FLUOXETINE Drug Interactions
Also known as: Fluoxetine
Fluoxetine is a type of antidepressant medication called a selective serotonin reuptake inhibitor (SSRI). It is used to treat conditions like depression, obsessive-compulsive disorder (OCD), bulimia nervosa, and panic disorder by helping to restore the balance of a natural substance called serotonin in the brain.FLUOXETINE has 12 documented drug interactions in our database, including 0 contraindicated, 6 major, 3 moderate, and 3 minor interactions.
0
Contraindicated
6
Major
3
Moderate
3
Minor
Fluoxetine is a potent inhibitor of CYP2D6, which is a primary enzyme responsible for the metabolism of carvedilol. This inhibition can lead to significantly increased plasma concentrations of carvedilol, raising the risk of adverse effects such as severe bradycardia, hypotension, and heart block.
Mechanism
Fluoxetine inhibits the cytochrome P450 2D6 (CYP2D6) enzyme. Carvedilol is metabolized by CYP2D6, so fluoxetine reduces carvedilol's metabolism, increasing its systemic exposure and pharmacodynamic effects.
Clinical Management
Concomitant use should generally be avoided or managed with extreme caution. If co-administration is necessary, carvedilol dosage should be significantly reduced and the patient closely monitored for signs of bradycardia, hypotension, and heart block. Consider using an alternative antidepressant with minimal CYP22D6 inhibition (e.g., sertraline, escitalopram) or a beta-blocker not primarily metabolized by CYP2D6 (e.g., atenolol, bisoprolol).
The co-administration of nebivolol and fluoxetine can lead to significantly increased plasma concentrations of nebivolol. This interaction can result in enhanced beta-adrenergic blockade, potentially causing severe bradycardia, hypotension, or heart block.
Mechanism
Fluoxetine is a potent inhibitor of the cytochrome P450 2D6 (CYP2D6) enzyme. Nebivolol is metabolized by CYP2D6, and its metabolism is inhibited by fluoxetine, leading to reduced clearance and elevated systemic exposure of nebivolol.
Clinical Management
Close monitoring for signs and symptoms of excessive beta-blockade (e.g., bradycardia, hypotension, dizziness) is essential. A reduction in the nebivolol dose may be necessary, or an alternative beta-blocker not primarily metabolized by CYP2D6 (e.g., atenolol, bisoprolol, nadolol) should be considered if the combination cannot be avoided. If an alternative SSRI is needed, sertraline or escitalopram, which have minimal CYP2D6 inhibition, could be considered.
Fluoxetine is a potent inhibitor of CYP2D6, which is the primary enzyme responsible for the metabolism of metoprolol. This interaction can significantly increase metoprolol plasma concentrations, potentially leading to enhanced beta-blockade effects such as severe bradycardia, hypotension, and heart block.
Mechanism
Fluoxetine inhibits the cytochrome P450 2D6 (CYP2D6) enzyme, thereby reducing the metabolic clearance of metoprolol, a substrate of CYP2D6. This pharmacokinetic interaction leads to elevated systemic exposure to metoprolol.
Clinical Management
If concomitant use is unavoidable, consider using an alternative antidepressant with minimal CYP2D6 inhibition (e.g., sertraline, escitalopram) or an alternative beta-blocker primarily cleared renally (e.g., atenolol, nadolol). If metoprolol and fluoxetine are co-administered, closely monitor the patient for signs and symptoms of excessive beta-blockade (e.g., bradycardia, hypotension, dizziness) and reduce the metoprolol dose as necessary.
Fluoxetine can significantly increase the plasma concentrations of metoprolol, a beta-blocker. This interaction can lead to severe bradycardia, hypotension, and potentially heart block, increasing the risk of adverse cardiovascular events.
Mechanism
Fluoxetine is a potent inhibitor of the cytochrome P450 2D6 (CYP2D6) enzyme. Metoprolol is primarily metabolized by CYP2D6, so fluoxetine inhibits its metabolism, leading to reduced clearance and increased systemic exposure of metoprolol.
Clinical Management
Avoid concurrent use if possible. If co-administration is necessary, closely monitor the patient for signs of bradycardia, hypotension, and other beta-blocker adverse effects. A significant dose reduction of metoprolol may be required, or consider switching to a beta-blocker with minimal CYP2D6 metabolism (e.g., atenolol, bisoprolol) or an antidepressant with minimal CYP2D6 inhibition (e.g., sertraline, escitalopram).
Fluoxetine, a potent CYP2D6 inhibitor, can significantly increase plasma concentrations of propranolol, a beta-blocker primarily metabolized by CYP2D6. This interaction can lead to profound bradycardia, hypotension, and other symptoms of beta-blockade.
Mechanism
Fluoxetine inhibits the cytochrome P450 2D6 (CYP2D6) enzyme, which is a primary metabolic pathway for propranolol. This pharmacokinetic interaction reduces propranolol clearance, leading to elevated systemic exposure.
Clinical Management
If co-administration is necessary, close monitoring for signs of excessive beta-blockade (e.g., bradycardia, hypotension, fatigue) is essential. A lower starting dose of propranolol may be required, and dose adjustments should be made cautiously based on clinical response and tolerability. Consider using an alternative beta-blocker less dependent on CYP2D6 metabolism (e.g., atenolol, nadolol) or an antidepressant with less CYP2D6 inhibitory potential (e.g., sertraline).
The combination of timolol and fluoxetine can lead to significantly increased plasma concentrations of timolol, potentially causing severe bradycardia, hypotension, and heart block. This interaction is particularly concerning given timolol's non-selective beta-blocking effects and systemic absorption even with ophthalmic administration.
Mechanism
Fluoxetine is a potent inhibitor of the cytochrome P450 2D6 (CYP2D6) enzyme. Timolol is primarily metabolized by CYP2D6, so fluoxetine inhibits its metabolism, leading to reduced clearance and increased systemic exposure to timolol.
Clinical Management
Close monitoring for signs and symptoms of beta-blockade toxicity (e.g., bradycardia, hypotension, dizziness, fatigue) is essential. A lower starting dose of timolol or an alternative beta-blocker not metabolized by CYP2D6 (e.g., atenolol, bisoprolol, nadolol) should be considered. If the combination is necessary, dose adjustments for timolol may be required, and ECG monitoring is advisable.
Fluoxetine, a potent CYP2D6 inhibitor, can increase plasma concentrations of pindolol, which is partially metabolized by CYP2D6. This interaction may lead to enhanced beta-blockade effects, potentially causing bradycardia, hypotension, or heart block.
Mechanism
Fluoxetine inhibits the cytochrome P450 2D6 (CYP2D6) enzyme, which is involved in the metabolism of pindolol. This inhibition reduces pindolol clearance, leading to increased systemic exposure and enhanced pharmacodynamic effects.
Clinical Management
Monitor patients closely for signs of enhanced beta-blockade, including bradycardia, hypotension, and dizziness, especially when initiating or adjusting fluoxetine. Consider using a beta-blocker less dependent on CYP2D6 metabolism (e.g., atenolol, bisoprolol, nadolol) or an antidepressant with less CYP2D6 inhibition (e.g., sertraline, escitalopram) if close monitoring is not feasible or if adverse effects occur.
Fluoxetine, a potent CYP2D6 inhibitor, can increase plasma concentrations of labetalol, which is partially metabolized by CYP2D6. This can lead to an increased risk of beta-blocker adverse effects such as bradycardia, hypotension, and heart block.
Mechanism
Fluoxetine inhibits the cytochrome P450 2D6 (CYP2D6) enzyme, reducing the metabolism of labetalol, a substrate for this enzyme. This pharmacokinetic interaction leads to higher systemic exposure to labetalol.
Clinical Management
Monitor patients closely for signs and symptoms of beta-blockade, including bradycardia, hypotension, and dizziness, especially when initiating or adjusting fluoxetine. Consider a lower starting dose of labetalol or a dose reduction if co-administered with fluoxetine. If possible, consider alternative beta-blockers that are not primarily metabolized by CYP2D6 (e.g., atenolol, nadolol, bisoprolol) or SSRIs with less CYP2D6 inhibition (e.g., sertraline, escitalopram).
Fluoxetine is a potent CYP2D6 inhibitor, which can increase plasma concentrations of acebutolol. This interaction may lead to enhanced beta-blockade effects such as bradycardia, hypotension, and heart block, particularly in susceptible patients.
Mechanism
Fluoxetine inhibits the cytochrome P450 2D6 (CYP2D6) enzyme, which is involved in the metabolism of acebutolol. This inhibition reduces acebutolol clearance, leading to elevated systemic exposure.
Clinical Management
Monitor patients closely for signs and symptoms of excessive beta-blockade, including bradycardia, hypotension, and dizziness. Consider using alternative SSRIs with minimal CYP2D6 inhibition (e.g., sertraline, escitalopram) or an alternative beta-blocker not primarily metabolized by CYP2D6 (e.g., atenolol, nadolol). If co-administration is necessary, a lower dose of acebutolol may be required.
Atenolol is primarily renally cleared and its metabolism is minimally affected by CYP2D6 inhibition. Therefore, fluoxetine, a potent CYP2D6 inhibitor, is unlikely to cause a significant pharmacokinetic interaction leading to increased atenolol levels. However, both drugs can independently cause bradycardia, so additive pharmacodynamic effects are theoretically possible.
Mechanism
Fluoxetine is a potent inhibitor of CYP2D6. Atenolol is primarily eliminated renally and is not significantly metabolized by CYP2D6, thus its plasma levels are not expected to be significantly altered by fluoxetine. The potential for interaction is primarily pharmacodynamic, as both drugs can cause bradycardia.
Clinical Management
No specific dose adjustments for atenolol are typically required when co-administered with fluoxetine due to a lack of significant pharmacokinetic interaction. Monitor patients for additive bradycardia, especially if they are predisposed to this condition. If bradycardia occurs, consider dose adjustment of either medication or alternative agents.
The interaction between nadolol and fluoxetine is considered minor. While fluoxetine is a potent CYP2D6 inhibitor, nadolol is primarily renally cleared with minimal CYP2D6 involvement, reducing the risk of pharmacokinetic interaction. However, both drugs can independently cause bradycardia, so additive pharmacodynamic effects are theoretically possible.
Mechanism
Fluoxetine is a potent inhibitor of CYP2D6. However, nadolol is primarily eliminated via renal excretion, with minimal metabolism by CYP2D6, thus its plasma levels are not significantly affected by CYP2D6 inhibition. Both drugs can cause bradycardia, leading to a potential additive pharmacodynamic effect.
Clinical Management
Generally, no specific dose adjustments are required for nadolol when co-administered with fluoxetine due to nadolol's renal clearance. However, clinicians should monitor patients for signs of excessive bradycardia or hypotension, especially when initiating or significantly changing doses of either medication. If symptomatic bradycardia occurs, consider dose reduction or alternative agents.
Fluoxetine is a potent CYP2D6 inhibitor, but bisoprolol is primarily cleared renally with minimal CYP2D6 involvement. Therefore, a clinically significant pharmacokinetic interaction via CYP2D6 inhibition is unlikely. Both drugs can independently cause bradycardia, so additive pharmacodynamic effects are theoretically possible, though less likely to be significant.
Mechanism
Fluoxetine inhibits CYP2D6, but bisoprolol metabolism is not significantly dependent on CYP2D6. Both drugs can exert bradycardic effects, leading to a theoretical additive pharmacodynamic effect.
Clinical Management
Routine monitoring for expected therapeutic effects and adverse reactions of both medications is recommended. Specific dose adjustments due to this interaction are generally not necessary. Patients should be advised to report any symptoms of excessive bradycardia or hypotension.
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