Cancer Drug Interactions from Radboud UMC and University of Liverpool

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

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Potential Interaction

Tegafur/Gimeracil/Oteracil

Acenocoumarol

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Acenocoumarol is mainly metabolised by CYP2C9 and to a lesser extent by CYP1A2 and CYP2C19. 5-fluorouracil, the active compound of tegafur, may increase acenocoumarol plasma concentrations due to inhibition of CYP2C9. No formal interaction studies have been conducted. Increased prothrombin time (PT) and internationalised normal ratio (INR) values have been reported in patients treated with warfarin in combination with tegafur, oteracil and gimeracil. A similar effect may occur after coadministration with acenocoumarol. The clinical relevance of these interactions is unknown. Coadministration should be approached with caution. Monitoring for acenocoumarol toxicity and INR/PT is recommended.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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). Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce UGTs.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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%). 5-fluorouracil, the active compound of tegafur, may increase agomelatine plasma concentrations due to inhibition of CYP2C9. However, no clinically relevant effect on agomelatine exposure is expected.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway. Although no pharmacokinetic interaction is expected, alendronic acid should be separated from food or other medicinal products and patients must wait at least 30 minutes after taking alendronic acid before taking any other oral medicinal product.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this elimination pathway.

Description:

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Do Not Coadminister

Tegafur/Gimeracil/Oteracil

Allopurinol

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Allopurinol is converted to oxipurinol by xanthine oxidase and aldehyde oxidase. Allopurinol is also an inhibitor of xanthine oxidase. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway. However, based on non-clinical data allopurinol may inhibit the phosphorylation of 5-fluorouracil. As a result 5-fluorouracil efficacy may decrease. The clinical relevance of this interaction is unknown. Monitoring of 5-fluorouracil efficacy and, if available, 5-fluourouracil plasma concentrations is recommended.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. 5-fluorouracil, the active compound of tegafur, may increase alosetron plasma concentrations due to inhibition of CYP2C9. However, no clinically relevant effect on alosetron exposure is expected.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway. The effect of coadministration of tegafur, oteracil and gimeracil with a proton pump inhibitor on tegafur and 5-fluorouracil (the active compound of tegafur) has been studied. After coadministration, 5-fluorouracil exposure decreased by 7% and tegafur exposure increased by 11%. No clinically relevant effect of aluminium hydroxide on tegafur and 5-fluorouracil exposure is expected.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce these CYPs, UGTs or P-gp.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. 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). Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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). Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. 5-fluorouracil, the active compound of tegafur, may increase amitriptyline plasma concentration due to inhibition of CYP2C9. However, no clinically relevant effect on amitriptyline exposure is expected.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

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Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interfere with this 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

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. The effect of coadministration of tegafur, oteracil and gimeracil with a proton pump inhibitor on tegafur and 5-fluorouracil (the active compound of tegafur) has been studied. After coadministration, 5-fluorouracil exposure decreased by 7% and tegafur exposure increased by 11%. No clinically relevant effect of antacids on tegafur and 5-fluorouracil exposure is expected.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. 5-fluorouracil, the active compound of tegafur, is an inhibitor of CYP2C9 and may increase apixaban concentrations. However, no clinically relevant effect on apixaban exposure is expected.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. During treatment, aprepitant is a moderate inhibitor of CYP3A4. After treatment, aprepitant is a weak inducer of CYP3A4, CYP2C9 and UGT. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4 or CYP2D6.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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)). Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce these CYPs or UGTs.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce these CYPs.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4, P-gp or OATP1B1.

Description:

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Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

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 by xanthine oxidase. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do 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

Tegafur/Gimeracil/Oteracil

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. Azithromycin is also an inhibitor of P-gp, but the clinical relevance of P-gp inhibition by azithromycin is unknown. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this metabolic or elimination pathway.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

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Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

Bendroflumethiazide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic 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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this pathway. However, in patients receiving cyclophosphamide, methotrexate and 5-fluorouracil (the active compound of tegafur), addition of thiazide diuretics resulted in a more pronounced decrease in the number of granulocytes when compared to patients not receiving thiazides. Therefore, care should be taken and due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP2D6 or CYP3A4.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this pathway.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this metabolic or elimination pathway.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic or elimination pathway.

Description:

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Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

Bosentan

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Bosentan is a substrate and weak inducer of CYP3A4 and CYP2C9. 5-fluorouracil, the active compound of tegafur, may increase bosentan plasma concentrations due to inhibition of CYP2C9. No formal interaction studies have been conducted. The clinical relevance of this interaction is unknown and care should be taken if coadministered. No a priori dose adjustment is needed. However, monitoring for bosentan toxicity should be considered. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are not metabolised by CYP3A4 or CYP2C9.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce these CYPs.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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). Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4 or UGTs.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

Carbamazepine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Carbamazepine is primarily metabolized by CYP3A4 and to a lesser extent by CYP2C8. Carbamazepine is also an inducer of CYPs 2C8 (strong), 2C9 (strong), 3A4 (strong), 1A2 (weak), 2B6, UGT1A1 and P-gp (moderate). Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. 5-fluorouracil, the active compound of tegafur, may increase carvedilol concentrations due to CYP2C9 inhibition. However, no clinically relevant effect on carvedilol exposure is expected. Carvedilol is also an inhibitor of P-gp, but the clinical relevance of P-gp inhibition by carvedilol is unknown. Tegafur, oteracil, gimeracil and 5-flurouracil are not transported by P-gp.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

Cefalexin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cefalexin is predominantly eliminated unchanged renally by glomerular filtration and tubular secretion via OAT1 and MATE1. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this metabolic or elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

Celecoxib

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Celecoxib is primarily metabolised by CYP2C9. 5-fluorouracil, the active compound of tegafur, may increase celecoxib plasma concentrations due to inhibition of CYP2C9. No formal interaction studies have been conducted. The clinical relevance of this interaction is unknown and care should be taken if coadministered. No a priori dose adjustment is needed. However, monitoring for celecoxib toxicity should be considered.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. In vitro studies have shown that chloramphenicol can inhibit metabolism mediated by CYPs 3A4 (strong), 2C19 (strong) and 2D6 (weak). Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP2D6.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP2D6 or CYP1A2.

Description:

See Summary

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

Chlortalidone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic 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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway. However, in patients receiving cyclophosphamide, methotrexate and 5-fluorouracil (the active compound of tegafur), addition of thiazide diuretics resulted in a more pronounced decrease in the number of granulocytes when compared to patients not receiving thiazides. Therefore, care should be taken and due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

Ciclosporin (Cyclosporine)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ciclosporin is a substrate of CYP3A4 and P-gp and also inhibits CYP3A4 and OATP1B1. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

Cimetidine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Cimetidine is metabolised by CYP450 enzymes. 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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway. However, the EU product label warns for a decreased clearance of 5-fluourouracil. As a result 5-fluorouracil concentrations may increase. The clinical relevance of this interaction is unknown. Monitoring for 5-fluorouracil toxicity and, if available, 5-fluorouracil plasma concentrations may be required. Furthermore, the effect of coadministration of tegafur, oteracil and gimeracil with a proton pump inhibitor on tegafur and 5-fluorouracil (the active compound of tegafur) has been studied. After coadministration, 5-fluorouracil exposure decreased by 7% and tegafur exposure increased by 11%. No clinically relevant effect of cimetidine on tegafur and 5-fluorouracil exposure is expected.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Ciprofloxacin is also a weak to moderate inhibitor of CYP3A4 and a strong inhibitor of CYP1A2. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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%). Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce these CYPs.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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 and is also an inhibitor of CYP3A4 (strong) and P-gp. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP2D6.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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 and in vitro data suggest that it is a CYP3A4 inhibitor. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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

Tegafur/Gimeracil/Oteracil

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. In vitro data suggest that clofazimine is a CYP3A4 inhibitor. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce OATs.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce these CYPs.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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 an inhibitor of CYP2C8 (strong), CYP2B6 (weak) and of CYP2C9 (in vitro) at high concentrations. The clinical relevance of CYP2C9 inhibition is unknown. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4 or UGTs.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce these CYPs. However, due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. The metabolite morphine is a substrate of P-gp. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4, CYP2D6, UGTs or P-gp.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4 or P-gp.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. 5-fluorouracil, the active compound of tegafur, is an inhibitor of CYP2C9. However, as dapsone is metabolised through multiple CYP enzymes, no clinically relevant effect on dapsone exposure is expected.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP2D6.

Description:

See Summary

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

Desogestrel

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Desogestrel is a prodrug which is activated to etonogestrel by CYP2C9 (and possibly CYP2C19); the metabolism of etonogestrel is mediated by CYP3A4. 5-fluorouracil, the active compound of tegafur, may increase desogestrel plasma concentrations and decrease etonogestrel concentrations due to inhibition of CYP2C9. No formal interaction studies have been conducted. The clinical relevance of this interaction is unknown and care should be taken if coadministered. No a priori dose adjustment is needed. The addition of a barrier method as a second form of contraception should be considered while taking desogestrel in combination with Teysuno.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

Dexamethasone

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dexamethasone is a substrate of CYP3A4. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4. Furthermore, dexamethasone has been described as a weak inducer of CYP3A4. However, the clinical relevance of this interaction is not known and the induction of CYP3A4 by dexamethasone has not yet been established.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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). Morphine is a substrate of P-gp. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce UGTs or P-gp.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4, CYP2C19 or UGTs.

Description:

See Summary

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

Diclofenac

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Diclofenac is partly glucuronidated by UGT2B7 and partly oxidised by CYP2C9. 5-fluorouracil, the active compound of tegafur, may increase diclofenac plasma concentrations due to inhibition of CYP2C9. No formal interaction studies have been conducted. The clinical relevance of this interaction is unknown and care should be taken if coadministered. No a priori dose adjustment is needed. However, monitoring for diclofenac toxicity should be considered.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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 renally eliminated via OATP4C1 and P-gp. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce OATP4C1 or P-gp.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4 or UGTs.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Diltiazem is also an inhibitor of CYP3A4 (moderate) and P-gp, but the clinical relevance of P-gp inhibition by diltiazem is unknown. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. 5-fluorouracil, the active compound of tegafur, may increase diphenhydramine concentrations due to CYP2C9 inhibition. However, no clinically relevant effect on diphenhydramine exposure is expected. Diphenhydramine is also a weak inhibitor of CYP2D6. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce UGTs.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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%). Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4, CYP2D6 or UGTs.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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 tegafur, oteracil, gimeracil or the active compound 5-fluorouracil, or to be affected if coadministered with tegafur, oteracil, gimeracil or the active compound 5-fluorouracil.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP2C19 or CYP2D6.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

Dronabinol

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Dronabinol is mainly metabolised by CYP2C9 and to a lesser extent by CYP3A4. 5-fluorouracil, the active compound of tegafur, may increase dronabinol plasma concentrations due to inhibition of CYP2C9. No formal interaction studies have been conducted. The clinical relevance of this interaction is unknown and care should be taken if coadministered. No a priori dose adjustment is needed. However, monitoring for dronabinol toxicity should be considered.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do 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

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP2D6 or CYP1A2.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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). Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4 or P-gp.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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). Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP1A2, CYP2C8 or UGTs.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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). Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this metabolic or elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Erythromycin is an inhibitor of CYP3A4 (moderate) and P-gp. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce these CYPs.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway. Furthermore, the effect of coadministration of tegafur, oteracil and gimeracil with a proton pump inhibitor on tegafur and 5-fluorouracil (the active compound of tegafur) has been studied. After coadministration, 5-fluorouracil exposure decreased by 7% and tegafur exposure increased by 11%. No clinically relevant effect of esomeprazole on tegafur and 5-fluorouracil exposure is expected.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4, CYP1A2 or UGTs.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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%). Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this metabolic or elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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). 5-fluorouracil, the active compound of tegafur, may increase ethinylestradiol plasma concentrations due to inhibition of CYP2C9. However, no clinically relevant effect on ethinylestradiol exposure is expected.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4 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

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are 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

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce UGTs.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce OATs. Furthermore, the effect of coadministration of tegafur, oteracil and gimeracil with a proton pump inhibitor on tegafur and 5-fluorouracil (the active compound of tegafur) has been studied. After coadministration, 5-fluorouracil exposure decreased by 7% and tegafur exposure increased by 11%. No clinically relevant effect of famotidine on tegafur and 5-fluorouracil exposure is expected.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce P-gp.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic or elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

Flucloxacillin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Flucloxacillin is mainly renally eliminated partly by glomerular filtration and partly by active secretion via OAT1. Flucloxacillin is described as a CYP3A4 inducer. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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 and is also an inhibitor of CYPs 3A4 (moderate), 2C9 (moderate) and 2C19 (strong). Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this pathway.

Description:

See Summary

Do Not Coadminister

Tegafur/Gimeracil/Oteracil

Flucytosine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but is contraindicated as both flucytosine and tegafur are metabolised to 5-fluorouracil. Coadministration would lead to additive 5-fluorouracil toxicity. A minimum washout period of 7 days is recommended between administration of Teysuno and flucytosine. Flucytosine is metabolised to 5-fluorouracil (5-FU). 5-FU is further metabolised by dihydropyrimidine dehydrogenase (DPD) to an inactive metabolite.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4 or CYP2C19.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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 also a strong inhibitor of CYP2D6 and CYP2C19. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP2D6.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

Fluvastatin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Fluvastatin is mainly metabolised by CYP2C9 (75%) and to a lesser extent by CYP3A4 (20%) and CYP2C8 (5%). 5-fluorouracil, the active compound of tegafur, may increase fluvastatin plasma concentrations due to inhibition of CYP2C9. No formal interaction studies have been conducted. The clinical relevance of this interaction is unknown and care should be taken if coadministered. No a priori dose adjustment is needed. However, monitoring for fluvastatin toxicity should be considered. Fluvastatin also potentially inhibits CYP2C9, but the clinical relevance of CYP2C9 inhibition is unknown. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Fluvoxamine is also an inhibitor of CYPs 1A2 (strong), 2C19 (strong), 3A4 (moderate), 2C9 (weak-moderate) and 2D6 (weak). Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. 5-fluorouracil, the active compound of tegafur, may increase formoterol concentrations due to CYP2C9 inhibition. However, as multiple CYP450 and UGT enzymes catalyse the transformation the potential for a pharmacokinetic interaction is low.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Aprepitant is mainly metabolized by CYP3A4 and to a lesser extent by CYP1A2 and CYP2C19. During treatment, aprepitant is a moderate inhibitor of CYP3A4. After treatment, aprepitant is a weak inducer of CYP3A4, CYP2C9 and UGT. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

Potential Interaction

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway. Phenytoin is mainly metabolized by CYP2C9 and to a lesser extent by CYP2C19. 5-fluorouracil, the active compound of tegafur, may increase phenytoin plasma concentrations due to inhibition of CYP2C9. No formal interaction studies have been conducted. The clinical relevance of this interaction is unknown. Phenytoin is a potent inducer of CYP3A4, UGT and P-gp. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway. Furthermore, a case report described an increase in serum phenytoin concentrations after coadministration with Teysuno. The clinical relevance is unknown. No a priori dose adjustment is needed. However, monitoring for phenytoin toxicity and, if available, phenytoin plasma concentrations is recommended.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. 5-fluorouracil, the active compound of tegafur, may increase gestodene plasma concentrations due to inhibition of CYP2C9. However, no clinically relevant effect on gestodene exposure is expected.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. 5-fluorouracil, the active compound of tegafur, may increase glibenclamide plasma concentration due to inhibition of CYP2C9. However, no clinical relevant effect on glibenclamide exposure is expected.

Description:

See Summary

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

Gliclazide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Gliclazide is metabolised mainly by CYP2C9 and to a lesser extent by CYP2C19. 5-fluorouracil, the active compound of tegafur, may increase gliclazide plasma concentrations due to inhibition of CYP2C9. No formal interaction studies have been conducted. The clinical relevance of this interaction is unknown and care should be taken if coadministered. No a priori dose adjustment is needed. However, monitoring for gliclazide toxicity should be considered.

Description:

See Summary

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

Glimepiride

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Glimepiride is mainly metabolised by CYP2C9. 5-fluorouracil, the active compound of tegafur, may increase glimepiride plasma concentrations due to inhibition of CYP2C9. No formal interaction studies have been conducted. The clinical relevance of this interaction is unknown and care should be taken if coadministered. No a priori dose adjustment is needed. However, monitoring for glimepiride toxicity should be considered.

Description:

See Summary

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

Glipizide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Glipizide is mainly metabolised by CYP2C9. 5-fluorouracil, the active compound of tegafur, may increase glipizide plasma concentrations due to inhibition of CYP2C9. No formal interaction studies have been conducted. The clinical relevance of this interaction is unknown and care should be taken if coadministered. No a priori dose adjustment is needed. However, monitoring for glipizide toxicity should be considered.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4 or P-gp.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

Grapefruit juice

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Grapefruit juice is known to inhibit CYP3A4 enzymes. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are not substrates of CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere 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 CYPs. Tegafur is metabolised to the active compound 5-fluorouracil by CYP2A6. Griseofulvin may decrease tegafur concentrations by inhibiting CYP2A6. Concentrations of 5-fluorouracil may increase. The clinical relevance of this interaction is unknown. If coadministered, monitoring for 5-fluorouracil toxicity may be required.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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). Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. In vitro studies have suggested that hydralazine is a mixed enzyme inhibitor, which may weakly inhibit CYP3A4 and CYP2D6. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

Hydrochlorothiazide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Hydrochlorothiazide is not metabolised and is cleared by the kidneys via OAT1. OAT1/3 are the major transporters of loop and thiazide diuretics. Secretion of these diuretics into the urinary tract by transporters in the proximal tubular cells is necessary for the diuretic effect in later tubule segments. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway. However, in patients receiving cyclophosphamide, methotrexate and 5-fluorouracil (the active compound of tegafur), addition of thiazide diuretics resulted in a more pronounced decrease in the number of granulocytes when compared to patients not receiving thiazides. Therefore, care should be taken and due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP2D6 or CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce UGTs.

Description:

See Summary

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are 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

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are 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

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

Ibuprofen

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Ibuprofen is metabolised mainly by CYP2C9 and to a lesser extent by CYP2C8 and direct glucuronidation. 5-fluorouracil, the active compound of tegafur, may increase ibuprofen plasma concentrations due to inhibition of CYP2C9. No formal interaction studies have been conducted. The clinical relevance of this interaction is unknown and care should be taken if coadministered. No a priori dose adjustment is needed. However, monitoring for ibuprofen toxicity should be considered.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4 or CYP2D6.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce these CYPs.

Description:

See Summary

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

Indapamide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic 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. 5-fluorouracil, the active compound of tegafur, may increase indapamide plasma concentrations due to inhibition of CYP2C9. However, no clinically relevant effect on indapamide exposure is expected. In patients receiving cyclophosphamide, methotrexate and 5-fluorouracil (the active compound of tegafur), addition of thiazide diuretics resulted in a more pronounced decrease in the number of granulocytes when compared to patients not receiving thiazides. Therefore, care should be taken and due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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

Tegafur/Gimeracil/Oteracil

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

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are 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

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

See Summary

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

Irbesartan

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Irbesartan is metabolised by glucuronidation and oxidation (mainly CYP2C9). 5-fluorouracil, the active compound of tegafur, may increase irbesartan plasma concentrations due to inhibition of CYP2C9. No formal interaction studies have been conducted. The clinical relevance of this interaction is unknown and care should be taken if coadministered. No a priori dose adjustment is needed. However, monitoring for irbesartan toxicity should be considered.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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 and is also an inhibitor of CYP3A4 (strong), CYP2C9 (weak), P-gp and BCRP. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

Ketoconazole

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ketoconazole is a substrate of CYP3A4. Ketoconazole is also an inhibitor of CYP3A4 (strong) and P-gp. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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). Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce UGTs.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP2C19 or CYP3A4. Furthermore, the effect of coadministration of tegafur, oteracil and gimeracil with a proton pump inhibitor on tegafur and 5-fluorouracil (the active compound of tegafur) has been studied. After coadministration, 5-fluorouracil exposure decreased by 7% and tegafur exposure increased by 11%. No clinically relevant effect of lansoprazole on tegafur and 5-fluorouracil exposure is expected.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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). Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP2D6.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4 or UGTs.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

Levonorgestrel (Emergency Contraception)

Quality of Evidence: Very Low

Summary:

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP1A2 or CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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 and is a weak inhibitor of CYP3A4. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this unspecified metabolic pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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

Tegafur/Gimeracil/Oteracil

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

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4, CYP2C8 or P-gp.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4 or CYP2D6.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this unspecified metabolic pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce UGTs.

Description:

See Summary

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

Losartan

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Losartan is converted to its active metabolite mainly by CYP2C9 in the range of clinical concentrations. 5-fluorouracil, the active compound of tegafur, may increase losartan plasma concentrations due to inhibition of CYP2C9. No formal interaction studies have been conducted. The clinical relevance of this interaction is unknown and care should be taken if coadministered. No a priori dose adjustment is needed. However, monitoring for losartan toxicity should be considered.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. 5-fluorouracil, the active compound of tegafur, may increase macitentan plasma concentrations due to inhibition of CYP2C9. However, no clinically relevant effect on macitentan exposure is expected.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, glimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP2D6.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

Medroxyprogesterone (non-depot)

Quality of Evidence: Very Low

Summary:

Description:

See Summary

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

Mefenamic acid

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Mefenamic acid is metabolised by CYP2C9 and glucuronidated by UGT2B7 and UGT1A9. 5-fluorouracil, the active compound of tegafur, may increase mefenamic acid plasma concentrations due to inhibition of CYP2C9. However, no formal interaction studies have been conducted. The clinical relevance of this interaction is unknown and care should be taken if coadministered. No a priori dose adjustment is needed. However, monitoring for mefenamic acid toxicity should be considered.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

Metamizole

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. 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%). Metamizole is also an inducer of CYP3A4. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce OCTs or MATEs.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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 tegafur, oteracil, gimeracil or the active compound 5-fluorouracil, or to be affected if coadministered with tegafur, oteracil, gimeracil or the active compound 5-fluorouracil.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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). Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP2D6.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP2D6.

Description:

See Summary

Potential Interaction

Tegafur/Gimeracil/Oteracil

Metronidazole

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Metronidazole is eliminated via glomerular filtration. 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). Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this metabolic or elimination pathway. However, exposure of 5-fluorouracil, the active compound of tegafur, may increase after coadministration with metronidazole due to decreased clearance of 5-fluorouracil. The clinical relevance of this interaction is unknown. If coadministration is unavoidable, monitor closely for 5-fluorouracil toxicity and, if available, 5-fluorouracil plasma concentrations.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP2D6 or CYP1A2.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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 CYP2D6 and CYP1A2, and to a lesser extent by CYP3A4. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce these CYPs.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Miconazole is also an inhibitor of CYP2C9 (moderate) and CYP3A4 (strong). Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

Midazolam (parenteral)

Quality of Evidence: Very Low

Summary:

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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%). Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this metabolic or elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce these CYPs.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. 5-fluorouracil, the active compound of tegafur, may increase montelukast concentrations due to CYP2C9 inhibition. However, no clinically relevant effect on montelukast exposure is expected.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce UGTs or P-gp.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce UGTs.

Description:

See Summary

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce UGTs or OATs. However, due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

See Summary

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

Naproxen

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Naproxen is mainly glucuronidated by UGT2B7 (major) and demethylated to desmethylnaproxen by CYP2C9 (major) and CYP1A2. 5-fluorouracil, the active compound of tegafur, may increase naproxen plasma concentrations due to inhibition of CYP2C9. No formal interaction studies have been conducted. The clinical relevance of this interaction is unknown and care should be taken if coadministered. No a priori dose adjustment is needed. However, monitoring for naproxen toxicity should be considered.

Description:

See Summary

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

Nateglinide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Nateglinide is mainly metabolised by CYP2C9 (70%) and to a lesser extent by CYP3A4 (30%). 5-fluorouracil, the active compound of tegafur, may increase nateglinide plasma concentrations due to inhibition of CYP2C9. No formal interaction studies have been conducted. The clinical relevance of this interaction is unknown and care should be taken if coadministered. No a priori dose adjustment is needed. However, monitoring for nateglinide toxicity should be considered.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP2D6.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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 and is also a strong inhibitor of CYP3A4. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Nicardipine is also a weak inhibitor of CYP3A4. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

Nimesulide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Nimesulide is extensively metabolised in the liver following multiple pathways including CYP2C9. 5-fluorouracil, the active compound of tegafur, may increase nimesulide plasma concentrations due to inhibition of CYP2C9. No formal interaction studies have been conducted. The clinical relevance of this interaction is unknown and care should be taken if coadministered. No a priori dose adjustment is needed. However, monitoring for nimesulide toxicity should be considered.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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%). Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interfere with this metabolic or elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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). Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. 5-fluorouracil, the active compound of tegafur, may increase norgestimate plasma concentrations due to inhibition of CYP2C9. However, no clinically relevant effect on norgestimate exposure is expected.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4 or UGTs.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP2D6.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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). Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP1A2, CYP2D6 or UGTs.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway. Furthermore, the effect of coadministration of tegafur, oteracil and gimeracil with a proton pump inhibitor on tegafur and 5-fluorouracil (the active compound of tegafur) has been studied. After coadministration, 5-fluorouracil exposure decreased by 7% and tegafur exposure increased by 11%. No clinically relevant effect of omeprazole on tegafur and 5-fluorouracil exposure is expected.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce these CYPs or P-gp.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce UGTs.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

Oxcarbazepine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Oxcarbazepine is extensively metabolized to the active metabolite monohydroxyderivate (MHD) through cytosolic enzymes. Both oxcarbazepine and MHD are inducers of CYP3A4 (moderate) and CYP3A5 and are inhibitors of CYP2C19. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce UGTs.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4 or CYP2D6.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic or elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

Palonosetron

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Palonosetron is metabolised mainly by CYP3A4 and to a lesser extent by CYP2D6 and CYP1A2. Palonosetron is also a substrate of P-gp. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce these CYPs or P-gp.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. 5-fluorouracil, the active compound of tegafur, may increase pantoprazole plasma concentrations due to inhibition of CYP2C9. However, no clinically relevant effect on pantoprazole exposure is expected. Furthermore, the effect of coadministration of tegafur, oteracil and gimeracil with a proton pump inhibitor on tegafur and 5-fluorouracil (the active compound of tegafur) has been studied. After coadministration, 5-fluorouracil exposure decreased by 7% and tegafur exposure increased by 11%. No clinically relevant effect of pantoprazole on tegafur and 5-fluorouracil exposure is expected.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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). Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce these CYPs or UGTs.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

Peginterferon alfa-2a

Quality of Evidence: Very Low

Summary:

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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). Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. 5-fluorouracil, the active compound of tegafur, may increase perazine concentrations due to CYP2C9 inhibition. However, no clinically relevant effect on perazine exposure is expected.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP2D6.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP2D6.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP2B6 or CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

See Summary

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

Phenobarbital (Phenobarbitone)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Phenobarbital is metabolized by CYP2C19 and CYP2C9 (major) and to a lesser extent by CYP2E1. 5-fluorouracil, the active compound of tegafur, may increase phenobarbital plasma concentrations due to inhibition of CYP2C9. No formal interaction studies have been conducted. The clinical relevance of this interaction is unknown and care should be taken if coadministered. No a priori dose adjustment is needed. However, monitoring for phenobarbital toxicity and, if available, phenobarbital plasma concentrations should be considered. Phenobarbital is a strong inducer of CYPs 3A4, 2C9, 2C8 and UGTs. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

Potential Interaction

Tegafur/Gimeracil/Oteracil

Phenprocoumon

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Phenprocoumon is mainly metabolised by CYP2C9 and CYP3A4. 5-fluorouracil, the active compound of tegafur, may increase phenprocoumon plasma concentrations due to inhibition of CYP2C9. No formal interaction studies have been conducted. Increased prothrombin time (PT) and internationalised normal ratio (INR) values have been reported in patients treated with warfarin in combination with tegafur, oteracil and gimeracil. A similar effect may occur after coadministration with phenprocoumon. The clinical relevance of these interactions is unknown. Therefore, coadministration should be approached with caution. Monitoring for phenprocoumon toxicity and INR/PT is recommended.

Description:

See Summary

Potential Interaction

Tegafur/Gimeracil/Oteracil

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. 5-fluorouracil, the active compound of tegafur, may increase phenytoin plasma concentrations due to inhibition of CYP2C9. No formal interaction studies have been conducted. The clinical relevance of this interaction is unknown. Phenytoin is a potent inducer of CYP3A4, UGT and P-gp. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway. Furthermore, a case report described an increase in serum phenytoin concentrations after coadministration with Teysuno. The clinical relevance is unknown. No a priori dose adjustment is needed. However, monitoring for phenytoin toxicity and, if available, phenytoin plasma concentrations is recommended.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP4F2.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce these CYPs.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic or elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. 5-fluorouracil, the active compound of tegafur, may increase pioglitazone plasma concentration due to inhibition of CYP2C9. However, no clinically relevant effect on pioglitazone is expected.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP2D6.

Description:

See Summary

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

Piroxicam

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Piroxicam is primarily metabolised by CYP2C9. 5-fluorouracil, the active compound of tegafur, may increase piroxicam plasma concentrations due to inhibition of CYP2C9. No formal interaction studies have been conducted. The clinical relevance of this interaction is unknown and care should be taken if coadministered. No a priori dose adjustment is needed. However, monitoring for piroxicam toxicity should be considered.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. 5-fluorouracil, the active compound of tegafur, may increase pitavastatin plasma concentration due to inhibition of CYP2C9. However, no clinically relevant effect on pitavastatin exposure is expected.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Posaconazole is also a strong inhibitor of CYP3A4. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. 5-fluorouracil, the active compound of tegafur, may increase prasugrel plasma concentrations due to inhibition of CYP2C9. However, no clinically relevant effect on prasugrel exposure is expected.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYPs or OATP1B1.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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). Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP2D6 or CYP2C19.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP2D6.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce these CYPs.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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). Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce these CYPs or UGTs.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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 a substrate of P-gp. 5-fluorouracil, the active compound of tegafur, may increase quinidine plasma concentrations due to inhibition of CYP2C9. However, no clinically relevant effect on quinidine exposure is expected. Quinidine is also an inhibitor of CYP2D6 (strong), CYP3A4 (weak) and P-gp (moderate). Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway. Furthermore, the effect of coadministration of tegafur, oteracil and gimeracil with a proton pump inhibitor on tegafur and 5-fluorouracil (the active compound of tegafur) has been studied. After coadministration, 5-fluorouracil exposure decreased by 7% and tegafur exposure increased by 11%. No clinically relevant effect of rabeprazole on tegafur and 5-fluorouracil exposure is expected.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce OATs. Furthermore, the effect of coadministration of tegafur, oteracil and gimeracil with a proton pump inhibitor on tegafur and 5-fluorouracil (the active compound of tegafur) has been studied. After coadministration, 5-fluorouracil exposure decreased by 7% and tegafur exposure increased by 11%. No clinically relevant effect of ranitidine on tegafur and 5-fluorouracil exposure is expected.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Ranolazine is a weak inhibitor of P-gp, CYP3A4 and CYP2D6. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. In vitro data indicate reboxetine to be a weak inhibitor of CYP3A4 but in vivo data showed no inhibitory effect on CYP3A4. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP2C8, CYP3A4 or OATP1B1.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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

No Interaction Expected

Tegafur/Gimeracil/Oteracil

Rifabutin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Rifabutin is metabolised by CYP3A4 and via deacetylation. Rifabutin is also a strong CYP3A4 and P-gp inducer. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

Rifampicin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Rifampicin is metabolised via deacetylation and is also a strong CYP3A4 and P-gp inducer. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

Rifapentine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Rifapentine is metabolised via deacetylation and is also a strong CYP3A4, CYP2C8 and P-gp inducer. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP2D6, CYP3A4 or P-gp.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic or elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. 5-fluorouracil, the active compound of tegafur, may increase rosiglitazone plasma concentrations due to inhibition of CYP2C9. However, no clinically relevant effect on rosiglitazone exposure is expected.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce OATP1B1 or BCRP.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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 tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4 or P-gp.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP2D6 or CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. 5-fluorouracil, the active compound of tegafur, may increase sertraline concentrations due to inhibition of CYP2C9. However, no clinically relevant effect on sertraline exposure is expected.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. 5-fluorouracil, the active compound of tegafur, may increase sildenafil plasma concentrations due to inhibition of CYP2C9. However, no clinically relevant effect on sildenafil exposure is expected.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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 also a substrate of BCRP and the active metabolite is a substrate of OATP1B1. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4, OATP1B1 or BCRP.

Description:

See Summary

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4 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

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic or elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this unspecified metabolic pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

St John's Wort

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. St John’s wort is a P-gp and CYP3A4 inducer. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are not substrates of P-gp or CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

Sulfadiazine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. In vitro studies suggest a role of CYP2C9 in sulfadiazine metabolism. 5-fluorouracil, the active compound of tegafur, may increase sulfadiazine plasma concentrations due to inhibition of CYP2C9. No formal interaction studies have been conducted. The clinical relevance of this interaction is unknown and care should be taken if coadministered. No a priori dose adjustment is needed. However, monitoring for sulfadiazine toxicity should be considered.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

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. 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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway. However, due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4 or CYP2D6.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Telithromycin is also an inhibitor of CYP3A4 (strong) and P-gp, but the clinical relevance of P-gp inhibition is unknown. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce UGTs.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce UGTs.

Description:

See Summary

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

Terbinafine

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Terbinafine is metabolised by CYPs 1A2, 2C9, 3A4 and to a lesser extent by CYP2C8 and CYP2C19. 5-fluorouracil, the active compound of tegafur, may increase terbinafine plasma concentrations due to inhibition of CYP2C9. No formal interaction studies have been conducted. The clinical relevance of this interaction is unknown and care should be taken if coadministered. No a priori dose adjustment is needed. However, monitoring for terbinafine toxicity should be considered. Terbinafine is also a moderate-strong inhibitor of CYP2D6. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are not substrates of CYP2D6.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP1A2.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP2D6 or CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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 and mild inhibitor of CYP3A4. Ticagrelor is also a substrate of P-gp. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP2D6.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

Tolbutamide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Tolbutamide is mainly metabolised by CYP2C9 and to a lesser extent by CYP2C8 and CYP2C19. 5-fluorouracil, the active compound of tegafur, may increase tolbutamide plasma concentrations due to inhibition of CYP2C9. No formal interaction studies have been conducted. The clinical relevance of this interaction is unknown and care should be taken if coadministered. No a priori dose adjustment is needed. However, monitoring for tolbutamide toxicity should be considered.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP2D6 or CYP3A4.

Description:

See Summary

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

Torasemide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. Torasemide is metabolised mainly by CYP2C9. 5-fluorouracil, the active compound of tegafur, may increase torasemide plasma concentrations due to inhibition of CYP2C9. No formal interaction studies have been conducted. The clinical relevance of this interaction is unknown and care should be taken if coadministered. No a priori dose adjustment is needed. However, monitoring for torasemide toxicity should be considered. Furthermore, OAT1/3 are the major transporters of loop and thiazide diuretics. Secretion of these diuretics into the urinary tract by transporters in the proximal tubular cells is necessary for the diuretic effect in later tubule segments. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce OATs.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce these CYPs.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4.

Description:

See Summary

Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

Trimethoprim/Sulfamethoxazole

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but care should be taken. 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. 5-fluorouracil, the active compound of tegafur, may increase trimethoprim and sulfamethoxazole plasma concentrations due to inhibition of CYP2C9. No formal interaction studies have been conducted. The clinical relevance of this interaction is unknown and care should be taken if coadministered. No a priori dose adjustment is needed. However, monitoring for trimethoprim and sulfamethoxazole toxicity should be considered. 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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are not substrates of these enzymes or transporters.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP2D6.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP2D6 or P-gp.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce these CYPs.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

Valproic acid (Valproate)

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Valproic acid is primarily metabolized by glucuronidation (50%) and mitochondrial beta-oxidation (30-40%). To a lesser extent (10%) valproic acid is metabolized by CYP2C9 and CYP2C19. Valproic acid is also an inhibitor of CYP2C9. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. 5-fluoruouracil, the active compound of tegafur, may increase venlafaxine concentrations due to CYP2C9 inhibition. However, no clinically relevant effect on venlafaxine exposure is expected.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. 5-fluorouracil, the active compound of tegafur, may increase verapamil plasma concentrations due to inhibition of CYP2C9. However, no clinically relevant effect on verapamil exposure is expected. Verapamil is also an inhibitor of CYP3A4 (moderate) and P-gp (strong). Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this pathway.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. 5-fluorouracil, the active compound of tegafur, may increase voriconazole plasma concentrations due to inhibition of CYP2C9. However, no clinically relevant effect on voriconazole exposure is expected. Voriconazole is also a strong inhibitor of CYP3A4 and a weak inhibitor of CYPs 2C9, 2C19 and 2B6. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are not substrates of these CYPs.

Description:

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Potential Interaction

Tegafur/Gimeracil/Oteracil

Warfarin

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but should be approached with caution. Warfarin is a mixture of enantiomers which are metabolised by different cytochromes. R-warfarin is primarily metabolised by CYP1A2 and CYP3A4. S-warfarin (more potent) is metabolised by CYP2C9. 5-fluorouracil, the active compound of tegafur, may increase warfarin plasma concentrations due to inhibition of CYP2C9. No formal interaction studies have been conducted. Increased prothrombin time (PT) and internationalised normal ratio (INR) values have been reported in patients treated with warfarin in combination with tegafur, oteracil and gimeracil. The clinical relevance of these interactions is unknown. Coadministration should be approached with caution. Monitoring for warfarin toxicity and INR/PT is recommended.

Description:

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Potential Weak Interaction

Tegafur/Gimeracil/Oteracil

Xipamide

Quality of Evidence: Very Low

Summary:

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic 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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway. However, in patients receiving cyclophosphamide, methotrexate and 5-fluorouracil (the active compound of tegafur), addition of thiazide diuretics resulted in a more pronounced decrease in the number of granulocytes when compared to patients not receiving thiazides. Therefore, care should be taken and due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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). Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not interact with this metabolic pathway.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil are unlikely to interfere with this elimination pathway.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. 5-fluorouracil, the active compound of tegafur, may increase zolpidem concentrations due to CYP2C9 inhibition. However, no clinically relevant effect on zolpidem exposure is expected.

Description:

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No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP3A4 or CYP2C8.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce these CYPs.

Description:

See Summary

No Interaction Expected

Tegafur/Gimeracil/Oteracil

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. Tegafur, oteracil, gimeracil or the active compound 5-fluorouracil do not inhibit or induce CYP2D6, CYP3A4 or UGTs.

Description:

See Summary