Coadministration has not been studied but as entecavir and acetazolamide are both eliminated by similar renal transporters, caution is warranted. Acetazolamide is predominantly excreted unchanged via active renal tubular secretion and may competitively inhibit the renal transporters OAT1 and OAT3. Entecavir is eliminated primarily in the urine by glomerular filtration and tubular secretion by OAT1. As entecavir can be nephrotoxic, renal function monitoring is recommended.

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. Entecavir is not expected to interact with this pathway.

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 clinically significant interaction is unlikely. Agomelatine is metabolised predominantly by CYP1A2. Entecavir is not hepatically metabolised and the potential for interactions via this route is low. Entecavir is eliminated primarily in the urine by glomerular filtration and tubular 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 entecavir.

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. Entecavir does not interact with these pathways.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as allopurinol is converted to oxipurinol by xanthine oxidase and aldehyde oxidase. Entecavir is not hepatically metabolised and the potential for interactions via this route is low. Entecavir is eliminated primarily in the urine by glomerular filtration and tubular 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 based on metabolism and clearance a clinically significant interaction is unlikely. Entecavir is mainly excreted unchanged by the kidney by both glomerular filtration and active transport. 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. Entecavir is eliminated renally via glomerular filtration and active renal secretion by both organic anions and cations transporters. 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. Entecavir is eliminated renally via glomerular filtration and active renal secretion by both organic anions and cations transporters. Atazanavir 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. Entecavir is eliminated renally via glomerular filtration and active renal secretion by both organic anions and cations transporters. Atazanavir/cobicistat 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. Entecavir is mainly excreted unchanged by the kidney by both glomerular filtration and active transport. 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. Entecavir is mainly excreted unchanged by the kidney by both glomerular filtration and active transport. Baricitinib does not inhibit these pathways.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Entecavir is eliminated primarily in the urine by glomerular filtration and tubular secretion by OAT1. In vitro data suggest that bezafibrate inhibits the renal transporter OAT1 but a clinically relevant drug interaction with entecavir 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. Entecavir is not hepatically metabolised and the potential for interactions via this route is low. In vitro data indicate that bisoprolol inhibits OCT2, whereas entecavir is eliminated primarily in the urine by glomerular filtration and tubular 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. Entecavir is not hepatically metabolised and the potential for interactions via this route is low. Entecavir is eliminated primarily in the urine by glomerular filtration and tubular 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. Entecavir is eliminated primarily in the urine by glomerular filtration and tubular secretion by OAT1.

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. Entecavir does not interfere with these pathways.

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. Entecavir does not interact with this pathway. 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. Entecavir is not hepatically metabolised and the potential for interactions via this route is low. Entecavir is eliminated primarily in the urine by glomerular filtration and tubular 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. Entecavir is mainly excreted unchanged by the kidney by both glomerular filtration and active transport. 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. Entecavir is not hepatically metabolised and the potential for interactions via this route is low. Entecavir is eliminated primarily in the urine by glomerular filtration and tubular secretion by OAT1.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ceftaroline is excreted predominantly by renal glomerular filtration, with no significant active renal tubular secretion. Entecavir is eliminated primarily in the urine by glomerular filtration and tubular secretion by OAT1. There is little potential for an interaction with entecavir via competition for active renal transport mechanisms.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Celecoxib is metabolised mainly by CYP2C9. Entecavir is not hepatically metabolised and the potential for interactions via this route is low. Entecavir is eliminated primarily in the urine by glomerular filtration and tubular 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. Entecavir is not hepatically metabolised and the potential for interactions via this route is low. Entecavir is eliminated primarily in the urine by glomerular filtration and tubular 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. Entecavir is not hepatically metabolised and the potential for interactions via this route is low. Entecavir is eliminated primarily in the urine by glomerular filtration and tubular 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. Cilazapril is mainly eliminated unchanged by the kidneys. Entecavir 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 entecavir 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. Entecavir is not hepatically metabolised and the potential for interactions via this route is low. Entecavir is eliminated primarily in the urine by glomerular filtration and tubular 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. Colchicine is metabolized by CYP3A4. Entecavir is not hepatically metabolised and the potential for interactions via this route is low. Entecavir is eliminated primarily in the urine by glomerular filtration and tubular secretion by OAT1.

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. Entecavir is not hepatically metabolised and the potential for interactions via this route is low. There is little potential for an interaction with entecavir via modulation of, or competition for, metabolic pathways. Entecavir is eliminated primarily in the urine by glomerular filtration and tubular secretion by OAT1.

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. Entecavir is not hepatically metabolised and the potential for interactions via this route 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. Entecavir is eliminated primarily in the urine by glomerular filtration and tubular 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. Entecavir 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 the metabolism and clearance a clinically significant interaction is unlikely. Entecavir is eliminated renally via glomerular filtration and active renal secretion by both organic anion and cation transporters. Darunavir/ritonavir is unlikely to inhibit OATs at clinically relevant concentrations.

Coadministration has not been studied but based on the metabolism and clearance a clinically significant interaction is unlikely. Entecavir is eliminated renally via glomerular filtration and active renal secretion by both organic anions and cations transporters. Darunavir/cobicistat is unlikely to inhibit OATs at clinically relevant concentrations. Emtricitabine and tenofovir alafenamide are unlikely to significantly interact with entecavir.

Coadministration has not been studied but based on the metabolism and clearance a clinically significant interaction is unlikely. Entecavir is eliminated renally via glomerular filtration and active renal secretion by both organic anions and cations transporters. Darunavir/cobicistat 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. 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. Entecavir is not hepatically metabolised and the potential for interactions via this route is low. Entecavir is eliminated primarily in the urine by glomerular filtration and tubular 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. Entecavir is not hepatically metabolised and the potential for interactions via this route is low.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Desvenlafaxine is metabolised by CYP3A4. Entecavir is not hepatically metabolised and the potential for interactions via this route is low. Entecavir is eliminated primarily in the urine by glomerular filtration and tubular 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. Entecavir is not hepatically metabolised and the potential for interactions via this route is low. Entecavir is eliminated primarily in the urine by glomerular filtration and tubular 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. Diphenhydramine is mainly metabolized by CYP2D6. Entecavir is not hepatically metabolised and the potential for interactions via this route is low. Entecavir is eliminated primarily in the urine by glomerular filtration and tubular 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 clinically significant interaction is unlikely. No pharmacokinetic interactions between entecavir and lamivudine were observed. Coadministration of entecavir and lamivudine was studied in healthy subjects. Entecavir Cmax decreased by 2%, while AUC and Cmin increased by 7% and 14%, respectively. Lamivudine AUC and Cmin increased by 3% and 14%, respectively, while Cmax increased by 1%. Dolutegravir is primarily metabolized by UGT1A1, with some contribution from CYP3A, and is an inhibitor of OCT2. Entecavir is not hepatically metabolized and the potential for interactions via this route is low. Entecavir is eliminated primarily in the urine by glomerular filtration and tubular secretion by OAT1.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Entecavir is eliminated renally via glomerular filtration and active renal secretion by both organic anions and cations transporters. Dolutegravir is not expected to inhibit OATs. In vitro data indicate that dolutegravir inhibits OCT, but is unlikely to cause a clinically relevant drug interaction with entecavir. Rilpivirine does not interact with this elimination pathway.

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

Coadministration has not been studied but based on the metabolism and clearance a clinically significant interaction is unlikely. Entecavir is eliminated renally via glomerular filtration and active renal secretion by both organic anions and cations transporters. Doravirine does not interfere with entecavir elimination. No pharmacokinetic interaction was observed with lamivudine. No significant pharmacokinetic interactions were observed when tenofovir-DF (300 mg once daily) was coadministered with entecavir (1 mg once daily). There was no change in tenofovir AUC, Cmax or Cmin and no change in entecavir Cmax or Cmin; however, entecavir AUC increased by 13%.

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. Entecavir is not hepatically metabolised and the potential for interactions via this route is low. Entecavir is eliminated primarily in the urine by glomerular filtration and tubular 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. Entecavir is not hepatically metabolised and the potential for interactions via this route is low. Entecavir is eliminated primarily in the urine by glomerular filtration and tubular 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. Entecavir is not hepatically metabolised and the potential for interactions via this route is low. Entecavir is eliminated primarily in the urine by glomerular filtration and tubular 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. Doxycycline is excreted in the urine and faeces as unchanged active substance. Between 40-60% of an administered dose can be accounted for in the urine. Studies have indicated that administration of doxycycline at the usual recommended doses does not lead to excessive accumulation in patients with renal impairment. Entecavir is eliminated primarily in the urine by glomerular filtration and tubular secretion by OAT1. There is little potential for a clinically significant interaction with entecavir via competition for renal elimination transport mechanisms.

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. Entecavir is not hepatically metabolised and the potential for interactions via this route is low. Entecavir is eliminated primarily in the urine by glomerular filtration and tubular 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. Entecavir is not hepatically metabolised and the potential for interactions via this route 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. Entecavir is not hepatically metabolised and the potential for interactions via this route 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. Entecavir is not hepatically metabolised and the potential for interactions via this route is low. Entecavir is eliminated primarily in the urine by glomerular filtration and tubular 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. Dutasteride is mainly metabolized by CYP3A4. Entecavir is not hepatically metabolised and the potential for interactions via this route is low. Entecavir is eliminated primarily in the urine by glomerular filtration and tubular 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). Entecavir is not hepatically metabolised and the potential for interactions via this route is low. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Elbasvir and grazoprevir are both significantly hepatically metabolised. Entecavir is not hepatically metabolised and the potential for interactions via this route is low. Entecavir is mainly excreted unchanged by the kidney by both glomerular filtration and active transport.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. No effect of entecavir on elvitegravir, cobicistat, emtricitabine or tenofovir-DF is expected. Entecavir is eliminated primarily in the urine by glomerular filtration and tubular secretion by OAT1. Elvitegravir/cobicistat is unlikely to inhibit OATs and OCTs at clinically relevant concentrations. Emtricitabine and tenofovir-DF are unlikely to significantly interact with entecavir.

Coadministration with emtricitabine/tenofovir-DF has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely.  Entecavir is eliminated renally via glomerular filtration and active renal secretion by both organic anion and cation transporters. No interaction is expected with emtricitabine and no significant pharmacokinetic interactions were observed when tenofovir-DF (300 mg once daily) was coadministered with entecavir (1 mg once daily). There was no change in entecavir Cmax or Cmin; however, entecavir AUC increased by 13%.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Etizolam is metabolized predominantly via CYP3A4 with minor contributions from CYP2C18 and CYP2C19. Entecavir is not hepatically metabolized and the potential for interactions via this route is low. Entecavir is eliminated primarily in the urine by glomerular filtration and tubular secretion by OAT1.