressants should be monitored for extrapyramidal symptoms, neuroleptic malignant Syndrome, or serotonin syndrome.
    Opioid Agonists CNS Depressants can increase the CNS depressant effects of Opioid Aggonists. Management: When possible, avoid concomitant use opioid agonists and other CNS depressants. Combining these agents is not recommended unless there are other options. Limit the amount and duration of each drug when combined.
    OxyCODONE CNS Depressants can increase OxyCODONE's CNS depressant effects. When possible, avoid the simultaneous use of oxycodone and other CNS depressants. Combining these agents is not recommended unless there are other options. Limit the amount and duration of each drug when combined.
    PARoxetine Could increase the toxic/adverse effects of Tricyclic Antidepressants. PARoxetine can increase serum levels of TricyclicAntidepressants. Management: If possible, consider alternatives to this combination. When a TCA is used with paroxetine, monitor for any adverse effects such as serotonin syndrome or QT-interval prolongation.
    Perampanel CNS Depressants may have a greater CNS depressant effect. Perampanel and any other CNS depressant drug should be used in combination. Patients who take perampanel together with any other drug should not engage in complex or high-risk activities until they have had experience with the combination.
    Pramlintide Anticholinergic Agents may have an enhanced anticholinergic effect. These effects are only for the GI tract.
    QuiNIDine Tricyclic Antidepressants could increase the QTc-prolonging effects of QuiNIDine. QuiNIDine could increase serum levels of Tricyclic Antepressants. Management: The drug interactions monographs for drugs listed as an exception to this monograph will discuss the management of these drugs in greater detail.
    Secretin Secretin's therapeutic effects may be diminished by anticholinergic agents. Concomitant use: Secretin and anticholinergic agents should be avoided. Stop using anticholinergic drugs for at least five half-lives before administering secretin.
    Sertraline Could increase the toxic/adverse effects of Tricyclic Antidepressants. Sertraline can increase serum levels of Tricyclic Antepressants. Management: If possible, consider alternatives to this combination. When sertraline is used with a tricyclic antidepressant (TCA), monitor for adverse effects, including serotonin syndrome or QT-interval prolongation.
    Sodium Oxybate CNS Depressants may have a greater depressant effect if taken in combination. Management: Look for alternatives to the combination use. If you must combine use, reduce the dose of any one or more drugs. It is not recommended to combine sodium oxybate and alcohol, or any sedative hypnotics.
    St John's Wort May increase metabolism of tricyclic antidepressants. The possibility of serotonin syndrome could theoretically increase.
    Suvorexant CNS Depressants can increase the CNS depressant effects of Suvorexant. Management: Suvorexant or any other CNS depressionant can be reduced in doses. Suvorexant should not be taken with alcohol. It is also not recommended to take suvorexant along with any other drugs for insomnia.
    Tapentadol CNS Depressants may increase the CNS depressant effects. Tapentadol, benzodiazepines and other CNS depressants should be avoided when possible. Combining these agents is not recommended unless there are other options. Limit the amount and duration of each drug when combined.
    Zolpidem CNS Depressants can increase the CNS depressant effects of Zolpidem. Management: For men who also take CNS depressants, reduce the adult Intermezzo brand sublingual Zolpidem dose to 1.75mg. For women, no dose adjustment is advised. Avoid using CNS depressants at night; do not use alcohol.

    Risk Factor X (Avoid Combination)

     
    Aclidinium Anticholinergic Agents may have an enhanced anticholinergic effect.
    Azelastine (Nasal) CNS Depressants could increase the CNS depressant effects of Azelastine.
    Bromopride Might increase the toxic/adverse effects of Tricyclic Antidepressants.
    Bromperidol CNS Depressants may increase the CNS depressant effects.
    Cimetropium Cimetropium may have an anticholinergic effect that can be enhanced by the use of anticholinergic agents.
    Dapoxetine Can increase the toxic/adverse effects of Serotonin Activators.
    Dronedarone Tricyclic Antidepressants can increase Dronedarone's arrhythmogenic effects. Management: The drug interactions monographs for drugs listed as an exception to this monograph provide more information.
    Eluxadoline Eluxadoline may cause constipation by using anticholinergic agents.
    Glycopyrrolate (Oral Inhalation) Anticholinergic agents may increase the anticholinergic effects of Glycopyrrolate (Oral inhalation).
    Glycopyrronium (Topical) Anticholinergic Agents may have an enhanced anticholinergic effect.
    Iobenguane Radiopharmaceutical Products Tricyclic Antidepressants can decrease the therapeutic effects of Iobenguane Radiopharmaceutical Products. Management: Stop using any drug that could inhibit or interfere catecholamine transport and uptake for at most 5 biological half-lives prior to iobenguane Administration. These drugs should not be administered until 7 days following each iobenguane dosage.
    Oral Inhalation with Ipratropium Anticholinergic Agents may have an enhanced anticholinergic effect.
    Levosulpiride Anticholinergic Agents can reduce the therapeutic effects of Levosulpiride.
    Methylene Blue Tricyclic Antidepressants could increase the serotonergic effects of Methylene Blue. This could lead to serotonin syndrome.
    Methylene Blue This may increase the serotonergic effects of Serotonin Activators. This could lead to serotonin syndrome.
    Monoamine Oxidase Inhibitors This may increase the serotonergic effects of Tricyclic Antidepressants. This could lead to serotonin syndrome. Although methylene blue is expected to interact with linezolid via this mechanism, management guidelines differ from those for other monoamine-oxidase inhibitors. For more information, refer to monographs pertaining to these agents. Exceptions: Linezolid; Methylene Blue; Tedizolid.
    Orphenadrine Orphenadrine may be more effective against CNS depression than other drugs.
    Oxatomide Anticholinergic Agents may have an enhanced anticholinergic effect.
    Oxomemazine CNS Depressants may increase the CNS depressant effects.
    Paraldehyde Paraldehyde may be enhanced by CNS depressants.
    Potassium Chloride Potassium Chloride may have an ulcerogenic effect that can be exacerbated by anticholinergic agents. Treatment: Patients taking drugs that have significant anticholinergic effects should not consume any oral dose form of potassium chloride.
    Potassium Citrate Potassium Citrate may be more ulcerogenic if it is given to anticholinergic agents.
    Revefenacin Revefenacin may be enhanced by anticholinergic agents.
    Thalidomide CNS Depressants can increase Thalidomide's CNS depressant effects.
    Tiotropium Anticholinergic agents may increase the anticholinergic effects of Tiotropium.
    Umeclidinium Anticholinergic Agents may have an enhanced anticholinergic effect.

Monitoring parameters :

  • Monitor serum sodium in at-risk populations as clinically indicated)
  • Evaluate:
    • mental status,
    • suicidal thoughts and ideation especially at the beginning of therapy and after any dose adjustment,
    • anxiety,
    • social functioning,
    • mania,
    • panic attacks or other unusual changes in behavior.
  • Monitor:
    • heart rate,
    • blood pressure and
    • ECG in older adults and patients with preexisting heart disease
    • electrolyte panel to assess the risk of conduction abnormalities
    • blood glucose
    • weight and BMI
    • Observe for involuntary movements and signs of Parkinson's disease
    • tardive dyskinesias
    • ejaculatory and erectile dysfunction
    • galactorrhea
    • changes in libido and menstruation

 

Administration :

It should be taken with the evening meals to reduce the gastrointestinal side effects and sedation.

 

Mechanism of action of Amoxapine:

Amoxapine increases synaptic serotonin levels and norepinephrine concentrations in the central nervous systems by inhibiting their reuptake through the presynaptic neural membrane pump. Its metabolite 7OH-amoxapine is similar to antipsychotic drugs in that it has significant dopamine receptor blocking ability.

The process takes between 1 and 2 weeks.antidepressant effectIt may take up to 6 weeks for maximum results to be observed. It works wellabsorbedAbsorption is quick. 95% of the drug's active ingredient is protein-bound. It is widely used.MetabolizedThrough hepatic hydrolysis.

 It contains two metabolites: 7-hydroxyamoxapine (7OH-amoxapine), and 8-hydroxyamoxapine (OH-amoxapine), which form glucuronides through the process of conjugation. Thehalf-life eliminationIt takes 8 hours. The half-life of its metabolite 8 hydroxyamoxapine is 30 hours. The drug takes approximately 90 minutes to reach its destination. peak serum concentrationIt isexcretedIn the urine.

 

 

Amoxapine International Brands:

  • Adisen
  • Asendin
  • Defanyl
  • Demolox
  • Oxcap

Brands in Pakistan:

No brands available in Pakistan.

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