Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Aceclofenac is metabolised by CYP2C9. The potential for hepatically metabolised interactions with adefovir is low. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1.

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. Adefovir is not expected to interact with this pathway.

Coadministration has not been studied, but based on metabolism and clearance a clinically significant interaction is unlikely. Agomelatine is metabolised predominantly by CYP1A2. The potential for hepatically metabolised interactions with adefovir is low. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. [Note, agomelatine is contraindicated in hepatic impairment as increases in exposure of up to 140-times have been seen in cirrhotic patients.]

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Albiglutide is a protein for which the expected metabolic pathway is degradation to small peptides and individual amino acids by ubiquitous proteolytic enzymes. Albiglutide slows gastric emptying, but this is unlikely to have a clinically relevant effect on adefovir.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Alcohol is metabolized by alcohol dehydrogenase and aldehyde dehydrogenase. Acute alcohol use inhibits CYP2E1. Chronic use may induce CYP2E1 and to a lesser extent CYP3A4 but this is unlikely to be clinically relevant. Adefovir does not interact with these pathways.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Alirocumab is a monoclonal IgG antibody. Elimination is similar to endogenous IgG and occurs primarily via proteolytic catabolism throughout the body. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Allopurinol is converted to oxipurinol by xanthine oxidase and aldehyde oxidase. The potential for hepatically metabolised interactions with adefovir is low. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. [Note, the European SmPC and US Prescribing Information for allopurinol recommend a reduced dose in hepatic impairment.]

Coadministration has not been studied but concentrations of both may be altered. Amikacin is eliminated renally by glomerular filtration and adefovir is eliminated renally both via glomerular filtration and active renal secretion by OAT1. As both drugs can be nephrotoxic, renal function monitoring is required.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Amphotericin B is eliminated unchanged via urinary and biliary excretion (biliary excretion is lower with lipid formulated amphotericin).

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. Anakinra does not interact with this pathway. Anakinra is an IL-1 receptor antagonist and is eliminated by glomerular filtration and subsequent tubular metabolism.

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). The potential for hepatically metabolised interactions with adefovir is low.Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. Atazanavir/ritonavir is unlikely to inhibit OATs at clinically relevant concentrations.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. Atazanavir is unlikely to inhibit OATs at clinically relevant concentrations.

Coadministration has not been studied but based on the metabolism and clearance a clinically significant drug-drug interaction is unlikely as adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. Atazanavir/cobicistat is unlikely to inhibit OATs at clinically relevant concentrations. Cobicistat has been shown to decrease estimated creatinine clearance due to inhibition of tubular secretion of creatinine without affecting actual renal glomerular function. Atazanavir/cobicistat should not be coadministered with adefovir in patients with creatinine clearance less than 70 ml/min.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. Bamlanivimab and etesevimab are IgG1 monoclonal antibodies and are likely to be eliminated via intracellular catabolism, similarly to endogenous IgG.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. Baricitinib does not inhibit OATs.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. In vitro data suggest that bezafibrate inhibits the renal transporter OAT1 but a clinically relevant drug interaction with adefovir is unlikely in the observed range of clinical concentrations. [Note, the European SmPC for bezafibrate contraindicates its use in significant hepatic disease.]

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bisoprolol is partly metabolized by CYP3A4 and CYP2D6 and partly eliminated unchanged in the urine. The potential for hepatically metabolised interactions with adefovir is low. In vitro data indicate that bisoprolol inhibits OCT2, however an interaction is unlikely as adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. [Note, the European product label for bisoprolol recommends a maximum of 10 mg in severe hepatic impairment whereas the US Prescribing Information recommends an initial 2.5 mg in hepatic impairment with caution in further dose titration.]

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction Is unlikely. Black cohosh does not appear to be a potent modulator of human drug metabolism. Standardized black cohosh supplements, when taken at recommended doses, pose little risk for herb-drug interactions. The potential for hepatically metabolised interactions with adefovir is low. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1.

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. Unlike cidofovir, brincidofovir is not a substrate of OATs and therefore is less likely to accumulate in the kidney thereby reducing the potential for nephrotoxicity. Furthermore, the administration of oral brincidofovir leads to cidofovir plasma concentrations <1% of those observed after IV cidofovir. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1, however given that brincidofovir is not a substrate of this transporter no pharmacokinetic interaction is expected. 

Coadministration has not been formally studied but based on current knowledge of the effect of vaccines on drug disposition a clinically significant interaction is considered unlikely.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as candesartan is mainly eliminated unchanged via urine and bile. [Note, use of candesartan in severe hepatic impairment is contraindicated in the European SmPC; the US Prescribing Information recommends caution in moderate hepatic impairment.]

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. Adefovir does not interfere with these pathways.

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 adefovir may compete for these metabolic pathways. The clinical relevance of this interaction is unknown.

Coadministration has not been studied. Capreomycin is predominantly excreted in the urine as unchanged drug. As capreomycin may potentially compete with adefovir for renal elimination transport mechanisms, levels of either drug may hypothetically be raised. Renal function should be monitored as clinically appropriate.

Coadministration has not been studied but based on metabolism and clearance a clinically significant pharmacokinetic interaction is unlikely. Carfentanil is expected to be metabolized by CYP3A4/5. The potential for hepatically metabolized interactions with adefovir is low. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. However, carfentanil is an extremely strong opiate, reported to be up to 10,000 times more potent than morphine, and multiple deaths have resulted from its use. Advise patients to avoid.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Carvedilol undergoes glucuronidation via UGTs 1A1, 2B4 and 2B7, with additional metabolism via CYP2D6 and to a lesser extent by CYPs 2C9 and 1A2. The potential for hepatically metabolised interactions with adefovir is low. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. [Note, the US Prescribing Information contraindicates carvedilol in patients with severe liver impairment and the European SmPC contraindicates it in patients with hepatic dysfunction.]

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. Casirivimab and imdevimab are IgG1 monoclonal antibodies and are likely to be eliminated via intracellular catabolism, similarly to endogenous IgG. Casirivimab and imdevimab are not renally excreted. Interactions with concomitant medications that are renally excreted are unlikely.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Caspofungin undergoes spontaneous chemical degradation and metabolism via a non CYP-mediated pathway. [Note, no dose adjustment is required in patients with normal hepatic function but a dose reduction of caspofungin daily dose to 35 mg is recommended for adults with moderate hepatic impairment. There is no clinical experience in adults with severe hepatic impairment.]

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cat’s claw is a CYP3A4 inhibitor; the potential for hepatically metabolised interactions with adefovir is low. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Celecoxib is metabolised mainly by CYP2C9. The potential for hepatically metabolised interactions with adefovir is low. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. [Note, use in patients with severe liver impairment is contraindicated in the European SmPC and not recommended in the US Prescribing Information. In patients with moderate liver impairment (serum albumin 25-35 g/L, Child-Pugh Class B), celecoxib treatment should be started at half the recommended dose.]

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Chlorpromazine is a substrate of CYPs 2D6 (major), 1A2, and 3A4 in vitro. The potential for hepatically metabolised interactions with adefovir is low. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. [Note, the European SmPC for chlorpromazine advises that its use should be avoided in patients with hepatic dysfunction.]

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Chlorprothixene is metabolised by CYP2D6. The potential for hepatically metabolised interactions with adefovir is low. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. [Note, although no interaction is anticipated, ECG monitoring is mandatory prior to treatment with chlorprothixene.]

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ciclosporin is mainly metabolized by CYP3A4. The potential for hepatically metabolised interactions with adefovir is low. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. Adefovir and ciclosporin can be coadministered with routine therapeutic drug monitoring of ciclosporin as concentrations may alter as a result of improved liver function.

Coadministration has not been studied. Cidofovir is eliminated renally via glomerular filtration and active renal secretion by OAT1 and OAT3. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. Concentrations of both drugs may increase due to competition for renal elimination. Both drugs are nephrotoxic therefore monitor renal function closely.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cilazapril is mainly eliminated unchanged by the kidneys. Adefovir is predominantly eliminated unchanged via active renal tubular secretion. [Note, in patients with cirrhosis, a maximum dose of 0.5 mg/day is recommended as significant hypotension may occur.]

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Clofazimine is largely excreted unchanged in the faeces, both as unabsorbed drug and via biliary excretion. As renal excretion has a minor role in clofazimine elimination, interaction with lamivudine via competition for renal elimination pathways is unlikely. [Note, the US Prescribing Information for clofazimine recommends to avoid clofazimine in patients with hepatic impairment (Child-Pugh Class A, B, and C) unless the benefit outweighs the risk.]

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Clopidogrel is a prodrug that is converted to its active metabolites via CYPs 3A4, 2B6, 2C19 and 1A2. The potential for hepatically metabolised interactions with adefovir is low. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. [Note, the European SmPC for clopidogrel contraindicates its use in severe hepatic impairment but the US Prescribing Information states no dose alteration.]

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. The metabolism of conjugated estrogens is complex and involves CYP3A4 isoenzymes and glucuronidation in the liver. The potential for hepatically metabolised interactions with adefovir is low.

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. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cyclophosphamide is activated (major pathway) to 4-hydroxycyclophosphamide by CYPs 2B6 (major), 2C9 and 3A4. Inactivation (minor, 10%) to the neurotoxic chloroacetaldehyde metabolite is performed mainly by CYP3A4. Adefovir is not expected to interact with these pathways.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. Darunavir/ritonavir is unlikely to inhibit OATs at clinically relevant concentrations. 

Coadministration has not been studied and is contraindicated. Symtuza, which contains tenofovir (derived from tenofovir alafenamide), should not be used concomitantly with adefovir dipivoxil.

Coadministration has not been studied but based on the metabolism and clearance a clinically significant interaction is unlikely as adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. Darunavir/cobicistat is unlikely to inhibit OATs at clinically relevant concentrations. Cobicistat has been shown to decrease estimated creatinine clearance due to inhibition of tubular secretion of creatinine without affecting actual renal glomerular function. Darunavir/cobicistat should not be coadministered with adefovir in patients with creatinine clearance less than 70 ml/min.

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. The potential for hepatically metabolised interactions with adefovir is low. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. [Note, delamanid is not recommended in patients with moderate to severe hepatic impairment.]

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is not anticipated and contraceptive efficacy is unlikely to be affected. Ethinylestradiol is mainly metabolized by hydroxylation with CYP3A4 and CYP2C9. Desogestrel is a prodrug that requires activation to etonogestrel by CYP2C9 (and possibly CYP2C19); the metabolism of etonogestrel is mediated by CYP3A4. The potential for hepatically metabolised interactions with adefovir is low. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Desvenlafaxine is a substrate of CYP3A4. The potential for hepatically metabolised interactions with adefovir is low. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1.

Coadministration has not been studied but based on the metabolism and clearance a clinically significant interaction is unlikely. Dexketoprofen is mainly glucuronidated, with CYP mediated metabolism (CYP2C8/9) playing a minor role. The potential for hepatically metabolised interactions with adefovir is low. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. [Note, use in patients with severe hepatic impairment (Child-Pugh class C) is contraindicated in the European product label for dexketoprofen.]

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Diamorphine is rapidly metabolized by sequential deacetylation to morphine which is then mainly glucuronidated to morphine-3-glucuronide (UGT2B7>UGT1A1) and, to a lesser extent, to the pharmacologically active morphine-6-glucuronide (UGT2B7>UGT1A1). The potential for hepatically metabolised interactions with adefovir is low. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Diclofenac is partly glucuronidated by UGT2B7 and partly oxidized by CYP2C9. The potential for hepatically metabolised interactions with adefovir is low. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1.

Results from clinical studies show that coadministration of adefovir (10 mg or 60 mg once daily) and enteric coated didanosine (400 mg) had no significant effect on the pharmacokinetics of didanosine or adefovir.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Diphenhydramine is mainly metabolized by CYP2D6. The potential for hepatically metabolised interactions with adefovir is low. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. [Note, diphenhydramine should be used with caution in patients with moderate to severe hepatic impairment.]

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

Coadministration with dolutegravir/lamivudine has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Dolutegravir is primarily metabolized by UGT1A1, with some contribution from CYP3A, and is an inhibitor of OCT2. The potential for hepatically metabolized interactions with adefovir is low. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. Coadministration of adefovir dipivoxil (10 mg once daily) and lamivudine (100 mg once daily) did not alter the pharmacokinetic profile of either drug. However, as adefovir is nephrotoxic, renal function should be monitored and lamivudine dosage adjusted accordingly.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. Dolutegravir is not expected to inhibit this renal transporter. Rilpivirine does not interact with this elimination pathway.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. Doravirine does not inhibit renal transporters.

Coadministration has not been studied and is not recommended. Tenofovir-DF and adefovir dipivoxil should not be coadministered.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dosulepin is extensively metabolised in the liver, likely by CYP2D6 (major) and CYP3A4. The potential for hepatically metabolised interactions with adefovir is low. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. [Note: Dosulepin should be used with caution in mild to moderate hepatic impairment and avoided in severe hepatic impairment.]

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Doxazosin is metabolized mainly by CYP3A4. The potential for hepatically metabolised interactions with adefovir is low. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. [Note, the European SmPC does not recommend doxazosin in severe hepatic impairment; the US Prescribing Information has a caution for use in hepatic impairment.]

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Doxepin is metabolized mainly by CYP2C19 to nordoxepin, an active metabolite. In addition, doxepin and nordoxepin are metabolized by CYP2D6. The potential for hepatically metabolised interactions with adefovir is low. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. [Note, the European and US product labels for doxepin advise caution and monitoring in patients with hepatic impairment as a dosage reduction may be required.]

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Doxylamine is metabolized primarily by CYP2D6, CYP1A2, and CYP2C9. The potential for hepatically metabolised interactions with adefovir is low. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Estradiol is metabolized by CYP3A4 and CYP1A2 and is glucuronidated. Drospirenone is metabolised in part by CYP3A4. The potential for hepatically metabolised interactions with adefovir is low. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely and contraceptive efficacy is unlikely to be affected. Ethinylestradiol is mainly metabolized by hydroxylation with CYP3A4 and CYP2C9. Drospirenone is metabolised in part by CYP3A4. The potential for hepatically metabolised interactions with adefovir is low. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Duloxetine is metabolized by CYP2D6 and CYP1A2. The potential for hepatically metabolised interactions with adefovir is low. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. [Note, duloxetine is contraindicated in patients with hepatic impairment as concentrations may increase due to decreased clearance of duloxetine.]

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as dutasteride is mainly metabolized by CYP3A4. The potential for hepatically metabolised interactions with adefovir is low. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. [Note, the European SmPC (but not the US Prescribing Information) cautions against dutasteride use in mild to moderate hepatic impairment and contraindicates it in severe hepatic impairment.]

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Estradiol is metabolized by CYP3A4 and CYP1A2 and is glucuronidated. Dydrogesterone is metabolized to dihydrodydrogesterone (possibly via CYP3A4). The potential for hepatically metabolised interactions with adefovir is low.

No pharmacokinetic interaction was observed with efavirenz (600 mg once daily) and adefovir (60 mg, 6-fold higher than that recommended for the treatment of chronic hepatitis B).

Emtricitabine/tenofovir-DF and adefovir dipivoxil should not be coadministered. Coadministration of adefovir dipivoxil and tenofovir-DF decreased adefovir AUC and Cmax by 11% and 7%; tenofovir AUC and Cmax decreased by 2% and 1%.

Coadministration of adefovir (10 mg once daily) and entecavir (1 mg once daily) was studied in 26 uninfected subjects. AUC, Cmax and C24 of entecavir and adefovir were unchanged. The combination can be considered for the treatment of complex HBV, but as both drugs are renally excreted by active tubular secretion, consider monitoring renal function.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Note, there is a concern of hepatotoxic adverse events in patients with HBV receiving anti-TNF agents. Use with caution and monitor liver enzymes and HBV viral load. [Note, due to the possible risk of hepatitis B (HBV) reactivation, patients should be tested for HBV infection before initiating treatment with etanercept. Patients who test positive for HBV infection should be discussed with a physician with expertise in the treatment of HBV.]