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.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Acenocoumarol is mainly metabolised by CYP2C9 and to a lesser extent by CYP1A2 and CYP2C19. Abiraterone is an inhibitor of CYPs 1A2, 2C9 and 2C19 in vitro but the in vivo effects have yet to be determined. However, clinically significant interactions are unlikely.

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). Abiraterone does not inhibit or induce UGT1A6.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as agomelatine is metabolised predominantly via CYP1A2 (90%), with a small proportion metabolised by CYP2C9 and CYP2C19 (10%). Although abiraterone is an inhibitor of CYPs 1A2, 2C9 and 2C19 in vitro, a clinically relevant interaction is unlikely.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Alfentanil undergoes extensive CYP3A4 metabolism. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically relevant effect on alfentanil is expected.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Alfuzosin is metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected.

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 the faeces. P-gp is a major determinant of aliskiren bioavailability. Abiraterone does not inhibit or induce P-gp.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as allopurinol is converted to oxipurinol by xanthine oxidase and aldehyde oxidase. Abiraterone not interfere with this metabolic pathway. 

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. Although abiraterone is an inhibitor of CYPs 2C9, 3A4 and 1A2 in vitro, no clinically significant effect on alosetron is expected.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Alprazolam is mainly metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect on alprazolam is expected.

Coadministration has not been studied but care should be taken. Aluminium hydroxide is not metabolised by CYPs. Abiraterone is unlikely to interfere with this elimination pathway. However, the solubility of abiraterone is pH dependent and exposure may be altered by coadministration with acid-reducing agents. The clinical relevance of this interaction is unknown. If coadministration is clinically necessary, abiraterone should be administered at least 2 hours before or 4 hours after antacids.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ambrisentan is metabolised 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. Abiraterone is an inhibitor of CYP2C19 and CYP3A4 in vitro. Since CYP2C19 and CYP3A4 are only minor pathways, a clinically relevant interaction is unlikely.

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

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. Abiraterone is unlikely to interfere with this elimination pathway.

Coadministration has not been studied but is not recommended. Amiodarone is metabolised by CYP2C8 and CYP3A4. Abiraterone is a weak inhibitor of CYP2C8 and may increase concentrations of amiodarone. Therefore, coadministration is not recommended and selection of an alternate concomitant medicinal product, with no or minimal metabolism via CYP2C8 should be considered. Close monitoring for amiodarone toxicity is recommended. Furthermore, the major metabolite of amiodarone, desethylamiodarone, is an inhibitor of CYPs 3A4 (weak), 2C9 (moderate), 2D6 (moderate), 2C19 (weak), 1A1 (strong) and 2B6 (moderate) and P-gp (strong). Concentrations of abiraterone may increase due to inhibition of CYP3A4. When coadministered with the strong CYP3A4 inhibitor, ketoconazole, abiraterone AUC increased by 15%. Therefore, an interaction with CYP3A4 inhibitors is not likely to be clinically significant. Note: due to the long half-life of amiodarone, interactions can be observed for several months after discontinuation of amiodarone.

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). Abiraterone is unlikely to significantly affect amisulpride elimination. 

Coadministration has not been studied but should be approached with caution. Amitriptyline is metabolised predominantly by CYP2D6 and CYP2C19, with a small proportion metabolised by CYPs 3A4, 1A2 and 2C9. Abiraterone is an in vitro inhibitor of CYPs 1A2, 2C9, 2C19 and 3A4 but a clinically relevant effect due to the inhibition of these CYPs is unlikely. Abiraterone is also an inhibitor of CYP2D6 and may increase concentrations of amitriptyline. Coadministration should be approached with caution. If treatment with amitriptyline cannot be interrupted, the dose of amitriptyline should be reduced. Consider monitoring of amitriptyline and nortriptyline plasma concentrations, if available.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Amlodipine is metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as amoxicillin is mainly excreted in the urine by glomerular filtration and tubular secretion. In vitro data indicate that amoxicillin is a substrate of OAT3. Abiraterone is unlikely to interfere with amoxicillin renal elimination.

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. Abiraterone does 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.

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. Abiraterone is unlikely to significantly inhibit ampicillin renal elimination.

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. Abiraterone does not interfere with this metabolic pathway.

Coadministration has not been studied but care should be taken. Antacids are not metabolised by CYPs. Abiraterone is unlikely to interfere with this elimination pathway. However, the solubility of abiraterone is pH dependent and exposure may be altered by coadministration with acid-reducing agents. The clinical relevance of this interaction is unknown. If coadministration is clinically necessary, abiraterone should be administered at least 2 hours before or 4 hours after antacids.

Coadministration has not been studied. Apixaban is metabolised by CYP3A4 and to a lesser extent by CYPs 1A2, 2C8, 2C9 and 2C19. Apixaban is also a substrate of P-gp and BCRP. Abiraterone is a weak inhibitor of CYP2C8 and may increase apixaban concentrations. As the clinical relevance of this interaction is unknown, monitoring for apixaban toxicity may be required.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Aprepitant is mainly metabolised by CYP3A4 and to a lesser extent by CYP1A2 and CYP2C19. Although abiraterone is an in vitro inhibitor of CYP3A4 and CYP2C19, no clinically relevant effect on aprepitant exposure is expected. During treatment, aprepitant is a moderate inhibitor of CYP3A4 and may increase abiraterone concentrations during the three days of coadministration. Since CYP3A4 is a minor pathway, a clinically relevant effect due to CYP3A4 inhibition is not likely. Furthermore, after treatment aprepitant is a weak inducer of CYP3A4, CYP2C9 and UGT. Concentrations of abiraterone may decrease due to weak induction of CYP3A4, but this is not considered to be clinically significant.

Coadministration has not been studied but should be approached with caution. Aripiprazole is metabolised by CYP3A4 and CYP2D6. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of aripiprazole. Coadministration should be approached with caution. If treatment with aripiprazole cannot be interrupted, a dose reduction of aripiprazole should be considered.

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)). Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of asenapine. Since CYP2D6 is only a minor pathway, a clinically relevant interaction is unlikely.

Coadministration has not been studied. Astemizole is metabolised by CYPs 2D6, 2J2 and 3A4. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of astemizole. As the clinical relevance of this interaction is unknown, monitoring may be required.

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. Abiraterone does not interfere with this elimination pathway.

Coadministration has not been studied but care should be taken. Atorvastatin is metabolised by CYP3A4 and is a substrate of P-gp and OATP1B1. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically relevant effect due to CYP3A4 inhibition is expected. Abiraterone is also an inhibitor of OATP1B1 in vitro and may increase concentrations of atorvastatin. As the clinical relevance of this interaction is unknown, consider starting with the lowest dose of atorvastatin and titrate up to the desired clinical effect whilst monitoring for toxicity.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Azithromycin is mainly eliminated via biliary excretion with animal data suggesting this may occur via P-gp and MRP2. Azithromycin is also an inhibitor of P-gp. However, the clinical relevance of P-gp inhibition by azithromycin is unknown. Abiraterone does not interfere with this pathway and no effect on abiraterone concentrations is expected. 

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bedaquiline is metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected.

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. There is no evidence that bendroflumethiazide inhibits or induces CYP450 enzymes and therefore is unlikely to impact abiraterone. However, coadministration may increase risk of hypokalaemia and monitoring may be required.

Coadministration has not been studied but should be approached with caution. Bepridil is metabolised by CYP2D6 (major) and CYP3A4. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of bepridil. Coadministration should be approached with caution. If treatment with bepridil cannot be interrupted, the dose should be reduced by at least 50% as bepridil has a narrow therapeutic index.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Betamethasone is metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as half of bezafibrate dose is eliminated unchanged in the urine. 

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. 

Coadministration has not been studied but should be approached with caution. Bisoprolol is partly metabolised by CYP3A4 and CYP2D6, and partly eliminated unchanged in the urine. Abiraterone is an inhibitor of CYP2D6 (moderate) and CYP3A4 (in vitro), and may increase concentrations of bisoprolol. Coadministration should be approached with caution. Monitoring of blood pressure and heart rate is recommended.

Coadministration has not been studied but care should be taken. Bosentan is metabolised by CYP3A4 and CYP2C9. Although abiraterone is an in vitro inhibitor of CYP3A4 and CYP2C9, no clinically relevant effect due to inhibition of these CYPs is expected. Furthermore, bosentan is a weak inducer of CYP3A4 and CYP2C9. Concentrations of abiraterone may decrease due to induction of CYP3A4. This is unlikely to be clinically relevant, but monitoring of abiraterone efficacy may be required.

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 with CYP2D6 or CYP1A2 also potentially playing a role. Abiraterone is a moderate inhibitor of CYP2D6, but since this is a minor pathway, a clinically relevant interaction is unlikely.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Budesonide is metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected.

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). Abiraterone does not inhibit or induce UGTs. However, abiraterone is an inhibitor of CYP3A4 in vitro but no clinically significant effect is expected. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bupropion is primarily metabolised by CYP2B6. Abiraterone does not inhibit or induce CYP2B6.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Buspirone is metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected.

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. 

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. 

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. Abiraterone does not interfere with this elimination pathway. 

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. Abiraterone does not interfere with captopril elimination.

Coadministration has not been studied but is contraindicated. Carbamazepine is primarily metabolised by CYP3A4 and to a lesser extent by CYP2C8. Although abiraterone is an in vitro inhibitor of CYP3A4, no clinically relevant effect due to CYP3A4 inhibition is expected. Abiraterone is also a weak inhibitor of CYP2C8, but since CYP2C8 is a minor pathway, a clinically relevant effect due to CYP2C8 inhibition is unlikely. Carbamazepine is an inducer of CYPs 2C8 (strong), 2C9 (strong), 3A4 (strong), 1A2 (weak), 2B6 and UGT1A1. Carbamazepine may significantly decrease concentrations of abiraterone due to CYP3A4 induction. A decrease in exposure can lead to decreased efficacy. Coadministration of CYP3A4 inducers should be avoided, or selection of an alternate concomitant medicinal product, with no or minimal potential to induce CYP3A4 should be considered. If coadministration is unavoidable, a dose increase of abiraterone may be required. Closely monitor abiraterone efficacy. Consider monitoring of abiraterone plasma concentrations, if available.

Coadministration has not been studied but should be approached with caution. Carvedilol undergoes glucuronidation via UGTs 1A1, 2B4 and 2B7, and metabolism via CYP2D6 and to a lesser extent by CYPs 2C9 and 1A2. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of carvedilol. Coadministration should be approached with caution. Monitoring of blood pressure and heart rate is recommended.

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. Abiraterone does not interact with this metabolic pathway. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cefalexin is predominantly renally eliminated as unchanged drug by glomerular filtration and tubular secretion via OAT1 and MATE1. Abiraterone does not interfere with cefalexin renal elimination.

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. Abiraterone does not interfere with this elimination pathway.

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. Abiraterone does not interfere with this elimination pathway.

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. Abiraterone does not interfere with this elimination pathway.

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

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. Abiraterone does not interfere with this elimination pathway.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Celecoxib is primarily metabolised by CYP2C9. Abiraterone is an inhibitor of CYP2C9 in vitro but the in vivo effect has yet to be determined. However, a clinically relevant interaction is unlikely.

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 inhibits OCT2. Abiraterone is not transported by OCT2 and is unlikely to interfere with the elimination of cetirizine.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Chloramphenicol is predominately glucuronidated. Abiraterone does not interact with this pathway. In vitro studies have shown that chloramphenicol can inhibit metabolism mediated by CYPs 3A4 (strong), 2C19 (strong) and 2D6 (weak). Abiraterone concentrations may increase due to CYP3A4 inhibition. However, the clinical relevance of this interaction is unknown. Coadministration with ketoconazole, a strong CYP3A4 inhibitor, increased abiraterone exposure by 15%. Therefore, no clinically relevant effect is expected after coadministration with chloramphenicol. Ocular use: Although chloramphenicol is systemically absorbed when used topically in the eye, the absorbed concentrations are unlikely to cause a clinically relevant interaction.

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. Although abiraterone is an in vitro inhibitor of CYP3A4, no clinically relevant effect on chlordiazepoxide exposure is expected.

Coadministration has not been studied. Chlorphenamine is predominantly metabolised in the liver via CYP2D6. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of chlorphenamine. As the clinical relevance of this interaction is unknown, careful monitoring of side effects is advised. A dose reduction of chlorphenamine should also be considered.

Coadministration has not been studied but should be approached with caution. Chlorpromazine is metabolised mainly by CYP2D6, but also by CYP1A2. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of chlorpromazine. Coadministration should be approached with caution. If treatment with chlorpromazine cannot be interrupted, the dose of chlorpromazine should be reduced by at least 50% as chlorpromazine has a narrow therapeutic index. Monitor closely for chlorpromazine toxicity.

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. Abiraterone is unlikely to interfere with this elimination pathway. 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. Abiraterone does not inhibit or induce OATs. However, coadministration may increase the risk of hypokalaemia and monitoring may be required.

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. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically relevant effect on ciclosporin exposure is expected. Ciclosporin is also an inhibitor of CYP3A4 and may increase concentrations of abiraterone. When coadministered with the strong CYP3A4 inhibitor, ketoconazole, abiraterone AUC increased by 15%. Therefore, an interaction with CYP3A4 inhibitors is not likely to be clinically significant.

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. 

Coadministration has not been studied but care should be taken. Cimetidine is metabolised by CYP450 enzymes. Abiraterone is an inhibitor of CYP2D6 (moderate) and CYP2C8 (weak) and may increase concentrations of cimetidine. Monitoring for cimetidine toxicity may be required. Cimetidine is also a weak inhibitor of CYPs 3A4, 1A2, 2D6 and 2C19. Abiraterone concentrations may increase due to CYP3A4 inhibition, but since CYP3A4 is a minor pathway, a clinical relevant effect is unlikely. Furthermore, in vitro data indicate that cimetidine inhibits OAT1 and OCT2 but at concentrations much higher than the observed clinical concentrations. Abiraterone does not interact with this pathway. However, the solubility of abiraterone is pH dependent and exposure may be altered by coadministration with acid-reducing agents. The clinical relevance of this interaction is unknown. If coadministration is clinically necessary, abiraterone should be administered at the moment at which acid secretion is less inhibited, which is just before a new dose of cimetidine. Even with optimal timing of abiraterone intake, monitoring of abiraterone plasma concentrations should be considered, if available.

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 also metabolised and partially cleared through the bile and intestine. Abiraterone does not interfere with the elimination of ciprofloxacin. Ciprofloxacin is a weak to moderate inhibitor of CYP3A4 and a strong inhibitor of CYP1A2. No clinically relevant effect on abiraterone is expected due to CYP1A2 inhibition but concentrations of abiraterone may increase due to inhibition of CYP3A4. However, when coadministered with the strong CYP3A4 inhibitor, ketoconazole, abiraterone AUC increased by 15%. An interaction with CYP3A4 inhibitors is not likely to be clinically significant.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cisapride is metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected. 

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%). Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of citalopram. However, since CYP2D6 mediated metabolism is only a minor pathway, a clinically relevant interaction is unlikely.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Clarithromycin is metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, a clinically relevant effect is not expected. Clarithromycin is also an inhibitor of CYP3A4 (strong) and P-gp. Abiraterone concentrations may increase due to CYP3A4 inhibition. However, when coadministered with the strong CYP3A4 inhibitor, ketoconazole, abiraterone AUC increased by 15%. A similar effect may occur with clarithromycin. No clinically relevant effect on abiraterone exposure is expected.

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. Abiraterone does not interact with this pathway. 

Coadministration has not been studied. Clemastine is predominantly metabolised in the liver via CYP2D6. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of clemastine. As the clinical relevance of this interaction is unknown, careful monitoring of side effects is advised. A dose reduction of clemastine should also be considered.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Clindamycin is metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically relevant effect is expected.

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

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. Abiraterone does not interfere with this elimination pathway. In vitro data suggest that clofazimine is a CYP3A4 inhibitor and may increase abiraterone concentrations. However, when coadministered with the strong CYP3A4 inhibitor, ketoconazole, abiraterone AUC increased by 15%. An interaction with CYP3A4 inhibitors is not likely to be clinically relevant.

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. Abiraterone does not interfere with clofibrate elimination.

Coadministration has not been studied but should be approached with caution. 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. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of clomipramine and desmethylclomipramine. Coadministration should be approached with caution. Careful monitoring of side effects is advised and a dose reduction of clomipramine should be considered.

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 a weak inhibitor of OCT2 and is unlikely to interact with abiraterone elimination. In addition, abiraterone does not interfere with clonidine elimination.

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. Abiraterone is an in vitro inhibitor of CYP3A4. Abiraterone is also an in vitro inhibitor of CYP1A2 and CYP2C19 but the in vivo effect has yet to be determined. However, a clinically relevant effect on clopidogrel exposure is not expected. 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. Abiraterone is not metabolised by these CYPs.

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. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically relevant effect on clorazepate exposure is expected.

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. Abiraterone does not interact with this elimination pathway.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Clozapine is metabolised mainly by CYP1A2 and CYP3A4, and to a lesser extent by CYP2C19 and CYP2D6. Abiraterone is an in vitro inhibitor of CYP3A4 and CYP2C19, but a clinically relevant effect due to inhibition of these CYPs is not expected. Abiraterone is also a moderate inhibitor of CYP2D6 and may increase concentrations of clozapine. Since CYP2D6 is only a minor pathway, a clinically relevant interaction is unlikely.

Coadministration has not been studied. Codeine is converted via CYP2D6 to morphine, an active metabolite with analgesic and opioid properties. Morphine is further metabolised by conjugation with glucuronic acid to morphine-3-glucuronide (inactive) and morphine-6-glucuronide (active). Morphine is also a substrate of P-gp. Furthermore, codeine is converted via CYP3A4 to norcodeine, an inactive metabolite. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically relevant effect is expected through this pathway. However, abiraterone is a moderate inhibitor of CYP2D6. Concentrations of codeine may increase and thus concentrations of the active metabolite, morphine, may decrease due to inhibition of CYP2D6. Therefore, the analgesic effect of codeine may be reduced.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Colchicine is metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected.

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. Abiraterone does not interact with this elimination pathway.

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. Abiraterone does not inhibit or induce P-gp.

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. Abiraterone does not interfere with this elimination pathway.

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. Abiraterone is a moderate inhibitor of CYP2D6 and a weak inhibitor of CYP2C8. Concentrations of dapsone may increase due to inhibition of CYP2D6 and CYP2C8. As the clinical relevance of this interaction is unknown, monitoring for dapsone toxicity may be required.

Coadministration has not been studied but should be approached with caution. Desipramine is metabolised by CYP2D6. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of desipramine. Coadministration should be approached with caution. If treatment with desipramine cannot be interrupted, the dose of desipramine should be reduced by at least 50% as desipramine has a narrow therapeutic index.

Coadministration is contraindicated if abiraterone is used for treatment of hormone-sensitive cancer. If used for hormone insensitive tumours the following information is applicable. Coadministration has not been studied and is unlikely due to the differing target populations. Based on metabolism and clearance a clinically significant interaction is unlikely. Desogestrel is a prodrug which is activated to etonogestrel by CYP2C9 (and possibly CYP2C19); the metabolism of etonogestrel is mediated by CYP3A4. Abiraterone is an in vitro inhibitor of CYPs 2C9, 2C19 and 3A4, but no clinically relevant effect on desogestrel exposure is expected.

Coadministration has not been studied but care should be taken. Dexamethasone is a substrate of CYP3A4. Although abiraterone is an in vitro inhibitor of CYP3A4, no clinically relevant effect on dexamethasone exposure is expected. Furthermore, dexamethasone has been described as an inducer of CYP3A4 and may possibly decrease abiraterone concentrations. The clinical relevance of CYP3A4 induction by dexamethasone has not yet been established. Monitoring of abiraterone efficacy may be required. Monitoring of abiraterone plasma concentrations should be considered, if available.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dextropropoxyphene is mainly metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically relevant effect is expected.  

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 also a substrate of P-gp. Abiraterone does not interact with this pathway.

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 CYPC19) and to temazepam (mainly by CYP3A4). Temazepam is mainly glucuronidated. Although abiraterone is an in vitro inhibitor of CYP3A4 and CYP2C19, no clinically relevant effect on diazepam exposure is expected.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Diclofenac is partly glucuronidated by UGT2B7 and partly oxidised by CYP2C9. Abiraterone is an inhibitor of CYP2C9 in vitro but the in vivo effect has yet to be determined. However, a clinically relevant interaction is unlikely.

Coadministration has not been studied. Digoxin is renally eliminated via the renal transporters OATP4C1 and P-gp. Abiraterone does not interfere with digoxin elimination. However, coadministration with abiraterone can lead to hypokalaemia, which may increase the risk of digoxin toxicity. Close monitoring of serum potassium is recommended.

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. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically relevant effect is expected.

Coadministration has not been studied but care should be taken. Diltiazem is metabolised by CYP3A4 and CYP2D6. Abiraterone is an inhibitor of CYP2D6 (moderate) and CYP3A4 (in vitro), and may increase concentrations of diltiazem. Coadministration should be approached with caution. If treatment with diltiazem cannot be interrupted, the dose of diltiazem should be reduced. Monitor for diltiazem toxicity. Diltiazem is also a moderate inhibitor of CYP3A4 and may increase concentrations of abiraterone. When coadministered with the strong CYP3A4 inhibitor, ketoconazole, abiraterone AUC increased by 15%. Therefore, an interaction with CYP3A4 inhibitors is not likely to be clinically relevant.

Coadministration has not been studied. Diphenhydramine is mainly metabolised by CYP2D6 and to a lesser extent by CYPs 1A2, 2C9 and 2C19. Abiraterone is an in vitro inhibitor of CYPs 1A2, 2C9 and 2C19 but a clinically relevant effect on diphenhydramine exposure due to inhibition of these CYPs is unlikely. Abiraterone is also a moderate inhibitor of CYP2D6 and may increase concentrations of diphenhydramine. As the clinical relevance of this interaction is unknown, careful monitoring of side effects is advised. A dose reduction of diphenhydramine should also be considered. Diphenhydramine is a weak inhibitor of CYP2D6, but abiraterone is not metabolised by CYP2D6.

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. Abiraterone does not inhibit or induce UGT1A.

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. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically relevant effect is expected.

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%). Abiraterone is a moderate inhibitor of CYP2D6. Since CYP2D6 mediated metabolism is only a minor pathway, a clinically relevant interaction is unlikely. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Domperidone is mainly metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected. 

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 abiraterone, or to be affected if co-administered with abiraterone.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Doxazosin is metabolised mainly by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect on doxazosin is expected.

Coadministration has not been studied but should be approached with caution. 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. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of doxepin and nordoxepin. Coadministration should be approached with caution. If treatment with doxepin cannot be interrupted, the dose of doxepin should be reduced by at least 50% as doxepin has a narrow therapeutic index.

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. Abiraterone does not interact with this pathway. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dronabinol is mainly metabolised by CYP2C9 and to a lesser extent by CYP3A4. Although abiraterone is an inhibitor of CYP2C9 and CYP3A4 in vitro, no clinically significant effect is expected.

Coadministration is contraindicated if abiraterone is used for treatment of hormone-sensitive cancer. If used for hormone insensitive tumours the following information is applicable. Coadministration has not been studied and is unlikely due to the differing target populations. Based on metabolism and clearance a clinically significant interaction is unlikely. Drospirenone is metabolised to a minor extent via CYP3A4. Although abiraterone is an in vitro inhibitor of CYP3A4, no clinically relevant effect on drospirenone exposure is expected.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dulaglutide is degraded by endogenous endopeptidases. Dulaglutide delays gastric emptying and could possibly decrease the absorption rate of concomitantly administered oral drugs. Since the efficacy of abiraterone is more likely to be correlated to trough plasma concentrations instead of maximum plasma concentrations, the clinical relevance of delayed absorption is considered to be limited.

Coadministration has not been studied but should be approached with caution. Duloxetine is metabolised by CYP2D6 and CYP1A2. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of duloxetine. Coadministration should be approached with caution. If treatment with duloxetine cannot be interrupted, the dose of duloxetine should be reduced by at least 50% as duloxetine has a narrow therapeutic index.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dutasteride is mainly metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected.

Coadministration is contraindicated if abiraterone is used for treatment of hormone-sensitive cancer. If used for hormone insensitive tumours the following information is applicable. Coadministration has not been studied and is unlikely due to the differing target populations. Based on metabolism and clearance a clinically significant interaction is unlikely. Dydrogesterone is metabolised to dihydrodydrogesterone (possibly via CYP3A4). Although abiraterone is an in vitro inhibitor of CYP3A4, no clinically relevant effect on dydrogesterone exposure is expected.

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 by P-gp. Although abiraterone is an inhibitor of CYP3A4 in vitro, a clinically relevant interaction is unlikely.

Coadministration has not been studied. Eltrombopag is metabolised by cleavage conjugation (via UGT1A1 and UGT1A3) and oxidation (via CYP1A2 and CYP2C8). Abiraterone is a weak inhibitor of CYP2C8 and may increase concentrations of eltrombopag. As the clinical relevance of this interaction is unknown, monitoring may be required.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Enalapril is hydrolysed to enalaprilat which is eliminated renally (possibly via OATs). Abiraterone is an inhibitor of OATP1B1 in vitro.  However, since different OATs appear to be involved in enalapril elimination, a clinically relevant interaction is unlikely. 

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. Abiraterone does not interact with this metabolic pathway.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as eprosartan is largely excreted in bile and urine as unchanged drug. 

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. Abiraterone does not interact with this elimination pathway.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Erythromycin is metabolised by CYP3A4 and is a substrate of P-gp. Abiraterone is an inhibitor of CYP3A4 in vitro but a clinically relevant effect on erythromycin exposure is unlikely. Erythromycin is also an inhibitor of CYP3A4 (moderate) and P-gp. Concentrations of abiraterone may increase due to CYP3A4 inhibition. However, when coadministered with the strong CYP3A4 inhibitor, ketoconazole, abiraterone AUC increased by 15%. An interaction with CYP3A4 inhibitors is not likely to be clinically relevant.

Coadministration has not been studied. Escitalopram is metabolised by CYPs 2C19 (37%), 2D6 (28%) and 3A4 (35%) to form N-desmethylescitalopram. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of escitalopram. As the clinical relevance of this is interaction is unknown, monitoring of side effects is recommended.

Coadministration has not been studied but care should be taken. Esomeprazole is metabolised by CYP2C19 and CYP3A4. Although abiraterone is an in vitro inhibitor of CYP3A4 and CYP2C19, a clinically relevant effect on esomeprazole exposure is unlikely. However, the solubility of abiraterone is pH dependent and exposure may be altered by coadministration with acid-reducing agents. The clinical relevance of this interaction is unknown. If coadministration is clinically necessary, abiraterone should be administered at the moment at which acid secretion is less inhibited, which is just before a new dose of esomeprazole. Even with optimal timing of abiraterone intake, monitoring of abiraterone plasma concentrations should be considered, if available. 

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. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected.

Coadministration is contraindicated if abiraterone is used for treatment of hormone-sensitive cancer. If used for hormone insensitive tumours the following information is applicable. Coadministration has not been studied and is unlikely due to the differing target populations. Based on metabolism and clearance a clinically significant interaction is unlikely. Estradiol is metabolised by CYP3A4, CYP1A2 and is glucuronidated. Although abiraterone is an in vitro inhibitor of CYP3A4 and CYP1A2, no clinically relevant effect on estradiol exposure is expected.

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

Coadministration is contraindicated if abiraterone is used for treatment of hormone-sensitive cancer. If used for hormone insensitive tumours the following information is applicable. Coadministration has not been studied and is unlikely due to the differing target populations. Based on metabolism and clearance a clinically significant interaction is unlikely. Ethinylestradiol undergoes oxidation (CYP3A4>CYP2C9), sulfation and glucuronidation (UGT1A1). Although abiraterone is an in vitro inhibitor of CYP3A4, no clinically relevant effect on ethinylestradiol exposure is expected.

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

Coadministration is contraindicated if abiraterone is used for treatment of hormone-sensitive cancer. If used for hormone insensitive tumours the following information is applicable. Coadministration has not been studied and is unlikely due to the differing target populations. Based on metabolism and clearance a clinically significant interaction is unlikely. Etonogestrel is metabolised by CYP3A4. Although abiraterone is an in vitro inhibitor of CYP3A4, no clinically relevant effect on etonogestrel exposure is expected.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Everolimus is metabolised via CYP3A4 and is a substrate of P-gp. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically relevant effect on everolimus exposure is expected.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Exenatide is cleared mainly by glomerular filtration. Exenatide delays gastric emptying and could possibly decrease the absorption rate of concomitantly administered oral drugs. Since the efficacy of abiraterone is more likely to be correlated to trough plasma concentrations instead of maximum plasma concentrations, the clinical relevance of delayed absorption is considered to be limited.

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. Abiraterone does not interact with these pathways

Coadministration has not been studied but care should be taken. Famotidine is excreted via OAT1/OAT3. Abiraterone is unlikely to interact with this elimination pathway. However, the solubility of abiraterone is pH dependent and exposure may be altered by coadministration with acid-reducing agents. The clinical relevance of this interaction is unknown. If coadministration is clinically necessary, abiraterone should be administered at the moment at which acid secretion is less inhibited, which is just before a new dose of famotidine. Even with optimal timing of abiraterone intake, monitoring of abiraterone plasma concentrations should be considered, if available.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Felodipine is metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected. 

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. Abiraterone does not interact with this pathway.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fentanyl undergoes extensive CYP3A4 metabolism. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically relevant effect is expected. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fexofenadine undergoes negligible metabolism and is mainly eliminated unchanged in the faeces. Abiraterone does not interfere with this elimination pathway.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Finasteride is metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected.

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

Coadministration has not been studied but should be approached with caution. Flecainide is metabolised mainly via CYP2D6, with a proportion (approximately 30%) of the parent drug also renally eliminated unchanged. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of flecainide. Coadministration should be approached with caution. If treatment with flecainide cannot be interrupted, the dose should be reduced by at least 50% as flecainide has a narrow therapeutic index.

Coadministration has not been studied. Flucloxacillin is mainly renally eliminated partly by glomerular filtration and partly by active secretion via OAT1. Abiraterone does not interact with this metabolic pathway. However, flucloxacillin has been described as a CYP3A4 inducer and may decrease concentrations of abiraterone. As the clinical relevance of this interaction is unknown, monitoring of abiraterone efficacy may be required.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fluconazole is renally excreted. Abiraterone does not interact with this elimination pathway. However, fluconazole is an inhibitor of CYPs 3A4 (moderate), 2C9 (moderate) and 2C19 (strong). Concentrations of abiraterone may increase due to inhibition of CYP3A4. When coadministered with the strong CYP3A4 inhibitor, ketoconazole, abiraterone AUC increased by 15%. An interaction with CYP3A4 inhibitors is not likely to be clinically relevant.

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

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 CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected.

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. Although abiraterone is an inhibitor of CYP3A4 and CYP2C19 in vitro, no clinically significant effects are expected.

Coadministration has not been studied but should be approached with caution. Fluoxetine is metabolised by CYPs 2D6 and 2C9 and to a lesser extent by CYPs 2C19 and 3A4 to form norfluoxetine. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of fluoxetine. Coadministration should be approached with caution. If treatment with fluoxetine cannot be interrupted, the dose of fluoxetine should be reduced by at least 50% as fluoxetine has a narrow therapeutic index. Monitor closely for fluoxetine toxicity. Furthermore, fluoxetine is a strong inhibitor of CYP2D6 and CYP2C19. Abiraterone is not metabolised by these CYPs.

Coadministration has not been studied but should be approached with caution. Fluphenazine is metabolised by CYP2D6. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of fluphenazine. Coadministration should be approached with caution. If treatment with fluphenazine cannot be interrupted, the dose of fluphenazine should be reduced by at least 50% as fluphenazine has a narrow therapeutic index.

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. Abiraterone is a moderate inhibitor of CYP2D6 and weak inhibitor of CYP2C8. However, since flurazepam does not have a narrow therapeutic index, clinically relevant interactions are unlikely.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fluticasone is metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fluvastatin is mainly metabolised by CYP2C9 (75%) and to a lesser extent by CYP3A4 (20%) and CYP2C8 (5%). Although abiraterone is an in vitro inhibitor of CYP3A4 and CYP2C9, a clinically relevant effect on fluvastatin exposure is not expected. Abiraterone is also a weak inhibitor of CYP2C8, but since CYP2C8 is a minor pathway, no clinically significant interaction is expected. Furthermore, fluvastatin potentially inhibits CYP2C9. However, the clinical relevance of CYP2C9 inhibition is unknown. Abiraterone is not metabolised by CYP2C9.

Coadministration has not been studied but should be approached with caution. Fluvoxamine is metabolised mainly by CYP2D6 and to a lesser extent by CYP1A2. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of fluvoxamine. Coadministration should be approached with caution. If treatment with fluvoxamine cannot be interrupted, the dose of fluvoxamine should be reduced by at least 50% as fluvoxamine has a narrow therapeutic index. Monitor closely for fluvoxamine toxicity. Fluvoxamine is also an inhibitor of CYPs 1A2 (strong), 2C19 (strong), 3A4 (moderate), 2C9 (weak-moderate) and 2D6 (weak). Concentrations of abiraterone may increase due to inhibition of CYP3A4. When coadministered with the strong CYP3A4 inhibitor, ketoconazole, abiraterone AUC increased by 15%. Therefore, an interaction with CYP3A4 inhibitors is not likely to be clinically relevant.

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. Abiraterone does not interact with this elimination pathway.

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

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. Abiraterone does not interact with this metabolic pathway. Aprepitant is mainly metabolised by CYP3A4 and to a lesser extent by CYP1A2 and CYP2C19. Although abiraterone is an in vitro inhibitor of CYP3A4 and CYP2C19, no clinically relevant effect on aprepitant exposure is expected. During treatment, aprepitant is a moderate inhibitor of CYP3A4 and may increase abiraterone concentrations during the three days of coadministration. Since CYP3A4 is a minor pathway, a clinically relevant effect due to CYP3A4 inhibition is not likely. Furthermore, after treatment aprepitant is a weak inducer of CYP3A4, CYP2C9 and UGT. Concentrations of abiraterone may decrease due to weak induction of CYP3A4, but this is not considered to be clinically significant.

Coadministration has not been studied but should be avoided. Fosphenytoin is rapidly converted to the active metabolite phenytoin. Phenytoin is mainly metabolised by CYP2C9 and to a lesser extent by CYP2C19. Although abiraterone is an in vitro inhibitor of CYP2C9 and CYP2C19, a clinically relevant effect on fosphenytoin exposure is unlikely. Furthermore, phenytoin is a potent inducer of CYP3A4, UGT and P-gp. Concentrations of abiraterone may decrease due to induction of CYP3A4. A decrease in exposure can lead to decreased efficacy. Coadministration of CYP3A4 inducers should be avoided, or selection of an alternate concomitant medicinal product, with no or minimal potential to induce CYP3A4 should be considered. If coadministration is unavoidable, the dose of abiraterone may need to be increased. Closely monitor abiraterone efficacy. Consider monitoring of abiraterone plasma concentrations, if available.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic 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. Abiraterone does not interact with this elimination pathway. However, coadministration may increase the risk of hypokalaemia and monitoring may be required.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as gabapentin is eliminated mainly by glomerular filtration. Abiraterone does not interfere with this elimination pathway.

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

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. Abiraterone does not interact with this elimination pathway. 

Coadministration is contraindicated if abiraterone is used for treatment of hormone-sensitive cancer. If used for hormone insensitive tumours the following information is applicable. Coadministration has not been studied and is unlikely due to the differing target populations. 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. Although abiraterone is an in vitro inhibitor of CYPs 3A4, 2C9 and 2C19, no clinically relevant effect on gestodene exposure is expected.

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. Although abiraterone is an inhibitor of CYP3A4 and CYP2C9 in vitro, no clinically significant effect is expected.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Gliclazide is metabolised mainly by CYP2C9 and to a lesser extent by CYP2C19. Abiraterone is an inhibitor of CYP2C9 and CYP2C29 in vitro but the in vivo effect has yet to be determined. However, a clinically relevant interaction is unlikely.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Glimepiride is mainly metabolised by CYP2C9. Abiraterone is an inhibitor of CYP2C9 in vitro but the in vivo effect has yet to be determined. However, a clinically relevant interaction is unlikely.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Glipizide is mainly metabolised by CYP2C9. Abiraterone is an inhibitor of CYP2C9 in vitro but the in vivo effect has yet to be determined. However, a clinically relevant interaction is unlikely.

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. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Grapefruit juice is a known inhibitor of CYP3A4 and may increase concentrations of abiraterone. When coadministered with the strong CYP3A4 inhibitor, ketoconazole, abiraterone AUC increased by 15%. Therefore, an interaction with CYP3A4 inhibitors is not likely to be clinically significant.

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

Coadministration has not been studied and is contraindicated. Less than 1% of a griseofulvin dose is excreted unchanged via the kidneys. Abiraterone does not interfere with griseofulvin elimination pathway. However, griseofulvin is a liver microsomal enzyme inducer and may lower plasma levels, and therefore reduce the efficacy, of concomitantly administered medicinal products metabolised by CYP3A4. Concentrations of abiraterone may decrease due to induction of CYP3A4. A decrease in exposure can lead to decreased efficacy. Coadministration should be avoided, or selection of an alternate concomitant medicinal product, with no or minimal potential to induce CYP3A4 should be considered. If coadministration is unavoidable, a dose increase of abiraterone may be required. Consider monitoring of abiraterone plasma concentrations, if available.

Coadministration has not been studied. Haloperidol has a complex metabolism as it undergoes glucuronidation (UGTs 2B7>1A4 and 1A9), carbonyl reduction as well as oxidative metabolism (CYP3A4 and CYP2D6). Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of haloperidol. As the clinical relevance of this interaction is unknown, careful monitoring of side effects is advised. A dose reduction of haloperidol should also be considered.

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. Abiraterone does not interact with this metabolic pathway.

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. Although in vitro studies have suggested that hydralazine is a mixed enzyme inhibitor, which may weakly inhibit CYP3A4 and CYP2D6, it is not expected that this will lead to a clinical relevant interaction with abiraterone. 

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Hydrochlorothiazide is not metabolised but is cleared by the kidneys via OAT1. OAT1/3 are the major transporters of loop and thiazide diuretics. Secretion of these diuretics into the urinary tract by transporters in the proximal tubular cells is necessary for the diuretic effect in later tubule segments. Significant interactions are not expected with abiraterone. However, coadministration may increase the risk of hypokalaemia and monitoring may be required.

Coadministration has not been studied but should be approached with caution. Hydrocodone is metabolised by CYP2D6 to hydromorphone and by CYP3A4 to norhydrocodone, both of which have analgesic effects. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of hydrocodone. Coadministration should be approached with caution. If treatment with hydrocodone cannot be interrupted, the dose should be reduced by at least 50% as hydrocodone has a narrow therapeutic index. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Hydrocortisone is metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected.

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

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. Abiraterone does not inhibit or induce UGT2B7. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Hydroxyurea is not a substrate of CYP enzymes or P-gp. 

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. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ibuprofen is metabolised mainly by CYP2C9 and to a lesser extent by CYP2C8 and direct glucuronidation. Abiraterone is a weak inhibitor of CYP2C8, but since ibuprofen does not have a narrow therapeutic index, a clinically relevant interaction is unlikely.

Coadministration has not been studied but should be approached with caution. Iloperidone is metabolised by CYP3A4 and CYP2D6. Abiraterone is an inhibitor of CYP2D6 (moderate) and CYP3A4 (in vitro) and may increase concentrations of iloperidone. Coadministration should be approached with caution. If treatment with iloperidone cannot be interrupted, the dose of iloperidone should be reduced by at least 50% as iloperidone has a narrow therapeutic index.

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

Coadministration has not been studied. Imipramine is metabolised by CYPs 3A4, 2C19 and 1A2 to desipramine. Imipramine and desipramine are both metabolised by CYP2D6. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of imipramine and desipramine. Coadministration should be approached with caution. If treatment with imipramine cannot be interrupted, the dose should be reduced by at least 50% as imipramine has a narrow therapeutic index.

Coadministration has not been studied but care should be taken. Indapamide is extensively metabolised by CYP450. Abiraterone is a moderate inhibitor of CYP2D6 and a weak inhibitor of CYP2C8. As the clinical relevance of this interaction is unknown, monitoring for indapamide toxicity may be required. 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. Abiraterone does not inhibit or induce OATs. However, coadministration may increase the risk of hypokalaemia and monitoring may be required.

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

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Interleukin-2 is mainly eliminated by glomerular filtration. 

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. Abiraterone does not interact with this metabolic pathway.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Irbesartan is metabolised by glucuronidation and oxidation (mainly CYP2C9). Abiraterone is an inhibitor of CYP2C9 in vitro, but the in vivo effect has yet to be determined. However, a clinically relevant interaction is unlikely.

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

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. Abiraterone does not interact with this metabolic pathway. 

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. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Itraconazole is metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4, no clinically relevant effect on itraconazole exposure is expected. Furthermore, itraconazole is an inhibitor of CYP3A4 (strong), CYP2C9 (weak), P-gp and BCRP. Concentrations of abiraterone may increase due to inhibition of CYP3A4, but this is unlikely to be clinically significant. When coadministered with the strong CYP3A4 inhibitor, ketoconazole, abiraterone AUC increased by 15%. An interaction with CYP3A4 inhibitors is not likely to be clinically relevant.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ivabradine is metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected. 

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. Abiraterone does not interfere with this elimination pathway.

Ketoconazole is a substrate of CYP3A4. Although abiraterone is an in vitro inhibitor of CYP3A4, no clinically relevant effect on ketoconazole exposure is expected. Ketoconazole is an inhibitor of CYP3A4 (strong) and P-gp. Abiraterone concentrations may increase due to CYP3A4 inhibition. However, when coadministered with ketoconazole, abiraterone AUC increased by 15%. An interaction with CYP3A4 inhibitors is not likely to be clinically relevant.

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). Abiraterone does not inhibit or induce UGT1A1 or UGT2B7

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Lacidipine is metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect on lacidipine is expected.

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. 

Coadministration has not been studied but care should be taken. Lansoprazole is mainly metabolised by CYP2C19 and to lesser extent by CYP3A4. Although abiraterone is an in vitro inhibitor of CYP3A4 and CYP2C19, a clinically relevant effect on lansoprazole exposure is unlikely. However, the solubility of abiraterone is pH dependent and exposure may be altered by coadministration with acid-reducing agents. The clinical relevance of this interaction is unknown. If coadministration is clinically necessary, abiraterone should be administered at the moment at which acid secretion is less inhibited, which is just before a new dose of lansoprazole. Even with optimal timing of abiraterone intake, monitoring of abiraterone plasma concentrations should be considered, if available.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Lercanidipine is mainly metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as 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. Abiraterone does not interfere with this elimination pathway.

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). Abiraterone does not interact with this elimination pathway. 

Coadministration has not been studied but should be approached with caution. Levomepromazine is metabolised by CYP2D6. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of levomepromazine. Coadministration should be approached with caution. If treatment with levomepromazine cannot be interrupted, the dose of levomepromazine should be reduced by at least 50% as levomepromazine has a narrow therapeutic index.

Coadministration is contraindicated if abiraterone is used for treatment of hormone-sensitive cancer. If used for hormone insensitive tumours the following information is applicable. Coadministration has not been studied and is unlikely due to the differing target populations. Based on metabolism and clearance a clinically significant interaction is unlikely. Levonorgestrel is metabolised by CYP3A4 and is glucuronidated to a minor extent. Although abiraterone is an in vitro inhibitor of CYP3A4, no clinically relevant effect on levonorgestrel exposure is expected.

Coadministration is contraindicated if abiraterone is used for treatment of hormone-sensitive cancer. However, the use of levonorgestrel as emergency contraception is a relative contraindication due to the risk of a pregnancy while having a hormone-sensitive tumour. Therefore, the following information is applicable: Coadministration has not been studied and is unlikely due to the differing target populations. Based on metabolism and clearance a clinically significant interaction is unlikely. Levonorgestrel is metabolised by CYP3A4 and is glucuronidated to a minor extent. Although abiraterone is an in vitro inhibitor of CYP3A4, no clinically relevant effect on levonorgestrel exposure is expected.

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. Abiraterone does not interfere with levothyroxine metabolism. 

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. Although abiraterone is an inhibitor of CYP1A2 and CYP3A4 in vitro, no clinically significant effect is expected.

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. Although abiraterone is an in vitro inhibitor of CYP3A4, a clinically relevant interaction is unlikely. Furthermore, linagliptin is a weak inhibitor of CYP3A4 and may increase concentrations of abiraterone. When coadministered with the strong CYP3A4 inhibitor, ketoconazole, abiraterone AUC increased by 15%. Therefore, an interaction with CYP3A4 inhibitors is not likely to be clinically relevant.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as liraglutide is degraded by endogenous endopeptidases. Abiraterone does not interfere with this elimination pathway.

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

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. In patients receiving abiraterone, the use of live vaccines for immunisation is not contraindicated.

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. Abiraterone is a weak inhibitor CYP2C8. However, due to the wide therapeutic index of loperamide, this interaction is unlikely to be clinically relevant.

Coadministration has not been studied. Loratadine is metabolised mainly by CYP3A4 and to a lesser extent by CYP2D6. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of loratadine. As the clinical relevance of this interaction is unknown, careful monitoring of side effects is advised. A dose reduction of loratadine should also be considered.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Lorazepam is eliminated by non-CYP mediated pathways and no effect on plasma concentrations is expected when coadministered with abiraterone. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Lormetazepam is mainly glucuronidated. Abiraterone does not interact with this metabolic pathway.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Losartan is converted to its active metabolite mainly by CYP2C9 in the range of clinical concentrations. Although abiraterone is an inhibitor of CYP2C9 in vitro, a clinically relevant interaction is unlikely.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Lovastatin is metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected. 

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. Although abiraterone is a weak inhibitor of CYP2C8, no clinically significant effect is expected as multiple pathways are involved.

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. Abiraterone does not interfere with this elimination pathway.

Coadministration has not been studied but should be approached with caution. Maprotiline is mainly metabolised by CYP2D6. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of maprotiline. Coadministration should be approached with caution. If treatment with maprotiline cannot be interrupted, the dose of maprotiline should be reduced by at least 50% as maprotiline has a narrow therapeutic index.

Coadministration is contraindicated if abiraterone is used for treatment of hormone-sensitive cancer. If used for hormone insensitive tumours the following information is applicable. Coadministration has not been studied and is unlikely due to the differing target populations. Based on metabolism and clearance a clinically significant interaction is unlikely. Medroxyprogesterone is metabolised by CYP3A4. Although abiraterone is an in vitro inhibitor of CYP3A4, no clinically relevant effect on medroxyprogesterone exposure is expected.

Coadministration is contraindicated if abiraterone is used for treatment of hormone-sensitive cancer. If used for hormone insensitive tumours the following information is applicable. Coadministration has not been studied and is unlikely due to the differing target populations. Based on metabolism and clearance a clinically significant interaction is unlikely. Medroxyprogesterone is metabolised by CYP3A4. Although abiraterone is an in vitro inhibitor of CYP3A4, no clinically relevant effect on medroxyprogesterone exposure is expected.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Mefenamic acid is metabolised by CYP2C9 and glucuronidated by UGT2B7 and UGT1A9. Abiraterone is an inhibitor of CYP2C9 in vitro but the in vivo effect has yet to be determined. However, a clinically relevant interaction is unlikely.

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. 

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. Abiraterone does not interfere with this elimination pathway. 

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. Abiraterone does not interfere with this pathway. 

Coadministration has not been studied but should be avoided. 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%). Abiraterone does not interact with this metabolic pathway. However, metamizole is an inducer of CYP3A4 and may decrease abiraterone concentrations. A decrease in exposure may lead to decreased efficacy. Coadministration of CYP3A4 inducers should be avoided, or selection of an alternate concomitant medicinal product, with no or minimal potential to induce CYP3A4 should be considered. If coadministration is unavoidable, a dose increase of abiraterone may be required. Consider close monitoring of abiraterone plasma concentrations, if available.

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. Abiraterone does not inhibit or induce these OCTs or MATEs.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Methadone is demethylated by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically relevant effect on methadone is expected.

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. It is unlikely to affect the disposition of abiraterone, or to be altered by coadministration with abiraterone.

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. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Methylprednisolone is metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected.

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). Abiraterone is a moderate inhibitor of CYP2D6. However, since CYP2D6 mediated metabolism is only a minor pathway, a clinically relevant interaction is unlikely.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic 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. Abiraterone does not inhibit or induce OATs. However, coadministration may increase the risk of hypokalaemia and monitoring may be required.

Coadministration has not been studied but should be approached with caution. Metoprolol is mainly metabolised by CYP2D6. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of metoprolol. Coadministration should be approached with caution. Monitoring of blood pressure and heart rate is recommended.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Metronidazole is eliminated via glomerular filtration. Abiraterone is unlikely to interfere with this elimination pathway. Elevated plasma concentrations have been reported for some CYP3A substrates (e.g. tacrolimus, cyclosporine) with metronidazole. However, metronidazole did not increase concentrations of several CYP3A probe drugs (e.g. midazolam, alprazolam). The mechanism of the interaction with CYP3A has not yet been identified. When coadministered with the strong CYP3A4 inhibitor, ketoconazole, abiraterone AUC increased by 15%. Therefore, an interaction with CYP3A4 inhibitors is not likely to be clinically relevant.

Coadministration has not been studied but should be approached with caution. Mexiletine is metabolised mainly by CYP2D6 and to a lesser extent by CYP1A2. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of mexiletine. Coadministration should be approached with caution. If treatment with mexiletine cannot be interrupted, the dose should be reduced by at least 50% as mexiletine has a narrow therapeutic index.

Coadministration has not been studied but should be approached with caution. Mianserin is metabolised by CYP2D6, CYP1A2, and to a lesser extent by CYP3A4. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of mianserin. Coadministration should be approached with caution. If treatment with mianserin cannot be interrupted, the dose of mianserin should be reduced by at least 50% as mianserin has a narrow therapeutic index.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Miconazole is extensively metabolised by the liver. Abiraterone is unlikely to interact with this unspecified metabolic pathway. Furthermore, miconazole is an inhibitor of CYP2C9 (moderate) and CYP3A4 (strong). Concentrations of abiraterone may increase due to inhibition of CYP3A4. However, when coadministered with the strong CYP3A4 inhibitor, ketoconazole, abiraterone AUC increased by 15%. An interaction with CYP3A4 inhibitors is not likely to be clinically relevant. Dermal application: No interaction is expected with abiraterone, since miconazole is used topically and systemic exposure is limited.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Midazolam is metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect on midazolam is expected.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Midazolam is metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect on midazolam is expected.

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%). Abiraterone is unlikely to interfere with this pathway.

Coadministration has not been studied. Mirtazapine is metabolised to 8-hydroxymirtazapine by CYP2D6 and CYP1A2, and to N-desmethylmirtazapine mainly by CYP3A4. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of mirtazapine. Coadministration should be approached with care. As the clinical relevance of this interaction is unknown, monitoring may be required.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Mometasone is metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected.

Coadministration has not been studied. Montelukast is mainly metabolised by CYP2C8 and to a lesser extent by CYPs 3A4 and 2C9. Abiraterone is a weak inhibitor of CYP2C8 and may increase concentrations of montelukast. However, due to the wide therapeutic index of montelukast, this interaction is unlikely to be clinically relevant, but monitoring may be required.

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. Abiraterone does not interact with this metabolic pathway.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Mycophenolate is mainly glucuronidated by UGT1A9 and UGT2B7. Abiraterone does not interact with this metabolic pathway. In addition, inhibition of OAT1/OAT3 renal transporters by mycophenolic acid (active metabolite) is unlikely to interfere with abiraterone elimination. 

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. Abiraterone does not interact with this elimination pathway.

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. Abiraterone does not interact with this pathway.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Naproxen is mainly glucuronidated by UGT2B7 (major) and demethylated to desmethylnaproxen by CYP2C9 (major) and CYP1A2. Abiraterone is an inhibitor of CYP2C9 in vitro but the in vivo effect has yet to be determined. However, a clinically relevant interaction is unlikely.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Nateglinide is mainly metabolised by CYP2C9 (70%) and to a lesser extent by CYP3A4 (30%). Although abiraterone is an inhibitor of CYP3A4 and CYP2C9 in vitro, no clinically significant effect is expected.

Coadministration has not been studied but should be approached with caution. Nebivolol metabolism involves CYP2D6. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of nebivolol. Coadministration should be approached with caution. Monitoring of blood pressure and heart rate is recommended.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Nefazodone is metabolised mainly by CYP3A4. Abiraterone is an in vitro inhibitor of CYP3A4, but a clinically relevant effect on nefazodone exposure is unlikely. Nefazodone is also a strong inhibitor of CYP3A4 and may increase concentrations of abiraterone. When coadministered with the strong CYP3A4 inhibitor, ketoconazole, abiraterone AUC increased by 15%. A similar effect may occur with nefazodone. Therefore, an interaction with CYP3A4 inhibitors is not likely to be clinically significant.

Coadministration has not been studied. Nicardipine is metabolised mainly by CYP3A4 and to a lesser extent by CYP2D6 and CYP2C8. Abiraterone is an inhibitor of CYPs 2D6 (moderate), 2C8 (weak) and 3A4 (in vitro), and may increase concentrations of nicardipine. As the clinical relevance of this interaction is unknown, monitoring of blood pressure may be required. Furthermore, nicardipine is a weak inhibitor of CYP3A4 and may increase concentrations of abiraterone. When coadministered with the strong CYP3A4 inhibitor, ketoconazole, abiraterone AUC increased by 15%. An interaction with CYP3A4 inhibitors is not likely to be clinically relevant.

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. Abiraterone does not interact with this metabolic pathway. In addition, nicotinic acid and its metabolites do not inhibit CYP-mediated reactions in vitro and therefore are unlikely to impact abiraterone exposure.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Nifedipine is metabolised mainly by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Nimesulide is extensively metabolised in the liver following multiple pathways including CYP2C9. Abiraterone is an inhibitor of CYP2C9 in vitro but the in vivo effect has yet to be determined. However, a clinically significant interaction is unlikely.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Nisoldipine is metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Nitrendipine is extensively metabolised mainly by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected. 

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%). Abiraterone does not interact with these pathways. 

Coadministration is contraindicated if abiraterone is used for treatment of hormone-sensitive cancer. If used for hormone insensitive tumours the following information is applicable. Coadministration has not been studied and is unlikely due to the differing target populations. Based on metabolism and clearance a clinically significant interaction is unlikely. Norelgestromin is metabolised to norgestrel (possibly by CYP3A4). Although abiraterone is an in vitro inhibitor of CYP3A4, no clinically relevant effect on norelgestromin exposure is expected.

Coadministration is contraindicated if abiraterone is used for treatment of hormone-sensitive cancer. If used for hormone insensitive tumours the following information is applicable. Coadministration has not been studied and is unlikely due to the differing target populations. 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. Abiraterone does not interact with this metabolic pathway.

Coadministration is contraindicated if abiraterone is used for treatment of hormone-sensitive cancer. If used for hormone insensitive tumours the following information is applicable. Coadministration has not been studied and is unlikely due to the differing target populations. 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. Abiraterone is an inhibitor of CYP2D6 (moderate) and CYP2C8 (weak). Since norgestimate does not have a narrow therapeutic index, a clinically relevant interaction is unlikely.

Coadministration is contraindicated if abiraterone is used for treatment of hormone-sensitive cancer. If used for hormone insensitive tumours the following information is applicable. Coadministration has not been studied and is unlikely due to the differing target populations. Based on metabolism and clearance a clinically significant interaction is unlikely. Norgestrel is a racemic mixture with levonorgestrel being biologically active. Norgestrel is mainly metabolised by CYP3A4 and is glucuronidated to a minor extent. Although abiraterone is an in vitro inhibitor of CYP3A4, no clinically relevant effect on norgestrel exposure is expected.

Coadministration has not been studied but should be approached with caution. Nortriptyline is metabolised mainly by CYP2D6. Abiraterone is an inhibitor of CYP2D6 and may increase concentrations of nortriptyline. Coadministration should be approached with caution. If treatment with nortriptyline cannot be interrupted, the dose of nortriptyline should be reduced by at least 50% as nortriptyline has a narrow therapeutic index. Consider monitoring of nortriptyline plasma concentrations, if available.

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.

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. Abiraterone is unlikely to interfere with this pathway. 

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). Abiraterone does not inhibit or induce CYP1A2 or UGTs in vivo. However, abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of olanzapine. Since CYP2D6 is a minor pathway, no clinically relevant effect on olanzapine exposure is expected.

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 via multiple OATs. Abiraterone does not interfere with this elimination pathway. 

Coadministration has not been studied but care should be taken. Omeprazole is mainly metabolised by CYP2C19 and to a lesser extent by CYP3A4. Although abiraterone is an in vitro inhibitor of CYP2C19 and CYP3A4, no clinically relevant effect on omeprazole exposure is expected. However, the solubility of abiraterone is pH dependent and exposure may be altered by coadministration with acid-reducing agents. The clinical relevance of this interaction is unknown. If coadministration is clinically necessary, abiraterone should be administered at the moment at which acid secretion is less inhibited, which is just before a new dose of omeprazole. Even with optimal timing of abiraterone intake, monitoring of abiraterone plasma concentrations should be considered, if available.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction unlikely. Ondansetron is metabolised mainly by CYP1A2, CYP3A4 and to a lesser extent by CYP2D6. Ondansetron is also a substrate of P-gp. Abiraterone is a moderate inhibitor of CYP2D6. However, since CYP2D6-mediated metabolism is only a minor pathway, a clinically relevant interaction is unlikely.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Oxazepam is mainly glucuronidated. Abiraterone does not interact with this metabolic pathway. 

Coadministration has not been studied but should be avoided. Oxcarbazepine is extensively metabolised to the active metabolite monohydroxyderivate (MHD) through cystolic enzymes. Abiraterone does not interact with this pathway. Both oxcarbazepine and MHD are inducers of CYP3A4 (moderate) and CYP3A5 and are inhibitors of CYP2C19. Concentrations of abiraterone may decrease due to CYP3A4 induction. A decrease in exposure can lead to decreased efficacy. Coadministration of CYP3A4 inducers should be avoided, or selection of an alternate concomitant medicinal product, with no or minimal potential to induce CYP3A4 should be considered. If coadministration is unavoidable, the dose of abiraterone may need to be increased. Closely monitor abiraterone efficacy. Consider monitoring of abiraterone plasma concentrations, if available.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Oxprenolol is largely metabolised via glucuronidation. Abiraterone does not interact with this metabolic pathway. 

Coadministration has not been studied. Oxycodone is metabolised principally to noroxycodone via CYP3A and oxymorphone via CYP2D6. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of oxycodone. If treatment with oxycodone cannot be interrupted, a dose reduction should be considered. Careful monitoring of side effects is recommended.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Paliperidone is primarily eliminated renally (possibly via OCT) with minimal metabolism occurring via CYP2D6 and CYP3A4. Abiraterone is a moderate inhibitor of CYP2D6, however since this is only a minor pathway, a clinically relevant interaction is unlikely.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction unlikely. Palonosetron is metabolised mainly by CYP2D6 and to a lesser extent by CYP3A4 and CYP1A2. Abiraterone is a moderate inhibitor of CYP2D6. However, since CYP2D6-mediated metabolism is only a minor pathway, a clinically relevant interaction is unlikely.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as pamidronic acid is not metabolised and is cleared as unchanged drug via urine.

Coadministration has not been studied but care should be taken. Pantoprazole is mainly metabolised by CYP2C19 and to lesser extent by CYPs 3A4, 2D6 and 2C9. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of pantoprazole. Since CYP2D6 is only a minor pathway, a clinically relevant effect on pantoprazole exposure is unlikely. However, the solubility of abiraterone is pH dependent and exposure may be altered by coadministration with acid-reducing agents. The clinical relevance of this interaction is unknown. If coadministration is clinically necessary, abiraterone should be administered at the moment at which acid secretion is less inhibited, which is just before a new dose of pantoprazole. Even with optimal timing of abiraterone intake, monitoring of abiraterone plasma concentrations should be considered, if available.

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. Abiraterone does not interact with this elimination pathway. 

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). There is no evidence that abiraterone inhibits or induces UGT1A9 and CYP2E1.

Coadministration has not been studied but should be approached with caution. Paroxetine is mainly metabolised by CYP2D6. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of paroxetine. Coadministration should be approached with caution. If treatment with paroxetine cannot be interrupted, the dose of paroxetine should be reduced by at least 50% as paroxetine has a narrow therapeutic index. Monitor closely for paroxetine toxicity. Paroxetine is also an inhibitor of CYP2D6 (strong) and CYP2C9. Abiraterone is not metabolised by these CYPs.

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

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). Abiraterone does not interfere with the elimination of penicillins.

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. Abiraterone is a moderate inhibitor of CYP2D6. Since CYP2D6 is only a minor pathway, a clinically relevant interaction is unlikely. Furthermore, abiraterone is an in vitro inhibitor of CYPs 3A4, 2C19 and 2C9, but no clinically significant effect on perazine exposure is expected.

Coadministration has not been studied. The metabolism of periciazine has not been well characterized but is likely to involve CYP2D6. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of periciazine. Coadministration should be approached with caution. If treatment with periciazine cannot be interrupted, the dose should be reduced by at least 50% as periciazine has a narrow therapeutic index.

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 probably via CYP3A4 and is metabolised to other inactive metabolites. Elimination occurs predominantly via the urine. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect on perindopril is expected.

Coadministration has not been studied but should be approached with caution. Perphenazine is metabolised by CYP2D6. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of perphenazine. Coadministration should be approached with caution. If treatment with perphenazine cannot be interrupted, the dose of perphenazine should be reduced by at least 50% as perphenazine has a narrow therapeutic index.

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. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected.

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. Abiraterone does not interact with these metabolic pathways.

Coadministration has not been studied but should be avoided. Phenobarbital is metabolised by CYP2C19 and CYP2C9 (major) and to a lesser extent by CYP2E1. Abiraterone is an in vitro inhibitor of CYP2C19 and CYP2C9 but the in vivo effect has yet to be determined. Concentrations of phenobarbital may increase due to inhibition of CYP2C19 and CYP2C9, but this is unlikely to be clinically relevant. However, phenobarbital is a strong inducer of CYPs 3A4, 2C9, 2C8 and UGTs. Concentrations of abiraterone may significantly decrease due to CYP3A4 induction. A decrease in exposure can lead to decreased efficacy. Coadministration of CYP3A4 inducers should be avoided, or selection of an alternate concomitant medicinal product, with no or minimal potential to induce CYP3A4 should be considered. If coadministration is unavoidable, a dose increase of abiraterone may be required. Closely monitor abiraterone efficacy. Consider monitoring of abiraterone plasma concentrations, if available. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Phenprocoumon is metabolised by CYP2C9 and CYP3A4. Although abiraterone is an in vitro inhibitor of CYP3A4 and CYP2C9, no clinically relevant effect on phenprocoumon exposure is expected.

Coadministration has not been studied but should be avoided. Phenytoin is mainly metabolised by CYP2C9 and to a lesser extent by CYP2C19. Although abiraterone is an in vitro inhibitor of CYP2C9 and CYP2C19, a clinically relevant effect on phenytoin exposure is unlikely. Furthermore, phenytoin is a potent inducer of CYP3A4, UGT and P-gp. Concentrations of abiraterone may decrease due to induction of CYP3A4. A decrease in exposure can lead to decreased efficacy. Coadministration of CYP3A4 inducers should be avoided, or selection of an alternate concomitant medicinal product, with no or minimal potential to induce CYP3A4 should be considered. If coadministration is unavoidable, the dose of abiraterone may need to be increased. Closely monitor abiraterone efficacy. Consider monitoring of abiraterone plasma concentrations, if available.

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. Abiraterone does not inhibit or induce CYP4F2. 

Coadministration has not been studied but should be approached with caution. Pimozide is mainly metabolised by CYP3A4 and CYP2D6, and to a lesser extent by CYP1A2. Abiraterone is a moderate inhibitor of CYP2D6 and may increase pimozide concentrations. Coadministration should be approached with caution. If treatment with pimozide cannot be interrupted, the dose of pimozide should be reduced by at least 50% as pimozide has a narrow therapeutic index.

Coadministration has not been studied. Pindolol is partly metabolised to hydroxymetabolites (possibly via CYP2D6) and partly eliminated unchanged in the urine. Abiraterone is a moderate inhibitor of CYP2D6. However, as multiple pathways are involved, clinically relevant interactions are unlikely. However, monitoring of blood pressure and heart rate is recommended.

Coadministration has been studied but care should be taken. Pioglitazone is metabolised mainly by CYP2C8 and to a lesser extent by CYPs 3A4, 1A2 and 2C9. Abiraterone is an inhibitor of CYP2C8 and may increase concentrations of pioglitazone. In healthy volunteers, coadministration of abiraterone and pioglitazone increased pioglitazone AUC by 46%. The AUC of the active metabolites, MIII and MIV, decreased by 10%. Monitoring of blood glucose levels and pioglitazone toxicity may be required.

Coadministration has not been studied but should be approached with caution. The metabolism of pipotiazine has not been well described but may involve CYP2D6. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of pipotiazine. Coadministration should be approached with caution. If treatment with pipotiazine cannot be interrupted, the dose of pipotiazine should be reduced by at least 50% as pipotiazine has a narrow therapeutic index.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Piroxicam is primarily metabolised by CYP2C9. Abiraterone is an inhibitor of CYP2C9 in vitro but the in vivo effect has yet to be determined. However, a clinically relevant interaction is unlikely.

Coadministration has not been studied. Pitavastatin is metabolised by UGT1A3 and UGT2B7 with minimal metabolism by CYP2C9 and CYP2C8. Pitavastatin is also a substrate of OATP1B1. Abiraterone is a weak inhibitor of CYP2C8 and an inhibitor of OATP1B1 in vitro. Therefore concentrations of abiraterone may slightly increase. As the clinical relevance of this interaction is unknown, monitoring may be required.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Posaconazole is metabolised by UGTs and is a substrate of P-gp. Abiraterone does not interact with this metabolic pathway. Posaconazole is a strong inhibitor of CYP3A4 and may increase abiraterone concentrations. When coadministered with the strong CYP3A4 inhibitor, ketoconazole, abiraterone AUC increased by 15%. An interaction with CYP3A4 inhibitors is not likely to be clinically relevant.

Coadministration has not been studied but based on limited data available an interaction appears unlikely. Potassium is renally eliminated. 

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. Although abiraterone is an in vitro inhibitor of CYPs 3A4, 2C9 and 2C19, no clinically relevant effect on prasugrel exposure is expected.

Coadministration has not been studied but care should be taken. Pravastatin is metabolised by CYP3A4 and is a substrate of OATP1B1. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically relevant effect due to CYP3A4 inhibition is expected. Abiraterone is also an inhibitor of OATP1B1 in vitro and may increase concentrations of pravastatin. As the clinical relevance of this interaction is unknown, consider starting with the lowest dose of pravastatin and titrate up to the desired clinical effect whilst monitoring for toxicity.

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. Abiraterone does not interact with this metabolic pathway.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Prednisolone undergoes hepatic metabolism via CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect on prednisolone is expected.

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. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect on prednisone is expected.

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). Abiraterone does not interfere with this elimination pathway.

Coadministration has not been studied. Prochlorperazine is metabolised by CYP2D6 and CYP2C19. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of prochlorperazine. As the clinical relevance of this interaction is unknown, monitoring for toxicity may be required.

Coadministration has not been studied. Promethazine is metabolised by CYP2D6. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of promethazine. As the clinical relevance of this interaction is unknown, careful monitoring of side effects is advised. A dose reduction of promethazine should also be considered.

Coadministration has not been studied but should be approached with caution. Propafenone is metabolised mainly by CYP2D6 and to a lesser extent by CYP1A2 and CYP3A4. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of propafenone. Coadministration should be approached with caution. If treatment with propafenone cannot be interrupted, the dose should be reduced by at least 50% as propafenone has a narrow therapeutic index.

Coadministration has not been studied. 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). Abiraterone is a moderate inhibitor of CYP2D6. However, since CYP2D6 mediated metabolism is only a minor pathway, a clinically relevant interaction is unlikely. However, monitoring of blood pressure and heart rate is recommended.

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. Abiraterone does not interfere with these metabolic or elimination pathways. 

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

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Quetiapine is primarily metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect on quetiapine is expected.

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. Abiraterone does not interfere with this renal transporter. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Quinidine is metabolised by CYP3A4 and to a lesser extent by CYP2C9 and CYP2E1. Quinidine is also a substrate of P-gp. Abiraterone is an inhibitor of CYP3A4 and CYP2C9 (in vitro). However, this is unlikely to lead to a clinically relevant effect on quinidine exposure. Quinidine is an inhibitor of CYP2D6 (strong), CYP3A4 (weak) and P-gp (moderate). Concentrations of abiraterone may increase due to inhibition of CYP3A4. When coadministered with the strong CYP3A4 inhibitor, ketoconazole, abiraterone AUC increased by 15%. Therefore, an interaction with CYP3A4 inhibitors is not likely to be clinically relevant.

Coadministration has not been studied but care should be taken. Rabeprazole is mainly metabolised via non-enzymatic reduction and to lesser extent by CYP2C19 and CYP3A4. Although abiraterone is an in vitro inhibitor of CYP3A4 and CYP2C19, a clinically relevant effect on rabeprazole exposure is unlikely. However, the solubility of abiraterone is pH dependent and exposure may be altered by coadministration with acid-reducing agents. The clinical relevance of this interaction is unknown. If coadministration is clinically necessary, abiraterone should be administered at the moment at which acid secretion is less inhibited, which is just before a new dose of rabeprazole. Even with optimal timing of abiraterone intake, monitoring of abiraterone plasma concentrations should be considered, if available.

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 probably via CYP3A4, and is metabolised to the diketopiperazine ester, diketopiperazine acid and the glucuronides of ramipril and ramiprilat. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected.

Coadministration has not been studied but care should be taken. Ranitidine is excreted via OAT1/OAT3. Abiraterone is unlikely to interact with this elimination pathway. However, the solubility of abiraterone is pH dependent and exposure may be altered by coadministration with acid-reducing agents. The clinical relevance of this interaction is unknown. If coadministration is clinically necessary, abiraterone should be administered at the moment at which acid secretion is less inhibited, which is just before a new dose of ranitidine. Even with optimal timing of abiraterone intake, monitoring of abiraterone plasma concentrations should be considered, if available.

Coadministration has not been studied but based on metabolism and clearance a clinically relevant interaction is unlikely. Ranolazine is primarily metabolised by CYP3A4 and to a lesser extent by CYP2D6. Ranolazine is also a substrate of P-gp. Although abiraterone is an in vitro inhibitor of CYP3A4, no clinically relevant effect due to CYP3A4 inhibition is expected. Abiraterone is also a moderate inhibitor of CYP2D6 and may increase concentrations of ranolazine. Since CYP2D6 is a minor pathway, no clinically relevant effect on ranolazine exposure is expected. Furthermore, ranolazine is a weak inhibitor of P-gp, CYP3A4 and CYP2D6. No clinically significant effect on abiraterone exposure is expected.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Reboxetine is metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect on reboxetine is expected.

Coadministration has not been studied but should be approached with caution. Repaglinide is metabolised by CYP2C8 and CYP3A4 with clinical data indicating it is a substrate of OATP1B1. Abiraterone is a weak inhibitor of CYP2C8; it is also an inhibitor of OATP1B1 in vitro but the in vivo effect has yet to be determined. Concentrations of repaglinide may increase due to inhibition of both CYP2C8 and OATP1B1. Coadministration is not recommended and selection of an alternate concomitant medicinal product, with no or minimal metabolism via CYP2C8 should be considered. If used concomitantly, close monitoring of blood glucose levels in addition to signs of repaglinide toxicity is recommended.

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. Abiraterone does not interact with this metabolic pathway. 

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

Coadministration has not been studied and is contraindicated. Rifabutin is metabolised by CYP3A and via deacetylation. Abiraterone is an inhibitor of CYP3A4 but this is unlikely to be clinically relevant. However, rifabutin is an inducer of CYP3A4 and may significantly decrease abiraterone concentrations. A decrease in abiraterone exposure can lead to decreased efficacy. Selection of an alternative medication with no or minimal enzyme or transporter induction potential is recommended. If coadministration is unavoidable, a dose increase of abiraterone may be required. Consider close monitoring of abiraterone plasma concentrations, if available. 

Coadministration is contraindicated. Rifampicin is metabolised via deacetylation. Abiraterone does not interfere with this metabolic pathway. However, rifampicin is a strong CYP3A4 and P-gp inducer. In healthy volunteers, coadministration of abiraterone and rifampicin decreased abiraterone AUC and Cmax by 45%. A decrease in abiraterone exposure can lead to decreased efficacy. Selection of an alternative medication with no or minimal enzyme or transporter induction potential is recommended. If coadministration is unavoidable, a dose increase of abiraterone may be required. The FDA suggest increasing the dose to 1000 mg twice daily, which is based on pharmacokinetic data, not on clinical outcome. Consider monitoring of abiraterone plasma concentrations, if available. After discontinuation of rifampicin, the effect of the interaction can maintain for up to several weeks. 

Coadministration has not been studied but is contraindicated. Rifapentine is metabolised via deacetylation. Abiraterone does not interfere with this metabolic pathway. However, rifapentine is a strong CYP3A4, CYP2C8 and P-gp inducer. Concentrations of rifapentine may significantly decrease due to CYP3A4 induction. A decrease in abiraterone exposure can lead to decreased efficacy. Selection of an alternative medication with no or minimal enzyme or transporter induction potential is recommended. If coadministration is unavoidable, a dose increase of abiraterone may be required. Consider monitoring of abiraterone plasma concentrations, if available. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Rifaximin is mainly excreted in the faeces, almost entirely as unchanged drug. Abiraterone does not interact with this metabolic pathway. 

Coadministration has not been studied but should be approached with caution. Risperidone is metabolised by CYP2D6 and to a lesser extent by CYP3A4. Risperidone is also a substrate of P-gp. Abiraterone is an inhibitor of CYP2D6 (moderate) and CYP3A4 (in vitro) and may increase concentrations of risperidone. Coadministration should be approached with caution. If treatment with risperidone cannot be interrupted, the dose of risperidone should be reduced by at least 50% as risperidone has a narrow therapeutic index.

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. Although abiraterone is an in vitro inhibitor of CYP3A4, no clinically relevant effect on rivaroxaban exposure is expected. Abiraterone does not inhibit or induce CYP2J2, P-gp, and BCRP.

Coadministration has not been studied but should be approached with caution. Rosiglitazone is metabolised mainly by CYP2C8 and to a lesser extent by CYP2C9. Abiraterone is a weak inhibitor of CYP2C8 and may increase concentrations of rosiglitazone. Coadministration is not recommended and selection of an alternate concomitant medicinal product, with no or minimal metabolism via CYP2C8 should be considered. Patients should be closely monitored for signs of rosiglitazone toxicity. Close monitoring of blood glucose levels is also recommended.

Coadministration has not been studied but care should be taken. Rosuvastatin is largely excreted unchanged in the faeces via OATP1B1 and is a substrate of BCRP. Abiraterone is an inhibitor of OATP1B1 in vitro and may increase concentrations of rosuvastatin. As the clinical relevance of this interaction is unknown, consider starting with the lowest dose of rosuvastatin and titrate up to the desired clinical effect whilst monitoring for toxicity.

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. Abiraterone does not interact with this metabolic pathway.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Salmeterol is metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4, the systemic absorption of salmeterol after bronchial administration is low and a clinically relevant interaction is unlikely.

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. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected. 

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 faeces and also in other secretions. No clinically significant interactions are known. 

Coadministration has not been studied but should be approached with caution. Sertindole is metabolised by CYP2D6 and CYP3A4. Abiraterone is an inhibitor of CYP2D6 (moderate) and CYP3A4 (in vitro), and may increase concentrations of sertindole. Coadministration should be approached with caution. If treatment with sertindole cannot be interrupted, the dose of sertindole should be reduced by at least 50% as sertindole has a narrow therapeutic index.

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. Abiraterone is a moderate inhibitor of CYP2D6, but since CYP2D6 mediated metabolism is only a minor pathway, a clinically relevant interaction is unlikely.

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. Abiraterone is an inhibitor of CYP2C9 and CYP3A4 in vitro but a clinically significant effect is not expected.

Coadministration has not been studied but care should be taken. Simvastatin is metabolised by CYP3A4. Simvastatin is also a substrate of BCRP and the active metabolite is a substrate of OATP1B1. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically relevant effect due to CYP3A4 inhibition is expected. Abiraterone is also an inhibitor of OATP1B1 in vitro and may increase concentrations of the active metabolite. As the clinical relevance of this interaction is unknown, consider starting with the lowest dose of simvastatin and titrate up to the desired clinical effect whilst monitoring for toxicity.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Sirolimus is metabolised by CYP3A4 and is a substrate of P-gp. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Sitagliptin is primarily eliminated in the urine as unchanged drug (active secretion by OAT3, OATP4C1, and P-gp) with metabolism by CYP3A4 representing a minor elimination pathway. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected.

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. There is little potential for sodium nitroprusside to affect the disposition of abiraterone, or to be affected if co-administered with abiraterone. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as sotalol is excreted unchanged via renal elimination. 

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. Abiraterone does not interact with this elimination pathway. 

Coadministration has not been studied and is contraindicated. Based on metabolism and clearance a pharmacokinetic interaction is unlikely. Spironolactone is partly metabolised by the flavin containing monooxygenases. Abiraterone does not affect this metabolic pathway. However, spironolactone binds to the androgen receptor and may increase prostate specific antigen levels; therefore coadministration should be avoided.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Stanozolol undergoes hepatic metabolism. Abiraterone is a moderate inhibitor of CYP2D6 and weak inhibitor of CYP2C8. However, since stanozolol has a wide therapeutic index, a clinically relevant interaction is unlikely.

Coadministration has not been studied and should be avoided. St John’s wort may cause significant and unpredictable decreases in the plasma concentrations of abiraterone due to induction of CYP3A4. 

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. Streptokinase is unlikely to affect the disposition of abiraterone, or to be affected if coadministered with abiraterone.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. In vitro studies suggest a role of CYP2C9 in sulfadiazine metabolism. Abiraterone is an inhibitor of CYP2C9 in vitro but the in vivo effect has yet to be determined. However, a clinically relevant interaction is unlikely.

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. Abiraterone does not interfere with this elimination pathway.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Tacrolimus is metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically relevant effect on tacrolimus exposure is expected. Tacrolimus is also an in vitro inhibitor of CYP3A4 and OATP1B1 but produced modest inhibition of CYP3A4 and OATP1B1 in the range of clinical concentrations. Concentrations of abiraterone may increase due to inhibition of CYP3A4. When coadministered with the strong CYP3A4 inhibitor, ketoconazole, abiraterone AUC increased by 15%. Therefore, an interaction with CYP3A4 inhibitors is not likely to be clinically significant.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Tadalafil is metabolised by CYP3A4. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect is expected.

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. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of tamsulosin. However, since CYP2D6 mediated metabolism is only a minor pathway, a clinically relevant interaction is unlikely.

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. Abiraterone does not interact with this elimination pathway.

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. Although abiraterone is an inhibitor of CYP3A4 in vitro, a clinically relevant effect on telithromycin exposure is unlikely. Telithromycin is also an inhibitor of CYP3A4 (strong) and P-gp. Concentrations of abiraterone may increase due to CYP3A4 inhibition. When coadministered with the strong CYP3A4 inhibitor, ketoconazole, abiraterone AUC increased by 15%. A similar effect may occur with telithromycin. Therefore, an interaction with CYP3A4 inhibitors is not likely to be clinically significant.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Temazepam is mainly glucuronidated. Abiraterone does not interact with this metabolic pathway. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Terbinafine is metabolised by CYPs 1A2, 2C9, 3A4 and to a lesser extent by CYPs 2C8 and 2C19. Abiraterone is a weak inhibitor of CYP2C8, however since this is only a minor pathway, a clinically relevant interaction is unlikely.

Coadministration is contraindicated if abiraterone is used for treatment of hormone-sensitive cancer. If used for hormone insensitive tumours the following information is applicable. Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Testosterone is metabolised by CYP3A4. Although abiraterone is an in vitro inhibitor of CYP3A4, no clinically relevant effect on testosterone exposure is expected.

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. Abiraterone does not interfere with this elimination pathway.

No clinically significant interaction was observed when abiraterone was coadministered with theophylline. In patients with metastatic castration-resistant prostate cancer, coadministration of abiraterone plus prednisone with theophylline increased theophylline AUC by 8%.

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

Coadministration has not been studied but should be approached with caution. Thioridazine is metabolised by CYP2D6 and to a lesser extent by CYP3A4. Abiraterone is a moderate inhibitor of CYP2D6 and may increase concentrations of thioridazine. Coadministration should be approached with caution. If treatment with thioridazine cannot be interrupted, the dose of thioridazine should be reduced by at least 50% as thioridazine has a narrow therapeutic index.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ticagrelor undergoes extensive CYP3A4 metabolism. Although abiraterone is an inhibitor of CYP3A4 in vitro, no clinically significant effect on ticagrelor is expected. Furthermore, ticagrelor is a weak inhibitor of CYP3A4. No clinically significant effect on abiraterone is expected. 

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. Abiraterone is a moderate inhibitor of CYP2D6. However, the systemic absorption of timolol after ocular administration is low. Therefore, a clinically relevant interaction is unlikely. 

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. Abiraterone does not interact with this elimination pathway.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Tolbutamide is mainly metabolised by CYP2C9 and to a lesser extent by CYP2C8 and CYP2C19. Abiraterone is a weak inhibitor of CYP2C8, but since CYP2C8 mediated metabolism is only a minor pathway, a clinically relevant interaction is unlikely.