Cancer Drug Interactions from Radboud UMC and University of Liverpool

No Interaction Expected

Tamoxifen

Acarbose

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. After ingestion of acarbose, the majority of active unchanged drug remains in the lumen of the gastrointestinal tract to exert its pharmacological activity and is metabolised by intestinal enzymes and by the microbial flora. Tamoxifen does not interact with this metabolic pathway.

Description:

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Potential Interaction

Tamoxifen

Acenocoumarol

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but is not recommended. Acenocoumarol is mainly metabolised by CYP2C9 and to a lesser extent by CYP1A2 and CYP2C19. Tamoxifen does not inhibit or induce CYPs. Vitamin K antagonists are used in patients that are at risk of venous thromboembolic events and tamoxifen is associated with an increased risk of venous thromboembolic events, although the exact mechanism of the interaction is unknown. Therefore, coadministration of acenocoumarol and tamoxifen is not recommended. If coadministration is unavoidable, monitor closely for INR/PT and signs of bleeding.

Description:

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No Interaction Expected

Tamoxifen

Acetylsalicylic acid (Aspirin)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Aspirin is rapidly deacetylated to form salicylic acid and then further metabolised by glucuronidation (by several UGTs, major UGT1A6). Tamoxifen does not inhibit or induce UGTs.

Description:

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No Interaction Expected

Tamoxifen

Agomelatine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Agomelatine is metabolised predominantly via CYP1A2 (90%), with a small proportion metabolised by CYP2C9 and CYP2C19 (10%). Tamoxifen does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Tamoxifen

Alendronic acid

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Alendronic acid is not metabolised and is cleared from the plasma by uptake into bone and elimination via renal excretion. Tamoxifen is unlikely to interfere with this elimination pathway. Although no pharmacokinetic interaction is expected, alendronic acid should be separated from food or other medicinal products and patients must wait at least 30 minutes after taking alendronic acid before taking any other oral medicinal product.

Description:

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No Interaction Expected

Tamoxifen

Alfentanil

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Alfentanil undergoes extensive CYP3A4 metabolism. Tamoxifen does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Tamoxifen

Alfuzosin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Alfuzosin is metabolised by CYP3A. Tamoxifen does not inhibit or induce CYPs.

Description:

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Potential Weak Interaction

Tamoxifen

Aliskiren

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Aliskiren is minimally metabolised and is mainly excreted unchanged in faeces. Aliskiren is also a substrate of P-gp. Tamoxifen is an inhibitor of P-gp and may increase concentrations of aliskiren. The clinical relevance of this interaction is unknown. Monitoring for aliskiren toxicity and blood pressure may be required.

Description:

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No Interaction Expected

Tamoxifen

Allopurinol

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Allopurinol is converted to oxipurinol by xanthine oxidase and aldehyde oxidase. Allopurinol is also an inhibitor of xanthine oxidase. Tamoxifen does not interact with this metabolic pathway.

Description:

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No Interaction Expected

Tamoxifen

Alosetron

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. In vitro data indicate that alosetron is metabolised by CYPs 2C9, 3A4 and 1A2. Tamoxifen does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Tamoxifen

Alprazolam

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Alprazolam is mainly metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Tamoxifen

Aluminium hydroxide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Aluminium hydroxide is not metabolised.

Description:

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Potential Weak Interaction

Tamoxifen

Ambrisentan

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Ambrisentan is metabolized by glucuronidation via UGTs 1A3, 1A9 and 2B7 and to a lesser extent by CYP3A4 and CYP2C19. Tamoxifen does not inhibit or induce CYPs or UGTs. Ambrisentan is also a substrate of P-gp. Tamoxifen is an inhibitor of P-gp and may increase concentrations of ambrisentan. The clinical relevance of this interaction is unknown. Monitoring for ambrisentan toxicity and blood pressure may be required.

Description:

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No Interaction Expected

Tamoxifen

Amikacin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Amikacin is eliminated by glomerular filtration. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Tamoxifen

Amiloride

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Amiloride is eliminated unchanged in the kidney. In vitro data indicate that amiloride is a substrate of OCT2. Tamoxifen is unlikely to interfere with this elimination pathway and does not inhibit or induce OCTs.

Description:

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Potential Interaction

Tamoxifen

Amiodarone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Amiodarone is metabolised by CYP3A4 and CYP2C8. Tamoxifen does not inhibit or induce CYPs. The major metabolite of amiodarone, desethylamiodarone, is an inhibitor of CYPs 3A4 (weak), 2C9 (moderate), 2D6 (moderate), 2C19 (weak), 1A1 (strong), 2B6 (moderate) and P-gp (strong). Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. The active metabolite of amiodarone may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. As the active metabolites, 4-hydroxytamoxifen and endoxifen, are much more potent than tamoxifen, a decrease of those plasma concentrations may lead to decreased efficacy. Close monitoring of tamoxifen efficacy is recommended. Monitor endoxifen plasma concentrations, if available.

Description:

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No Interaction Expected

Tamoxifen

Amisulpride

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Amisulpride is weakly metabolised and is primarily eliminated renally (possibly via OCT). Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Tamoxifen

Amitriptyline

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Amitriptyline is metabolised predominantly by CYP2D6 and CYP2C19, with a small proportion metabolised by CYPs 3A4, 1A2 and 2C9. Tamoxifen does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Tamoxifen

Amlodipine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Amlodipine is metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Tamoxifen

Amoxicillin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Amoxicillin is mainly excreted in the urine by glomerular filtration and tubular secretion. In vitro data indicate that amoxicillin is a substrate of OAT3. Tamoxifen is unlikely to interfere with this elimination pathway and does not inhibit or induce OATs.

Description:

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Potential Weak Interaction

Tamoxifen

Amphotericin B

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Amphotericin B is not appreciably metabolised and is eliminated to a large extent in the bile. Tamoxifen does not interfere with this elimination pathway. However, the European SPC for amphotericin B states that concomitant use of amphotericin B and antineoplastic agents can increase the risk of renal toxicity, bronchospasm and hypotension. Monitoring may be required.

Description:

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No Interaction Expected

Tamoxifen

Ampicillin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Renal clearance of ampicillin occurs partly by glomerular filtration and partly by tubular secretion. Tamoxifen is unlikely to interfere with this elimination pathway. About 20-40% of an oral dose may be excreted unchanged in the urine in 6 hours. After parenteral use about 60-80% is excreted in the urine within 6 hours.

Description:

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No Interaction Expected

Tamoxifen

Anidulafungin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Anidulafungin is not metabolised hepatically but undergoes chemical degradation at physiological temperatures. Tamoxifen does not interact with this metabolic pathway.

Description:

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No Interaction Expected

Tamoxifen

Antacids

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Antacids are not metabolised by CYPs. Tamoxifen is unlikely to interfere with this unspecified metabolic pathway.

Description:

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Potential Weak Interaction

Tamoxifen

Apixaban

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Apixaban is a substrate of P-gp and BCRP and is metabolised by CYP3A4 and to a lesser extent by CYPs 1A2, 2C8, 2C9 and 2C19. Tamoxifen does not inhibit or induce CYPs or BCRP. Tamoxifen is an inhibitor of P-gp and may increase apixaban concentrations. The clinical relevance of this interaction is unknown. Monitoring for apixaban toxicity and anti-Xa activity may be required.

Description:

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Potential Interaction

Tamoxifen

Aprepitant

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Aprepitant is mainly metabolized by CYP3A4 and to a lesser extent by CYP1A2 and CYP2C19. Tamoxifen does not inhibit or induce CYPs. During treatment, aprepitant is a moderate inhibitor of CYP3A4. Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Aprepitant may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. As the active metabolites, 4-hydroxytamoxifen and endoxifen, are much more potent than tamoxifen, a decrease of those plasma concentrations may lead to decreased efficacy. No a priori dose adjustment for tamoxifen is necessary during the few days of coadministration. Moreover, after treatment aprepitant is a weak inducer of CYP3A4, CYP2C9 and UGT. Aprepitant may decrease tamoxifen concentrations due to CYP3A4, UGT1A4 and UGT2B7 induction. Therefore, concentrations of the active metabolites of tamoxifen, 4-hydroxytamoxifen and endoxifen, may increase. The clinical relevance of this interaction is unknown. Monitoring for granisetron toxicity may be required.

Description:

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No Interaction Expected

Tamoxifen

Aripiprazole

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Aripiprazole is metabolised by CYP3A4 and CYP2D6. Tamoxifen does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Tamoxifen

Asenapine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Asenapine is metabolised by glucuronidation (UGT1A4) and oxidative metabolism (CYPs 1A2 (major), 3A4 (minor) and 2D6 (minor)). Tamoxifen does not inhibit or induce CYPs or UGTs.

Description:

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No Interaction Expected

Tamoxifen

Astemizole

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Astemizole is metabolised by CYPs 2D6, 2J2 and 3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Tamoxifen

Atenolol

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Atenolol is mainly eliminated unchanged in the kidney, predominantly by glomerular filtration. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

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Potential Weak Interaction

Tamoxifen

Atorvastatin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Atorvastatin is metabolised by CYP3A4 and is a substrate of P-gp and OATP1B1. Tamoxifen is an inhibitor of P-gp and may increase atorvastatin concentrations. In post marketing research, infrequent cases of hyperlipidaemia have been reported during therapy with tamoxifen. The clinical relevance of this interaction is unknown. Monitoring for atorvastatin toxicity, triglycerides and cholesterol may be required.

Description:

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No Interaction Expected

Tamoxifen

Azathioprine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Azathioprine is converted to 6-mercaptopurine which is metabolised analogously to natural purines by xanthine oxidase. Tamoxifen does not interact with this metabolic pathway.

Description:

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Potential Weak Interaction

Tamoxifen

Azithromycin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Azithromycin is mainly eliminated via biliary excretion; animal data suggest this may occur via P-gp and MRP2. Tamoxifen is an inhibitor of P-gp and may increase azithromycin concentrations. As the clinical relevance of this interaction is unknown, monitoring for azithromycin toxicity may be required. Azithromycin is also an inhibitor of P-gp, but the clinical relevance of P-gp inhibition by azithromycin is unknown. Tamoxifen is not transported by P-gp.

Description:

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No Interaction Expected

Tamoxifen

Beclometasone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Beclometasone is a pro-drug which is not metabolised by CYP450, but is hydrolysed via esterase enzymes to the highly active metabolite beclometasone-17-monopropionate. Tamoxifen does not interact with this metabolic pathway.

Description:

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No Interaction Expected

Tamoxifen

Bedaquiline

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bedaquiline is metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Tamoxifen

Bendroflumethiazide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bendroflumethiazide is mainly eliminated by hepatic metabolism (70%) and excreted unchanged in the urine (30%) via OAT1 and OAT3. Tamoxifen is unlikely to interfere with this metabolic or elimination pathway and does not inhibit or induce OATs. In vitro data indicate that bendroflumethiazide inhibits these renal transporters, but a clinically significant interaction is unlikely in the range of observed clinical concentrations.

Description:

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No Interaction Expected

Tamoxifen

Bepridil

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bepridil is metabolised by CYP2D6 (major) and CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Tamoxifen

Betamethasone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Betamethasone is metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

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Potential Weak Interaction

Tamoxifen

Bezafibrate

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Half of a bezafibrate dose is eliminated unchanged in the urine. In vitro data suggest that bezafibrate inhibits the renal transporter OAT1. Tamoxifen is unlikely to interfere with this elimination pathway. However, in post marketing research infrequent cases of hyperlipidaemia have been reported during therapy with tamoxifen. The clinical relevance of this interaction is unknown. Monitoring of triglycerides and cholesterol may be required.

Description:

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No Interaction Expected

Tamoxifen

Bisacodyl

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bisacodyl is converted to an active metabolite by intestinal and bacterial enzymes. Absorption from the gastrointestinal tract is minimal and the small amount absorbed is excreted in the urine as the glucuronide. Tamoxifen is unlikely to interfere with this metabolic or elimination pathway.

Description:

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No Interaction Expected

Tamoxifen

Bisoprolol

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bisoprolol is partly metabolised by CYP3A4 and CYP2D6, and partly eliminated unchanged in the urine. Tamoxifen does not inhibit or induce CYPs and is unlikely to interfere with this elimination pathway.

Description:

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Potential Interaction

Tamoxifen

Bosentan

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but is not recommended. Bosentan is a substrate and weak inducer of CYP3A4 and CYP2C9. Tamoxifen does not inhibit or induce CYPs. However, tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Bosentan may decrease tamoxifen concentrations and increase concentrations of the active metabolites of tamoxifen. The net effect on the exposure to tamoxifen and the active metabolites is unknown and therefore the clinical relevance of this interaction cannot be determined. Coadministration is not recommended. If coadministration is unavoidable, closely monitor tamoxifen toxicity. Monitor endoxifen plasma concentrations, if available.

Description:

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No Interaction Expected

Tamoxifen

Bromazepam

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bromazepam undergoes oxidative biotransformation. Interaction studies indicate that CYP3A4 plays a minor role in bromazepam metabolism, but other cytochromes such as CYP2D6 or CYP1A2 may also play a role. Tamoxifen does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Tamoxifen

Budesonide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Budesonide is metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Tamoxifen

Buprenorphine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Buprenorphine undergoes both N-dealkylation to form norbuprenorphine (via CYP3A4) and glucuronidation (via UGT2B7 and UGT1A1). Tamoxifen does not inhibit or induce CYPs or UGTs.

Description:

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Do Not Coadminister

Tamoxifen

Bupropion

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be avoided. Bupropion is primarily metabolised by CYP2B6 and is a strong inhibitor of CYP2D6. Tamoxifen does not inhibit or induce CYPs. However, tamoxifen is metabolised by CYP2D6 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Bupropion may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. Tamoxifen product labels state that after coadministration with paroxetine, a strong CYP2D6 inhibitor, endoxifen concentrations decreased by 64%. A decrease in endoxifen plasma concentrations may lead to decreased efficacy as endoxifen is much more potent than tamoxifen. Coadministration should be avoided. If coadministration is unavoidable, closely monitor tamoxifen efficacy. Monitor endoxifen plasma concentrations, if available.

Description:

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No Interaction Expected

Tamoxifen

Buspirone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Buspirone is metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Tamoxifen

Calcium

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Calcium is eliminated through faeces, urine and sweat. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Tamoxifen

Candesartan

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Candesartan is mainly eliminated unchanged via urine and bile. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Tamoxifen

Capreomycin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Capreomycin is predominantly excreted via the kidneys as unchanged drug. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Tamoxifen

Captopril

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Captopril is largely excreted in the urine by OAT1. Tamoxifen is unlikely to interfere with this elimination pathway and does not inhibit or induce OATs.

Description:

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Do Not Coadminister

Tamoxifen

Carbamazepine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be avoided. Carbamazepine is primarily metabolized by CYP3A4 and to a lesser extent by CYP2C8. Tamoxifen does not inhibit or induce CYPs. Moreover, carbamazepine is an inducer of CYPs 2C8 (strong), 2C9 (strong), 3A4 (strong), 1A2 (weak), 2B6, UGT1A1 and P-gp (moderate). Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Carbamazepine may decrease tamoxifen concentrations and increase concentrations of the active metabolites of tamoxifen. After coadministration with rifampicin, a strong CYP3A4 inducer, tamoxifen exposure decreased by 84%. Concentrations of N-desmethyltamoxifen, 4-hydroxytamoxifen and endoxifen were decreased by 69%, 73% and 69%, respectively. A similar effect may occur after coadministration with carbamazepine. A decrease in exposure can lead to decreased efficacy. Coadministration should be avoided. If coadministration is unavoidable, closely monitor tamoxifen efficacy. Monitor endoxifen plasma concentrations, if available.

Description:

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No Interaction Expected

Tamoxifen

Carvedilol

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Carvedilol undergoes glucuronidation via UGTs 1A1, 2B4 and 2B7, and additional metabolism via CYP2D6 and to a lesser extent by CYPs 2C9 and 1A2. Carvedilol is also an inhibitor of P-gp, but the clinical relevance of P-gp inhibition by carvedilol is unknown. Tamoxifen does not interact with this metabolic pathway.

Description:

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No Interaction Expected

Tamoxifen

Caspofungin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Caspofungin undergoes spontaneous chemical degradation and metabolism via a non CYP-mediated pathway. Tamoxifen does not interact with this metabolic pathway.

Description:

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No Interaction Expected

Tamoxifen

Cefalexin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cefalexin is predominantly eliminated unchanged renally by glomerular filtration and tubular secretion via OAT1 and MATE1. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Tamoxifen

Cefazolin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cefazolin is predominantly excreted unchanged in the urine, mainly by glomerular filtration with some renal tubular secretion via OAT3. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Tamoxifen

Cefixime

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cefixime is renally excreted predominantly by glomerular filtration. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Tamoxifen

Cefotaxime

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cefotaxime is partially metabolised by non-specific esterases. Most of a dose of cefotaxime is excreted in the urine - about 60% as unchanged drug and a further 24% as desacetyl-cefotaxime, an active metabolite. In vitro studies indicate that OAT3 participates in the renal elimination of cefotaxime. Tamoxifen is unlikely to interfere with this metabolic or elimination pathway.

Description:

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No Interaction Expected

Tamoxifen

Ceftazidime

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ceftazidime is excreted predominantly by renal glomerular filtration. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Tamoxifen

Ceftriaxone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ceftriaxone is eliminated mainly as unchanged drug, approximately 60% of the dose being excreted in the urine predominantly by glomerular filtration and the remainder via the biliary and intestinal tracts. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Tamoxifen

Celecoxib

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Celecoxib is primarily metabolised by CYP2C9. Tamoxifen does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Tamoxifen

Cetirizine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cetirizine is only metabolised to a limited extent and is eliminated unchanged in the urine through both glomerular filtration and tubular secretion. In vitro data indicate that cetirizine is also an inhibitor of OCT2. Tamoxifen is unlikely to interfere with this metabolic or elimination pathway.

Description:

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Potential Weak Interaction

Tamoxifen

Chloramphenicol

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Chloramphenicol is predominantly glucuronidated. Tamoxifen does not inhibit or induce UGTs. In vitro studies have shown that chloramphenicol can inhibit metabolism mediated by CYPs 3A4 (strong), 2C19 (strong) and 2D6 (weak). Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Chloramphenicol may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. As the active metabolites, 4-hydroxytamoxifen and endoxifen, are much more potent than tamoxifen, a decrease of those plasma concentrations may lead to decreased efficacy. Close monitoring of tamoxifen efficacy should be considered. Monitor endoxifen plasma concentrations, if available. Ocular use: Although chloramphenicol is systemically absorbed when used topically in the eye, the absorbed concentrations are unlikely to cause a clinically significant interaction.

Description:

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No Interaction Expected

Tamoxifen

Chlordiazepoxide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Chlordiazepoxide is extensively metabolised by CYP3A4 but does not inhibit or induce cytochromes. Tamoxifen does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Tamoxifen

Chlorphenamine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Chlorphenamine is predominantly metabolised in the liver via CYP2D6. Tamoxifen does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Tamoxifen

Chlorpromazine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Chlorpromazine is metabolised mainly by CYP2D6, but also by CYP1A2. Tamoxifen does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Tamoxifen

Chlortalidone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Chlortalidone is mainly excreted unchanged in the urine and faeces. OAT1/3 are the major transporters of loop and thiazide diuretics. Secretion of these diuretics into the urinary tract by transporters in the proximal tubular cells is necessary for the diuretic effect in later tubule segments. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

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Potential Interaction

Tamoxifen

Ciclosporin (Cyclosporine)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Ciclosporin is a substrate of CYP3A4 and P-gp and also inhibits CYP3A4 and OATP1B1. Tamoxifen is an inhibitor of P-gp and may increase ciclosporin concentrations. The clinical relevance of this interaction is unknown. Monitor for ciclosporin toxicity and, if available, ciclosporin plasma concentrations. Furthermore, tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Ciclosporin may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. As the active metabolites, 4-hydroxytamoxifen and endoxifen, are much more potent than tamoxifen, a decrease of those plasma concentrations may lead to decreased efficacy. Close monitoring of tamoxifen efficacy is recommended. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

No Interaction Expected

Tamoxifen

Cilazapril

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cilazapril is mainly eliminated unchanged by the kidneys. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

Potential Interaction

Tamoxifen

Cimetidine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Cimetidine is metabolised by CYP450 enzymes. Tamoxifen does not inhibit or induce CYPs. In vitro data indicate that cimetidine inhibits OAT1 and OCT2 but at concentrations much higher than the observed clinical concentrations. Cimetidine is also a weak inhibitor of CYPs 3A4, 1A2, 2D6 and 2C19. Tamoxifen is metabolised by CYP2D6 and CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Cimetidine may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. As the active metabolites, 4-hydroxytamoxifen and endoxifen, are much more potent than tamoxifen, a decrease of those plasma concentrations may lead to decreased efficacy. Close monitoring of tamoxifen efficacy is recommended. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

Potential Interaction

Tamoxifen

Ciprofloxacin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Ciprofloxacin is primarily eliminated unchanged by the kidneys by glomerular filtration and tubular secretion via OAT3. It is also metabolised and partially cleared through the bile and intestine. Tamoxifen is unlikely to interfere with this metabolic or elimination pathway. Ciprofloxacin is also a weak to moderate inhibitor of CYP3A4 and a strong inhibitor of CYP1A2. Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Ciprofloxacin may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. As the active metabolites, 4-hydroxytamoxifen and endoxifen, are much more potent than tamoxifen, a decrease of those plasma concentrations may lead to decreased efficacy. Close monitoring of tamoxifen efficacy is recommended. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

No Interaction Expected

Tamoxifen

Cisapride

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cisapride is metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Citalopram

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Citalopram is metabolised by CYPs 2C19 (38%), 2D6 (31%) and 3A4 (31%). Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Clarithromycin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be avoided. Clarithromycin is metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs. Clarithromycin is also an inhibitor of CYP3A4 (strong) and P-gp. Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Clarithromycin may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. As the active metabolites, 4-hydroxytamoxifen and endoxifen, are much more potent than tamoxifen, a decrease of those plasma concentrations may lead to decreased efficacy. Coadministration should be avoided. If coadministration is unavoidable, closely monitor tamoxifen efficacy. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

No Interaction Expected

Tamoxifen

Clavulanic acid

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Clavulanic acid is extensively metabolised (likely non-CYP mediated pathway) and excreted in the urine by glomerular filtration. Tamoxifen is unlikely to interfere with this metabolic or elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Clemastine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Clemastine is predominantly metabolised in the liver via CYP2D6. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Clindamycin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Clindamycin is metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs. In vitro data suggest that clindamycin is a CYP3A4 inhibitor. Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Clindamycin may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. As the active metabolites, 4-hydroxytamoxifen and endoxifen, are much more potent than tamoxifen, a decrease of those plasma concentrations may lead to decreased efficacy. Close monitoring of tamoxifen efficacy should be considered. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

No Interaction Expected

Tamoxifen

Clobetasol

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely with the topical use of clobetasol.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Clofazimine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Clofazimine is largely excreted unchanged in the faeces. Tamoxifen is unlikely to interfere with this elimination pathway. In vitro data suggest that clofazimine is a CYP3A4 inhibitor. Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Clofazimine may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. As the active metabolites, 4-hydroxytamoxifen and endoxifen, are much more potent than tamoxifen, a decrease of those plasma concentrations may lead to decreased efficacy. Close monitoring of tamoxifen efficacy should be considered. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Clofibrate

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Clofibrate is hydrolysed to an active metabolite, clofibric acid. Excretion of clofibric acid glucuronide is possibly performed via OAT1. Tamoxifen is unlikely to interfere with this metabolic or elimination pathway. However, in post marketing research infrequent cases of hyperlipidemia have been reported during therapy with tamoxifen. The clinical relevance of this interaction is unknown. Monitoring of triglycerides and cholesterol may be required.

Description:

See Summary

No Interaction Expected

Tamoxifen

Clomipramine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Clomipramine is metabolised by CYPs 3A4, 1A2 and 2C19 to desmethylclomipramine, an active metabolite which has a higher activity than the parent drug. In addition, clomipramine and desmethylclomipramine are metabolised by CYP2D6. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Clonidine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Approximately 70% of administered clonidine is excreted in the urine, mainly in the form of the unchanged parent drug (40-60% of the dose). Clonidine is also a weak inhibitor of OCT2. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Clopidogrel

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Clopidogrel is a prodrug and is converted to its active metabolite mainly through CYP2C19 with CYPs 3A4, 2B6 and 1A2 playing a minor role. Moreover, clopidogrel is an inhibitor of CYP2C8 (strong), CYP2B6 (weak) and of CYP2C9 (in vitro) at high concentrations. The clinical relevance of CYP2C9 inhibition is unknown. Tamoxifen does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Clorazepate

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Clorazepate is rapidly converted to nordiazepam which is then metabolised to oxazepam by CYP3A4. Oxazepam is mainly glucuronidated. Tamoxifen does not inhibit or induce CYPs or UGTs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Cloxacillin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cloxacillin is metabolised to a limited extent, and the unchanged drug and metabolites are excreted in the urine by glomerular filtration and renal tubular secretion. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Clozapine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Clozapine is metabolised mainly by CYP1A2 and CYP3A4, and to a lesser extent by CYP2C19 and CYP2D6. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Codeine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Codeine is converted via CYP2D6 to morphine, an active metabolite with analgesic and opioid properties. Morphine is further metabolized by conjugation with glucuronic acid to morphine-3-glucuronide (inactive) and morphine-6-glucuronide (active). Codeine is converted via CYP3A4 to norcodeine, an inactive metabolite. Additionally, the metabolite morphine is a substrate of P-gp. Tamoxifen does not inhibit or induce CYPs or UGTs. However, tamoxifen is an inhibitor of P-gp and may increase morphine concentrations. The clinical relevance of this interaction is unknown. Monitoring for morphine toxicity may be required.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Colchicine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Colchicine is metabolised by CYP3A4 and is a substrate of P-gp. Tamoxifen is an inhibitor of P-gp and may increase colchicine concentrations. The clinical relevance of this interaction is unknown. Monitoring for colchicine toxicity may be required.

Description:

See Summary

No Interaction Expected

Tamoxifen

Cycloserine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cycloserine is predominantly excreted renally via glomerular filtration. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Dabigatran

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Dabigatran is transported via P-gp and is renally excreted. Tamoxifen is an inhibitor of P-gp and may increase dabigatran concentrations. The clinical relevance of this interaction is unknown. Monitoring for dabigatran toxicity and ecarine clotting time (ECT) or diluted thrombin time (dTT) may be required.

Description:

See Summary

No Interaction Expected

Tamoxifen

Dalteparin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dalteparin is excreted largely unchanged via the kidneys. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Dapsone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Metabolism of dapsone is mainly by N-acetylation with a component of N-hydroxylation and is via multiple CYP450 enzymes. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Desipramine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Desipramine is metabolised by CYP2D6. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Desogestrel

Quality of Evidence: Very Low

Summary:

The efficacy of hormonal contraceptives and tamoxifen may both decrease if coadministered. Therefore, coadministration of hormones in hormone-sensitive cancer is contraindicated. In addition, tamoxifen is associated with an increased risk of venous thromboembolic events as are hormonal contraceptives. Desogestrel is a prodrug which is activated to etonogestrel by CYP2C9 (and possibly CYP2C19); the metabolism of etonogestrel is mediated by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Dexamethasone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dexamethasone is a substrate of CYP3A4. Tamoxifen does not inhibit or induce CYPs. Furthermore, dexamethasone has been described as a weak inducer of CYP3A4 but the clinical relevance of this interaction is not known. Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Dexamethasone may decrease tamoxifen concentrations and increase concentrations of the active metabolites of tamoxifen. If an interaction occurs the exposure to the active metabolite increases which will not negatively influence the efficacy of tamoxifen.

Description:

See Summary

No Interaction Expected

Tamoxifen

Dextropropoxyphene

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dextropropoxyphene is mainly metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Diamorphine (diacetylmorphine)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Diamorphine is rapidly metabolised by sequential deacetylation to morphine which is then mainly glucuronidated to morphine-3-glucuronide (UGT2B7>UGT1A1) and, to a lesser extent, to the pharmacologically active morphine-6-glucuronide (UGT2B7>UGT1A1). Additionally, morphine is a substrate of P-gp. Tamoxifen does not inhibit or induce UGTs. However, tamoxifen is an inhibitor of P-gp and may increase morphine concentrations. The clinical relevance of this interaction is unknown. Monitoring for morphine toxicity may be required.

Description:

See Summary

No Interaction Expected

Tamoxifen

Diazepam

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Diazepam is metabolised to nordiazepam (by CYP3A4 and CYP2C19) and to temazepam (mainly by CYP3A4). Temazepam is mainly glucuronidated. Tamoxifen does not inhibit or induce CYPs or UGTs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Diclofenac

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Diclofenac is partly glucuronidated by UGT2B7 and partly oxidised by CYP2C9. Tamoxifen does not inhibit or induce CYPs or UGTs.

Description:

See Summary

Potential Interaction

Tamoxifen

Digoxin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Digoxin is eliminated renally via OATP4C1 and P-gp. Tamoxifen is an inhibitor of P-gp and may increase digoxin concentrations. The clinical relevance of this interaction is unknown. Monitor for digoxin toxicity and, if available, digoxin plasma concentrations.

Description:

See Summary

No Interaction Expected

Tamoxifen

Dihydrocodeine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dihydrocodeine undergoes predominantly direct glucuronidation, with CYP3A4 mediated metabolism accounting for only 5-10% of the overall metabolism. Tamoxifen does not inhibit or induce CYPs or UGTs.

Description:

See Summary

Potential Interaction

Tamoxifen

Diltiazem

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Diltiazem is metabolised by CYP3A4 and CYP2D6. Tamoxifen does not inhibit or induce CYPs. Diltiazem is also an inhibitor of CYP3A4 (moderate) and P-gp, but the clinical relevance of P-gp inhibition by diltiazem is unknown. Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Diltiazem may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. As the active metabolites, 4-hydroxytamoxifen and endoxifen, are much more potent than tamoxifen, a decrease of those plasma concentrations may lead to decreased efficacy. Close monitoring of tamoxifen efficacy is recommended. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

Potential Interaction

Tamoxifen

Diphenhydramine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Diphenhydramine is mainly metabolised by CYP2D6 and to a lesser extent by CYPs 1A2, 2C9 and 2C19. Tamoxifen does not inhibit or induce CYPs. Moreover, diphenhydramine is a weak inhibitor of CYP2D6. Tamoxifen is metabolised by CYP2D6 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Diphenhydramine may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. As the active metabolites, 4-hydroxytamoxifen and endoxifen, are much more potent than tamoxifen, a decrease of those plasma concentrations may lead to decreased efficacy. Monitoring for tamoxifen efficacy is recommended. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

No Interaction Expected

Tamoxifen

Dipyridamole

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dipyridamole is glucuronidated by many UGTs, specifically those of the UGT1A subfamily. Tamoxifen does not inhibit or induce UGTs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Disopyramide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Disopyramide is metabolised by CYP3A4 (25%) and 50% of the drug is eliminated unchanged in the urine. Tamoxifen does not inhibit or induce CYPs and is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Dolasetron

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dolasetron is converted by carbonyl reductase to its active metabolite, hydrodolasetron, which is mainly glucuronidated (60%) and metabolised by CYP2D6 (10-20%) and CYP3A4 (<1%). Tamoxifen does not inhibit or induce CYPs or UGTs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Domperidone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Domperidone is mainly metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Dopamine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dopamine is metabolised in the liver, kidneys, and plasma by monoamine oxidase (MAO) and catechol-O-methyltransferase to inactive compounds. About 25% of a dose of dopamine is metabolised to norepinephrine within the adrenergic nerve terminals. There is little potential for dopamine to affect disposition of tamoxifen, or to be affected if coadministered with tamoxifen.

Description:

See Summary

No Interaction Expected

Tamoxifen

Doxazosin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Doxazosin is metabolised mainly by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Doxepin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Doxepin is metabolised to nordoxepin (a metabolite with comparable pharmacological activity as the parent compound) mainly by CYP2C19. In addition, doxepin and nordoxepin are metabolised by CYP2D6. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Doxycycline

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Doxycycline is excreted in the urine and faeces as unchanged active substance. Tamoxifen is unlikely to interfere with this elimination pathway. Between 40-60% of an administered dose can be accounted for in the urine.

Description:

See Summary

No Interaction Expected

Tamoxifen

Dronabinol

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dronabinol is mainly metabolised by CYP2C9 and to a lesser extent by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Drospirenone

Quality of Evidence: Very Low

Summary:

The efficacy of hormonal contraceptives and tamoxifen may both decrease if coadministered. Therefore, coadministration of hormones in hormone-sensitive cancer is contraindicated. In addition, tamoxifen is associated with an increased risk of venous thromboembolic events as are hormonal contraceptives. Drospirenone is metabolised to a minor extent via CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Dulaglutide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dulaglutide is degraded by endogenous endopeptidases. Tamoxifen does not interact with this metabolic pathway. Dulaglutide delays gastric emptying and could possibly decrease the absorption rate of concomitantly administered oral drugs. The clinical relevance of delayed absorption is considered to be limited.

Description:

See Summary

No Interaction Expected

Tamoxifen

Duloxetine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Duloxetine is metabolised by CYP2D6 and CYP1A2. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Dutasteride

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dutasteride is mainly metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Dydrogesterone

Quality of Evidence: Very Low

Summary:

The efficacy of hormonal contraceptives and tamoxifen may both decrease if coadministered. Therefore, coadministration of hormones in hormone-sensitive cancer is contraindicated. In addition, tamoxifen is associated with an increased risk of venous thromboembolic events as are hormonal contraceptives. Dydrogesterone is metabolised to dihydrodydrogesterone (possibly via CYP3A4). Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Edoxaban

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Edoxaban is partially metabolised by CYP3A4 (<10%) and is transported via P-gp. Tamoxifen is an inhibitor of P-gp and may increase edoxaban concentrations. The clinical relevance of this interaction is unknown. Monitoring for edoxaban toxicity and anti-Xa activity may be required.

Description:

See Summary

No Interaction Expected

Tamoxifen

Eltrombopag

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Eltrombopag is metabolised by cleavage conjugation (via UGT1A1 and UGT1A3) and oxidation (via CYP1A2 and CYP2C8). Tamoxifen does not inhibit or induce CYPs or UGTs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Enalapril

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Enalapril is hydrolysed to enalaprilat which is eliminated renally (possibly via OATs). Tamoxifen is unlikely to interfere with this metabolic or elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Enoxaparin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Enoxaparin does not undergo cytochrome metabolism but is desulphated and depolymerised in the liver and is predominantly renally excreted. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Eprosartan

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Eprosartan is largely excreted in bile and urine as unchanged drug. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Ertapenem

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ertapenem is mainly eliminated through the kidneys by glomerular filtration with tubular secretion playing a minor role. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

Potential Interaction

Tamoxifen

Erythromycin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Erythromycin is a substrate of CYP3A4 and P-gp. Tamoxifen is an inhibitor of P-gp and may increase erythromycin concentrations. The clinical relevance of this interaction is unknown. Monitoring for erythromycin toxicity may be required. Moreover, erythromycin is an inhibitor of CYP3A4 (moderate) and P-gp. Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Erythromycin may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. As the active metabolites, 4-hydroxytamoxifen and endoxifen, are much more potent than tamoxifen, a decrease of those plasma concentrations may lead to decreased efficacy. Close monitoring of tamoxifen efficacy is recommended. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

No Interaction Expected

Tamoxifen

Escitalopram

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Escitalopram is metabolised by CYPs 2C19 (37%), 2D6 (28%) and 3A4 (35%) to form N-desmethylescitalopram. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Esomeprazole

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Esomeprazole is metabolised by CYP2C19 and CYP3A4. Esomeprazole is also an inhibitor of CYP2C19. Tamoxifen does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Estazolam

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Estazolam is metabolised to its major metabolite 4-hydroxyestazolam via CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Estradiol

Quality of Evidence: Very Low

Summary:

The efficacy of hormonal contraceptives and tamoxifen may both decrease if coadministered. Therefore, coadministration of hormones in hormone-sensitive cancer is contraindicated. In addition, tamoxifen is associated with an increased risk of venous thromboembolic events as are hormonal contraceptives. Estradiol is metabolised by CYP3A4, CYP1A2 and is glucuronidated. Tamoxifen does not inhibit or induce CYPs or UGTs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Ethambutol

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ethambutol is partly metabolised by alcohol dehydrogenase (20%) and partly eliminated unchanged in the faeces (20%) and urine (50%). Tamoxifen is unlikely to interfere with this metabolic or elimination pathway.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Ethinylestradiol

Quality of Evidence: Very Low

Summary:

The efficacy of hormonal contraceptives and tamoxifen may both decrease if coadministered. Therefore, coadministration of hormones in hormone-sensitive cancer is contraindicated. In addition, tamoxifen is associated with an increased risk of venous thromboembolic events as are hormonal contraceptives. Ethinylestradiol undergoes oxidation (CYP3A4>CYP2C9), sulfation and glucuronidation (UGT1A1). Tamoxifen does not inhibit or induce CYPs or UGTs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Ethionamide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ethionamide is extensively metabolised in the liver; animal studies suggest involvement of flavin-containing monooxygenases. Tamoxifen does not interact with this metabolic pathway.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Etonogestrel

Quality of Evidence: Very Low

Summary:

Description:

See Summary

Potential Interaction

Tamoxifen

Everolimus (Immunosuppressant)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Everolimus is mainly metabolised by CYP3A4 and is a substrate of P-gp. Tamoxifen is an inhibitor of P-gp and may increase everolimus concentrations. The clinical relevance of this interaction is unknown. Monitor for everolimus toxicity and, if available, everolimus plasma concentrations.

Description:

See Summary

No Interaction Expected

Tamoxifen

Exenatide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Exenatide is cleared mainly by glomerular filtration. Tamoxifen is unlikely to interfere with exenatide renal elimination. Exenatide delays gastric emptying and could possibly decrease the absorption rate of concomitantly administered oral drugs. The clinical relevance of delayed absorption is considered to be limited.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Ezetimibe

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Ezetimibe is glucuronidated by UGTs 1A1 and 1A3 and to a lesser extent by UGTs 2B15 and 2B7. Tamoxifen does not inhibit or induce UGTs. However, in post marketing research infrequent cases of hyperlipidemia have been reported during therapy with tamoxifen. The clinical relevance of this interaction is unknown. Monitoring of triglycerides and cholesterol may be required.

Description:

See Summary

No Interaction Expected

Tamoxifen

Famotidine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Famotidine is excreted via OAT1/OAT3. Tamoxifen does not inhibit or induce OATs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Felodipine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Felodipine is metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Fenofibrate

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Fenofibrate is hydrolysed to an active metabolite, fenofibric acid. In vitro data suggest that fenofibric acid inhibits OAT3. Tamoxifen does not interact with this metabolic pathway. However, in post marketing research infrequent cases of hyperlipidemia have been reported during therapy with tamoxifen. The clinical relevance of this interaction is unknown. Monitoring of triglycerides and cholesterol may be required.

Description:

See Summary

No Interaction Expected

Tamoxifen

Fentanyl

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fentanyl undergoes extensive CYP3A4 metabolism. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Fexofenadine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Fexofenadine is a substrate of P-gp. Tamoxifen is an inhibitor of P-gp and may increase concentrations of fexofenadine. The clinical relevance of this interaction is unknown. Monitoring for fexofenadine toxicity may be required.

Description:

See Summary

No Interaction Expected

Tamoxifen

Finasteride

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Finasteride is metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Fish oils

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. In post marketing research infrequent cases of hyperlipidemia have been reported during therapy with tamoxifen. The clinical relevance of this interaction is unknown. Monitoring of triglycerides and cholesterol may be required.

Description:

See Summary

No Interaction Expected

Tamoxifen

Flecainide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Flecainide is metabolised mainly via CYP2D6, with a proportion (approximately 30%) of the parent drug also eliminated unchanged renally. Tamoxifen does not inhibit or induce CYPs and is unlikely to interfere with this elimination pathway.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Flucloxacillin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Flucloxacillin is mainly renally eliminated partly by glomerular filtration and partly by active secretion via OAT1. Tamoxifen is unlikely to interfere with this elimination pathway and does not inhibit or induce OATs. Flucloxacillin is also described as a CYP3A4 inducer. Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Flucloxacillin may decrease tamoxifen concentrations and increase concentrations of the active metabolites of tamoxifen. The net effect on the exposure to tamoxifen and the active metabolites is unknown and therefore the clinical relevance of this interaction cannot be determined. Moreover, the mechanism of CYP3A4 induction by flucloxacillin is unknown. Close monitoring of tamoxifen efficacy and endoxifen plasma concentrations should be considered.

Description:

See Summary

Potential Interaction

Tamoxifen

Fluconazole

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Fluconazole is cleared primarily by renal excretion and is also an inhibitor of CYPs 3A4 (moderate), 2C9 (moderate) and 2C19 (strong). Tamoxifen is unlikely to interfere with this elimination pathway. Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Fluconazole may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. In a simulation study fluconazole appeared to increase tamoxifen concentrations by 6%. The clinical relevance of this simulation is unknown. As the active metabolites, 4-hydroxytamoxifen and endoxifen, are much more potent than tamoxifen, a decrease of those plasma concentrations may lead to decreased efficacy. Close monitoring of tamoxifen efficacy is recommended. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

No Interaction Expected

Tamoxifen

Flucytosine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a interaction is unlikely. Flucytosine is metabolised to 5-fluorouracil (5-FU). 5-FU is further metabolised by dihydropyrimidine dehydrogenase (DPD) to an inactive metabolite. Tamoxifen does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Fludrocortisone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fludrocortisone is metabolised in the liver to inactive metabolites, possibly via CYP3A. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Flunitrazepam

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Flunitrazepam is metabolised mainly via CYP3A4 and CYP2C19. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Fluoxetine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be avoided. Fluoxetine is mainly metabolised by CYP2D6 and CYP2C9 and to a lesser extent by CYP2C19 and CYP3A4 to form norfluoxetine. Tamoxifen does not inhibit or induce CYPs. Fluoxetine is also a strong inhibitor of CYP2D6 and CYP2C19. Tamoxifen is metabolised by CYP2D6 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Fluoxetine may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. Tamoxifen product labels state that after coadministration with paroxetine, a strong CYP2D6 inhibitor, endoxifen concentrations decreased by 64%. A decrease in endoxifen plasma concentrations may lead to decreased efficacy as endoxifen is much more potent than tamoxifen. Coadministration should be avoided. If coadministration is unavoidable, closely monitor tamoxifen efficacy. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

No Interaction Expected

Tamoxifen

Fluphenazine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fluphenazine is metabolised by CYP2D6. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Flurazepam

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. The metabolism of flurazepam is most likely CYP-mediated. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Fluticasone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fluticasone is metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Fluvastatin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Fluvastatin is mainly metabolised by CYP2C9 (75%) and to a lesser extent by CYP3A4 (20%) and CYP2C8 (5%). Fluvastatin also potentially inhibits CYP2C9, but the clinical relevance of CYP2C9 inhibition is unknown. Tamoxifen does not interact with this metabolic pathway. However, in post marketing research infrequent cases of hyperlipidemia have been reported during therapy with tamoxifen. The clinical relevance of this interaction is unknown. Monitoring of triglycerides and cholesterol may be required.

Description:

See Summary

Potential Interaction

Tamoxifen

Fluvoxamine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Fluvoxamine is metabolised mainly by CYP2D6 and to a lesser extent by CYP1A2. Tamoxifen does not inhibit or induce CYPs. Fluvoxamine is also an inhibitor of CYPs 1A2 (strong), 2C19 (strong), 3A4 (moderate), 2C9 (weak-moderate) and 2D6 (weak). Tamoxifen is metabolised by CYP3A4 and CYP2D6 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Fluvoxamine may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. As the active metabolites, 4-hydroxytamoxifen and endoxifen, are much more potent than tamoxifen, a decrease of those plasma concentrations may lead to decreased efficacy. Close monitoring of tamoxifen efficacy is recommended. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

No Interaction Expected

Tamoxifen

Fondaparinux

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fondaparinux does not undergo cytochrome metabolism but is eliminated predominantly renally. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Formoterol

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Formoterol is eliminated primarily by direct glucuronidation, with O-demethylation (by CYPs 2D6, 2C19, 2C9, and 2A6) followed by further glucuronidation. As multiple CYP450 and UGT enzymes catalyse the transformation the potential for a pharmacokinetic interaction is low.

Description:

See Summary

Potential Interaction

Tamoxifen

Fosaprepitant

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Fosaprepitant is rapidly, almost completely, converted to the active metabolite aprepitant. Tamoxifen does not interact with this metabolic pathway. Aprepitant is mainly metabolized by CYP3A4 and to a lesser extent by CYP1A2 and CYP2C19. Tamoxifen does not inhibit or induce CYPs. During treatment, aprepitant is a moderate inhibitor of CYP3A4. Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Aprepitant may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. As the active metabolites, 4-hydroxytamoxifen and endoxifen, are much more potent than tamoxifen, a decrease of those plasma concentrations may lead to decreased efficacy. No a priori dose adjustment for tamoxifen is necessary during the few days of coadministration. Moreover, after treatment aprepitant is a weak inducer of CYP3A4, CYP2C9 and UGT. Aprepitant may decrease tamoxifen concentrations due to CYP3A4, UGT1A4 and UGT2B7 induction. Therefore, concentrations of the active metabolites of tamoxifen, 4-hydroxytamoxifen and endoxifen, may increase. The clinical relevance of this interaction is unknown. Monitoring for granisetron toxicity may be required.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Fosphenytoin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be avoided. Fosphenytoin is rapidly converted to the active metabolite phenytoin. Tamoxifen does not interact with this metabolic pathway. Phenytoin is mainly metabolized by CYP2C9 and to a lesser extent by CYP2C19. Tamoxifen does not inhibit or induce CYPs. Phenytoin is a potent inducer of CYP3A4, UGT and P-gp. Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Phenytoin may decrease tamoxifen concentrations and increase concentrations of the active metabolites of tamoxifen. After coadministration with rifampicin, a strong CYP3A4 inducer, tamoxifen exposure decreased by 84%. Concentrations of N-desmethyltamoxifen, 4-hydroxytamoxifen and endoxifen were decreased by 69%, 73% and 69%, respectively. A similar effect may occur after coadministration with fosphenytoin. Moreover, concentrations of the active metabolites of tamoxifen may further decrease due to induction of UGT1A4 and UGT2B7 by phenytoin. The clinical relevance of UGT induction is unknown. A decrease in exposure can lead to decreased efficacy. Therefore, coadministration should be avoided. If coadministration is unavoidable, closely monitor tamoxifen efficacy. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

No Interaction Expected

Tamoxifen

Furosemide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Furosemide is glucuronidated mainly in the kidney (UGT1A9) and to a lesser extent in the liver (UGT1A1). A large proportion of furosemide is also eliminated unchanged renally (via OATs). OAT1/3 are the major transporters of loop and thiazide diuretics. Secretion of these diuretics into the urinary tract by transporters in the proximal tubular cells is necessary for the diuretic effect in later tubule segments. In vitro data indicate that furosemide is also an inhibitor of the renal transporters OAT1/OAT3. Tamoxifen is unlikely to interfere with this metabolic or elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Gabapentin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Gabapentin is cleared mainly by glomerular filtration. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Gemfibrozil

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Gemfibrozil is metabolised by UGT2B7. Moreover, gemfibrozil is an inhibitor of CYP2C8 (strong), OATP1B1 and OAT3. In vitro data indicate gemfibrozil to be a strong inhibitor of CYP2C9 but in vivo data showed no clinically relevant effect on CYP2C9. Tamoxifen does not interact with this metabolic pathway. However, in post marketing research infrequent cases of hyperlipidemia have been reported during therapy with tamoxifen. The clinical relevance of this interaction is unknown. Monitoring of triglycerides and cholesterol may be required.

Description:

See Summary

No Interaction Expected

Tamoxifen

Gentamicin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Gentamicin is eliminated unchanged predominantly via glomerular filtration. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Gestodene

Quality of Evidence: Very Low

Summary:

The efficacy of hormonal contraceptives and tamoxifen may both decrease if coadministered. Therefore, coadministration of hormones in hormone-sensitive cancer is contraindicated. In addition, tamoxifen is associated with an increased risk of venous thromboembolic events as are hormonal contraceptives. Gestodene is metabolised by CYP3A4 and to a lesser extent by CYP2C9 and CYP2C19. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Glibenclamide (Glyburide)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Glibenclamide is mainly metabolised by CYP3A4 and to a lesser extent by CYP2C9. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Gliclazide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Gliclazide is metabolised mainly by CYP2C9 and to a lesser extent by CYP2C19. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Glimepiride

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Glimepiride is mainly metabolised by CYP2C9. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Glipizide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Glipizide is mainly metabolised by CYP2C9. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Granisetron

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Granisetron is metabolised by CYP3A4 and is a substrate of P-gp. Tamoxifen is an inhibitor of P-gp and may increase granisetron concentrations. The clinical relevance of this interaction is unknown. Monitoring for granisetron toxicity may be required.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Grapefruit juice

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but is contraindicated. Grapefruit juice is known to inhibit CYP3A4 enzymes. Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Grapefruit juice may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. As the active metabolites, 4-hydroxytamoxifen and endoxifen, are much more potent than tamoxifen, a decrease of those plasma concentrations may lead to decreased efficacy. Therefore, coadministration is contraindicated.

Description:

See Summary

Potential Interaction

Tamoxifen

Green tea

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Tamoxifen concentrations may be increased after coadministration with EGCG. The clinical relevance of this interaction is unknown. Increased tamoxifen concentrations may result in decreased concentrations of its active metabolites. As the active metabolites, 4-hydroxytamoxifen and endoxifen, are much more potent than tamoxifen, decrease of those plasma concentrations may lead to decreased efficacy. Try to avoid intake of green tea during treatment with tamoxifen.

Description:

See Summary

Potential Interaction

Tamoxifen

Griseofulvin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Less than 1% of a griseofulvin dose is excreted unchanged via the kidneys. Tamoxifen is unlikely to interfere with this metabolic or elimination pathway. Griseofulvin is also a liver microsomal enzyme inducer and may lower plasma levels, and reduce the efficacy of concomitantly administered medicinal products that are metabolised by CYPs, such as tamoxifen. Tamoxifen is metabolised by CYP2D6 and CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Griseofulvin may decrease tamoxifen concentrations and increase concentrations of the active metabolites of tamoxifen. The net effect on the exposure to tamoxifen and the active metabolites is unknown and therefore the clinical relevance of this interaction cannot be determined. Monitoring for tamoxifen toxicity is recommended. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

No Interaction Expected

Tamoxifen

Haloperidol

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Haloperidol has a complex metabolism as it undergoes glucuronidation (UGTs 2B7>1A4, 1A9), carbonyl reduction as well as oxidative metabolism (CYP3A4 and CYP2D6). Tamoxifen does not inhibit or induce CYPs or UGTs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Heparin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Heparin is thought to be eliminated via the reticuloendothelial system. Tamoxifen does not interact with this metabolic pathway.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Hydralazine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Hydralazine is metabolised via primary oxidative metabolism and acetylation. Tamoxifen does not interact with this metabolic pathway. In vitro studies have suggested that hydralazine is a mixed enzyme inhibitor, which may weakly inhibit CYP3A4 and CYP2D6. Tamoxifen is metabolised by CYP3A4 and CYP2D6 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Hydralazine may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. As the active metabolites, 4-hydroxytamoxifen and endoxifen, are much more potent than tamoxifen, a decrease of those plasma concentrations may lead to decreased efficacy. Monitoring of tamoxifen efficacy and endoxifen plasma concentrations should be considered.

Description:

See Summary

No Interaction Expected

Tamoxifen

Hydrochlorothiazide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Hydrochlorothiazide is not metabolised and is cleared by the kidneys via OAT1. OAT1/3 are the major transporters of loop and thiazide diuretics. Secretion of these diuretics into the urinary tract by transporters in the proximal tubular cells is necessary for the diuretic effect in later tubule segments. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Hydrocodone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Hydrocodone is metabolised by CYP2D6 to hydromorphone and by CYP3A4 to norhydrocodone, both of which have analgesic effects. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Hydrocortisone (oral)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Hydrocortisone is metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Hydrocortisone (topical)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely with the topical use of hydrocortisone.

Description:

See Summary

No Interaction Expected

Tamoxifen

Hydromorphone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Hydromorphone is eliminated via glucuronidation, mainly by UGT2B7. Tamoxifen does not inhibit or induce UGTs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Hydroxyurea (Hydroxycarbamide)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Hydroxyurea is metabolised in the liver and cleared via the lungs. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Hydroxyzine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Hydroxyzine is partly metabolised by alcohol dehydrogenase and partly by CYP3A4. Tamoxifen does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Ibandronic acid

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ibandronic acid is not metabolised and is cleared from the plasma by uptake into bone and elimination via renal excretion. Tamoxifen is unlikely to interfere with ibandronic acid elimination pathway. Although no pharmacokinetic interaction is expected, ibandronic acid should be taken after an overnight fast (at least 6 hours) and before the first food or drink of the day. Medicinal products and supplements should be similarly avoided prior to taking ibandronic acid. Fasting should be continued for at least 30 minutes after taking ibandronic acid.

Description:

See Summary

No Interaction Expected

Tamoxifen

Ibuprofen

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ibuprofen is metabolised mainly by CYP2C9 and to a lesser extent by CYP2C8 and direct glucuronidation. Tamoxifen does not inhibit or induce CYPs or UGTs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Iloperidone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Iloperidone is metabolised by CYP3A4 and CYP2D6. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Imipenem/Cilastatin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Imipenem/cilastatin are eliminated by glomerular filtration and to a lesser extent by active tubular secretion. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Imipramine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Imipramine is metabolised by CYPs 3A4, 2C19 and 1A2 to desipramine. Imipramine and desipramine are both metabolised by CYP2D6. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Indapamide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Indapamide is extensively metabolised by CYP450s. OAT1/3 are the major transporters of loop and thiazide diuretics. Secretion of these diuretics into the urinary tract by transporters in the proximal tubular cells is necessary for the diuretic effect in later tubule segments. Tamoxifen does not inhibit or induce CYPs or OATs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Insulin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely.

Description:

See Summary

No Interaction Expected

Tamoxifen

Interferon alpha

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely.

Description:

See Summary

No Interaction Expected

Tamoxifen

Interleukin 2 (Aldesleukin)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Interleukin-2 is mainly eliminated by glomerular filtration. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Ipratropium bromide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. A small proportion of an inhaled ipratropium dose is systemically absorbed (6.9%). Metabolism is via ester hydrolysis and conjugation. Tamoxifen does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Irbesartan

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Irbesartan is metabolised by glucuronidation and oxidation (mainly CYP2C9). Tamoxifen does not inhibit or induce OATs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Iron supplements

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely.

Description:

See Summary

No Interaction Expected

Tamoxifen

Isoniazid

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Isoniazid is acetylated in the liver to form acetylisoniazid which is then hydrolysed to isonicotinic acid and acetylhydrazine. Tamoxifen does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Isosorbide dinitrate

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. In vitro studies suggest that CYP3A4 has a role in nitric oxide formation from isosorbide dinitrate. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Itraconazole

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be avoided. Itraconazole is primarily metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs. Itraconazole is also an inhibitor of CYP3A4 (strong), CYP2C9 (weak), P-gp and BCRP. Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Itraconazole may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. In a simulation study itraconazole appeared to increase tamoxifen concentrations by 1%. The clinical relevance of this simulation is unknown. As the active metabolites, 4-hydroxytamoxifen and endoxifen, are much more potent than tamoxifen, a decrease of those plasma concentrations may lead to decreased efficacy. Coadministration should be avoided. If coadministration is unavoidable, closely monitor tamoxifen efficacy. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

No Interaction Expected

Tamoxifen

Ivabradine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ivabradine is metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Kanamycin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Kanamycin is eliminated unchanged predominantly via glomerular filtration. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Ketoconazole

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be avoided. Ketoconazole is a substrate of CYP3A4. Tamoxifen does not inhibit or induce CYPs. Moreover, ketoconazole is an inhibitor of CYP3A4 (strong) and P-gp. Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Ketoconazole may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. As the active metabolites, 4-hydroxytamoxifen and endoxifen, are much more potent than tamoxifen, a decrease of those plasma concentrations may lead to decreased efficacy. Coadministration should be avoided. If coadministration is unavoidable, closely monitor tamoxifen efficacy. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

No Interaction Expected

Tamoxifen

Labetalol

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Labetalol is mainly glucuronidated (via UGT1A1 and UGT2B7). Tamoxifen does not inhibit or induce UGTs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Lacidipine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Lacidipine is metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Lactulose

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Metabolism of lactulose to lactic acid occurs via gastro-intestinal microbial flora only. Tamoxifen does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Lansoprazole

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Lansoprazole is mainly metabolised by CYP2C19 and to a lesser extent by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Lercanidipine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Lercanidipine is mainly metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Levocetirizine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Less than 14% of a dose of levocetirizine is metabolised. Levocetirizine is mainly eliminated unchanged in the urine through both glomerular filtration and tubular secretion. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Levofloxacin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Levofloxacin is renally eliminated mainly by glomerular filtration and active secretion (possibly OCT2). Tamoxifen is unlikely to interfere with this elimination pathway and does not inhibit or induce OCTs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Levomepromazine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Levomepromazine is metabolised by CYP2D6. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Levonorgestrel

Quality of Evidence: Very Low

Summary:

The efficacy of hormonal contraceptives and tamoxifen may both decrease if coadministered. Therefore, coadministration of hormones in hormone-sensitive cancer is contraindicated. In addition, tamoxifen is associated with an increased risk of venous thromboembolic events as are hormonal contraceptives. Levonorgestrel is mainly metabolised by CYP3A4 and is glucuronidated to a minor extent. Tamoxifen does not inhibit or induce CYPs or UGTs.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Levonorgestrel (Emergency Contraception)

Quality of Evidence: Very Low

Summary:

The efficacy of hormonal contraceptives and tamoxifen may both decrease if coadministered. Therefore, coadministration of hormones in hormone-sensitive cancer is contraindicated. In addition, tamoxifen is associated with an increased risk of venous thromboembolic events as are hormonal contraceptives. Levonorgestrel is mainly metabolised by CYP3A4 and is glucuronidated to a minor extent. Tamoxifen does not inhibit or induce CYPs or UGTs.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Levothyroxine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Levothyroxine is metabolised by deiodination (by enzymes of deiodinase family) and glucuronidation. Tamoxifen does not interact with this metabolic pathway. However, there are post marketing reports of T4 elevations in postmenopausal patients taking tamoxifen that may be explained by increases in thyroid-binding globulin. These elevations were not accompanied by clinical hyperthyroidism. Monitoring for T4 concentrations may be required.

Description:

See Summary

No Interaction Expected

Tamoxifen

Lidocaine (Lignocaine)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. CYP1A2 is the predominant enzyme involved in lidocaine metabolism in the range of therapeutic concentrations with a minor contribution from CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Potential Interaction

Tamoxifen

Linagliptin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Linagliptin is mainly eliminated as parent compound in faeces with metabolism by CYP3A4 representing a minor metabolic pathway. Linagliptin is also a substrate of P-gp. Tamoxifen is an inhibitor of P-gp and may increase concentrations of linagliptin. The clinical relevance of this interaction is unknown. Monitoring for linagliptin toxicity may be required. Linagliptin is also a weak inhibitor of CYP3A4. Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Linagliptin may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. As the active metabolites, 4-hydroxytamoxifen and endoxifen, are much more potent than tamoxifen, a decrease of those plasma concentrations may lead to decreased efficacy. Close monitoring of tamoxifen efficacy is recommended. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

No Interaction Expected

Tamoxifen

Linezolid

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Linezolid undergoes non-CYP mediated metabolism. Tamoxifen is unlikely to interfere with this unspecified metabolic pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Liraglutide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Liraglutide is degraded by endogenous endopeptidases. Tamoxifen does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Lisinopril

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Lisinopril is eliminated unchanged renally via glomerular filtration. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Lithium

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Lithium is mainly eliminated unchanged through the kidneys. Lithium is freely filtered at a rate that is dependent upon the glomerular filtration rate. No pharmacokinetic interaction is expected.

Description:

See Summary

No Interaction Expected

Tamoxifen

Live vaccines

Quality of Evidence: Very Low

Summary:

Coadministration of live vaccines (such as BCG vaccine; measles, mumps and rubella vaccines; varicella vaccines; typhoid vaccines; rotavirus vaccines; yellow fever vaccines; oral polio vaccine) has not been studied. In patients, who are receiving cytotoxics or other immunosuppressant drugs, use of live vaccines for immunisation is contraindicated. If coadministration is judged clinically necessary, use with extreme caution since generalised infections can occur. However, tamoxifen is not an immunosuppressant, immunomodulatory or bone marrow toxic drug. Therefore, no pharmacodynamic interaction is expected with live vaccines.

Description:

See Summary

No Interaction Expected

Tamoxifen

Loperamide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Loperamide is mainly metabolised by CYP3A4 and CYP2C8 and is a substrate of P-gp. Tamoxifen is an inhibitor of P-gp and may increase loperamide concentrations. However, since loperamide has a broad therapeutic index, no clinically relevant effect on loperamide exposure is expected.

Description:

See Summary

No Interaction Expected

Tamoxifen

Loratadine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Loratadine is metabolised mainly by CYP3A4 and to a lesser extent by CYP2D6. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Lorazepam

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Lorazepam undergoes non-CYP-mediated elimination. Tamoxifen is unlikely to interfere with this unspecified metabolic pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Lormetazepam

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Lormetazepam is mainly glucuronidated. Tamoxifen does not inhibit or induce UGTs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Losartan

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Losartan is converted to its active metabolite mainly by CYP2C9 in the range of clinical concentrations. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Lovastatin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Lovastatin is metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs. However, in post marketing research infrequent cases of hyperlipidemia have been reported during therapy with tamoxifen. The clinical relevance of this interaction is unknown. Monitoring of triglycerides and cholesterol may be required.

Description:

See Summary

No Interaction Expected

Tamoxifen

Macitentan

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Macitentan is metabolised mainly by CYP3A4 and to a lesser extent by CYPs 2C19, 2C9 and 2C8. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Magnesium

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Magnesium is eliminated in the kidney, mainly by glomerular filtration. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Maprotiline

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Maprotiline is mainly metabolised by CYP2D6. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Medroxyprogesterone (depot)

Quality of Evidence: Very Low

Summary:

The efficacy of hormonal contraceptives and tamoxifen may both decrease if coadministered. Therefore, coadministration of hormones in hormone-sensitive cancer is contraindicated. In addition, tamoxifen is associated with an increased risk of venous thromboembolic events as are hormonal contraceptives. Medroxyprogesterone is metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs. Furthermore, medroxyprogesterone reduces the plasma concentration of N-desmethyl tamoxifen, but not that of tamoxifen. The clinical relevance of this interaction is unknown.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Medroxyprogesterone (non-depot)

Quality of Evidence: Very Low

Summary:

The efficacy of hormonal contraceptives and tamoxifen may both decrease if coadministered. Therefore, coadministration of hormones in hormone-sensitive cancer is contraindicated. In addition, tamoxifen is associated with an increased risk of venous thromboembolic events as are hormonal contraceptives. Medroxyprogesterone is metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs. Furthermore, medroxyprogesterone reduces the plasma concentration of N-desmethyl tamoxifen, but not that of tamoxifen. The clinical relevance of this interaction is unknown.

Description:

See Summary

No Interaction Expected

Tamoxifen

Mefenamic acid

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Mefenamic acid is metabolised by CYP2C9 and glucuronidated by UGT2B7 and UGT1A9. Tamoxifen does not inhibit or induce CYPs or UGTs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Megestrol acetate

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Megestrol acetate is mainly eliminated in the urine. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Meropenem

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Meropenem is primarily eliminated by the kidney with in vitro data suggesting it is a substrate of the renal transporters OAT3>OAT1. Tamoxifen is unlikely to interfere with this elimination pathway and does not inhibit or induce OATs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Mesalazine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Mesalazine is metabolised to N-acetyl-mesalazine by N-acetyltransferase. Tamoxifen does not interact with this metabolic pathway.

Description:

See Summary

Potential Interaction

Tamoxifen

Metamizole

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but is not recommended. Metamizole is metabolised by hydrolysis to the active metabolite MAA in the gastrointestinal tract. Metamizole is metabolised in serum and excreted via urine (90%) and faeces (10%). Tamoxifen is unlikely to interfere with this metabolic or elimination pathway. However, metamizole is an inducer of CYP3A4. Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Metamizole may decrease tamoxifen concentrations and increase concentrations of the active metabolites of tamoxifen. The net effect on the exposure to tamoxifen and the active metabolites is unknown and therefore the clinical relevance of this interaction cannot be determined. Coadministration is not recommended. If coadministration is unavoidable, monitor closely for tamoxifen toxicity. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

No Interaction Expected

Tamoxifen

Metformin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Metformin is mainly eliminated unchanged in the urine and is a substrate of OCT1, OCT2, OCT3, MATE1 and MATE2K. Tamoxifen does not inhibit or induce OCTs or MATEs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Methadone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Methadone is demethylated by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Methyldopa

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Methyldopa is excreted in urine largely by glomerular filtration, primarily unchanged and as the mono-O-sulfate conjugate. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Methylphenidate

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Methylphenidate is not metabolised by CYP450s to a clinically relevant extent and does not inhibit or induce CYP450s. Therefore, there is little potential for methylphenidate to affect disposition of tamoxifen, or to be affected if coadministered with tamoxifen.

Description:

See Summary

No Interaction Expected

Tamoxifen

Methylprednisolone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Methylprednisolone is metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Metoclopramide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Metoclopramide is partially metabolised by the CYP450 system (mainly CYP2D6). Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Metolazone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Metolazone is largely excreted unchanged in the urine. OAT1/3 are the major transporters of loop and thiazide diuretics. Secretion of these diuretics into the urinary tract by transporters in the proximal tubular cells is necessary for the diuretic effect in later tubule segments. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Metoprolol

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Metoprolol is mainly metabolised by CYP2D6. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Metronidazole

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Metronidazole is eliminated via glomerular filtration. Tamoxifen is unlikely to interfere with this elimination pathway. Elevated plasma concentrations have been reported for some CYP3A substrates (e.g. tacrolimus, ciclosporin) with metronidazole. However, metronidazole did not increase concentrations of several CYP3A probe drugs (e.g. midazolam, alprazolam). Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Metronidazole may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. As the active metabolites, 4-hydroxytamoxifen and endoxifen, are much more potent than tamoxifen, a decrease of those plasma concentrations may lead to decreased efficacy. Close monitoring of tamoxifen efficacy should be considered. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

No Interaction Expected

Tamoxifen

Mexiletine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Mexiletine is metabolised mainly by CYP2D6 and to a lesser extent by CYP1A2. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Mianserin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Mianserin is metabolised by CYPs 2D6 and 1A2, and to a lesser extent by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Miconazole

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be avoided. Miconazole is extensively metabolized by the liver. Tamoxifen is unlikely to interfere with this unspecified metabolic pathway. Moreover, miconazole is an inhibitor of CYP2C9 (moderate) and CYP3A4 (strong). Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Miconazole may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. As the active metabolites, 4-hydroxytamoxifen and endoxifen, are much more potent than tamoxifen, a decrease of those plasma concentrations may lead to decreased efficacy. Coadministration should be avoided. If coadministration is unavoidable, closely monitor tamoxifen efficacy. Monitor endoxifen plasma concentrations, if available. Note: after dermal application miconazole is only minimally absorbed. Therefore, no clinically relevant interaction is expected.

Description:

See Summary

No Interaction Expected

Tamoxifen

Midazolam (oral)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Midazolam is metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Midazolam (parenteral)

Quality of Evidence: Very Low

Summary:

Description:

See Summary

No Interaction Expected

Tamoxifen

Milnacipran

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Milnacipran is mainly eliminated unchanged (50%), and as glucuronides (30%) and oxidative metabolites (20%). Tamoxifen does not interact with this elimination or metabolic pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Mirtazapine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Mirtazapine is metabolised to 8-hydroxymirtazapine by CYP2D6 and CYP1A2, and to N-desmethylmirtazapine mainly by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Mometasone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Mometasone is metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Montelukast

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Montelukast is mainly metabolised by CYP2C8 and to a lesser extent by CYPs 3A4 and 2C9. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Morphine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Morphine is mainly glucuronidated to morphine-3-glucuronide (UGT2B7>UGT1A1) and, to a lesser extent, to the pharmacologically active morphine-6-glucuronide (UGT2B7>UGT1A1). Additionally, morphine is a substrate of P-gp. Tamoxifen does not inhibit or induce UGTs. However, tamoxifen is an inhibitor of P-gp and may increase morphine concentrations. The clinical relevance of this interaction is unknown. Monitoring for morphine toxicity may be required.

Description:

See Summary

No Interaction Expected

Tamoxifen

Moxifloxacin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Moxifloxacin is predominantly glucuronidated by UGT1A1. Tamoxifen does not inhibit or induce UGTs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Mycophenolate

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Mycophenolate is mainly glucuronidated by UGT1A9 and UGT2B7. The active metabolite of mycophenolate, mycophenolic acid, is an inhibitor of OAT1/OAT3. Tamoxifen does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Nadroparin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Nadroparin is excreted renally by a nonsaturable mechanism. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Nandrolone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Nandrolone is metabolised in the liver by alpha-reductase. Tamoxifen does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Naproxen

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Naproxen is mainly glucuronidated by UGT2B7 (major) and demethylated to desmethylnaproxen by CYP2C9 (major) and CYP1A2. Tamoxifen does not inhibit or induce CYPs or UGTs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Nateglinide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Nateglinide is mainly metabolised by CYP2C9 (70%) and to a lesser extent by CYP3A4 (30%). Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Nebivolol

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Nebivolol metabolism involves CYP2D6. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Nefazodone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be avoided. Nefazodone is metabolised mainly by CYP3A4. Tamoxifen does not inhibit or induce CYPs. Nefazodone is also a strong inhibitor of CYP3A4. Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Nefazodone may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. As the active metabolites, 4-hydroxytamoxifen and endoxifen, are much more potent than tamoxifen, a decrease of those plasma concentrations may lead to decreased efficacy. Coadministration should be avoided. If coadministration is unavoidable, closely monitor tamoxifen efficacy. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

Potential Interaction

Tamoxifen

Nicardipine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Nicardipine is metabolised mainly by CYP3A4 and to a lesser extent by CYP2D6 and CYP2C8. Tamoxifen does not inhibit or induce CYPs. Moreover, nicardipine is a weak inhibitor of CYP3A4. Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Nicardipine may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. As the active metabolites, 4-hydroxytamoxifen and endoxifen, are much more potent than tamoxifen, a decrease of those plasma concentrations may lead to decreased efficacy. Close monitoring of tamoxifen efficacy is recommended. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

No Interaction Expected

Tamoxifen

Nicotinamide (Niacinamide)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Nicotinamide is converted to N-methylnicotinamide by nicotinamide methyltransferase which in turn is metabolised by xanthine oxidase and aldehyde oxidase. Tamoxifen does not interact with this metabolic pathway.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Nifedipine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Nifedipine is metabolised mainly by CYP3A4. Tamoxifen does not inhibit or induce CYPs. However, an in vitro study showed that nifedipine inhibited the formation of N-desmethyltamoxifen and may therefore decrease the exposure of the metabolite endoxifen (30 to 100-fold more potent than tamoxifen). The clinical relevance of this interaction is unknown. Close monitoring of tamoxifen efficacy may be required. Monitoring of endoxifen plasma concentrations should be considered, if available.

Description:

See Summary

No Interaction Expected

Tamoxifen

Nimesulide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Nimesulide is extensively metabolised in the liver following multiple pathways including CYP2C9. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Nisoldipine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Nisoldipine is metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Nitrendipine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Nitrendipine is extensively metabolised mainly by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Nitrofurantoin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Nitrofurantoin is partly metabolised in the liver via glucuronidation and N-acetylation and partly eliminated in the urine as unchanged drug (30-40%). Tamoxifen does not inhibit or induce UGTs and is unlikely to interfere with this elimination pathway.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Norelgestromin

Quality of Evidence: Very Low

Summary:

The efficacy of hormonal contraceptives and tamoxifen may both decrease if coadministered. Therefore, coadministration of hormones in hormone-sensitive cancer is contraindicated. In addition, tamoxifen is associated with an increased risk of venous thromboembolic events as are hormonal contraceptives. Norelgestromin is metabolised to norgestrel (possibly by CYP3A4). Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Norethisterone (Norethindrone)

Quality of Evidence: Very Low

Summary:

The efficacy of hormonal contraceptives and tamoxifen may both decrease if coadministered. Therefore, coadministration of hormones in hormone-sensitive cancer is contraindicated. In addition, tamoxifen is associated with an increased risk of venous thromboembolic events as are hormonal contraceptives. Norethisterone is extensively biotransformed, first by reduction and then by sulfate and glucuronide conjugation. Tamoxifen does not interact with this metabolic pathway.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Norgestimate

Quality of Evidence: Very Low

Summary:

The efficacy of hormonal contraceptives and tamoxifen may both decrease if coadministered. Therefore, coadministration of hormones in hormone-sensitive cancer is contraindicated. In addition, tamoxifen is associated with an increased risk of venous thromboembolic events as are hormonal contraceptives. Norgestimate is rapidly deacetylated to the active metabolite which is further metabolised via CYP450. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Norgestrel

Quality of Evidence: Very Low

Summary:

The efficacy of hormonal contraceptives and tamoxifen may both decrease if coadministered. Therefore, coadministration of hormones in hormone-sensitive cancer is contraindicated. In addition, tamoxifen is associated with an increased risk of venous thromboembolic events as are hormonal contraceptives. Norgestrel is a racemic mixture with levonorgestrel being biologically active. Levonorgestrel is mainly metabolized by CYP3A4 and is glucuronidated to a minor extent. Tamoxifen does not inhibit or induce CYPs or UGTs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Nortriptyline

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Nortriptyline is metabolised mainly by CYP2D6. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Nystatin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Systemic absorption of nystatin from oral or topical dosage forms is not significant. No drug interactions are expected.

Description:

See Summary

No Interaction Expected

Tamoxifen

Ofloxacin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ofloxacin is renally eliminated unchanged by glomerular filtration and active tubular secretion via both cationic and anionic transport systems. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Olanzapine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Olanzapine is metabolised mainly by CYP1A2 (major) and CYP2D6, but also by glucuronidation (UGT1A4). Tamoxifen does not inhibit or induce CYPs or UGTs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Olmesartan

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Olmesartan medoxomil is de-esterified to the active metabolite olmesartan which is eliminated in the faeces and urine. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Omeprazole

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Omeprazole is mainly metabolised by CYP2C19 and to a lesser extent by CYP3A4. Omeprazole is also an inducer of CYP1A2 and an inhibitor of CYP2C19. Tamoxifen does not interact with this metabolic pathway.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Ondansetron

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Ondansetron is metabolised mainly by CYP1A2 and CYP3A4 and to a lesser extent by CYP2D6. Tamoxifen does not inhibit or induce CYPs. Additionally, ondansetron is a substrate of P-gp. Tamoxifen is an inhibitor of P-gp and may increase concentrations of ondansetron. The clinical relevance of this interaction is unknown. Monitoring for ondansetron toxicity may be required.

Description:

See Summary

No Interaction Expected

Tamoxifen

Oxazepam

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Oxazepam is mainly glucuronidated. Tamoxifen does not inhibit or induce UGTs.

Description:

See Summary

Potential Interaction

Tamoxifen

Oxcarbazepine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but is not recommended. Oxcarbazepine is extensively metabolized to the active metabolite monohydroxyderivate (MHD) through cytosolic enzymes. Tamoxifen does not interact with this metabolic pathway. Both oxcarbazepine and MHD are inducers of CYP3A4 (moderate) and CYP3A5 and are inhibitors of CYP2C19. Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Oxcarbazepine may decrease tamoxifen concentrations and increase concentrations of the active metabolites of tamoxifen. The net effect on the exposure to tamoxifen and the active metabolites is unknown and therefore the clinical relevance of this interaction cannot be determined. Coadministration is not recommended. If coadministration is unavoidable, closely monitor tamoxifen toxicity. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

No Interaction Expected

Tamoxifen

Oxprenolol

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Oxprenolol is largely metabolised via glucuronidation. Tamoxifen does not inhibit or induce UGTs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Oxycodone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Oxycodone is metabolised principally to noroxycodone via CYP3A and oxymorphone via CYP2D6. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Paliperidone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Paliperidone is primarily eliminated renally (possibly via OCT) with minimal metabolism occurring via CYP2D6 and CYP3A4. Tamoxifen does not inhibit or induce CYPs and is unlikely to interfere with this elimination pathway.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Palonosetron

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Palonosetron is metabolised mainly by CYP3A4 and to a lesser extent by CYP2D6 and CYP1A2. Tamoxifen does not inhibit or induce CYPs. Additionally, palonosetron is a substrate of P-gp. Tamoxifen is an inhibitor of P-gp and may increase concentrations of palonosetron. The clinical relevance of this interaction is unknown. Monitoring for palonosetron toxicity may be required.

Description:

See Summary

No Interaction Expected

Tamoxifen

Pamidronic acid

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Pamidronic acid is not metabolised and is cleared from the plasma by uptake into bone and elimination via renal excretion. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Pantoprazole

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Pantoprazole is mainly metabolised by CYP2C19 and to a lesser extent by CYPs 3A4, 2D6 and 2C9. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Para-aminosalicylic acid

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Para-aminosalicylic acid and its acetylated metabolite are mainly excreted in the urine by glomerular filtration and tubular secretion. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Paracetamol (Acetaminophen)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Paracetamol is mainly metabolised by glucuronidation (via UGTs 1A9 (major), 1A6, 1A1, and 2B15), sulfation and, to a lesser extent, by oxidation (CYPs 2E1 (major), 1A2, 3A4 and 2D6). Tamoxifen does not inhibit or induce CYPs or UGTs.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Paroxetine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be avoided. Paroxetine is mainly metabolised by CYP2D6. Tamoxifen does not inhibit or induce CYPs. Paroxetine is also an inhibitor of CYP2D6 (strong) and CYP2C9. Tamoxifen is metabolised by CYP2D6 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Paroxetine may increase tamoxifen concentrations and decrease concentrations of the active metabolites of the tamoxifen. Tamoxifen product labels state that after coadministration with paroxetine, a strong CYP2D6 inhibitor, endoxifen concentrations decreased by 64%. A decrease in endoxifen plasma concentrations may lead to decreased efficacy as endoxifen is much more potent than tamoxifen. Coadministration should be avoided. If coadministration is unavoidable, closely monitor tamoxifen efficacy. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

No Interaction Expected

Tamoxifen

Peginterferon alfa-2a

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely.

Description:

See Summary

No Interaction Expected

Tamoxifen

Penicillins

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Penicillins are mainly eliminated in the urine (20% by glomerular filtration and 80% by tubular secretion via OAT). Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Perazine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Perazine is mainly metabolised by CYPs 1A2, 3A4 and 2C19, and to a lesser extent by CYPs 2C9, 2D6 and 2E1, with oxidation via FMO3. Tamoxifen does not inhibit or induce CYPs or FMO3.

Description:

See Summary

No Interaction Expected

Tamoxifen

Periciazine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. The metabolism of periciazine has not been well characterized but is likely to involve CYP2D6. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Perindopril

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Perindopril is hydrolysed to the active metabolite perindoprilat and is metabolised to other inactive metabolites. Elimination occurs predominantly via the urine. Tamoxifen is unlikely to interfere with this metabolic or elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Perphenazine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Perphenazine is metabolised by CYP2D6. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Pethidine (Meperidine)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Pethidine is metabolised mainly by CYP2B6 and to a lesser extent by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Phenelzine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Phenelzine is primarily metabolised by oxidation via monoamine oxidase and to a lesser extent by acetylation. Tamoxifen does not interact with this metabolic pathway.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Phenobarbital (Phenobarbitone)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be avoided. Phenobarbital is metabolized by CYP2C19 and CYP2C9 (major pathway) and to a lesser extent by CYP2E1. Tamoxifen does not inhibit or induce CYPs. Phenobarbital is a strong inducer of CYPs 3A4, 2C9, 2C8 and UGTs. Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Phenobarbital may decrease tamoxifen concentrations and increase concentrations of the active metabolites of tamoxifen. After coadministration with rifampicin, a strong CYP3A4 inducer, tamoxifen exposure decreased by 84%. Concentrations of N-desmethyltamoxifen, 4-hydroxytamoxifen and endoxifen were decreased by 69%, 73% and 69%, respectively. A similar effect may occur after coadministration with phenobarbital. Moreover, concentrations of the active metabolites of tamoxifen may further decrease due to induction of UGT1A4 and UGT2B7 by phenobarbital. The clinical relevance of UGT induction is unknown. A decrease in exposure can lead to decreased efficacy. Therefore, coadministration should be avoided. If coadministration is unavoidable, closely monitor tamoxifen efficacy. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

Potential Interaction

Tamoxifen

Phenprocoumon

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Phenprocoumon is mainly metabolised by CYP2C9 and CYP3A4. Tamoxifen does not inhibit or induce CYPs. Vitamin K antagonists are used in patients that are at risk of venous thromboembolic events and tamoxifen is associated with an increased risk of venous thromboembolic events, although the exact mechanism of the interaction is unknown. Therefore, coadministration of phenprocoumon and tamoxifen is not recommended. If coadministration is unavoidable, monitor closely for INR/PT and signs of bleeding.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Phenytoin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be avoided. Phenytoin is mainly metabolized by CYP2C9 and to a lesser extent by CYP2C19. Tamoxifen does not inhibit or induce CYPs. Phenytoin is a potent inducer of CYP3A4, UGT and P-gp. Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Phenytoin may decrease tamoxifen concentrations and increase concentrations of the active metabolites of tamoxifen. After coadministration with rifampicin, a strong CYP3A4 inducer, tamoxifen exposure decreased by 84%. Concentrations of N-desmethyltamoxifen, 4-hydroxytamoxifen and endoxifen were decreased by 69%, 73% and 69%, respectively. A similar effect may occur after coadministration with fosphenytoin. Moreover, concentrations of the active metabolites of tamoxifen may further decrease due to induction of UGT1A4 and UGT2B7 by phenytoin. The clinical relevance of UGT induction is unknown. A decrease in exposure can lead to decreased efficacy. Therefore, coadministration should be avoided. If coadministration is unavoidable, closely monitor tamoxifen efficacy. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

No Interaction Expected

Tamoxifen

Phytomenadione (Vitamin K)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. An in vitro study found that the only CYP450 enzyme involved in phytomenadione metabolism was CYP4F2. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Pimozide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Pimozide is mainly metabolised by CYP3A4 and CYP2D6 and to a lesser extent by CYP1A2. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Pindolol

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Pindolol is partly metabolised to hydroxymetabolites (possibly via CYP2D6) and partly eliminated unchanged in the urine. Tamoxifen does not inhibit or induce CYPs and is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Pioglitazone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Pioglitazone is metabolised mainly by CYP2C8 and to a lesser extent by CYPs 3A4, 1A2 and 2C9. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Pipotiazine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. The metabolism of pipotiazine has not been well described but may involve CYP2D6. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Piroxicam

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Piroxicam is primarily metabolised by CYP2C9. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Pitavastatin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Pitavastatin is metabolised by UGTs 1A3 and 2B7 with minimal metabolism by CYPs 2C9 and 2C8. Moreover, pitavastatin is a substrate of OATP1B1. Tamoxifen does not inhibit or induce CYPs, UGTs or OATP1B1. However, in post marketing research infrequent cases of hyperlipidemia have been reported during therapy with tamoxifen. The clinical relevance of this interaction is unknown. Monitoring of triglycerides and cholesterol may be required.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Posaconazole

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be avoided. Posaconazole is primarily metabolised by UGTs and is a substrate of P-gp. Tamoxifen is an inhibitor of P-gp and may increase posaconazole concentrations. The clinical relevance of this interaction is unknown. Moreover, posaconazole is a strong inhibitor of CYP3A4. Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Posaconazole may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. As the active metabolites, 4-hydroxytamoxifen and endoxifen, are much more potent than tamoxifen, a decrease of those plasma concentrations may lead to decreased efficacy. Coadministration should be avoided. If coadministration is unavoidable, closely monitor tamoxifen efficacy. Monitor endoxifen plasma concentrations, if available. Monitoring for posaconazole toxicity may be required.

Description:

See Summary

No Interaction Expected

Tamoxifen

Potassium

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on limited data available an interaction appears unlikely. Potassium is eliminated renally. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Prasugrel

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Prasugrel is a prodrug and is converted to its active metabolite mainly by CYP3A4 and CYP2B6 and to a lesser extent by CYP2C9 and CYP2C19. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Pravastatin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Pravastatin is minimally metabolised via CYP enzymes and is a substrate of OATP1B1. Tamoxifen does not inhibit or induce CYPs or OATP1B1. However, in post marketing research infrequent cases of hyperlipidemia have been reported during therapy with tamoxifen. The clinical relevance of this interaction is unknown. Monitoring of triglycerides and cholesterol may be required.

Description:

See Summary

No Interaction Expected

Tamoxifen

Prazosin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Prazosin is extensively metabolised, primarily by demethylation and conjugation. Tamoxifen does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Prednisolone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Prednisolone undergoes hepatic metabolism via CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Prednisone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Prednisone is converted to the active metabolite prednisolone by 11-B-hydroxydehydrogenase. Prednisolone is then metabolised by CYP3A4. Tamoxifen does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Pregabalin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Pregabalin is cleared mainly by glomerular filtration (90% as unchanged drug). Tamoxifen does not interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Prochlorperazine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Prochlorperazine is metabolised by CYP2D6 and CYP2C19. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Promethazine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Promethazine is metabolised by CYP2D6. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Propafenone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Propafenone is metabolised mainly by CYP2D6 and to a lesser extent by CYP1A2 and CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Propranolol

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Propranolol is metabolised by 3 routes (aromatic hydroxylation by CYP2D6, N-dealkylation followed by side chain hydroxylation via CYPs 1A2, 2C19, 2D6, and direct glucuronidation). Tamoxifen does not inhibit or induce CYPs or UGTs.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Prucalopride

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Prucalopride is minimally metabolised and mainly eliminated renally, partly by active secretion by renal transporters. Additionally, prucalopride is a substrate of P-gp. Tamoxifen is an inhibitor of P-gp and may increase prucalopride concentrations. The clinical relevance of this interaction is unknown. Monitoring for prucalopride toxicity may be required.

Description:

See Summary

No Interaction Expected

Tamoxifen

Pyrazinamide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Pyrazinamide is mainly metabolised by xanthine oxidase. Tamoxifen does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Pyridoxine (Vitamin B6)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely.

Description:

See Summary

No Interaction Expected

Tamoxifen

Quetiapine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Quetiapine is primarily metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Quinapril

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Quinapril is de-esterified to the active metabolite quinaprilat which is eliminated primarily by renal excretion via OAT3. Tamoxifen is unlikely to interfere with this metabolic or elimination pathway.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Quinidine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be avoided. Quinidine is mainly metabolised by CYP3A4 and to a lesser extent by CYP2C9 and CYP2E1. Tamoxifen does not inhibit or induce CYPs. Quinidine is also a substrate of P-gp. Tamoxifen is an inhibitor of P-gp and may increase concentrations of quinidine. The clinical relevance of this interaction is unknown. Monitoring for quinidine toxicity may be required. Furthermore, quinidine is an inhibitor of CYP2D6 (strong), CYP3A4 (weak) and P-gp (moderate). Tamoxifen is metabolised by CYP3A4 and CYP2D6 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Quinidine may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. Tamoxifen product labels state that after coadministration with paroxetine, a strong CYP2D6 inhibitor, endoxifen concentrations decreased by 64%. A decrease in endoxifen plasma concentrations may lead to decreased efficacy as endoxifen is much more potent than tamoxifen. Coadministration should be avoided. If coadministration is unavoidable, closely monitor tamoxifen efficacy. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

No Interaction Expected

Tamoxifen

Rabeprazole

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Rabeprazole is mainly metabolised via non-enzymatic reduction and to a lesser extent by CYP2C19 and CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Ramipril

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ramipril is hydrolysed to the active metabolite ramiprilat, and is metabolised to the diketopiperazine ester, diketopiperazine acid and the glucuronides of ramipril and ramiprilat. Tamoxifen is unlikely to interfere with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Ranitidine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ranitidine is excreted via OAT1/OAT3. Tamoxifen does not inhibit or induce OATs.

Description:

See Summary

Potential Interaction

Tamoxifen

Ranolazine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Ranolazine is primarily metabolized by CYP3A4 and to a lesser extent by CYP2D6. Tamoxifen does not inhibit or induce CYPs. Ranolazine is a substrate of P-gp. Tamoxifen is an inhibitor of P-gp and may increase concentrations of ranolazine. The clinical relevance of this interaction is unknown. Monitoring for ranolazine toxicity and blood pressure may be required. Moreover, ranolazine is a weak inhibitor of P-gp, CYP3A4 and CYP2D6. Tamoxifen is metabolised by CYP2D6 and CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Ranolazine may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. As the active metabolites, 4-hydroxytamoxifen and endoxifen, are much more potent than tamoxifen, a decrease of those plasma concentrations may lead to decreased efficacy. Close monitoring of tamoxifen efficacy is recommended. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

No Interaction Expected

Tamoxifen

Reboxetine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Reboxetine is metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs. In vitro data indicate reboxetine to be a weak inhibitor of CYP3A4 but in vivo data showed no inhibitory effect on CYP3A4. No clinically relevant effect on tamoxifen or its active metabolites is expected.

Description:

See Summary

No Interaction Expected

Tamoxifen

Repaglinide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Repaglinide is metabolised by CYP2C8 and CYP3A4, with clinical data indicating it is a substrate of the hepatic transporter OATP1B1. Tamoxifen does not inhibit or induce CYPs or OATP1B1.

Description:

See Summary

No Interaction Expected

Tamoxifen

Retinol (Vitamin A)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Vitamin A esters are hydrolysed by pancreatic enzymes to retinol, which is then absorbed and re-esterified. Some retinol is stored in the liver but retinol not stored in the liver undergoes glucuronide conjugation and subsequent oxidation to retinal and retinoic acid. Tamoxifen does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Riboflavin (Vitamin B2)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Rifabutin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be avoided. Rifabutin is metabolised by CYP3A4 and via deacetylation. Tamoxifen does not inhibit or induce CYPs. Rifabutin is also a strong CYP3A4 and P-gp inducer. Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Rifabutin may decrease tamoxifen concentrations and increase concentrations of the active metabolites of tamoxifen. After coadministration with rifampicin, a strong CYP3A4 inducer, tamoxifen exposure decreased by 84%. Concentrations of N-desmethyltamoxifen, 4-hydroxytamoxifen and endoxifen were decreased by 69%, 73% and 69%, respectively. A similar effect may occur after coadministration with rifabutin. A decrease in exposure can lead to decreased efficacy. Therefore, coadministration should be avoided. If coadministration is unavoidable, closely monitor tamoxifen efficacy. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Rifampicin

Quality of Evidence: Very Low

Summary:

Coadministration has been studied and should be avoided. Rifampicin is metabolised via deacetylation. Tamoxifen does not interact with this metabolic pathway. Rifampicin is also a strong CYP3A4 and P-gp inducer. Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Rifampicin will decrease tamoxifen concentrations and increase concentrations of the active metabolites of tamoxifen. In breast cancer patients (n=4), coadministration of tamoxifen (20 mg or 40 mg daily) with rifampicin (600 mg daily for 15 days), decreased tamoxifen exposure by 84%. Exposure of tamoxifen metabolites N-desmethyltamoxifen, 4-hydroxytamoxifen and endoxifen also decreased by 69%, 73% and 69%, respectively. A decrease in exposure can lead to decreased efficacy. Therefore, coadministration should be avoided. If coadministration is unavoidable, closely monitor tamoxifen efficacy. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Rifapentine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be avoided. Rifapentine is metabolised via deacetylation. Tamoxifen does not interact with this metabolic pathway. Rifapentine is also a strong CYP3A4, CYP2C8 and P-gp inducer. Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Rifapentine may decrease tamoxifen concentrations and increase concentrations of the active metabolites of tamoxifen. After coadministration with rifampicin, a strong CYP3A4 inducer, tamoxifen exposure decreased by 84%. Concentrations of N-desmethyltamoxifen, 4-hydroxytamoxifen and endoxifen were decreased by 69%, 73% and 69%, respectively. A similar effect may occur after coadministration with rifapentine. A decrease in exposure can lead to decreased efficacy. Therefore, coadministration should be avoided. If coadministration is unavoidable, closely monitor tamoxifen efficacy. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

No Interaction Expected

Tamoxifen

Rifaximin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Rifaximin is mainly excreted in faeces, almost entirely as unchanged drug. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Risperidone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Risperidone is metabolised by CYP2D6 and to a lesser extent by CYP3A4. Tamoxifen does not inhibit or induce CYPs. Furthermore, risperidone is a substrate of P-gp. Tamoxifen is an inhibitor of P-gp and may increase concentrations of risperidone. The clinical relevance of this interaction is unknown. Monitoring for risperidone toxicity may be required.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Rivaroxaban

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Rivaroxaban is partly metabolised in the liver (by CYP3A4, CYP2J2 and hydrolytic enzymes) and partly eliminated unchanged in urine. Moreover, rivaroxaban is substrate of P-gp and BCRP. Tamoxifen is an inhibitor of P-gp and may increase rivaroxaban concentrations. The clinical relevance of this interaction is unknown. Monitoring for rivaroxaban toxicity may be required.

Description:

See Summary

No Interaction Expected

Tamoxifen

Rosiglitazone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Rosiglitazone is metabolised mainly by CYP2C8 and to a lesser extent by CYP2C9. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Rosuvastatin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Rosuvastatin is largely excreted unchanged in the faeces via OATP1B1 and is a substrate of BCRP. Tamoxifen does not inhibit or induce OATP1B1 or BCRP. However, in post marketing research infrequent cases of hyperlipidemia have been reported during therapy with tamoxifen. The clinical relevance of this interaction is unknown. Monitoring of triglycerides and cholesterol may be required.

Description:

See Summary

No Interaction Expected

Tamoxifen

Salbutamol

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Salbutamol is metabolised to the inactive salbutamol-4’-O-sulphate. Tamoxifen does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Salmeterol

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Salmeterol is metabolised by CYP3A4. The systemic exposure of salmeterol is low. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Saxagliptin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Saxagliptin is mainly metabolised by CYP3A4 and is a substrate of P-gp. Tamoxifen is an inhibitor of P-gp and may increase saxagliptin concentrations. The clinical relevance of this interaction is unknown. Monitoring for saxagliptin toxicity may be required.

Description:

See Summary

No Interaction Expected

Tamoxifen

Senna

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Senna glycosides are hydrolysed by colonic bacteria in the intestinal tract and the active anthraquinones liberated into the colon. Excretion occurs in the urine and the faeces and also in other secretions. No clinically significant interactions are known.

Description:

See Summary

No Interaction Expected

Tamoxifen

Sertindole

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Sertindole is metabolised by CYP2D6 and CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Sertraline

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Sertraline is mainly metabolised by CYP2B6 and to a lesser extent by CYPs 2C9, 2C19, 2D6 and 3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Sildenafil (Pulmonary Arterial Hypertension)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Sildenafil is metabolised mainly by CYP3A4 and to a lesser extent by CYP2C9. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Simvastatin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Simvastatin is metabolised by CYP3A4. Moreover, simvastatin is a substrate of BCRP, and the active metabolite is a substrate of OATP1B1. Tamoxifen does not inhibit or induce CYPs, BCRP or OATP1B1. However, in post marketing research infrequent cases of hyperlipidemia have been reported during therapy with tamoxifen. The clinical relevance of this interaction is unknown. Monitoring of triglycerides and cholesterol may be required.

Description:

See Summary

Potential Interaction

Tamoxifen

Sirolimus

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Sirolimus is metabolised by CYP3A4 and is a substrate of P-gp. Tamoxifen is an inhibitor of P-gp and may increase sirolimus concentrations. The clinical relevance of this interaction is unknown. Monitor for sirolimus toxicity and, if available, sirolimus plasma concentrations.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Sitagliptin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Sitagliptin is primarily eliminated in urine as unchanged drug (active secretion by OAT3, OATP4C1, and P-gp) and metabolism by CYP3A4 represents a minor metabolic pathway. Tamoxifen is an inhibitor of P-gp and may increase sitagliptin concentrations. The clinical relevance of this interaction is unknown. Monitoring for sitagliptin toxicity may be required.

Description:

See Summary

No Interaction Expected

Tamoxifen

Sodium nitroprusside

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Sodium nitroprusside is rapidly metabolised, likely by interaction with sulfhydryl groups in the erythrocytes and tissues. Cyanogen (cyanide radical) is produced which is converted to thiocyanate in the liver by the enzyme thiosulfate sulfurtransferase. Tamoxifen does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Sotalol

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Sotalol is excreted unchanged via renal elimination. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Spectinomycin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Spectinomycin is predominantly eliminated unchanged in the kidneys via glomerular filtration. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Spironolactone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Spironolactone is partly metabolised by the flavin containing monooxygenases. Tamoxifen does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Stanozolol

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Stanozolol undergoes hepatic metabolism. Tamoxifen is unlikely to interfere with this unspecified metabolic pathway.

Description:

See Summary

Do Not Coadminister

Tamoxifen

St John's Wort

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but is contraindicated. St John’s wort is a P-gp and CYP3A4 inducer. Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. St John’s Wort may decrease tamoxifen concentrations and increase concentrations of the active metabolites of tamoxifen. After coadministration with rifampicin, a strong CYP3A4 inducer, tamoxifen exposure decreased by 84%. Concentrations of N-desmethyltamoxifen, 4-hydroxytamoxifen and endoxifen were decreased by 69%, 73% and 69%, respectively. A similar effect may occur after coadministration with St John’s Wort. A decrease in exposure can lead to decreased efficacy. Therefore, coadministration is contraindicated.

Description:

See Summary

No Interaction Expected

Tamoxifen

Streptokinase

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Like other proteins, streptokinase is metabolised proteolytically in the liver and eliminated via the kidneys. Tamoxifen does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Streptomycin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Streptomycin is eliminated by glomerular filtration. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Sulfadiazine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. In vitro studies suggest a role of CYP2C9 in sulfadiazine metabolism. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Sulpiride

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Sulpiride is mainly excreted in the urine and faeces as unchanged drug. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Tacrolimus

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Tacrolimus is metabolised mainly by CYP3A4. Tamoxifen does not inhibit or induce CYPs. Tacrolimus is also an inhibitor of CYP3A4 and OATP1B1 in vitro but produced modest inhibition of CYP3A4 and OATP1B1 in the range of clinical concentrations. Therefore, no clinically relevant effect on tamoxifen exposure is expected.

Description:

See Summary

No Interaction Expected

Tamoxifen

Tadalafil (Pulmonary Arterial Hypertension)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Tadalafil is metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Tamsulosin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Tamsulosin is metabolised mainly by CYP3A4 and to a lesser extent by CYP2D6. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Tazobactam

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Tazobactam is excreted as unchanged drug (approximately 80%) and inactive metabolite (approximately 20%) in the urine. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Telithromycin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be avoided. Telithromycin is metabolised by CYP3A4 (50%) with the remaining 50% metabolised via non-CYP mediated pathways. Tamoxifen does not inhibit or induce CYPs. Telithromycin is also an inhibitor of CYP3A4 (strong) and P-gp. The clinical relevance of P-gp inhibition is unknown. Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Telithromycin may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. As the active metabolites, 4-hydroxytamoxifen and endoxifen, are much more potent than tamoxifen, a decrease of those plasma concentrations may lead to decreased efficacy. Coadministration should be avoided. If coadministration is unavoidable, closely monitor tamoxifen efficacy. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

No Interaction Expected

Tamoxifen

Telmisartan

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Telmisartan is mainly glucuronidated by UGT1A3. Tamoxifen does not inhibit or induce UGTs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Temazepam

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Temazepam is mainly glucuronidated. Tamoxifen does not inhibit or induce UGTs.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Terbinafine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be avoided. Terbinafine is metabolised by CYPs 1A2, 2C9, 3A4 and to a lesser extent by CYP2C8 and CYP2C19. Tamoxifen does not inhibit or induce CYPs. Terbinafine is also a moderate-strong inhibitor of CYP2D6. Tamoxifen is metabolised by CYP2D6 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Terbinafine may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. Tamoxifen product labels state that after coadministration with paroxetine, a strong CYP2D6 inhibitor, endoxifen concentrations decreased by 64%. A decrease in endoxifen plasma concentrations may lead to decreased efficacy as endoxifen is much more potent than tamoxifen. Coadministration should be avoided. If coadministration is unavoidable, closely monitor tamoxifen efficacy. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Testosterone

Quality of Evidence: Very Low

Summary:

Tamoxifen is used for hormone-sensitive tumours. Coadministration with testosterone is contraindicated as testosterone is a precursor of estradiol and could, therefore, potentially interfere with tamoxifen pharmacologic action. In addition, tamoxifen is associated with an increased risk of venous thromboembolic events as is estradiol. Testosterone is metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Tetracycline

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Tetracycline is eliminated unchanged primarily by glomerular filtration. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Theophylline

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Theophylline is mainly metabolised by CYP1A2. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Thiamine (Vitamin B1)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely.

Description:

See Summary

No Interaction Expected

Tamoxifen

Thioridazine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Thioridazine is metabolised by CYP2D6 and to a lesser extent by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Tiapride

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Tiapride is excreted largely unchanged in urine. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

Potential Interaction

Tamoxifen

Ticagrelor

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Ticagrelor is a substrate of CYP3A4 and P-gp. Tamoxifen is an inhibitor of P-gp and may increase ticagrelor concentrations. The clinical relevance of this interaction wis unknown. Monitoring for ticagrelor toxicity and thrombocytes aggregation test may be required. Furthermore, ticagrelor is a weak inhibitor of CYP3A4. Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Ticagrelor may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. As the active metabolites, 4-hydroxytamoxifen and endoxifen, are much more potent than tamoxifen, a decrease of those plasma concentrations may lead to decreased efficacy. Close monitoring of tamoxifen efficacy is recommended. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

No Interaction Expected

Tamoxifen

Timolol

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Timolol is predominantly metabolised in the liver by CYP2D6. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Tinzaparin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Tinzaparin is renally excreted as unchanged or almost unchanged drug. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Tolbutamide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Tolbutamide is mainly metabolised by CYP2C9 and to a lesser extent by CYPs 2C8 and 2C19. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Tolterodine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Tolterodine is primarily metabolised by CYP2D6 with CYP3A4 playing a minor role. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Torasemide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Torasemide is metabolised mainly by CYP2C9. Furthermore, OAT1/3 are the major transporters of loop and thiazide diuretics. Secretion of these diuretics into the urinary tract by transporters in the proximal tubular cells is necessary for the diuretic effect in later tubule segments. Tamoxifen does not inhibit or induce CYPs or OATs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Tramadol

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Tramadol is metabolised by CYPs 3A4, 2B6, and 2D6. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Trandolapril

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Trandolapril is hydrolysed to trandolaprilat. Tamoxifen does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Tranexamic acid

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Tranexamic acid is mainly cleared by glomerular filtration. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Tranylcypromine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Tranylcypromine is hydroxylated and acetylated. Tamoxifen does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Trazodone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Trazodone is primarily metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Triamcinolone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Triamcinolone is metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Triazolam

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Triazolam is metabolised by CYP3A4. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Trimethoprim/Sulfamethoxazole

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Trimethoprim is primarily eliminated by the kidneys through glomerular filtration and tubular secretion. To a lesser extent (approximately 30%) trimethoprim is metabolised by CYP enzymes (in vitro data suggest CYPs 3A4, 1A2 and 2C9). Sulfamethoxazole is metabolised by CYP2C9. Furthermore, trimethoprim is a weak CYP2C8 inhibitor and in vitro data also suggest that trimethoprim is an inhibitor of OCT2 and MATE1. Sulfamethoxazole is a weak inhibitor of CYP2C9. Tamoxifen does not interact with these metabolic pathways.

Description:

See Summary

No Interaction Expected

Tamoxifen

Trimipramine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Trimipramine is metabolised mainly by CYP2D6. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Tropisetron

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Tropisetron is metabolised mainly by CYP2D6. Tamoxifen does not inhibit or induce CYPs. Additionally, tropisetron is a substrate of P-gp. Tamoxien is an inhibitor of P-gp and may increase concentrations of tropisetron. The clinical relevance of this interaction is unknown. Monitoring for tropisetron toxicity may be required.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Ulipristal

Quality of Evidence: Very Low

Summary:

The efficacy of hormonal contraceptives and tamoxifen may both decrease if coadministered. Therefore, coadministration of hormones in hormone-sensitive cancer is contraindicated. In addition, tamoxifen is associated with an increased risk of venous thromboembolic events as are hormonal contraceptives. Ulipristal is mainly metabolised by CYP3A4 and to a lesser extent by CYP1A2 and CYP2D6. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Valproic acid (Valproate)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Valproic acid is primarily metabolized by glucuronidation (50%) and mitochondrial beta-oxidation (30-40%). To a lesser extent (10%) valproic acid is metabolized by CYP2C9 and CYP2C19. In addition, valproic acid is an inhibitor of CYP2C9. Tamoxifen does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Valsartan

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Valsartan is eliminated unchanged mostly through biliary excretion. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Vancomycin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Vancomycin is excreted unchanged via glomerular filtration. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Venlafaxine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Venlafaxine is mainly metabolised by CYP2D6 and to a lesser extent by CYPs 3A4, 2C19 and 2C9. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

Potential Interaction

Tamoxifen

Verapamil

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Verapamil is metabolised mainly by CYP3A4 and to a lesser extent by CYPs 1A2, 2C8 and 2C9. Tamoxifen does not inhibit or induce CYPs. Verapamil is also an inhibitor of CYP3A4 (moderate) and P-gp (strong). Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Verapamil may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. As the active metabolites, 4-hydroxytamoxifen and endoxifen, are much more potent than tamoxifen, a decrease of those plasma concentrations may lead to decreased efficacy. Close monitoring of tamoxifen efficacy is recommended. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

Potential Weak Interaction

Tamoxifen

Vildagliptin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Vildagliptin is inactivated via non-CYP mediated hydrolysis and is a substrate of P-gp. Tamoxifen is an inhibitor of P-gp and may increase vildagliptin concentrations. The clinical relevance of this interaction is unknown. Monitoring for vildagliptin toxicity may be required.

Description:

See Summary

No Interaction Expected

Tamoxifen

Vitamin E

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely.

Description:

See Summary

Do Not Coadminister

Tamoxifen

Voriconazole

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be avoided. Voriconazole is metabolised by CYP2C19 (major pathway) and to a lesser extent by CYP3A4 and CYP2C9. Tamoxifen does not inhibit or induce CYPs. Voriconazole is also a strong inhibitor of CYP3A4 and a weak inhibitor of CYPs 2C9, 2C19 and 2B6. Tamoxifen is metabolised by CYP3A4 to the 30- to 100-fold more potent metabolites 4-hydroxytamoxifen and endoxifen. Voriconazole may increase tamoxifen concentrations and decrease concentrations of the active metabolites of tamoxifen. In a simulation study voriconazole appeared to increase tamoxifen concentrations by 45%. The clinical relevance of this simulation is unknown. As the active metabolites, 4-hydroxytamoxifen and endoxifen, are much more potent than tamoxifen, a decrease of those plasma concentrations may lead to decreased efficacy. Coadministration should be avoided. If coadministration is unavoidable, closely monitor tamoxifen efficacy. Monitor endoxifen plasma concentrations, if available.

Description:

See Summary

Potential Interaction

Tamoxifen

Warfarin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Warfarin is a mixture of enantiomers which are metabolised by different cytochromes. R-warfarin is primarily metabolised by CYP1A2 and CYP3A4. S-warfarin (more potent) is metabolised by CYP2C9. Tamoxifen does not inhibit or induce CYPs. Vitamin K antagonists are used in patients that are at risk of venous thromboembolic events and tamoxifen is associated with an increased risk of venous thromboembolic events, although the exact mechanism of the interaction is unknown. Therefore, coadministration of warfarin and tamoxifen is not recommended. If coadministration is unavoidable, monitor closely for INR/PT and signs of bleeding.

Description:

See Summary

No Interaction Expected

Tamoxifen

Xipamide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Approximately 90% of xipamide is excreted in the urine, mainly as unchanged drug (~50%) and glucuronides (30%). OAT1/3 are the major transporters of loop and thiazide diuretics. Secretion of these diuretics into the urinary tract by transporters in the proximal tubular cells is necessary for the diuretic effect in later tubule segments. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Zaleplon

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Zaleplon is mainly metabolised by aldehyde oxidase and to a lesser extent by CYP3A4. Tamoxifen does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Ziprasidone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Approximately two thirds of ziprasidone metabolic clearance is by reduction, with less than one third by CYP enzymes (mainly CYP3A4). Tamoxifen does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Zoledronic acid

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Zoledronic acid is not metabolised and is cleared from the plasma by uptake into bone and elimination via renal excretion. Tamoxifen is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tamoxifen

Zolpidem

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Zolpidem is metabolised mainly by CYP3A4 and to a lesser extent by CYPs 2C9, 2C19, 2D6 and 1A2. Tamoxifen does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Tamoxifen

Zopiclone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Zopiclone is metabolised mainly by CYP3A4 and to a lesser extent by CYP2C8. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Zotepine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Zotepine is mainly metabolised by CYP3A4 and to a lesser extent by CYP1A2 and CYP2D6. Tamoxifen does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Tamoxifen

Zuclopenthixol

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Zuclopenthixol is metabolised by sulphoxidation, N-dealkylation (via CYP2D6 and CYP3A4) and glucuronidation. Tamoxifen does not interact with this metabolic pathway.

Description:

See Summary