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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Acamprosate is eliminated unchanged in the urine.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Acetazolamide is primarily excreted unchanged via the kidneys, there is therefore little potential for interaction with nevirapine 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. Aclidinium bromide is rapidly and extensively hydrolyzed (non-enzymatic and enzymatic transformation by esterases and butylrylcholineesterases) to its pharmacologically inactive metabolites with only a minor role for CYP metabolism.

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

No clinically relevant drug-drug interaction is expected. No interaction was observed at doses of adefovir 6- to 12-fold higher than that recommended for the treatment of chronic hepatitis B. Adefovir and nevirapine may be coadministered without dose adjustments. 

This interaction has not been studied. Based on the metabolism/elimination and toxicity profiles of both drugs, there is little potential for interaction. Adrenaline is rapidly inactivated, mostly in the liver by catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO). There is therefore little potential for interaction with nevirapine via modulation of, or competition for metabolic or elimination pathways.

Coadministration has not been studied but based on metabolic data there is little potential for pharmacokinetic interactions. African potato was shown to inhibit CYP3A4 and P-gp in vitro and to activate PXR suggesting that inhibition may occur initially followed by induction of CYP3A4 and P-gp when used for extended periods. However coadministration of African potato with efavirenz in healthy volunteers did not result in significant pharmacokinetic changes. Similarly, no significant effect is expected on the pharmacokinetics of nevirapine.

Coadministration has not been studied. In vitro studies have demonstrated that CYP3A4 is involved in formation of the active metabolite albendazole sulfoxide. When antiepileptics (phenytoin, carbamazepine and phenobarbital) were coadministered with albendazole, significantly reduced levels of the active metabolite albendazole sulfoxide were observed, apparently due to induction of CYP3A4. Similarly, coadministration with nevirapine could reduce albendazole exposure; however, the clinical relevance is unknown as the antihelmintic action is thought to be mainly intra-intestinal.

Coadministration has not been studied but based on metabolism and clearance, as well as limited drug-drug interaction data, a clinically significant interaction is unlikely. Nevirapine is metabolized by CYP3A4 and CYP2B6. In vitro human microsomal studies and limited in vivo drug-drug interaction data indicate that albuvirtide has no inhibiting or inducing properties on P450 enzymes. Induction of CYP3A4 by nevirapine is unlikely to affect albuvirtide, a peptide which is eliminated by catabolism to its constituent amino acids.

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

If taken at the same time, it is likely that food and beverages (including mineral water), calcium supplements, antacids, and some oral medicinal products will interfere with absorption of alendronate. Therefore, patients must wait at least 30 minutes after taking alendronate before taking any other oral medicinal product.

Coadministration has not been studied but based on metabolism and clearance, a clinically significant interaction is unlikely. Aloe vera is only a weak inhibitor of CYPs in vitro and therefore is unlikely to cause clinically significant interactions. It does not inhibit P-gp and there is no evidence to suggest it impacts UGTs.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ambrisentan is mainly glucuronidated by UGT1A9, UGT2B7, UGT1A3 and is metabolized to a lesser extent by CYP3A4. Ambrisentan is also a substrate of P-gp and OATP1B1. Induction of CYP3A4 by NVP is unlikely to significantly impact ambrisentan exposure as CYP3A4 does not play a major role in ambrisentan metabolism.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Aminophylline is a complex of theophylline and ethylenediamine and is given for its theophylline activity. Theophylline is mainly metabolized by CYP1A2.

Coadministration may decrease amiodarone concentrations. Dose adjustment may be needed due to possible decrease in clinical effect.

Amodiaquine is metabolised mainly by CYP2C8 to N-desethylamodiaquine, an active metabolite but less potent than the parent compound. Coadministration of nevirapine (200 mg twice daily with zidovudine/lamivudine) and amodiaquine (600 once daily with artesunate) decreased the AUCs of amodiaquine and desethylamodiaquine by 29% and 33%, respectively. This may negatively impact the effectiveness of artesunate/amodiaquine in patients receiving nevirapine. The mechanism for this interaction is unclear as nevirapine is not thought to inhibit CYP2C8 in the range of clinical concentrations. In addition, coadministration of these drugs may increase the risk of hepatotoxicity through additive toxicity. Careful clinical monitoring for efficacy and toxicity is recommended.

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

Nevirapine may be administered with or without antacid. When nevirapine (200 mg) was administered with antacid (Maalox 30 ml), nevirapine AUC was comparable to that observed under fasting conditions. Coadministration with antacids containing calcium carbonate has not been studied.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Thymoglobulins are cleared by the reticuloendothelial system.

Coadministration has not been studied. Apixaban is metabolized by CYP3A4 and to a lesser extent by CYP1A2, CYP2C8, CYP2C9 and CYP2C19. Nevirapine could potentially decrease apixaban exposure resulting in diminished efficacy.

Coadministration has not been studied. Apomorphine is metabolized by several pathways that include mainly glucuronidation and sulfation and to a lesser extent N-demethylation. Although some NNRTIs have the potential to induce glucuronidation, the clinical relevance of such an interaction is unknown considering the numerous pathways contributing to apomorphine metabolism. No a priori dosage adjustment is required.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Argatroban undergoes metabolism in the liver via hydroxylation and aromatization. In vitro studies indicate that CYP3A4 plays a role in argatroban metabolism however, human drug-drug interactions studies suggest that metabolism via CYP3A4 is not a major elimination pathway in vivo. Erythromycin (a strong CYP3A4 inhibitor) had no effect on argatroban pharmacokinetics and pharmacodynamics and it is unlikely that nevirapine will significantly reduce argatroban exposure due to induction of CYP3A4.

Coadministration has not been studied. Aripiprazole is metabolized by CYP3A4 and CYP2D6. Nevirapine could potentially decrease aripiprazole concentrations. Monitor therapeutic effect and adjust aripiprazole dosage if needed. The European SPC advises doubling the aripiprazole dose when given with potent inducers of CYP3A4, such as nevirapine.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely with vitamin C when given alone or in multivitamins. Ascorbic acid is oxidised to dehydroascorbic acid where some is metabolised to oxalic acid and the inactive ascorbate-2-sulphate. Large doses are rapidly excreted in the urine when in excess of the requirements of the body. There is therefore little potential for interaction with nevirapine via modulation of, or competition for metabolic pathways.

Coadministration has not been studied. Asenapine is metabolized by glucuronidation (UGT1A4) and oxidative metabolism (mainly CYP1A2, with minor contributions from CYP3A4 and CYP2D6). Nevirapine could potentially decrease asenapine concentrations by induction of CYP3A4, although to a moderate extent. No a priori dosage adjustment is recommended.

This interaction has not been studied. Based on the metabolic profiles of both drugs, there is little potential for pharmacokinetic interaction. Limited data suggest that asparaginase is likely to be eliminated by the reticuloendothelial system.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Aspirin is rapidly deacetylated to salicylic acid and then further metabolized mainly by glucuronidation (by several UGT, major UGT1A6).

Coadministration has not been studied. Astemizole is metabolized by CYPs 2D6, 2J2 and 3A4. Nevirapine, an inducer of CYP3A4, could potentially decrease astemizole exposure. Monitor clinical effect.

Coadministration of nevirapine with atazanavir is contraindicated as it increases nevirapine exposure and decreases atazanavir exposure. There is potential risk for nevirapine-associated toxicity due to increased nevirapine exposures, whereas the decreased atazanavir exposure may result in loss of therapeutic effect and development of resistance.

Coadministration is not recommended and may result in a loss of therapeutic effect of atazanavir/cobicistat and development of resistances. In addition, coadministration may increase the risk for nevirapine associated adverse reactions due to increased nevirapine exposure.

Coadministration of nevirapine with atazanavir/ritonavir is contraindicated as it increases nevirapine exposure and decreases atazanavir exposure. There is potential risk for nevirapine-associated toxicity due to increased nevirapine exposures, whereas the decreased atazanavir exposure may result in loss of therapeutic effect and development of resistance.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as atenolol is mainly eliminated unchanged by the kidney, both by glomerular filtration and active secretion via the renal transporters OCT2 and MATE1.

Coadministration has not been studied. Atorvastatin is metabolised mainly by CYP3A4. Based on drug-drug interaction studies with other NNRTIs and considering that nevirapine is a weak CYP3A4 inducer, coadministration is predicted to minimally impact atorvastatin exposure. No a priori dosage adjustment of atorvastatin is needed due to coadministration with nevirapine. However, treatment with statins requires periodic monitoring of lipid values and the atorvastatin dose should be adjusted based on the clinical response.

This interaction has not been studied. Based on the metabolism/elimination profiles of both drugs, there is little potential for interaction when atropine is used either systemically or as eye drops. Although metabolism of atropine is not fully elucidated, up to 50% is excreted unchanged via the kidneys. There is therefore little potential for clinically significant interactions with nevirapine via modulation of, or competition for metabolic pathways.

Coadministration has not been studied but is not recommended. Avanafil is primarily metabolized by CYP3A4 and concentrations (and efficacy) may decrease due to induction of CYP3A4 by nevirapine.

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

Coadministration of bedaquiline (400 mg single dose) and nevirapine (200 mg twice daily for 4 weeks) in HIV-infected patients had no clinically relevant effect on bedaquiline exposure (AUC increased by 3%, Cmax decreased by 20%). Coadministration of bedaquiline (400 mg, once daily loading dose; 200 mg once daily maintenance dose) with nevirapine had no significant effect on the pharmacokinetics of bedaquiline (17% increase in AUC) or on the bedaquiline M2 metabolite. No dosage adjustment of bedaquiline is required. There are no clinical data on the safety and efficacy of bedaquiline when co-administered with antiretroviral agents.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Belatacept is a protein that undergoes non-CYP mediated metabolism in the liver.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Benazepril is rapidly hydrolyzed to its active metabolite benazeprilat which is eliminated predominantly renally.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bendroflumethiazide is mainly eliminated by hepatic metabolism, although the exact pathway is not known. It is unlikely that CYP enzymes are involved in this process and no transporter interactions have been described. There is no evidence that bendroflumethiazide inhibits or induces CYP450 enzymes.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Benznidazole undergoes non-CYP mediated metabolism and partly CYP mediated metabolism. Renal elimination of unchanged benznidazole appears to be minimal and there is little potential for an interaction via competition for renal elimination pathways.

Coadministration has not been studied. Bepridil is metabolised mainly by CYP2D6 and to a lesser extent by CYP3A4. Nevirapine, an inducer of CYP3A4, could potentially decrease bepridil exposure. No a priori dose adjustment is recommended, but the therapeutic effect should be monitored.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Betahistine is metabolized by monoamine oxidase. Betahistine does not induce or inhibit CYP450 enzymes.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Betrixaban is largely eliminated unchanged through biliary secretion via P-gp. In vitro data indicate that nevirapine does not induce or inhibit P-gp in the range of clinical concentrations.

Coadministration has not been studied but based on metabolism and clearance a clinically significant pharmacokinetic interaction is unlikely as bevacizumab is metabolized via proteolytic catabolism. 

Biktarvy (bictegravir, emtricitabine, tenofovir alafenamide) is indicated for use as a complete regimen for the treatment of HIV 1 infection and should not be administered with other antiretroviral products. In addition, nevirapine is an inducer of CYP3A4 and is expected to decrease bictegravir exposure which may result in loss of therapeutic effect and development of resistance.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Although limited human data suggest biperiden undergoes hydroxylation in the liver, there are no known or documented interactions with other drugs that have an effect on metabolism or transport.

Coadministration has not been studied. Bisoprolol is partly metabolized by CYP3A4 and CYP2D6 and partly eliminated unchanged in the urine. Nevirapine could potentially decrease bisoprolol exposure, although to a moderate extent. No a priori dosage adjustment is required.

Coadministration has not been studied but based on metabolism and clearance, a clinically significant interaction is unlikely. No effect on nevirapine is expected as black cohosh had no significant effect on the pharmacokinetics of midazolam (a CYP3A4 substrate) or digoxin (a P-gp substrate).

Coadministration has not been studied. Bromazepam undergoes oxidative biotransformation. Drug-drug interaction studies indicate that CYP3A4 plays a minor role in bromazepam metabolism, but other cytochromes such as CYP2D6 or CYP1A2 may play a role. Bromazepam does not inhibit CYP3A4.Nevirapine could potentially decrease bromazepam concentrations although to a moderate extent. No a priori dosage adjustment is required.

Coadministration has not been studied. Bupivacaine is predominantly metabolized by CYP3A4. CYP3A4 inducers such as nevirapine may decrease levels of bupivacaine and potentially decrease its efficacy. The clinical relevance of this interaction is unknown.

Coadministration has not been studied. Buspirone is metabolized by CYP3A4 but does not inhibit CYP3A4. Nevirapine could potentially decrease buspirone concentrations. Monitor the clinical response and increase dosage of buspirone if needed.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Canagliflozin is primarily metabolised by UGT1A9 and UGT2B4 which are not affected by nevirapine.

Coadministration has not been studied. Cannabidiol is mainly metabolized by CYP3A4 and CYP2C19 and is unlikely to significantly inhibit or induce CYPs and therefore no effect is expected on nevirapine. However, nevirapine induces CYP3A4 which decrease cannabidiol exposure. A careful dose increase in cannabidiol might be needed. In addition, a careful titration might be needed within the two weeks following cessation of nevirapine.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. THC, the principal psychoactive constituent of cannabis, is metabolized mainly by CYP2C9 and to a lesser extent by CYP3A4; nevirapine does not inhibit or induce CYP2C9.

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 may decrease carbamazepine and nevirapine concentrations. Dose adjustment may be needed due to possible decrease in clinical effect.

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 nevirapine. 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. In vitro studies have shown that chloramphenicol can inhibit metabolism mediated by CYP3A4. Coadministration of chloramphenicol may potentially increase levels of nevirapine via this mechanism, increasing the risk of adverse events. The clinical significance of this interaction is unknown. Ocular use: Although chloramphenicol is systemically absorbed when used topically in the eye, the concentrations used are unlikely to cause a clinically significant interaction.

Coadministration has not been studied. Chloroquine undergoes CYP mediated metabolism by CYPs 2C8, 3A4 and 2D6, and is also eliminated unchanged via the kidney (50%). Nevirapine could potentially decrease chloroquine exposure due to induction CYP3A4, although to a moderate extent due to the multiple elimination pathways. No dosage adjustment is recommended but monitor the efficacy of the antimalarial.

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. Nevirapine is unlikely to have clinically significant effect on ciclesonide metabolism.

Coadministration may decrease ciclosporin concentrations. Dose adjustment may be needed due to possible decrease in clinical effect.

Coadministration has no effect on cimetidine and increases nevirapine Cmin by 7%. No dose adjustments required.

Coadministration has not been studied. Cisapride is metabolised mainly by CYP3A4. Nevirapine, an inducer of CYP3A4, may decrease cisapride concentrations. A dose adjustment may be needed due to a possible decrease in clinical effect.

Coadministration has not been studied. Citalopram is metabolized by CYPs 2C19 (38%), 2D6 (31%) and 3A4 (31%). Nevirapine could potentially decrease citalopram concentrations, although to a moderate extent. No a priori dosage adjustment is recommended.

Coadministration of nevirapine (200 mg twice daily) with clarithromycin (500 mg twice daily) decreased clarithromycin AUC (31%), Cmax (23%) and Cmin (57%), and increased 14-OH-clarithromycin AUC (42%) and Cmax (47%) with no change in Cmin. Compared to historical controls, there were increases in nevirapine Cmin (28%), AUC (26%) and Cmax (24%). Close monitoring for hepatic abnormalities is recommended. As the clarithromycin metabolite has reduced activity against Mycobacterium avium-intracellulare complex, overall activity may be altered and alternatives to clarithromycin, such as azithromycin, should be considered.

Coadministration has not been studied. Clindamycin is metabolized by CYP3A4 and some metabolites have antibacterial activity. Nevirapine could potentially decrease clindamycin exposure which could impact efficacy.

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. Nevirapine induces CYP3A4 and CYP2B6 which may decrease clobazam exposure. Monitor for anticonvulsant effect and adjust clobazam dosage if needed. Clobazam is unlikely to affect nevirapine.

This interaction has not been studied. Based on the metabolism/elimination and toxicity profiles of both drugs, there is little potential for interaction. In vitro studies have suggested that CYP3A4 does not affect conversion of clomifene to its active metabolite, and that this transformation is likely to be mediated via CYP2D6. There is therefore little potential for nevirapine to affect this metabolic pathway.

Coadministration has not been studied. Clomipramine is metabolized by CYPs 3A4, 1A2 and 2C19 to desmethylclomipramine, an active metabolite which has a higher activity than the parent drug. In addition, clomipramine and desmethylclomipramine are metabolized by CYP2D6. Nevirapine could potentially decrease clomipramine concentrations but increase the formation of the active metabolite. The clinical relevance is unknown. Monitor clinical effect.

Coadministration may decrease clonazepam concentrations. Dose adjustment may be needed due to possible decrease in clinical effect.

Coadministration has not been studied. Clopidogrel is a prodrug that is converted to its active metabolites via CYPs 3A4, 2B6, 2C19 and 1A2. Nevirapine is likely to increase the amount of active metabolites through induction of CYP3A4. In vitro data suggest that clopidogrel inhibits CYP2B6 and could potentially increase nevirapine concentrations. Use with caution and with monitoring of clinical and side effects.

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 nevirapine could potentially decrease codeine exposure and increase the conversion to norcodeine, a metabolite that does not have analgesic properties. Codeine is converted to morphine (active metabolite) via CYP2D6 and inactivated to codeine-6-glucuronide via glucuronidation (major pathway) as well as to norcodeine via CYP3A4. No a priori dosage adjustment is recommended but monitoring the analgesic effect may be considered.

Colchicine is a substrate of CYP3A4 and P-gp. Coadministration with nevirapine (an inducer of CYP3A4) has not been studied but may reduce colchicine concentrations. The clinical relevance of this potential interaction is unknown.

Coadministration has not been studied. No interaction is expected 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. In vitro studies have shown rifampicin (an enzyme inducer) increased metabolism of vitamin D and introduction of 6',7'-dihydroxybergamottin (a CYP3A4 inhibitor in grapefruit juice) reversed the effects of rifampicin on vitamin D clearance. These studies suggest that inducers of CYP3A4 (such as nevirapine) may increase metabolism of vitamin D and therefore reduce its effect. However, no effect of antiretroviral therapy on the response to vitamin D supplementation was found in a PK modelling study.

Coadministration of a constituent of Piper cubeba (piperine 20 mg) and nevirapine (200 mg) to 8 HIV-negative subjects increased nevirapine AUC and Cmin by 170% and 146%, respectively. However, the treatments were well tolerated and no a priori dose adjustment of nevirapine is required.

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.

Coadministration may decrease cyclophosphamide concentrations. Dose adjustment may be needed due to possible decrease in clinical effect.

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. Cyproterone acetate is metabolized by CYP3A4 and concentrations may decrease due to induction of CYP3A4 by nevirapine. A dose adjustment of cyproterone may be required.

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 nevirapine.

In vitro studies showed that dapsone did not affect the formation of nevirapine hydroxylated metabolites. No data on the effect of nevirapine on dapsone.

Coadministration has not been studied. Darifenacin is metabolized by CYP3A4 and CYP2D6 and could potentially decrease darifenacin exposure due to induction of CYP3A4. Monitor the effect.

Coadministration has not been studied and is not recommended because it is expected to decrease darunavir/cobicistat exposure which may result in loss of therapeutic effect and development of resistance to darunavir. 

Symtuza (darunavir, cobicistat, emtricitabine, tenofovir alafenamide) is indicated for use as a complete regimen for the treatment of HIV-1 infection and should not be administered with other antiretroviral products. Furthermore, coadministration with nevirapine is expected to decrease darunavir/cobicistat exposure which may result in loss of therapeutic effect and development of resistance to darunavir.

Note: this interaction was studied using a darunavir/ritonavir dose lower than that licensed. Coadministration of nevirapine (200 mg twice daily) and darunavir/ritonavir (400/100 mg twice daily) increased nevirapine AUC (27%), Cmax (18%) and Cmin (47%). Based on between study comparison, darunavir Cmax, AUC and Cmin increased by 40%, 24% and 2%, respectively. These differences are not considered to be clinically relevant and no adjustments to the licensed doses are required.

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. No clinically relevant decrease in delamanid exposure was observed with efavirenz (a moderate inducer of CY3A4). As nevirapine is a moderate-weak inducer of CYP3A4, a clinically relevant decrease in delamanid exposure is not expected.

Desogestrel is a prodrug that requires activation to etonogestrel. Activation to etonogestrel is by CYP2C9 (and possibly CYP2C19); the metabolism of etonogestrel is mediated by CYP3A4. Coadministration of nevirapine and desogestrel was administered as a COC to HIV+ women (n=18). Serum progesterone was less 1.0 ng/ml in all subjects and nevirapine C12 concentrations increased by 17% but this was not statistically significant. When compared to values obtained from administration without nevirapine to HIV-negative women (n=14), etonogestrel trough concentrations decreased by 22%. This small pharmacokinetic change did not impact contraceptive efficacy based on measured serum progesterone levels.

Coadministration with a desogestrel-containing progestogen-only pill (POP) has not been studied but is not expected to affect the contraceptive efficacy of desogestrel. Desogestrel is a prodrug that requires activation to etonogestrel. Activation to etonogestrel is by CYP2C9 (and possibly CYP2C19); the metabolism of etonogestrel is mediated by CYP3A4. The coadministration of nevirapine and a combined oral contraceptive containing desogestrel and ethinylestradiol resulted in 12% decrease in etonogestrel Cmin. This small pharmacokinetic change did not impact the contraceptive efficacy of the contraceptive based on measured serum progesterone levels. Similarly, nevirapine is not expected to reduce the contraceptive efficacy of a desogestrel-containing POP.

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 nevirapine.

Coadministration has not been studied but nevirapine could potentially decrease dihydrocodeine exposure. Dihydrocodeine is converted to dihydromorphine (active metabolite) via CYP2D6, to dihydrocodeine-6-glucuronide via UGT2B7 (major pathway) and to nordihydrocodeine via CYP3A4. The analgesic effect appears to be primarily due to the parent compound. Monitoring for analgesic effect and for signs of opiate toxicity may be required as clinically indicated.

Coadministration has not been studied. Dihydroergotamine is a substrate and inhibitor of CYP3A4. Nevirapine is metabolized by CYP3A4. Dihydroergotamine is unlikely to have a clinically significant effect on nevirapine. However, nevirapine is a weak-moderate inducer of CYP3A4 and could potentially decrease dihydroergotamine exposure. If coadministration is necessary, use with caution and monitor for clinical effect.

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 may decrease diltiazem concentrations. Dose adjustment may be needed due to possible decrease in clinical effect.

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. Nevirapine does not inhibit or induce these UGTs.

Coadministration may decrease disopyramide concentrations. Dose adjustment may be needed due to possible decrease in clinical effect.

Coadministration with CYP3A inducers (i.e. efavirenz, etravirine, nevirapine) may decrease concentrations of docetaxel.

Coadministration has not been studied. Dofetilide is metabolized to a small degree by CYP3A4 and therefore nevirapine could potentially decrease dofetilide exposure. Dose adjustment may be needed and should be done with caution due to the narrow therapeutic index of dofetilide.

Coadministration has not been studied. Nevirapine, an inducer of CYP3A4, could potentially decrease dolutegravir concentrations. The US Prescribing Information advises that coadministration should be avoided because there are insufficient data to make dosing recommendations. However, the European SPC recommends a dolutegravir dose of 50 mg twice daily with nevirapine, except in the presence of integrase class resistance when alternative combinations that do not include nevirapine should be considered.

Triumeq (dolutegravir, abacavir, lamivudine) is indicated for use as a complete regimen for the treatment of HIV-1 infection and coadministration with nevirapine is not recommended. Nevirapine, an inducer of CYP3A4, could potentially decrease dolutegravir concentrations. However, in specific clinical situations where an intensification of HIV treatment is needed, coadministration with nevirapine would be possible from a pharmacokinetic standpoint if an additional dolutegravir 50 mg tablet, separated by 12 hours from Triumeq, is taken. Note, the bioavailability of lamivudine has been shown to be significantly reduced in a dose dependent manner by sorbitol which is present in liquid formulations such as nevirapine oral suspension.

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 nevirapine would be possible from a pharmacokinetic standpoint. The European product label for Dovato recommends an additional 50 mg tablet of dolutegravir should be administered, approximately 12 hours after Dovato, during coadministration as nevirapine, an inducer of CYP3A4, could potentially decrease dolutegravir concentrations. Note, the bioavailability of lamivudine has been shown to be significantly reduced in a dose dependent manner by sorbitol which is present in liquid formulations such as nevirapine oral suspension.

Juluca (dolutegravir/rilpivirine) is indicated for use as a complete regimen for the treatment of HIV-1 infection and should not be administered with other antiretroviral products. Furthermore, coadministration may decrease dolutegravir and rilpivirine concentrations and combining two NNRTIs (i.e., nevirapine and rilpivirine) has not been shown to be beneficial.

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.

Doravirine should not be administered with another NNRTI. Furthermore, coadministration is expected to decrease doravirine exposure.

Delstrigo (doravirine, lamivudine, tenofovir-DF) is indicated for use as a complete regimen for the treatment of HIV 1 infection and must not be administered with other antiretroviral products. Furthermore, coadministration is expected to decrease doravirine exposure.

Coadministration has not been studied. Doxazosin is metabolised mainly by CYP3A4 and concentrations may decrease due to induction of CYP3A4 by nevirapine. Monitor clinical effect. For the treatment of benign prostatic hyperplasia (BPH), depending on the patient’s urodynamics and BPH symptomatology, doxazosin dose may be increased from 1 mg/day to 2 mg/day and thereafter 4 mg/day with a maximum recommended dose of 8 mg/day. The recommended titration interval is 1-2 weeks with routine blood pressure monitoring.

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.)

Coadministration has not been studied. Although metabolism of doxycycline is thought to be minimal and the mechanisms are not fully elucidated, metabolic enzyme inducers such as barbiturates, carbamazepine, and phenytoin have been found to decrease the half-life of doxycycline, which may result in sub-therapeutic concentrations. As nevirapine induces metabolism mediated by some CYP450 enzymes, an interaction with doxycycline can not be ruled out.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dronabinol is metabolised mainly by CYP2C9 and to a lesser extent by CYP3A4. Nevirapine does not inhibit or induce CYP2C9.

Coadministration with a drospirenone-containing combined oral contraceptive (COC) has not been studied but is not expected to impair the contraceptive efficacy of drospirenone/ethinylestradiol. Drospirenone is metabolised in part by CYP3A4. Coadministration of nevirapine with an oral contraceptive containing ethinylestradiol/norethindrone moderately decreased ethinylestradiol AUC (20%) and norethindrone AUC (19%). Similarly, nevirapine is not expected to significantly impair drospirenone pharmacokinetics and contraceptive efficacy when administered as a COC.

Coadministration with drospirenone as hormone replacement therapy (HRT) has not been studied. CYP3A4 contributes to drospirenone metabolism. Coadministration is predicted to decrease drospirenone exposure. In addition, exposure of estrogens/estradiol administered as part of HRT may also decrease. Monitor for signs of hormone deficiency.

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. Dydrogesterone is metabolized to dihydrodydrogesterone (possibly via CYP3A4). Coadministration is predicted to decrease dydrogesterone exposure. In addition, exposure of estrogens/estradiol administered as part of HRT may also decrease. Monitor for signs of hormone deficiency.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Edoxaban is a substrate for P-gp and in vitro data indicate that nevirapine does not induce or inhibit P-glycoprotein in the range of clinical concentrations.

Coadministration of nevirapine (200 mg twice daily) with efavirenz (600 mg once daily) decreased efavirenz AUC (28%), Cmax (12%) and Cmin (32%), with no significant effect on nevirapine pharmacokinetics. Coadministration is not recommended because of additive toxicity and no benefit in terms of efficacy over either NNRTI alone.

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 and must not be administered with other antiretroviral products. Genvoya should not be used in conjunction with non-nucleoside reverse transcriptase inhibitors due to potential drug-drug interactions including altered and/or suboptimal pharmacokinetics of cobicistat, elvitegravir and/or the coadministered antiretroviral products.

Stribild (elvitegravir, cobicistat, emtricitabine, tenofovir-DF) is indicated for use as a complete regimen for the treatment of HIV 1 infection and must not be administered with other antiretroviral products. Stribild should not be used in conjunction with non-nucleoside reverse transcriptase inhibitors due to potential drug-drug interactions including altered and/or suboptimal pharmacokinetics of cobicistat, elvitegravir, and/or the coadministered antiretroviral products.

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. Nevirapine is unlikely to affect the metabolism of empagliflozin and empagliflozin is unlikely to affect nevirapine concentrations as it does not inhibit or induce CYPs and does not inhibit UGTs. 

Based on the results of in vitro experiments and the known elimination pathways of emtricitabine, the potential for CYP450 mediated interactions involving emtricitabine with other medicinal products is low. Nevirapine trough concentrations in 7 HIV+ subjects receiving nevirapine (200 mg twice daily) with tenofovir/emtricitabine were comparable to historical values.

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

Coadministration with emtricitabine/tenofovir-DF has not been studied. Based on metabolism and clearance a clinically significant interaction with emtricitabine is unlikely. Tenofovir and nevirapine plasma levels remain unchanged when co-administered.  Emtricitabine/tenofovir-DF and nevirapine can be co-administered without dose adjustments.

Coadministration has not been studied but based on the metabolism and clearance a clinically significant interaction is unlikely. Entecavir is eliminated renally via glomerular filtration and active renal secretion by both organic anion and cation transporters.

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. Eplerenone is metabolized by CYP3A4. Nevirapine could potentially decrease eplerenone exposure due to induction of CYP3A4 and thereby reduce the efficacy of eplerenone.

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. Ergometrine is metabolized by CYP3A4. Nevirapine is metabolized by CYP3A4. Ergometrine is unlikely to affect CYPs. However, nevirapine is a weak-moderate inducer of CYP3A4 and could potentially decrease ergometrine exposure. If coadministration is necessary, use with caution and monitor for clinical effect.

Coadministration has not been studied. Ergotamine is metabolized by CYP3A4. Nevirapine is metabolized by CYP3A4. Ergotamine is unlikely to affect CYPs. However, nevirapine is a weak-moderate inducer of CYP3A4 and could potentially decrease ergotamine exposure. If coadministration is necessary, use with caution and monitor for clinical effect.

Erythromycin significantly inhibited the formation of nevirapine hydroxylated metabolites. There is the potential for an interaction.

Coadministration has not been studied. Escitalopram is metabolized by CYPs 2C19 (37%), 2D6 (28%) and 3A4 (35%) to form N-desmethylescitalopram. Nevirapine could potentially decrease escitalopram concentrations although to a moderate extent. No a priori dosage adjustment is recommended.

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 nevirapine concentrations although to a limited extent. No a priori dose adjustment is recommended but HIV infection (e.g. viral load, CD4 count) should be monitored.

Coadministration has not been studied. Estazolam is metabolized to its major metabolite 4-hydroxyestazolam via CYP3A4. Nevirapine, an inducer of CYP3A4, could potentially decrease estazolam exposure. Monitor clinical effect and withdrawal symptoms.

Coadministration with estradiol as hormone replacement therapy (HRT) has not been studied. Estradiol is metabolized by CYP3A4, CYP1A2 and is glucuronidated. Nevirapine, an inducer of CYP3A4, could potentially decrease estradiol exposure. Monitor for signs of estrogen deficiency.

Coadministration of nevirapine (200 mg twice daily) with an oral contraceptive containing ethinylestradiol/norethindrone (0.035 mg/1 mg once daily) decreased ethinylestradiol AUC (20%) and had no effect on Cmax; norethindrone AUC and Cmax decreased by 19% and 16%, respectively. The effect on nevirapine pharmacokinetics was not significant. Of note: a study examining the effectiveness of ethinylestradiol/norgestrel (30/300 µg) in 196 HIV-infected women taking nevirapine compared with 206 HIV infected women in Uganda and South Africa not yet on antiretrovirals found no significant differences in ovulation or pregnancy rates in the presence or absence of nevirapine. Taken together, these data seem to indicate that nevirapine is unlikely to impair the efficacy of contraception. 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 may decrease ethosuximide concentrations. Dose adjustment may be needed due to possible decrease in clinical effect.

Coadministration has not been studied. Etidocaine is metabolized by CYP3A4. Inducers of CYP3A4, such as nevirapine, may decrease concentrations of etidocaine and potentially decrease its efficacy. The clinical relevance of this interaction is unknown.

Coadministration with an etonogestrel-containing progestogen-only implant has not been assessed in pharmacokinetic studies. Data from a small number of subjects (n=7) with etonogestrel implants showed that nevirapine had no effect on etonogestrel concentrations (7% increase) when compared to a control group of subjects (n=22). Etonogestrel is metabolized by CYP3A4. Efavirenz has been shown to impair the contraceptive efficacy of both etonogestrel and levonorgestrel containing implants. However, nevirapine did not have significant effect on levonorgestrel concentrations (another progestogen metabolized by CYP3A4) following use with a levonorgestrel implant and there were no report of unintended pregnancies. In addition, drug-drug interactions studies with progestogen COCs have shown in general a modest effect of nevirapine on the pharmacokinetics of the progestogens. Taken together, these findings suggest that nevirapine is likely to maintain the contraceptive efficacy of etonogestrel when administered as an implant.

Coadministration with the etonogestrel as a combined vaginal ring (CVR) has not been studied but is not expected to impair the contraceptive efficacy of etonogestrel/ethinylestradiol. Etonogestrel is metabolized by CYP3A4.  Coadministration of nevirapine with an oral contraceptive containing ethinylestradiol/norethindrone moderately decreased ethinylestradiol AUC (20%) and norethindrone AUC (19%). In addition, nevirapine did not have significant effect on levonorgestrel concentrations following use with a levonorgestrel implant and no unintended pregnancies were reported. Similarly, nevirapine is not expected to significantly impair etonogestrel and ethinylestradiol pharmacokinetics and contraceptive efficacy when administered as a CVR.

Coadministration decreased etravirine AUC by 55% and Cmax by 36%. Coadministration is contraindicated as it significantly decreases etravirine concentrations. Combining two NNRTIs has not been shown to be beneficial.

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 nevirapine given that CYP3A4 is already induced by nevirapine.

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. Fentanyl undergoes extensive CYP3A4 metabolism. Coadministration could decrease fentanyl concentrations due to induction of CYP3A4, which could decrease opioid efficacy or, possibly, lead to a withdrawal syndrome in a patient who had developed physical dependence to fentanyl. When using fentanyl with CYP3A4 inducers, monitor patients closely at frequent intervals and consider increasing the opioid dosage if needed to maintain adequate analgesia or if symptoms of opioid withdrawal occur. Discontinuation of a concomitantly used CYP3A4 inducer may increase in fentanyl concentrations which could result in a fatal overdose of fentanyl. When discontinuing CYP3A4 inducers in fentanyl-treated patients, monitor patients closely at frequent intervals and consider dosage reduction of fentanyl until stable drug effects are achieved. 

Coadministration has not been studied. Fesoterodine is rapidly hydrolysed to its active metabolite which is subsequently metabolized by CYP2D6 and CYP3A4. Concentrations of the active metabolite of fesoterodine are likely to decrease due to induction of CYP3A4. Monitor the effect.

Coadministration has not been studied. Flibanserin is primarily metabolized by CYP3A4 and to a lesser extent by CYP2C19. Etravirine (a moderate inducer of CYP3A4) decreased flibanserin exposure by approximately 21%. Coadministration with nevirapine (also an inducer of CYP3A4) is expected to decrease flibanserin exposure.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. 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) but is unlikely to alter nevirapine exposure as bosentan (moderate inducer) had no effect on nevirapine exposure in a drug-drug interaction study.

Coadministration of nevirapine (200 mg twice daily) with fluconazole (200 mg once daily) had no effect on fluconazole AUC, Cmax or Cmin but increased nevirapine exposure by ~100% when compared to historic data. Caution should be used because of the risk of increased exposure to nevirapine and patients should be monitored closely for nevirapine-associated adverse events.

Coadministration has not been studied. Flunisolide undergoes CYP3A4-mediated metabolism and coadministration may decrease flunisolide concentrations. Monitor steroid effect and adjust dosage if needed. 

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 nevirapine 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.

Data from a cohort of HIV+ patients showed that coadministration of fluvoxamine could increase nevirapine concentrations as coadministration signficantly reduced nevirapine apparent oral clearance by 34%. No effect of nevirapine on fluvoxamine concentrations was seen. When used in combination, caution is advised, especially with high doses of fluvoxamine as the effect of fluvoxamine appeared to be dose-dependent.

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 nevirapine 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 is not expected to impair the contraceptive efficacy of gestodene/ethinylestradiol. Gestodene is metabolized by CYP3A4 and to a lesser extent by CYP2C9 and CYP2C19. Coadministration of nevirapine with a COC containing ethinylestradiol/norethindrone moderately decreased ethinylestradiol AUC (20%) and norethindrone AUC (19%). Similarly, nevirapine is not expected to significantly impair gestodene pharmacokinetics and contraceptive efficacy when administered as a COC.

Coadministration has not been studied but based on metabolism and clearance, a clinically significant interaction is unlikely. Although gingerols moderately inhibit CYP3A4 in vitro this is unlikely to impact the exposure of nevirapine.

Coadministration has not been studied. Inconsistent findings have been reported from clinical drug interaction studies with CYP3A4 substrates, but could reduce exposure of non-boosted protease inhibitors or non-nucleoside reverse transcriptase inhibitors. No a priori dose adjustment is recommended, but monitor nevirapine concentrations (if available).

Coadministration has not been studied and is not recommended. Concentrations of glecaprevir/pibrentasvir may decrease due to CYP3A4 induction by nevirapine which may lead to reduced therapeutic effect.

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.

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 nevirapine.

Coadministration has not been studied. Haloperidol undergoes glucuronidation (UGT2B7 > 1A4, 1A9), carbonyl reduction and oxidative metabolism (CYP3A4, CYP2D6). Nevirapine could potentially decrease haloperidol exposure. No a priori dosage adjustment is recommended.

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 nevirapine.

This interaction has not been studied. In vitro studies have suggested that hydralazine is a mixed enzyme inhibitor, which may weakly inhibit CYP3A4 and CYP2D6. There is little potential for clinically significant interactions with nevirapine via these mechanisms.

Coadministration has not been studied but may decrease hydrocortisone concentrations. A dose adjustment of hydrocortisone may be required.

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 not a substrate of P-gp.