Cancer Drug Interactions from Radboud UMC and University of Liverpool

No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic pathway.

Description:

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No Interaction Expected

Etoposide

Acenocoumarol

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Acenocoumarol is mainly metabolised by CYP2C9 and to a lesser extent by CYP1A2 and CYP2C19. Etoposide does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Etoposide

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). Etoposide does not inhibit or induce UGTs.

Description:

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No Interaction Expected

Etoposide

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%). Etoposide does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Etoposide

Alendronic acid

Quality of Evidence: Very Low

Summary:

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

Description:

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No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Etoposide

Aliskiren

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Aliskiren is minimally metabolised and is mainly excreted unchanged in faeces. Aliskiren is also a substrate of P-gp. Etoposide does not interact with this elimination pathway.

Description:

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No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic pathway.

Description:

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No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this metabolic pathway.

Description:

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No Interaction Expected

Etoposide

Ambrisentan

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ambrisentan is metabolized by glucuronidation via UGTs 1A3, 1A9 and 2B7 and to a lesser extent by CYP3A4 and CYP2C19. Ambrisentan is also a substrate of P-gp. Etoposide does not inhibit or induce CYPs, UGTs or P-gp.

Description:

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No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Etoposide

Amiodarone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Amiodarone is metabolised by CYP3A4 and CYP2C8. Etoposide 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). Concentrations of etoposide may increase due to CYP3A4 and P-gp inhibition. After coadministration with ketoconazole, a strong CYP3A4 inhibitor, etoposide exposure increased by 20%. Therefore, a clinically relevant effect on etoposide exposure is not expected due to coadministration with amiodarone.

Description:

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No Interaction Expected

Etoposide

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 renally eliminated (possibly via OCT). Etoposide is unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

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Potential Weak Interaction

Etoposide

Amphotericin B

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Amphotericin B is not appreciably metabolised but is eliminated to a large extent in the bile. Etoposide does not interfere with this metabolic or elimination pathway. However, the European SPC for amphotericin 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

Etoposide

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. 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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic pathway.

Description:

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No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this metabolic pathway.

Description:

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No Interaction Expected

Etoposide

Apixaban

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. 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. Etoposide does not inhibit or induce CYPs, P-gp or BCRP.

Description:

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No Interaction Expected

Etoposide

Aprepitant

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Aprepitant is mainly metabolized by CYP3A4 and to a lesser extent by CYP1A2 and CYP2C19. Etoposide does not inhibit or induce CYPs. During treatment, aprepitant is a moderate inhibitor of CYP3A4 and may increase etoposide concentrations. After coadministration with ketoconazole, a strong CYP3A4 inhibitor, etoposide exposure increased by 20%. A clinically relevant effect on etoposide exposure is not expected due CYP3A4 inhibition. Moreover, after treatment aprepitant is a weak inducer of CYP3A4, CYP2C9 and UGT. Etoposide concentrations may decrease due to CYP3A4 induction. However, this is considered to be not clinically relevant.

Description:

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No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Etoposide

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)). Etoposide does not inhibit or induce CYPs or UGTs.

Description:

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No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Etoposide

Atorvastatin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Atorvastatin is metabolised by CYP3A4 and is a substrate of P-gp and OATP1B1. Etoposide does not inhibit or induce CYPs, P-gp or OATP1B1.

Description:

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Potential Weak Interaction

Etoposide

Azathioprine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Azathioprine is converted to 6-mercaptopurine which is metabolised analogously to natural purines. Etoposide does not interact with this metabolic pathway. However, due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.

Description:

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No Interaction Expected

Etoposide

Azithromycin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Azithromycin is mainly eliminated via biliary excretion; animal data suggest this may occur via P-gp and MRP2. Etoposide is unlikely to interfere with this elimination pathway. Azithromycin is also an inhibitor of P-gp. Etoposide is an in vitro substrate of P-gp and etoposide concentrations may increase. However, no clinically relevant effect on etoposide exposure is expected.

Description:

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No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic pathway.

Description:

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No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Etoposide

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. In vitro data indicate that bendroflumethiazide inhibits these renal transporters but a clinically significant interaction is unlikely in the range of observed clinical concentrations. Etoposide does not interact with this metabolic or elimination pathway.

Description:

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No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Etoposide

Bezafibrate

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Half of a bezafibrate dose is eliminated unchanged in the urine. In vitro data suggest that bezafibrate inhibits the renal transporter OAT1. Etoposide does not interact with this pathway.

Description:

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No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic pathway.

Description:

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No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic or elimination pathway.

Description:

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Potential Weak Interaction

Etoposide

Bosentan

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Bosentan is a substrate of CYP3A4 and CYP2C9. Etoposide does not inhibit or induce CYPs. Bosentan is also a weak inducer of CYP3A4 and CYP2C9. Concentrations of etoposide may decrease due to induction of CYP3A4. The clinical relevance of this interaction is unknown. Monitoring of etoposide efficacy may be required if coadministered.

Description:

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No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Etoposide

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). Etoposide does not inhibit or induce CYPs or UGTs.

Description:

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No Interaction Expected

Etoposide

Bupropion

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bupropion is primarily metabolised by CYP2B6 and is a strong inhibitor of CYP2D6. Etoposide does not interact with this pathway.

Description:

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No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce OATs.

Description:

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Potential Interaction

Etoposide

Carbamazepine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Carbamazepine is primarily metabolized by CYP3A4 and to a lesser extent by CYP2C8. Etoposide does not inhibit or induce CYPs. Carbamazepine is also an inducer of CYPs 2C8 (strong), 2C9 (strong), 3A4 (strong), 1A2 (weak), 2B6, UGT1A1 and P-gp (moderate). Concentrations of etoposide may decrease due to induction of CYP3A4. Coadministration with phenytoin is associated with decreased etoposide exposure and therefore reduced efficacy. A similar effect may occur after coadministration with carbamazepine. Selection of an alternate concomitant medicinal product, with no or minimal potential to induce CYP3A4 is recommended. Etoposide is also a substrate of P-gp in vitro. Concentrations of etoposide may decrease due to P-gp induction by carbamazepine, but the clinical relevance of this interaction is unknown. Furthermore, coadministration may lead to decreased seizure control due to pharmacokinetic interactions between etoposide and carbamazepine. If coadministration is unavoidable, closely monitor etoposide and carbamazepine efficacy. Monitor carbamazepine plasma concentrations, if available.

Description:

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No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs or UGTs. Carvedilol is also an inhibitor of P-gp, but the clinical relevance of P-gp inhibition by carvedilol is unknown. Although etoposide is a substrate of P-gp in vitro, no clinically relevant interaction is expected.

Description:

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No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic pathway.

Description:

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No Interaction Expected

Etoposide

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 renally eliminated unchanged by glomerular filtration and tubular secretion via OAT1 and MATE1. Etoposide is unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Etoposide

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. Etoposide does not interact with this pathway.

Description:

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No Interaction Expected

Etoposide

Chloramphenicol

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Chloramphenicol is predominantly glucuronidated. Etoposide 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). Concentrations of etoposide may increase due to inhibition of CYP3A4 by chloramphenicol. After coadministration with ketoconazole, a strong CYP3A4 inhibitor, etoposide exposure increased by 20%. Therefore, a clinically relevant effect on etoposide exposure is not expected due to coadministration with chloramphenicol.

Description:

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No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

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No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

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Potential Interaction

Etoposide

Ciclosporin (Cyclosporine)

Quality of Evidence: Low

Summary:

Coadministration should be approached with caution. Ciclosporin is a substrate of CYP3A4 and P-gp. Etoposide does not inhibit or induce CYPs or P-gp. Ciclosporin is also inhibits CYP3A4 and OATP1B1. Concentrations of etoposide may increase due to inhibition of CYP3A4. After coadministration with ketoconazole, a strong CYP3A4 inhibitor, etoposide exposure increased by 20%. However, after coadministration with high dose ciclosporin A (blood level >2000 ng/L) patients experienced a 60% higher etoposide AUC compared to coadministration with low dose ciclosporin (blood level <2000 ng/L). However, this difference was only significant if corrected for dose. If coadministration is unavoidable, monitor closely for etoposide toxicity. A dose decrease of 50% for intravenous etoposide with high dose cyclosporin is recommended. For oral etoposide or low dose cyclosporin a dose decrease may be required.

Description:

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No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Etoposide

Cimetidine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cimetidine is metabolised by CYP450 enzymes. Etoposide 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. Concentrations of etoposide may increase due to inhibition of CYP3A4. After coadministration with ketoconazole, a strong CYP3A4 inhibitor, etoposide exposure increased by 20%. Therefore, a clinically relevant effect on etoposide exposure is not expected due to coadministration with cimetidine.

Description:

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No Interaction Expected

Etoposide

Ciprofloxacin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ciprofloxacin is primarily eliminated unchanged in the kidneys by glomerular filtration and tubular secretion via OAT3. It is metabolised and partially cleared through the bile and intestine. Etoposide does not interact with this metabolic or elimination pathway. Ciprofloxacin is also a weak to moderate inhibitor of CYP3A4 and a strong inhibitor of CYP1A2. Concentrations of etoposide may increase due to inhibition of CYP3A4. After coadministration with ketoconazole, a strong CYP3A4 inhibitor, etoposide exposure increased by 20%. Therefore, a clinically relevant effect on etoposide exposure is not expected due to coadministration with ciprofloxacin.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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%). Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Clarithromycin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Clarithromycin is metabolised by CYP3A4. Etoposide does not inhibit or induce CYPs. Clarithromycin is also an inhibitor of CYP3A4 (strong) and P-gp and may increase concentrations of etoposide. After coadministration with ketoconazole, a strong CYP3A4 and P-gp inhibitor, etoposide exposure increased by 20%. Therefore, a clinically relevant effect on etoposide exposure is not expected due to coadministration with clarithromycin.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Clindamycin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Clindamycin is metabolised by CYP3A4. Etoposide does not inhibit or induce CYPs. In vitro data suggest that clindamycin is also a CYP3A4 inhibitor and may increase concentrations of etoposide. After coadministration with ketoconazole, a strong CYP3A4 inhibitor, etoposide exposure increased by 20%. Therefore, a clinically relevant effect on etoposide exposure is not expected due to coadministration with clindamycin.

Description:

See Summary

No Interaction Expected

Etoposide

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

No Interaction Expected

Etoposide

Clofazimine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Clofazimine is largely excreted unchanged in the faeces. Etoposide is unlikely to interfere with this elimination pathway. In vitro data suggest that clofazimine is a CYP3A4 inhibitor and may increase concentrations of etoposide. After coadministration with ketoconazole, a strong CYP3A4 inhibitor, etoposide exposure increased by 20%. Therefore, a clinically relevant effect on etoposide exposure is not expected due to coadministration with clofazimine.

Description:

See Summary

No Interaction Expected

Etoposide

Clofibrate

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Clofibrate is hydrolysed to an active metabolite, clofibric acid. Excretion of clofibric acid glucuronide is possibly performed via OAT1. Etoposide does not inhibit or induce OATs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Clomipramine and desmethylclomipramine are both metabolised by CYP2D6. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interact with this pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Clopidogrel is also an inhibitor of CYP2C8 (strong), CYP2B6 (weak) and of CYP2C9 (in vitro) at high concentrations. The clinical relevance of CYP2C9 inhibition is unknown. Etoposide does not interact with this pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs or UGTs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

Potential Weak Interaction

Etoposide

Clozapine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Clozapine is metabolised mainly by CYP1A2 and CYP3A4, and to a lesser extent by CYP2C19 and CYP2D6. Etoposide does not inhibit or induce CYPs. However, due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.

Description:

See Summary

No Interaction Expected

Etoposide

Codeine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. 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. Etoposide does not inhibit or induce CYPs, UGTs or P-gp.

Description:

See Summary

No Interaction Expected

Etoposide

Colchicine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Colchicine is metabolised by CYP3A4 and is a substrate of P-gp. Etoposide does not inhibit or induce CYPs or P-gp.

Description:

See Summary

No Interaction Expected

Etoposide

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 renally excreted via glomerular filtration. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

Dabigatran

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dabigatran is transported via P-gp and is renally excreted. Etoposide does not interact with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Desogestrel

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Desogestrel is a prodrug which is activated to etonogestrel by CYP2C9 (and possibly CYP2C19); the metabolism of etonogestrel is mediated by CYP3A4. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Dexamethasone

Quality of Evidence: Very Low

Summary:

Dexamethasone is a substrate of CYP3A4. Etoposide does not inhibit or induce CYPs. Dexamethasone has also been described as a weak inducer of CYP3A4 and could possibly decrease etoposide plasma concentrations. The clinical relevance of this interaction is not known and induction of CYP3A4 by dexamethasone has not yet been established. However, in paediatric patients (n=57), coadministration of etoposide (150 mg/m²/day for 3 days or 100 mg/m²/day for 5 days) and dexamethasone (5 mg/m²/day) had no significant effect on etoposide pharmacokinetics.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Diamorphine (diacetylmorphine)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. 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. Etoposide does not inhibit or induce CYPs or P-gp.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs or UGTs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs or UGTs.

Description:

See Summary

No Interaction Expected

Etoposide

Digoxin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Digoxin is eliminated renally via OATP4C1 and P-gp. Etoposide does not inhibit or induce OATP4C1 or P-gp.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs or UGTs.

Description:

See Summary

No Interaction Expected

Etoposide

Diltiazem

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Diltiazem is metabolised by CYP3A4 and CYP2D6. Etoposide 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. Concentrations of etoposide may increase due to CYP3A4 and P-gp inhibition. After coadministration with ketoconazole, a strong CYP3A4 inhibitor, etoposide exposure increased by 20%. Therefore, a clinically relevant effect on etoposide exposure is not expected due to coadministration with diltiazem.

Description:

See Summary

No Interaction Expected

Etoposide

Diphenhydramine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Diphenhydramine is mainly metabolised by CYP2D6 and to a lesser extent by CYPs 1A2, 2C9 and 2C19. Diphenhydramine is also a weak inhibitor of CYP2D6. Etoposide does not interact with this pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce UGTs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic or elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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%). Etoposide does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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 etoposide, or to be affected if coadministered with etoposide.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Doxepin and nordoxepin are both metabolised by CYP2D6. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Between 40-60% of an administered dose can be accounted for in the urine. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Drospirenone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Drospirenone is metabolised to a minor extent via CYP3A4. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide 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

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Dydrogesterone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dydrogesterone is metabolised to dihydrodydrogesterone (possibly via CYP3A4). Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Edoxaban

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Edoxaban is partially metabolised by CYP3A4 (<10%) and is transported via P-gp. Etoposide does not inhibit or induce CYPs or P-gp.

Description:

See Summary

No Interaction Expected

Etoposide

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). Etoposide does not inhibit or induce CYPs or UGTs.

Description:

See Summary

No Interaction Expected

Etoposide

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 renally eliminated (possibly via OATs). Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic or elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

Erythromycin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Erythromycin is a substrate of CYP3A4 and P-gp. Etoposide does not inhibit or induce CYPs or P-gp. Erythromycin is also an inhibitor of CYP3A4 (moderate) and P-gp and may increase concentrations of etoposide. After coadministration with ketoconazole, a strong CYP3A4 and P-gp inhibitor, etoposide exposure increased by 20%. Therefore, a clinically relevant effect on etoposide exposure is not expected due to coadministration with erythromycin.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not interact with this pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Estradiol

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Estradiol is metabolised by CYP3A4, CYP1A2 and is glucuronidated. Etoposide does not inhibit or induce CYPs or UGTs.

Description:

See Summary

No Interaction Expected

Etoposide

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%). Etoposide does not interact with this metabolic or elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

Ethinylestradiol

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ethinylestradiol undergoes oxidation (CYP3A4>CYP2C9), sulfation and glucuronidation (UGT1A1). Etoposide does not inhibit or induce CYPs or UGTs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Etoposide

Etonogestrel

Quality of Evidence: Very Low

Summary:

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

Description:

See Summary

Potential Weak Interaction

Etoposide

Everolimus (Immunosuppressant)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Everolimus is mainly metabolised by CYP3A4 and is a substrate of P-gp. Etoposide does not inhibit or induce CYPs or P-gp. However, due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway. 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

No Interaction Expected

Etoposide

Ezetimibe

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ezetimibe is glucuronidated by UGTs 1A1 and 1A3 and to a lesser extent by UGTs 2B15 and 2B7. Etoposide does not inhibit or induce UGTs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce OATs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Fenofibrate

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fenofibrate is hydrolysed to an active metabolite, fenofibric acid. In vitro data suggest that fenofibric acid inhibits OAT3. Etoposide does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Fexofenadine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fexofenadine is a substrate of P-gp. Etoposide does not inhibit or induce P-gp.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Fish oils

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

Etoposide

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 renally eliminated unchanged. Etoposide does not interact with this metabolic or elimination pathway.

Description:

See Summary

Potential Weak Interaction

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway. However, flucloxacillin is described as a CYP3A4 inducer and may decrease etoposide concentrations, but the mechanism and clinical relevance of this interaction is unknown. Monitoring of etoposide efficacy may be required.

Description:

See Summary

No Interaction Expected

Etoposide

Fluconazole

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fluconazole is cleared primarily by renal excretion. Etoposide is unlikely to interfere with this elimination pathway. Fluconazole is also an inhibitor of CYPs 3A4 (moderate), 2C9 (moderate) and 2C19 (strong). Concentrations of etoposide may increase due to inhibition of CYP3A4. After coadministration with ketoconazole, a strong CYP3A4 inhibitor, etoposide exposure increased by 20%. Therefore, a clinically relevant effect on etoposide exposure is not expected due to coadministration with fluconazole.

Description:

See Summary

Potential Weak Interaction

Etoposide

Flucytosine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Flucytosine is metabolised to 5-fluorouracil (5-FU). 5-FU is further metabolised by dihydropyrimidine dehydrogenase to an inactive metabolite. Etoposide does not interfere with this elimination pathway. However, 5-FU binds to the enzyme thymidylate synthase resulting in DNA damage. This mechanism occurs in all fast-dividing cells including bone marrow cells, resulting in haematological toxicity. Etoposide also induces haematological toxicity which could be enhanced by the use of flucytosine. Due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Fluoxetine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fluoxetine is mainly metabolised by CYP2D6 and CYP2C9 and to a lesser extent by CYP2C19 and CYP3A4 to form norfluoxetine. Fluoxetine is a strong inhibitor of CYP2D6 and CYP2C19. Etoposide does not interact with this pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Fluvastatin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fluvastatin is mainly metabolised by CYP2C9 (75%) and to a lesser extent by CYP3A4 (20%) and CYP2C8 (5%). Fluvastatin potentially inhibits CYP2C9. However, the clinical relevance of CYP2C9 inhibition is unknown. Etoposide does not interact with this pathway.

Description:

See Summary

No Interaction Expected

Etoposide

Fluvoxamine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fluvoxamine is metabolised mainly by CYP2D6 and to a lesser extent by CYP1A2. Etoposide 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). Etoposide concentrations may increase due to CYP3A4 inhibition. After coadministration with ketoconazole, a strong CYP3A4 inhibitor, etoposide exposure increased by 20%. Therefore, a clinically relevant effect on etoposide exposure is not expected due to coadministration with fluvoxamine.

Description:

See Summary

No Interaction Expected

Etoposide

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 predominantly renally eliminated. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Moreover, etoposide does not inhibit or induce CYPs or UGTs.

Description:

See Summary

No Interaction Expected

Etoposide

Fosaprepitant

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fosaprepitant is rapidly, almost completely, converted to the active metabolite aprepitant. Etoposide does not interact with this metabolic pathway. Aprepitant is mainly metabolized by CYP3A4 and to a lesser extent by CYP1A2 and CYP2C19. Etoposide does not inhibit or induce CYPs. During treatment, aprepitant is a moderate inhibitor of CYP3A4 and may increase etoposide concentrations. After coadministration with ketoconazole, a strong CYP3A4 inhibitor, etoposide exposure increased by 20%. A clinically relevant effect on etoposide exposure is not expected due CYP3A4 inhibition. Moreover, after treatment aprepitant is a weak inducer of CYP3A4, CYP2C9 and UGT. Etoposide concentrations may decrease due to CYP3A4 induction. However, this is considered to be not clinically relevant.

Description:

See Summary

Potential Interaction

Etoposide

Fosphenytoin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Fosphenytoin is rapidly converted to the active metabolite phenytoin. Etoposide does not interact with this metabolic pathway. Phenytoin is mainly metabolized by CYP2C9 and to a lesser extent by CYP2C19. Etoposide does not inhibit or induce CYPs. Phenytoin is a potent inducer of CYP3A4, UGT and P-gp. Concentrations of etoposide may decrease due to induction of CYP3A4 and P-gp. Coadministration with phenytoin is associated with decreased etoposide exposure and therefore reduced efficacy. Selection of an alternate concomitant medicinal product, with no or minimal potential to induce CYP3A4 is recommended. Furthermore, coadministration may lead to decreased seizure control due to pharmacokinetic interactions between etoposide and fosphenytoin. If coadministration is unavoidable, closely monitor etoposide and phenytoin efficacy. Monitor phenytoin plasma concentrations, if available.

Description:

See Summary

No Interaction Expected

Etoposide

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 renally eliminated unchanged (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. Etoposide does not interact with this pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

Gemfibrozil

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Gemfibrozil is metabolised by UGT2B7. Gemfibrozil is also 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. Etoposide does not interact with this pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

Gestodene

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Gestodene is metabolised by CYP3A4 and to a lesser extent by CYP2C9 and CYP2C19. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Granisetron

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Granisetron is metabolised by CYP3A4 and is a substrate of P-gp. Etoposide does not inhibit or induce CYPs or P-gp.

Description:

See Summary

Do Not Coadminister

Etoposide

Grapefruit juice

Quality of Evidence: Very Low

Summary:

Coadministration should be avoided. Grapefruit juice is known to inhibit CYP3A4 enzymes and may increase etoposide concentrations. After coadministration with ketoconazole, a strong CYP3A4 inhibitor, etoposide exposure increased by 20%. After coadministration of grapefruit juice and etoposide, etoposide exposure decreased by 26.2%. However, interindividual variability was large in all treatment groups and the effect of grapefruit juice on etoposide exposure is considered to be unpredictable. Therefore, coadministration should be avoided.

Description:

See Summary

No Interaction Expected

Etoposide

Green tea

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

Potential Weak Interaction

Etoposide

Griseofulvin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Less than 1% of a griseofulvin dose is excreted unchanged via the kidneys. Etoposide does not interact with this elimination pathway. Griseofulvin is also a liver microsomal enzyme inducer and may lower plasma levels, and therefore reduce the efficacy of concomitantly administered medicinal products that are metabolised by CYP3A4, such as etoposide. The clinical relevance of this interaction is unknown. Monitoring of etoposide efficacy may be required if coadministered.

Description:

See Summary

No Interaction Expected

Etoposide

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). Etoposide does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Etoposide

Hydralazine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Hydralazine is metabolised via primary oxidative metabolism and acetylation. Etoposide 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. Etoposide concentrations may increase due to CYP3A4 inhibition. After coadministration with ketoconazole, a strong CYP3A4 inhibitor, etoposide exposure increased by 20%. Therefore, a clinically relevant effect on etoposide exposure is not expected due to coadministration with hydralazine.

Description:

See Summary

No Interaction Expected

Etoposide

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 but 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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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

Etoposide

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. Etoposide does not inhibit or induce UGTs.

Description:

See Summary

Potential Weak Interaction

Etoposide

Hydroxyurea (Hydroxycarbamide)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Hydroxyurea is metabolised in the liver and cleared via the lungs and kidneys. Etoposide is unlikely to interfere with this elimination pathway. However, due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Etoposide

Ibandronic acid

Quality of Evidence: Very Low

Summary:

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

Etoposide

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. Etoposide does not inhibit or induce CYPs or UGTs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs or OATs.

Description:

See Summary

No Interaction Expected

Etoposide

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

Potential Weak Interaction

Etoposide

Interferon alpha

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. However, due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.

Description:

See Summary

Potential Weak Interaction

Etoposide

Interleukin 2 (Aldesleukin)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Interleukin-2 is mainly eliminated by glomerular filtration. Etoposide is unlikely to interfere with this elimination pathway. However, due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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). Etoposide does not inhibit or induce UGTs or CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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

Etoposide

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. Etoposide does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Itraconazole

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Itraconazole is primarily metabolised by CYP3A4. Etoposide does not inhibit or induce CYPs. Itraconazole is also an inhibitor of CYP3A4 (strong), CYP2C9 (weak), P-gp and BCRP. Concentrations of etoposide may increase due to inhibition of CYP3A4 and P-gp. After coadministration with ketoconazole, a strong CYP3A4 inhibitor and P-gp, etoposide exposure increased by 20%. Therefore, a clinically relevant effect on etoposide exposure is not expected due to coadministration with itraconazole.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

Ketoconazole

Quality of Evidence: Very Low

Summary:

Ketoconazole is a substrate of CYP3A4. Etoposide does not inhibit or induce CYPs. Ketoconazole is also an inhibitor of CYP3A4 (strong) and P-gp. In patients (n=32), coadministration of etoposide (escalating oral dose starting at 50 mg every other day) and ketoconazole (200 mg daily) increased etoposide exposure by 20%. Therefore, no clinically relevant effect on etoposide exposure is expected.

Description:

See Summary

No Interaction Expected

Etoposide

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). Etoposide does not inhibit or induce UGTs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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). Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Levonorgestrel

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Levonorgestrel is mainly metabolised by CYP3A4 and is glucuronidated to a minor extent. Etoposide does not inhibit or induce CYPs or UGTs.

Description:

See Summary

No Interaction Expected

Etoposide

Levonorgestrel (Emergency Contraception)

Quality of Evidence: Very Low

Summary:

Description:

See Summary

No Interaction Expected

Etoposide

Levothyroxine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Levothyroxine is metabolised by deiodination (by enzymes of deiodinase family) and glucuronidation. Etoposide does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Linagliptin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Linagliptin is mainly eliminated as parent compound in faeces with metabolism by CYP3A4 representing a minor elimination pathway. Linagliptin is also a substrate of P-gp. Etoposide does not inhibit or induce CYPs or P-gp. Linagliptin is a weak inhibitor of CYP3A4 and may increase etoposide concentrations. After coadministration with ketoconazole, a strong CYP3A4 inhibitor, etoposide exposure increased by 20%. Therefore, a clinically relevant effect on etoposide exposure is not expected due to coadministration with linagliptin.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this unspecified metabolic pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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 renally eliminated unchanged via glomerular filtration. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Therefore, no pharmacokinetic interaction is expected.

Description:

See Summary

Do Not Coadminister

Etoposide

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.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs or P-gp.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this unspecified metabolic pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce UGTs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Lovastatin

Quality of Evidence: Very Low

Summary:

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

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Medroxyprogesterone (depot)

Quality of Evidence: Very Low

Summary:

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

Description:

See Summary

No Interaction Expected

Etoposide

Medroxyprogesterone (non-depot)

Quality of Evidence: Very Low

Summary:

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs or UGTs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic pathway.

Description:

See Summary

Potential Weak Interaction

Etoposide

Metamizole

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. 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%). Etoposide does not interact with this metabolic or elimination pathway. However, metamizole is an inducer of CYP3A4 and may decrease etoposide exposure. The clinical relevance of this interaction is unknown. Monitoring for etoposide efficacy may be required if coadministered.

Description:

See Summary

No Interaction Expected

Etoposide

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 OCT1/2/3, MATE1 and MATE2K. Etoposide does not inhibit or induce OCTs or MATEs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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 etoposide, or to be affected if coadministered with etoposide.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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). Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Metronidazole

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Metronidazole is eliminated via glomerular filtration. Etoposide 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). After coadministration with ketoconazole, a strong CYP3A4 inhibitor, etoposide exposure increased by 20%. Therefore, no clinically relevant effect on etoposide exposure is expected.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Miconazole

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Miconazole is extensively metabolized by the liver. Etoposide is unlikely to interfere with this unspecified metabolic pathway. Miconazole is also an inhibitor of CYP2C9 (moderate) and CYP3A4 (strong). Concentrations of etoposide may increase due to inhibition of CYP3A4. After coadministration with ketoconazole, a strong CYP3A4 inhibitor, etoposide exposure increased by 20%. Therefore, a clinically relevant effect on etoposide exposure is not expected due to coadministration with miconazole.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Midazolam (parenteral)

Quality of Evidence: Very Low

Summary:

Description:

See Summary

No Interaction Expected

Etoposide

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%). Etoposide does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Morphine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Morphine is mainly glucuronidated to morphine-3-glucuronide (UGT2B7>UGT1A1) and to a lesser extent, to the pharmacologically active morphine-6-glucuronide (UGT2B7>UGT1A1). Morphine is also a substrate of P-gp. Etoposide does not inhibit or induce UGTs or P-gp.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce UGTs.

Description:

See Summary

Potential Weak Interaction

Etoposide

Mycophenolate

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Mycophenolate is mainly glucuronidated by UGT1A9 and UGT2B7. The active metabolite of mycophenolate, mycophenolic acid, is an inhibitor of OAT1/OAT3. Etoposide does not interact with this pathway. However, due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.

Description:

See Summary

No Interaction Expected

Etoposide

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 renally excreted by a nonsaturable mechanism. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs or UGTs.

Description:

See Summary

No Interaction Expected

Etoposide

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%). Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Nefazodone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Nefazodone is metabolised mainly by CYP3A4. Etoposide does not inhibit or induce CYPs. Nefazodone is also a strong inhibitor of CYP3A4 and may increase etoposide concentrations. After coadministration with ketoconazole, a strong CYP3A4 inhibitor, etoposide exposure increased by 20%. Therefore, a clinically relevant effect on etoposide exposure is not expected due to coadministration with nefazodone.

Description:

See Summary

No Interaction Expected

Etoposide

Nicardipine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Nicardipine is metabolised mainly by CYP3A4 and to a lesser extent by CYP2D6 and CYP2C8. Etoposide does not inhibit or induce CYPs. Nicardipine is also a weak inhibitor of CYP3A4 and may increase etoposide concentrations. After coadministration with ketoconazole, a strong CYP3A4 inhibitor, etoposide exposure increased by 20%. Therefore, a clinically relevant effect on etoposide exposure is not expected due to coadministration with nicardipine.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Etoposide

Nifedipine

Quality of Evidence: Very Low

Summary:

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

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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%). Etoposide does not interact with this metabolic or elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

Norelgestromin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Norelgestromin is metabolised to norgestrel (possibly by CYP3A4). Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Norethisterone (Norethindrone)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Norethisterone is extensively biotransformed, first by reduction and then by sulfate and glucuronide conjugation. Etoposide does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Etoposide

Norgestimate

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Norgestimate is rapidly deacetylated to the active metabolite which is further metabolised via CYP450. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Norgestrel

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Norgestrel is a racemic mixture with levonorgestrel being biologically active. Levonorgestrel is mainly metabolized by CYP3A4 and is glucuronidated to a minor extent. Etoposide does not inhibit or induce CYPs or UGTs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Therefore, no drug interactions are expected.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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). Etoposide does not inhibit or induce CYPs or UGTs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this metabolic or elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not interact with this pathway.

Description:

See Summary

No Interaction Expected

Etoposide

Ondansetron

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ondansetron is metabolised mainly by CYP1A2 and CYP3A4 and to a lesser extent by CYP2D6. Ondansetron is also a substrate of P-gp. Etoposide does not inhibit or induce CYPs or P-gp.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce UGTs.

Description:

See Summary

Potential Interaction

Etoposide

Oxcarbazepine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Oxcarbazepine is extensively metabolized to the active metabolite monohydroxyderivate (MHD) through cytosolic enzymes. Etoposide does not interact with this metabolic pathway. Both oxcarbazepine and MHD are inducers of CYP3A4 (moderate) and CYP3A5 and are inhibitors of CYP2C19. Concentrations of etoposide may decrease due to induction of CYP3A4. The clinical relevance of this interaction is unknown. Selection of an alternate concomitant medicinal product, with no or minimal potential to induce CYP3A4 is recommended. Furthermore, coadministration may lead to decreased seizure control due to pharmacokinetic interactions between etoposide and oxcarbazepine. If coadministration is unavoidable, closely monitor etoposide and oxcarbazepine efficacy. Monitor oxcarbazepine plasma concentrations, if available.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce UGTs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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 renally eliminated (possibly via OCT) with minimal metabolism occurring via CYP2D6 and CYP3A4. Etoposide does not interact with this metabolic or elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

Palonosetron

Quality of Evidence: Very Low

Summary:

Palonosetron is metabolised mainly by CYP3A4 and to a lesser extent by CYP2D6 and CYP1A2. Palonosetron is also a substrate of P-gp. Etoposide does not inhibit or induce CYPs or P-gp. After coadministration of Akynzeo (palonosetron and netupitant), etoposide exposure was not changed by a clinically relevant extent.

Description:

See Summary

No Interaction Expected

Etoposide

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 but is cleared from the plasma by uptake into bone and elimination via renal excretion. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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). Etoposide does not inhibit or induce CYPs or UGTs.

Description:

See Summary

No Interaction Expected

Etoposide

Paroxetine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Paroxetine is mainly metabolised by CYP2D6. Paroxetine is also an inhibitor of CYP2D6 (strong) and CYP2C9. Etoposide does not interact with this pathway.

Description:

See Summary

Potential Weak Interaction

Etoposide

Peginterferon alfa-2a

Quality of Evidence: Very Low

Summary:

Description:

See Summary

No Interaction Expected

Etoposide

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). Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs or FMO3.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic pathway.

Description:

See Summary

Potential Interaction

Etoposide

Phenobarbital (Phenobarbitone)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Phenobarbital is metabolized by CYP2C19 and CYP2C9 (major) and to a lesser extent by CYP2E1. Etoposide does not interact with this metabolic pathway. Phenobarbital is also a strong inducer of CYPs 3A4, 2C9, 2C8 and UGTs. Concentrations of etoposide may decrease due to induction of CYP3A4. Coadministration with phenytoin is associated with decreased etoposide exposure and therefore reduced efficacy. A similar effect may occur after coadministration with phenobarbital. Selection of an alternate concomitant medicinal product, with no or minimal potential to induce CYP3A4 is recommended. Furthermore, coadministration may lead to decreased seizure control due to pharmacokinetic interactions between etoposide and phenobarbital. If coadministration is unavoidable, closely monitor etoposide and phenobarbital efficacy. Monitor phenobarbital plasma concentrations, if available.

Description:

See Summary

No Interaction Expected

Etoposide

Phenprocoumon

Quality of Evidence: Very Low

Summary:

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

Description:

See Summary

Potential Interaction

Etoposide

Phenytoin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Phenytoin is mainly metabolized by CYP2C9 and to a lesser extent by CYP2C19. Etoposide does not inhibit or induce CYPs. Phenytoin is a potent inducer of CYP3A4, UGT and P-gp. Concentrations of etoposide may decrease due to induction of CYP3A4 and P-gp. Coadministration with phenytoin is associated with decreased etoposide exposure and therefore reduced efficacy. Selection of an alternate concomitant medicinal product, with no or minimal potential to induce CYP3A4 is recommended. Furthermore, coadministration may lead to decreased seizure control due to pharmacokinetic interactions between etoposide and phenytoin. If coadministration is unavoidable, monitor closely for etoposide and phenytoin efficacy. Monitor phenytoin plasma concentrations, if available.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic or elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Pitavastatin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Pitavastatin is metabolised by UGTs 1A3 and 2B7 with minimal metabolism by CYPs 2C9 and 2C8. Pitavastatin is also a substrate of OATP1B1. Etoposide does not inhibit or induce CYPs, UGTs or OATP1B1.

Description:

See Summary

No Interaction Expected

Etoposide

Posaconazole

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Posaconazole is primarily metabolised by UGTs and is a substrate of P-gp. Etoposide does not inhibit or induce UGTs or P-gp. Posaconazole is also a strong inhibitor of CYP3A4 and may increase concentrations of etoposide. After coadministration with ketoconazole, a strong CYP3A4 inhibitor, etoposide exposure increased by 20%. Therefore, a clinically relevant effect on etoposide exposure is not expected due to coadministration with posaconazole.

Description:

See Summary

No Interaction Expected

Etoposide

Potassium

Quality of Evidence: Very Low

Summary:

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

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Pravastatin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Pravastatin is minimally metabolised via CYP enzymes and is a substrate of OATP1B1. Etoposide does not inhibit or induce CYPs or OATP1B1.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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). Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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). Etoposide does not inhibit or induce CYPs or UGTs.

Description:

See Summary

No Interaction Expected

Etoposide

Prucalopride

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Prucalopride is minimally metabolised and mainly renally eliminated, partly by active secretion by renal transporters. Prucalopride is also a substrate of P-gp. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

Quinidine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Quinidine is mainly metabolised by CYP3A4 and to a lesser extent by CYP2C9 and CYP2E1. Quinidine is also a substrate of P-gp. Etoposide does not inhibit or induce CYPs or P-gp. Quinidine is an inhibitor of CYP2D6 (strong), CYP3A4 (weak) and P-gp (moderate). Concentrations of etoposide may increase due to inhibition of CYP3A4 and P-gp. After coadministration with ketoconazole, a strong CYP3A4 and P-gp inhibitor, etoposide exposure increased by 20%. Therefore, a clinically relevant effect on etoposide exposure is not expected due to coadministration with quinidine.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce OATs.

Description:

See Summary

No Interaction Expected

Etoposide

Ranolazine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ranolazine is primarily metabolized by CYP3A4 and to a lesser extent by CYP2D6. Ranolazine is also a substrate of P-gp. Etoposide does not inhibit or induce CYPs or P-gp. Moreover, ranolazine is a weak inhibitor of P-gp, CYP3A4 and CYP2D6. Concentrations of etoposide may increase due to inhibition of CYP3A4 and P-gp. After coadministration with ketoconazole, a strong CYP3A4 and P-gp inhibitor, etoposide exposure increased by 20%. Therefore, a clinically relevant effect on etoposide exposure is not expected due to coadministration with ranolazine.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide 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. Therefore, no clinically relevant effect on etoposide exposure is expected.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs or OATP1B1.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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

Potential Interaction

Etoposide

Rifabutin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Rifabutin is metabolised by CYP3A4 and via deacetylation. Etoposide does not interact with this metabolic pathway. Rifabutin is also a strong CYP3A4 and P-gp inducer and may decrease etoposide concentrations. The clinical relevance of this interaction is unknown. Coadministration should be approached with caution. Selection of an alternate concomitant medicinal product, with no or minimal potential to induce CYP3A4 is recommended. If coadministration is clinically unavoidable, closely monitor etoposide efficacy.

Description:

See Summary

Potential Interaction

Etoposide

Rifampicin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Rifampicin is metabolised via deacetylation. Etoposide is unlikely to interfere with this metabolic pathway. Rifampicin is also a strong CYP3A4 and P-gp inducer and may decrease etoposide concentrations. The clinical relevance of this interaction is unknown. Coadministration should be approached with caution. Selection of an alternate concomitant medicinal product, with no or minimal potential to induce CYP3A4 is recommended. If coadministration is clinically unavoidable, closely monitor etoposide efficacy.

Description:

See Summary

Potential Interaction

Etoposide

Rifapentine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Rifapentine is metabolised via deacetylation. Etoposide is unlikely to interfere with this metabolic pathway. Rifapentine is also a strong CYP3A4, CYP2C8 and P-gp inducer. Etoposide exposure may decrease due to CYP3A4 and P-gp induction. The clinical relevance of this interaction is unknown. Coadministration should be approached with caution. Selection of an alternate concomitant medicinal product, with no or minimal potential to induce CYP3A4 is recommended. If coadministration is clinically unavoidable, closely monitor etoposide efficacy.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

Risperidone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Risperidone is metabolised by CYP2D6 and to a lesser extent by CYP3A4. Risperidone is also a substrate of P-gp. Etoposide does not inhibit or induce CYPs or P-gp.

Description:

See Summary

No Interaction Expected

Etoposide

Rivaroxaban

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Rivaroxaban is partly metabolised in the liver (by CYP3A4, CYP2J2 and hydrolytic enzymes) and partly eliminated unchanged in urine. Rivaroxaban is also a substrate of P-gp and BCRP. Etoposide does not interact with this metabolic or elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Rosuvastatin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Rosuvastatin is largely excreted unchanged in the faeces via OATP1B1 and is a substrate of BCRP. Etoposide does not inhibit or induce OATP1B1 or BCRP.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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 and etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Saxagliptin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Saxagliptin is mainly metabolised by CYP3A4 and is a substrate of P-gp. Etoposide does not inhibit or induce CYPs or P-gp.

Description:

See Summary

No Interaction Expected

Etoposide

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

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Simvastatin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Simvastatin is metabolised by CYP3A4. Simvastatin is a substrate of BCRP, and the active metabolite is a substrate of OATP1B1. Etoposide does not inhibit or induce CYPs, BCRP or OATP1B1.

Description:

See Summary

Potential Weak Interaction

Etoposide

Sirolimus

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Sirolimus is metabolised by CYP3A4 and is a substrate of P-gp. Etoposide does not inhibit or induce CYPs or P-gp. However, due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.

Description:

See Summary

No Interaction Expected

Etoposide

Sitagliptin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. 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. Etoposide is unlikely to interfere with this metabolic or elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this unspecified metabolic pathway.

Description:

See Summary

Do Not Coadminister

Etoposide

St John's Wort

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be avoided. St John’s wort is a P-gp and CYP3A4 inducer and may decrease etoposide concentrations. The clinical relevance of this interaction is unknown. Therefore, coadministration should be avoided. Selection of an alternate concomitant medicinal product, with no or minimal potential to induce CYP3A4 is recommended. If coadministration is clinically unavoidable, closely monitor etoposide efficacy.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

Potential Weak Interaction

Etoposide

Tacrolimus

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Tacrolimus is metabolised mainly by CYP3A4. Etoposide 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 etoposide exposure is expected. However, due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

Telithromycin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Telithromycin is metabolised by CYP3A4 (50%) with the remaining 50% metabolised via non-CYP mediated pathways. Etoposide does not interact with this metabolic pathway. Telithromycin is also an inhibitor of CYP3A4 (strong) and P-gp and may increase concentrations of etoposide. After coadministration with ketoconazole, a strong CYP3A4 and P-gp inhibitor, etoposide exposure increased by 20%. Therefore, a clinically relevant effect on etoposide exposure is not expected due to coadministration with telithromycin.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce UGTs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce UGTs.

Description:

See Summary

No Interaction Expected

Etoposide

Terbinafine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Terbinafine is metabolised by CYPs 1A2, 2C9, 3A4 and to a lesser extent by CYP2C8 and CYP2C19. Terbinafine is also a moderate-strong inhibitor of CYP2D6. Etoposide does not interact with this pathway.

Description:

See Summary

No Interaction Expected

Etoposide

Testosterone

Quality of Evidence: Very Low

Summary:

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

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

Ticagrelor

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ticagrelor is a substrate of CYP3A4 and P-gp. Etoposide does not inhibit or induce CYPs or P-gp. Ticagrelor is also a mild inhibitor of CYP3A4 and may increase concentrations of etoposide. After coadministration with ketoconazole, a strong CYP3A4 inhibitor, etoposide exposure increased by 20%. Therefore, a clinically relevant effect on etoposide exposure is not expected due to coadministration with ticagrelor.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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 CYP2C8 and CYP2C19. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. 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. Etoposide does not inhibit or induce CYPs or OATs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Tropisetron

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Tropisetron is metabolised mainly by CYP2D6. Tropisetron is also a substrate of P-gp. Etoposide does not inhibit or induce CYPs or P-gp.

Description:

See Summary

No Interaction Expected

Etoposide

Ulipristal

Quality of Evidence: Very Low

Summary:

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

Description:

See Summary

Potential Interaction

Etoposide

Valproic acid (Valproate)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. 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. Valproic acid is also an inhibitor of CYP2C9. Etoposide does not interact with this metabolic pathway. However, coadministration may lead to decreased seizure control due to pharmacokinetic interactions between etoposide and valproic acid. If coadministration is unavoidable, closely monitor etoposide and valproic acid efficacy. Monitor valproic acid plasma concentrations, if available.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

Verapamil

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Verapamil is metabolised mainly by CYP3A4 and to a lesser extent by CYPs 1A2, 2C8 and 2C9. Etoposide does not inhibit or induce CYPs. Verapamil is also an inhibitor of CYP3A4 (moderate) and P-gp (strong) and may increase etoposide concentrations. After coadministration with ketoconazole, a strong CYP3A4 inhibitor, etoposide exposure increased by 20%. Therefore, a clinically relevant effect on etoposide exposure is not expected due to coadministration with verapamil.

Description:

See Summary

No Interaction Expected

Etoposide

Vildagliptin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Vildagliptin is inactivated via non-CYP mediated hydrolysis and is a substrate of P-gp. Etoposide does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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

No Interaction Expected

Etoposide

Voriconazole

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Voriconazole is metabolised by CYP2C19 (major) and to a lesser extent by CYP3A4 and CYP2C9. Etoposide does not inhibit or induce CYPs. Voriconazole is also a strong inhibitor of CYP3A4 and a weak inhibitor of CYPs 2C9, 2C19 and 2B6. Concentrations of etoposide may increase due to inhibition of CYP3A4. After coadministration with ketoconazole, a strong CYP3A4 inhibitor, etoposide exposure increased by 20%. Therefore, a clinically relevant effect on etoposide exposure is not expected due to coadministration with voriconazole.

Description:

See Summary

Potential Interaction

Etoposide

Warfarin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. 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. Etoposide does not inhibit or induce CYPs. However, coadministration of warfarin and etoposide may result in elevated international normalized ratio (INR). Close monitoring of INR is recommended.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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). Etoposide does not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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 but is cleared from the plasma by uptake into bone and elimination via renal excretion. Etoposide is unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not inhibit or induce CYPs.

Description:

See Summary

No Interaction Expected

Etoposide

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. Etoposide does not interact with this metabolic pathway.

Description:

See Summary