Clinical studies have shown no clinically significant interactions between abacavir and zidovudine.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic 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. Zidovudine is metabolized by UGT2B7 and UGT1A9. However, when used for the prophylaxis of acute graft versus host disease, coadministration can increase the risk of developing anaemia.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Abemaciclib is metabolized by CYP3A4. Zidovudine does not interact with this pathway. However, due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Abiraterone is metabolized by CYP3A4 and SULT2A1. Zidovudine does not interact with these metabolic pathways.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Abrocitinib is mainly metabolized by CYP2C19 and CYP2C9, and to a lesser extent by CYP3A4 and CYP2B6. Zidovudine is metabolized by UGT2B7 and UGT1A9. Abrocitinib is not expected to have a clinically relevant effect on UGTs.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Acalabrutinib is metabolized by CYP3A4. Zidovudine does not interact with this pathway. However, due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Acamprosate is eliminated unchanged in the urine both via glomerular filtration and active secretion (exact transporter unknown, possibly OATs or OCTs). Zidovudine and acamprosate may compete for tubular secretion, which could lead to increased levels of either drug. The clinical relevance of this interaction is unknown.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as acenocoumarol is mainly metabolized by CYP2C9.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. However, agranulocytosis, thrombocytopenia, leukopenia, and aplastic anaemia, bone marrow depression, pancytopenia have been reported with acetazolamide therapy. Anaemia, neutropenia and leucopenia can be expected to occur in patients receiving zidovudine. If concomitant treatment with potentially myelosuppressive drugs is necessary then extra care should be taken in monitoring renal function and haematological parameters.

No significant interaction was observed when zidovudine (500 mg/day) and aciclovir were coadministered to 20 HIV-infected subjects.

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 zidovudine should be separated by 4 hours. [Note: this interaction is not specific for zidovudine, but for any oral medication taken with activated charcoal.]

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Adalimumab is a monoclonal IgG antibody. Elimination is similar to endogenous IgG and occurs primarily via proteolytic catabolism throughout the body. However, coadministration can increase the risk of developing anaemia.

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 zidovudine via modulation of, or competition for metabolic or elimination pathways.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Afatinib is mainly eliminated unchanged in the faeces. Zidovudine is metabolized by UGT2B7 and UGT1A9.

Coadministration has not been studied but based on the metabolic data there is little potential for pharmacokinetic interactions.

Concomitant treatment with potentially myelosuppressive drugs such as albendazole may increase the risk of adverse reactions to zidovudine. If concomitant therapy with these drugs is necessary then extra care should be taken in monitoring haematological parameters.

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. Zidovudine is metabolized by UGTs. An interaction is unlikely as albuvirtide is 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 pharmacokinetic interaction is unlikely. Alectinib is metabolised by CYP3A4 to an active metabolite (M4), which is also metabolised by CYP3A4. Zidovudine is metabolized by UGT2B7 and UGT1A9. However, caution is advised as coadministration can increase the risk of developing anaemia.

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. Zidovudine is metabolized by UGT2B7 and UGT1A9. 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.

Coadministration has not been studied but based on metabolism and clearance a clinically significant pharmacokinetic interaction is unlikely. Alpelisib is primarily metabolized by enzymatic hydrolysis to an inactive metabolite, with a minor contribution from CYP3A4. Zidovudine is metabolized by UGT2B7 and UGT1A9. However, caution is needed as the combined use of these medications can increase the risk of anemia.

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. Zidovudine is metabolized by UGT2B7 and UGT1A9. Alprostadil is unlikely to affect UGT 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. Zidovudine does not interfere with 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 has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as amiodarone is metabolized by CYP3A4.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Amivantamab is a monoclonal IgG1 and is eliminated primarily via intracellular catabolism similarly to endogenous IgG. Zidovudine is metabolized by UGT2B7 and UGT1A9. However, caution is needed as the combined used of these drugs can increase the risk of anaemia.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Amodiaquine is mainly metabolized by CYP2C8 to N-desethylamodiaquine, an active metabolite but less potent than the parent compound. However, use with caution as coadministration of these drugs can increase the risk of haematotoxicity. Closely monitor haematological parameters.

Concomitant treatment, especially acute therapy, with potentially nephrotoxic or myelosuppressive drugs (e.g. amphotericin) may also increase the risk of adverse reactions to zidovudine. Monitor renal function and haematological parameters and consider dose reduction if required.

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 pharmacokinetic interaction is unlikely. Anakinra is an IL-1 receptor antagonist which is predominantly cleared renally by glomerular filtration and subsequent tubular metabolism. Zidovudine is metabolized by UGT2B7 and UGT1A9. However, caution is advised due to the risk of additive haematological toxicity and haematological parameters should be monitored if coadministered.

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 based on metabolism and clearance a clinically significant interaction is unlikely. Apalutamide is primarily metabolized by CYP2C8 and CYP3A4.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Apixaban is metabolized by CYP3A4 and to a lesser extent by CYP1A2, CYP2C8, CYP2C9 and CYP2C19.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Apremilast is metabolized by multiple pathways involving hydrolysis, glucuronidation and oxidation by CYP3A4. Apremilast has no inhibitory or inducing effects on CYPs or drug transporters. Zidovudine does not interact with apremilast’s elimination pathways. 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 but based on metabolism and clearance a clinically significant interaction is unlikely. Aprepitant is mainly metabolized by CYP3A4 and to a lesser extent by CYPs 1A2 and 2C19. Zidovudine is metabolized by UGT2B7 and UGT1A9. Aprepitant shows a weak inducing effect on UGT on day 8 which is clinically insignificant by two weeks and no clinically significant effect on zidovudine is expected.

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.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Arsenic trioxide is hydrolysed to arsenious acid (the pharmacologically active metabolite) which is then methylated to less cytotoxic metabolites primarily in the liver (non-CYP mediated). Arsenious acid is also oxidated to arsenic acid, which may occur in numerous tissues via enzymatic or nonenzymatic processes. Zidovudine is metabolized by UGT2B7 and UGT1A9 and is unlikely to affect arsenic trioxide metabolism. Arsenic trioxide is unlikely to affect UGT2B7 or UGT1A9. Anaemia, neutropenia and leucopenia can be expected to occur in patients receiving zidovudine. Due to the risk of additive haematological toxicity, extra care should be taken in monitoring haematological parameters.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Asciminib is metabolised by several pathways, including CYP3A4, UGT2B7 and UGT2B17. Zidovudine is metabolized by UGT2B7 and UGT1A9. However, caution is advised as coadministration can increase the risk of haematological toxicity.

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 zidovudine 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 zidovudine 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.

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 pharmacokinetic interaction is unlikely. Aspirin is rapidly deacetylated to salicylic acid and then further metabolized mainly by glucuronidation (by several UGT, major UGT1A6) whereas zidovudine is glucuronidated by UGT2B7. However, there is increased risk of haematological toxicity when zidovudine is coadministered with non-steroidal anti-inflammatory drugs.

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 but based on metabolism and clearance a clinically significant interaction is unlikely. No clinically significant drug interactions were observed when atazanavir alone (400 mg once daily) was coadministered with lamivudine/zidovudine (150/300 mg twice daily). Zidovudine Cmax and AUC both increased by 5% but Cmin decreased by 31%. There was no change in the AUC of zidovudine glucuronide, but Cmax and Cmin decreased by 5% and 18%.

Coadministration with zidovudine alone has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. No clinically significant drug interactions were observed when atazanavir alone (400 mg once daily) was coadministered with lamivudine/zidovudine (150/300 mg twice daily). Zidovudine Cmax and AUC both increased by 5% but Cmin decreased by 31%. There was no change in the AUC of zidovudine glucuronide, but Cmax and Cmin decreased by 5% and 18%.

Coadministration with atazanavir/cobicistat has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Coadministration with atazanavir alone had no significant effect on zidovudine concentrations and cobicistat is not expected to have a significant impact on the pharmacokinetics of zidovudine.

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 pharmacokinetic interaction is unlikely. Atezolizumab is eliminated through catabolism. Zidovudine is metabolized by UGT2B7 and UGT1A9. No pharmacokinetic interaction is expected, however, caution is advised as coadministration can potentially increase the risk of developing anaemia.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Atogepant is metabolized primarily by CYP3A4 and is a substrate of OATP. Zidovudine is metabolized by UGT2B7 and UGT1A9.

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

Coadministration increased zidovudine AUC by ~30-35% but had no effect on atovaquone exposure. The clinical significance of the increase in zidovudine exposure is unknown, but routine dose modification is not warranted. Use with caution as coadministration of these drugs can increase the risk of haematotoxicity. Closely monitor haematological parameters.

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 zidovudine 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. Avanafil is primarily metabolized by CYP3A4. 

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Avapritinib is predominantly mediated by CYP3A4 and to a minor extent by CYP2C9. Zidovudine is metabolized by UGT2B7 and UGT1A9. However, caution is advised as coadministration can increase the risk of developing anaemia.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Avatrombopag is mainly metabolized by CYP2C9 and CYP3A4. Zidovudine is metabolized by UGT2B7 and UGT1A9.

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 based on metabolism and clearance a pharmacokinetic interaction is unlikely. Axitinib is metabolized primarily by CYP3A4 and to a lesser extent by CYP1A2, CYP2C19 and UGT1A1. Zidovudine is metabolized by UGT2B7 and UGT1A9. Axitinib does not inhibit or induce UGTs. However, caution is advised as coadministration can increase the risk of developing anaemia.

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 pharmacokinetic 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. Zidovudine is metabolised by UGT2B7 and UGT1A9. Anaemia, neutropenia and leucopenia can be expected to occur in patients receiving zidovudine. Due to the risk of additive haematological toxicity, extra care should be taken in monitoring haematological parameters.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Azathioprine is metabolized to 6-mercaptopurine which is further inactivated by xanthine oxidase and thiopurine methyltransferase. However, use with caution as coadministration of these drugs can increase the risk of haematotoxicity.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic 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. Zidovudine is metabolized by UGT2B7 and UGT1A9. Baricitinib is not expected to have a clinically relevant effect on drugs metabolised by UGT enzymes. However, caution is advised due to the risk of additive haematological toxicity and haematological parameters should be monitored if coadministered.

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 but based on metabolism and clearance a clinically significant interaction is unlikely. Bazedoxifene is glucuronidated by UGT1A1/8/10 and conjugated estrogens are metabolized by CYP3A4, CYP1A2 and are glucuronidated. Zidovudine does not interact with these metabolic pathways.

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. Zidovudine is metabolized by UGT2B7 and UGT1A9.

Coadministration has not been studied but based on metabolism and clearance a clinically pharmacokinetic interaction is unlikely. Bempedoic acid is glucuronidated by UGT2B7 and also converted to an active metabolite by aldo-keto reductase. However, caution is needed as coadministration may increase the risk of haematotoxicity. Closely monitor haematological parameters.

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 pharmacokinetic interaction is unlikely. Bendamustine is metabolised by multiple routes including hydrolysis (main), glutathione conjugation and hepatic metabolism via CYP1A2. Zidovudine is metabolized by UGT2B7 and UGT1A9. However, coadministration can increase the risk of haematological toxicity.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bendroflumethiazide is eliminated by hepatic metabolism (70%, exact pathway not known) and excreted unchanged in the urine (30%) via OAT1 and OAT3.

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. Zidovudine is metabolized by UGT2B7 and UGT1A9.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic 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. The most severe adverse effects associated with benznidazole are bone marrow depression, thrombocytopenic purpura, and agranulocytosis. Anaemia, neutropenia and leucopenia can be expected to occur in patients receiving zidovudine. If concomitant treatment with potentially nephrotoxic or myelosuppressive drugs is necessary then extra care should be taken in monitoring renal function and haematological parameters.

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. Zidovudine is metabolized by UGT2B7 and UGT1A9. Beta-alanine is unlikely to affect UGT2B7 or UGT1A9.

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

Coadministration has not been studied but based on metabolism and clearance, a clinically significant interaction is unlikely. Betamethasone is metabolized by CYP3A4.

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 as betrixaban is largely eliminated unchanged through biliary secretion via P-gp.

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 but based on metabolism and clearance a clinically significant interaction is unlikely. Bicalutamide is metabolized by CYP3A4 and UGT1A9. Zidovudine is metabolized by UGT2B7 and UGT1A9. Bicalutamide inhibited UGT1A9 in vitro but a clinically significant effect on zidovudine is not expected.

Biktarvy (bictegravir, emtricitabine, tenofovir alafenamide) is indicated for use as a complete regimen for the treatment of HIV 1 infection. However, in specific clinical situations where an intensification of HIV treatment is needed, coadministration with zidovudine would be possible from a pharmacokinetic standpoint.

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. Zidovudine is metabolized by UGT2B7 and UGT1A9. Bilastine is unlikely to affect UGTs.

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. Zidovudine is metabolized by UGT2B7 and UGT1A9.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Binimetinib is primarily metabolised by UGT1A1 and the active metabolite M3 is metabolised by CYP1A2 and CYP2C19. Zidovudine is metabolized by UGT2B7 and UGT1A9. However, coadministration can increase the risk of haematological toxicity.

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 limited information concerning the metabolism and clearance of biperiden, there is little potential for clinically significant interaction. Limited human data suggest biperiden undergoes hydroxylation in the liver.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic 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. Zidovudine is metabolized by UGT2B7 and UGT1A9. Bismuth subsalicylate is unlikely to affect zidovudine metabolism.

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 pharmacokinetic interaction is unlikely. The metabolic pathway of blinatumomab has not been characterized. Like other protein therapeutics, blinatumomab is expected to be degraded into small peptides and amino acids via catabolic pathways. However, due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Bosutinib is metabolized by CYP3A4. Zidovudine does not interact with this pathway. However, due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.

Coadministration has not been studied but based on metabolism and clearance a 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. Zidovudine is metabolized by UGT2B7 and UGT1A9. BCAAs are unlikely to affect UGT2B7 or UGT1A9.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. 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 zidovudine. MMAE is a substrate of CYP3A4 and P-gp but zidovudine does not interfere with these pathways. 

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Brexpiprazole is predominantly metabolised by CYP3A4 and CYP2D6. Zidovudine is metabolized by UGT2B7 and UGT1A9. However, caution is advised due to the risk of additive haematological toxicity and haematological parameters should be monitored if coadministered.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Brigatinib is metabolised by CYP2C8 and CYP3A4. Zidovudine is metabolized by UGT2B7 and UGT1A9. However, coadministration can increase the risk of haematological toxicity.

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. Brincidofovir is a prodrug converted to cidofovir which is eliminated renally via glomerular filtration and active renal secretion by OAT1 and OAT3. When brincidofovir is coadministered to patients being treated with zidovudine, they should be closely monitored for zidovudine-induced haematological toxicity.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Brinzolamide is mainly metabolised by CYP3A4, and to a lesser extent by CYPs 2A6, 2C8 and 2C9. Zidovudine is metabolized by UGT2B7 and UGT1A9. Zidovudine is unlikely to inhibit or induce CYPs. Brinzolamide is unlikely to affect UGT2B7 or UGT1A9.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bromocriptine is metabolised by CYP3A4. Zidovudine is metabolized by UGT2B7 and UGT1A9. Bromocriptine is unlikely to affect UGTs.

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%). Zidovudine is metabolized by UGT2B7 and UGT1A9.

This interaction has not been studied. Based on the metabolism/elimination and toxicity profiles of both drugs, there is little potential for interaction. Bupivacaine is predominantly metabolized via CYP3A4.

No significant effect of buprenorphine on zidovudine pharmacokinetics was observed in opioid-dependent subjects receiving buprenorphine and zidovudine when compared to values obtained from 17 non-opioid treated subjects.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Busulfan is metabolised through conjugation with glutathione (spontaneous and GST-mediated) and then by hepatic oxidation (likely CYP3A4-mediated). Zidovudine is metabolized by UGT2B7 and UGT1A9. Zidovudine is unlikely to affect busulfan metabolism. Busulfan is unlikely to affect UGTs. However, coadministration should be avoided due to potential additive myelosuppression.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Cabazitaxel is metabolized by CYP3A4. Zidovudine does not interact with this pathway. However, due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cabergoline is extensively metabolized by the liver predominantly via hydrolysis (non-CYP mediated metabolism).

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).

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

Cabenuva (cabotegravir LA, rilpivirine LA) 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 zidovudine would be possible from a pharmacokinetic standpoint. 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 but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Cabozantinib is metabolized by CYP3A4. Zidovudine does not interact with this pathway. However, due to the risk of additive haematological toxicity, haematological parameters should be monitored if coadministered.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Caffeine is mainly metabolised by CYP1A2. Zidovudine is metabolized by UGT2B7 and UGT1A9 and does not affect CYP1A2. Caffeine is unlikely to affect UGTs.

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. Zidovudine 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 zidovidine.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Canakinumab is an IL-1 beta monoclonal antibody and is eliminated via intracellular catabolism. Zidovudine is metabolized by UGT2B7 and UGT1A9. However, caution is advised due to the risk of additive haematological toxicity and haematological parameters should be monitored if coadministered.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cannabidiol is mainly metabolized by CYP3A4 and CYP2C19 and is unlikely to significantly inhibit CYPs or UGTs in the range of doses in clinical use.

Coadministration has not been studied. Capecitabine is activated by sequential enzyme reactions to fluorouracil. Dihydropyrimidine dehydrogenase plays a role in fluorouracil metabolism. Nucleoside analogues such as zidovudine may compete for these metabolic pathways. The clinical relevance of this interaction is unknown. However, the risk of haematological toxicity may be potentially increased as both drugs can cause myelosuppression. Closely monitor haematological parameters.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Capmatinib is primarily metabolized by CYP3A4. Zidovudine is metabolized by UGT2B7 and UGT1A9.

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

Coadministration has not been studied but may increase carbamazepine concentrations due to competition for glucuronidation (carbamazepine is glucuronidated by UGT2B7). The clinical relevance of this interaction is unknown as the importance of glucuronidation in the overall metabolic process of carbamazepine is controversial.

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. Zidovudine is metabolized by UGT2B7 and UGT1A9.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Carboplatin is excreted primarily by renal glomerular filtration and therefore there is little potential for a pharmacokinetic interaction. However, myelosuppression as a result of carboplatin treatment is closely related to renal clearance of the drug. Therefore, in patients with abnormal renal function, or who are receiving concomitant therapy with nephrotoxic drugs, myelosuppression may be more severe and prolonged. Anaemia, neutropenia and leucopenia can be expected to occur in patients receiving zidovudine. If concomitant treatment with potentially nephrotoxic or myelosuppressive drugs is necessary then extra care should be taken in monitoring renal function and haematological parameters.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Carfilzomib is rapidly metabolized, mainly by peptidase cleavage and epoxide hydrolysis with CYP-mediated metabolism representing a minor pathway. Zidovudine is metabolized by UGT2B7 and UGT1A9. However, caution is advised due to the risk of additive haematological toxicity and haematological parameters should be monitored if coadministered.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Metabolism of cariprazine and its major active metabolites is mediated mainly by CYP3A4 with a minor contribution from CYP2D6. Zidovudine is metabolized by UGT2B7 and UGT1A9. Cariprazine is unlikely to affect UGTs. However, caution is advised due to the risk of additive haematological toxicity and haematological parameters should be monitored if coadministered.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cat’s claw was demonstrated to strongly inhibit CYP3A4 in vitro but has also been shown to induce CYP3A4 activity in vitro. No interaction is expected as zidovudine does not undergo CYP3A4 metabolism.

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). Zidovudine is metabolised by UGT2B7 and UGT1A9.

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. Cefixime 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. 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. Zidovudine is metabolized by UGT2B7 and UGT1A9.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely as celecoxib is metabolised mainly by CYP2C9. However, there is increased risk of haematological toxicity when zidovudine is coadministered with non-steroidal anti-inflammatory drugs.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Cemiplimab is primarily metabolised through catabolic pathways and drug-drug interactions are not expected. Zidovudine is metabolized by UGT2B7 and UGT1A9. However, coadministration can increase the risk of developing anaemia.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cenobamate is primarily glucuronidated by UGT2B7 and to a lesser extent by UGT2B4. CYP3A4 contributes to cenobamate metabolism but to a minor extent.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Ceritinib is metabolized by CYP3A4. Zidovudine is metabolized by UGT2B7 and UGT1A9. However, coadministration can increase the risk of developing anaemia.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic 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. Zidovudine is metabolized by UGT2B7 and UGT1A9. However, coadministration can increase the risk of developing anaemia.

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 evaluated in clinical studies. Chloramphenicol and zidovudine are glucuronidated via the same route, predominantly by UGT2B7. In vitro studies have demonstrated that chloramphenicol can decrease the glucuronidation of zidovudine, and that zidovudine can decrease the glucuronidation of chloramphenicol. This could potentially lead to increased levels of either drug, although the clinical consequence is not known. As both chloramphenicol and zidovudine can cause myelosuppression, monitoring of haematological parameters is recommended.

Coadministration with a chlormadinone-containing combined oral contraceptive (COC) has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Chlormadinone undergoes extensive hepatic metabolism by hydroxylation (likely CYP mediated). Ethinylestradiol is also metabolized by hydroxylation and glucuronidation. Zidovudine does not interact with these metabolic pathways.

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.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cinacalcet is metabolized by multiple CYP enzymes, mainly CYP3A4, CYP2D6 and CYP1A2. Zidovudine is metabolized by UGT2B7 and UGT1A9.

Coadministration of clarithromycin (500 mg twice daily)  and zidovudine (100 mg every 4 hours) reduced zidovudine AUC by 12% (range 34% decrease to 14% increase). This is unlikely to be clinically significant but the European SPC for zidovudine advises to administer clarithromycin and zidovudine at least 2 h apart.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Clobazam is metabolised by CYP3A4 (major) and CYP2B6 and CYP2C19 (minor) to the active metabolite N-desmethylclobazam, which is metabolised by CYP2C19.

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

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

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Cobimetinib is metabolised by CYP3A4 and UGT2B7. Zidovudine is metabolized by UGT2B7 and UGT1A9. However, coadministration can increase the risk of developing anaemia.

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. Zidovudine is metabolised by UGT2B7 and UGT1A9. Coenzyme Q10 is unlikely to have a clinically significant effect on substrates of CYP3A4, UGTs and P-gp.

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

Coadministration has not been studied. Colesevelam is not absorbed from the gastrointestinal tract, is not metabolised and does not affect CYP enzymes. Zidovudine is metabolised by UGT2B7 and UGT1A9. However, given that colesevelam can reduce the gastrointestinal absorption of some drugs, colesevelam should be administered at least four hours before or after zidovudine 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 zidovudine, 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. Zidovudine is metabolized by UGT2B7 and UGT1A9. Collagen hydrolysate is unlikely to affect UGT2B7 or UGT1A9.

Coadministration with conjugated estrogens as hormone replacement therapy (HRT) has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Conjugated estrogens are metabolized by CYP3A4, CYP1A2 and are glucuronidated. Zidovudine does not interact with these metabolic pathways. In addition, no interaction is expected with progestogens administered as part of HRT. 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 based on metabolism and clearance a pharmacokinetic interaction is unlikely. Copanlisib is metabolised by CYP3A (~90%) and CYP1A1 (~10%). Zidovudine is metabolized by UGT2B7 and UGT1A9. Zidovudine is unlikely to inhibit or induce CYPs. Copanlisib does not inhibit or induce UGTs. However, caution is advised due to the risk of additive haematological toxicity and haematological parameters should be monitored if coadministered.

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. Zidovudine is metabolized by UGT2B7 and UGT1A9. Creatine is unlikely to affect UGT2B7 or UGT1A9.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Crizotinib is mainly metabolized by CYP3A4. Zidovudine is metabolized by UGT2B7 and UGT1A9. However, coadministration can increase the risk of developing anaemia.

Coadministration has not been studied but based on metabolism and clearance, a clinically significant interaction is unlikely. There is no evidence to suggest that Piper cubeba impacts UGTs.

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 pharmacokinetic interaction is unlikely. The metabolism of cyclizine has not been fully described but may involve CYP2D6. Zidovudine is metabolized by UGT2B7 and UGT1A9. No pharmacokinetic interaction is expected, however, caution is advised as coadministration can potentially increase the risk of developing anaemia.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cyproterone acetate is metabolized by CYP3A4.

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. Zidovudine is metabolised by UGT2B7 and UGT1A9.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Dabrafenib is metabolized by CYP3A4 and CYP2C8 and the active metabolites are metabolized by CYP3A4. Zidovudine is metabolized by UGT2B7 and UGT1A9. However, coadministration can increase the risk of developing anaemia.

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. Zidovudine is metabolized by UGT2B7 and UGT1A9.

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 zidovudine.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Zidovudine is metabolized by UGT2B7 and UGT1A9. 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 of dapsone and zidovudine had no effect on the pharmacokinetics of either drug. However, concomitant treatment, especially acute therapy, with potentially nephrotoxic or myelosuppressive drugs (e.g. dapsone) may also increase the risk of adverse reactions to zidovudine. Monitor renal function and haematological parameters and consider dose reduction if required.

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 pharmacokinetic interaction is unlikely. Daratumumab, is an IgG1 monoclonal antibody and is likely to be eliminated via intracellular catabolism, similarly to endogenous IgG. Zidovudine is metabolized by UGT2B7 and UGT1A9. However, coadministration can increase the risk of developing anaemia.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Daridorexant is mainly metabolised by CYP3A4. Zidovudine is metabolized by UGT2B7 and UGT1A9.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Darifenacin is metabolized by CYP3A4 and CYP2D6.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Darolutamide is primarily metabolised by CYP3A4, and to a lesser extent by UGT1A9 and UGT1A1, and is a substrate of P-gp. Zidovudine is metabolized by UGT2B7 and UGT1A9.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as zidovudine is primarily renally excreted.

Symtuza (darunavir, cobicistat, emtricitabine, tenofovir alafenamide) is indicated for use as a complete regimen for the treatment of HIV-1 infection. However, in specific clinical situations where an intensification of HIV treatment is needed, coadministration with zidovudine would be possible from a pharmacokinetic standpoint. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as zidovudine is primarily renally excreted.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely.  A clinical study reported that antiretroviral regimens containing zidovudine had no effect on the pharmacokinetics of liposomal daunorubicin. After administration of daunorubicin, myelosuppression can be expected in all patients. In patients treated with medicinal products influencing the bone marrow function (e. g. antiretroviral agents) the possibility of a marked disorder of hematopoiesis should be considered and the dose of daunorubicin should be modified if required. Anaemia, neutropenia and leucopenia can be expected to occur in patients receiving zidovudine. If concomitant treatment with potentially myelosuppressive drugs is necessary, care should be taken in monitoring haematological parameters.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic 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. Zidovudine is metabolised by UGT2B7 and UGT1A9. Anaemia, neutropenia and leucopenia can be expected to occur in patients receiving zidovudine. Due to the risk of additive haematological toxicity, extra care should be taken in monitoring haematological parameters.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Deferasirox is mainly glucuronidated by UGT1A1 and to a lesser extent by UGT1A3; CYP-mediated metabolism appears to be minor (~8%). Zidovudine is metabolized by UGT2B7 and UGT1A9. Deferasirox is unlikely to affect UGT2B7 or UGT1A9. However, caution is advised due to the risk of additive haematological toxicity and haematological parameters should be monitored if coadministered.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. 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%). Zidovudine is metabolized by UGT2B7 and UGT1A9. Deflazacort and 21-desdeflazacort do not inhibit or induce UGT2B7 or UGT1A9. Zidovudine is unlikely to affect CYP3A4.

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. Zidovudine does not affect CYP enzymes.

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. Zidovudine is metabolized by UGT2B7 and UGT1A9.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Desmopressin undergoes no significant hepatic metabolism and is not a substrate for CYP enzymes. Zidovudine is metabolized by UGT2B7 and UGT1A9. No metabolic drug interactions are expected with desmopressin.

Coadministration with a desogestrel-containing combined oral contraceptive (COC) has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Desogestrel is a prodrug which is activated to etonogestrel by CYP2C9 (and possible CYP2C19); the metabolism of etonogestrel is mediated by CYP3A4. Ethinylestradiol is mainly metabolized by hydroxylation.

Coadministration with a desogestrel-containing progestogen-only pill (POP) has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Desogestrel is a prodrug which is activated to etonogestrel by CYP2C9 (and possible CYP2C19); the metabolism of etonogestrel is mediated by CYP3A4.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dexamethasone is metabolized by CYP3A4. Dexamethasone and its metabolites are excreted in the urine.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dexamethasone is metabolized by CYP3A4. Dexamethasone and its metabolites are excreted in the urine.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Dexketoprofen is mainly excreted as glucuronide conjugates; CYP2C8/9 plays a minor role in metabolism. Zidovudine is metabolized by UGT2B7 and UGT1A9. Zidovudine is unlikely to affect UGTs or CYPs. Dexketoprofen is unlikely to affect UGTs. However, there is increased risk of haematological toxicity when zidovudine is coadministered with non-steroidal anti-inflammatory drugs.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dexlansoprazole is mainly metabolized by CYP2C19 (major) and CYP3A4 (minor).

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dextromethorphan is metabolized by CYP2D6. Zidovudine is metabolized by UGT2B7 and UGT1A9. Zidovudine is unlikely to inhibit or induce CYP2D6. Dextromethorphan is unlikely to affect UGTs.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Diclofenac is partly glucuronidated by UGT2B7 and partly oxidized by CYP2C9. However, there is increased risk of haematological toxicity when zidovudine is coadministered with non-steroidal anti-inflammatory drugs.

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 zidovudine.

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

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Dimethyl fumarate is metabolized by esterases before entering the blood stream. Further metabolism occurs though the TCA cycle. Zidovudine is metabolised by UGT2B7 and UGT1A9. Dimethyl fumarate is unlikely to have a clinically significant effect on substrates of CYPs, UGTs and P-gp. However, anaemia, neutropaenia and leucopaenia can be expected to occur in patients receiving zidovudine. If concomitant treatment with potentially myelosuppressive drugs is necessary then extra care should be taken in monitoring haematological parameters.

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, whereas zidovudine is glucuronidated by UGT2B7.

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

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 zidovudine would be possible from a pharmacokinetic standpoint. No interaction is expected with dolutegravir or tenofovir-DF. Coadministration of zidovudine (200 mg single dose) and lamivudine (300 mg twice daily) to 12 asymptomatic HIV-infected adult patients increased zidovudine Cmax and AUC by 28% and 13%, but had no effect on the pharmacokinetics of lamivudine.

Triumeq (dolutegravir, abacavir, lamivudine) can be used 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 zidovudine would be possible from a pharmacokinetic standpoint. Coadministration of single doses of abacavir (600 mg), lamivudine (150 mg), and zidovudine (300 mg) showed no clinically relevant changes in the pharmacokinetics of abacavir. Lamivudine AUC decreased by 15% and zidovudine AUC increased by 10% with concurrent abacavir. No clinically significant alterations in lamivudine or zidovudine pharmacokinetics were observed with coadministration of zidovudine (200 mg, single dose) and lamivudine (300 mg single dose).

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 zidovudine would be possible from a pharmacokinetic standpoint. The European product label for Dovato advises that no dose adjustment is necessary with zidovudine. No interaction is expected with dolutegravir. No clinically significant alterations in lamivudine or zidovudine pharmacokinetics were observed with coadministration of zidovudine (200 mg, single dose) and lamivudine (300 mg single dose).

Juluca (dolutegravir/rilpivirine) is indicated for use as a complete regimen for the treatment of HIV-1 infection. However, in specific clinical situations where an intensification of HIV treatment is needed, coadministration with zidovudine would be possible from a pharmacokinetic standpoint as no clinically relevant drug-drug interaction is expected.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Donepezil is metabolized by CYP3A4 and to a lesser extent by CYP2D6. Zidovudine does not interact with this metabolic pathway.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Doravirine is metabolized by CYP3A4. Zidovudine does not interfere with CYP450 mediated metabolism.

Delstrigo (doravirine, lamivudine, tenofovir-DF) is indicated for use as a complete regimen for the treatment of HIV 1 infection. However, in specific clinical situations where an intensification of HIV treatment is needed, coadministration with zidovudine would be possible from a pharmacokinetic standpoint. Coadministration of zidovudine with doravirine or tenofovir-DF has not been studied, but a clinically significant interaction is unlikely. Coadministration of zidovudine (200 mg single dose) and lamivudine (300 mg twice daily) to 12 asymptomatic HIV-infected adult patients increased zidovudine Cmax and AUC by 28% and 13%, but had no effect on the pharmacokinetics of lamivudine.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic 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.) However, concomitant treatment, especially acute therapy, with potentially nephrotoxic or myelosuppressive drugs (e.g. doxorubicin) may also increase the risk of adverse reactions to zidovudine. The European SPC for zidovudine recommends that if concomitant therapy is necessary to monitor renal function and haematological parameters and consider dose reduction if required. The US Prescribing Information for zidovudine advises to avoid concomitant use since an antagonistic relationship has been demonstrated in vitro .

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

Coadministration 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. Zidovudine is metabolized by UGT2B7 and UGT1A9.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dronedarone is primarily metabolized by CYP3A4. Zidovudine does not interfere with this metabolic pathway.

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

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

Coadministration with a drospirenone progestogen-only pill (POP) has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Drospirenone is metabolized to a minor extent via CYP3A4. Zidovudine does not interact with this metabolic pathway.

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. Zidovudine is metabolised by UGT2B7 and UGT1A9.

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. Zidovudine is metabolized by UGT2B7 and UGT1A9.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Durvalumab is an IgG1 monoclonal antibody and is likely to be eliminated via intracellular catabolism, similarly to endogenous IgG. Zidovudine is metabolized by UGT2B7 and UGT1A9. However, coadministration can increase the risk of developing anaemia.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Duvelisib is primarily metabolized by CYP3A4. Zidovudine is metabolized by UGT2B7 and UGT1A9. However, coadministration can increase the risk of developing anaemia.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ecdysterone has poor bioavailability and is predominantly metabolised once it reaches the gut microbiota. Unchanged ecdysterone and ecdysterone metabolites are excreted in both urine and faeces. Zidovudine is metabolized by UGT2B7 and UGT1A9. Ecdysterone is unlikely to affect UGT2B7 or UGT1A9.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Edoxaban is minimally metabolised by hydrolysis (mediated by carboxylesterase 1), conjugation, or oxidation by CYP3A4/5 (<10%). Edoxaban is eliminated primarily as unchanged drug in urine.