This interaction has not been studied. Based on the metabolism/elimination and toxicity profiles of both drugs, there is little potential for interaction. Capreomycin is predominantly excreted via the kidneys as unchanged drug.

Coadministration has not been studied but is expected to decrease maraviroc concentrations due to induction of CYP3A4. Maraviroc dose should be increased to 600 mg twice daily when co-administered with carbamazepine in the absence of a potent CYP3A4 inhibitor. The US Prescribing Information contraindicates coadministration in patients with creatinine clearance less than 30 ml/min or on haemodialysis.

Coadministration has not been studied. Carbimazole is a pro-drug which undergoes rapid and virtually complete metabolism to the active metabolite, thiamazole (also known as methimazole). Despite this potential hepatic metabolism very few data exist on carbimazole drug interactions. Thiamazole has been shown to have inhibitory effects on CYP3A4 in vitro, however, the clinical relevance of this for maraviroc is unclear.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Carboplatin is excreted primarily by renal glomerular filtration and therefore there is little potential for a pharmacokinetic interaction.

Coadministration has not been studied. Cat’s claw is a strong inhibitor of CYP3A4 in vitro but has also been shown to induce CYP3A4 activity in vitro. Increased concentrations of atazanavir, saquinavir and ritonavir were reported in a patient receiving Cat’s claw. Similar increases would be expected for other CYP3A4 substrates, such as maraviroc. Coadministration should be avoided.

This interaction has not been studied. Based on the metabolism/elimination and toxicity profiles of both drugs, there is little potential for interaction. Cefalexin is predominantly eliminated unchanged via the kidneys.

This interaction has not been studied. Based on the metabolism/elimination and toxicity profiles of both drugs, there is little potential for interaction. Cefazolin is predominantly eliminated unchanged via the kidneys.

This interaction has not been studied. Based on the metabolism/elimination and toxicity profiles of both drugs, there is little potential for interaction. Approximately 50% of the absorbed dose is excreted unchanged in the urine; there is no evidence of metabolism of cefixime in vivo. In vitro studies have shown that cefixime does not inhibit/induce major cytochrome P450 metabolic enzymes, and would not be expected to cause clinically significant interactions with other drugs, which are metabolized by CYP450 enzymes.

This interaction has not been studied. Based on the metabolism/elimination and toxicity profiles of both drugs, there is little potential for interaction. Cefotaxime is predominantly eliminated unchanged via the kidneys.

This interaction has not been studied. Based on the metabolism/elimination and toxicity profiles of both drugs, there is little potential for interaction. Ceftazidime is predominantly eliminated unchanged via renal glomerular filtration.

This interaction has not been studied. Based on the metabolism/elimination and toxicity profiles of both drugs, there is little potential for interaction. Ceftriaxone is eliminated mainly as unchanged drug; approximately 60% of the dose being excreted in the urine, almost exclusively by glomerular filtration, and the remainder via the biliary and intestinal tracts.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cetuximab is a monoclonal IgG antibody. Elimination is similar to endogenous IgG and occurs primarily via proteolytic catabolism throughout the body.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Chloramphenicol is predominantly metabolised via UGTs (in particular UGT2B7) but maraviroc does not inhibit or induce UGT enzymes. Maraviroc is metabolized by CYP3A4. In vitro studies have shown that chloramphenicol can inhibit metabolism mediated by CYP3A4 but this is unlikely to cause a clinically significant interaction with maraviroc.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Chlorphenamine is predominantly metabolized in the liver via CYP2D6.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ciclesonide is a pro-drug activated by esterases in the lungs to des-ciclesonide which then undergoes CYP3A4-mediated metabolism. Maraviroc does not interact with ciclesonide metabolism.

Coadministration has not been studied but could potentially increase maraviroc concentrations. Maraviroc is metabolized by CYP3A4 and is a substrate of OATP1B. Ciclosporin is an inhibitor of CYP3A4 and OATPs.

Coadministration has not been studied. Ciprofloxacin is primarily eliminated unchanged by the kidneys by glomerular filtration and tubular secretion via OAT3. It is also metabolized and partially cleared through the bile and intestine. Maraviroc does not interfere with ciprofloxacin elimination. However, ciprofloxacin is a moderate inhibitor of CYP3A4 and could increase maraviroc exposure. No dosage adjustment of maraviroc is needed in presence of moderate inhibitors of CYP3A4.

Decrease maraviroc dose to 150 mg twice daily. Coadministration has not been studied, but would be expected to increase maraviroc concentrations. The European SmPC for maraviroc recommends when coadministering clarithromycin and maraviroc to patients with impaired renal function (creatinine clearance less than 80 ml/min), maraviroc should be reduced to 150 mg once daily. The US Prescribing Information recommends 150 mg twice daily for patients with creatinine clearance of 30-80 ml/min and contraindicates coadministration in patients with creatinine clearance less than 30 ml/min or on haemodialysis.

Coadministration has not been studied. Clobazam is metabolised by CYP3A4 (major) and CYP2B6 and CYP2C19 (minor) to the active metabolite N-desmethylclobazam, which is metabolised by CYP2C19. Clobazam is a weak inducer and could potentially decrease maraviroc exposure although to a limited extent. Maraviroc does not induce or inhibit CYP450 enzymes and therefore is unlikely to impact clobazam. 

Coadministration has not been studied. Clofazimine is largely excreted unchanged in the faeces, both as unabsorbed drug and via biliary excretion. Maraviroc is unlikely to affect clofazimine, however, clofazimine is a moderate inhibitor of CYP3A4 and may increase maraviroc concentrations.

This interaction has not been studied. Based on the metabolism/elimination and toxicity profiles of both drugs, there is little potential for interaction. CYP2D6 is thought to have a role in clomifene metabolism.

This interaction has not been studied. Based on the metabolism/elimination and toxicity profiles of both drugs, there is little potential for interaction. Cloxacillin is metabolised to a limited extent, and the unchanged drug and metabolites are excreted in the urine by glomerular filtration and renal tubular secretion.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely with vitamin D when given with calcium or in a multivitamin preparation. Metabolism of vitamin D to active metabolites occurs in the liver and kidneys, and is thought to involve CYP3A4 and CYP24A1. There is little potential for interaction with maraviroc via modulation of, or competition for, metabolic pathways.

Coadministration has not been studied. Several constituents of Piper cubeba were shown to inhibit CYP3A4 in vitro, and could potentially increase the exposure of maraviroc. No a priori dosage adjustment of maraviroc is needed.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely with cyanocobalamin when given alone or in multivitamins. Cyanocobalamin undergoes enterohepatic recycling and is excreted almost entirely in the urine.

This interaction has not been studied. Based on the metabolism/elimination and toxicity profiles of both drugs, there is little potential for interaction. Cycloserine is predominantly excreted renally via glomerular filtration.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cyproterone acetate is metabolized by CYP3A4 and does not inhibit CYPs when used at doses lower than 100 mg three times per day. Maraviroc does not inhibit or induce CYP450 enzymes.

In vitro studies have shown maraviroc to inhibit P-glycoprotein, but it does not significantly affect the pharmacokinetics of digoxin (a P-gp substrate) in vivo. A clinically significant increase in exposure of dabigatran (also a P-gp substrate) is unlikely, but cannot be excluded.

This interaction has not been studied. Based on the metabolism/elimination and toxicity profiles of both drugs, there is little potential for interaction.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dapagliflozin is primarily metabolised by UGT1A9 which is not affected by maraviroc.

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

Coadministration has not been studied. Maraviroc is metabolized by CYP3A4. When coadministered with darunavir/cobicistat, maraviroc should be dosed at 150 mg twice daily. The European SmPC for maraviroc recommends when coadministering potent CYP3A inhibitors and maraviroc to patients with impaired renal function (creatinine clearance less than 80 ml/min), maraviroc should be reduced to 150 mg once daily. The US Prescribing Information recommends 150 mg twice daily for patients with creatinine clearance of 30-80 ml/min and contraindicates coadministration in patients with creatinine clearance less than 30 ml/min or on haemodialysis.

Symtuza (darunavir, cobicistat, emtricitabine, tenofovir alafenamide) is indicated for use as a complete regimen for the treatment of HIV-1 infection. However, in specific clinical situations where an intensification of HIV treatment is needed, coadministration with maraviroc (dosed at 150 mg twice daily) would be possible from a pharmacokinetic standpoint. Maraviroc is metabolized by CYP3A4 and concentrations may increase due to inhibition of CYP3A4 by darunavir/cobicistat. A pharmacokinetic interaction between maraviroc and emtricitabine or tenofovir alafenamide is not expected.

Decrease maraviroc to 150 mg twice daily when coadministered. Coadministration of darunavir/ritonavir (600/100 mg twice daily) and maraviroc (150 mg twice daily) increased maraviroc AUC (4-fold), Cmax (2.3-fold) and Cmin (8-fold). Darunavir and ritonavir pharmacokinetics were similar to historical data. The European SmPC for maraviroc recommends when coadministering darunavir/ritonavir and maraviroc to patients with impaired renal function (creatinine clearance less than 80 ml/min), maraviroc should be reduced to 150 mg once daily. The US Prescribing Information recommends 150 mg twice daily for patients with creatinine clearance of 30-80 ml/min and contraindicates coadministration in patients with creatinine clearance less than 30 ml/min or on haemodialysis.

Coadministration has not been studied. Dasatinib is metabolized by CYP3A4 and concentrations are unlikely to be affected by maraviroc. Dasatinib is a weak inhibitor of CYP3A4 and therefore could potentially increase maraviroc exposure, although to a moderate extent.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. An in vitro study has shown that daunorubicin was able to inhibit metabolism mediated by CYP3A4, but was unlikely to cause clinically significant drug interactions via this mechanism.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Delamanid is primarily metabolised by albumin to DM-6705; metabolism of DM-6705 to other metabolites is thought to involve pathways mediated by CYP enzymes, including CYP3A4. Maraviroc does not affect CYP enzymes.

Coadministration with a desogestrel-containing combined oral contraceptive (COC) has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Desogestrel is a prodrug which is activated to etonogestrel by CYP2C9 (and possible CYP2C19); the metabolism of etonogestrel is mediated by CYP3A4. Maraviroc is unlikely to alter concentrations of etonogestrel through induction/inhibition of the cytochrome P450s responsible for activation and/or metabolism. Maraviroc (100 mg twice daily) had no effect on the AUC and Cmax of ethinylestradiol when coadministered with a COC containing ethinylestradiol/levonorgestrel. 

Coadministration with a desogestrel-containing progestogen-only pill (POP) has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Desogestrel is a prodrug which is activated to etonogestrel by CYP2C9 (and possible CYP2C19); the metabolism of etonogestrel is mediated by CYP3A4. Maraviroc is unlikely to alter concentrations of etonogestrel through induction/inhibition of the cytochrome P450s responsible for activation and/or metabolism.

This interaction has not been studied. Based on limited data concerning the metabolism/elimination and toxicity profile of diethylcarbamazine, there is little potential for interaction with maraviroc.

Maraviroc 300 mg twice daily and digoxin can be coadministered without dose adjustment. In vitro results suggest that maraviroc could inhibit P-gp in the gut. However, maraviroc did not significantly affect the pharmacokinetics of digoxin in vivo, indicating maraviroc may not significantly inhibit or induce P-gp clinically. Coadministration of digoxin (0.25 mg single dose) and maraviroc (300 mg twice daily) had no significant effect on digoxin AUC or Cmax. Maraviroc concentrations were not measured, but no interaction is expected. The effect of maraviroc 600 mg twice daily on digoxin has not been studied.

Coadministration has not been studied. Dihydroergotamine is a substrate and inhibitor of CYP3A4 and could potentially increase maraviroc concentrations. However, no a priori dosage adjustment is recommended for maraviroc.

This interaction has not been studied. Based on the metabolism/elimination and toxicity profiles of both drugs, there is little potential for interaction. Diloxanide furoate is largely hydrolysed under the combined action of bacterial and gut esterases and consequently glucuronidated. No clinically-significant drug interactions are known, and significant interactions with antiretrovirals are unlikely.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dipyridamole is glucuronidated by many UGTs, specifically those of the UGT1A subfamily. Maraviroc does not inhibit or induce these UGTs.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as dofetilide is mainly excreted unchanged in urine.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Maraviroc is metabolized by CYP3A4, however, dolutegravir is not expected to inhibit or induce CYP450 enzymes at clinically relevant concentrations.

Triumeq (dolutegravir/abacavir/lamivudine) is indicated for use as a complete regimen for the treatment of HIV 1 infection. However, in specific clinical situations where an intensification of HIV treatment is needed, coadministration with maraviroc (dosed at 300 mg twice daily) would be possible from a pharmacokinetic standpoint. Maraviroc is metabolized by CYP3A4. Dolutegravir is not expected to inhibit or induce CYP450 enzymes at clinically relevant concentrations and no interaction is expected with abacavir. Coadministration of maraviroc (300 mg twice daily) and lamivudine/zidovudine (150/300 mg twice daily) increased lamivudine AUC (14%) and Cmax (16%), but is not considered to be clinically significant. Maraviroc concentrations were not measured, but no effect is expected.

Dovato (dolutegravir/lamivudine) is indicated for use as a complete regimen for the treatment of HIV 1 infection. However, in specific clinical situations where an intensification of HIV treatment is needed, coadministration with maraviroc (dosed at 300 mg twice daily) would be possible from a pharmacokinetic standpoint. Maraviroc is metabolized by CYP3A4. Dolutegravir is not expected to inhibit or induce CYP450 enzymes at clinically relevant concentrations. Coadministration of maraviroc (300 mg twice daily) and lamivudine/zidovudine (150/300 mg twice daily) increased lamivudine AUC (14%) and Cmax (16%), but is not considered to be clinically significant. Maraviroc concentrations were not measured, but no effect is expected.

Juluca (dolutegravir/rilpivirine) is indicated for use as a complete regimen for the treatment of HIV-1 infection. However, in specific clinical situations where an intensification of HIV treatment is needed, coadministration with maraviroc (dosed at 300 mg twice daily) would be possible from a pharmacokinetic standpoint as no clinically relevant drug-drug interaction is expected. Maraviroc is metabolized by CYP3A4. Dolutegravir and rilpivirine are not expected to inhibit or induce CYP enzymes at clinically relevant concentrations. 

This interaction has not been studied. Based on the metabolism/elimination and toxicity profiles of both drugs there is little potential for interaction. Dopamine is metabolised in the liver, kidneys, and plasma by monoamine oxidase (MAO) and catechol-O-methyltransferase to inactive compounds. About 25% of a dose of dopamine is metabolised to norepinephrine within the adrenergic nerve terminals. There is little potential for dopamine to affect disposition of antiretrovirals, or to be affected if co-administered with antiretrovirals.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Doravirine and maraviroc are metabolized by CYP3A4, but neither drug has any inhibitory or inducing effects on P450 enzymes. Therefore, no significant interactions are expected between doravirine and maraviroc.

Delstrigo (doravirine, lamivudine, tenofovir-DF) is indicated for use as a complete regimen for the treatment of HIV-1 infection. However, in specific clinical situations where an intensification of HIV treatment is needed, coadministration with maraviroc (dosed at 300 mg twice daily) would be possible from a pharmacokinetic standpoint. No clinically relevant drug-drug interaction is expected between maraviroc and doravirine. Coadministration of maraviroc (300 mg twice daily) and lamivudine/zidovudine (150/300 mg twice daily) increased lamivudine AUC (14%) and Cmax (16%), but is not considered to be clinically significant. Maraviroc concentrations were not measured, but no effect is expected. Coadministration of maraviroc (300 mg twice daily) and tenofovir-DF (300 mg once daily) had no significant effect on maraviroc AUC or Cmax. Tenofovir concentrations were not measured, but no effect is expected.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Doxorubicin is mainly eliminated in the bile by P-gp and BCRP and does not undergo CYP-mediated metabolism. (Some product labels suggest doxorubicin is a substrate of CYP3A4, however, there are no strong data supporting the role of CYP3A4 in doxorubicin metabolism.)

This interaction has not been studied. Based on the metabolism/elimination and toxicity profiles of both drugs, there is little potential for interaction. No significant metabolism of doxycycline occurs, it is cleared intact by renal and biliary mechanisms.

Coadministration with a drospirenone-containing combined oral contraceptive (COC) has not been studied. Drospirenone is metabolized to a minor extent via CYP3A4. Ethinylestradiol is mainly metabolized by hydroxylation. Maraviroc does not interact with these metabolic pathways.

Coadministration with drospirenone as hormone replacement therapy (HRT) has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Drospirenone is metabolized to a minor extent via CYP3A4. Maraviroc does not induce or inhibit CYPs. In addition, no interaction is expected with estradiol or estrogens administered as part of HRT.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as dulaglutide is presumed to be degraded by general protein catabolism pathways. Dulaglutide delays gastric emptying and has the potential to impact the rate of absorption of concomitantly administered oral medicinal products. However, interaction studies did not result in any clinically relevant effects and no dose adjustment of comedications is recommended.

Coadministration with dydrogesterone as hormone replacement therapy (HRT) has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dydrogesterone is metabolized to dihydrodydrogesterone (possibly via CYP3A4). Maraviroc does not induce or inhibit CYPs. In addition, no interaction is expected with estradiol or estrogens administered as part of HRT.

Coadministration has not been studied but may decrease maraviroc concentrations. Echinacea has a selective effect on CYP3A4 activity (inhibition of intestinal CYP3A4 and induction of hepatic CYP3A4) and its effect on the net exposure of a CYP3A4 substrate will depend on the extraction of the drug at the intestinal and hepatic sites. Since maraviroc has a moderate intestinal extraction echinacea may cause a modest reduction in maraviroc plasma concentrations.

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

Maraviroc dose should be increased to 600 mg twice daily when co-administered with efavirenz in the ABSENCE of a PI or other potent CYP3A4 inhibitor. Maraviroc dose should be decreased to 150 mg twice daily when co-administered with efavirenz in the PRESENCE of a PI (other than tipranavir/ritonavir where the dose should be 600 mg twice daily). Coadministration of efavirenz alone decreased maraviroc exposure by ~50%. Coadministration with a boosted PI increased maraviroc exposure by up to 5.0-fold. The US Prescribing Information contraindicates coadministration in patients with creatinine clearance less than 30 ml/min or on haemodialysis.

This interaction has not been studied. Based on the metabolism/elimination and toxicity profiles of both drugs, there is little potential for interaction. Eflornithine is predominantly eliminated unchanged via the kidneys.

Genvoya (elvitegravir, cobicistat, emtricitabine, tenofovir alafenamide) is indicated for use as a complete regimen for the treatment of HIV 1 infection. However, in specific clinical situations where an intensification of HIV treatment is needed, coadministration with maraviroc (dosed at 150 mg twice daily) would be possible from a pharmacokinetic standpoint.

Stribild (elvitegravir, cobicistat, emtricitabine, tenofovir-DF) is indicated for use as a complete regimen for the treatment of HIV 1 infection. However, in specific clinical situations where an intensification of HIV treatment is needed, coadministration with maraviroc (dosed at 150 mg twice daily) would be possible from a pharmacokinetic standpoint.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Empagliflozin is mainly glucuronidated by UGTs 1A3, 1A8, 1A9 and 2B7. It is a substrate of P-gp and BCRP, and also a substrate of the renal transporter OAT3 and the hepatic transporters OATP1B1 and OATP1B3. Maraviroc is unlikely to affect the metabolism of empagliflozin and empagliflozin is unlikely to affect maraviroc concentrations as it does not inhibit or induce CYPs and does not inhibit UGTs. 

No significant interaction expected. Maraviroc and NRTIs can be co-administered without dose adjustment.

Coadministration had not been studied. Tenofovir alafenamide exposure is not expected to be affected by maraviroc nor is it expected to affect the metabolic and excretion pathways relevant to maraviroc. The recommended dose of Descovy for HIV-1 treatment is 200/25 mg once daily.

Coadministration with emtricitabine/tenofovir-DF has not been studied. No clinically significant interaction is expected with emtricitabine. Coadministration of maraviroc (300 mg twice daily) and tenofovir-DF (300 mg once daily) had no significant effect on maraviroc AUC or Cmax. Tenofovir concentrations were not measured, but no effect is expected. Maraviroc and NRTIs can be co-administered without dose adjustment.

This interaction has not been studied. Based on the metabolism/elimination and toxicity profiles of both drugs, there is little potential for interaction. Ephedrine is predominantly eliminated unchanged via the kidneys.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Eplerenone is metabolized by CYP3A4 but maraviroc does not inhibit or induce CYP3A4.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Epoprostenol is rapidly hydrolyzed in the blood.

Coadministration has not been studied. Ergotamine is a substrate and inhibitor of CYP3A4 and could potentially increase maraviroc concentrations. However, no a priori dosage adjustment is recommended for maraviroc.

Coadministration has not been studied. Eslicarbazepine is partly eliminated unchanged renally and partly glucuronidated by UGT2B4. Eslicarbazepine is a weak/moderate inducer of CYP3A4 and therefore could decrease maraviroc exposure as it is metabolized by CYP3A4. 

Coadministration with estradiol as hormone replacement therapy (HRT) has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Estradiol is metabolized by CYP3A4, CYP1A2 and is glucuronidated. Maraviroc does not inhibit or induce CYPs and UGTs.

Coadministration of a non-licensed dose of maraviroc (100 mg twice daily) and an oral contraceptive (ethinylestradiol/levonorgestrel 0.03/0.15 mg once daily) had no effect on the AUC and Cmax of either ethinylestradiol or levonorgestrel. Maraviroc pharmacokinetics were with in the range seen in male subjects. Note, use of ethinylestradiol as part of gender affirming treatment is not recommended due to thrombotic risks.

This interaction has not been studied. Based on the metabolism/elimination and toxicity profiles of both drugs, there is little potential for interaction. Ethionamide is extensively metabolized in the liver, animal studies suggest involvement of flavin-containing monooxygenases. Ethionamide does not affect metabolism mediated by CYP450 enzymes in vitro.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Etidocaine is metabolized by CYP3A4, but maraviroc does not inhibit or induce drug metabolizing enzymes.

Coadministration with an etonogestrel-containing progestogen-only implant has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Etonogestrel is metabolised by CYP3A4 but maraviroc does not inhibit or induce CYP450 enzymes.

Coadministration with etonogestrel as a combined vaginal ring (CVR) has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Etonogestrel is metabolised by CYP3A4. Ethinylestradiol is mainly metabolized by hydroxylation. Maraviroc does not inhibit or induce CYP450 enzymes. Maraviroc (100 mg twice daily) had no effect on the AUC and Cmax of ethinylestradiol when coadministered with a COC containing ethinylestradiol/levonorgestrel.

Etravirine decreases maraviroc AUC and Cmax by 53% and 60% respectively. Coadministration of etravirine with darunavir/ritonavir increased maraviroc AUC and Cmax by 210% and 77% respectively. Maraviroc had no significant effect on etravirine, darunavir or ritonavir pharmacokinetics. When coadministered with etravirine and boosted PIs, the recommended dose of maraviroc is 150 mg twice daily (coadministration with etravirine and fosamprenavir/ritonavir is not recommended in the European SPC). When coadministered with etravirine in the absence of a potent CYP3A4 inhibitor, the recommended dose of maraviroc is 600 mg twice daily. No dose adjustment for etravirine is necessary. The US Prescribing Information contraindicates coadministration in patients with creatinine clearance less than 30 ml/min or on haemodialysis.

Coadministration has not been studied but based on metabolism and clearance, a clinically significant interaction is unlikely. Eucalyptus is only a weak inhibitor of CYP3A4 and is unlikely to impact the exposure of maraviroc.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Everolimus is metabolized by CYP3A4 and concentrations are unlikely to be affected by maraviroc.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Evolocumab is a monoclonal IgG antibody. Elimination is similar to endogenous IgG and occurs primarily via proteolytic catabolism throughout the body.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fesoterodine is rapidly hydrolysed to its active metabolite which is subsequently metabolized by CYP2D6 and CYP3A4. Maraviroc does not inhibit or induce CYPs.

Coadministration has not been studied. Flibanserin is primarily metabolized by CYP3A4 and has been shown to moderately increase the exposure of simvastatin, a CYP3A4 substrate. Thus, flibanserin could potentially increase maraviroc exposure. No a priori dosage adjustment of maraviroc is recommended.

Coadministration has not been studied. Flucloxacillin is mainly eliminated renally, partly by glomerular filtration and partly by active secretion via OAT1. Flucloxacillin is thought to be a weak inducer of CYP3A4 particularly at higher doses (>2-3 g daily). A modest reduction in maraviroc concentrations may be observed but this is unlikely to be clinically relevant unless flucloxacillin is prescribed at higher doses for a prolonged course (> 10-14 days).

Population PK studies suggest that a dose adjustment of maraviroc is not required.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Flunisolide undergoes CYP3A4-mediated metabolism. Maraviroc does not interact with flunisolide metabolism.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fluorouracil is metabolised via the same mechanisms as endogenous uracil, including via dihydropyrimidine dehydrogenase. There is therefore little potential for an interaction with maraviroc via modulation of, or competition for metabolic pathways.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fluphenazine is metabolised by CYP2D6.

No dose adjustment of maraviroc required. Coadministration with statins has not been studied, but no interaction is expected.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Folic acid is metabolized to dihydrofolic acid and tetrahydrofolic acid with the aid of reduced diphosphopyridine nucleotide and folate reductases.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely when folic acid is administered in a multivitamin preparation. Folic acid is metabolized to dihydrofolic acid and tetrahydrofolic acid with the aid of reduced diphosphopyridine nucleotide and folate reductases.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fondaparinux does not undergo cytochrome metabolism but is eliminated predominantly renally.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fosinopril is hydrolysed by esterases in the GI mucosa and liver. Fosinopril does not inhibit or induce CYP450 enzymes.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as gabapentin is cleared mainly by glomerular filtration.

Coadministration has not been studied. Garlic supplements have been shown to decrease unboosted saquinavir AUC by 50% in a clinical trial and there is a case report of treatment failure due to garlic cloves (six garlic cloves three times weekly) decreasing ritonavir-boosted atazanavir trough concentrations by ~70%. Similarly, concentrations of maraviroc could be decreased via induction of CYP3A4 and/or P-gp. Patients should be advised against the use of garlic supplements.

This interaction has not been studied. Based on the metabolism/elimination and toxicity profiles of both drugs, there is little potential for interaction. Gentamicin is predominantly eliminated unchanged via the kidneys.

Coadministration with a gestodene-containing combined oral contraceptive (COC) has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Gestodene is metabolized by CYP3A4 and to a lesser extent by CYP2C9 and CYP2C19. Ethinylestradiol is mainly metabolized by hydroxylation. Maraviroc does not inhibit or induce CYP450 enzymes at clinically relevant concentrations. Maraviroc (100 mg twice daily) had no effect on the AUC and Cmax of ethinylestradiol when coadministered with a COC containing ethinylestradiol/levonorgestrel.

Coadministration has not been studied. Gingerols moderately inhibit CYP3A4 in vitro and could potentially increase the exposure of maraviroc, although to a modest extent. No a priori dosage adjustment of maraviroc is needed.

Coadministration has not been studied but may decrease maraviroc concentrations through induction of CYP3A4 by Ginkgo biloba. The magnitude and clinical relevance of this potential interaction is difficult to predict as inconsistent findings have been reported from clinical drug interaction studies with CYP3A4 substrates.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Any increase in maraviroc concentrations due to inhibition of P-gp by glecaprevir/pibrentasvir is unlikely to be clinically relevant in patients with normal renal function.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Glyceryl trinitrate is metabolised by aldehyde dehydrogenase-2. Glyceryl trinitrate is not known to induce or inhibit CYP450 enzymes.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Glycopyrronium bromide is mainly eliminated renally (active secretion via organic cation transporter) and is also partly hydroxylated via multiple CYPs. Inhibition or induction of its metabolism is unlikely to result in a significant change in exposure.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Goldenseal has been shown to inhibit CYP3A4 in vitro, however, no significant effect of golden seal root on indinavir pharmacokinetics was observed in a study in HIV-negative subjects. Interactions with other drugs metabolized by CYP3A4 are unlikely.

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

Coadministration has not been studied but may increase in maraviroc concentrations through inhibition of CYP3A4 and possibly P-glycoprotein. The magnitude of the potential interaction is difficult to predict as the effect of grapefruit juice is concentration, dose and preparation dependent and varies widely across brands, but as grapefruit juice inhibits intestinal CYP3A4 and maraviroc has a moderate intestinal extraction, the interaction is likely to be modest.

This interaction has not been studied. Griseofulvin is a liver microsomal enzyme inducer and may lower plasma levels (and therefore reduce the efficacy) of concomitantly administered medicinal products that are metabolized by cytochrome P450 3A4, such as maraviroc.

Coadministration has not been studied but could potentially increase maraviroc concentrations through inhibition of P-gp by haloperidol.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Heparin is thought to be eliminated via the reticuloendothelial system.

Coadministration has not been studied. In vitro data indicate that extracts of hops activate PXR and induce expression of CYP3A4, CYP2B6 and MDR1 genes to a degree similar to that of St John's wort. However, a pharmacokinetic study with a standardised hop extract showed no clinically relevant effect on CYPs 2C9, 1A2, and 2D6 and suggested only minor induction of CYP3A4/5 (AUC of alprazolam, a CYP3A4/5 substrate, decreased by ~8%). Based on these results, hop extracts are unlikely to have a clinically significant effect on maraviroc.

Coadministration has not been studied. Based the metabolism/elimination and toxicity profiles of both drugs there is little potential for pharmacokinetic interaction. Caution should be used when administering maraviroc in patients with a history of postural hypotension or on concomitant medicinal products known to lower blood pressure, and those at increased risk of cardiovascular events.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Hydroxyurea undergoes metabolism via non-CYP mediated metabolism and is unlikely to affect concentrations of maraviroc.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. No drug interaction studies have been conducted with ibalizumab: based on ibalizumab’s mechanism of action and target-mediated drug disposition, drug-drug interactions are not expected. Maraviroc undergoes hepatic metabolism whereas ibalizumab, a monoclonal antibody binding to the CD4 receptor, is likely to be eliminated via intracellular catabolism similarly to other monoclonal antibodies. Dose modifications of ibalizumab are not required when administered with any other antiretroviral.

Ibandronic acid should be taken after an overnight fast (at least 6 hours) and before the first food or drink of the day. Medicinal products and supplements should be similarly avoided prior to taking ibandronic acid. Fasting should be continued for at least 30 minutes after taking ibandronic acid.