FLUVOXAMINE MALEATE Drug Interactions
Also known as: Fluvoxamine Maleate
Fluvoxamine Maleate is a type of antidepressant medication called a Selective Serotonin Reuptake Inhibitor (SSRI). It works by helping to balance certain natural substances in the brain, and it is primarily used to treat Obsessive Compulsive Disorder (OCD) by reducing repetitive thoughts and behaviors.FLUVOXAMINE MALEATE has 12 documented drug interactions in our database, including 0 contraindicated, 1 major, 7 moderate, and 4 minor interactions.
0
Contraindicated
1
Major
7
Moderate
4
Minor
Coadministration of fluvoxamine with propranolol can significantly increase propranolol plasma concentrations, leading to enhanced beta-blockade effects. This can manifest as severe bradycardia, hypotension, and potentially heart block, increasing the risk of adverse cardiovascular events.
Mechanism
Fluvoxamine is a potent inhibitor of CYP1A2 and CYP2C19, both of which are involved in the metabolism of propranolol. Inhibition of these enzymes reduces propranolol clearance, leading to elevated systemic exposure.
Clinical Management
Avoid concurrent use if possible. If coadministration is necessary, initiate propranolol at a lower dose and monitor the patient closely for signs of bradycardia, hypotension, and other symptoms of excessive beta-blockade. Consider therapeutic drug monitoring for propranolol or using an alternative beta-blocker that is not metabolized by CYP1A2 or CYP2C19.
Coadministration of carvedilol and fluvoxamine may lead to increased plasma concentrations of carvedilol, potentially enhancing its beta-blocking effects. This can result in symptoms such as bradycardia, hypotension, and dizziness, particularly in susceptible patients.
Mechanism
Fluvoxamine is a potent inhibitor of CYP1A2 and CYP2C19. While carvedilol is primarily metabolized by CYP2D6, it also undergoes metabolism by CYP2C9, CYP1A2, and CYP3A4. Inhibition of CYP1A2 by fluvoxamine could reduce the clearance of carvedilol, leading to elevated systemic exposure.
Clinical Management
Monitor patients for signs and symptoms of increased beta-blockade, including bradycardia, hypotension, and dizziness, especially when fluvoxamine is initiated or its dose is changed. A carvedilol dose reduction may be necessary if adverse effects occur. Consider using alternative antidepressants with less CYP1A2 inhibitory activity if close monitoring is not feasible.
Coadministration of fluvoxamine and pindolol can increase pindolol plasma concentrations, potentially leading to enhanced beta-blockade effects such as bradycardia, hypotension, or heart block. This interaction is primarily due to fluvoxamine's inhibition of CYP1A2, which is involved in pindolol's metabolism.
Mechanism
Fluvoxamine is a potent inhibitor of cytochrome P450 1A2 (CYP1A2). Pindolol is metabolized, in part, by CYP1A2, thus fluvoxamine can decrease the metabolism and increase the plasma levels of pindolol.
Clinical Management
Monitor patients closely for signs and symptoms of increased beta-blockade, including bradycardia, hypotension, and dizziness. A reduction in pindolol dosage may be necessary if adverse effects occur, or consider alternative antidepressants with less CYP1A2 inhibitory potential.
Coadministration of nebivolol with fluvoxamine may increase nebivolol plasma concentrations, potentially leading to enhanced beta-blockade effects such as bradycardia and hypotension. This interaction is due to fluvoxamine's inhibition of CYP2D6, the primary enzyme responsible for nebivolol's metabolism.
Mechanism
Nebivolol is primarily metabolized by CYP2D6. Fluvoxamine is a known inhibitor of CYP2D6, though not as potent as fluoxetine or paroxetine. Inhibition of nebivolol's metabolism by fluvoxamine can lead to increased systemic exposure and accumulation of nebivolol.
Clinical Management
Monitor patients closely for signs and symptoms of excessive beta-blockade, including bradycardia, hypotension, and dizziness, especially when initiating fluvoxamine or increasing its dose. A lower starting dose of nebivolol or dose reduction may be necessary if coadministration cannot be avoided. Consider alternative antidepressants with minimal CYP2D6 inhibition if significant adverse effects occur.
Coadministration of labetalol and fluvoxamine may increase labetalol plasma concentrations, potentially leading to enhanced beta-blockade effects such as bradycardia and hypotension. Both drugs can independently cause bradycardia, leading to additive effects.
Mechanism
Fluvoxamine is a potent inhibitor of CYP1A2 and CYP2C19. While labetalol is primarily metabolized by glucuronidation, it also undergoes some metabolism via CYP2D6, and to a lesser extent, CYP1A2 and CYP2C19. Inhibition of these CYP enzymes by fluvoxamine could reduce labetalol clearance.
Clinical Management
Monitor patients for signs and symptoms of increased beta-blockade, including bradycardia, hypotension, and dizziness. Consider using the lowest effective dose of labetalol or an alternative antidepressant with less CYP inhibition, such as sertraline or escitalopram, if close monitoring is not feasible. Dose adjustment of labetalol may be necessary.
Coadministration of fluvoxamine with metoprolol may increase metoprolol plasma concentrations, leading to enhanced beta-blockade effects such as bradycardia, hypotension, and heart block. While fluvoxamine is primarily a CYP1A2 and CYP2C19 inhibitor, metoprolol is mainly metabolized by CYP2D6, suggesting a lower risk of significant pharmacokinetic interaction than with potent CYP2D6 inhibitors. However, both drugs can independently cause bradycardia, and additive pharmacodynamic effects are possible.
Mechanism
Metoprolol is primarily metabolized by CYP2D6. Fluvoxamine is a potent inhibitor of CYP1A2 and CYP2C19, and a moderate inhibitor of CYP2D6. Inhibition of metoprolol's metabolism by fluvoxamine's CYP2D6 inhibitory activity, even if moderate, can increase metoprolol plasma levels. Additionally, both drugs can cause bradycardia, leading to potential additive pharmacodynamic effects.
Clinical Management
Monitor patients closely for signs and symptoms of excessive beta-blockade, including bradycardia, hypotension, and dizziness, especially when initiating or adjusting fluvoxamine or metoprolol doses. Consider using the lowest effective dose of metoprolol or choosing an alternative beta-blocker with minimal CYP2D6 metabolism (e.g., atenolol, nadolol) if close monitoring is not feasible or if adverse effects occur. Dose reduction of metoprolol may be necessary.
Coadministration of fluvoxamine with timolol may increase timolol plasma concentrations, potentially leading to enhanced beta-blockade effects such as bradycardia and hypotension. This interaction is primarily due to fluvoxamine's inhibition of CYP1A2, which is involved in timolol metabolism.
Mechanism
Fluvoxamine is a potent inhibitor of CYP1A2. Timolol is metabolized by CYP2D6 and to a lesser extent by CYP1A2. Inhibition of CYP1A2 by fluvoxamine can reduce timolol clearance, leading to elevated systemic levels.
Clinical Management
Monitor patients for signs and symptoms of increased beta-blockade, including bradycardia, hypotension, and fatigue. Consider using a lower dose of timolol or an alternative antidepressant with less CYP1A2 inhibitory activity if adverse effects occur. If timolol is used topically, remind patients about systemic absorption and potential for interaction.
The co-administration of acebutolol and fluvoxamine may lead to an increased risk of bradycardia and hypotension. While acebutolol is primarily metabolized by CYP2D6, fluvoxamine is a potent inhibitor of CYP1A2 and CYP2C19, and a moderate inhibitor of CYP2D6, which could potentially increase acebutolol plasma concentrations.
Mechanism
Fluvoxamine is a moderate inhibitor of CYP2D6, the primary enzyme responsible for acebutolol's metabolism to diacetolol. This inhibition could decrease acebutolol clearance, leading to elevated systemic exposure and enhanced beta-adrenergic blockade.
Clinical Management
Monitor patients closely for signs and symptoms of bradycardia and hypotension, especially when initiating or adjusting fluvoxamine dose. Consider using a lower starting dose of acebutolol or an alternative antidepressant with less CYP2D6 inhibitory potential if clinically appropriate. Regular blood pressure and heart rate monitoring are recommended.
Atenolol is primarily renally cleared and not significantly metabolized by cytochrome P450 enzymes, including those inhibited by fluvoxamine. Therefore, a significant pharmacokinetic interaction is unlikely. However, both drugs can independently cause bradycardia, so additive pharmacodynamic effects are theoretically possible, though generally not clinically significant with atenolol.
Mechanism
Atenolol is eliminated largely unchanged by the kidneys, with minimal hepatic metabolism. Fluvoxamine is a potent inhibitor of CYP1A2 and CYP2C19, but these enzymes are not primary pathways for atenolol metabolism.
Clinical Management
No specific dose adjustments are typically required for atenolol when co-administered with fluvoxamine due to the lack of significant pharmacokinetic interaction. Monitor for additive pharmacodynamic effects such as excessive bradycardia or hypotension, especially in sensitive patients, although this is rare given atenolol's elimination profile.
Nadolol is primarily renally cleared, and its metabolism is not significantly impacted by CYP450 enzymes. Therefore, fluvoxamine, a potent CYP1A2 and CYP2C19 inhibitor, is unlikely to cause a significant pharmacokinetic interaction with nadolol.
Mechanism
Nadolol is predominantly eliminated via renal excretion as unchanged drug, with minimal hepatic metabolism. Fluvoxamine's inhibitory effects on CYP1A2 and CYP2C19 enzymes would not significantly alter nadolol's pharmacokinetics.
Clinical Management
No specific dose adjustments or enhanced monitoring are generally required for this combination due to the minimal pharmacokinetic interaction. However, clinicians should always monitor patients for expected therapeutic effects and adverse reactions of both medications, especially if other interacting drugs are present or renal function is impaired.
Fluvoxamine is not a significant inhibitor of CYP2D6, the primary enzyme responsible for metoprolol metabolism. Therefore, a clinically significant pharmacokinetic interaction leading to increased metoprolol levels is unlikely.
Mechanism
Metoprolol is primarily metabolized by CYP2D6. Fluvoxamine is a potent inhibitor of CYP1A2 and CYP2C19, but not CYP2D6. Thus, fluvoxamine is not expected to significantly alter the metabolism or plasma concentrations of metoprolol.
Clinical Management
No specific dose adjustments for metoprolol are typically required when co-administered with fluvoxamine. However, as both drugs can independently affect heart rate, general monitoring for bradycardia or hypotension is prudent, especially in sensitive patients. If adverse effects occur, consider alternative SSRIs with minimal CYP inhibition or monitor metoprolol levels if clinically indicated.
Bisoprolol is primarily renally cleared and not significantly metabolized by CYP450 enzymes inhibited by fluvoxamine (CYP1A2, CYP2C19). Therefore, a significant pharmacokinetic interaction is unlikely. However, both drugs can independently cause bradycardia, so an additive pharmacodynamic effect is theoretically possible.
Mechanism
Fluvoxamine is a potent inhibitor of CYP1A2 and CYP2C19. Bisoprolol is primarily eliminated renally with minimal CYP450 metabolism, thus fluvoxamine's inhibitory effects are not expected to significantly alter bisoprolol plasma levels. An additive pharmacodynamic effect on heart rate is possible.
Clinical Management
Generally, no specific dose adjustments are required for bisoprolol when co-administered with fluvoxamine due to the lack of significant pharmacokinetic interaction. Monitor patients for signs of excessive bradycardia or hypotension, especially if they are sensitive to either medication, though this is considered a low risk.
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