Strong enzymatic inhibitors

Abemaciclib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Use of strong CYP3A4 inhibitors together with abemaciclib should be avoided. If strong CYP3A4 inhibitors need to be co-administered, the dose of abemaciclib should be reduced, followed by careful monitoring of toxicity.

Abiraterone [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Co-administration of abiraterone and ketoconazole, a strong inhibitor of CYP3A4, had no clinically meaningful effect on the pharmacokinetics of abiraterone.

Acalabrutinib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Co-administration of strong CYP3A inhibitors with Calquence may lead to increased acalabrutinib exposure and consequently a higher risk for toxicity. Concomitant use with strong CYP3A inhibitors should be avoided.

Acalabrutinib [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Co-administration of strong P-gp inhibitors with Calquence may lead to increased acalabrutinib exposure. Concomitant use with strong P-gp inhibitors should be avoided.

Aceclofenac, strong CYP2C9 inhibitors

The CYP2C9 inhibition may increase the plasma concentrations of aceclofenac

Acenocoumarol [1], strong CYP2C9 inhibitors ---> SmPC of [1] of eMC

The potent CYP2C9 inhibition may increase the plasma concentrations of acenocoumarol

Afatinib [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Increased exposure to afatinib. It is recommended to administer strong P-gp inhibitors using staggered dosing, preferably 6 hours or 12 hours apart from afatinib

Agomelatine [1], strong CYP1A2 inhibitors ---> SmPC of [1] of EMA

The strong CYP1A2 inhibition may increase the plasma concentrations of agomelatine. Co-administration of agomelatine with potent CYP1A2 inhibitors is contraindicated.

Ajmaline, strong CYP2D6 inhibitors

The strong CYP2D6 inhibition may increase the plasma concentrations of ajmaline.

Alectinib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Appropriate monitoring is recommended for patients taking concomitant strong CYP3A inhibitors

Alfentanyl [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

Alfentanil is metabolised mainly via the human cytochrome P450 3A4 enzyme. In vitro data suggest that cytochrome P450 3A4 enzyme inhibitors may inhibit the metabolism of alfentanil

Alfuzosin [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

The strong CYP3A4 inhibition may increase the plasma concentrations of alfuzosin

Aliskiren [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

The concomitant use of aliskiren with ciclosporin and itraconazole, two highly potent P-gp inhibitors, and other potent P-gp inhibitors (e.g. quinidine), is contraindicated

Aliskiren/amlodipine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Concomitant use of amlodipine with strong or moderate CYP3A4 inhibitors may give rise to significant increase in amlodipine exposure. Clinical monitoring and dose adjustment may thus be required.

Aliskiren/amlodipine [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

The concomitant use of aliskiren with ciclosporin and itraconazole, two highly potent P-gp inhibitors, and other potent P-gp inhibitors (e.g. quinidine), is contraindicated

Aliskiren/amlodipine/hydrochlorothiazide [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Concomitant use of amlodipine with strong or moderate CYP3A4 inhibitors may give rise to significant increase in amlodipine exposure. Clinical monitoring and dose adjustment may thus be required.

Aliskiren/amlodipine/hydrochlorothiazide, strong P-gp inhibitors ---> SmPC of [aliskiren] of EMA

The concomitant use of aliskiren with ciclosporin and itraconazole, two highly potent P-gp inhibitors, and other potent P-gp inhibitors (e.g. quinidine), is contraindicated

Aliskiren/hydrochlorothiazide [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Concomitant use of aliskiren and P-gp potent inhibitors is contraindicated

Alitretinoin [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

Co-administration of alitretinoin with CYP3A4 inhibitors such as ketoconazole increases the plasma level of alitretinoin and dose reduction may be required. The effects of other inhibitors of CYP3A4 have not been studied.

Allopurinol/lesinurad [1], strong CYP2C9 inhibitors ---> SmPC of [1] of EMA

Lesinurad exposure is increased when it is co-administered with inhibitors of CYP2C9. Therefore, it is recommended that Duzallo should be used with caution in patients taking moderate inhibitors of CYP2C9.

Alprazolam [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

Compounds that inhibit certain hepatic enzymes (particularly cytochrome P450 3A4) may increase the concentration of alprazolam and enhance its activity.

Ambrisentan [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Steady-state administration of ketoconazole (a strong inhibitor of CYP3A4) did not result in a clinically significant increase in exposure to ambrisentan

Amiodarone, strong CYP2C8 inhibitors

The CYP2C8 inhibitors may inhibit the amiodarone metabolism and increase its plasma concentrations

Amiodarone, strong CYP3A4 inhibitors

The CYP3A4 inhibitors may inhibit the amiodarone metabolism and increase its plasma concentrations. It is recommended to avoid the CYP3A4 inhibitors (e. g. grapefruit juice)

Amitriptyline, strong CYP2D6 inhibitors

The CYP2D6 inhibition may increase the plasma concentrations of amitriptyline. Concomitant use should be avoided

Amlodipine, strong CYP3A4 inhibitors ---> SmPC of [amlodipine/valsartan] of EMA

Concomitant use of amlodipine with strong or moderate CYP3A4 inhibitors may give rise to significant increase in amlodipine exposure. Clinical monitoring and dose adjustment may thus be required.

Amlodipine/valsartan [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Concomitant use of amlodipine with strong or moderate CYP3A4 inhibitors may give rise to significant increase in amlodipine exposure. Clinical monitoring and dose adjustment may thus be required.

Amlodipine/valsartan/hydrochlorothiazide [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Concomitant use of amlodipine with strong or moderate CYP3A4 inhibitors may give rise to significant increase in amlodipine exposure.

Amprenavir [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

The strong CYP3A4 inhibition may increase the plasma concentrations of amprenavir

Anagrelide [1], strong CYP1A2 inhibitors ---> SmPC of [1] of EMA

Anagrelide is primarily metabolised by CYP1A2. It is known that CYP1A2 is inhibited by several medicinal products, and such medicinal products could theoretically adversely influence the clearance of anagrelide.

Apalutamide [1], strong CYP2C8 inhibitors ---> SmPC of [1] of EMA

No initial dose adjustment is necessary when Erleada is co-administered with a strong inhibitor of CYP2C8 (e.g., gemfibrozil, clopidogrel) however, a reduction of the Erleada dose based on tolerability should be considered

Apalutamide [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

No initial dose adjustment is necessary when Erleada is co-administered with a strong inhibitor of CYP3A4 (e.g., ketoconazole, ritonavir, clarithromycin) however, a reduction of the Erleada dose based on tolerability should be considered

Apixaban [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

The use of apixaban is not recommended in patients receiving concomitant systemic treatment with strong inhibitors of both CYP3A4 and P-gp

Apixaban [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

The use of apixaban is not recommended in patients receiving concomitant systemic treatment with strong inhibitors of both CYP3A4 and P-gp

Apremilast [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

There was no clinically meaningful drug-drug interaction between ketoconazole and apremilast. Apremilast can be co-administered with a potent CYP3A4 inhibitor such as ketoconazole.

Aprepitant [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Concomitant administration of aprepitant with active substances that inhibit CYP3A4 activity should be approached cautiously, as the combination is expected to result several-fold in increased plasma concentrations of aprepitant

Aripiprazole [1], strong CYP2D6 inhibitors ---> SmPC of [1] of EMA

Strong inhibitors of CYP2D6 may increase the AUC of aripiprazole. A dose reduction should, therefore, be applied

Aripiprazole [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Strong inhibitors of CYP3A4 may increase the AUC of aripiprazole. A dose reduction should, therefore, be applied

Artemether, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of artemether

Artemether/lumefantrine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

The concurrent oral administration of potent CYP3A4 inhibitors with artemether/lumefantrine led to a modest increase in artemether, DHA, and lumefantrine exposure. A dose adjustment is considered unnecessary

Artesunate [1], strong glucuronidation inhibitors ---> SmPC of [1] of EMA

Co-administration of intravenous artesunate with strong inhibitors of UGT enzymes (e.g. axitinib, vandetanib, imatinib, diclofenac) may increase plasma exposures to DHA. Co-administration should be avoided if possible.

Astemizole, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of astemizole and prolong the QT interval. The co-administration is contraindicated

Atazanavir/cobicistat [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Co-administration of EVOTAZ with medicinal products that inhibit CYP3A may result in increased plasma concentration of atazanavir and/or cobicistat.

Atazanavir/cobicistat [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Concentrations of dabigatran may be affected upon coadministration with EVOTAZ. The mechanism of interaction is P-gp inhibition by atazanavir and cobicistat. Clinical monitoring is recommended when dabigatran is co-administered with P-gp inhibitors.

Atenolol/nifedipine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

Drugs known to inhibit the cytochrome P450 3A4 system when administered orally with nifedipine may substantial increase the systemic bioavailability of nifedipine due to a decreased first pass metabolism and a decreased elimination

Atomoxetine, strong CYP2D6 inhibitors

The CYP2D6 inhibition may increase the AUC of atomoxetine ca. 6- to 8-fold. There is the potential for an increased risk of QT interval prolongation

Atorvastatin [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

Potent CYP3A4 inhibitors have been shown to lead to markedly increased concentrations of atorvastatin. Co-administration of potent CYP3A4 inhibitors should be avoided if possible.

Atorvastatin [1], strong P-gp inhibitors ---> SmPC of [1] of eMC

Inhibitors of transport proteins can increase the systemic exposure of atorvastatin

Avacopan [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Strong CYP3A4 enzyme inhibitors should be used with caution in patients who are being treated with avacopan.

Avanafil [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Avanafil is predominantly metabolised by CYP3A4. The strong CYP3A4 inhibitors may increase the exposition of avanafil. Co-administration of avanafil with potent CYP3A4 inhibitors is contraindicated

Avapritinib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Co-administration with strong or moderate CYP3A inhibitors should be avoided because it may increase the plasma concentration of avapritinib

Avatrombopag [1], strong CYP2C9 inhibitors ---> SmPC of [1] of EMA

These patients should be evaluated on the day of the procedure for an unexpectedly high increase in platelet count

Avatrombopag [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

These patients should be evaluated on the day of the procedure for an unexpectedly high increase in platelet count

Axitinib [1], strong CYP1A2 inhibitors ---> SmPC of [1] of EMA

CYP1A2 and CYP2C19 constitute minor (< 10%) pathways in axitinib metabolism. Caution should be exercised due to the risk of increased axitinib plasma concentrations in patients taking strong inhibitors of these isozymes.

Axitinib [1], strong CYP2C19 inhibitors ---> SmPC of [1] of EMA

Axitinib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Co-administration of axitinib with strong CYP3A4/5 inhibitors may increase axitinib plasma concentrations. Selection of concomitant medicinal products with no or minimal CYP3A4/5 inhibition potential is recommended.

Azelastine, strong CYP2D6 inhibitors

Patients treated with known CYP2D6 inhibitors should be controlled due to the probability of experiencing side effects.

Barnidipine, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of barnidipine. Barnidipine should not be concomitantly prescribed with strong CYP3A4 inhibitors.

Beclometasone/formoterol/glycopyrronium [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Beclometasone is less dependent on CYP3A metabolism than some other corticosteroids; however, the possibility of systemic effects with concomitant use of strong CYP3A inhibitors (e.g. ritonavir, cobicistat) cannot be excluded

Bedaquiline [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Due to the potential risk of adverse reactions due to an increase in systemic exposure, prolonged co-administration of bedaquiline and moderate or strong CYP3A4 inhibitors used systemically for more than 14 consecutive days should be avoided.

Bendamustine [1], strong CYP1A2 inhibitors ---> SmPC of [1] of eMC

Bendamustine metabolism involves cytochrome P450 (CYP) 1A2 isoenzyme. Therefore, the potential for interaction with CYP1A2 inhibitors

Bezafibrate, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of bezafibrate

Bictegravir/emtricitabine/tenofovir alafenamide [1], strong BCRP inhibitors ---> SmPC of [1] of EMA

Co-administration of Biktarvy with other medicinal products that inhibit P-gp and BCRP may increase the absorption and plasma concentration of tenofovir alafenamide.

Bictegravir/emtricitabine/tenofovir alafenamide [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Co-administration of bictegravir with medicinal products that potently inhibit both CYP3A and UGT1A1, such as atazanavir, may significantly increase plasma concentrations of bictegravir, therefore co-administration is not recommended.

Bictegravir/emtricitabine/tenofovir alafenamide [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Co-administration of Biktarvy with other medicinal products that inhibit P-gp and BCRP may increase the absorption and plasma concentration of tenofovir alafenamide.

Bictegravir/emtricitabine/tenofovir alafenamide [1], strong UGT1A1 inhibitors ---> SmPC of [1] of EMA

Bilastine [1], strong P-gp inhibitors ---> SmPC of [1] of eMC

Concomitant intake of bilastine, substrate for P-gp, may likewise have the potential to increase plasma concentrations of bilastine.

Bimatoprost/timolol [1], strong CYP2D6 inhibitors ---> SmPC of [1] of EMA

Potentiated systemic beta-blockade (e.g., decreased heart rate, depression) has been reported during combined treatment with CYP2D6 inhibitors and timolol.

Boceprevir [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Boceprevir is partly metabolized by CYP3A4/5. Co-administration of boceprevir with medicines that inhibit CYP3A4/5 could increase exposure to boceprevir

Boceprevir [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Boceprevir has been shown to be a p-glycoprotein (P-gp) and breast cancer resistant protein (BCRP) substrate in vitro .There is potential for inhibitors of these transporters to increase concentrations of boceprevir

Bortezomib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

The strong CYP3A4 inhibition may increase the AUC of bortezomib. Patients should be closely monitored when given bortezomib in combination with potent CYP3A4 inhibitors

Bosentan [1], strong CYP2C9 inhibitors ---> SmPC of [1] of EMA

The influence of CYP2C9 inhibitors on bosentan concentration has not been studied. The combination should be used with caution.

Bosentan [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

The strong CYP3A4 inhibition may increase the plasma concentrations of bosentan. Co-administration is not recommended

Bosutinib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

The concomitant use of bosutinib with potent CYP3A inhibitors should be avoided, as an increase in bosutinib plasma levels will occur. Selection of an alternate concomitant medicine with no or minimal CYP3A enzyme inhibition potential is recommended.

Brentuximab vedotin [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

The combination of brentuximab with a strong CYP3A4 inhibitor increased the exposure to the antimicrotubule agent MMAE and may increase the incidence of neutropenia.

Brentuximab vedotin [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

The combination of brentuximab with a strong P-gp inhibitor increased the exposure to the antimicrotubule agent MMAE and may increase the incidence of neutropenia.

Brexpiprazole [1], strong CYP2D6 inhibitors ---> SmPC of [1] of EMA

Based on results of interaction studies, dose adjustment of brexpiprazole to half the dose is recommended when administered concomitantly with strong CYP2D6 inhibitors (quinidine, paroxetine, and fluoxetine).

Brexpiprazole [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Based on results of interaction studies, dose adjustment of brexpiprazole to half the dose is recommended when administered concomitantly with strong CYP3A4 inhibitors

Brigatinib [1], strong CYP2C8 inhibitors ---> SmPC of [1] of EMA

No dose adjustment is required during coadministration with strong CYP2C8 inhibitors.

Brigatinib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

The concomitant use of Alunbrig with strong CYP3A inhibitors should be avoided.

Brinzolamide [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

It is expected that inhibitors of CYP3A4 will inhibit the metabolism of brinzolamide by CYP3A4. Caution is advised if CYP3A4 inhibitors are given concomitantly.

Brinzolamide/brimonidine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

It is expected that inhibitors of CYP3A4 will inhibit the metabolism of brinzolamide by CYP3A4. Caution is advised if CYP3A4 inhibitors are given concomitantly.

Brinzolamide/timolol [1], strong CYP2D6 inhibitors ---> SmPC of [1] of EMA

Potentiated systemic beta-blockade (e.g., decreased heart rate, depression) has been reported during combined treatment with CYP2D6 inhibitors and timolol.

Brinzolamide/timolol [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

It is expected that inhibitors of CYP3A4 will inhibit the metabolism of brinzolamide by CYP3A4. Caution is advised if CYP3A4 inhibitors are given concomitantly.

Bromocriptine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

Bromocriptine is both a substrate and an inhibitor of CYP3A4. Caution should therefore be used when co-administering drugs which are strong inhibitors and/or substrates of this enzyme

Brotizolam, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of brotizolam

Budesonide [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Co-treatment with potent CYP3A inhibitors may cause a marked increase of the plasma concentration of budesonide and is expected to increase the risk of systemic adverse reactions. Therefore, concomitant use should be avoided

Budesonide/formoterol [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Potent inhibitors of CYP3A4 are likely to markedly increase plasma levels of budesonide and concomitant use should be avoided.

Buflomedil, strong CYP2D6 inhibitors

The risk of neurological adverse effects increases if buflomedil is administered with CYP2D6 inhibitors to patients with renal or hepatic disorder

Buprenorphine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

CYP3A4 inhibitors may inhibit the metabolism of buprenorphine resulting in increased Cmax and AUC of buprenorphine and norbuprenorphine.

Buprenorphine/naloxone [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Medicines that inhibit the enzyme CYP3A4 may give rise to increased concentrations of buprenorphine. A reduction of the buprenorphine/naloxone dose may be needed.

Buspirone [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

If buspirone is administered with a potent CYP3A4 inhibitor, the initial dose should be lowered and only increased gradually after medical evaluation

Cabazitaxel [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Repeated administration of ketoconazole, a strong CYP3A inhibitor, decreased cabazitaxel clearance. Therefore concomitant administration of strong CYP3A inhibitors should be avoided as an increase of plasma concentrations of cabazitaxel may occur

Cabergoline, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of cabergoline. The co-administration is contraindicated

Cabozantinib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Co-administration of cabozantinib with strong CYP3A4 inhibitors (increased plasma cabozantinib exposure (AUC) should be approached with caution.

Caffeine [1], strong CYP1A2 inhibitors ---> SmPC of [1] of EMA

Cytochrome P450 1A2 (CYP1A2) is the major enzyme involved in the metabolism of caffeine in humans. Therefore, caffeine has the potential to interact with active substances that inhibit CYP1A2

Calcium antagonists, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of the calcium antagonist

Cannabidiol [1], strong glucuronidation inhibitors ---> SmPC of [1] of EMA

Caution should be taken when co-administering drugs that are known inhibitors of these UGTs. Dose reduction of cannabidiol and/or the inhibitor may be necessary when given in combination.

Carbamazepine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

Co-administration of carbamazepine with inhibitors of CYP 3A4 may result in increased carbamazepine plasma concentrations which could induce adverse reactions.

Cariprazine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Metabolism of cariprazine and its major active metabolites is mediated mainly by CYP3A4. The co-administration of cariprazine with strong or moderate inhibitors of CYP3A4 is contraindicated

Carisoprodol, strong CYP2C19 inhibitors

The strong CYP2C19 inhibition may increase the plasma concentrations of carisoprodol

Carvedilol, strong CYP2C9 inhibitors

The strong CYP2C9 inhibition may increase plasma levels of carvedilol

Carvedilol, strong CYP2D6 inhibitors

The strong CYP2D6 inhibition may increase plasma levels of carvedilol

Carvedilol, strong P-gp inhibitors

Inhibition of P-glycoprotein may lead to increased bioavailability of oral carvedilol

Celecoxib [1], strong CYP2C9 inhibitors ---> SmPC of [1] of EMA

Concomitant treatment of celecoxib with CYP2C9 inhibitors could result in further increases in celecoxib exposure.

Ceritinib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

If it is not possible to avoid concomitant use with strong CYP3A inhibitors, reduce the ceritinib dose by approximately one third, rounded to the nearest multiple of the 150 mg dosage strength.

Ceritinib [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Based on in vitro data, ceritinib is a substrate of the efflux transporter P-glycoprotein (P-gp). If ceritinib is administered with medicinal products that inhibit P-gp, an increase in ceritinib concentration is likely.

Chlorpromazine, strong CYP1A2 inhibitors

The strong CYP1A2 inhibition may increase the plasma levels of chlorpromazine (small therapeutic range)

Chlorprothixene, strong CYP2D6 inhibitors

Medicinal drugs that inhibit the CYP2D6 may increase plasma levels of chlorprothixene. The combination has to be avoided

Ciclesonide [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

The concomitant administration of ciclesonide with potent inhibitors of CYP 3A4 should be avoided unless the benefit outweighs the increased risk of systemic side effects of corticosteroids.

Cilostazol [1], strong CYP2C19 inhibitors ---> SmPC of [1] of EMA

Cilostazol is extensively metabolised by CYP3A4 and CYP2C19 and to a lesser extent CYP1A2. Drugs inhibiting CYP2C19 increase the total pharmacological activity and could have the potential to enhance the undesirable effects of cilostazol.

Cilostazol [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Cilostazol is extensively metabolised by CYP3A4 and CYP2C19 and to a lesser extent CYP1A2. Drugs inhibiting CYP3A4 increase the total pharmacological activity and could have the potential to enhance the undesirable effects of cilostazol.

Cinacalcet [1], strong CYP1A2 inhibitors ---> SmPC of [1] of EMA

In vitro data indicate that cinacalcet is in part metabolised by CYP1A2. Smoking induces CYP1A2. Dose adjustment may be necessary when concomitant treatment with strong CYP1A2 inhibitors is initiated or discontinued.

Cinacalcet [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Cinacalcet is metabolised in part by the enzyme CYP3A4. Co-administration of a strong inhibitor of CYP3A4 may increase cinacalcet levels. Dose adjustment of cinacalcet may be required

Cinitapride, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of cinitapride

Cisapride, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of cisapride and prolong the QT interval. The co-administration is contraindicated

Citalopram [1], strong CYP2C19 inhibitors ---> SmPC of [1] of eMC

The strong CYP2C19 inhibition may increase the plasma concentrations of citalopram. Caution should be exercised when used concomitantly with CYP2C19 inhibitors

Clarithromycin, strong CYP3A4 inhibitors

Strong CYP3A4 inhibitors may increase the plasma concentrations of clarithromycin

Clobazam [1], strong CYP2C19 inhibitors ---> SmPC of [1] of eMC

The potent CYP2C19 inhibition may increase the exposure to the active metabolite of clobazam. Dosage adjustment of clobazam may be necessary

Clobetasol, strong CYP3A4 inhibitors

The co-administration of clobetasol with CYP3A4 inhibitors inhibits the metabolism of corticosteroid and increases its systemic bioavailability

Clobetasone [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

Co-administered drugs that can inhibit CYP3A4 have been shown to inhibit the metabolism of corticosteroids leading to increased systemic exposure.

Clomipramine [1], strong CYP2D6 inhibitors ---> SmPC of [1] of eMC

Clomipramine is metabolised by cytochrome P450 2D6 and the plasma concentration of clomipramine may therefore be increased by drugs that are either substrates and/or inhibitors of this P450 isoform.

Clonazepam, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of clonazepam

Clopidogrel [1], strong CYP2C19 inhibitors ---> SmPC of [1] of EMA

Since clopidogrel is metabolised to its active metabolite partly by CYP2C19, use of medicinal products that inhibit the activity of this enzyme would be expected to result in reduced drug levels of the active metabolite of clopidogrel.

Clopidogrel, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may decrease plasma concentrations of the active metabolite and the effect of clopidogrel. The co-administration should be discouraged

Clopidogrel/acetylsalicylic acid [1], strong CYP2C19 inhibitors ---> SmPC of [1] of EMA

Cloprednol, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of cloprednol

Clozapine [1], strong CYP1A2 inhibitors ---> SmPC of [1] of eMC

Concomitant administration of substances known to inhibit the activity of some cytochrome P450 isozymes (CYP1A2) may increase the levels of clozapine, and the dose of clozapine may need to be reduced to prevent undesirable effects.

Cobicistat [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Co-administration of cobicistat with medicinal products that inhibit CYP3A may result in increased plasma concentration of cobicistat.

Cobimetinib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Avoid concurrent use of strong CYP3A inhibitors during treatment with cobimetinib. If concomitant use of a strong CYP3A inhibitor is unavoidable, patients should be carefully monitored for safety.

Codergocrin, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the exposition to codergocrin, which may cause a dopaminergic effect. Concomitant use should be avoided

Colchicine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

Colchicine is contraindicated in patients with renal or hepatic impairment who are taking a P-glycoprotein inhibitor

Colchicine [1], strong P-gp inhibitors ---> SmPC of [1] of eMC

Colchicine is contraindicated in patients with renal or hepatic impairment who are taking a P-glycoprotein or a strong CYP3A4 inhibitor

Conjugated oestrogens/bazedoxifene [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

In a clinical drug-drug interaction study, repeat administration of 200 mg itraconazole, a strong CYP3A4 inhibitor, had minimal impact on the pharmacokinetics of CE and bazedoxifene when administered with a single dose of CE 0.45 mg/bazedoxifene 20 mg.

Contraceptives, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the concentrations of the steroid.

Corticosteroids, strong CYP3A4 inhibitors

Co-administered drugs that can inhibit CYP3A4 have been shown to inhibit the metabolism of corticosteroids leading to increased systemic exposure.

Crisaborole [1], strong CYP1A2 inhibitors ---> SmPC of [1] of EMA

Based on in vitro data, concomitant administration of Staquis and CYP1A2 inhibitors (e.g., ciprofloxacin, fluvoxamine) can increase systemic crisaborole concentrations

Crisaborole [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Based on in vitro data, concomitant administration of Staquis and CYP3A4 inhibitors (e.g., ketoconazole, itraconazole, erythromycin, clarithromycin, ritonavir) can increase systemic crisaborole concentrations

Crizotinib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Coadministration of crizotinib with strong CYP3A inhibitors may increase crizotinib plasma concentrations. Therefore, the concomitant use of strong CYP3A inhibitors should be avoided.

Cyclophosphamide, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may decrease the efficacy of cyclophosphamide (prodrug)

Cyclosporine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

All inhibitors of CYP3A4 and/or P-glycoprotein may lead to increased levels of cyclosporine.

Cyclosporine [1], strong P-gp inhibitors ---> SmPC of [1] of eMC

All inhibitors of CYP3A4 and/or P-glycoprotein may lead to increased levels of cyclosporine.

CYP450, strong cytokine inhibitors ---> SmPC of [tocilizumab] of EMA

The expression of hepatic CYP450 enzymes is suppressed by cytokines, such as IL-6, that stimulate chronic inflammation. Thus, CYP450 expression may be reversed when potent cytokine inhibitory therapy, such as tocilizumab, is introduced.

Cyproterone [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

Since cyproterone acetate is metabolised by CYP3A4, it is expected strong inhibitors of CYP3A4 inhibit the metabolism of cyproterone acetate.

Dabigatran etexilate [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Dabigatran etexilate is a substrate for the efflux transporter P-gp. Close clinical surveillance (looking for signs of bleeding or anaemia) is required when dabigatran is co-administered with strong P-gp inhibitors.

Dabigatran [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Dabrafenib [1], strong CYP2C8 inhibitors ---> SmPC of [1] of EMA

Dabrafenib is a substrate for the metabolising enzymes CYP2C8. Medicines that are strong inhibitors of CYP2C8 are therefore likely to increase dabrafenib concentrations. Use caution if strong inhibitors are coadministered with dabrafenib.

Dabrafenib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Dabrafenib is a substrate for the metabolising enzymes CYP3A4. Medicines that are strong inhibitors of CYP3A4 are therefore likely to increase dabrafenib concentrations. Use caution if strong inhibitors are coadministered with dabrafenib.

Daclatasvir [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Strong inhibitors of CYP3A4 may increase the plasma levels of daclatasvir. Dose adjustment of daclatasvir is recommended when coadministered with strong inhibitors of CYP3A4

Daclatasvir [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Coadministration of medicines that inhibit P-gp activity is likely to a have limited effect on daclatasvir exposure.

Dapoxetine [1], strong CYP2D6 inhibitors ---> SmPC of [1] of eMC

The Cmax of the active fraction may be increased by approximately 50% and the AUC of the active fraction may be doubled if taken dapoxetine with potent CYP2D6 inhibitors

Dapoxetine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

The strong CYP3A4 inhibition may increase the plasma concentrations of dapoxetine. Concomitant use of dapoxetine and potent CYP3A4 inhibitors is contraindicated

Daridorexant [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

No clinical study was conducted with a strong CYP3A4 inhibitor. Concomitant use of QUVIVIQ with strong inhibitors of CYP3A4 (e.g., itraconazole, clarithromycin, ritonavir) is contraindicated

Darifenacin [1], strong CYP2D6 inhibitors ---> SmPC of [1] of EMA

Concomitant treatment with potent CYP2D6 inhibitors results in an increase in darifenacin exposure

Darifenacin [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Concomitant treatment of darifenacin with potent CYP3A4 inhibitors is contraindicated

Darifenacin [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Concomitant treatment of darifenacin with potent P-glycoprotein inhibitors should be avoided.

Darolutamide [1], strong BCRP inhibitors ---> SmPC of [1] of EMA

Darolutamide is a substrate of CYP3A4, P-gp and breast cancer resistance protein (BCRP). No clinically relevant drug-drug interaction is expected in case of CYP3A4, P-gp or BCRP inhibitor administration.

Darolutamide [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Darolutamide [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Darolutamide [1], strong UGT1A9 inhibitors ---> SmPC of [1] of EMA

No clinically relevant drug-drug interaction is expected in case of UGT1A9 inhibitor administration. Darolutamide may be given concomitantly with UGT1A9 inhibitors.

Darunavir/cobicistat, strong CYP3A4 inhibitors ---> SmPC of [darunavir] of EMA

Co-administration of darunavir and cobicistat with other medicinal products that inhibit CYP3A may result in increased plasma concentrations of darunavir and cobicistat. Co-administration with strong CYP3A4 inhibitors is not recommended

Darunavir/cobicistat/emtricitabine/tenofovir alafenamide [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Co-administration of Symtuza and other medicinal products that inhibit CYP3A may decrease the clearance of darunavir and cobicistat and may result in increased plasma concentrations of darunavir and cobicistat

Darunavir/cobicistat/emtricitabine/tenofovir alafenamide [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Co-administration of tenofovir alafenamide with other medicinal products that inhibit P-gp (e.g., cobicistat, ritonavir, ciclosporin) are expected to increase the absorption and plasma concentration of tenofovir alafenamide.

Darunavir/ritonavir, strong CYP3A4 inhibitors ---> SmPC of [darunavir] of EMA

Co-administration of darunavir and ritonavir with other medicinal products that inhibit CYP3A may decrease the clearance of darunavir and ritonavir. Co-administration with strong CYP3A4 inhibitors is not recommended and caution is warranted

Dasabuvir with ombitasvir/paritaprevir/ritonavir, strong CYP3A4 inhibitors ---> SmPC of [ombitasvir/paritaprevir/r

Co-administration of ombitasvir/paritaprevir/ritonavir with or without dasabuvir with medicinal products that are strong inhibitors of CYP3A4 is expected to increase paritaprevir plasma concentrations. The coadministration is contraindicated

Dasabuvir [1], strong CYP2C8 inhibitors ---> SmPC of [1] of EMA

Co-administration of dasabuvir with medicinal products that inhibit CYP2C8 (e.g. teriflunomide, deferasirox) may increase dasabuvir plasma concentrations. Strong CYP2C8 inhibitors are contraindicated with dasabuvir

Dasabuvir [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Dasabuvir is a substrate of P-gp and BCRP and its major metabolite M1 is a substrate of OCT1 in vitro. Inhibition of P-gp and BCRP is not expected to show clinically relevant increases in exposures of dasabuvir

Dasatinib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

In vitro studies indicate that dasatinib is a CYP3A4 substrate. Concomitant use of dasatinib and medicinal products which potently inhibit CYP3A4 may increase exposure to dasatinib. Systemic administration of a potent CYP3A4 inhibitor is not recommended.

Daunorubicin, strong CYP3A4 inhibitors

Daunorubicin is mainly metabolized in the liver; each accompanying medication influencing liver function may also influence the metabolism or pharmacokinetics of daunorubicin and as a consequence influence efficacy and/or toxicity.

Daunorubicin, strong P-gp inhibitors

Deflazacort, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of glucocorticoid

Delamanid [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Co-administration of delamanid with a strong inhibitor of CYP3A (lopinavir/ritonavir) was associated with 30% higher exposure to the metabolite M-6705, which has been associated with QTc prolongation.

Desipramine, strong CYP2D6 inhibitors

The CYP2D6 inhibition may increase plasma concentrations of desipramine, which has a narrow therapeutic index

Dextromethorphan, strong CYP2D6 inhibitors

The strong CYP2D6 inhibition may increase the plasma concentrations of dextromethorphan

Dextromethorphan/quinidine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Concomitant administration of medicines that inhibit CYP3A4 can be expected to increase plasma levels of quinidine, which could increase risk relating to QTc prolongation. Strong and moderate CYP3A4 inhibitors should be avoided during treatment.

Diazepam, strong CYP2C19 inhibitors

The strong CYP2C19 inhibition may increase the plasma concentrations of diazepam

Diazepam, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of diazepam

Diclofenac, strong CYP2C9 inhibitors

The strong CYP2C9 inhibition may increase the plasma concentrations of diclofenac

Dienogest, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma levels of dienogest

Digitoxin, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma levels of digitoxin

Digitoxin, strong P-gp inhibitors

The strong inhibition of P-glycoprotein may increase the plasma concentrations of digitoxin

Digoxin [1], strong P-gp inhibitors ---> SmPC of [1] of eMC

Digoxin is a substrate of P-glycoprotein. Thus, inhibitors of P-glycoprotein may increase blood concentrations of digoxin by enhancing its absorption and/or by reducing its renal clearance

Dihydroergotamine, strong CYP3A4 inhibitors

Concomitant use of dihydroergotamine with strong CYP3A4 inhibitors may increase the effect of dihydroergotamine (acute ergotism and vasospastic ischemia) and is contraindicated

Dihydroergotoxine, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the exposition to dihydroergotoxine, which may cause a dopaminergic effect. Concomitant use should be avoided

Dihydropyridines, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of dihydropyridine. Caution is recommended

Diltiazem [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

A moderate (less than 2-fold) increase of diltiazem plasma concentration in cases of co-administration with a stronger CYP3A4 inhibitor has been documented.

Disopyramide [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

There is evidence that phosphodiesterase Type 5 inhibitors may be potentially associated with a risk of QT prolongation. Concomitant administration of disopyramide with such drugs may potentially enhance this QT prolongation effect and is not recommended

Docetaxel [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

In case of combination of docetaxel with CYP3A4 inhibitors, the occurrence of docetaxel adverse reactions may increase, as a result of reduced metabolism

Dofetilide [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

The strong CYP3A4 inhibition may increase the plasma concentrations of dofetilide. The co-administration is contraindicated

Dolutegravir [1], strong UGT1A1 inhibitors ---> SmPC of [1] of EMA

Dolutegravir is eliminated mainly through metabolism by UGT1A1. Co-administration of dolutegravir and other medicinal products that inhibit these enzymes may increase dolutegravir plasma concentration

Dolutegravir/abacavir/lamivudine [1], strong BCRP inhibitors ---> SmPC of [1] of EMA

Co-administration of dolutegravir/abacavir/lamivudine and other drugs that inhibit BCRP may increase dolutegravir plasma concentration.

Dolutegravir/abacavir/lamivudine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Co-administration of dolutegravir/abacavir/lamivudine and other drugs that inhibit CYP3A4 may increase dolutegravir plasma concentration.

Dolutegravir/abacavir/lamivudine [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Co-administration of dolutegravir/abacavir/lamivudine and other drugs that inhibit P-gp may increase dolutegravir plasma concentration.

Dolutegravir/abacavir/lamivudine [1], strong UGT1A1 inhibitors ---> SmPC of [1] of EMA

Co-administration of dolutegravir/abacavir/lamivudine and other drugs that inhibit UGT1A1 may increase dolutegravir plasma concentration.

Dolutegravir/abacavir/lamivudine [1], strong UGT1A3 inhibitors ---> SmPC of [1] of EMA

Co-administration of dolutegravir/abacavir/lamivudine and other drugs that inhibit UGT1A3 may increase dolutegravir plasma concentration.

Dolutegravir/abacavir/lamivudine [1], strong UGT1A9 inhibitors ---> SmPC of [1] of EMA

Co-administration of dolutegravir/abacavir/lamivudine and other drugs that inhibit UGT1A9 may increase dolutegravir plasma concentration.

Dolutegravir/rilpivirine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Rilpivirine is primarily metabolised by cytochrome P450 (CYP)3A. Co-administration of rilpivirine and medicinal products that inhibit CYP3A has been observed to increase the plasma concentrations of rilpivirine

Dolutegravir/rilpivirine [1], strong UGT1A1 inhibitors ---> SmPC of [1] of EMA

Domperidone [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

In vitro data suggest that the concomitant use of drugs that significantly inhibit CYP3A4 may result in increased plasma levels of domperidone.

Donepezil [1], strong CYP2D6 inhibitors ---> SmPC of [1] of eMC

The strong CYP2D6 inhibition may increase the plasma concentrations of donepezil.

Donepezil [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

The strong CYP3A4-inhibition may increase the plasma levels of donepezil

Doravirine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Co-administration of doravirine and medicinal products that are inhibitors of CYP3A may result in increased plasma concentrations of doravirine. However, no dose adjustment is needed when doravirine is co-administered with CYP3A inhibitors.

Doravirine/lamivudine/tenofovir disoproxil [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Co-administration of doravirine/lamivudine/tenofovir disoproxil and medicinal products that are inhibitors of CYP3A may result in increased plasma concentrations of doravirine. However, no dose adjustment is needed

Dorzolamide/timolol [1], strong CYP2D6 inhibitors ---> SmPC of [1] of eMC

Potentiated systemic beta-blockade (e.g., decreased heart rate, depression) has been reported during combined treatment with CYP2D6 inhibitors and timolol.

Doxepin, strong CYP2D6 inhibitors

Doxepin is metabolised by cytochrome P450 (CYP) 2D6. Inhibitors of CYP2D6 may increase the plasma concentration of doxepin when administered concomitantly.

Doxorubicine [1], strong P-gp inhibitors ---> SmPC of [1] of eMC

Concomitant administration of inhibitors of CYP450 and/or Pgp might lead to increased plasma concentrations of doxorubicin and thereby increased toxicity.

Dronedarone [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Concomitant use of dronedarone with strong CYP3A4 inhibitors increases dronedarone exposure. The combination of dronedarone with strong CYP3A4 inhibitors is contraindicated

Droperidol [1], strong CYP1A2 inhibitors ---> SmPC of [1] of eMC

Substances inhibiting the activity of cytochrome P450 iso-enzyme CYP1A2 could decrease the rate at which droperidol is metabolised and prolong its pharmacological action.

Droperidol [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

Substances inhibiting the activity of cytochrome P450 iso-enzyme CYP3A4 could decrease the rate at which droperidol is metabolised and prolong its pharmacological action.

Drospirenone/estetrol [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Concomitant administration of strong CYP3A4 inhibitors can increase plasma concentrations of oestrogens or progestogens or both.

Duloxetine [1], strong CYP1A2 inhibitors ---> SmPC of [1] of EMA

YENTREVE should not be used in combination with CYP1A2 inhibitors, like fluvoxamine, ciprofloxacin or enoxacin since the combination results in elevated plasma concentrations of duloxetine

Dutasteride [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

Long-term combination of dutasteride with drugs that are potent inhibitors of the enzyme CYP3A4 may increase serum concentrations of dutasteride.

Duvelisib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Duvelisib dose should be reduced to 15 mg twice daily when co-administered with a strong CYP3A4 inhibitor

Ebastine, strong CYP3A4 inhibitors

The co-administration with CYP3A4 inhibitors may increase the plasma levels of ebastine and should be done with caution

Edoxaban [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

The use of edoxaban with other P-gp inhibitors including HIV protease inhibitors has not been studied.

Efavirenz [1], strong CYP2B6 inhibitors ---> SmPC of [1] of EMA

Efavirenz exposure may be increased when given with medicinal products (for example, ritonavir) or food (for example, grapefruit juice), which inhibit CYP3A4 or CYP2B6 activity.

Efavirenz [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Efavirenz exposure may be increased when given with medicinal products (for example, ritonavir) or food (for example, grapefruit juice), which inhibit CYP3A4 or CYP2B6 activity.

Elbasvir/grazoprevir [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Co-administration of ZEPATIER with strong CYP3A inhibitors increases elbasvir and grazoprevir plasma concentrations, and co-administration is not recommended

Elbasvir/grazoprevir [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Co-administration of ZEPATIER with P-gp inhibitors is expected to have a minimal effect on the plasma concentrations of ZEPATIER.

Eletriptan [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

In clinical studies with potent inhibitors of CYP3A4 significant increases in eletriptan Cmax and AUC were observed. Eletriptan should not be used together with potent CYP3A4 inhibitors

Eliglustat [1], strong CYP2D6 inhibitors ---> SmPC of [1] of EMA

A dose of eliglustat 84 mg once daily should be considered when a strong CYP2D6 inhibitor is used concomitantly in intermediate and extensive metabolisers

Eliglustat [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Eliglustat is contraindicated in patients who are CYP2D6 poor metabolisers (PMs) taking a strong CYP3A inhibitor

Eltrombopag [1], strong CYP1A2 inhibitors ---> SmPC of [1] of EMA

Medicinal products that inhibit a single enzyme are unlikely to significantly affect plasma eltrombopag concentrations

Eltrombopag [1], strong CYP2C8 inhibitors ---> SmPC of [1] of EMA

Medicinal products that inhibit a single enzyme are unlikely to significantly affect plasma eltrombopag concentrations

Eltrombopag [1], strong UGT1A1 inhibitors ---> SmPC of [1] of EMA

Medicinal products that inhibit a single enzyme are unlikely to significantly affect plasma eltrombopag concentrations

Eltrombopag [1], strong UGT1A3 inhibitors ---> SmPC of [1] of EMA

Medicinal products that inhibit a single enzyme are unlikely to significantly affect plasma eltrombopag concentrations

Eluxadoline [1], strong OATP1B1 inhibitors ---> SmPC of [1] of EMA

Co-administration of OATP1B1 inhibitors with eluxadoline may increase exposure to eluxadoline. Eluxadoline should not be administered concomitantly with such medicinal products

Elvitegravir [1], strong UGT1A1 inhibitors ---> SmPC of [1] of EMA

Co-administration of elvitegravir with medicinal products that are potent inhibitors of UGT1A1/3 may result in increased elvitegravir plasma concentrations and dose modifications may be required.

Elvitegravir [1], strong UGT1A3 inhibitors ---> SmPC of [1] of EMA

Co-administration of elvitegravir with medicinal products that are potent inhibitors of UGT1A1/3 may result in increased elvitegravir plasma concentrations and dose modifications may be required.

Elvitegravir, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase plasma levels of elvitegravir

Elvitegravir/cobicistat/emtricitabine/tenofovir disoproxil [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Co-administration of elvitegravir/cobicistat/emtricitabine/tenofovir with medicinal products that inhibit CYP3A may decrease the clearance of cobicistat, resulting in increased cobicistat plasma concentrations.

Emtricitabine/rilpivirine/tenofovir disoproxil [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Co-administration of emtricitabine/rilpivirine/tenofovir with medicinal products that inhibit CYP3A enzyme activity has been observed to increase rilpivirine plasma concentrations.

Emtricitabine/tenofovir alafenamide [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Co-administration of Descovy with other medicinal products that inhibit P-gp (e.g., cobicistat, ritonavir, ciclosporin) are expected to increase the absorption and plasma concentration of tenofovir alafenamide.

Encorafenib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Concomitant administration of encorafenib with strong CYP3A4 inhibitors should be avoided (due to increased encorafenib exposure and potential increase in toxicity, see section 5.2).

Enfortumab vedotin [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Patients receiving concomitant strong CYP3A4 inhibitors should be monitored more closely for signs of toxicities.

Entrectinib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Co-administration of strong and moderate CYP3A inhibitors (including, but not limited to, ritonavir, saquinavir, ketoconazole, itraconazole, voriconazole, posaconazole, grapefruit or Seville oranges) should be avoided.

Entrectinib [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Caution is advised when treatment with strong or moderate P-gp inhibitors (e.g. verapamil, nifedipine, felodipine, fluvoxamine, paroxetine) are co-administered with entrectinib due to risk of increased entrectinib exposure

Enzalutamide [1], strong CYP2C8 inhibitors ---> SmPC of [1] of EMA

CYP2C8 plays an important role in the elimination of enzalutamide. A strong CYP2C8 inhibitor increased AUC of enzalutamide. Strong inhibitors of CYP2C8 are to be avoided or used with caution during enzalutamide treatment.

Enzalutamide [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

CYP3A4 plays a minor role in the metabolism of enzalutamide. No dose adjustment is necessary when enzalutamide is co-administered with inhibitors of CYP3A4.

Eplerenone [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

Strong CYP3A4 inhibitors may increase the AUC of eplerenone. The concomitant use of eplerenone with strong CYP3A4 inhibitors is contra-indicated

Ergot derivatives, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of ergot derivate

Eribulin [1], strong OATP inhibitors ---> SmPC of [1] of EMA

The inhibition of hepatic transport proteins may increase the plasma concentrations of eribulin. Co-administration is not recommended

Eribulin [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

The inhibition of hepatic transport proteins may increase the plasma concentrations of eribulin. Co-administration is not recommended

Erlotinib [1], strong CYP1A2 inhibitors ---> SmPC of [1] of EMA

Caution should be exercised when potent CYP1A2 inhibitors are combined with erlotinib. If adverse reactions related to erlotinib are observed, the dose of erlotinib may be reduced.

Erlotinib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Erlotinib is metabolised in the liver by the hepatic cytochromes in humans, primarily CYP3A4 and to a lesser extent by CYP1A2. Potent inhibitors of CYP3A4 activity decrease erlotinib metabolism and increase erlotinib plasma concentrations.

Erlotinib [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Erlotinib is a substrate for the P-glycoprotein active substance transporter. Concomitant administration of inhibitors of Pgp may lead to altered distribution and/or altered elimination of erlotinib.

Escitalopram [1], strong CYP2C19 inhibitors ---> SmPC of [1] of eMC

Caution should be exercised when used escitalopram concomitantly with CYP2C19 inhibitors. A reduction in the dose of escitalopram may be necessary based on monitoring of side-effects during concomitant treatment.

Esomeprazole [1], strong CYP2C19 inhibitors ---> SmPC of [1] of EMA

Esomeprazole is metabolised by CYP2C19 and CYP3A4. Concomitant administration of esomeprazole and a CYP3A4 inhibitor resulted in an increased exposure (AUC) to esomeprazole. A dose adjustment of esomeprazole is not regularly required

Estrogens, strong CYP3A4 inhibitors ---> SmPC of [conjugated oestrogens/bazedoxifene] of EMA

Inhibitors of CYP3A4 may increase plasma concentrations of oestrogens and may result in adverse reactions.

Ethinyl estradiol, strong CYP3A4 inhibitors

Increase in plasma hormone levels associated with co-administered drug

Ethinylestradiol/norgestimate [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

Increase in plasma hormone levels associated with co-administered drug

Ethosuximide, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of ethosuximide, which has a narrow therapeutic margin

Etonogestrel, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of etonogestrel

Etravirine [1], strong CYP2C19 inhibitors ---> SmPC of [1] of EMA

Etravirine is metabolised by CYP3A4, CYP2C9 and CYP2C19. Medicinal products that inhibit CYP3A4, CYP2C9 or CYP2C19 may decrease the clearance of etravirine and may result in increased plasma concentrations of etravirine.

Etravirine [1], strong CYP2C9 inhibitors ---> SmPC of [1] of EMA

Etravirine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Everolimus [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Large increase in everolimus concentration is expected. Concomitant treatment of everolimus and potent CYP3A4 inhibitors is not recommended.

Everolimus [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Large increase in everolimus concentration is expected. Concomitant treatment of everolimus and potent PgP inhibitors is not recommended.

Exemestane [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

In a clinical pharmacokinetic study, the specific inhibition of CYP 3A4 showed no significant effects on the pharmacokinetics of exemestane.

Ezetimibe/atorvastatin [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

Potent CYP3A4 inhibitors have been shown to lead to markedly increased concentrations of atorvastatin. Coadministration of potent CYP3A4 inhibitors should be avoided if possible.

Ezetimibe/simvastatine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

Potent inhibitors of cytochrome P450 3A4 with simvastatine increase the risk of myopathy and rhabdomyolysis. The co-administration of simvastatine with potent inhibitors of CYP3A4 is contraindicated

Fedratinib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Concomitant administration of Inrebic with strong CYP3A4 inhibitors increases Inrebic exposure. Increased exposure of Inrebic may increase the risk of adverse reactions.

Felodipine, strong CYP3A4 inhibitors ---> SmPC of [felodipine/metoprolol] of eMC

Enzyme inhibiting substances of cytochrome P450 isoenzyme 3A4 may increase in felodipine plasma concentrations

Felodipine/metoprolol, strong CYP2D6 inhibitors

CYP2D6 inhibitors may increase the plasma levels of metoprolol

Felodipine/metoprolol, strong CYP3A4 inhibitors

It has been shown that inhibitors of cytochrome P450-3A4 system increase the plasma concentrations of felodipine. The concomitant use with strong CYP3A4 inhibitors should be avoided

Felodipine/ramipril [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

The strong CYP3A4 inhibition may increase the plasma levels of felodipine. The co-administration of felodipine with strong CYP3A4 inhibitors should be avoided

Fenofibrate/simvastatin [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Potent inhibitors of cytochrome P450 3A4 increase the risk of myopathy and rhabdomyolysis by increasing the concentration of HMG-CoA reductase inhibitory activity in plasma during simvastatin therapy. Concomitant use is contraindicated

Fentanyl [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

The concomitant use of fentanyl with strong CYP3A4 inhibitors may result in increased fentanyl plasma concentrations, potentially causing serious adverse drug reactions including fatal respiratory depression.

Fesoterodine [1], strong CYP2D6 inhibitors ---> SmPC of [1] of EMA

Co-administration of fesoterodine and a potent CYP2D6 inhibitor may result in increased exposure and adverse events. A dose reduction to 4 mg may be needed

Fesoterodine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

The maximum dose of fesoterodine should be restricted to 4 mg when used concomitantly with potent CYP3A4 inhibitors

Fidaxomicin [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Fidaxomicin is a substrate of P-gp. Co-administration of potent inhibitors of P-gp increases fidaxomicin exposure. Co-administration of potent inhibitors of P-gp is not recommended.

Finasteride [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

It is probable that inhibitors and inducers of CYP3A4 will affect the plasma concentration of finasteride. However, based on established safety margins, any increase due to concomitant use of such inhibitors is unlikely to be of clinical significance.

Fingolimod [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Co-administration of fingolimod with CYP3A4 inhibitors may increase the fingolimod exposure. Caution should be exercised with substances that may inhibit CYP3A4

Flecainide [1], strong CYP2D6 inhibitors ---> SmPC of [1] of eMC

Concurrent use of drugs inhibiting the iso-enzyme CYP2D6 can increase plasma concentrations of flecainide

Flunitrazepam, strong CYP3A4 inhibitors

Substances that inhibit hepatic enzymes may enhance the effect of benzodiazepines. Interactions with strong CYP3A4 inhibitors cannot be excluded

Fluoxetine, strong CYP2D6 inhibitors

The strong CYP2D6 inhibition may increase plasma concentrations of fluoxetine

Fluphenazine, strong CYP2D6 inhibitors

The co-administration of fluphenazine with drugs that may increase the plasma levels of fluphenazine should be avoided

Flurazepam, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of flurazepam

Fluticasone furoate [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Caution is recommended when co-administering fluticasone furoate with potent CYP3A4 inhibitors as an increase in systemic exposure cannot be ruled out.

Fluticasone furoate/umeclidinium/vilanterol [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Caution is advised when co-administering with strong CYP3A4 inhibitors as there is potential for increased systemic exposure to both fluticasone furoate and vilanterol, which could lead to an increased potential for adverse reactions.

Fluticasone furoate/vilanterol [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Caution is advised when co-administering with strong CYP 3A4 inhibitors as there is potential for increased systemic exposure to both fluticasone furoate and vilanterol, and concomitant use should be avoided.

Fluticasone furoate/vilanterol [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Clinical pharmacology studies with a specific P-gp inhibitor and fluticasone furoate have not been conducted.

Fluticasone [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

The strong CYP3A4 inhibition may increase the plasma concentrations of fluticasone. Concomitant use is not recommended

Fluvastatin [1], strong CYP2C9 inhibitors ---> SmPC of [1] of eMC

There are multiple, alternative cytochrome P450 (CYP450) pathways for fluvastatin biotransformation and thus fluvastatin metabolism is relatively insensitive to CYP450 inhibition.

Fluvastatin [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

Given the minimal involvement of the enzyme CYP3A4 in the metabolism of fluvastatin, it is expected that CYP3A4 inhibitors (e.g. ketoconazole, ciclosporin) are unlikely to affect the bioavailability of fluvastatin.

Formoterol/glycopyrronium/budesonide [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

The metabolism of budesonide is primarily mediated by CYP3A4. Co-treatment with strong CYP3A inhibitors are expected to increase the risk of systemic side effects, and should be avoided

Fosamprenavir, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of amprenavir

Fosaprepitant [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Concomitant administration of fosaprepitant with active substances that inhibit CYP3A4 activity should be approached cautiously as the combination is expected to result in increased plasma concentrations of aprepitant

Fosphenytoin [1], strong CYP2C19 inhibitors ---> SmPC of [1] of eMC

Phenytoin is mainly metabolized in the liver by the CYP2C9 and CYP2C19 enzymes. Inhibition of phenytoin metabolism may produce significant increases in plasma phenytoin concentrations and increase the risk of phenytoin toxicity.

Fosphenytoin [1], strong CYP2C9 inhibitors ---> SmPC of [1] of eMC

Fostamatinib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Concomitant use of fostamatinib with strong CYP3A4 inhibitors increases exposure to R406 (the major active metabolite), which may increase the risk of adverse reactions.

Fostemsavir [1], strong BCRP inhibitors ---> SmPC of [1] of EMA

Fostemsavir may be co-administered with strong CYP3A4, BCRP and/or P-gp inhibitors without dose adjustment based on the results of clinical drug interaction studies with cobicistat and ritonavir.

Fostemsavir [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Fostemsavir may be co-administered with strong CYP3A4, BCRP and/or P-gp inhibitors without dose adjustment based on the results of clinical drug interaction studies with cobicistat and ritonavir.

Fostemsavir [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Fostemsavir may be co-administered with strong CYP3A4, BCRP and/or P-gp inhibitors without dose adjustment based on the results of clinical drug interaction studies with cobicistat and ritonavir.

Fulvestrant [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Dose adjustment is not necessary in patients who are receiving fulvestrant and CYP3A4 inhibitors or inducers concomitantly.

Gadoxetate [1], strong OATP inhibitors ---> SmPC of [1] of eMC

As transport of gadoxetate to the liver may be mediated by OATP transporters it cannot be excluded that potent OATP inhibitors could cause drug interactions reducing the hepatic contrast effect.

Gadoxetic acid, strong OATP inhibitors [2] ---> SmPC of [2] of eMC

As transport of gadoxetate to the liver may be mediated by OATP transporters it cannot be excluded that potent OATP inhibitors could cause drug interactions reducing the hepatic contrast effect.

Galantamine [1], strong CYP2D6 inhibitors ---> SmPC of [1] of eMC

The co-administration of galantamine with strong CYP2D6 inhibitors may increase the bioavailability of galantamine and the incidence of cholinergic adverse reactions, predominantly nausea and vomiting.

Galantamine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

The co-administration of galantamine with strong CYP3A4 inhibitors may increase the bioavailability of galantamine and the incidence of cholinergic adverse reactions, predominantly nausea and vomiting.

Gefitinib [1], strong CYP2D6 inhibitors ---> SmPC of [1] of EMA

There are no data on concomitant treatment with an inhibitor of CYP2D6 but potent inhibitors of this enzyme might cause increased plasma concentrations of gefitinib in CYP2D6 extensive metabolisers by about 2-fold

Gefitinib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Concomitant administration with potent inhibitors of CYP3A4 activity may increase gefitinib plasma concentrations. The increase may be clinically relevant since adverse reactions are related to dose and exposure.

Gilteritinib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Caution is required when prescribing gilteritinib with medicines that are strong inhibitors of CYP3A and/or P-gp because they can increase gilteritinib exposure. Alternative medicines that do not strongly inhibit CYP3A and/or P-gp should be considered.

Gilteritinib [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Glasdegib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Caution should be used when administering concomitantly with strong CYP3A4 inhibitors as an increase in glasdegib plasma concentration may occur.

Glibenclamide, strong CYP2C9 inhibitors

The strong CYP2C9 inhibition may increase the plasma concentrations of glibenclamide, which has a narrow therapeutic margin

Glimepiride [1], strong CYP2C9 inhibitors ---> SmPC of [1] of eMC

Glimepiride is metabolized by cytochrome P450 2C9 (CYP2C9). Its metabolism is known to be influenced by concomitant administration of CYP2C9 inhibitors (e.g. fluconazole).

Glycopyrronium/indacaterol/mometasone [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

However, there may be a potential for increased systemic exposure to mometasone furoate when strong CYP3A4 inhibitors (e.g. ketoconazole, itraconazole, nelfinavir, ritonavir, cobicistat) are co-administered.

Glycopyrronium/indacaterol/mometasone [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Due to the very low plasma concentration achieved after inhaled dosing, clinically significant interactions with mometasone furoate are unlikely.

Granisetron [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

As granisetron is metabolised by hepatic cytochrome P450 drug-metabolising enzymes (CYP1A1 and CYP3A4), inhibitors of these enzymes may change the clearance and, hence, the half-life of granisetron.

Guanfacin [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Co-administration of Intuniv with moderate and strong CYP3A4/5 inhibitors elevates plasma guanfacine concentrations and increases the risk of adverse reactions such as hypotension, bradycardia, and sedation.

Halofantrine, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of halofantrine

Haloperidol [1], strong CYP2D6 inhibitors ---> SmPC of [1] of eMC

Inhibition of the CYP2D6 by another drug may result in increased haloperidol concentrations and an increased risk of adverse events, including QT-prolongation.

Haloperidol [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

Inhibition of the CYP3A4 by another drug may result in increased haloperidol concentrations and an increased risk of adverse events, including QT-prolongation.

Hemp extract, strong CYP3A4 inhibitors

The co-administration may increase the Cmax and THC and CBD.

Hydrocortisone [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Potent CYP 3A4 inhibitors can inhibit the metabolism of hydrocortisone, and thus increase blood levels.

Hydroxyzine, strong CYP3A4 inhibitors

The strong inhibition of CYP3A4 may increase the plasma levels of hydroxycine

Ibrutinib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Ibrutinib is primarily metabolised by cytochrome P450 enzyme 3A4. Concomitant use of ibrutinib and medicinal products that strongly inhibit CYP3A4 can increase ibrutinib exposure and should be avoided.

Ibuprofen, strong CYP2C9 inhibitors

The potent CYP2C9 inhibition may increase the plasma concentrations of ibuprofen

Ifosfamide, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of ifosfamide, which has a narrow therapeutic margin

Iloperidone, strong CYP2D6 inhibitors

The strong CYP2D6 inhibition may increase the plasma concentrations of iloperidone

Iloperidone, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of iloperidone

Imatinib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Substances that inhibit the cytochrome P450 isoenzyme CYP3A4 activity could decrease metabolism and increase imatinib concentrations. Caution should be taken when administering imatinib with inhibitors of the CYP3A4 family.

Imipramine, strong CYP2D6 inhibitors

The CYP2D6 inhibition may increase plasma concentrations of imipramine (narrow therapeutic index)

Indacaterol, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of indacaterol

Indacaterol/mometasone [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

There may be a potential for increased systemic exposure to mometasone furoate when strong CYP3A4 inhibitors (e.g. ketoconazole, itraconazole, nelfinavir, ritonavir, cobicistat) are co-administered.

Indinavir [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

The metabolism of indinavir is mediated by the cytochrome P450 enzyme CYP3A4. Therefore, other substances that either share this metabolic pathway or modify CYP3A4 activity may influence the pharmacokinetics of indinavir.

Irinotecan [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Co-administration of ONIVYDE with other inhibitors of CYP3A4 may increase systemic exposure of ONIVYDE.

Isavuconazole [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

No dose adjustment of CRESEMBA is necessary when co-administered with strong CYP3A4/5 inhibitors, however caution is advised as adverse drug reactions may increase

Isradipine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

Caution should be exercised when co-administering isradipine with strong CYP3A inhibitors

Itraconazol [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

Potent inhibitors of CYP3A4 may increase the bioavailability of itraconazole.

Ivabradine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

The concomitant use of ivabradine and potent CYP3A4 inhibitors increases plasma concentrations of ivabradine (may be associated with the risk of excessive bradycardia). The concomitant use of ivabradine with these medicinal products is contraindicated

Ivacaftor [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Ivacaftor is a sensitive CYP3A substrate. A reduction of the Kalydeco dose to 150 mg twice a week is recommended for co-administration with strong CYP3A inhibitors

Ivacaftor/tezacaftor/elexacaftor [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

The dose of IVA/TEZ/ELX and ivacaftor should be reduced when co-administered with strong CYP3A inhibitors (see Table 1 in section 4.2 and section 4.4).

Ixabepilone, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of ixabepilone. The coadministration should be avoided

Ixazomib [1], strong CYP1A2 inhibitors ---> SmPC of [1] of EMA

No dose modification is required for ixazomib with co-administration of strong CYP1A2 inhibitors.

Ixazomib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

No dose modification is required for ixazomib with co-administration of strong CYP3A inhibitors.

Ketoconazole [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Potent inhibitors of CYP3A4 may increase the bioavailability of Ketoconazole HRA, these drugs should be used with caution when co-administered with Ketoconazole HRA and patients should be monitored closely for signs and symptoms of adrenal insufficiency.

Lacidipine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

Lacidipine is known to be metabolised by cytochrome CYP3A4 and, therefore, significant inhibitors and inducers of CYP3A4 administered concurrently may interact with the metabolism and elimination of lacidipine.

Lacosamide [1], strong CYP2C9 inhibitors ---> SmPC of [1] of EMA

Caution is recommended in concomitant treatment of lacosamide with strong inhibitors of CYP2C9, which may lead to increased systemic exposure of lacosamide.

Lacosamide [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Caution is recommended in concomitant treatment of lacosamide with strong inhibitors of CYP3A4, which may lead to increased systemic exposure of lacosamide.

Lamivudine/raltegravir [1], strong UGT1A1 inhibitors ---> SmPC of [1] of EMA

Co-administration of lamivudine/raltegravir with medicinal products that are known to be potent UGT1A1 inhibitors (e.g., atazanavir) may increase plasma levels of raltegravir.

Lansoprazole [1], strong P-gp inhibitors ---> SmPC of [1] of eMC

Lansoprazole has been observed to inhibit the transport protein, P-glycoprotein (P-gp)in vitro .The clinical relevance of this is unknown.

Lapatinib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Lapatinib is predominantly metabolised by CYP3A. The strong CYP3A4 inhibition increases the exposition to lapatinib. Co-administration of lapatinib with strong inhibitors of CYP3A4 should be avoided.

Lapatinib [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Lapatinib is a substrate for the transport proteins Pgp and BCRP. Inhibitors of these proteins may alter the exposure and/or distribution of lapatinib

Larotrectinib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Larotrectinib is a substrate of cytochrome P450 (CYP) 3A, P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP). Co-administration of VITRAKVI with strong CYP3A inhibitors, P-gp and BCRP inhibitors may increase larotrectinib plasma levels

Latanoprost/timolol [1], strong CYP2D6 inhibitors ---> SmPC of [1] of eMC

Potentiated systemic beta-blockade (e.g. decreased heart rate, depression) has been reported during combined treatment with CYP2D6 inhibitors (e.g. quinidine, fluoxetine, paroxetine) and timolol.

Ledipasvir/sofosbuvir [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Co-administration with medicinal products that inhibit P-gp and/or BCRP may increase ledipasvir and sofosbuvir plasma concentrations without increasing GS-331007 plasma concentration

Lefamulin [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Medicinal products that are strong CYP3A and P-gp inhibitors may alter absorption of lefamulin and therefore increase lefamulin plasma concentrations. Co- administration is contraindicated

Lefamulin [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Medicinal products that are strong CYP3A and P-gp inhibitors may alter absorption of lefamulin and therefore increase lefamulin plasma concentrations. Co- administration is contraindicated

Lercanidipine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

The strong CYP3A4 inhibition increases plasma concentrations of lercanidipine. Co-administration of lercanidipine with inhibitors of CYP3A4 should be avoided

Levobupivacaine [1], strong CYP1A2 inhibitors ---> SmPC of [1] of eMC

In vitro studies indicate that the CYP3A4 isoform and CYP1A2 isoform mediate the metabolism of levobupivacaine. Metabolism of levobupivacaine may be affected by CYP3A4 inhibitors and CYP1A2 inhibitors

Levobupivacaine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

Linagliptin [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Clinically relevant interactions would not be expected with CYP3A4 inhibitors.

Linagliptin [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Clinically relevant interactions would not be expected with P-glycoprotein inhibitors.

Liposome-encapsulated doxorubicin-citrate complex [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Plasma levels of doxorubicin and its metabolite, doxorubicinol, may be increased when doxorubicin is administered with cyclosporine, verapamil, paclitaxel or other agents that inhibit P-glycoprotein (P-Gp).

Lomitapide [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

The strong CYP3A4 inhibition may increase lomitapide AUC. The combination of lomitapide with strong CYP3A4 inhibitors is contra-indicated

Loperamide, strong P-gp inhibitors

The P-glycoprotein inhibition may increase the plasma levels of loperamide

Lopinavir, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition increases the plasma concentrations of lopinavir

Loratadine, strong CYP2D6 inhibitors

The strong CYP2D6 inhibition may increase the plasma concentrations of loratadine.

Loratadine, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of loratadine

Lorlatinib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

CYP3A4/5 inhibitors may increase lorlatinib plasma concentrations and should be avoided

Lornoxicam, strong CYP2C9 inhibitors

Lornoxicam interacts with known inhibitors and inductors of CYP2C9 isoenzymes

Lovastatine, strong CYP3A4 inhibitors

Strong CYP3A4 inhibitors may increase the plasma levels of lovastatin and the risk of myopathy and rhabdomyolysis. The co-administration of strong CYP3A4 inhibitors and lovastatin is contraindicated

Loxapine [1], strong CYP1A2 inhibitors ---> SmPC of [1] of EMA

Concomitant use of loxapine with CYP1A2 inhibitors should be avoided, if possible.

Lumacaftor/ivacaftor [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

When initiating lumacaftor/ivacaftor in patients taking strong CYP3A inhibitors, the dose should be reduced to one tablet daily for the first week of treatment to allow for the steady state induction effect of lumacaftor.

Lumefantrine, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of lumefantrine

Lurasidone [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Lurasidone and its active metabolite ID-14283 are primarily metabolised by CYP3A4. Lurasidone is contraindicated with strong CYP3A4 inhibitors

Lusutrombopag [1], strong BCRP inhibitors ---> SmPC of [1] of EMA

A potential interaction with either P-gp or BCRP inhibitors cannot be excluded, but no dose adjustment is necessary at the recommended clinical dosage of 3 mg in adults.

Lusutrombopag [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

A potential interaction with either P-gp or BCRP inhibitors cannot be excluded, but no dose adjustment is necessary at the recommended clinical dosage of 3 mg in adults.

Macimorelin [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Co-administration of a CYP3A4 inhibitor may increase the macimorelin plasma concentration, and this, in turn, could yield higher plasma GH levels. Based on current understanding, this is unlikely to decrease the specificity of the test.

Macitentan [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Caution should be exercised when macitentan (by CYP3A4 metabolized) is administered concomitantly with strong CYP3A4 inhibitors

Manidipine, strong CYP3A4 inhibitors

Manidipine should not be administered with CYP3A4 inhibitors

Maprotiline, strong CYP2D6 inhibitors

The strong CYP2D6 inhibition may increase plasma concentrations of maprotiline (narrow therapeutic index)

Maraviroc [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Maraviroc is a substrate of cytochrome P450 CYP3A4. Co-administration of maraviroc with medicinal products that inhibit CYP3A4 may increase maraviroc plasma concentrations. Dose adjustment of maraviroc is recommended

Mefloquine, strong CYP3A4 inhibitors [2] ---> SmPC of [2] of eMC

Inhibitors of the isoenzyme CYP3A4 may modify the pharmacokinetics/metabolism of mefloquine, leading to an increase in mefloquine plasma concentration.

Melagatran, strong P-gp inhibitors

The strong inhibition of P-glycoprotein may increase the exposure to melagatran

Melatonin [1], strong CYP1A2 inhibitors ---> SmPC of [1] of EMA

CYP1A2 inhibitors such as quinolones may give rise to increased melatonin exposure.

Melitracen, strong CYP2D6 inhibitors

The strong CYP2D6 inhibition may increase plasma concentrations of melitracen

Mequitazine, strong CYP2D6 inhibitors

Mequitazine should not be used with CYP2D6 inhibitor drugs. The increased plasma levels of mequitazine may increase the risk of QT interval prolongation

Metformin/saxagliptin/dapagliflozin [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Co-administration of saxagliptin with the potent inhibitor of CYP3A4/5 ketoconazole, increased the Cmax and AUC of saxagliptin by 62% and 2.5-fold. These pharmacokinetic effects are not clinically meaningful and do not require dose adjustment.

Methadone [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

Methadone clearance is decreased when co-administered with drugs which inhibit CYP3A4 activity, since the metabolism of methadone is mediated by the CYP3A4 isoenzyme.

Methadone, strong P-gp inhibitors

Methadone is substrate of P-glycoprotein. Medicinal products that the substrate inhibit (quinidine, verapamil) may increase plasma concentrations of methadone

Methylergometrine, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of methylergometrine. The concomitant use should be avoided

Methylphenidate, strong CYP2D6 inhibitors

The strong CYP2D6 inhibition may increase the plasma concentrations of methylphenidate

Methylprednisolone, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of glucocorticoid

Methysergide, strong CYP3A4 inhibitors [2] ---> SmPC of [2] of eMC

The concomitant use of cytochrome P450 3A (CYP3A) inhibitors, since this can result in an elevated exposure to methysergide and ergot toxicity (vasospasm and ischemia of the extremities and other tissues).

Metoclopramide, strong CYP2D6 inhibitors

The strong CYP2D6 inhibition may increase the plasma levels of metoclopramide

Metoprolol, strong CYP2D6 inhibitors

The strong CYP2D6 inhibition may increase the plasma levels of metoprolol.

Mexiletine [1], strong CYP1A2 inhibitors ---> SmPC of [1] of EMA

Co-administration of mexiletine with a hepatic enzyme inhibitor (CYP1A2 inhibitor; CYP2D6 inhibitor) significantly increases mexiletine exposure and thus the associated risk of adverse reactions to mexiletine.

Mexiletine [1], strong CYP2D6 inhibitors ---> SmPC of [1] of EMA

Mianserin, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of mianserin

Midazolam [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Midazolam is metabolized by CYP3A4. Inhibitors of CYP3A4 have the potential to increase the plasma concentrations and, subsequently, the effects of midazolam thus requiring dose adjustments accordingly.

Midostaurin [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Strong CYP3A4 inhibitors may increase midostaurin blood concentrations.

Mifepristone [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

On the basis of this drug's metabolism by CYP3A4, it is possible that strong CYP3A4 inhibitors may inhibit its metabolism (increasing serum levels of mifepristone).

Mirabegron [1], strong CYP2D6 inhibitors ---> SmPC of [1] of EMA

Interaction of mirabegron with a known CYP2D6 inhibitor is not expected and was not studied.

Mirabegron [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

The strong CYP3A4 inhibition may increase the exposition of mirabegron. No dose-adjustment is needed when mirabegron is combined with inhibitors of CYP3A and/or P-gp.

Mirabegron [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

The strong inhibition of P-gp may increase the exposition of mirabegron. No dose-adjustment is needed when mirabegron is combined with inhibitors of P-gp.

Mirtazapine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

The strong CYP3A4 inhibition may increase the plasma concentrations of mirtazapine

Mizolastine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

Concurrent use of other potent inhibitors or substrates of hepatic oxidation (cytochrome P450 3A4) with mizolastine should be approached with caution.

Moclobemide, strong CYP2D6 inhibitors

Moclobemide should not be co-administered with drugs that may inhibit its hepatic metabolism (e. g. cimetidine, fluoxetine)

Mometasone [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

There may be a potential for increased systemic exposure to mometasone furoate when strong CYP3A4 inhibitors are co-administered

Naftidrofuryl, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase plasma concentrations of naftidrofuryl

Naldemedine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Concomitant use of naldemedine with strong CYP3A inhibitors leads to an increase in naldemedine exposure and may increase the risk of adverse reactions. Concomitant use with strong CYP3A inhibitors should be avoided.

Naldemedine [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Concomitant use of P-gp inhibitors such as cyclosporine may increase plasma concentrations of naldemedine. If naldemedine is used with strong P-gp inhibitors, monitor for adverse reactions.

Nalmefene [1], strong UGT2B7 inhibitors ---> SmPC of [1] of EMA

Co-administration with medicinal products that are potent inhibitors of the UGT2B7 enzyme may significantly increase the exposure to nalmefene.

Naloxegol [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Concomitant use of naloxegol with CYP3A4 inhibitors increases naloxegol exposition. Concomitant use of naloxegol with strong CYP3A4 inhibitors is contraindicated

Naproxen/esomeprazole, strong CYP2C19 inhibitors ---> SmPC of [esomeprazole] of EMA

Nateglinide [1], strong CYP2C9 inhibitors ---> SmPC of [1] of EMA

Particular caution is recommended when nateglinide is co-administered with potent inhibitors of CYP2C9, or in patients known to be poor metabolisers for CYP2C9.

Nateglinide [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Interaction studies with a 3A4 inhibitor have not been carried out in vivo.

Nebivolol [1], strong CYP2D6 inhibitors ---> SmPC of [1] of eMC

The CYP2D6 inhibition may lead to increased plasma levels of nebivolol (metabolized by CYP2D6) that is associated with an increased risk of excessive bradycardia and adverse events.

Nelfinavir [1], strong CYP2C19 inhibitors ---> SmPC of [1] of EMA

Co-administration of nelfinavir with inhibitors of CYP2C19 may be expected to reduce the conversion of nelfinavir to its major active metabolite M8 (tert-butyl hydroxy nelfinavir) with a concomitant increase in plasma nelfinavir levels

Nelfinavir [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Coadministration of nelfinavir and a strong inhibitor of CYP3A, ketoconazole, resulted in a 35 % increase in nelfinavir plasma AUC. The changes in nelfinavir concentrations are not considered clinically significant and no dose adjustment is needed

Neratinib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Concomitant treatment with strong CYP3A4 and P-gp inhibitors should be avoided due to risk of increased exposure to neratinib

Neratinib [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Concomitant treatment with strong CYP3A4 and P-gp inhibitors should be avoided due to risk of increased exposure to neratinib

Netupitant/palonosetron [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Netupitant is mainly metabolized by CYP3A4; therefore, co-administration with medicinal products that inhibit CYP3A4 may increase netupitant plasma levels. Consequently, co-administration with strong CYP3A4 inhibitors should be approached with caution

Nicardipine, strong CYP3A4 inhibitors [2] ---> SmPC of [2] of eMC

Nicardipine is metabolized by cytochrome P450 3A4. Concomitant administration of nicardipine with inhibitors of cytochrome P450 3A4 may alter the plasma levels of nicardipine.

Nifedipine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

Nifedipine is metabolised via the cytochrome P450 3A4 system. Therefore, there are theoretical interactions with drugs that are known to inhibit this enzyme

Nilotinib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Significant prolongation of the QT interval may occur when nilotinib is inappropriately taken with strong CYP3A4 inhibitors. Prolongation of the QT interval may expose patients to the risk of fatal outcome.

Nilutamide, strong CYP2C19 inhibitors

The potent CYP2C19 inhibition may increase the plasma concentrations of nilutamide

Nilvadipine, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of nilvadipine. Caution is recommended

Nimodipine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

Upon co-administration of nimodipine with CYP3A4 inhibitors the blood pressure should be monitored and, if necessary, an adaptation in the nimodipine dose should be considered.

Nintedanib [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

If co-administered with nintedanib, potent P-gp inhibitors may increase exposure to nintedanib. In such cases, patients should be monitored closely for tolerability of nintedanib.

Nisoldipine, strong CYP3A4 inhibitors

The co-administration of nisoldipine with medicinal products that inhibit the cytochrome P450 3A4-system may increase the bioavailability of nisoldipine. Concomitant use is contraindicated

Nitisinone [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Nitisinone is metabolised in vitro by CYP 3A4 and dose-adjustment may therefore be needed when nitisinone is co-administered with inhibitors of this enzyme.

Nitrendipine, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of nitrendipine

Norgestimate, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of norgestimate

Nortriptyline, strong CYP2D6 inhibitors

Concomitant use of nortriptyline with drugs increasing the metabolism and plasma levels of nortriptyline should be avoided

Olanzapine [1], strong CYP1A2 inhibitors ---> SmPC of [1] of EMA

Since olanzapine is metabolised by CYP1A2, substances that can specifically inhibit this isoenzyme may increase olanzapine concentration

Olaparib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Known strong or moderate CYP3A inhibitors are not recommended with olaparib

Olaparib [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

In vitro olaparib is a substrate for the efflux transporter P-gp and therefore P-gp inhibitors may increase exposure to olaparib

Olmesartan medoxomil/amlodipine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

Concomitant use of amlodipine with strong or moderate CYP3A4 inhibitors may give rise to significant increase in amlodipine exposure.

Ombitasvir/paritaprevir/ritonavir [1], strong BCRP inhibitors ---> SmPC of [1] of EMA

Potent inhibitors of P-gp, BCRP, OATP1B1 and/or OATP1B3 have the potential to increase the exposure to paritaprevir.

Ombitasvir/paritaprevir/ritonavir [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Ombitasvir/paritaprevir/ritonavir [1], strong OATP1B1 inhibitors ---> SmPC of [1] of EMA

Potent inhibitors of P-gp, BCRP, OATP1B1 and/or OATP1B3 have the potential to increase the exposure to paritaprevir.

Ombitasvir/paritaprevir/ritonavir [1], strong OATP1B3 inhibitors ---> SmPC of [1] of EMA

Potent inhibitors of P-gp, BCRP, OATP1B1 and/or OATP1B3 have the potential to increase the exposure to paritaprevir.

Ombitasvir/paritaprevir/ritonavir [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Potent inhibitors of P-gp, BCRP, OATP1B1 and/or OATP1B3 have the potential to increase the exposure to paritaprevir.

Omeprazole [1], strong CYP2C19 inhibitors ---> SmPC of [1] of eMC

Concomitant administration of omeprazole and a CYP2C19 inhibitor, increased the omeprazole exposure.

Omeprazole [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

Concomitant administration of omeprazole and a CYP3A4 inhibitor, increased the omeprazole exposure.

Opipramol, strong CYP2D6 inhibitors

The strong CYP2D6 inhibition may increase the plasma concentrations of opipramol.

Osilodrostat [1], strong inhibitors ---> SmPC of [1] of EMA

Caution is advised when co-administered medicinal products that strongly inhibit multiple enzymes are introduced or discontinued during osilodrostat treatment

Osimertinib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Itraconazole (a strong CYP3A4 inhibitor) had no clinically significant effect on the exposure of osimertinib. Therefore, CYP3A4 inhibitors are not likely to affect the exposure of osimertinib.

Ospemifene [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Ketoconazole, a strong CYP3A4 inhibitor, increased the ospemifene AUC by 1.4-fold. This increase is not considered to be clinically significant. There is no reason to expect that strong CYP3A4 inhibitors would cause a clinically meaningful change

Oxybutynine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

As oxybutynin is metabolised by cytochrome P 450 isoenzyme CYP 3A4, interactions with medicinal products that inhibit this isoenzyme cannot be ruled out.

Oxycodone [1], strong CYP2D6 inhibitors ---> SmPC of [1] of eMC

Strong CYP2D6 inhibitors may have an effect on the elimination of oxycodone.

Ozanimod [1], strong CYP2C8 inhibitors ---> SmPC of [1] of EMA

Caution should be exercised for concomitant use of ozanimod with strong CYP2C8 inhibitors (e.g. gemfibrozil, clopidogrel).

Paclitaxel [1], strong CYP2C8 inhibitors ---> SmPC of [1] of EMA

The metabolism of paclitaxel is catalysed, in part, by cytochrome P450 isoenzymes CYP2C8 and CYP3A4. Therefore, caution should be exercised when administering paclitaxel concomitantly with medicines known to inhibit either CYP2C8 or CYP3A4.

Paclitaxel [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Palbociclib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Strong inhibitors of CYP3A4 may lead to increased toxicity. Concomitant use of strong CYP3A inhibitors during treatment with palbociclib should be avoided.

Panobinostat [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

In patients who take concomitant medicinal products which are strong CYP3A and/or Pgp inhibitors, the dose of panobinostat should be reduced

Panobinostat [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

In patients who take concomitant medicinal products which are strong CYP3A and/or Pgp inhibitors, the dose of panobinostat should be reduced

Parecoxib [1], strong CYP2C9 inhibitors ---> SmPC of [1] of EMA

The strong CYP2C9 inhibition may increase the plasma levels of valdecoxib

Parecoxib, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma levels of valdecoxib

Paroxetine [1], strong CYP2D6 inhibitors ---> SmPC of [1] of eMC

When paroxetine is to be co-administered with a known drug metabolising inhibitor, consideration should be given to using paroxetine doses at the lower end of the range.

Pazopanib [1], strong BCRP inhibitors ---> SmPC of [1] of EMA

Concomitant treatment with strong inhibitors of breast cancer resistance protein (BCRP) should be avoided due to risk of increased exposure to pazopanib

Pazopanib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Concomitant treatment with strong inhibitors of CYP3A4 should be avoided due to risk of increased exposure to pazopanib

Pazopanib [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Concomitant treatment with strong inhibitors of P-glycoprotein (P-gp) should be avoided due to risk of increased exposure to pazopanib

Pemigatinib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

A strong CYP3A4 inhibitor (itraconazole 200 mg once daily) increased pemigatinib AUC geometric mean by 88 % (90 % CI of 75 %, 103 %), which may increase the incidence and severity of adverse reactions with pemigatinib.

Perampanel [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

In healthy subjects, the CYP3A4 inhibitor ketoconazole (400 mg once daily for 10 days) increased perampanel AUC by 20% and prolonged perampanel half-life by 15% (67.8 h vs 58.4 h).

Perazine, strong CYP2D6 inhibitors

The co-administration of perazine (metabolized by CYP2D6) with medicines that its metabolism inhibit should be avoided

Perphenazine, strong CYP2D6 inhibitors

Concomitant use of perphenazine with drugs inhibiting the metabolism of perphenazine is not recommended.

Phenprocoumon, strong CYP2C9 inhibitors

The strong CYP2C9 inhibition may increase plasma concentrations of phenprocoumon

Phenytoin, strong CYP2C19 inhibitors ---> SmPC of [fosphenytoin] of eMC

Phenytoin, strong CYP2C9 inhibitors ---> SmPC of [fosphenytoin] of eMC

Pimozide [1], strong CYP1A2 inhibitors ---> SmPC of [1] of eMC

As CYP1A2 may also contribute to the metabolism of pimozide, prescribers should be aware of the theoretical potential for drug interactions with inhibitors of this enzymatic system.

Pimozide [1], strong CYP2D6 inhibitors ---> SmPC of [1] of eMC

Potent inhibitors of the CYP2D6 will inhibit the metabolism of pimozide, resulting in elevated pimozide plasma levels. Concomitant use of pimozide with drugs known to be inhibitors of cytochrome CYP2D6 is contraindicated

Pimozide [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

Potent inhibitors of the CYP3A4 will inhibit the metabolism of pimozide, resulting in markedly elevated pimozide plasma levels. Concomitant use of pimozide with drugs known to be inhibitors of cytochrome CYP3A4 is contraindicated

Pioglitazone [1], strong CYP2C8 inhibitors ---> SmPC of [1] of EMA

Pioglitazone should be used with caution during concomitant administration of cytochrome P450 2C8 inhibitors (e.g. gemfibrozil). Glycaemic control should be monitored closely.

Pioglitazone/metformin [1], strong CYP2C8 inhibitors ---> SmPC of [1] of EMA

Pioglitazone should be used with caution during concomitant administration of cytochrome P450 2C8 inhibitors (e.g. gemfibrozil) or inducers (e.g. rifampicin). Glycaemic control should be monitored closely.

Piperaquine/artenimol [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Concomitant treatment with medicinal products which inhibit CYP3A4 may lead to a marked increase of piperaquine plasma concentration resulting in an exacerbation of the effect on QTc

Pirfenidone [1], strong CYP1A2 inhibitors ---> SmPC of [1] of EMA

In vitro in vivo extrapolations indicate that strong and selective inhibitors of CYP1A2 (e.g. enoxacin) have the potential to increase the exposure to pirfenidone by approximately 2 to 4-fold.

Pitavastatin, strong CYP3A4 inhibitors

Itraconazol and Saint John's wort, strong inhibitors of CYP3A4, had no clinically meaningful effect on the plasma concentrations of pitavastatin.

Pixantrone [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Based on in vitro studies, pixantrone was found to be a substrate for the membrane transport proteins P-gp/BCRP and OCT1 and agents which inhibit these transporters have the potential to decrease hepatic uptake and excretion efficiency of pixantrone.

Polatuzumab vedotin [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Patients receiving concomitant strong CYP3A4 inhibitors should be monitored more closely for signs of toxicities.

Pomalidomide [1], strong CYP1A2 inhibitors ---> SmPC of [1] of EMA

If strong inhibitors of CYP1A2 (e.g. ciprofloxacin, enoxacin and fluvoxamine) are co-administered with pomalidomide, reduce the dose of pomalidomide by 50%.

Pomalidomide [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Co-administration of pomalidomide with the strong CYP3A4/5 and P-gp inhibitor ketoconazole had no clinically relevant effect on exposure to pomalidomide.

Ponatinib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Caution should be exercised and a reduction of the starting dose should be considered with concurrent use of ponatinib with strong CYP3A inhibitors (modest increases in ponatinib systemic exposure are possible)

Posaconazole [1], strong glucuronidation inhibitors ---> SmPC of [1] of EMA

Posaconazole is metabolised via UDP glucuronidation (phase 2 enzymes) and is a substrate for p-glycoprotein (P-gp) efflux in vitro. Therefore, inhibitors of these clearance pathways may increase posaconazole plasma concentrations

Posaconazole [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Prajmalium, strong CYP2D6 inhibitors

The strong CYP2D6 inhibition may increase the plasma concentrations of prajmaline.

Pralsetinib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Co-administration of pralsetinib with strong CYP3A4 inhibitors or combined P-gp and strong CYP3A4 inhibitors can increase pralsetinib plasma concentrations, which may increase the incidence and severity of adverse reactions of pralsetinib.

Pranlukast, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of pranlukast

Prasugrel [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

CYP3A inhibitors are not anticipated to have a significant effect on the pharmacokinetics of the prasugrel active metabolite.

Pravastatine/fenofibrate [1], strong CYP2C9 inhibitors ---> SmPC of [1] of EMA

Absence of a significant pharmacokinetic interaction with pravastatin

Pravastatine/fenofibrate [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Absence of a significant pharmacokinetic interaction with pravastatin

Prazepam, strong CYP2C19 inhibitors

The potent CYP2C19 inhibition may increase the plasma concentrations of prazepam. Caution should be exercised

Prazepam, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of prazepam. Caution is recommended

Prednisolone, strong CYP3A4 inhibitors

Medicinal products that inhibit the hepatic metabolism of prednisolone may enhance the corticoid effect

Prednisone, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of prednisone

Primidone, strong CYP3A4 inhibitors

Agents which inhibit the CYP 450 3A4 enzyme system may result in increased plasma levels of concomitantly administered primidone and its metabolite phenobarbitone.

Procarbazine, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of procarbazine

Progesterone, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of progesterone

Propafenone, strong CYP2D6 inhibitors

The strong CYP2D6 inhibition may increase plasma levels of propafenone

Propafenone, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of propafenone, which has a narrow therapeutic margin

Propiverine, strong CYP3A4 inhibitors

Clinically relevant increases in serum propiverine may cause the coadministration of propiverine with CYP3A4 inhibitors (e. g. ketoconazole)

Prucalopride [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

The inhibition of P-glycoprotein may increase the systemic exposure to prucalopride. This effect is too small to be clinically relevant.

Quetiapine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

The strong CYP3A4 inhibition may increase the plasma concentrations of quetiapine. Concomitant use of quetiapine with CYP3A4 inhibitors is contraindicated.

Quinidine, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of quinidine and risk relating to QTc prolongation.

Quinine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

Quinine is metabolised via hepatic oxidative cytochrome P450, predominantly by CYP3A4. There is the potential for increased quinine toxicity with concurrent use of potent CYP3A4 inhibitors

Raltegravir [1], strong UGT1A1 inhibitors ---> SmPC of [1] of EMA

The strong inhibition of UGT1A1 may increase plasma levels of raltegravir

Ranolazine [1], strong CYP2D6 inhibitors ---> SmPC of [1] of EMA

Ranolazine is partially metabolised by CYP2D6; therefore, inhibitors of this enzyme may increase plasma concentrations of ranolazine. No dosage adjustment necessary.

Ranolazine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Ranolazine is a substrate of cytochrome CYP3A4. Inhibitors of CYP3A4 increase plasma concentrations of ranolazine. Combining ranolazine with potent CYP3A4 inhibitors is contraindicated

Ranolazine [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Ranolazine is a substrate for P-gp. Inhibitors of P-gp (e.g. ciclosporin, verapamil) increase plasma levels of ranolazine. Careful dose titration of Ranexa is recommended in patients treated with P-gp inhibitors. Down-titration of Ranexa may be required

Rasagiline [1], strong CYP1A2 inhibitors ---> SmPC of [1] of EMA

In vitro metabolism studies have indicated that cytochrome P450 1A2 (CYP1A2) is the major enzyme responsible for the metabolism of rasagiline. Thus, potent CYP1A2 inhibitors may alter rasagiline plasma levels and should be administered with caution.

Reboxetine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

The CYP3A4 inhibition may increase the plasma levels of reboxetine (narrow therapeutic margin and primarily metabolised by the CYP3A4). Reboxetine should not be given together with drugs known to inhibit CYP3A4

Regorafenib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

It is recommended to avoid concomitant use of strong inhibitors of CYP3A4 activity, as their influence on the steady-state exposure of regorafenib and its metabolites has not been studied.

Regorafenib [1], strong UGT1A9 inhibitors ---> SmPC of [1] of EMA

Co-administration of a strong UGT1A9 inhibitor during regorafenib treatment should be avoided, as their influence on the steady-state exposure of regorafenib and its metabolites has not been studied.

Remdesivir [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

In vitro, remdesivir is a substrate for esterases in plasma and tissue, drug metabolizing enzymes CYP2C8, CYP2D6, and CYP3A4, and is a substrate OATP1B1 and P-gp transporters. Strong inhibitors may result in increased remdesivir exposure.

Repaglinide [1], strong CYP2C8 inhibitors ---> SmPC of [1] of EMA

In vitro data indicate that repaglinide is metabolised predominantly by CYP2C8, but also by CYP3A4. Metabolism, and by that clearance of repaglinide, may be altered by substances which influence these cytochrome P-450 enzymes via inhibition.

Retapamulin [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

The strong CYP3A4 inhibition may increase the plasma concentrations of retapamulin. Caution is advised

Ribociclib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Concomitant use of strong CYP3A4 inhibitors should be avoided and an alternative concomitant medicinal product with less potential to inhibit CYP3A4 inhibition should be considered.

Rilpivirine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Riluzole [1], strong CYP1A2 inhibitors ---> SmPC of [1] of EMA

In vitro studies suggest that CYP1A2 is the principal isozyme involved in the initial oxidative metabolism of riluzole. Inhibitors of CYP1A2 could potentially decrease the rate of riluzole elimination

Rimegepant [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Inhibitors of CYP3A4 increase plasma concentrations of rimegepant. Concomitant administration of rimegepant with strong CYP3A4 inhibitors (e.g., clarithromycin, itraconazole, ritonavir) is not recommended

Rimonabant [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

The strong CYP3A4 inhibition may increase the exposition of rimonabant. Caution is advised during concomitant use of rimonabant and potent CYP3A4 inhibitors

Riociguat [1], strong BCRP inhibitors ---> SmPC of [1] of EMA

Concomitant use of riociguat with strong P-gp/BCRP inhibitors is not recommended

Riociguat [1], strong CYP1A1 inhibitors ---> SmPC of [1] of EMA

Drug-drug interactions by inhibition of CYP1A1 could result in increased riociguat exposure, especially in smokers. Strong CYP1A1 inhibitors should be used with caution

Riociguat [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Concomitant use of riociguat with strong P-gp/BCRP inhibitors is not recommended

Risperidone [1], strong CYP2D6 inhibitors ---> SmPC of [1] of eMC

It is expected that CYP 2D6 inhibitors increase the plasma concentrations of risperidone

Ritonavir, strong CYP2D6 inhibitors

The strong CYP2D6 inhibition may increase plasma concentrations of ritonavir (narrow therapeutic index)

Ritonavir, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of ritonavir

Rivaroxaban [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Active substances strongly inhibiting only one of the rivaroxaban elimination pathways, either CYP3A4 or P-gp, are expected to increase rivaroxaban plasma concentrations. This increase is not considered clinically relevant.

Rivaroxaban [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Roflumilast, strong CYP1A2 inhibitors

The potent CYP1A2 inhibition may increase the plasma concentrations of roflumilast

Roflumilast, strong CYP3A4 inhibitors

The strong CYP3A4 inhibition may increase the plasma concentrations of roflumilast

Ropinirole [1], strong CYP1A2 inhibitors ---> SmPC of [1] of eMC

Ropinirole is principally metabolised by the CYP1A2. A pharmacokinetic study revealed that ciprofloxacin increased the Cmax and AUC of ropinirole by 60% and 84% respectively, with a potential risk of adverse events.

Ropivacaine [1], strong CYP1A2 inhibitors ---> SmPC of [1] of eMC

The strong CYP1A2 inhibition may decrease the plasma clearance of ropivacaine. Prolonged administration of ropivacaine with strong CYP1A2 inhibitors should be avoided

Rosiglitazone [1], strong CYP2C8 inhibitors ---> SmPC of [1] of EMA

Rosiglitazone should be used with caution during concomitant administration of CYP2C8 inhibitors (e.g. gemfibrozil). Glycaemic control should be monitored closely.

Roxadustat [1], strong CYP2C8 inhibitors ---> SmPC of [1] of EMA

Roxadustat is a substrate of CYP2C8 and UGT1A9. Monitor Hb levels when initiating or discontinuing concomitant treatment with gemfibrozil, probenecid, other strong inhibitors or inducers of CYP2C8 or other strong inhibitors of UGT1A9.

Roxadustat [1], strong UGT1A9 inhibitors ---> SmPC of [1] of EMA

Rucaparib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Caution should be used for concomitant use of strong CYP3A4 inhibitors or inducers.

Rucaparib [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Caution is recommended when rucaparib is co-administered with medicinal products that are strong inhibitors of P-gp.

Rupatadine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

The concomitant administration of rupatadine with inhibitors of the isozyme CYP3A4 increases the systemic exposure to rupatadine. Rupatadine should be used with caution when it is administered concomitantly with inhibitors of CYP3A4.

Ruxolitinib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

The strong CYP3A4 inhibition may increase ruxolitinib exposition. When co-administering with strong CYP3A4 inhibitors the unit dose of ruxolitinib should be reduced

Salmeterol [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

The co-administration with strong CYP3A4 inhibitors with salmeterol may significant increase the plasma salmeterol exposure, what may cause a QTc interval prolongation. The co-administration should be avoided

Salmeterol/fluticasone propionate [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Co-treatment with potent CYP3A inhibitors, such as itraconazole, and moderate CYP3A inhibitors, such as erythromycin, is also expected to increase the systemic fluticasone propionate exposure and the risk of systemic undesirable effects.

Saquinavir [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Medicinal products that modify CYP3A4 activity may modify the pharmacokinetics of saquinavir.

Saquinavir [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Medicinal products that modify P-gp activity may modify the pharmacokinetics of saquinavir.

Saxagliptin [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

The strong CYP3A4 inhibition may increase the AUC of saxagliptin and decrease those of the principal metabolite

Saxagliptin/metformin [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Coadministration of saxagliptin with the potent inhibitor of CYP3A4/5 ketoconazole, increased the Cmax and AUC of saxagliptin by 62% and 2.5-fold, respectively, and the corresponding values for the active metabolite were decreased by 95% and 88%.

Selexipag [1], strong CYP2C8 inhibitors ---> SmPC of [1] of EMA

In the presence of 600 mg gemfibrozil, twice a day, a strong inhibitor of CYP2C8, exposure to selexipag increased approximately 2-fold. Concomitant administration of Uptravi with strong inhibitors of CYP2C8 (e.g., gemfibrozil) is contraindicated

Selexipag [1], strong UGT1A3 inhibitors ---> SmPC of [1] of EMA

The effect of strong inhibitors of UGT1A3 and UGT2B7 (valproic acid, probenecid, and fluconazole) on the exposure to selexipag has not been studied. A potential pharmacokinetic interaction with strong inhibitors of UGT1A3 and UGT2B7 cannot be excluded.

Selexipag [1], strong UGT2B7 inhibitors ---> SmPC of [1] of EMA

Selpercatinib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

If strong CYP3A and/or P-gp inhibitors, e. g. ketoconazole, itraconazole, voriconazole, ritonavir, saquinavir, telithromycin, posaconazole and nefazodone, have to be coadministered, the dose of selpercatinib should be reduced

Selpercatinib [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Selumetinib [1], strong CYP2C19 inhibitors ---> SmPC of [1] of EMA

Concomitant use of strong or moderate CYP3A4 or CYP2C19 inhibitors is not recommended and alternative agents should be considered.

Selumetinib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Concomitant use of strong or moderate CYP3A4 or CYP2C19 inhibitors is not recommended and alternative agents should be considered.

Sertindole, strong CYP2D6 inhibitors

The plasma concentration of sertindole is increased in patients concurrently taking potent CYP2D6 inhibitors; sertindole should therefore only be used concomitantly with CYP2D6 inhibitors with extreme caution.

Sertindole, strong CYP3A4 inhibitors

The concomitant administration of CYP3A inhibitors and sertindole is contraindicated, as this may lead to significant increases in sertindole levels

Sibutramine [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

Caution should be exercised on concomitant administration of sibutramine with drugs which affect CYP3A4 enzyme activity (increased plasma concentrations (AUC) of sibutramine active metabolites)

Silodosin [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

The strong CYP3A4 inhibition may increase the plasma levels of silodosin. Concomitant use of silodosin with potent CYP3A4 inhibitors is not recommended

Simeprevir [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Co-administration of simeprevir with moderate or strong inhibitors of CYP3A4 may significantly increase the plasma exposure of simeprevir. Co-administration of simeprevir with these inhibitors is not recommended.

Simvastatine, strong CYP3A4 inhibitors ---> SmPC of [fenofibrate/simvastatin] of EMA

The strong CYP3A4 inhibition may increase the plasma concentrations of simvastatine and the risk of myopathy and rhabdomyolysis. The co-administration is contraindicated

Sirolimus [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Inhibitors of CYP3A4 decrease the metabolism of sirolimus and increase sirolimus levels. Co-administration of sirolimus with strong inhibitors of CYP3A4 is not recommended

Sirolimus [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Inhibitors of P-gp may decrease the efflux of sirolimus from intestinal cells and increase sirolimus levels.

Sitagliptin [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

It is possible that potent CYP3A4 inhibitors (i.e. ketoconazole, itraconazole, ritonavir, clarithromycin) could alter the pharmacokinetics of sitagliptin in patients with severe renal impairment or ESRD.

Sitagliptin [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Meaningful interactions would not be expected with p-glycoprotein inhibitors.

Sitagliptin/metformin [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

It is possible that potent CYP3A4 inhibitors (i.e., ketoconazole, itraconazole, ritonavir, clarithromycin) could alter the pharmacokinetics of sitagliptin in patients with severe renal impairment or ESRD.

Sitaxentan [1], strong OATP inhibitors ---> SmPC of [1] of EMA

The extent of interaction with other OATP inhibitors (except cyclosporine) is unknown but could result in raised plasma levels of sitaxentan.

Sofosbuvir [1], strong BCRP inhibitors ---> SmPC of [1] of EMA

Co-administration of sofosbuvir with medicinal products that inhibit BCRP may increase sofosbuvir plasma concentration without increasing GS-331007 plasma concentration, thus sofosbuvir may be co-administered with BCRP inhibitors.

Sofosbuvir [1], strong P-gp inhibitors ---> SmPC of [1] of EMA

Co-administration of sofosbuvir with medicinal products that inhibit P-gp may increase sofosbuvir plasma concentration without increasing GS-331007 plasma concentration, thus sofosbuvir may be co-administered with P-gp inhibitors.

Sofosbuvir/velpatasvir/voxilaprevir [1], strong OATP1B1 inhibitors ---> SmPC of [1] of EMA

Medicinal products that are strong OATP1B inhibitors (e.g. ciclosporin) may substantially increase voxilaprevir plasma levels, the safety of which has not been established. Co-administration of strong OATP1B inhibitors with Vosevi is not recommended

Sofosbuvir/velpatasvir/voxilaprevir [1], strong OATP1B3 inhibitors ---> SmPC of [1] of EMA

Solifenacin [1], strong CYP3A4 inhibitors ---> SmPC of [1] of eMC

The CYP3A4 inhibition may increase the plasma levels of solifenacin. Simultaneous treatment of solifenacin and a potent CYP3A4 inhibitor is contra-indicated in patients with severe renal impairment or moderate hepatic impairment

Sonidegib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Sonidegib undergoes metabolism primarily by CYP3A4, and concomitant administration of strong inhibitors of CYP3A4 can increase sonidegib concentrations significantly. The sonidegib dose should be reduced to 200 mg every other day

Sorafenib [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Clinical pharmacokinetic interactions of sorafenib with CYP3A4 inhibitors are unlikely.

Stiripentol [1], strong CYP1A2 inhibitors ---> SmPC of [1] of EMA

In vitro studies suggested that stiripentol phase 1 metabolism is catalyzed by CYP1A2, CYP2C19 and CYP3A4. Caution is advised when combining stiripentol with other substances that inhibit one or more of these enzymes.

Stiripentol [1], strong CYP2C19 inhibitors ---> SmPC of [1] of EMA

Stiripentol [1], strong CYP3A4 inhibitors ---> SmPC of [1] of EMA

Strong BCRP inhibitors, talazoparib [2] ---> SmPC of [2] of EMA

Concomitant use of strong BCRP inhibitors (including but not limited to curcumin and cyclosporine) should be avoided.

Strong CYP1A2 inhibitors, tasimelteon [2] ---> SmPC of [2] of EMA

Caution should be used when administering tasimelteon in combination with strong CYP1A2 inhibitors because of a potentially large increase in tasimelteon exposure and greater risk of adverse reactions

Strong CYP1A2 inhibitors, theophylline

The strong CYP1A2 inhibition may increase plasma concentrations of theophylline

Strong CYP1A2 inhibitors, tizanidine [2] ---> SmPC of [2] of eMC

Concomitant administration of drugs known to inhibit the activity of CYP1A2 may increase the plasma levels of tizanidine. Co-administration of tizanidine inhibitors of CYP1A2 is not recommended

Strong CYP1A2 inhibitors, zolmitriptan [2] ---> SmPC of [2] of eMC

Based on the overall interaction profile, an interaction of zolmitriptan with inhibitors of the cytochrome P450 isoenzyme CYP1A2 cannot be excluded.

Strong CYP2A6 inhibitors, tegafur

The co-administration of a CYP2A6 inhibitor and tegafur should be avoided as effectiveness of tegafur can be decreased

Strong CYP2B6 inhibitors, thiotepa [2] ---> SmPC of [2] of EMA

Thiotepa appears to be metabolised via CYP2B6 and CYP3A4. Co-administration with inhibitors of CYP2B6 or CYP3A4 may increase the plasma concentrations of thiotepa and potentially decrease the concentrations of the active metabolite TEPA.

Strong CYP2C19 inhibitors, tasimelteon [2] ---> SmPC of [2] of EMA

Caution should be used when administering tasimelteon in combination with strong CYP2C19 inhibitors such as omeprazole because there is uncertainty regarding the involvement of CYP2C19 and the effect of coadministration has not been studied.

Strong CYP2C19 inhibitors, voriconazole [2] ---> SmPC of [2] of EMA

Voriconazole is metabolised by cytochrome P450 isoenzymes, CYP2C19, CYP2C9, and CYP3A4. Inhibitors of these isoenzymes may increase voriconazole plasma concentrations

Strong CYP2C8 inhibitors [1], tretinoin ---> SmPC of [1] of eMC

As tretinoin is metabolised by the hepatic P450 system, there is the potential for alteration of pharmacokinetics parameters in patients administered concomitant medications that are also inducers or inhibitors of this system.

Strong CYP2C8 inhibitors, treprostinil [2] ---> SmPC of [2] of EMA

Concomitant administration of cytochrome P450 (CYP2C8) enzyme inhibitors (as gemfibrozil) may lead to increased exposure (both Cmax and AUC) to treprostinil.

Strong CYP2C8 inhibitors, tucatinib [2] ---> SmPC of [2] of EMA

Co-administration of tucatinib with strong CYP2C8 inhibitors such as gemfibrozil should be avoided as this may result in increased risk of tucatinib toxicity

Strong CYP2C9 inhibitors, torasemid

The potent CYP2C9 inhibition may increase the plasma concentrations of torasemide

Strong CYP2C9 inhibitors, trimethoprim

The potent CYP2C9 inhibition may increase the plasma concentrations of trimethoprim

Strong CYP2C9 inhibitors, valdecoxib [2] ---> SmPC of [2] of EMA

The strong CYP2C9 inhibition may increase the plasma levels of valdecoxib

Strong CYP2C9 inhibitors, voriconazole [2] ---> SmPC of [2] of EMA

Voriconazole is metabolised by cytochrome P450 isoenzymes, CYP2C19, CYP2C9, and CYP3A4. Inhibitors of these isoenzymes may increase voriconazole plasma concentrations

Strong CYP2C9 inhibitors, vortioxetine [2] ---> SmPC of [2] of EMA

The strong CYP2C9 inhibition may increase the AUC of vortioxetine. It is caution recommended with CYP2D6 poor metabolisers

Strong CYP2C9 inhibitors, zafirlukast

The strong CYP2C9 inhibition may increase plasma concentrations of zafirlukast

Strong CYP2D6 inhibitors, tamoxifen [2] ---> SmPC of [2] of eMC

Concomitant medications that inhibit CYP2D6 may lead to reduced concentrations of the active metabolite endoxifen. Therefore, potent inhibitors of CYP2D6 should whenever possible be avoided during tamoxifen treatment

Strong CYP2D6 inhibitors, tamsulosin

The strong CYP2D6 inhibition may increase the plasma concentrations of tamsulosin

Strong CYP2D6 inhibitors, tetrabenazine [2] ---> SmPC of [2] of eMC

Inhibitors of CYP2D6 may result in increased plasma concentrations of the active metabolite dihydrotetrabenazine, why they should only be combined with caution. A reduction of the tetrabenazine dose may be necessary.

Strong CYP2D6 inhibitors, thiethylperazine

The strong CYP2D6 inhibition may increase the plasma concentrations of thiethylperazine

Strong CYP2D6 inhibitors, thioridazine

The CYP2D6 inhibition may increase the plasma levels of thioridazine and the risk of QT interval prolongation. The co-administration is contraindicated

Strong CYP2D6 inhibitors, timolol ---> SmPC of [bimatoprost/timolol] of EMA

Potentiated systemic beta-blockade (e.g., decreased heart rate, depression) has been reported during combined treatment with CYP2D6 inhibitors and timolol.

Strong CYP2D6 inhibitors, tolperisone

The strong CYP2D6 inhibition may increase the plasma concentrations of tolperisone

Strong CYP2D6 inhibitors, tolterodine [2] ---> SmPC of [2] of eMC

Concomitant treatment with fluoxetine (a potent CYP2D6 inhibitor) does not result in a clinically significant interaction since tolterodine and its CYP2D6-dependent metabolite, 5-hydroxymethyl tolterodine are equipotent.

Strong CYP2D6 inhibitors, tramadol

The strong CYP2D6 inhibition may increase the plasma concentrations of tramadol

Strong CYP2D6 inhibitors, travoprost/timolol [2] ---> SmPC of [2] of EMA

Potentiated systemic beta-blockade (e.g., decreased heart rate, depression) has been reported during combined treatment with CYP2D6 inhibitors and timolol.

Strong CYP2D6 inhibitors, tricyclic antidepressant

Strong CYP2D6 inhibitors should not be used concomitantly with tricyclic antidepressants

Strong CYP2D6 inhibitors, trimipramine

The strong CYP2D6 inhibition may increase plasma concentrations of trimipramine

Strong CYP2D6 inhibitors, umeclidinium [2] ---> SmPC of [2] of EMA

Based on the magnitude of these changes, no clinically relevant drug interaction is expected when umeclidinium is co-administered with CYP2D6 inhibitors or when administered to subjects genetically deficient in CYP2D6 activity (poor metabolisers).

Strong CYP2D6 inhibitors, umeclidinium/vilanterol [2] ---> SmPC of [2] of EMA

No clinically relevant drug interaction is expected when umeclidinium is co-administered with CYP2D6 inhibitors

Strong CYP2D6 inhibitors, vernakalant [2] ---> SmPC of [2] of EMA

No dose adjustment of vernakalant is required on the basis of CYP2D6 metaboliser status, or when vernakalant is administered concurrently with 2D6 inhibitors.

Strong CYP2D6 inhibitors, vortioxetine [2] ---> SmPC of [2] of EMA

Depending on individual patient response, a lower dose of vortioxetine may be considered if strong CYP2D6 inhibitor is added to vortioxetine treatment

Strong CYP2D6 inhibitors, zuclopenthixol [2] ---> SmPC of [2] of eMC

Since zuclopenthixol is partly metabolised by CYP2D6 concomitant use of drugs known to inhibit this enzyme may lead to higher than expected plasma concentrations of zuclopenthixol, increasing the risk of adverse effects and cardiotoxicity.

Strong CYP3A4 inhibitors, sufentanil [2] ---> SmPC of [2] of EMA

Sufentanil is primarily metabolised by the CYP3A4. Ketoconazole, a potent CYP3A4 inhibitor, can significantly increase the systemic exposure to sublingual sufentanil. Similar effects with other potent CYP3A4 inhibitors cannot be excluded.

Strong CYP3A4 inhibitors, sunitinib [2] ---> SmPC of [2] of EMA

Administration of sunitinib with potent CYP3A4 inhibitors may increase sunitinib concentrations. Combination with CYP3A4 inhibitors should therefore be avoided

Strong CYP3A4 inhibitors, tacrolimus [2] ---> SmPC of [2] of EMA

Concomitant use of substances known to inhibit CYP3A4 may affect the metabolism of tacrolimus and thereby increase tacrolimus blood levels.

Strong CYP3A4 inhibitors, tadalafil [2] ---> SmPC of [2] of EMA

Caution should be exercised when prescribing tadalafil to patients using potent CYP3A4 inhibitors as increased tadalafil exposure (AUC) has been observed if the medicinal products are combined

Strong CYP3A4 inhibitors, tamsulosin

The strong CYP3A4 inhibition may increase the plasma concentrations of tamsulosin

Strong CYP3A4 inhibitors, tasimelteon [2] ---> SmPC of [2] of EMA

Tasimelteon exposure was increased by approximately 50% when co-administered with ketoconazole (strong CYP3A4 inhibitor) 400 mg (after 5 days of ketoconazole 400 mg per day).

Strong CYP3A4 inhibitors, telaprevir [2] ---> SmPC of [2] of EMA

Co-administration of telaprevir and medicinal products that inhibit CYP3A may increase telaprevir plasma concentrations.

Strong CYP3A4 inhibitors, telithromycin [2] ---> SmPC of [2] of EMA

Due to a potential to increase the QT interval, telithromycin (contraindicated in patients with severe renal or hepatic insufficiency) should be used with care in patients concomitantly treated with potent CYP 3A4 inhibitors

Strong CYP3A4 inhibitors, telmisartan/amlodipine [2] ---> SmPC of [2] of EMA

It cannot be ruled out that strong inhibitors of CYP3A4 may increase the plasma concentrations of amlodipine. Amlodipine should be used with caution together with CYP3A4 inhibitors.

Strong CYP3A4 inhibitors, temsirolimus [2] ---> SmPC of [2] of EMA

Strong CYP3A4 inhibitors may increase blood concentrations of the active moieties, temsirolimus and its metabolite, sirolimus. Therefore, concomitant treatment with agents that have strong CYP3A4 inhibition potential should be avoided.

Strong CYP3A4 inhibitors, terfenadine

The strong CYP3A4 inhibition may increase the terfenadine plasma levels and prolong the QT interval (risk of life-threatening arrythmias). The combination is contraindicated

Strong CYP3A4 inhibitors, tezacaftor/ivacaftor [2] ---> SmPC of [2] of EMA

When co-administered with strong CYP3A inhibitors, the dose should be adjusted to one Symkevi tablet twice a week, taken approximately 3 to 4 days apart.

Strong CYP3A4 inhibitors, ticagrelor [2] ---> SmPC of [2] of EMA

Co-administration of ticagrelor with strong CYP3A4 inhibitors is contraindicated, as co-administration may lead to a substantial increase in exposure to ticagrelor

Strong CYP3A4 inhibitors, tipranavir [2] ---> SmPC of [2] of EMA

The strong CYP3A4 inhibition may increase the plasma concentrations of tipranavir

Strong CYP3A4 inhibitors, tivozanib [2] ---> SmPC of [2] of EMA

The co-administration of tivozanib with a potent CYP3A4 inhibitor, ketoconazole (400 mg once daily), had no influence on tivozanib serum concentrations (Cmax or AUC); therefore, tivozanib exposure is unlikely to be altered by CYP3A4 inhibitors.

Strong CYP3A4 inhibitors, tofacitinib [2] ---> SmPC of [2] of EMA

XELJANZ exposure is increased when coadministered with potent inhibitors of CYP3A4 (e.g., ketoconazole)

Strong CYP3A4 inhibitors, tolterodine [2] ---> SmPC of [2] of eMC

Concomitant systemic medication with potent CYP3A4 inhibitors is not recommended due to increased serum concentrations of tolterodine in poor CYP2D6 metabolisers with (subsequent) risk of overdosage

Strong CYP3A4 inhibitors, tolvaptan [2] ---> SmPC of [2] of EMA

Tolvaptan plasma concentrations have been increased by up to 5.4-fold area under time-concentration curve (AUC) after the administration of strong CYP3A4 inhibitors. Caution should be exercised in co-administering CYP3A4 inhibitors with tolvaptan

Strong CYP3A4 inhibitors, toremifene [2] ---> SmPC of [2] of EMA

Theoretically the metabolism of toremifene is inhibited by drugs known to inhibit the CYP3A enzyme system which is reported to be responsible for its main metabolic pathways. Concomitant use should be carefully considered.

Strong CYP3A4 inhibitors, trabectedin [2] ---> SmPC of [2] of EMA

Concomitant use of a strong CYP3A4 inhibitor with trabectedin may increase the plasma exposure of trabectedin. Concomitant use should be avoided. If the combination is needed, close monitoring of toxicities

Strong CYP3A4 inhibitors, tramadol

The strong CYP3A4 inhibition may increase the plasma concentrations of tramadol

Strong CYP3A4 inhibitors, trandolapril/verapamil [2] ---> SmPC of [2] of eMC

Clinically significant interactions have been reported with inhibitors of CYP3A4 causing elevation of plasma levels of verapamil. Patients should be monitored for drug interactions.

Strong CYP3A4 inhibitors, trastuzumab emtansine [2] ---> SmPC of [2] of EMA

Concomitant use of strong CYP3A4 inhibitors with trastuzumab emtansine should be avoided due to the potential for an increase in DM1 exposure and toxicity.

Strong CYP3A4 inhibitors, trazodone [2] ---> SmPC of [2] of eMC

It is likely that potent CYP3A4 inhibitors may lead to substantial increases in trazodone plasma concentrations. The co-administration of trazodone and potent CYP3A4 inhibitors should be avoided where possible.

Strong CYP3A4 inhibitors, triazolam

The strong CYP3A4 inhibition may increase the plasma concentrations of triazolam

Strong CYP3A4 inhibitors, trofosfamide

The inhibition of CYP3A4 may increase the formation of a trofosfamide metabolite which is related with nephrotoxicity and CNS toxicity

Strong CYP3A4 inhibitors, tucatinib [2] ---> SmPC of [2] of EMA

A clinical drug interaction study found that co-administration of a single dose of 300 mg tucatinib with itraconazole (a strong CYP3A inhibitor) resulted in an increase in tucatinib concentrations

Strong CYP3A4 inhibitors, ulipristal [2] ---> SmPC of [2] of EMA

Administration of the moderate or potent CYP3A4 inhibitor increased Cmax and AUC of ulipristal acetate. Co-administration of moderate or potent CYP3A4 inhibitors and ulipristal acetate is not recommended

Strong CYP3A4 inhibitors, umeclidinium/vilanterol [2] ---> SmPC of [2] of EMA

Concomitant administration of strong CYP3A4 inhibitors may inhibit the metabolism of, and increase the systemic exposure to, vilanterol. Care is advised

Strong CYP3A4 inhibitors, upadacitinib [2] ---> SmPC of [2] of EMA

Upadacitinib exposure is increased when co-administered with strong CYP3A4 inhibitors. Consider alternatives to strong CYP3A4 inhibitor medications when used in the long-term.

Strong CYP3A4 inhibitors, valdecoxib

Plasma exposure (AUC) to valdecoxib was increased 38% when co-administered with ketoconazole (CYP3A4 inhibitor).

Strong CYP3A4 inhibitors, vandetanib [2] ---> SmPC of [2] of EMA

In healthy subjects, no clinically significant interaction was shown between vandetanib (a single dose of 300 mg) and the potent CYP3A4 inhibitor, itraconazole

Strong CYP3A4 inhibitors, vardenafil [2] ---> SmPC of [2] of EMA

The concomitant use of potent CYP3A4 inhibitors can be expected to increase vardenafil plasma levels. Concomitant use of vardenafil with potent CYP3A4 inhibitors should be avoided

Strong CYP3A4 inhibitors, vemurafenib [2] ---> SmPC of [2] of EMA

Vemurafenib should be used with caution in combination with potent inhibitors of CYP3A4, glucuronidation and/or transport proteins

Strong CYP3A4 inhibitors, venetoclax [2] ---> SmPC of [2] of EMA

Concomitant use of venetoclax with strong CYP3A inhibitors at initiation and during the dose-titration phase is contraindicated due to increased risk for TLS

Strong CYP3A4 inhibitors, venlafaxine [2] ---> SmPC of [2] of eMC

Concomitant use of CYP3A4 inhibitors and venlafaxine may increase levels of venlafaxine and O-desmethylvenlafaxine. Therefore, caution is advised if a patient's therapy includes a CYP3A4 inhibitor and venlafaxine concomitantly.

Strong CYP3A4 inhibitors, verapamil [2] ---> SmPC of [2] of eMC

Clinically significant interactions have been reported with inhibitors of CYP3A4 causing elevation of plasma levels of verapamil hydrochloride, therefore, patients should be monitored for drug interactions.

Strong CYP3A4 inhibitors, vilanterol ---> SmPC of [umeclidinium/vilanterol] of EMA

Concomitant administration of strong CYP3A4 inhibitors may inhibit the metabolism of, and increase the systemic exposure to, vilanterol. Care is advised

Strong CYP3A4 inhibitors, vinblastine [2] ---> SmPC of [2] of eMC

Concurrent administration of vinblastine sulphate with an inhibitor of CYP 3A subfamily may cause an earlier onset and/or an increased severity of side-effects.

Strong CYP3A4 inhibitors, vinca alkaloids

The strong CYP3A4 inhibition may increase the plasma concentrations of the vinca alkaloid. The dosage should be reduced if necessary

Strong CYP3A4 inhibitors, vincristine [2] ---> SmPC of [2] of eMC

The metabolism of vinca alkaloids has been shown to be mediated by hepatic cytochrome P450 isoenzymes in the CYP3A subfamily. This metabolic pathway may be impaired in patients who are taking concomitant potent inhibitors of these isoenzymes

Strong CYP3A4 inhibitors, vindesine

Concurrent administration of vindesine with an inhibitor of CYP 3A subfamily may cause an earlier onset and/or an increased severity of side-effects.

Strong CYP3A4 inhibitors, vinflunine [2] ---> SmPC of [2] of EMA

The concomitant use of vinflunine and potent CYP3A4 inhibitors should be avoided since they may increase vinflunine and DVFL concentrations

Strong CYP3A4 inhibitors, vinorelbine [2] ---> SmPC of [2] of eMC

CYP3A4 is the main enzyme involved in the metabolism of vinorelbine, and the combination with a drug that inhibits this iso-enzyme can affect the concentration of vinorelbine

Strong CYP3A4 inhibitors, vorapaxar [2] ---> SmPC of [2] of EMA

Co-administration of ketoconazole with vorapaxar significantly increased the vorapaxar exposition. Concomitant use of vorapaxar with strong inhibitors of CYP3A should be avoided.

Strong CYP3A4 inhibitors, voriconazole [2] ---> SmPC of [2] of EMA

Voriconazole is metabolised by cytochrome P450 isoenzymes, CYP2C19, CYP2C9, and CYP3A4. Inhibitors of these isoenzymes may increase voriconazole plasma concentrations

Strong CYP3A4 inhibitors, vortioxetine [2] ---> SmPC of [2] of EMA

The strong CYP3A4 inhibition may increase the AUC of vortioxetine. No dosage adjustment necessary. It is caution recommended with CYP2D6 poor metabolisers

Strong CYP3A4 inhibitors, zanubrutinib [2] ---> SmPC of [2] of EMA

If a strong CYP3A inhibitor must be used (e.g., posaconazole, voriconazole, ketoconazole, itraconazole, clarithromycin, indinavir, lopinavir, ritonavir, telaprevir), reduce the BRUKINSA dose to 80 mg (one capsule) for the duration of the inhibitor use.

Strong CYP3A4 inhibitors, ziprasidone

It is unlikely that changes in pharmacokinetics (with the concomitant use of strong CYP3A4 inhibitors) be of clinical relevance. No dose adjustment is required

Strong CYP3A4 inhibitors, zolpidem

CYP3A4 inhibitors may increase the effect of zolpidem

Strong CYP3A4 inhibitors, zonisamide [2] ---> SmPC of [2] of EMA

Specific and non-specific CYP3A4 inhibitors appear to have no clinically relevant effect on zonisamide pharmacokinetic exposure parameters.

Strong CYP3A4 inhibitors, zopiclone [2] ---> SmPC of [2] of eMC

Since zopiclone is metabolised by the cytochrome P450 (CYP) 3A4, plasma levels of zopiclone may be increased when co-administered with CYP3A4 inhibitors

Strong glucuronidation inhibitors, vemurafenib [2] ---> SmPC of [2] of EMA

Vemurafenib should be used with caution in combination with potent inhibitors of CYP3A4, glucuronidation and/or transport proteins

Strong P-gp inhibitors, talazoparib [2] ---> SmPC of [2] of EMA

Concomitant use of strong P-gp inhibitors during treatment with talazoparib should be avoided.

Strong P-gp inhibitors, telaprevir [2] ---> SmPC of [2] of EMA

Co-administration of telaprevir and medicinal products that inhibit P-gp may increase telaprevir plasma concentrations.

Strong P-gp inhibitors, tenofovir alafenamide [2] ---> SmPC of [2] of EMA

Co-administration of Vemlidy with medicinal products that inhibit P-gp and/or BCRP may increase plasma concentration of tenofovir alafenamide. Co-administration of strong inhibitors of P-gp with Vemlidy is not recommended.

Strong P-gp inhibitors, ticagrelor

The strong inhibition of P-glycoprotein may increase ticagrelor exposure. The concomitant use should be made with caution

Strong P-gp inhibitors, tipranavir [2] ---> SmPC of [2] of EMA

Co-administration of tipranavir and medicinal products that inhibit P-gp may increase tipranavir plasma concentrations.

Strong P-gp inhibitors, trabectedin [2] ---> SmPC of [2] of EMA

Preclinical data have demonstrated that trabectedin is a substrate to P-gp. Concomitant administration of inhibitors of P-gp may alter trabectedin distribution and/or elimination.

Strong P-gp inhibitors, trametinib [2] ---> SmPC of [2] of EMA

As it cannot be excluded that strong inhibition of hepatic P-gp may result in increased levels of trametinib, caution is advised when coadministering trametinib with medicinal products that are strong inhibitors of P-gp

Strong P-gp inhibitors, umeclidinium [2] ---> SmPC of [2] of EMA

No clinically relevant drug interaction is expected when umeclidinium is co-administered with P-gp inhibitors

Strong P-gp inhibitors, umeclidinium/vilanterol [2] ---> SmPC of [2] of EMA

No clinically relevant drug interaction is expected when umeclidinium is co-administered with P-gp inhibitors

Strong P-gp inhibitors, vemurafenib [2] ---> SmPC of [2] of EMA

Vemurafenib should be used with caution in combination with potent inhibitors of CYP3A4, glucuronidation and/or transport proteins

Strong P-gp inhibitors, vinblastine

The strong inhibition of P-glycoprotein may increase the exposure to vinblastine

Strong P-gp inhibitors, vinca alkaloids

As vinca-alkaloids are known as substrates for P-glycoprotein, caution should be exercised when combining vinorelbine with strong modulators of this membrane transporter.

Strong P-gp inhibitors, vincristine [2] ---> SmPC of [2] of eMC

Strong P-gp inhibitors, vinorelbine [2] ---> SmPC of [2] of eMC

As vinca-alkaloids are known as substrates for P-glycoprotein, caution should be exercised when combining vinorelbine with strong modulators of this membrane transporter.

Strong P-gp inhibitors, vismodegib [2] ---> SmPC of [2] of EMA

Clinically significant PK interactions between vismodegib and P-gp inhibitors are not expected.

Strong P-gp inhibitors, ziprasidone

The co-administration of ziprasidone with P glycoprotein inhibitors may increase the plasma concentrations of ziprasidone

Strong UGT1A6 inhibitors, tapentadol [2] ---> SmPC of [2] of eMC

Concomitant administration of tapentadol with strong inhibitors of UGT1A6 may lead to increased systemic exposure of tapentadol

Strong UGT1A9 inhibitors, tapentadol [2] ---> SmPC of [2] of eMC

Concomitant administration of tapentadol with strong inhibitors of UGT1A9 may lead to increased systemic exposure of tapentadol

Strong UGT2B7 inhibitors, tapentadol [2] ---> SmPC of [2] of eMC

Concomitant administration of tapentadol with strong inhibitors of UGT2B7 may lead to increased systemic exposure of tapentadol

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