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. Pomalidomide does not interfere with this metabolic pathway.

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. Pomalidomide does not inhibit or induce CYPs.

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). Pomalidomide does not inhibit or induce UGTs.

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

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Alendronate is not metabolised but 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. Pomalidomide does not inhibit or induce CYPs.

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

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

Coadministration has not been studied but based on the metabolism and clearance a clinically significant interaction is unlikely. Allopurinol is converted to oxipurinol by xanthine oxidase and aldehyde oxidase. Pomalidomide 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. Pomalidomide does not inhibit or induce CYPs.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Aluminium hydroxide is not metabolised. Pomalidomide is unlikely to interact with this pathway.

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. Pomalidomide does not inhibit or induce CYPs, UGTs or P-gp.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Amiodarone is metabolised by CYP3A4 and CYP2C8. 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). Pomalidomide does not interact with this pathway.

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

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

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

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

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

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. Pomalidomide does not interfere with this metabolic pathway.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Antacids are not metabolised by CYPs. Pomalidomide does not interact with this pathway.

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

Coadministration has not been studied. Aprepitant is mainly metabolised by CYP3A4 and to a lesser extent by CYP1A2 and CYP2C19. Pomalidomide does not inhibit or induce CYPs. However, during treatment aprepitant is a weak-moderate inhibitor of CYP3A4 and a weak inhibitor of CYP2C9. After treatment aprepitant is an inducer of CYP3A4, CYP2C9 (weak) and UGT (weak). Pomalidomide concentrations may slightly alter during and after treatment with aprepitant due to CYP3A4 induction and inhibition. However, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inhibitor, ketoconazole (400 mg twice daily), increased pomalidomide mean AUC and Cmax by 18.8% and 7.3%, respectively. A clinically relevant effect is not expected during aprepitant treatment. Furthermore, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inducer, carbamazepine (200mg twice daily), decreased pomalidomide AUC and Cmax by 20% and 25%, respectively. A clinically relevant effect is not expected after aprepitant treatment. No a priori dose adjustment for pomalidomide is necessary but monitoring of pomalidomide efficacy may be required.

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

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 and 2D6 (minor)). Pomalidomide does not inhibit or induce CYPs or UGTs.

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

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. Pomalidomide not interfere with this elimination pathway.

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

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Azithromycin is mainly eliminated via biliary excretion; animal data suggest this may occur via P-gp and MRP2. Pomalidomide does not interact with this elimination pathway. However, azithromycin is an inhibitor of P-gp and may increase concentrations of pomalidomide. The clinical relevance of P-gp inhibition by azithromycin is unknown. Coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 and P-gp inhibitor, ketoconazole (400 mg twice daily), increased pomalidomide mean AUC and Cmax by 18.8% and 7.3%, respectively. Therefore, no clinically relevant effect is expected with azithromycin.

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

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

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

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

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

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

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. Pomalidomide does not interfere with this metabolic pathway.

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

Coadministration has not been studied. Bosentan is metabolised by CYP3A4 and CYP2C9. Pomalidomide does not inhibit or induce CYPs. Bosentan is also an inducer of CYP3A4 and CYP2C9. Concentrations of pomalidomide may decrease due to induction of CYP3A4. However, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inducer, carbamazepine (200mg twice daily), decreased pomalidomide AUC and Cmax by 20% and 25%, respectively. Therefore, a clinically significant effect is not expected with bosentan. No a priori dose adjustment for pomalidomide is necessary, but monitoring of pomalidomide 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, but other cytochromes such as CYP2D6 and CYP1A2 may play a role. Pomalidomide does not inhibit or induce CYPs.

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

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

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

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

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. Pomalidomide is unlikely to interfere with these elimination pathways.

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. Pomalidomide does not interact with this elimination pathway.

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. Pomalidomide 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. Pomalidomide does not interfere with this elimination pathway.

Carbamazepine is primarily metabolised by CYP3A4 and to a lesser extent by CYP2C8. Pomalidomide does not inhibit or induce CYPs. Carbamazepine is also an inducer of CYPs 2C8 (strong), 2C9 (strong), 3A4 (strong), 1A2 (weak), 2B6 and UGT1A1. Concentrations of pomalidomide may slightly decrease due to induction of CYP3A4. However, coadministration of pomalidomide (4 mg single dose) and carbamazepine (200mg twice daily) decreased pomalidomide AUC and Cmax by 20% and 25%, respectively. No a priori dose adjustment for pomalidomide is necessary, but monitoring of pomalidomide efficacy may be required.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Carvedilol undergoes glucuronidation via UGTs 1A1, 2B4 and 2B7, and additional metabolism via CYP2D6 and to a lesser extent by CYPs 2C9 and 1A2. Pomalidomide does not inhibit or induce CYPs or UGTs.

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. Pomalidomide 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 unchanged by glomerular filtration and tubular secretion via OAT1 and MATE1. Pomalidomide does not interfere with this elimination pathway.

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. Pomalidomide 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. Pomalidomide 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. Pomalidomide does not interfere with this elimination pathway.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ceftazidime is excreted predominantly by renal glomerular filtration. Pomalidomide 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. Pomalidomide 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. Pomalidomide does not inhibit or induce CYPs.

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 (possibly via OCT2). In vitro data indicate that cetirizine also inhibits OCT2. Pomalidomide is unlikely to interact with this pathway.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Chloramphenicol is predominantly glucuronidated. Pomalidomide does not inhibit or induce UGTs. Furthermore, in vitro studies have shown that chloramphenicol can inhibit metabolism mediated by CYPs 3A4 (strong), 2C19 (strong) and 2D6 (weak). Concentrations of pomalidomide may slightly increase due to inhibition of CYP3A4. However, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inhibitor, ketoconazole (400 mg twice daily), increased pomalidomide AUC and Cmax by 18.8 and 7.3%, respectively. Therefore, no clinically relevant effect is expected with chloramphenicol. No a priori dose adjustment for pomalidomide is necessary. Ocular use: Although chloramphenicol is systemically absorbed when used topically in the eye, the concentrations used are unlikely to cause a clinically significant 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. Pomalidomide does not inhibit or induce CYPs.

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

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

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

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. Pomalidomide does not inhibit or induce CYPs or P-gp. Ciclosporin is also an inhibitor of CYP3A4 and OATP1B1. Concentrations of pomalidomide may increase due to inhibition of CYP3A4. However, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inhibitor, ketoconazole (400 mg twice daily), increased pomalidomide mean AUC and Cmax by 18.8% and 7.3%, respectively. Therefore, a clinically relevant effect is not expected with ciclosporin. No a priori dose adjustment for pomalidomide is necessary.

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 (possibly via OATs). Pomalidomide 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 data indicate that cimetidine inhibits OAT1 and OCT2 but at concentrations much higher than the observed clinical concentrations. Cimetidine is also a weak inhibitor of several CYP-enzymes (CYPs 3A4, 1A2, 2D6 and 2C19 among others). Concentrations of pomalidomide may increase due to CYP3A4 inhibition. However, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inhibitor, ketoconazole (400 mg twice daily), increased pomalidomide mean AUC and Cmax by 18.8% and 7.3%, respectively. Therefore, a clinically relevant effect is not expected with cimetidine. No a priori dose adjustment for pomalidomide is necessary.

Coadministration has not been studied but is not recommended. 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. Pomalidomide does not interfere with this metabolic pathway. Ciprofloxacin is a weak to moderate inhibitor of CYP3A4 and a strong inhibitor of CYP1A2, and may increase concentrations of pomalidomide. Coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inhibitor, ketoconazole (400 mg twice daily), increased pomalidomide AUC and Cmax by 18.8% and 7.3%, respectively. Therefore, CYP3A4 inhibition is unlikely to cause a clinically relevant effect on pomalidomide exposure. However, coadministration of pomalidomide (4 mg single dose) and the CYP1A2 inhibitor, fluvoxamine (50 mg twice daily), plus the CYP3A4 inhibitor, ketoconazole (200 mg twice daily), increased pomalidomide AUC and Cmax by 145.7% and 106.7%, respectively, when compared to pomalidomide alone. In a second study the contribution of a CYP1A2 inhibitor alone was assessed. Coadministration of pomalidomide (4 mg single dose) and fluvoxamine (50 mg twice daily) increased pomalidomide mean exposure by 125% compared to pomalidomide alone. Coadministration with ciprofloxacin is not recommended. Selection of an alternate concomitant medicinal product with no or minimal potential to inhibit CYP1A2 should be considered. If coadministration is unavoidable, the dose of pomalidomide needs to be reduced by 50%. Close monitoring for pomalidomide toxicity is recommended. Monitor pomalidomide concentrations, if available.

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

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%). Pomalidomide does not inhibit or induce CYPs.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Clarithromycin is metabolised by CYP3A4. Pomalidomide does not inhibit or induce CYPs. Clarithromycin is also an inhibitor of CYP3A4 (strong) and P-gp, and may increase concentrations of pomalidomide. However, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 and P-gp inhibitor, ketoconazole (400 mg twice daily), increased pomalidomide mean AUC and Cmax by 18.8% and 7.3%, respectively. Therefore, no clinically relevant interaction is expected with clarithromycin.

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. Pomalidomide does not interact with this elimination pathway.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Clindamycin is metabolised by CYP3A4. Pomalidomide does not inhibit or induce CYPs. In vitro data suggest that clindamycin is also a CYP3A4 inhibitor and may slightly increase concentrations of pomalidomide. However, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inhibitor, ketoconazole (400 mg twice daily), increased pomalidomide mean AUC and Cmax by 18.8% and 7.3%, respectively. Therefore, a clinically relevant interaction is not expected with clindamycin.

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. Pomalidomide does not interfere with this elimination pathway. In vitro data suggest that clofazimine is also a CYP3A4 inhibitor and may slightly increase concentrations of pomalidomide. However, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inhibitor, ketoconazole (400 mg twice daily), increased pomalidomide mean AUC and Cmax by 18.8% and 7.3%, respectively. Therefore, a clinically relevant interaction is not expected with clofazimine.

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. Pomalidomide does not interact with this pathway.

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

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

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. Pomalidomide does not inhibit or induce CYPs. Furthermore, clopidogrel is an inhibitor of CYP2C8 (strong), CYP2B6 (weak) and of CYP2C9 (in vitro) at high concentrations. Pomalidomide 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. Pomalidomide does not interact with this metabolic pathway.

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. Pomalidomide does not interact with this elimination pathway.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Codeine is converted via CYP2D6 to morphine, an active metabolite with analgesic and opioid properties. Morphine is further metabolised by conjugation with glucuronic acid to morphine-3-glucuronide (inactive) and morphine-6-glucuronide (active). Codeine is converted via CYP3A4 to norcodeine, an inactive metabolite. The active metabolite morphine is also a substrate of P-gp. Pomalidomide does not inhibit or induce CYPs or P-gp.

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

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. Pomalidomide 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. Pomalidomide 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 via unsaturable glomerular filtration. Pomalidomide is unlikely to interfere with the renal excretion of dalteparin.

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 CYPs. Pomalidomide does not inhibit or induce CYPs.

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

Coadministration has not been studied. Desogestrel is a prodrug which is activated to etonogestrel by CYP2C9 (and possibly CYP2C19); the metabolism of etonogestrel is mediated by CYP3A4. Pomalidomide does not inhibit or induce CYPs. However, coadministration of combined oral contraception is contraindicated with pomalidomide. The potential impact of pomalidomide on the pharmacokinetics of combined oral contraceptives has not been clinically evaluated, but the effect of oral contraceptives can be reduced by the registered comedication, dexamethasone. An increased risk of venous thromboembolism was observed in patients with multiple myeloma taking pomalidomide, dexamethasone and combined oral contraception. Therefore, a switch to another effective contraception method is recommended. The risk of venous thromboembolism continues for 4-6 weeks after discontinuing combined oral contraception. The following can be considered to be examples of suitable methods of contraception: implant, levonorgestrel-releasing intrauterine system, medroxyprogesterone acetate depot, tubal sterilization, sexual intercourse with a vasectomised male partner only (vasectomy must be confirmed by two negative semen analyses) and ovulation inhibitory progesterone-only pills (i.e. desogestrel).

Dexamethasone is metabolised by CYP3A4. Pomalidomide does not inhibit or induce CYPs. Dexamethasone has also been described as CYP3A4 inducer and may decrease concentrations of pomalidomide. The induction effect of CYP3A4 by dexamethasone has yet to be established and the clinical relevance of this interaction is unknown. However, in patients with multiple myeloma, coadministration of pomalidomide (up to 4 mg) and dexamethasone (20-40 mg) had no effect on the pharmacokinetics of pomalidomide compared with pomalidomide administered alone.

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

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. Pomalidomide does not inhibit or induce UGTs or P-gp.

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

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. Pomalidomide does not inhibit or induce UGTs or CYPs.

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

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. Pomalidomide does not inhibit or induce CYPs or UGTs.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Diltiazem is metabolised by CYP3A4 and CYP2D6. Pomalidomide does not inhibit or induce CYPs. Diltiazem is also a moderate inhibitor of CYP3A4 and may increase pomalidomide exposure. However, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inhibitor, ketoconazole (400 mg twice daily), increased pomalidomide mean AUC and Cmax by 18.8% and 7.3%, respectively. Therefore, a clinically relevant effect is not expected with diltiazem. No a priori dose adjustment for pomalidomide is necessary.

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

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. Pomalidomide does not inhibit or induce UGTs.

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

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%). Pomalidomide does not interfere with this metabolic pathway.

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

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 pomalidomide, or to be affected by pomalidomide.

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

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

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. Pomalidomide does not interfere with this elimination 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. Pomalidomide does not inhibit of induce CYPs.

Coadministration has not been studied. Drospirenone is metabolised to a minor extent via CYP3A4. Pomalidomide does not inhibit or induce CYPs. However, coadministration of combined oral contraception is contraindicated with pomalidomide. The potential impact of pomalidomide on the pharmacokinetics of combined oral contraceptives has not been clinically evaluated, but the effect of oral contraceptives can be reduced by the registered comedication, dexamethasone. An increased risk of venous thromboembolism was observed in patients with multiple myeloma taking pomalidomide, dexamethasone and combined oral contraception. Therefore, a switch to another effective contraception method is recommended. The risk of venous thromboembolism continues for 4-6 weeks after discontinuing combined oral contraception. The following can be considered to be examples of suitable methods of contraception: implant, levonorgestrel-releasing intrauterine system, medroxyprogesterone acetate depot, tubal sterilization, sexual intercourse with a vasectomised male partner only (vasectomy must be confirmed by two negative semen analyses) and ovulation inhibitory progesterone-only pills (i.e. desogestrel).

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. 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. Duloxetine is metabolised by CYP2D6 and CYP1A2. Pomalidomide does not inhibit or induce CYPs.

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

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

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

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

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

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. Pomalidomide 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. Eprosartan is largely excreted in bile and urine as unchanged drug. Pomalidomide does not interact with this elimination pathway.

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. Pomalidomide 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 a substrate of CYP3A4 and P-gp. Pomalidomide does not inhibit or induce CYPs or P-gp. Erythromycin is also an inhibitor of CYP3A4 (moderate) and P-gp, and may increase concentrations of pomalidomide. However, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 and P-gp inhibitor, ketoconazole (400 mg twice daily), increased pomalidomide mean AUC and Cmax by nearly 18.8% and 7.3%, respectively. Therefore, a clinically relevant interaction is not expected with erythromycin. No a priori dose adjustment for pomalidomide is necessary.

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

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

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. Pomalidomide does not inhibit or induce CYPs.

Coadministration has not been studied. Estradiol is metabolised by CYP3A4, CYP1A2 and is glucuronidated. Pomalidomide does not inhibit or induce CYPs or UGTs. However, coadministration of combined oral contraception is contraindicated with pomalidomide. The potential impact of pomalidomide on the pharmacokinetics of combined oral contraceptives has not been clinically evaluated, but the effect of oral contraceptives can be reduced by the registered comedication, dexamethasone. An increased risk of venous thromboembolism was observed in patients with multiple myeloma taking pomalidomide, dexamethasone and combined oral contraception. Therefore, a switch to another effective contraception method is recommended. The risk of venous thromboembolism continues for 4-6 weeks after discontinuing combined oral contraception. The following can be considered to be examples of suitable methods of contraception: implant, levonorgestrel-releasing intrauterine system, medroxyprogesterone acetate depot, tubal sterilization, sexual intercourse with a vasectomised male partner only (vasectomy must be confirmed by two negative semen analyses) and ovulation inhibitory progesterone-only pills (i.e. desogestrel).

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%). Pomalidomide does not interact with this elimination pathway.

Coadministration has not been studied. Ethinylestradiol undergoes oxidation (CYP3A4>CYP2C9), sulfation and glucuronidation (UGT1A1). Pomalidomide does not inhibit or induce CYPs or UGTs. However, coadministration of combined oral contraception is contraindicated with pomalidomide. The potential impact of pomalidomide on the pharmacokinetics of combined oral contraceptives has not been clinically evaluated, but the effect of oral contraceptives can be reduced by the registered comedication, dexamethasone. An increased risk of venous thromboembolism was observed in patients with multiple myeloma taking pomalidomide, dexamethasone and combined oral contraception. Therefore, a switch to another effective contraception method is recommended. The risk of venous thromboembolism continues for 4-6 weeks after discontinuing combined oral contraception. The following can be considered to be examples of suitable methods of contraception: implant, levonorgestrel-releasing intrauterine system, medroxyprogesterone acetate depot, tubal sterilization, sexual intercourse with a vasectomised male partner only (vasectomy must be confirmed by two negative semen analyses) and ovulation inhibitory progesterone-only pills (i.e. desogestrel).

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

Coadministration has not been studied. Etonogestrel is metabolised by CYP3A4. Pomalidomide does not inhibit or induce CYPs. However, coadministration of combined oral contraception is contraindicated with pomalidomide. The potential impact of pomalidomide on the pharmacokinetics of combined oral contraceptives has not been clinically evaluated, but the effect of oral contraceptives can be reduced by the registered comedication, dexamethasone. An increased risk of venous thromboembolism was observed in patients with multiple myeloma taking pomalidomide, dexamethasone and combined oral contraception. Therefore, a switch to another effective contraception method is recommended. The risk of venous thromboembolism continues for 4-6 weeks after discontinuing combined oral contraception. The following can be considered to be examples of suitable methods of contraception: implant, levonorgestrel-releasing intrauterine system, medroxyprogesterone acetate depot, tubal sterilization, sexual intercourse with a vasectomised male partner only (vasectomy must be confirmed by two negative semen analyses) and ovulation inhibitory progesterone-only pills (i.e. desogestrel).

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

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

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. Pomalidomide does not inhibit or induce UGTs.

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

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

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. Pomalidomide 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. Pomalidomide does not inhibit or induce CYPs.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Finasteride is metabolised by CYP3A4. Pomalidomide does not inhibit or induce 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. Flecainide is metabolised mainly via CYP2D6, with a proportion (approximately 30%) of the parent drug also renally eliminated unchanged. Pomalidomide does not interact with this metabolic or elimination pathway.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Flucloxacillin is mainly renally eliminated partly by glomerular filtration and partly by active secretion via OAT1. Pomalidomide does not interfere with this elimination pathway. Furthermore, flucloxacillin has shown to induce CYP3A4, but this is unlikely to be clinically relevant.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fluconazole is cleared primarily by renal excretion. Pomalidomide does not interfere with this elimination pathway. Fluconazole is also an inhibitor of CYPs 3A4 (moderate), 2C9 (moderate) and 2C19 (strong). Concentrations of pomalidomide may slightly increase due to inhibition of CYP3A4. However, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inhibitor, ketoconazole (400 mg twice daily), increased pomalidomide mean AUC and Cmax by 18.8% and 7.3%, respectively. Therefore, a clinically relevant effect is not expected with fluconazole. No a priori dose adjustment for pomalidomide is necessary.

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

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

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. Pomalidomide does not inhibit or induce CYPs.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fluoxetine is metabolised by CYP2D6 and CYP2C9, and to a lesser extent by CYP2C19 and CYP3A4 to form norfluoxetine. Pomalidomide does not inhibit or induce CYPs.

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

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. Pomalidomide does not inhibit or induce CYPs.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fluticasone is metabolised by CYP3A4. Pomalidomide does not inhibit or induce CYPs. Note: A clinically significant interaction is also unlikely with the topical use of fluticasone.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fluvastatin is mainly metabolised by CYP2C9 (75%) and to a lesser extent by CYP3A4 (20%) and CYP2C8 (5%). Fluvastatin is also a potential inhibitor of CYP2C9. Pomalidomide does not interact with this pathway.

Coadministration is not recommended. Fluvoxamine is metabolised mainly by CYP2D6 and to a lesser extent by CYP1A2. Pomalidomide does not inhibit or induce CYPs. Fluvoxamine is also an inhibitor of CYPs 1A2, 2C19, 3A4, 2C9. Concentrations of pomalidomide may increase due to inhibition of CYP1A2 and CYP3A4. Coadministration of pomalidomide (4 mg single dose) and fluvoxamine (50 mg twice daily), plus the CYP3A4 inhibitor, ketoconazole (200 mg twice daily), increased pomalidomide AUC and Cmax by 145.7% and 106.7%, respectively, when compared to pomalidomide alone. In a second study the contribution of a CYP1A2 inhibitor alone was assessed. Coadministration of pomalidomide (4 mg single dose) and fluvoxamine (50 mg twice daily) increased pomalidomide mean exposure by 125% compared to pomalidomide alone. Therefore, coadministration with fluvoxamine is not recommended. Selection of an alternate concomitant medicinal product with no or minimal potential to inhibit CYP1A2 should be considered. If coadministration is unavoidable, the dose of pomalidomide needs to be reduced by 50%. Close monitoring for pomalidomide toxicity is recommended. Monitor pomalidomide concentrations, if available.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fondaparinux does not undergo cytochrome metabolism but is eliminated predominantly renally. Pomalidomide is unlikely to 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 CYP450 and UGT enzymes catalyse the transformation the potential for a pharmacokinetic interaction is low. Furthermore, pomalidomide does not inhibit or induce CYPs or UGTs.

Coadministration has not been studied. Fosaprepitant is rapidly, almost completely, converted to the active metabolite aprepitant. Aprepitant is mainly metabolised by CYP3A4 and to a lesser extent by CYP1A2 and CYP2C19. Pomalidomide does not inhibit or induce CYPs. However, during treatment aprepitant is a weak-moderate inhibitor of CYP3A4 and a weak inhibitor of CYP2C9. After treatment aprepitant is an inducer of CYP3A4, CYP2C9 (weak) and UGT (weak). Pomalidomide concentrations may slightly alter during and after treatment with aprepitant due to CYP3A4 induction and inhibition. However, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inhibitor, ketoconazole (400 mg twice daily), increased pomalidomide mean AUC and Cmax by 18.8% and 7.3%, respectively. A clinically relevant effect is not expected during fosaprepitant treatment. Furthermore, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inducer, carbamazepine (200mg twice daily), decreased pomalidomide AUC and Cmax by 20% and 25%, respectively. A clinically relevant effect is not expected after fosaprepitant treatment. No a priori dose adjustment for pomalidomide is necessary but monitoring of pomalidomide efficacy may be required.

Coadministration has not been studied. Fosphenytoin is rapidly converted to the active metabolite phenytoin. Phenytoin is mainly metabolised by CYP2C9 and to a lesser extent by CYP2C19. Pomalidomide does not interact with this metabolic pathway. Phenytoin is also a strong inducer of CYP3A4, UGT and P-gp. Concentrations of pomalidomide may slightly decrease due to induction of CYP3A4 and P-gp. However, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inducer, carbamazepine (200mg twice daily), decreased pomalidomide AUC and Cmax by 20% and 25%, respectively. Therefore, a clinically significant effect is not expected with phenytoin. No a priori dose adjustment for pomalidomide is necessary, but monitoring of pomalidomide efficacy may be required.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Furosemide is glucuronidated mainly in the kidney (UGT1A9) and to a lesser extent by in the liver (UGT1A1). A large proportion of furosemide is also eliminated unchanged renally (via OATs). In vitro data indicate that furosemide is also an inhibitor of OAT1/OAT3. Pomalidomide does not interfere with this elimination pathway.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Gabapentin is cleared mainly by glomerular filtration. Pomalidomide 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. Gemfibrozil is also an inhibitor of CYP2C8 (strong), OATP1B1 and OAT3. Furthermore, in vitro data indicate gemfibrozil to be a strong inhibitor of CYP2C9 but in vivo data showed no clinically relevant effect on CYP2C9. Pomalidomide 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. Pomalidomide does not interfere with this elimination pathway.

Coadministration has not been studied. Gestodene is metabolised by CYP3A4 and to a lesser extent by CYP2C9 and CYP2C19. Pomalidomide does not inhibit or induce CYPs. However, coadministration of combined oral contraception is contraindicated with pomalidomide. The potential impact of pomalidomide on the pharmacokinetics of combined oral contraceptives has not been clinically evaluated, but the effect of oral contraceptives can be reduced by the registered comedication, dexamethasone. An increased risk of venous thromboembolism was observed in patients with multiple myeloma taking pomalidomide, dexamethasone and combined oral contraception. Therefore, a switch to another effective contraception method is recommended. The risk of venous thromboembolism continues for 4-6 weeks after discontinuing combined oral contraception. The following can be considered to be examples of suitable methods of contraception: implant, levonorgestrel-releasing intrauterine system, medroxyprogesterone acetate depot, tubal sterilization, sexual intercourse with a vasectomised male partner only (vasectomy must be confirmed by two negative semen analyses) and ovulation inhibitory progesterone-only pills (i.e. desogestrel).

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. Pomalidomide does not inhibit or induce CYPs.

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. Pomalidomide does not inhibit or induce CYPs.

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

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

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. Pomalidomide does not inhibit of induce CYPs or P-gp.

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 pomalidomide. However, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inhibitor, ketoconazole (400 mg twice daily), increased pomalidomide mean AUC and Cmax by 18.8% and 7.3%, respectively. Therefore, a clinically relevant effect is not expected with grapefruit juice. No a priori dose adjustment for pomalidomide is necessary.

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

Coadministration has not been studied. Less than 1% of a griseofulvin dose is excreted unchanged via the kidneys. Pomalidomide does not interfere with this elimination pathway. Griseofulvin is also a liver microsomal enzyme inducer and may lower plasma levels, and therefore reduce the efficacy of concomitantly administered medicinal products that are metabolised by CYP3A4, such as pomalidomide. However, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inducer, carbamazepine (200mg twice daily), decreased pomalidomide AUC and Cmax by 20% and 25%, respectively. Therefore, a clinically significant effect is not expected with pomalidomide. No a priori dose adjustment for pomalidomide is necessary, but monitoring of pomalidomide efficacy may be required.

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

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. Pomalidomide 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. Pomalidomide does not interfere with this metabolic pathway. Although in vitro studies suggest 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 pomalidomide. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Hydrochlorothiazide is not metabolised but is cleared by the kidneys via OAT1. In vitro data indicate that hydrochlorothiazide is unlikely to inhibit OAT1 in the range of clinically significant. 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. Pomalidomide does not interfere with this elimination pathway.

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

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

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. Pomalidomide does not inhibit or induce UGTs.

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

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. Pomalidomide does not interact with this metabolic pathway.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction. Ibandronic acid is not metabolised but 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. Pomalidomide does not inhibit or induce CYPs or UGTs.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Imipenem/cilastatin are eliminated by glomerular filtration and to a lesser extent by active tubular secretion via OAT3. Pomalidomide does not interfere with this elimination pathway.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Indapamide is extensively metabolised by CYPs. Pomalidomide does not inhibit or induce 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 pharmacokinetic interaction is unlikely. However, due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.

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

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. Pomalidomide 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). Metabolites are excreted via bile (~80%) and urine (~20%). Pomalidomide does not inhibit or induce CYPs or UGTs.

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. Pomalidomide 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. Pomalidomide does not inhibit or induce CYPs.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Itraconazole is primarily metabolised by CYP3A4. Pomalidomide does not inhibit or induce CYPs. Itraconazole is also an inhibitor of CYP3A4 (strong), CYP2C9 (weak), P-gp and BCRP. Concentrations of pomalidomide may slightly increase due to inhibition of CYP3A4. However, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inhibitor, ketoconazole (400 mg twice daily), increased pomalidomide mean AUC and Cmax by 18.8% and 7.3%, respectively. Therefore, a clinically relevant effect is not expected with itraconazole. No a priori dose adjustment for pomalidomide is necessary.

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

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. Pomalidomide does not interfere with this elimination pathway.

Ketoconazole is a substrate of CYP3A4. Pomalidomide does not inhibit or induce CYPs. Ketoconazole is also an inhibitor of CYP3A4 (strong) and P-gp, and may slightly increase concentrations of pomalidomide. However, coadministration of pomalidomide (4 mg single dose) and ketoconazole (400 mg twice daily) increased pomalidomide mean AUC and Cmax by 18.8% and 7.3%, respectively. Therefore, a clinically relevant interaction is not expected. No a priori dose adjustment for pomalidomide is necessary.

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). Pomalidomide does not inhibit or induce UGTs.

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

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. Pomalidomide does not interact with this pathway.

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

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Less than 14% of a dose of levocetirizine is metabolised. Levocetirizine is mainly eliminated unchanged in the urine through both glomerular filtration and tubular secretion (possibly via OCT2). Pomalidomide is unlikely to interact 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). Pomalidomide does not interact with this elimination pathway.

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

Coadministration has not been studied. Levonorgestrel is metabolised by CYP3A4 and is glucuronidated to a minor extent. Pomalidomide does not inhibit or induce CYPs or UGTs. However, coadministration of combined oral contraception is contraindicated with pomalidomide. The potential impact of pomalidomide on the pharmacokinetics of combined oral contraceptives has not been clinically evaluated, but the effect of oral contraceptives can be reduced by the registered comedication, dexamethasone. An increased risk of venous thromboembolism was observed in patients with multiple myeloma taking pomalidomide, dexamethasone and combined oral contraception. Therefore, a switch to another effective contraception method is recommended. The risk of venous thromboembolism continues for 4-6 weeks after discontinuing combined oral contraception. The following can be considered to be examples of suitable methods of contraception: implant, levonorgestrel-releasing intrauterine system, medroxyprogesterone acetate depot, tubal sterilization, sexual intercourse with a vasectomised male partner only (vasectomy must be confirmed by two negative semen analyses) and ovulation inhibitory progesterone-only pills (i.e. desogestrel).

Coadministration has not been studied. Levonorgestrel is metabolised by CYP3A4 and is glucuronidated to a minor extent. Pomalidomide does not inhibit or induce CYPs or UGTs. However, coadministration of combined oral contraception is contraindicated with pomalidomide. The potential impact of pomalidomide on the pharmacokinetics of combined oral contraceptives has not been clinically evaluated, but the effect of oral contraceptives can be reduced by the registered comedication, dexamethasone. An increased risk of venous thromboembolism was observed in patients with multiple myeloma taking pomalidomide, dexamethasone and combined oral contraception. Therefore, a switch to another effective contraception method is recommended. The risk of venous thromboembolism continues for 4-6 weeks after discontinuing combined oral contraception. The following can be considered to be examples of suitable methods of contraception: implant, levonorgestrel-releasing intrauterine system, medroxyprogesterone acetate depot, tubal sterilization, sexual intercourse with a vasectomised male partner only (vasectomy must be confirmed by two negative semen analyses) and ovulation inhibitory progesterone-only pills (i.e. desogestrel).

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. Pomalidomide does not interact 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. Pomalidomide does not inhibit or induce CYPs.

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 metabolic pathway. Linagliptin is also a substrate of P-gp. Pomalidomide does not interfere with this metabolic or elimination pathway. Furthermore, linagliptin is an inhibitor of CYP3A4 and may slightly increase concentrations of pomalidomide. However, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inhibitor, ketoconazole (400 mg twice daily), increased pomalidomide mean AUC and Cmax by 18.8% and 7.3%, respectively. Therefore, a clinically relevant effect is not expected with linagliptin. No a priori dose adjustment for pomalidomide is necessary. No a priori dose adjustment for pomalidomide is necessary.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Linezolid undergoes non-CYP mediated metabolism. Pomalidomide 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. Liraglutide is degraded by endogenous endopeptidases. Pomalidomide does not interfere with this metabolic pathway.

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

Coadministration of live vaccines (such as BCG vaccine; measles, mumps and rubella vaccines; varicella vaccines; typhoid vaccines; rotavirus vaccines; yellow fever vaccines; oral polio vaccine) has not been studied. In patients, who are receiving cytotoxics or other immunosuppressant drugs, use of live vaccines for immunisation is contraindicated. If coadministration is judged clinically necessary, use with extreme caution since generalised infections can occur.

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. Pomalidomide does not inhibit or induce CYPs.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Lorazepam undergoes non-CYP mediated metabolism. Pomalidomide 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. Lormetazepam is mainly glucuronidated. Pomalidomide does not inhibit or induce UGTs.

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. Pomalidomide does not inhibit or induce CYPs.

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

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. Pomalidomide does not inhibit or induce CYPs.

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. Pomalidomide does not interfere with this elimination pathway.

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

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

Coadministration has not been studied. Medroxyprogesterone is metabolised by CYP3A4. Pomalidomide does not inhibit or induce CYPs. However, coadministration of combined oral contraception is contraindicated with pomalidomide. The potential impact of pomalidomide on the pharmacokinetics of combined oral contraceptives has not been clinically evaluated, but the effect of oral contraceptives can be reduced by the registered comedication, dexamethasone. An increased risk of venous thromboembolism was observed in patients with multiple myeloma taking pomalidomide, dexamethasone and combined oral contraception. Therefore, a switch to another effective contraception method is recommended. The risk of venous thromboembolism continues for 4-6 weeks after discontinuing combined oral contraception. The following can be considered to be examples of suitable methods of contraception: implant, levonorgestrel-releasing intrauterine system, medroxyprogesterone acetate depot, tubal sterilization, sexual intercourse with a vasectomised male partner only (vasectomy must be confirmed by two negative semen analyses) and ovulation inhibitory progesterone-only pills (i.e. desogestrel).

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. Pomalidomide does not inhibit or induce CYPs or UGTs.

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 (probably via OCT2). Pomalidomide does not interact with this elimination pathway.

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 OAT3>OAT1. Pomalidomide 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. Pomalidomide does not interfere with this pathway.

Coadministration has not been studied. Metamizole is metabolised by hydrolysis to the active metabolite MAA in the gastrointestinal tract. It is metabolised in serum and excreted via urine (90%) and faeces (10%). Pomalidomide does not interact with this metabolic pathway. Furthermore, metamizole is an inducer of CYP3A4 and may decrease concentrations of CYP3A4. However, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inducer, carbamazepine (200 mg twice daily), decreased pomalidomide AUC and Cmax by 20% and 25%, respectively. Therefore, a clinically relevant effect is not expected with metamizole. No a priori dose adjustment for pomalidomide is necessary but monitoring of pomalidomide efficacy may be required.

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 (via OCT2, MATE1 and MATE2). Pomalidomide does not interact with this elimination pathway.

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

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 pomalidomide or to be altered by pomalidomide.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Methylphenidate is not metabolised by CYPs to a clinically relevant extent and does not inhibit or induce CYPs.

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

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). Pomalidomide does not inhibit of induce CYPs.

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

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Metronidazole is eliminated via glomerular filtration. Pomalidomide does not interfere with this elimination pathway. Elevated plasma concentrations have been reported for some CYP3A substrates (e.g. tacrolimus, ciclosporin) with metronidazole, but metronidazole did not increase concentrations of several CYP3A probe drugs (e.g. midazolam, alprazolam). Since the mechanism of the interaction with CYP3A has yet to be identified, an interaction with pomalidomide cannot be excluded. However, coadministration of pomalidomide (4mg single dose) and the strong CYP3A4 inhibitor, ketoconazole (400 mg twice daily), increased pomalidomide mean AUC and Cmax by nearly 18.8% and 7.3%, respectively. Therefore, a clinically relevant interaction is not expected with metronidazole. No a priori dose adjustment for pomalidomide is necessary.

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

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Miconazole is extensively metabolised by the liver. Pomalidomide does not interfere with this metabolic pathway. Miconazole is also an inhibitor of CYP2C9 (moderate) and CYP3A4 (strong). Concentrations of pomalidomide may slightly increase due to inhibition of CYP3A4. However, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inhibitor, ketoconazole (400 mg twice daily), increased pomalidomide mean AUC and Cmax by 18.8% and 7.3%, respectively. Therefore, a clinically relevant effect is not expected with micoonazole. No a priori dose adjustment for pomalidomide is necessary. Note: after dermal application miconazole is only minimally absorbed. Therefore, no clinical relevant interaction is expected.

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

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

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%). Pomalidomide 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. Mirtazapine is metabolised to 8-hydroxymirtazapine by CYP2D6 and CYP1A2, and to N-desmethylmirtazapine mainly by CYP3A4. Pomalidomide does not inhibit or induce CYPs.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Mometasone is metabolised by CYP3A4. Pomalidomide does not inhibit or induce CYPs. Note: No clinically relevant interaction are expected with the topical use of mometasone.

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

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 by, to the pharmacologically active morphine-6-glucuronide (UGT2B7>UGT1A1). Morphine is also a substrate of P-gp. Pomalidomide does not inhibit or induce CYPs or P-gp.

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

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Nadroparin is renally excreted renally by a nonsaturable mechanism. Pomalidomide does not interact with this metabolic 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. Pomalidomide does not interact with this metabolic 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. Pomalidomide does not inhibit or induce UGTs or CYPs.

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%). Pomalidomide does not inhibit or induce CYPs.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Nefazodone is metabolised mainly by CYP3A4. Pomalidomide does not inhibit or induce CYPs. Nefazodone is also a strong inhibitor of CYP3A4, and may slightly increase concentrations of pomalidomide. However, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inhibitor, ketoconazole (400 mg twice daily), increased pomalidomide mean AUC and Cmax by 18.8% and 7.3%, respectively. Therefore, a clinically relevant effect is not expected with nefazodone. No a priori dose adjustment for pomalidomide is necessary.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Nicardipine is metabolised mainly by CYP3A4 and to a lesser extent by CYP2D6 and CYP2C8. Pomalidomide does not inhibit or induce CYPs. Nicardipine is also a weak inhibitor of CYP3A4 and may increase pomalidomide concentrations. However, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inhibitor, ketoconazole (400 mg twice daily), increased pomalidomide mean AUC and Cmax by 18.8% and 7.3%, respectively. Therefore, a clinically relevant effect is not expected with nicardipine. No a priori dose adjustment for pomalidomide is necessary.

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

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

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. Pomalidomide does not inhibit or induce CYPs.

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

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

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%). Pomalidomide does not interfere with this metabolic or elimination pathway.

Coadministration has not been studied. Norelgestromin is metabolised to norgestrel (possibly by CYP3A4). Pomalidomide does not inhibit or induce CYPs. However, coadministration of combined oral contraception is contraindicated with pomalidomide. The potential impact of pomalidomide on the pharmacokinetics of combined oral contraceptives has not been clinically evaluated, but the effect of oral contraceptives can be reduced by the registered comedication, dexamethasone. An increased risk of venous thromboembolism was observed in patients with multiple myeloma taking pomalidomide, dexamethasone and combined oral contraception. Therefore, a switch to another effective contraception method is recommended. The risk of venous thromboembolism continues for 4-6 weeks after discontinuing combined oral contraception. The following can be considered to be examples of suitable methods of contraception: implant, levonorgestrel-releasing intrauterine system, medroxyprogesterone acetate depot, tubal sterilization, sexual intercourse with a vasectomised male partner only (vasectomy must be confirmed by two negative semen analyses) and ovulation inhibitory progesterone-only pills (i.e. desogestrel).

Coadministration has not been studied. Norethindrone is extensively biotransformed, first by reduction and then by sulfate and glucuronide conjugation. Pomalidomide does not interact with this metabolic pathway. However, coadministration of combined oral contraception is contraindicated with pomalidomide. The potential impact of pomalidomide on the pharmacokinetics of combined oral contraceptives has not been clinically evaluated, but the effect of oral contraceptives can be reduced by the registered comedication, dexamethasone. An increased risk of venous thromboembolism was observed in patients with multiple myeloma taking pomalidomide, dexamethasone and combined oral contraception. Therefore, a switch to another effective contraception method is recommended. The risk of venous thromboembolism continues for 4-6 weeks after discontinuing combined oral contraception. The following can be considered to be examples of suitable methods of contraception: implant, levonorgestrel-releasing intrauterine system, medroxyprogesterone acetate depot, tubal sterilization, sexual intercourse with a vasectomised male partner only (vasectomy must be confirmed by two negative semen analyses) and ovulation inhibitory progesterone-only pills (i.e. desogestrel).

Coadministration has not been studied. Norgestimate is rapidly deacetylated to the active metabolite which is further metabolised via CYP450. Pomalidomide does not interact with this metabolic pathway. However, coadministration of combined oral contraception is contraindicated with pomalidomide. The potential impact of pomalidomide on the pharmacokinetics of combined oral contraceptives has not been clinically evaluated, but the effect of oral contraceptives can be reduced by the registered comedication, dexamethasone. An increased risk of venous thromboembolism was observed in patients with multiple myeloma taking pomalidomide, dexamethasone and combined oral contraception. Therefore, a switch to another effective contraception method is recommended. The risk of venous thromboembolism continues for 4-6 weeks after discontinuing combined oral contraception. The following can be considered to be examples of suitable methods of contraception: implant, levonorgestrel-releasing intrauterine system, medroxyprogesterone acetate depot, tubal sterilization, sexual intercourse with a vasectomised male partner only (vasectomy must be confirmed by two negative semen analyses) and ovulation inhibitory progesterone-only pills (i.e. desogestrel).

Coadministration has not been studied. Norgestrel is a racemic mixture with levonorgestrel being biologically active. Levonorgestrel is metabolised by CYP3A4 and is glucuronidated to a minor extent. Pomalidomide does not inhibit or induce CYPs or UGTs. However, coadministration of combined oral contraception is contraindicated with pomalidomide. The potential impact of pomalidomide on the pharmacokinetics of combined oral contraceptives has not been clinically evaluated, but the effect of oral contraceptives can be reduced by the registered comedication, dexamethasone. An increased risk of venous thromboembolism was observed in patients with multiple myeloma taking pomalidomide, dexamethasone and combined oral contraception. Therefore, a switch to another effective contraception method is recommended. The risk of venous thromboembolism continues for 4-6 weeks after discontinuing combined oral contraception. The following can be considered to be examples of suitable methods of contraception: implant, levonorgestrel-releasing intrauterine system, medroxyprogesterone acetate depot, tubal sterilization, sexual intercourse with a vasectomised male partner only (vasectomy must be confirmed by two negative semen analyses) and ovulation inhibitory progesterone-only pills (i.e. desogestrel).

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

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 (OAT/OCT). Pomalidomide does not interfere with this elimination 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). Pomalidomide does not inhibit or induce CYPs or UGTs.

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. Pomalidomide does not interfere with this elimination pathway.

Coadministration has not been studied but is not recommended. Omeprazole is mainly metabolised by CYP2C19 and to a lesser extent by CYP3A4. Pomalidomide does not inhibit or induce CYPs. Omeprazole is also an inducer of CYP1A2 and inhibits CYP2C19. Concentrations of pomalidomide may decrease due to induction of CYP1A2. Coadministration is not recommended as decreased exposure may lead to decreased efficacy. Coadministration of CYP1A2 inducers with pomalidomide has not been studied and the clinical relevance of this interaction is unknown. Selection of an alternate concomitant medication with no or minimal potential to induce CYP1A2 is recommended. If coadministration is unavoidable, monitor pomalidomide efficacy. Monitor pomalidomide concentrations, if available.

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

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

Coadministration has not been studied. Oxcarbazepine is extensively metabolised to the active metabolite monohydroxyderivate (MHD) through cystolic enzymes. Pomalidomide does not interact with this metabolic pathway. Both oxcarbazepine and MHD are inducers of CYP3A4 (moderate) and CYP3A5, and are inhibitors of CYP2C19. Concentrations of pomalidomide may slightly decrease due to induction of CYP3A4. However, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inducer, carbamazepine (200mg twice daily), decreased pomalidomide AUC and Cmax by 20% and 25%, respectively. Therefore, a clinically significant effect is not expected with oxcarbazepine. No a priori dose adjustment for pomalidomide is necessary, but monitoring of pomalidomide efficacy may be required.

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

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

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

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

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

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

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. Pomalidomide does not interfere 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, by oxidation (CYPs 2E1 (major), 1A2, 3A4 and 2D6). Pomalidomide does not inhibit or induce UGTs or CYPs.

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

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

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). Pomalidomide does not interfere with this pathway.

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. Pomalidomide does not inhibit or induce CYPs or FMO3.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Perindopril is hydrolysed to the active metabolite perindoprilat and is metabolised to other inactive metabolites. Elimination occurs predominantly via the urine (possibly via OAT). Pomalidomide does not interact with this elimination pathway.

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

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. Pomalidomide does not inhibit or induce CYPs.

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. Pomalidomide does not interfere with this metabolic pathway.

Coadministration has not been studied. Phenobarbital is metabolised by CYP2C19 and CYP2C9 (major), and to a lesser extent by CYP2E1. Pomalidomide does not inhibit or induce CYPs. Phenobarbital is also a strong inducer of CYPs 3A4, 2C9, 2C8 and UGTs. Concentrations of pomalidomide may slightly decrease due to induction of CYP3A4. However, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inducer, carbamazepine (200mg twice daily), decreased pomalidomide AUC and Cmax by 20% and 25%, respectively. Therefore, a clinically significant effect is not expected with phenobarbital. No a priori dose adjustment for pomalidomide is necessary, but monitoring of pomalidomide efficacy may be required.

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

Coadministration has not been studied. Phenytoin is mainly metabolised by CYP2C9 and to a lesser extent by CYP2C19. Pomalidomide does not inhibit or induce CYPs. Phenytoin is also a strong inducer of CYP3A4, UGT and P-gp. Concentrations of pomalidomide may slightly decrease due to induction of CYP3A4. However, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inducer, carbamazepine (200mg twice daily), decreased pomalidomide AUC and Cmax by 20% and 25%, respectively. Therefore, a clinically significant effect is not expected with phenytoin. No a priori dose adjustment for pomalidomide is necessary, but monitoring of pomalidomide efficacy may be required.

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. Pomalidomide does not inhibit or induce CYPs.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Pindolol is partly metabolised to hydroxymetabolites (possibly via CYP2D6) and partly eliminated unchanged in the urine (possibly via OCT2). Pomalidomide does not inhibit or induce CYPs or OCTs.

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

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

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

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Posaconazole is primarily metabolised by UGTs and is a substrate of P-gp. Pomalidomide does not inhibit or induce UGTs or P-gp. Posaconazole is also a strong inhibitor of CYP3A4 and may slightly increase concentrations of pomalidomide. However, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inhibitor, ketoconazole (400 mg twice daily), increased pomalidomide mean AUC and Cmax by 18.8% and 7.3%, respectively. Therefore, a clinically relevant effect is not expected with posaconazole. No a priori dose adjustment for pomalidomide is necessary.

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

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. Pomalidomide does not inhibit or induce CYPs.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Pravastatin is minimally metabolised (via CYP3A4) and is substrate of OATP1B1. Pomalidomide does not inhibit or induce CYPs or OATP1B1.

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. Pomalidomide is unlikely to 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. Pomalidomide does not inhibit or induce CYPs.

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. Pomalidomide does not interfere with this metabolic pathway.

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). Pomalidomide does not interfere with this elimination pathway.

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

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

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

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

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Pyrazinamide is mainly metabolised by xanthine oxidase. Pomalidomide 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. Pomalidomide does not inhibit or induce CYPs.

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. Pomalidomide does not interact elimination with this pathway.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Quinidine is mainly metabolised by CYP3A4 and to a lesser extent by CYP2C9 and CYP2E1. Quinidine is also a substrate of P-gp and an inhibitor of CYP2D6 (strong), CYP3A4 (weak) and P-gp (moderate). Pomalidomide does not interact with this pathway.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Rabeprazole is mainly metabolised via non-enzymatic reduction and to a lesser extent by CYP2C19 and CYP3A4. Pomalidomide does not interfere with this metabolic pathway.

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

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ranolazine is primarily metabolised by CYP3A4 and to a lesser extent by CYP2D6. Ranolazine is also substrate of P-gp. Pomalidomide does not inhibit or induce CYPs or P-gp. Furthermore, ranolazine is a weak inhibitor of P-gp, CYP3A4 and CYP2D6. Concentrations of pomalidomide may slightly increase due to inhibition of CYP3A4. However, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inhibitor, ketoconazole (400 mg twice daily), increased pomalidomide mean AUC and Cmax by 18.8% and 7.3%, respectively. Therefore, a clinically relevant effect is not expected on pomalidomide exposure. No a priori dose adjustment for pomalidomide is necessary.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Reboxetine is metabolised by CYP3A4. In vitro data indicate reboxetine to be a weak inhibitor of CYP3A4 but in vivo data showed no inhibitory effect on CYP3A4. Pomalidomide does not interact with this metabolic pathway. 

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

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. Pomalidomide 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. Rifabutin is metabolised by CYP3A and via deacetylation. Pomalidomide does not interact with this metabolic pathway. Rifabutin is also a strong CYP3A4 and P-gp inducer, and may decrease concentrations of pomalidomide. However, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inducer, carbamazepine (200mg twice daily), decreased pomalidomide AUC and Cmax by 20% and 25%, respectively. Therefore, a clinically significant effect is not expected with rifabutin. No a priori dose adjustment for pomalidomide is necessary, but monitoring of pomalidomide efficacy may be required.

Coadministration has not been studied. Rifampicin is metabolised via deacetylation. Pomalidomide does not interfere with this metabolic pathway. Rifampicin is also a strong CYP3A4 and P-gp inducer and may decrease concentrations of pomalidomide. However, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inducer, carbamazepine (200mg twice daily), decreased pomalidomide AUC and Cmax by 20% and 25%, respectively. Therefore, a clinically significant effect is not expected with rifampicin. No a priori dose adjustment for pomalidomide is necessary, but monitoring of pomalidomide efficacy may be required.

Coadministration has not been studied. Rifapentine is metabolised via deacetylation. Pomalidomide does not interfere with this metabolic pathway. Rifapentine is also a strong CYP3A4, CYP2C8 and P-gp inducer. Concentrations of pomalidomide may slightly decrease due to induction of CYP3A4 and P-gp. However, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inducer, carbamazepine (200mg twice daily), decreased pomalidomide AUC and Cmax by 20% and 25%, respectively. Therefore, a clinically significant effect is not expected with rifapentine. No a priori dose adjustment for pomalidomide is necessary, but monitoring of pomalidomide efficacy may be required.

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

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

Coadministration has not been studied but based on the 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 (by P-gp and BCRP). Pomalidomide does not interact with this metabolic or elimination pathway.

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

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

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. Pomalidomide 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. Pomalidomide does not inhibit or induce CYPs.

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

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

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

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. Pomalidomide does not inhibit or induce CYPs.

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. Pomalidomide does not inhibit or induce CYPs.

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

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Sitagliptin is primarily eliminated in urine as unchanged drug (active secretion by OAT3, OATP4C1 and P-gp) and metabolism by CYP3A4 represents a minor metabolic pathway. Pomalidomide does not interact with this metabolic or elimination pathway.

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

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

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. Pomalidomide does not interact with this elimination pathway.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Stanozolol undergoes hepatic metabolism. Pomalidomide does not interact with this metabolic pathway.

Coadministration has not been studied. St John’s Wort is a CYP3A4 and P-gp inducer. Concentrations of pomalidomide may slightly decrease due to induction of CYP3A4. However, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inducer, carbamazepine (200mg twice daily), decreased pomalidomide AUC and Cmax by 20% and 25%, respectively. Therefore, a clinically significant effect is not expected with St John’s Wort. No a priori dose adjustment for pomalidomide is necessary, but monitoring of pomalidomide efficacy may be required.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Streptomycin is eliminated by glomerular filtration. Pomalidomide does not interact 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. Pomalidomide does not inhibit or induce CYPs.

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. Pomalidomide does not interfere with this elimination pathway.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Tacrolimus is metabolised mainly by CYP3A4. Pomalidomide does not inhibit or induce CYPs. Tacrolimus is also an inhibitor of CYP3A4 and OATP1B1 in vitro but produced modest inhibition of CYP3A4 and OATP1B1 in the range of clinical concentrations. Tacrolimus could potentially increase pomalidomide concentrations due to CYP3A4 inhibition, although only to a modest extent. Coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inhibitor, ketoconazole (400 mg twice daily), increased pomalidomide mean AUC and Cmax by 18.8% and 7.3%, respectively. Therefore, a clinically relevant effect is not expected with tacrolimus. No a priori dose adjustment for pomalidomide is necessary. However, due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.

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

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. Pomalidomide does not inhibit or induce CYPs.

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. Pomalidomide does not interfere 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. Pomalidomide does not interact with this metabolic or elimination pathway. Telithromycin is also an inhibitor of CYP3A4 (strong) and P-gp, and may increase concentrations of pomalidomide. The clinical relevance of P-gp inhibition by telithromycin is unknown. Coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 and P-gp inhibitor, ketoconazole (400 mg twice daily), increased pomalidomide mean AUC and Cmax by 18.8% and 7.3%, respectively. Therefore, no clinically relevant effect is expected on pomalidomide exposure. No a priori dose adjustment for pomalidomide is necessary.

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

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Terbinafine is metabolised by CYPs 1A2, 2C9, 3A4 and to a lesser extent by CYP2C8 and CYP2C19. Pomalidomide does not inhibit or induce CYPs.

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

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. Pomalidomide does not interact with this elimination pathway.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Tiapride is excreted largely unchanged in urine. Pomalidomide 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 is metabolised by CYP3A4 and is a substrate of P-gp. Pomalidomide does not inhibit or induce CYPs or P-gp. Ticagrelor is also a weak inhibitor of CYP3A4 and may slightly increase concentrations of pomalidomide. However, coadministration of pomalidomide (4 mg single dose) and the strong CYP3A4 inhibitor, ketoconazole (400 mg twice daily), increased pomalidomide mean AUC and Cmax by 18.8% and 7.3%, respectively. Therefore, a clinically relevant effect is not expected with ticagrelor. No a priori dose adjustment for pomalidomide is necessary.

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. Pomalidomide does not inhibit or induce CYPs. Note: the systemic absorption of timolol after ocular administration is low. Therefore, a clinically relevant interaction via CYP2D6 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. Pomalidomide does not interfere 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 CYPs 2C8 and 2C19. Pomalidomide does not inhibit or induce CYPs.