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 microbial flora.

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 should be approached with caution. Alfentanil undergoes extensive CYP3A4 metabolism. Thalidomide does not inhibit or induce CYPs. However, thalidomide causes drowsiness and somnolence. Also, a thorough QT study with thalidomide has not been performed, therefore it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia. Due to the increased risk of additional sedative effects and bradycardia, coadministration with alfentanil should be approached with caution. If coadministration is clinically necessary, inform patients about the risks of coadministration. Dose reductions of alfentanil may be required. Closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Amiodarone is metabolised by CYP3A4 and CYP2C8. The major metabolite of amiodarone, desethylamiodarone, is an inhibitor of CYPs 3A4 (weak), 2C9 (moderate), 2D6 (moderate), 2C19 (weak), 1A1 (strong) and 2B6 (moderate) and P-gp (strong). Thalidomide does not interact with this pathway. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Furthermore, thalidomide has potential to induce bradycardia and coadministration with amiodarone should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG. Note: Due to the long half-life of amiodarone, interactions can be observed for several months after discontinuation of amiodarone.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Amitriptyline is metabolised predominantly by CYP2D6 and CYP2C19, with a small proportion metabolised by CYPs 3A4, 1A2 and 2C9. Thalidomide does not inhibit or induce CYPs. A thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with amitriptyline should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Astemizole is metabolised by CYPs 2D6, 2J2 and 3A4. Thalidomide does not inhibit or induce CYPs. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with astemizole should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Atenolol is mainly eliminated unchanged in the kidney, predominantly by glomerular filtration. Thalidomide is unlikely to interfere with this elimination pathway. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with atenolol should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

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. Thalidomide does not interact 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 pharmacokinetic interaction is unlikely. Azithromycin is mainly eliminated via biliary excretion; animal data suggest this may occur via P-gp and MRP2. Azithromycin is also an inhibitor of P-gp but the clinical relevance of P-gp inhibition by azithromycin is unknown. Thalidomide does not interact with this pathway. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with azithromycin should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Bedaquiline is metabolised by CYP3A4. Thalidomide does not inhibit or induce CYPs. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with bedaquiline should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Bepridil is metabolised by CYP2D6 (major) and CYP3A4. Thalidomide does not inhibit or induce CYPs. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with bepridil should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Bisoprolol is partly metabolised by CYP3A4 and CYP2D6, and partly eliminated unchanged in the urine. Thalidomide does not interact with this metabolic pathway. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with bisoprolol should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

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. Thalidomide is unlikely to interfere with these elimination pathways.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic 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. Thalidomide does not inhibit or induce CYPs or UGTs. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with carvedilol should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Chlorpromazine is metabolised mainly by CYP2D6, but also by CYP1A2. Thalidomide does not inhibit or induce CYPs. However, thalidomide causes drowsiness and somnolence. Also, a thorough QT study with thalidomide has not been performed, therefore it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia. Due to the increased risk of additional sedative effects and bradycardia, coadministration with chlorpromazine should be approached with caution. If coadministration is clinically necessary, inform patients about the risks of coadministration. Dose reductions of chlorpromazine may be required. Closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Ciprofloxacin is primarily eliminated unchanged in the kidneys by glomerular filtration and tubular secretion via OAT3. It is also metabolised and partially cleared through the bile and intestine. Ciprofloxacin is a weak to moderate inhibitor of CYP3A4 and a strong inhibitor of CYP1A2. Thalidomide does not interact with this pathway. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with ciprofloxacin should be approached with caution. If coadministration is unavoidable, monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Cisapride is metabolised by CYP3A4. Thalidomide does not inhibit or induce CYPs. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with cisapride should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Citalopram is metabolised by CYPs 2C19 (38%), 2D6 (31%) and 3A4 (31%). Thalidomide does not inhibit or induce CYPs. A thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with citalopram should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Clarithromycin is metabolised by CYP3A4 and is also an inhibitor of CYP3A4 (strong) and P-gp. Thalidomide does not interact with this pathway. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has a potential to induce bradycardia and coadministration with clarithromycin should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Clofazimine is largely excreted unchanged in the faeces. In vitro data suggest that clofazimine is a CYP3A4 inhibitor. Thalidomide does not interact with this pathway. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with clofazimine should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic 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. Thalidomide does not inhibit or induce CYPs. A thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with clomipramine should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

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. Thalidomide does not inhibit or induce CYPs. However, thalidomide causes drowsiness and somnolence. Also, a thorough QT study with thalidomide has not been performed, therefore it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia. Due to the increased risk of additional sedative effects and bradycardia, coadministration with clozapine should be approached with caution. If coadministration is clinically necessary, inform patients about the risks of coadministration. Dose reductions of clozapine may be required. Closely monitor heart rate and ECG. Furthermore, 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. Desipramine is metabolised by CYP2D6. Thalidomide does not inhibit or induce CYPs. A thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with desipramine should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

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

Coadministration has been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Digoxin is eliminated renally via OATP4C1 and P-gp. Thalidomide does not inhibit or induce OATP4C1 or P-gp. Furthermore, coadministration of single dose digoxin and multiple doses of thalidomide did not change the pharmacokinetics of either drug. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has a potential to induce bradycardia and coadministration with digoxin should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Diltiazem is metabolised by CYP3A4 and CYP2D6. Diltiazem is also a moderate inhibitor of CYP3A4. Thalidomide does not interact with this pathway. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with diltiazem should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Diphenhydramine is mainly metabolised by CYP2D6 and to a lesser extent by CYPs 1A2, 2C9 and 2C19. Diphenhydramine is also a weak inhibitor of CYP2D6. Thalidomide does not interact with this pathway. However, thalidomide causes drowsiness and somnolence. Also, a thorough QT study with thalidomide has not been performed, therefore it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia. Due to the increased risk of additional sedative effects and bradycardia, coadministration with diphenhydramine should be approached with caution. If coadministration is clinically necessary, inform patients about the risks of coadministration. Dose reductions of diphenhydramine may be required. Closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Disopyramide is metabolised by CYP3A4 (25%) and 50% of the drug is eliminated unchanged in the urine. Thalidomide does not interact with this metabolic or elimination pathway. However, a thorough QT study with thalidomide has not been performed. Therefore, it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has a potential to induce bradycardia and coadministration with disopyramide should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic 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%). Thalidomide does not inhibit or induce CYPs or UGTs. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with dolasetron should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Domperidone is mainly metabolised by CYP3A4. Thalidomide does not inhibit or induce CYPs. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with domperidone should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Erythromycin is a substrate of CYP3A4 and P-gp. Erythromycin is also an inhibitor of CYP3A4 (moderate) and P-gp. Thalidomide does not interact with this pathway. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with erythromycin should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Escitalopram is metabolised by CYPs 2C19 (37%), 2D6 (28%) and 3A4 (35%) to form N-desmethylescitalopram. Thalidomide does not inhibit or induce CYPs. A thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with escitalopram should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Fentanyl undergoes extensive CYP3A4 metabolism. Thalidomide does not inhibit or induce CYPs. However, thalidomide causes drowsiness and somnolence. Also, a thorough QT study with thalidomide has not been performed, therefore it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia. Due to the increased risk of additional sedative effects and bradycardia, coadministration with fentanyl should be approached with caution, especially with sublingual fentanyl administration. If coadministration is clinically necessary, inform patients about the risks of coadministration. Dose reductions of fentanyl may be required. Closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Flecainide is metabolised mainly via CYP2D6, with a proportion (approximately 30%) of the parent drug also renally eliminated unchanged. Thalidomide does not interact with this metabolic pathway. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with flecainide should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Fluconazole is cleared primarily by renal excretion and is also an inhibitor of CYPs 3A4 (moderate), 2C9 (moderate) and 2C19 (strong). Thalidomide does not interact with this pathway. However, a thorough QT study with thalidomide has not been performed but it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with fluconazole should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Fluphenazine is metabolised by CYP2D6. Thalidomide does not inhibit or induce CYPs. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with fluphenazine should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Granisetron is metabolised by CYP3A4 and is a substrate of P-gp. Thalidomide does not inhibit or induce CYPs or P-gp. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with granisetron should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Haloperidol has a complex metabolism as it undergoes glucuronidation (UGTs 2B7>1A4 and 1A9), carbonyl reduction, as well as oxidative metabolism (CYP3A4 and CYP2D6). Thalidomide does not inhibit or induce CYPs or UGTs. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with haloperidol should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but care should be taken. Heparin is thought to be eliminated via the reticuloendothelial system. Thalidomide does not interact with this metabolic pathway. Heparin may be indicated to treat the increased risk of thrombosis due to thalidomide administration. However, the use of heparin with thalidomide may increase the risk of bleeding. Therefore, care should be taken. Advise patients to observe for signs and symptoms of bleeding (e.g. petechiae, epistaxes, gastrointestinal bleedings) or bruising if coadministered.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Hydrocodone is metabolised by CYP2D6 to hydromorphone and by CYP3A4 to norhydrocodone, both of which have analgesic effects. Thalidomide does not inhibit or induce CYPs. However, thalidomide causes drowsiness and somnolence, and due to the increased risk of additional sedative effects, coadministration with hydrocodone should be approached with caution. If coadministration is clinically necessary, inform patients about the risks of coadministration. Dose reductions of hydrocodone may be required.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Hydroxyzine is partly metabolised by alcohol dehydrogenase and partly by CYP3A4. Thalidomide does not interact with this pathway. However, thalidomide causes drowsiness and somnolence. Also, a thorough QT study with thalidomide has not been performed, therefore it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia. Due to the increased risk of additional sedative effects and bradycardia, coadministration with hydroxyzine should be approached with caution. If coadministration is clinically necessary, inform patients about the risks of coadministration. Dose reductions of hydroxyzine may be required. Closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Ibandronic acid is not metabolised but is cleared from the plasma by uptake into bone and elimination via renal excretion. 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 pharmacokinetic interaction is unlikely. Iloperidone is metabolised by CYP3A4 and CYP2D6. Thalidomide does not inhibit or induce CYPs. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with iloperidone should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Imipramine is metabolised by CYPs 3A4, 2C19 and 1A2 to desipramine. Imipramine and desipramine are both metabolised by CYP2D6. Thalidomide does not inhibit or induce CYPs. A thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with imipramine should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Indapamide is extensively metabolised by CYP450s. OAT1/3 are the major transporters of loop and thiazide diuretics. Secretion of these diuretics into the urinary tract by transporters in the proximal tubular cells is necessary for the diuretic effect in later tubule segments. Thalidomide does not inhibit or induce CYPs or OATs. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with indapamide should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Ivabradine is metabolised by CYP3A4. Thalidomide does not inhibit or induce CYPs. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with ivabradine should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Ketoconazole is a substrate of CYP3A4 and also an inhibitor of CYP3A4 (strong) and P-gp. Thalidomide does not interact with this pathway. However, a thorough QT study with thalidomide has not been performed. Therefore, it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with ketoconazole should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but should be approached with caution. Levofloxacin is renally eliminated mainly by glomerular filtration and active secretion (possibly OCT2). Thalidomide is unlikely to interfere with this elimination pathway. However, coadministration may lead to an increased risk of peripheral neuropathy. Furthermore, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with levofloxacin should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Levomepromazine is metabolised by CYP2D6. Thalidomide does not inhibit or induce CYPs. However, thalidomide causes drowsiness and somnolence. Also, a thorough QT study with thalidomide has not been performed, therefore it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia. Due to the increased risk of additional sedative effects and bradycardia, coadministration with levomepromazine should be approached with caution. If coadministration is clinically necessary, inform patients about the risks of coadministration. Dose reductions of levomepromazine may be required. Closely monitor heart rate and ECG.

Coadministration has not been studied but is contraindicated. Levonorgestrel is mainly metabolised by CYP3A4 and is glucuronidated to a minor extent. Thalidomide does not inhibit or induce CYPs or UGTs. However, an increased risk of venous thromboembolism was observed in patients taking thalidomide in combination therapy. 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 (please note: risk of infection or bleeding), levonorgestrel-releasing intrauterine system (please note: risk of infection or bleeding), 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. CYP1A2 is the predominant enzyme involved in lidocaine metabolism in the range of therapeutic concentrations with a minor contribution from CYP3A4. Thalidomide does not inhibit or induce CYPs. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with lidocaine should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but should be approached with caution. 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. Thalidomide is unlikely to interfere with this elimination pathway. A thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with lithium should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Metformin is mainly eliminated unchanged in the urine and is a substrate of OCT1/2/3, MATE1 and MATE2K. Thalidomide is unlikely to interfere with this elimination pathway.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Methadone is demethylated by CYP3A4. Thalidomide does not inhibit or induce CYPs. Furthermore, a thorough QT study with thalidomide has not been performed. Therefore, it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide does have potential to induce bradycardia and coadministration should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

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. Thalidomide does not inhibit or induce OATs.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Metoprolol is mainly metabolised by CYP2D6. Thalidomide does not inhibit or induce CYPs. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with metoprolol should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Mexiletine is metabolised mainly by CYP2D6 and to a lesser extent by CYP1A2. Thalidomide does not inhibit or induce CYPs. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with mexiletine should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Miconazole is extensively metabolised by the liver. Miconazole is also an inhibitor of CYP2C9 (moderate) and CYP3A4 (strong). Thalidomide does not interact with this pathway. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with miconazole should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG. Note: After dermal application miconazole is only minimally absorbed. Therefore, no clinical relevant interaction is expected.

Coadministration has not been studied but should be approached with caution. Morphine is mainly glucuronidated to morphine-3-glucuronide (UGT2B7>UGT1A1) and to a lesser extent, to the pharmacologically active morphine-6-glucuronide (UGT2B7>UGT1A1). Morphine is also a substrate of P-gp. Thalidomide does not inhibit or induce CYPs, UGTs or P-gp. However, thalidomide causes drowsiness and somnolence. Also, a thorough QT study with thalidomide has not been performed, therefore it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia. Due to the increased risk of additional sedative effects and bradycardia, coadministration with morphine should be approached with caution. If coadministration is clinically necessary, inform patients about the risks of coadministration. Dose reductions of morphine may be required. Closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Moxifloxacin is predominantly glucuronidated by UGT1A1. Thalidomide does not inhibit or induce UGTs. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with moxifloxacin should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Nebivolol metabolism involves CYP2D6. Thalidomide does not inhibit or induce CYPs. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with nebivolol should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but is contraindicated. Norethisterone is extensively biotransformed, first by reduction and then by sulfate and glucuronide conjugation. Thalidomide does not interact with this pathway. Coadministration of single dose ethinylestradiol and multiple doses of thalidomide did not result in any changes to the pharmacokinetic profile of ethinylestradiol. However, an increased risk of venous thromboembolism was observed in patients taking thalidomide in combination therapy. 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 (please note: risk of infection or bleeding), levonorgestrel-releasing intrauterine system (please note: risk of infection or bleeding), 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. Nortriptyline is metabolised mainly by CYP2D6. Thalidomide does not inhibit or induce CYPs. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with nortriptyline should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Ofloxacin is renally eliminated unchanged by glomerular filtration and active tubular secretion via both cationic and anionic transport systems. Thalidomide is unlikely to interfere with this elimination pathway. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with ofloxacin should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Olanzapine is metabolised mainly by CYP1A2 (major) and CYP2D6, but also by glucuronidation (UGT1A4). Thalidomide does not inhibit or induce CYPs or UGTs. However, thalidomide causes drowsiness and somnolence. Also, a thorough QT study with thalidomide has not been performed, therefore it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia. Due to the increased risk of additional sedative effects and bradycardia, coadministration with olanzapine should be approached with caution. If coadministration is clinically necessary, inform patients about the risks of coadministration. Dose reductions of olanzapine may be required. Closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Ondansetron is metabolised mainly by CYP1A2 and CYP3A4, and to a lesser extent by CYP2D6. Ondansetron is also a substrate of P-gp. Thalidomide does not inhibit or induce CYPs or P-gp. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with ondansetron should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Oxprenolol is largely metabolised via glucuronidation. Thalidomide does not inhibit or induce UGTs. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with oxprenolol should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic 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. Thalidomide does not inhibit or induce CYPs or P-gp. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with palonosetron should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Perphenazine is metabolised by CYP2D6. Thalidomide does not inhibit or induce CYPs. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with perphenazine should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Pimozide is mainly metabolised by CYP3A4 and CYP2D6, and to a lesser extent by CYP1A2. Thalidomide does not inhibit or induce CYPs. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with pimozide should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Pindolol is partly metabolised to hydroxymetabolites (possibly via CYP2D6) and partly eliminated unchanged in the urine. Thalidomide does not interact with this metabolic pathway. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with pindolol should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. The metabolism of pipotiazine has not been well described but may involve CYP2D6. Thalidomide does not inhibit or induce CYPs. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with pipotiazine should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Posaconazole is primarily metabolised by UGTs and is a substrate of P-gp. Posaconazole is also a strong inhibitor of CYP3A4. Thalidomide does not interact with this pathway. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with posaconazole should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but should be approached with caution. 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. Thalidomide does not inhibit or induce CYPs. Prasugrel may be indicated to treat the increased risk of thrombosis due to thalidomide administration. However, the use of prasugrel with thalidomide may increase the risk of bleeding. Advise patients to observe for signs and symptoms of bleeding (e.g. petechiae, epistaxes, gastrointestinal bleedings) or bruising if coadministered. Furthermore, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with prasugrel should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Pravastatin is minimally metabolised via CYP enzymes and is a substrate of OATP1B1. Thalidomide 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. Thalidomide does not interact with this metabolic pathway.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Prochlorperazine is metabolised by CYP2D6 and CYP2C19. Thalidomide does not inhibit or induce CYPs. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia. Therefore, coadministration with prochlorperazine should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Promethazine is metabolised by CYP2D6. Thalidomide does not inhibit or induce CYPs. However, thalidomide causes drowsiness and somnolence. Also, a thorough QT study with thalidomide has not been performed, therefore it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia. Due to the increased risk of additional sedative effects and bradycardia, coadministration with promethazine should be approached with caution. If coadministration is clinically necessary, inform patients about the risks of coadministration. Dose reductions of promethazine may be required. Closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Propafenone is metabolised mainly by CYP2D6 and to a lesser extent by CYP1A2 and CYP3A4. Thalidomide does not inhibit or induce CYPs. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has a potential to induce bradycardia and coadministration with propafenone should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic 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). Thalidomide does not inhibit or induce CYPs or UGTs. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with propranolol should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

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. Thalidomide does not inhibit or induce OATs.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic 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. Quinidine is an inhibitor of CYP2D6 (strong), CYP3A4 (weak) and P-gp (moderate). Thalidomide does not interact with this pathway. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with quinidine should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Ranolazine is primarily metabolised by CYP3A4 and to a lesser extent by CYP2D6. Ranolazine is also a substrate of P-gp and weak inhibitor of P-gp, CYP3A4 and CYP2D6. Thalidomide does not interact with this pathway. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has a potential to induce bradycardia and coadministration with ranolazine should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

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 but also in other secretions. No clinically significant interactions are known.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Sertindole is metabolised by CYP2D6 and CYP3A4. Thalidomide does not inhibit or induce CYPs. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with sertindole should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Sotalol is excreted unchanged via renal elimination. Thalidomide is unlikely to interfere with this elimination pathway. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with sotalol should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Sulpiride is mainly excreted in the urine and faeces as unchanged drug. Thalidomide is unlikely to interfere with this elimination pathway. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has a potential to induce bradycardia and coadministration with sulpiride should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Thioridazine is metabolised by CYP2D6 and to a lesser extent by CYP3A4. Thalidomide does not inhibit or induce CYPs. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with thioridazine should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Tiapride is excreted largely unchanged in urine. Thalidomide is unlikely to interfere with this elimination pathway. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with tiapride should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but should be approached with caution. Ticagrelor is a substrate and weak inhibitor of CYP3A4. Ticagrelor is also a substrate of P-gp. Thalidomide does not interact with this pathway. Ticagrelor may be indicated to treat the increased risk of thrombosis due to thalidomide administration. However, the use of ticagrelor with thalidomide may increase the risk of bleeding. Advise patients to observe for signs and symptoms of bleeding (e.g. petechiae, epistaxes, gastrointestinal bleedings) or bruising if coadministered. Furthermore, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with ticagrelor should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Timolol is predominantly metabolised in the liver by CYP2D6. Thalidomide does not inhibit or induce CYPs. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with timolol should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG. Note: the systemic absorption of timolol after ocular administration is low. Therefore, a clinically relevant interaction is unlikely.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Tolterodine is primarily metabolised by CYP2D6 with CYP3A4 playing a minor role. Thalidomide does not inhibit or induce CYPs. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has a potential to induce bradycardia and coadministration with tolterodine should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Trandolapril is hydrolysed to trandolaprilat. Thalidomide does not interact with this pathway. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with trandolapril should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Trazodone is primarily metabolised by CYP3A4. Thalidomide does not inhibit or induce CYPs. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has a potential to induce bradycardia and coadministration with trazodone should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Tropisetron is metabolised mainly by CYP2D6. Tropisetron is also a substrate of P-gp. Thalidomide does not inhibit or induce CYPs or P-gp. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has a potential to induce bradycardia and coadministration with tropisetron should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Verapamil is metabolised mainly by CYP3A4 and to a lesser extent by CYPs 1A2, 2C8 and 2C9. Verapamil is also a moderate inhibitor of CYP3A4. Thalidomide does not interact with this pathway. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with verapamil should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Voriconazole is metabolised by CYP2C19 (major) and to a lesser extent by CYP3A4 and CYP2C9. Voriconazole is also a strong inhibitor of CYP3A4 and a weak inhibitor of CYPs 2C9, 2C19 and 2B6. Thalidomide does not interact with this pathway. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has potential to induce bradycardia and coadministration with voriconazole should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Zaleplon is mainly metabolised by aldehyde oxidase and to a lesser extent by CYP3A4. Thalidomide does not interact with this metabolic pathway. However, thalidomide causes drowsiness and somnolence, and due to the increased risk of additional sedative effects, coadministration with zaleplon should be approached with caution. If coadministration is clinically necessary, inform patients about the risks of coadministration. Dose reductions of zaleplon may be required.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Approximately two thirds of ziprasidone metabolic clearance is by reduction, with less than one third by CYP enzymes (mainly CYP3A4). Thalidomide does not interact with this metabolic pathway. However, a thorough QT study with thalidomide has not been performed and it’s currently unknown if thalidomide has an effect on the QT interval. Thalidomide has a potential to induce bradycardia and coadministration with ziprasidone should be approached with caution. If coadministration is unavoidable, closely monitor heart rate and ECG.