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. Abatacept is a fusion protein consisting of the extracellular domain of human CTLA-4 linked to a modified Fc portion of human IgG1 and is likely to be eliminated via proteolytic catabolism throughout the body. Nevirapine is metabolized by CYP3A4.

Coadministration has been studied but is not recommended as it is expected to reduce the efficacy of abemaciclib. Abemaciclib is metabolized by CYP3A4 and is a substrate of P-gp and BCRP. Efavirenz (a moderate CYP3A4 inducer) has been predicted to reduce abemaciclib AUC by 69% and to reduce the AUC of abemaciclib’s active metabolites (sum of 3 metabolites) by 52%. A similar effect is expected with nevirapine and therefore coadministration should be avoided.

Coadministration has not been studied and is not recommended. Abiraterone is metabolized by CYP3A4 and SULT2A1. Nevirapine induces CYP3A4 and may significantly decrease abiraterone concentrations and consequently reduce its efficacy. It is recommended to use an alternative antiretroviral agent devoid of inducing properties.

Coadministration has not been studied. Abrocitinib is metabolised predominantly by CYP2C19 and CYP2C9, and to a lesser extent by CYP3A4 and CYP2B6. Nevirapine is metabolized by CYP3A4. Abrocitinib is not expected to have a clinically relevant effect on CYP3A4. Nevirapine induces CYP3A4 and CYP2B6 and may decrease abrocitinib exposure, although to a limited extent given that nevirapine does not affect CYP2C19 and CYP2C9, the main metabolic pathway of abrocitinib.

Coadministration with etravirine has not been studied. PBPK modelling predicted efavirenz to reduce acalabrutinib exposure by 61%. Coadministration should be avoided due to the risk for lack of efficacy as a similar effect is expected with nevirapine. Note, the US label does not provide dosage recommendations in presence of moderate inducers of CYP3A4, such as nevirapine. However, the label mentions that if a strong CYP3A4 inducer cannot be avoided, the dose of acalabrutinib should be increased to 200 mg twice daily.

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. Activated charcoal absorbs substances in the stomach and intestines and may decrease absorption of orally administered medicines. If coadministration is required, administration of activated charcoal and nevirapine should be separated by 4 hours. [Note: this interaction is not specific for nevirapine, but for any oral medication taken with activated charcoal.]

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. Afatinib is mainly eliminated unchanged in the faeces and is a substrate of P-gp and BCRP. Coadministration with rifampicin (a strong inducer) decreased afatinib exposure by approximately 34%. However, the decrease in afatinib exposure is expected to be lower with nevirapine given that it is a moderate-weak inducer. No a priori dose adjustment of afatinib is needed.

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.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Alectinib is metabolised by CYP3A4 to an active metabolite (M4), which is also metabolised by CYP3A4. Alectinib does not inhibit CYP3A4 to a clinically relevant extent. Nevirapine is metabolized by CYP3A4 and induces CYP3A4 but is not expected to alter alectinib exposure to a significant extent. Coadministration with rifampicin (a strong CYP3A4 inducer) decreased the combined exposure of alectinib and M4 by only 18%.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Alemtuzumab is a monoclonal IgG antibody. Elimination is similar to endogenous IgG and occurs primarily via proteolytic catabolism throughout the body. Nevirapine is metabolized by CYP3A4. CYP-mediated drug interactions are not expected with alemtuzumab. Note, use of alemtuzumab (marketed as Lemtrada) for the treatment of relapsing remitting multiple sclerosis is contraindicated in patients with HIV infection as it causes prolonged reductions of CD4+ lymphocyte counts.

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. Alogliptin is primarily excreted unchanged in the urine and undergoes negligible CYP-mediated metabolism. Alogliptin was shown to have no inhibitory or inducing effect on CYPs at concentrations achieved with the recommended dose of 25 mg alogliptin.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Alpelisib is primarily metabolized by enzymatic hydrolysis to an inactive metabolite, with a minor contribution from CYP3A4. Nevirapine is metabolized by CYP3A4 and induces CYP3A4 but is not expected to cause a significant decrease in alpelisib exposure as CYP3A4 represents a minor pathway in alpelisib metabolism.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Following administration, ~80% of circulating alprostadil is rapidly metabolised in the lungs primarily by beta- and omega- oxidation and the resulting metabolites are mainly excreted in urine. Nevirapine is metabolized by CYP3A4. Alprostadil is unlikely to affect CYP enzymes.

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.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Amivantamab is a monoclonal IgG1 and is eliminated primarily via intracellular catabolism similarly to endogenous IgG. Nevirapine is metabolized by CYP3A4.

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.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Anakinra is an IL-1 receptor antagonist which is predominantly cleared renally by glomerular filtration and subsequent tubular metabolism. Nevirapine is metabolized by CYP3A4. Patients requiring treatment with anakinra may have elevated levels of cytokines (e.g., TNF-alpha, IL-1, IL-6, IL-10, IFN) which have been shown to suppress expression/activity of CYP3A4, CYP2C19, CYP2C9 and CYP1A2. Anakinra, per se, has no inhibitory or inducing effects on cytochromes. Anakinra will normalize cytochrome activity (via inhibition of IL-1) but no significant effect on nevirapine is expected and no a priori dose adjustment is required.

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 but is not recommended. Apalutamide is primarily metabolized by CYP2C8 and CYP3A4. Apalutamide concentrations may decrease as nevirapine was shown to reduce the exposure of amodiaquine, a CYP2C8 substrate. In addition, apalutamide is a strong inducer of CYP3A4 and could significantly reduce nevirapine exposure leading to loss of therapeutic effect and possible development of resistance.

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. Apremilast is metabolized by multiple pathways involving hydrolysis, glucuronidation and oxidation by CYP3A4. Coadministration with rifampicin (a strong CYP3A4 inducer) was shown to decrease substantially apremilast AUC by 72% and Cmax 43%. The product label for apremilast does not recommend coadministration with strong CYP3A4 inducers as it may reduce the efficacy of apremilast. Nevirapine is a moderate inducer and could potentially reduce apremilast exposure, although to a lower extent than rifampicin. Use with caution; monitoring of the clinical effect is warranted. Note: severe diarrhoea, nausea and vomiting can occur within the first few weeks after initiating apremilast treatment. Patients should be instructed to contact their healthcare provider if they experience severe diarrhoea, nausea or vomiting as this could potentially alter the absorption of orally administered antiretroviral drugs.

Coadministration has not been studied. Aprepitant is mainly metabolized by CYP3A4 and to a lesser extent by CYPs 1A2 and 2C19. Nevirapine is metabolized by CYP3A4. Aprepitant shows an initial inhibitory effect on CYP3A4 followed by a weak inducing effect from day 8 which is clinically insignificant by two weeks. Any transient change in nevirapine exposure is unlikely to be clinically significant. However, nevirapine is a weak-moderate CYP3A4 inducer and could potentially decrease aprepitant concentrations. Coadministration of oral aprepitant and rifampicin (a strong CYP3A4 inducer) decreased aprepitant exposure by 91% and product labels for aprepitant advise to avoid coadministration with strong CYP3A4 inducers. Although a reduced effect is expected with nevirapine, coadministration should be approached with caution due to a potential decrease in aprepitant exposure leading to reduced efficacy.

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. Asciminib is metabolised by several pathways, including CYP3A4, UGT2B7 and UGT2B17. Nevirapine is metabolized by CYP3A4. Asciminib is a weak inhibitor of CYP3A4 but is unlikely to cause a clinically significant increase in nevirapine exposure. Nevirapine induces CYP3A4 and may reduce asciminib exposure, although to a limited extent. Coadministration with rifampicin (a strong inducer) decreased asciminib exposure by 15%, although a more pronounced decrease is anticipated when asciminib is used at a higher dose. Use with caution.

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

Coadministration has not been studied but based on metabolism and clearance, a clinically significant interaction is unlikely. Ashwagandha extracts had no effect on CYP enzymes in vitro.

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/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 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 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 but based on metabolism and clearance a clinically significant interaction is unlikely. Atezolizumab is eliminated through catabolism. Nevirapine is metabolized by CYP3A4.

Coadministration has not been studied. Atogepant is metabolized primarily by CYP3A4 and is a substrate of OATP. Nevirapine is metabolized by CYP3A4. Atogepant is not expected to have a clinically relevant effect on drugs metabolized by CYP enzymes. Nevirapine is a weak-moderate CYP3A4 inducer and may decrease atogepant exposure. Atogepant AUC decreased by 60% with rifampicin (a strong CYP3A4 inducer) and by 25% with topiramate (a weak CYP3A4 inducer). No dose recommendations are given for coadministration with CYP3A4 inducers in the European product label for atogepant. For the treatment of episodic migraine, the American product label for atogepant recommends a once daily dose of 30 mg or 60 mg with CYP3A4 inducers and recommends to avoid use with CYP3A4 inducers if treatment is for chronic migraine.

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

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. Avapritinib is predominantly mediated by CYP3A4 and to a minor extent by CYP2C9. Nevirapine is metabolized by CYP3A4. Avapritinib was shown to inhibit and induce CYP3A4 in vitro but the net effect in vivo has not been studied. However, nevirapine induces CYP3A4 and may decrease avapritinib exposure. Coadministration with efavirenz (a moderate CYP3A4 inducer) is predicted to reduce avapritinib exposure by 62% at steady-state and a similar decrease is expected with nevirapine. Coadministration should be avoided.

Coadministration has not been studied. Avatrombopag is mainly metabolized by CYP2C9 and CYP3A4. Nevirapine is metabolized by CYP3A4. Avatrombopag does not inhibit or induce CYP3A. However, nevirapine is a weak-moderate inducer of CYP3A4 and could decrease avatrombopag exposure. Coadministration with rifampicin (a moderate CYP2C9 and strong CYP3A inducer) decreased avatrombopag exposure by 43%. Use with caution and monitor platelet counts and adjust dose as necessary.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Avelumab is primarily metabolized through catabolic pathways and drug-drug interactions are not expected.

Coadministration has not been studied but should be avoided. Axitinib is metabolized primarily by CYP3A4 and to a lesser extent by CYP1A2, CYP2C19 and UGT1A1. Nevirapine is metabolized by CYP3A4. Axitinib does not inhibit or induce CYP3A4. However, nevirapine induces CYP3A4 and may significantly decrease concentrations of axitinib. Coadministration of rifampicin (a strong CYP3A4 inducer) and axitinib reduced axitinib AUC by 79%. Coadministration is not recommended. If coadministration is unavoidable, the dose of axitinib should be increased gradually with careful monitoring of tolerability.

Coadministration has not been studied but based on metabolism and clearance, a clinically significant interaction is unlikely. Although in vitro data suggest that some harma alkaloids found in ayahuasca preparations have a weak/moderate inhibitory effect on CYP3A4, this 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. Azacitidine undergoes spontaneous hydrolysis and deamination mediated by cytidine deaminase. Urinary excretion is the primary route of elimination of azacitidine and/or its metabolites. Following cellular uptake, azacitidine is sequentially phosphorylated via phosphokinases activities to azacitidine triphosphate which is able to incorporate into DNA and RNA. Nevirapine is metabolised by CYP3A4. Azacitidine does not inhibit or induce CYP enzymes.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Baricitinib is mainly eliminated renally through glomerular filtration and active secretion via OAT3, P-gp, BCRP and MATE2-K, with CYP3A4 metabolism representing less than 10% of its overall metabolism. Nevirapine is metabolized by CYP3A4. Baricitinib is not expected to have a clinically relevant effect on drugs metabolised by CYP enzymes. Nevirapine is a weak-moderate inducer of CYP3A4 but coadministration with rifampicin (a strong inducer) did not significantly alter baricitinib exposure.

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 with bazedoxifene alone or coformulated with conjugated estrogens as hormone replacement therapy (HRT) has not been studied. Bazedoxifene is glucuronidated by UGT1A1/8/10 and conjugated estrogens are metabolized by CYP3A4, CYP1A2 and are glucuronidated. Coadministration is predicted to decrease exposure of bazedoxifene and conjugated estrogens. Monitor for signs of hormone deficiency.

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. Belimumab is a monoclonal IgG antibody. Elimination is similar to endogenous IgG and occurs primarily via proteolytic catabolism throughout the body. Nevirapine is metabolized by CYP3A4.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bempedoic acid is glucuronidated by UGT2B7 and also converted to an active metabolite by aldo-keto reductase. Nevirapine does not inhibit or induce UGT2B7.

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. Bendamustine is metabolised by multiple routes including hydrolysis (main), glutathione conjugation and hepatic metabolism via CYP1A2. Nevirapine is metabolized by CYP3A4 and is unlikely to inhibit or induce CYP1A2. Bendamustine does not inhibit or induce CYP enzymes.

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. Available information on the metabolism of benzatropine is limited but no clinically significant interactions are expected. Nevirapine is metabolized by CYP3A4.

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. Beta-alanine is a non-essential amino acid and dietary supplements enter the same physiological processes as endogenous beta-alanine. Excess beta-alanine is excreted in the urine by the kidneys. Nevirapine is metabolized by CYP3A4. Beta-alanine is unlikely to affect CYP3A4.

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 no clinically relevant drug interactions are expected with the topical use of betamethasone (for example, ointment, cream, lotion, emollient, foam).

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. 

Coadministration has not been studied. Bicalutamide is metabolized by CYP3A4 and UGT1A9. Nevirapine is metabolized by CYP3A4. Bicalutamide is a weak inhibitor of CYP3A4 but is unlikely to have a clinically significant effect on nevirapine. However, nevirapine is a moderate inducer of CYP3A4 and has the potential to decrease bicalutamide concentrations. Use with caution and monitor clinical effect.

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. Bilastine is mainly excreted unchanged and is a substrate of P-gp and OATP1A2. Nevirapine is metabolized by CYP3A4. Bilastine is unlikely to affect CYP3A4.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bimekizumab is an IgG1 monoclonal antibody and is likely to be eliminated via intracellular catabolism, similarly to endogenous IgG. Nevirapine is metabolized by CYP3A4.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Binimetinib is primarily metabolised by UGT1A1 and the active metabolite M3 is metabolised by CYP1A2 and CYP2C19. Nevirapine is metabolized by CYP3A4 and does not induce or inhibit UGTs, CYP1A2 and CYP2C19. Binimetinib is unlikely to affect CYP3A4.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Following absorption, vitamin B7 is stored in the liver, kidney and pancreas.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Following absorption, vitamin B7 is stored in the liver, kidney and pancreas.

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 but based on metabolism and clearance a clinically significant interaction is unlikely. Bismuth subsalicylate is largely hydrolysed in the stomach to form salicylic acid, which is rapidly absorbed, and insoluble bismuth salts, which are excreted unchanged in faeces. Nevirapine is metabolized by CYP3A4. Bismuth subsalicylate is unlikely to affect CYP3A4.

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 but based on metabolism and clearance a clinically significant interaction is unlikely. An indirect effect of blinatumomab on CYPs may occur due to transient release of cytokines during the first days of therapy which can inhibit CYP450 metabolism, however, this is unlikely to be clinically relevant. The metabolic pathway of blinatumomab has not been characterised. Like other protein therapeutics, blinatumomab is expected to be degraded into small peptides and amino acids via catabolic pathways.

Coadministration has not been studied but should be avoided. Bosutinib is metabolized by CYP3A4. Coadministration with rifampicin (a strong inducer) decreased bosutinib AUC by 94%. Increasing the dose of bosutinib when coadministering with strong or moderate CYP3A inducers, such as nevirapine, is unlikely to sufficiently compensate for the loss of exposure. Use an alternative antiretroviral drug with no inducing or inhibitory effects.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Branched chain amino acids (BCAAs) mainly undergo intracellular catabolism in skeletal muscle. Excess BCAAs and BCAA-derived metabolic products are excreted in the urine by the kidneys. Nevirapine is metabolized by CYP3A4. BCAAs are unlikely to affect CYP3A4.

Coadministration has not been studied. Brentuximab vedotin is an antibody-drug conjugate comprising a monoclonal antibody and monomethyl auristatin E (MMAE), a potent chemotherapeutic agent. The monoclonal antibody undergoes elimination via intracellular catabolism and does not interact with nevirapine. However, MMAE is a substrate of CYP3A4 and P-gp, therefore nevirapine may decrease concentrations of MMAE. Coadministration of brentuximab vedotin and the strong inducer rifampicin decreased MMAE AUC by 46%. A less pronounced interaction is expected with nevirapine. No a priori dose adjustment of brentuximab vedotin is necessary as the contribution of free MMAE to efficacy is minimal.

Coadministration has not been studied. Brexpiprazole is predominantly metabolised by CYP3A4 and CYP2D6. Nevirapine is metabolized by CYP3A4. Brexpiprazole is unlikely to have a clinically relevant effect on drugs metabolised by CYP enzymes. However, nevirapine is a moderate inducer of CYP3A4 and may decrease brexpiprazole exposure. Use with caution. Product labels for brexpiprazole recommend to double the brexpiprazole dose over 1 to 2 weeks when coadministered with a strong CYP3A4 inducer. A dose adjustment could also be considered, based on clinical response, when brexpiprazole is coadministered with nevirapine.

Coadministration has not been studied but should be avoided. Brigatinib is metabolised by CYP2C8 and CYP3A4. Nevirapine is a weak-moderate inducer of CYP3A4 and is predicted to decrease the exposure of brigatinib by approximately 50%. Avoid coadministration. The US product label for brigatinib mentions that if coadministration with a moderate CYP3A4 inducer is needed, the brigatinib once daily dose can be increased in 30 mg increments after 7 days of treatment with the current brigatinib dose as tolerated, up to a maximum of twice the brigatinib dose that was tolerated prior to initiating the moderate CYP3A4 inducer. After discontinuation of a moderate CYP3A4 inducer, resume the brigatinib dose that was tolerated prior to initiating the moderate CYP3A4 inducer.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Brimonidine is metabolized mainly by aldehyde oxidase.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Brincidofovir is a prodrug converted to cidofovir which is eliminated renally via glomerular filtration and active renal secretion by OAT1 and OAT3. Nevirapine does not affect this pathway.

Coadministration has not been studied. Brinzolamide is mainly metabolised by CYP3A4, and to a lesser extent by CYPs 2A6, 2C8 and 2C9. Nevirapine is metabolized by CYP3A4. Brinzolamide does not inhibit or induce CYP3A4. However, nevirapine is a CYP3A4 inducer and may decrease brinzolamide concentrations. The clinical relevance of this potential interaction is unknown and patients should be monitored for clinical effect.

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. Bromocriptine is metabolised by CYP3A4. Nevirapine is metabolized by CYP3A4. Bromocriptine is unlikely to affect CYP3A4 at clinically relevant concentrations. However, nevirapine is a CYP3A4 inducer and may decrease bromocriptine concentrations. Monitor patients for clinical effect.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bulevirtide is catabolized by peptidases and elimination occurs through binding to NTCP (a bile salt liver transporter serving as HDV/HBV entry receptor). Nevirapine does not have any inhibitory effect on NTCP.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bumetanide is hepatically metabolized and approximately 50-80% of bumetanide is excreted in the urine by OAT1 and OAT3, mainly as unchanged drug (~50%). Nevirapine is metabolized by CYP3A4.

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. Busulfan is metabolised through conjugation with glutathione (spontaneous and GST-mediated) and then by hepatic oxidation (likely CYP3A4-mediated). Nevirapine is metabolized by CYP3A4. Busulfan is unlikely to affect CYP3A4. However, nevirapine is a weak-moderate CYP3A4 inducer and may decrease busulfan concentrations. Monitor patients for busulfan efficacy and adjust dose if necessary.

Coadministration has not been studied and should be used with caution. Cabazitaxel is metabolized by CYP3A4. Coadministration with rifampicin (a strong CYP3A4 inducer) decreased cabazitaxel exposure by 17%. Nevirapine is a moderate inducer and, therefore, may cause less reduction in cabazitaxel exposure. Coadministration should be avoided but, if required, should be done with caution and monitoring of cabazitaxel efficacy.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cabergoline is extensively metabolized by the liver predominantly via hydrolysis (non-CYP mediated metabolism) and is a substrate of P-gp. In vitro data indicate that nevirapine does not induce or inhibit P-gp in the range of clinical concentrations. No effect on nevirapine is expected as cabergoline does not inhibit or induce drug metabolizing enzymes.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cabergoline is extensively metabolized by the liver predominantly via hydrolysis (non-CYP mediated metabolism) and is a substrate of P-gp. In vitro data indicate that nevirapine does not induce or inhibit P-gp in the range of clinical concentrations. No effect on nevirapine is expected as cabergoline does not inhibit or induce drug metabolizing enzymes.

Coadministration with intramuscular cabotegravir has not been studied but based on the drug-drug interaction study with oral cabotegravir and rifabutin (another moderate inducer), nevirapine has the potential to cause a modest reduction in cabotegravir exposure. Note, cabotegravir used as PrEP is not expected to be coadministered with antiretrovirals except in the case of breakthrough infection when an antiretroviral treatment should be initiated. Residual concentrations of cabotegravir may remain in the systemic circulation for prolonged periods (up to 12 months or longer) but are not expected to affect the exposure of antiretroviral drugs initiated after discontinuation of Apretude.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Nevirapine is a weak inducer. Based on drug-drug interaction studies with rifabutin (also a moderate inducer), the decrease in cabotegravir exposure is expected not to be clinically relevant. No dose adjustment is required with oral cabotegravir. Cabotegravir is not expected to alter concentrations of other antiretroviral products.

Coadministration is contraindicated due to the potential for loss of therapeutic effect and development of resistance. Nevirapine has enzyme inducing properties. Based on the drug-drug interaction study with rifabutin (a moderate inducer), the decrease in cabotegravir exposure after intramuscular administration is expected not to be clinically relevant. However, nevirapine has the potential to significantly reduce rilpivirine exposure. Residual concentrations of cabotegravir and rilpivirine may remain in the systemic circulation of patients for a prolonged period after discontinuation of intramuscular cabotegravir/rilpivirine but are not expected to affect exposure of antiretroviral drugs.

Coadministration has not been studied. Coadministration with rifampicin (a strong inducer) reduced cabozantinib AUC by 77%. Nevirapine is expected to reduce cabozantinib concentrations, but to a lesser extent than rifampicin. Avoid coadministration is possible and consider a non-inducing/inhibiting antiretroviral regimen. If coadministration with nevirapine is unavoidable, consider increasing cabozantinib dose by 20 mg as tolerated (do not exceed a daily dose of 80 mg). The US product label for cabozantinib recommends to resume the dose that was used prior to initiating the CYP3A4 inducer 2 to 3 days after discontinuation of the strong inducer.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Caffeine is mainly metabolised by CYP1A2. Nevirapine is metabolized by CYP3A4 and does not affect CYP1A2. Caffeine is unlikely to affect CYP3A4.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Calcitonin is primarily metabolized via proteolysis in the kidney. Nevirapine does not interfere with this pathway.

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

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Canakinumab is an IL-1 beta monoclonal antibody and is eliminated via intracellular catabolism. Nevirapine is metabolized by CYP3A4. Patients requiring treatment with anakinra may have elevated levels of cytokines (e.g., TNF-alpha, IL-1, IL-6, IL-10, IFN) which have been shown to suppress expression/activity of CYP3A4, CYP2C19, CYP2C9 and CYP1A2. Canakinumab, per se, has no inhibitory or inducing effects on cytochromes. Canakinumab will normalize cytochrome activity (via inhibition of IL-1) but no significant effect on nevirapine is expected and no a priori dose adjustment is required.

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.

Coadministration has not been studied and should be avoided. Capmatinib is primarily metabolized by CYP3A4. Nevirapine induces CYP3A4. Coadministration with efavirenz, another moderate inducer, was predicted to decrease capmatinib exposure by 44% and Cmax by 34%. Decreases in capmatinib exposure may decrease capmatinib anti-tumour activity. Nevirapine is metabolized by CYP3A4, but capmatinib is unlikely to have a clinically relevant effect on CYP3A4.

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. Carbocisteine is metabolized in the liver via acetylation, decarboxylation and sulfoxidation with up to 60% excreted unchanged in the urine. The likelihood of a clinically significant drug interaction is low and no studies have been performed. Nevirapine is metabolized by CYP3A4.

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 but based on metabolism and clearance a clinically significant interaction is unlikely. Carfilzomib is rapidly metabolized, mainly by peptidase cleavage and epoxide hydrolysis with CYP-mediated metabolism representing a minor pathway. Nevirapine is metabolized by CYP3A4 and is a weak-moderate inducer of CYP3A4. Carfilzomib is not expected to have a clinically relevant effect on drugs metabolised by CYPs and is unlikely to be affected by inhibitors and inducers of CYPs and P-gp.

Coadministration has not been studied and is not recommended. Metabolism of cariprazine and its major active metabolites is mediated mainly by CYP3A4 with a minor contribution from CYP2D6. Nevirapine is metabolized by CYP3A4. Cariprazine is unlikely to affect CYP3A4. However, nevirapine is a CYP3A4 inducer and is expected to decrease cariprazine exposure. Cariprazine and its metabolites have very long elimination half-lives and changes in dose may not be fully reflected in plasma for several weeks. The European product label for cariprazine contraindicates coadministration with strong and moderate CYP3A4 inducers, whereas the American product label does not recommend coadministration with CYP3A4 inducers. Refer to the cariprazine product labels for more information.

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.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cedazuridine is eliminated renally and converted to its epimer (which is then renally excreted). Nevirapine is metabolised by CYP3A4. Cedazuridine does not inhibit or induce CYP enzymes.

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. Cefuroxime is not metabolised and is excreted predominantly by renal glomerular filtration, with no significant active renal tubular secretion. Nevirapine is metabolized by CYP3A4.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cemiplimab is primarily metabolised through catabolic pathways and drug-drug interactions are not expected. Nevirapine is metabolized by CYP3A4.

Coadministration has not been studied and is not recommended. Cenobamate is primarily glucuronidated by UGT2B7 and to a lesser extent by UGT2B4. CYP3A4 contributes to cenobamate metabolism but to a minor extent. Nevirapine is metabolized by CYP3A4. Cenobamate is a dose-dependent inducer of CYP3A4 and was shown to reduce exposure of midazolam (a CYP3A4 substrate) by 72% at a dose of 200 mg daily and by 27% at a dose of 100 mg daily. Cenobamate is dose-titrated until the 200 mg maintenance dose is reached. Cenobamate at a daily dose of 200 mg or greater may significantly decrease nevirapine concentrations and may result in loss of therapeutic effect.

Coadministration has not been studied. Ceritinib is metabolized by CYP3A4. Nevirapine induces CYP3A4 and can reduce ceritinib exposure. Coadministration is not recommended.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Certolizumab pegol is an antibody Fab’ fragment conjugated with polyethylene glycol (PEG). The Fab’ fragment is expected to be degraded to peptides and amino acids by proteolysis; the PEG moiety is mainly excreted in urine without further metabolism. Nevirapine is metabolized by CYP3A4.

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 with a chlormadinone-containing combined oral contraceptive (COC) has not been studied but is not expected to impair the contraceptive efficacy of chlormadinone and ethinylestradiol. Chlormadinone undergoes extensive hepatic metabolism by hydroxylation (likely CYP mediated). 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 chlormadinone pharmacokinetics and contraceptive efficacy when administered as a COC.

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. Cinacalcet is metabolized by multiple CYP enzymes, mainly CYP3A4, CYP2D6 and CYP1A2. Nevirapine is metabolized by CYP3A4. Cinacalcet does not inhibit or induce CYP3A4. However, concentrations of cinacalcet may decrease due to induction of CYP3A4 by nevirapine. A dose adjustment of cinacalcet may be required to achieve the desired clinical effect. Monitoring of iPTH serum phosphorus and serum calcium is recommended when starting or discontinuing nevirapine.

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 should be avoided. Cobimetinib is metabolised by CYP3A4 and UGT2B7. Nevirapine induces CYP3A4 and may significantly decrease concentrations of cobimetinib thereby potentially reducing its efficacy.

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.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. The major route of elimination for coenzyme Q10 is by biliary and faecal excretion; only a small fraction is eliminated in the urine. Nevirapine is metabolised by CYP3A4. Coenzyme Q10 is unlikely to have a clinically significant effect on substrates of CYP3A4, UGTs and P-gp.

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. 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 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 has not been studied. Colesevelam is not absorbed from the gastrointestinal tract, is not metabolised and does not affect CYP enzymes. Nevirapine is metabolised by CYP3A4. However, given that colesevelam can reduce the gastrointestinal absorption of some drugs, colesevelam should be administered at least four hours before or after nevirapine to minimize the risk of reduced absorption.

Coadministration has not been studied. Colestyramine may delay or reduce the absorption of drugs. Administration of other drugs should be at least 1 hour before or 4-6 hours after colestyramine. [Note: this interaction is not specific for nevirapine, but for any medication taken with colestyramine.]

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Collagen hydrolysate is digested and absorbed as essential amino acids for use in essential physiological processes. Nevirapine is metabolized by CYP3A4. Collagen hydrolysate is unlikely to affect CYP3A4.

Coadministration with conjugated estrogens as hormone replacement therapy (HRT) has not been studied. Conjugated estrogens are metabolized by CYP3A4, CYP1A2 and are glucuronidated. Coadministration is predicted to decrease exposure of conjugated estrogens. In addition, exposure of progestogens administered as part of HRT may also decrease. Monitor for signs of hormone deficiency. Note, use of conjugated estrogens as part of gender affirming treatment should be avoided as they are associated with high thromboembolic risk.

Coadministration has not been studied but should be avoided. Copanlisib is metabolised by CYP3A (~90%) and CYP1A1 (~10%). Nevirapine is metabolized by CYP3A4. Copanlisib does not inhibit or induce CYP3A4. However, nevirapine is a CYP3A4 inducer and may decrease copanlisib concentrations. Coadministration of copanlisib (60 mg i.v. infusion) and a strong CYP inducer (rifampicin, 600 mg once daily for 12 days) decreased copanlisib AUC and Cmax by 60% and 12%, respectively. Avoid coadministration if possible.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Creatine monohydrate is not degraded during normal digestion and nearly 99% of orally ingested creatine monohydrate is either taken up by muscle or excreted in urine. Nevirapine is metabolized by CYP3A4. Creatine is unlikely to affect CYP3A4.

Coadministration has not been studied but should be avoided. Crizotinib is mainly metabolized by CYP3A4. Nevirapine induces CYP3A4 and therefore can reduce crizotinib exposure and potentially its efficacy.

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. Cyanocobalamin undergoes enterohepatic recycling and is excreted almost entirely in the urine.

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 has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. The metabolism of cyclizine has not been fully described but may involve CYP2D6. Nevirapine is metabolized by CYP3A4 and is unlikely to inhibit or induce CYP2D6.

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.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cytisine is primarily excreted renally as unchanged drug. There are no reports of CYP or transporter involvement and significant pharmacokinetic interactions are unlikely. Nevirapine is metabolised by CYP3A4.

Coadministration has not been studied but is not recommended. Dabrafenib is metabolized by CYP3A4 and CYP2C8 and the active metabolites are metabolized by CYP3A4. Nevirapine is metabolized by CYP3A4 and CYP2B6 and induces CYP3A4 and could potentially decrease dabrafenib exposure. In addition, dabrafenib is a strong inducer of CYP3A4 and CYP2B6 and has the potential to decrease nevirapine exposure which may decrease its therapeutic effect.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dacomitinib is metabolised by CYP2D6 (~26%) to O-desmethyl dacomitinib, an active metabolite with similar activity to dacomitinib, whilst CYP3A4 (~6%) contributes to the formation of other minor metabolites. Nevirapine is metabolized by CYP3A4. Dacomitinib does not inhibit or induce CYP3A4. Nevirapine induces CYP3A4 and may decrease dacomitinib concentrations. However, this is unlikely to be clinically significant as CYP3A4 contributes to dacomitinib metabolism only to a small degree.

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.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Nevirapine is metabolized by CYP3A4. Dapivirine is metabolized mainly by CYP3A4 and to a lesser extent by glucuronidation. However, the risk of drug-drug interactions is low with the dapivirine vaginal ring due to its low systemic exposure. Furthermore, dapivirine concentrations in vaginal fluid exceed the in vitro HIV IC99 by 1000-fold.

Coadministration has not been studied. Dapoxetine is metabolized by CYP2D6, CYP3A4 and flavin monooxygenase 1. Nevirapine could reduce dapoxetine exposure due to CYP3A4 induction although to a limited extent given that multiple metabolic pathways are involved in dapoxetine elimination. No a priori dose adjustment of dapoxetine is needed.

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 but based on metabolism and clearance a clinically significant interaction is unlikely. Daptomycin is eliminated renally.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Daratumumab, is an IgG1 monoclonal antibody and is likely to be eliminated via intracellular catabolism, similarly to endogenous IgG. Nevirapine is metabolized by CYP3A4 and CYP2B6.

Coadministration has not been studied. Daridorexant is mainly metabolised by CYP3A4. Nevirapine is metabolized by CYP3A4. Daridorexant is a weak inhibitor of CYP3A4 but is unlikely to have a clinically significant effect on nevirapine. However, nevirapine is a CYP3A4 inducer and may decrease daridorexant concentrations. Coadministration of daridorexant and efavirenz (600 mg once daily) decreased daridorexant AUC and Cmax by 61% and 35%, respectively. A similar effect is expected with nevirapine. Decreases in daridorexant exposure may lead to reduced efficacy, therefore patients should be monitored for clinical effect. A reduction in daridorexant exposure may be more clinically relevant for patients receiving the lower (25 mg) daridorexant dose than those receiving the higher dose (50 mg).

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. Darolutamide is primarily metabolised by CYP3A4, and to a lesser extent by UGT1A9 and UGT1A1, and is a substrate of P-gp. Nevirapine is metabolized by CYP3A4. Darolutamide is a weak inducer of CYP3A4 but is unlikely to have a clinically significant effect on nevirapine. However, nevirapine is an inducer of CYP3A4 and has the potential to decrease darolutamide concentrations. Use with caution and monitor clinical effect.

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.

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.

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. 

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. The primary route of decitabine metabolism is likely by cytidine deaminase. Decitabine is a prodrug and is activated intracellularly through sequential phosphorylation via phosphokinases activities to the active triphosphate. Nevirapine is metabolised by CYP3A4. Decitabine does not inhibit or induce CYP enzymes.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Deferasirox is mainly glucuronidated by UGT1A1 and to a lesser extent by UGT1A3; CYP-mediated metabolism appears to be minor (~8%). Nevirapine is metabolized by CYP3A4. Deferasirox is a weak inducer of CYP3A4 and was shown to reduce midazolam exposure by 17%, although it is unlikely to significantly decrease nevirapine concentrations. Nevirapine is unlikely to affect UGT1A1 or UGT1A3.

Coadministration has not been studied but should be avoided. Deflazacort is immediately metabolised by plasma esterases to the active metabolite (21-desdeflazacort) which is then metabolised mainly by CYP3A4 to several inactive metabolites which are excreted in the urine (~70%) and faeces (~30%). Nevirapine is metabolized by CYP3A4. Deflazacort and 21-desdeflazacort do not inhibit or induce CYP3A4. However, nevirapine is a weak-moderate CYP3A4 inducer and may decrease concentrations of 21-desdeflazacort. Coadministration of deflazacort with rifampicin (a strong CYP3A4 inducer) significantly decreased the exposure of 21-desdeflazacort by ~95%. The US product label for deflazacort recommends to avoid concomitant use of strong or moderate CYP3A4 inducers with deflazacort. The European product label recommends to increase the maintenance dose of deflazacort if coadministered with enzyme inducers.

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.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Desloratadine is metabolized to the active metabolite 3-hydroxydesloratadine, which is subsequently glucuronidated. The enzyme(s) responsible for the formation of the active metabolite have not been identified, but no clinically relevant interactions have been observed with inhibitors of CYP enzymes. Nevirapine is metabolized by CYP3A4. Desloratadine does not inhibit CYP3A4.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Desmopressin undergoes no significant hepatic metabolism and is not a substrate for CYP enzymes. Nevirapine is metabolized by CYP3A4. Desmopressin does not inhibit CYP enzymes and no metabolic drug interactions are 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.

Coadministration has not been studied. Dexamethasone is metabolized by CYP3A4 and concentrations may decrease due to the inducing effect of nevirapine. Nevirapine is metabolized by CYP3A4. Dexamethasone is a dose-dependent inducer of CYP3A4 and is a moderate CYP3A4 inducer at doses above 16 mg. However, dexamethasone is unlikely to alter nevirapine exposure as bosentan (another moderate inducer) had no effect on nevirapine exposure in a drug-drug interaction study. Monitor steroid effect.

Coadministration has not been studied. Dexamethasone is metabolized by CYP3A4 and concentrations may decrease due to the inducing effect of nevirapine. Nevirapine is metabolized by CYP3A4. Dexamethasone is a weak CYP3A4 inducer at a low dose and is unlikely to have a clinically significant effect on nevirapine.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dexketoprofen is mainly excreted as glucuronide conjugates; CYP2C8/9 plays a minor role in metabolism. Nevirapine is metabolized by CYP3A4. Nevirapine does not inhibit or induce UGTs or CYP2C8/9. Dexketoprofen is unlikely to affect CYP3A4.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Coadministration with medicinal products that alter gastric pH would not be expected to affect nevirapine absorption.

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

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. Dimethyl fumarate is metabolized by esterases before entering the blood stream. Further metabolism occurs though the TCA cycle. Nevirapine is metabolised by CYP3A4. Dimethyl fumarate is unlikely to have a clinically significant effect on substrates of CYPs, UGTs and P-gp.

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.

Dolutegravir/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 nevirapine would be possible from a pharmacokinetic standpoint. Product labels for dolutegravir/lamivudine/tenofovir-DF fixed dose combination recommend that an additional 50 mg tablet of dolutegravir should be administered, approximately 12 hours after the fixed dose combination, during coadministration with nevirapine. When nevirapine and lamivudine (150 mg twice daily) were coadministered, there were no changes to lamivudine apparent clearance and volume of distribution, suggesting no induction effect of nevirapine on lamivudine clearance. 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. No interaction is expected with tenofovir-DF

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.

Coadministration has not been studied. Donepezil is metabolized by CYP3A4 and to a lesser extent by CYP2D6. Nevirapine has inducing properties and therefore has the potential to reduce donepezil exposure. Adjust donepezil dosage if needed.

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. Doxylamine is metabolised primarily by CYP2D6, CYP1A2 and CYP2C9. Nevirapine does not affect these CYPs. Nevirapine is metabolized by CYP3A4. Doxylamine is unlikely to have a clinically significant effect on nevirapine.

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 has not been studied. Dronedarone is metabolized by CYP3A4 and is a moderate inhibitor of CYP3A4. Nevirapine is a moderate inducer of CYP3A4 and has the potential to decrease dronedarone concentrations. A dose adjustment may be needed due to the possible decrease in the clinical effect.

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 with a drospirenone progestogen-only pill (POP) has not been studied but is not expected to impair the contraceptive efficacy of drospirenone. Drospirenone is metabolized to a minor extent via CYP3A4. Coadministration of nevirapine and norethisterone/ethinylestradiol administered as a COC decreased norethisterone AUC (19%) and ethinylestradiol AUC (20%). Similarly, nevirapine is not expected to significantly impair drospirenone pharmacokinetics and contraceptive efficacy when administered as a POP.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Drotaverine is metabolised in the liver by O-deethylation. Clinically relevant pharmacokinetic interactions have not been reported. Nevirapine is metabolised by CYP3A4.

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 has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dupilumab is an IgG4 monoclonal antibody and is expected to be degraded into small peptides and amino acids via catabolic pathways in the same manner as endogenous IgG. Nevirapine is metabolized by CYP3A4. No metabolic drug interactions are expected with dupilumab.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Durvalumab is an IgG1 monoclonal antibody and is likely to be eliminated via intracellular catabolism, similarly to endogenous IgG. Nevirapine is metabolized by CYP3A4 and CYP2B6.