Coadministration has not been studied but based on metabolism and clearance a clinically significant pharmacokinetic interaction is unlikely. A high rate of virological failure and emergence of resistance have been reported with once daily regimens of abacavir with lamivudine and tenofovir-DF; the same problems may be seen if Descovy is administered with a third nucleoside analogue.

Coadministration has not been studied. Acamprosate is eliminated unchanged in the urine both via glomerular filtration and active secretion (renal transporter unknown, possibly OATs or OCTs). Tenofovir alafenamide is unlikely to compete with acamprosate for renal transporters as tenofovir alafenamide results in 90% lower systemic levels of tenofovir compared to tenofovir-DF. Emtricitabine 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 pharmacokinetic interaction is unlikely. After ingestion of acarbose, the majority of active unchanged drug remains in the lumen of the gastrointestinal tract to exert its pharmacological activity and is metabolised by intestinal enzymes and by the microbial flora. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Acenocoumarol is mainly metabolized by CYP2C9 and to a lesser extent by CYP1A2 and CYP2C19. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied. Acetazolamide is predominantly excreted unchanged via active renal tubular secretion. In vitro studies have shown acetazolamide may competitively inhibit renal transporters OAT1, OAT3 and OAT4. Inhibition of these renal transporters is unlikely to lead to significant increase in tenofovir as tenofovir alafenamide results in 90% lower systemic levels of tenofovir compared to tenofovir-DF. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied. Aciclovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. Emtricitabine and tenofovir alafenamide are unlikely to compete with aciclovir for renal transporters as emtricitabine is eliminated by different renal transporters and tenofovir alafenamide results in 90% lower systemic levels of tenofovir compared to tenofovir-DF. Dose Descovy according to the concomitant antiretroviral. 

Coadministration has not been studied but, based on metabolism and clearance, a clinically significant interaction is unlikely as acitretin undergoes isomerisation and glucuronidation. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Aclidinium bromide is rapidly and extensively hydrolyzed (non-enzymatic and enzymatic transformation by esterases and butylrylcholineesterases) to its pharmacologically inactive metabolites with only a minor role for CYP metabolism.

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

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Adrenaline is rapidly inactivated, mostly in the liver by catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO). Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied. African potato was shown to inhibit CYP3A4 and P-gp in vitro and to activate PXR suggesting that inhibition may occur initially followed by induction of CYP3A4 and P-gp when used for extended periods.  Tenofovir alafenamide (the prodrug of tenofovir) is a substrate of P-gp and its absorption may be decreased due to induction of intestinal P-gp by African potato. No effect on emtricitabine is expected.

Coadministration has not been studied, but based on metabolism and clearance a clinically significant interaction is unlikely as agomelatine is metabolised predominantly via CYP1A2. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. In vitro studies have shown that CYP3A4 and the flavine-containing monooxygenase system are involved in the formation of the active metabolite albendazole sulfoxide. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

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. Emtricitabine and tenofovir alafenamide are eliminated renally. An interaction is unlikely as albuvirtide is a peptide which is eliminated by catabolism to its constituent amino acids.

Coadministration has not been assessed in formal pharmacokinetic studies. Alcohol is metabolized by alcohol dehydrogenase and aldehyde dehydrogenase. The chronic use of alcohol may induce CYP2E1 and to a lesser extent CYP3A4. No a priori clinically relevant drug-drug interaction is anticipated. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied. Alcuronium is predominantly eliminated unchanged via the kidneys. As there are no available data determining whether excretion is via active tubular secretion or glomerular filtration, there is some potential for competition with emtricitabine for active renal transport mechanisms, which may lead to increased levels of either drug. This mechanism of interaction is unlikely to be relevant for tenofovir alafenamide as this prodrug results in 90% lower systemic levels of tenofovir compared to tenofovir-TF. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied. 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. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Alfentanil undergoes extensive CYP3A4 metabolism. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as alfuzosin is metabolized by CYP3A4. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Aliskiren is minimally metabolized and is mainly excreted unchanged in faeces. P-glycoprotein is a major determinant of aliskiren bioavailability. Significant interactions are not expected with emtricitabine and tenofovir alafenamide. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on the metabolism and clearance a clinically significant interaction is unlikely as allopurinol is converted to oxipurinol by xanthine oxidase and aldehyde oxidase. Emtricitabine and tenofovir alafenamide do not interfere with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Almotriptan is partly eliminated unchanged in the urine and partly metabolized mainly via monoamine oxidase-A and to a lesser extent by CYP3A4, CYP2D6 and flavin monooxygenase. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

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 pharmacokinetic interaction is unlikely. In vitro data indicate that alosetron is metabolized by CYPs 2C9, 3A4 and 1A2. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on the metabolism and clearance a clinically significant interaction is unlikely. Alprazolam is mainly metabolized by CYP3A4. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral. 

Coadministration has not been studied but based on the metabolism and clearance a clinically significant interaction is unlikely. Amantadine is mainly eliminated in the kidney by glomerular filtration and active secretion via OCT2. Emtricitabine and tenofovir derived from tenofovir alafenamide are unlikely to interfere with amantadine renal elimination as they are eliminated by different renal transporters. Dose Descovy according to the concomitant antiretroviral. 

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. Emtricitabine and tenofovir alafenamide do not interfere with ambrisentan metabolism.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as amikacin is eliminated renally by glomerular filtration. Coadministration with nephrotoxic agents is unlikely to be of concern for tenofovir alafenamide which results in 90% lower systemic levels of tenofovir compared to tenofovir-DF. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Amiloride is eliminated unchanged in the kidney. In vitro data indicate that amiloride is a substrate of OCT2. Emtricitabine and tenofovir derived from tenofovir alafenamide are unlikely to compete for renal elimination as they are eliminated by other renal transporters. Dose Descovy according to the concomitant antiretroviral.

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. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied. Amiodarone is metabolized by CYP3A4 and 2C8. Tenofovir alafenamide (the prodrug of tenofovir) is a substrate of P-gp and inhibitors of P-gp such as amiodarone are expected to increase the absorption of tenofovir alafenamide and thereby increase the systemic concentration. Consider dosing Descovy at a dose of 200/10 mg once daily (where available).

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Amisulpride is weakly metabolized and is primarily eliminated renally (possibly via OCT). Emtricitabine and tenofovir derived from tenofovir alafenamide are unlikely to significantly impair amisulpride elimination. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Amitriptyline is metabolised predominantly by CYP2D6 and CYP2C19. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Amlodipine is metabolized by CYP3A4. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Amodiaquine is metabolized mainly by CYP2C8. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as amoxicillin is mainly excreted in the urine by glomerular filtration and tubular secretion. In vitro data indicate that amoxicillin is a substrate of OAT3. Emtricitabine and tenofovir derived from tenofovir alafenamide are secreted by other renal transporters. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Amphetamine is metabolized by CYP2D6. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as amphotericin is not appreciably metabolized and is eliminated to a large extent in the bile. Coadministration with nephrotoxic agents is unlikely to be of concern for tenofovir alafenamide which results in 90% lower systemic levels of tenofovir compared to tenofovir-DF. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied. Renal clearance of ampicillin occurs partly by glomerular filtration and partly by tubular secretion; it is reduced by probenecid. About 20 to 40% of an oral dose may be excreted unchanged in the urine in 6 hours. After parenteral use about 60 to 80% is excreted in the urine within 6 hours. No interaction is expected with wit tenofovir alafenamide as it results in 90% lower systemic levels of tenofovir compared to tenofovir-DF. However, as emtricitabine is eliminated by renal tubular secretion, there is potential for competition with ampicillin for renal transporters, which could lead to increased levels of either drug when ampicillin is administered intravenously. When administered orally, there is little potential for significant interaction. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Anastrozole is mainly oxidized to hydroxyanastrozole by CYP3A4 (major) and glucuronidated via UGT1A4. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as anidulafungin is not metabolised hepatically but undergoes chemical degradation at physiological temperature. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dose Descovy according to the concomitant antiretroviral. 

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. 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 as apomorphine is metabolized by several pathways including glucuronidation, sulfation and to a lesser extent N-demethylation. Dose Descovy according to the concomitant antiretroviral. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Aprepitant is mainly metabolized by CYP3A4. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

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.

Aripiprazole Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Aripiprazole is metabolized by CYP3A4 and CYP2D6. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Artemisinins undergo rapid metabolism via several CYP450 (CYP3A4, 2A6, 2B6) and the active metabolite (dihydroartemisinin, which has greater potency than the parent drug) is further metabolism via UGT1A9 and 2B7. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral. 

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. Significant interactions are not expected with vitamin C given alone or in multivitamins and emtricitabine and tenofovir alafenamide. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Asenapine is metabolized by glucuronidation (UGT1A4) and oxidative metabolism (CYP1A2 (major) and CYP3A4, 2D6 (minor). Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Limited data suggest that asparaginase is likely to be eliminated by the reticulo-endothelial system. Less than 0.1% of a total injected dose is recovered in urine. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Aspirin is rapidly deacetylated to form salicylic acid which is further glucuronidated by several UGTs (major UGT1A6). In addition, coadministration with an NSAID is unlikely to be of concern for nephrotoxicity as tenofovir alafenamide results in 90% lower systemic levels of tenofovir compared to tenofovir-DF. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Aspirin is rapidly deacetylated to form salicylic acid which is further glucuronidated by several UGTs (major UGT1A6). Coadministration is unlikely to be of concern for nephrotoxicity as tenofovir alafenamide results in 90% lower systemic levels of tenofovir compared to tenofovir-DF. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as astemizole is metabolized by CYPs 2D6, 2J2 and 3A4. Dose Descovy according to the concomitant antiretroviral.

Coadministration with atazanavir alone has not been studied. Coadministration of atazanavir/ritonavir (300/100 mg once daily) and emtricitabine/tenofovir alafenamide (200/10 mg once daily) increased tenofovir AUC and Cmax by 162% and 112% (n=10). Coadministration of atazanavir/ritonavir (300/100 mg once daily) and tenofovir alafenamide alone (10 mg) increased tenofovir AUC and Cmax by 91% and 77%. Coadministration of atazanavir/cobicistat (300/150 mg once daily) and tenofovir alafenamide increased tenofovir alafenamide AUC and Cmax by 75% and 80%. No significant effects were observed on atazanavir pharmacokinetics. When administered with atazanavir/ritonavir or atazanavir/cobicistat for the treatment of HIV, the recommended dose of Descovy is 200/10 mg once daily (where available).

Coadministration with emtricitabine/TAF has not been studied. Coadministration of atazanavir/cobicistat (300/150 mg once daily) and tenofovir alafenamide increased tenofovir alafenamide AUC and Cmax by 75% and 80%. No significant effects were observed on atazanavir pharmacokinetics. When administered with atazanavir/cobicistat, the recommended dose of emtricitabine/tenofovir alafenamide is 200/10 mg once daily (where available). 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 emtricitabine in patients with creatinine clearance less than 70 ml/min.

Coadministration of atazanavir/ritonavir (300/100 mg once daily) and emtricitabine/tenofovir alafenamide (200/10 mg once daily) increased tenofovir AUC and Cmax by 162% and 112% (n=10). No significant effects were observed on atazanavir pharmacokinetics relative to historical controls. When administered with atazanavir/ritonavir, the recommended dose of Descovy is 200/10 mg once daily (where available).

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Atorvastatin is metabolized by CYP3A4. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Atovaquone is mainly eliminated unchanged in the faeces. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely 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 emtricitabine and tenofovir alafenamide via modulation of, or competition for metabolic pathways. Dose Descovy according to the concomitant antiretroviral.

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 clinically significant interaction is unlikely. Azathioprine is converted to 6-mercaptopurine which is metabolized analogously to natural purines. Emtricitabine and tenofovir alafenamide do not interfere with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Azithromycin is mainly eliminated via biliary excretion and animal data suggest this may occur via P-glycoprotein and MRP2. Emtricitabine and tenofovir alafenamide are not expected to interfere with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Baclofen is primarily eliminated by glomerular filtration. Dose Descovy according to the concomitant antiretroviral.

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 has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Beclometasone is a pro-drug which is not metabolised by CYP450, but is hydrolysed via esterase enzymes to the highly active metabolite beclometasone -17-monopropionate. Emtricitabine and tenofovir alafenamide do not interact with beclometasone metabolism. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bedaquiline is metabolised by CYP3A4 and mainly eliminated in faeces. There are no data on the safety and efficacy of bedaquiline when coadministered with antiretroviral agents. Dose Descovy according to the concomitant antiretroviral.

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

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bendroflumethiazide is mainly eliminated by hepatic metabolism (70%, exact pathway not known) and excreted unchanged in the urine (30%) via OAT1 and OAT3. In vitro data indicate that bendroflumethiazide inhibits these renal transporters but a clinically relevant drug interaction is unlikely in the range of observed clinical concentrations. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as benserazide is hydrolysed to trihydroxybenzylhydrazine. Dose Descovy according to the concomitant antiretroviral.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bepridil is metabolized by CYP2D6 (major) and 3A4. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Betamethasone is metabolized by CYP3A4. Emtricitabine and tenofovir alafenamide do not interact with betamethasone metabolism. Dose Descovy according to the concomitant antiretroviral.

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. Bexarotene is mainly metabolized by CYP3A4 and induces CYP3A4 (after repeated administration and especially at doses greater than 300 mg/m²/day). Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as half of bezafibrate dose is eliminated unchanged in the urine. In vitro data suggest that bezafibrate inhibits the renal transporter OAT1 but a clinically relevant drug interaction with tenofovir derived from tenofovir alafenamide is unlikely in the observed range of clinical concentrations. Dose Descovy according to the concomitant antiretroviral.

Biktarvy (bictegravir, emtricitabine, tenofovir alafenamide) is indicated for use as a complete regimen for the treatment of HIV 1 infection and should not be administered with other antiretroviral products. Furthermore, both products contain emtricitabine and tenofovir alafenamide and must not be administered with other products containing emtricitabine and tenofovir alafenamide.

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. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bisacodyl is converted to an active metabolite by intestinal and bacterial enzymes. Absorption from the gastrointestinal tract is minimal and the small amount absorbed is excreted in the urine as the glucuronide. Dose Descovy according to the concomitant antiretroviral.

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. Emtricitabine and tenofovir alafenamide are not expected to significantly interfere with bisoprolol elimination. Dose Descovy according to the concomitant antiretroviral. 

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

Coadministration has not been studied but based on the metabolism and clearance a clinically significant interaction is unlikely as bleomycin is inactivated by a cytosolic enzyme, bleomycin hydrolase. Furthermore, two third of the administered drug is excreted unchanged in urine probably by glomerular filtration. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bortezomib is mainly metabolized by CYP3A4 and CYP2C19 and to a lesser extent by CYPs 1A2, 2D6 and 2C9. Emtricitabine and tenofovir alafenamide do not interact with this pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as bosentan is metabolized by CYP3A4 and CYP2C9. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on the metabolism and clearance a clinically significant interaction is unlikely. Bromazepam undergoes oxidative biotransformation. Drug-drug interaction studies indicate that CYP3A4 plays a minor role in bromazepam metabolism, but other cytochromes such as CYP2D6 or CYP1A2 may play a role. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Budesonide is metabolized by CYP3A4. Emtricitabine and tenofovir alafenamide do not interact with budesonide metabolism. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bupivacaine is predominantly metabolized by CYP3A4. Renal excretion of unchanged bupivacaine is thought to account for approximately 1% of a dose therefore there is little potential for interaction with emtricitabine and tenofovir derived from tenofovir alafenamide. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Buprenorphine undergoes both N-dealkylation to form norbuprenorphine (via CYP3A4) and glucuronidation (via UGT2B7 and UGT1A1). Norbuprenorphine, an active metabolite, can further undergo glucuronidation (via UGT1A3 and UGT1A1). Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bupropion is primarily metabolized by CYP2B6. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on the metabolism and clearance a clinically significant interaction is unlikely. Buspirone is metabolized by CYP3A4. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral. 

Coadministration has not been studied but a clinically significant pharmacokinetic interaction is unlikely. Caffeine is mainly metabolized by CYP1A2. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

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

Coadministration has not been studied but a clinically significant pharmacokinetic interaction is unlikely. Calcium is eliminated through faeces, urine and sweat. Dose Descovy according to the concomitant antiretroviral.

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 emtricitabine or tenofovir alafenamide. Canagliflozin is a weak P-gp inhibitor but is unlikely to affect tenofovir alafenamide concentrations to a significant extent. Although an increased risk for bone fractures has been reported with canagliflozin (particularly in patients with a history of, or at high risk of, cardiovascular disease), coadministration with tenofovir alafenamide is unlikely to be problematic in terms of additive bone toxicity as tenofovir alafenamide results in 90% lower systemic exposure of tenofovir compared to tenofovir-DF.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Candesartan is mainly eliminated unchanged via urine and bile. Dose Descovy according to the concomitant antiretroviral.

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.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Tetrahydrocannabinol (THC, the psychoactive component of cannabis) is metabolized mainly by CYP2C9 and to a lesser extent by CYP3A4. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied. Capecitabine is activated by sequential enzyme reactions to fluorouracil. Dihydropyrimidine dehydrogenase plays a role in fluorouracil metabolism. Nucleoside/tide analogues such as emtricitabine and tenofovir alafenamide may compete for these metabolic pathways. The clinical relevance of this interaction is unknown. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied. Capreomycin is predominantly excreted via the kidneys as unchanged drug. As capreomycin may potentially compete with emtricitabine for renal elimination transport mechanisms, levels of either drug may increase. Renal function should be monitored as clinically appropriate. Note, coadministration with nephrotoxic agents is unlikely to be of concern for tenofovir alafenamide which results in 90% lower systemic levels of tenofovir compared to tenofovir-DF.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Captopril is largely excreted in the urine by OAT1. Emtricitabine and tenofovir alafenamide are unlikely to compete with captopril for renal transporters as emtricitabine is eliminated by different renal transporters and tenofovir alafenamide results in 90% lower systemic levels of tenofovir compared to tenofovir-DF. Dose Descovy according to the concomitant antiretroviral.

Coadministration is not recommended as it decreases tenofovir alafenamide plasma concentrations. Coadministration of carbamazepine (titrated from 100 mg to 300 mg twice a day) with emtricitabine/tenofovir alafenamide (200/25 mg once daily) decreased tenofovir alafenamide AUC and Cmax by 55% and 57%, respectively. However, data from a study with rifampicin suggest that use of tenofovir alafenamide 25 mg once daily with carbamazepine may be acceptable. Coadministration of emtricitabine/tenofovir alafenamide (200/25 mg once daily) and the strong inducer rifampicin (600 mg once daily) decreased plasma exposure of tenofovir alafenamide and tenofovir by ~55%. Intracellular tenofovir-DP AUC decreased by 36%, however, intracellular tenofovir-DP exposure was 4.2-fold higher than that achieved with standard dose tenofovir-DF alone (300 mg once daily). No interaction is expected with emtricitabine.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Carbidopa is partly metabolized and partly eliminated unchanged (30% of the total urinary excretion). Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but a clinically significant pharmacokinetic interaction is unlikely. Carbimazole is a pro-drug which undergoes rapid and virtually complete metabolism to the active metabolite, thiamazole (also known as methimazole). Emtricitabine and tenofovir alafenamide do not interact with carbimazole metabolism. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Carboplatin is excreted primarily by renal glomerular filtration and therefore there is little potential for a pharmacokinetic interaction. Coadministration with nephrotoxic agents is unlikely to be of concern for tenofovir alafenamide which results in 90% lower systemic levels of tenofovir compared to tenofovir-DF. Dose Descovy according to the concomitant antiretroviral.

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, and additionally metabolism via CYP2D6 and to a lesser extent by CYPs 2C9 and 1A2. Dose Descovy according to the concomitant antiretroviral. 

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. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral. 

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 emtricitabine and tenofovir alafenamide do not undergo CYP3A4 metabolism.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cefalexin is predominantly eliminated unchanged renally by glomerular filtration and tubular secretion via OAT1 and MATE1. Emtricitabine and tenofovir alafenamide are unlikely to compete with cephalexin for renal transporters as emtricitabine is eliminated by different renal transporters and tenofovir alafenamide results in 90% lower systemic levels of tenofovir compared to tenofovir-DF. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cefazolin is predominantly excreted unchanged in the urine, mainly by glomerular filtration with some renal tubular secretion via OAT3. OAT3 does not play a major role in tenofovir and emtricitabine renal elimination. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as cefixime is renally excreted predominantly by glomerular filtration. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cefotaxime is partially metabolized by non-specific esterases. Most of a dose of cefotaxime is excreted in the urine - about 60% as unchanged drug and a further 24% as desacetyl-cefotaxime, an active metabolite. In vitro studies indicate that OAT3 participates in the renal elimination of cefotaxime. Emtricitabine and tenofovir derived from tenofovir alafenamide are eliminated by other renal transporters. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as ceftazidime is excreted predominantly by renal glomerular filtration. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ceftriaxone is eliminated mainly as unchanged drug, approximately 60% of the dose being excreted in the urine predominantly by glomerular filtration and the remainder via the biliary and intestinal tracts. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Celecoxib is primarily metabolized by CYP2C9. In addition, coadministration with an NSAID is unlikely to be of concern for nephrotoxicity as tenofovir alafenamide results in 90% lower systemic levels of tenofovir compared to tenofovir-DF. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cetirizine is only metabolised to a limited extent and is eliminated unchanged in the urine through both glomerular filtration and tubular secretion. In vitro data indicate that cetirizine inhibits OCT2. Emtricitabine and tenofovir derived from tenofovir alafenamide are not transported by OCT2 and therefore no pharmacokinetic interaction is expected. Dose Descovy according to the concomitant antiretroviral.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Chlorambucil is almost completely metabolized (though little is known about chlorambucil metabolism in humans, it is most probably non-CYP mediated) and has extremely low urinary excretion. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Chloramphenicol is predominantly metabolised via UDP-glucuronyltransferases, in particular UGT2B7. Emtricitabine and tenofovir alafenamide do not interfere with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on the metabolism and clearance a clinically significant interaction is unlikely. Chlordiazepoxide is extensively metabolized by hepatic microsomal enzymes. Dose Descovy according to the concomitant antiretroviral. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Chloroquine undergoes CYP mediated metabolism by CYPs 2C8, 3A4 and 2D6, and is also eliminated unchanged via the kidney (50%). Emtricitabine and tenofovir alafenamide are not expected to cause a clinically relevant drug-drug interaction.  Dose Descovy according to the concomitant antiretroviral.

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. Since only 22% of a chlorphenamine dose is excreted unchanged in the urine, emtricitabine and tenofovir derived from tenofovir alafenamide are unlikely to interact with chlorphenamine. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Chlorpromazine is metabolized mainly by CYP2D6, but also by CYP1A2. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Chlortalidone is mainly excreted unchanged in the urine and faeces. Dose Descovy according to the concomitant antiretroviral.

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. Coadministration of ciclosporin, a potent P-gp inhibitor, is expected to increase plasma concentrations of tenofovir alafenamide. The recommended dose of Descovy is 200/10 mg once daily (where available). Of note: ciclosporin can impair renal function but this is unlikely to be problematic as tenofovir alafenamide results in 90% lower systemic levels of tenofovir compared to tenofovir-DF. 

Coadministration has not been studied but based on the metabolism and clearance a clinically significant interaction is unlikely as cidofovir is eliminated renally via glomerular filtration and active renal secretion by OAT1, OAT3. Tenofovir alafenamide is unlikely to compete with cidofovir for renal transporters or to be of concern when coadministered with nephrotoxic agents such as cidofovir as tenofovir alafenamide results in 90% lower systemic levels of tenofovir compared to tenofovir-DF. Dose Descovy according to the concomitant antiretroviral.

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. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. In vitro data indicate that cimetidine inhibits OAT1 and OCT2 at concentrations much higher than the observed clinical concentrations and therefore no interaction is expected with tenofovir derived from tenofovir alafenamide or emtricitabine. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ciprofloxacin is primarily eliminated unchanged through the kidneys by glomerular filtration and tubular secretion via OAT3. It is also metabolized and partially cleared through the bile and intestine. Emtricitabine and tenofovir derived from tenofovir alafenamide do not interfere with this pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cisapride is metabolized by CYP3A4. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cisatracurium undergoes mainly (80% of overall elimination) spontaneous degradation in plasma and tissues at physiological pH and temperature. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied. Cisplatin is eliminated renally via OCT2 and MATE1. Cisplatin and emtricitabine could potentially compete for MATE1 which could slow their elimination. Close monitoring of renal function is recommended. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Citalopram is metabolized by CYP2C19 (38%), 2D6 (31%) and 3A4 (31%). Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied. Clarithromycin is metabolized by CYP3A4. Tenofovir alafenamide (the prodrug of tenofovir) is a substrate of P-gp and inhibitors of P-gp such as clarithromycin are expected to increase the absorption of tenofovir alafenamide and thereby increase the systemic concentration. Consider dosing Descovy at a dose of 200/10 mg once daily (where available).

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Clavulanic acid is extensively metabolized (likely non CYP mediated pathway) and excreted in the urine by glomerular filtration. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Clindamycin is metabolized by CYP3A4. Emtricitabine and tenofovir alafenamide are unlikely to interfere with this pathway. Dose Descovy according to the concomitant antiretroviral.

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.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dose Descovy according to the concomitant antiretroviral.

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. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Clofibrate is hydrolyzed to an active metabolite, clofibric acid. Excretion of clofibric acid glucuronide is possibly performed via OAT1. Tenofovir alafenamide is unlikely to compete with the elimination of clofibrate as tenofovir alafenamide results in 90% lower systemic levels of tenofovir compared to tenofovir-DF and emtricitabine is eliminated by other renal transporters. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. In vitro studies have suggested that transformation of clomifene to its active metabolite is likely to be mediated via CYP2D6. Renal excretion of clomifene is thought to account for approximately 8% of an oral dose therefore there is little potential for an interaction with emtricitabine and tenofovir derived from tenofovir alafenamide. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Clomipramine is metabolized by CYP3A4, 1A2 and 2C19 to desmethylclomipramine, an active metabolite which has a higher activity than the parent drug. In addition, clomipramine and desmethylclomipramine are metabolized by CYP2D6. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Clonazepam is metabolized by CYP3A4. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Approximately 70% of administered clonidine is excreted in the urine, mainly in form of the unchanged parent drug (40-60% of the dose). Clonidine is a weak inhibitor of OCT2 but is unlikely to interact with emtricitabine and tenofovir derived from tenofovir alafenamide which are eliminated by different renal transporters. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Clopidogrel is a prodrug and is converted to its active metabolite via CYPs 3A4, 2B6, 2C19 and 1A2. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on the metabolism and clearance a clinically significant interaction is unlikely. Clorazepate is rapidly converted to nordiazepam which is then metabolized to oxazepam by CYP3A4. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cloxacillin is metabolised to a limited extent. As total renal elimination is approximately 35% of a dose, there is little potential for significant interactions with emtricitabine or tenofovir (derived from tenofovir alafenamide) via competition for renal transporters. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Clozapine is metabolized by CYPs 1A2, 2C19, 3A4, and to a lesser extent by CYPs 2C9 and 2D6. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cocaine is metabolized by several pathways (CYP and non CYP mediated), with metabolism to norcocaine by CYP3A4 being less than 10% of the overall metabolic clearance. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Codeine undergoes predominantly direct glucuronidation with CYP3A4 mediated metabolism accounting for only 10-15% of the overall metabolism. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as colchicine is metabolized by CYP3A4. Dose Descovy according to the concomitant antiretroviral.

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. Significant interactions are not expected with emtricitabine and tenofovir alafenamide. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied. Piperine, a component of Piper cubeba, inhibits intestinal P-gp. Tenofovir alafenamide is a substrate of P-gp and absorption of tenofovir alafenamide could potentially increase. However, since the clinical relevance of this effect has not been evaluated, Descovy should be dosed according to the concomitant antiretroviral agent and not based on a potential effect of Piper cubeba on P-gp substrates. No effect on emtricitabine exposure is expected.

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. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cyclophosphamide is metabolized by two pathways. Activation (major pathway) to 4-hydroxycyclophosphamide is catalyzed by CYPs 2B6 (major), 2C9 and 3A4. Inactivation (minor, 10%) to the neurotoxic chloroacetaldehyde metabolite is performed mainly by CYP3A4. Emtricitabine and tenofovir alafenamide do not interfere with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cycloserine is predominantly excreted renally via glomerular filtration. Dose Descovy according to the concomitant antiretroviral.

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. Cytarabine is metabolized by cytidine deaminase. Emtricitabine and tenofovir alafenamide do not interfere with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dabigatran is not metabolized by CYP450 enzymes and is mainly cleared by glomerular filtration. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dacarbazine undergoes activation to MTIC primarily via CYP1A2 and to a lesser extent by CYP2E1, with CYP1A1 having a role in extrahepatic metabolism. In vitro data indicate that dacarbazine is a substrate of the renal transporter OAT1. Emtricitabine and tenofovir are unlikely to compete for active renal transport as emtricitabine is eliminated by different renal transporters and tenofovir alafenamide results in 90% lower systemic levels of tenofovir compared to tenofovir-DF. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on the metabolism and clearance a clinically significant interaction is unlikely. No dose adjustment of daclatasvir is required. Dose Descovy according to the concomitant antiretroviral. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dactinomycin is minimally metabolized. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance, a clinically significant interaction is unlikely. Dalteparin is excreted largely unchanged via the kidneys. Dose Descovy according to the concomitant antiretroviral.

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 emtricitabine or tenofovir alafenamide.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Metabolism of dapsone is mainly by N-acetylation with a component of N-hydroxylation, and is via multiple CYP P450 enzymes. Dose Descovy according to the concomitant antiretroviral.

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 with emtricitabine/tenofovir alafenamide has not been studied. Coadministration with darunavir/cobicistat (800/150 mg once daily) and tenofovir alafenamide alone (25 mg once daily) increased tenofovir AUC and Cmax by 224% and 216%, respectively. No significant effects were observed on darunavir pharmacokinetics with either darunavir/ritonavir or darunavir/cobicistat. The recommended dose of Descovy for HIV-1 treatment is 200/10 mg once daily (where available).

Symtuza (darunavir, cobicistat, emtricitabine, tenofovir alafenamide) is indicated for use as a complete regimen for the treatment of HIV-1 infection and should not be administered with other antiretroviral products. Furthermore, Symtuza contains emtricitabine and tenofovir alafenamide must not be administered with other products containing emtricitabine and tenofovir alafenamide.

Coadministration of darunavir/ritonavir (800/100 mg once daily) with emtricitabine/tenofovir alafenamide (200/10 mg, once daily) increased tenofovir AUC and Cmax by 105% and 142% (n-10). No significant effects were observed on darunavir pharmacokinetics relative to historical controls. The recommended dose of Descovy for HIV-1 treatment is 200/10 mg once daily (where available).

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dasatinib is metabolized by CYP3A4. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dose Descovy according to the concomitant antiretroviral.

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. Emtricitabine and tenofovir alafenamide do not affect CYP enzymes.

Coadministration has not been studied but based on metabolism and clearance a clinically significant pharmacokinetic interaction is unlikely. Denosumab is not eliminated via hepatic metabolism but follows the immunoglobulin clearance pathway. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Desflurane is almost exclusively eliminated unchanged by the lungs. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as desipramine is metabolized by CYP2D6. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

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 that requires activation to etonogestrel. Activation to etonogestrel is by CYP2C9 (and possible CYP2C19); the metabolism of etonogestrel is mediated by CYP3A4. Ethinylestradiol is mainly metabolized by hydroxylation. Emtricitabine and tenofovir alafenamide do not interact with these metabolic pathways. Dose Descovy according to the concomitant antiretroviral.

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 that requires activation to etonogestrel. Activation to etonogestrel is by CYP2C9 (and possible CYP2C19); the metabolism of etonogestrel is mediated by CYP3A4. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dexmedetomidine undergoes extensive hepatic metabolism through direct glucuronidation (mainly via UGT1A4, 2B10) and cytochrome P450 (mainly CYP2A6). Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as dextropropoxyphene is mainly metabolized by CYP3A4. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

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). Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on the metabolism and clearance a clinically significant interaction is unlikely. Diazepam is metabolized to nordiazepam (by CYPs 3A4 and 2C19) and to temazepam (mainly by CYP3A4). Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral. 

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. In addition, coadministration with an NSAID is unlikely to be of concern for nephrotoxicity as tenofovir alafenamide results in 90% lower systemic levels of tenofovir compared to tenofovir-DF. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Diethylcarbamazine is mainly excreted unchanged in the urine. A clinically significant interaction is not expected with tenofovir alafenamide which results in 90% lower systemic levels of tenofovir compared to tenofovir-DF. Also, there is little potential for interaction with emtricitabine. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant pharmacokinetic interaction is unlikely. Digoxin is eliminated renally via the renal transporters OATP4C1 and P-glycoprotein, whereas emtricitabine and tenofovir alafenamide are excreted by different renal transporters. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dihydrocodeine is converted to dihydromorphine (active metabolite) via CYP2D6, to dihydrocodeine-6-glucuronide via UGT2B7 (major pathway) and to nordihydrocodeine via CYP3A4. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as dihydroergotamine is metabolized by CYP3A4. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Diloxanide furoate is largely hydrolysed under the combined action of bacterial and gut esterases and subsequently glucuronidated. No clinically-significant drug interactions are known, and significant interactions with antiretrovirals are unlikely. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Diltiazem is metabolized by CYP3A4 and CYP2D6. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Diphenhydramine is mainly metabolized by CYP2D6. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

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.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Disopyramide is metabolized by CYP3A4 (25%) and 50% of the drug is eliminated unchanged in the urine. In vitro data suggest that disopyramide weakly inhibits the renal transporter OCT2 in rats. Emtricitabine and tenofovir derived from tenofovir alafenamide are not transported by OCT2 and therefore are unlikely to be affected by disopyramide. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Disulfiram is reduced to diethyldithiocarbamic acid, is conjugated with glucuronic acid, oxidised to sulphate, methylated and decomposed to diethylamine and carbon disulphide. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as docetaxel is metabolized by CYP3A4. Emtricitabine and tenofovir alafenamide are not expected to interfere with docetaxel metabolism. Dose Descovy according to the concomitant antiretroviral.

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 has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dolasetron is converted by carbonyl reductase to its active metabolite, hydrodolasetron, which is mainly glucuronidated (60%) and metabolized by CYP2D6 (10-20%) and CYP3A4 (<1%). Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration of dolutegravir (50 mg once daily) with emtricitabine/tenofovir alafenamide (200/10 mg, once daily) increased tenofovir AUC and Cmax by 25% and 10% (n=10). No significant effects were observed on dolutegravir pharmacokinetics relative to historical controls. Coadministration of dolutegravir (50 mg once daily) and tenofovir alafenamide/emtricitabine/elvitegravir/cobicistat (10/200/150/150 mg) had no significant effect on the pharmacokinetics of dolutegravir and tenofovir alafenamide. The recommended dose of Descovy for HIV-1 treatment is 200/25 mg once daily.

Triumeq (dolutegravir, abacavir, lamivudine) is indicated for use as a complete regimen for the treatment of HIV-1 infection. Triumeq contains lamivudine and should not be taken with medicinal products containing emtricitabine due to the risk for intracellular interactions between cytidine analogues, such as lamivudine and emtricitabine.

Dovato (dolutegravir/lamivudine) is indicated for use as a complete regimen for the treatment of HIV-1 infection. Dovato contains lamivudine and should not be taken with medicinal products containing emtricitabine due to the risk for intracellular interactions between cytidine analogues, such as lamivudine and emtricitabine.

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 emtricitabine/tenofovir alafenamide would be possible from a pharmacokinetic standpoint. Coadministration of dolutegravir (50 mg once daily) with emtricitabine/tenofovir alafenamide (200/10 mg, once daily) increased tenofovir AUC and Cmax by 25% and 10% (n=10). No significant effects were observed on dolutegravir pharmacokinetics relative to historical controls. Coadministration of rilpivirine (25 mg once daily) and tenofovir alafenamide (25 mg once daily) had no significant effect on the pharmacokinetics of rilpivirine and tenofovir alafenamide. No interaction is expected with emtricitabine. When given with dolutegravir or rilpivirine, the recommended dose of Descovy (emtricitabine/tenofovir alafenamide) is 200/25 mg once daily.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Domperidone is mainly metabolized by CYP3A4. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant pharmacokinetic interaction is unlikely. 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. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Doravirine is metabolized by CYP3A4. Emtricitabine and tenofovir alafenamide do 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 and must not be administered with other antiretroviral products. Furthermore, Delstrigo contains lamivudine and tenofovir-DF and should not be administered products containing emtricitabine or tenofovir alafenamide.

Coadministration has not been studied but based on metabolism and clearance a clinically significant pharmacokinetic interaction is unlikely. Doxazosin is metabolized mainly by CYP3A4. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Doxepin is metabolized to nordoxepin (a metabolite with comparable pharmacological activity as the parent compound) mainly by CYP2C19. In addition, doxepin and nordoxepin are metabolized by CYP2D6. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied, but based on metabolism and clearance a clinically significant interaction is unlikely. Doxorubicin is mainly eliminated in the bile by P-gp and BCRP and does not undergo CYP-mediated metabolism. (Some product labels suggest doxorubicin is a substrate of CYP3A4, however, there are no strong data supporting the role of CYP3A4 in doxorubicin metabolism.) Dose Descovy according to the concomitant antiretroviral.

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. There is therefore little potential for a clinically significant interaction with emtricitabine and tenofovir (derived from tenofovir alafenamide) via competition for renal elimination transport mechanisms. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Droloxifene is mainly glucuronidated. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dronabinol is mainly metabolized by CYP2C9 and to a lesser extent by CYP3A4. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration with a drospirenone-containing combined oral contraceptive (COC) 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. Ethinylestradiol is mainly metabolized by hydroxylation. Emtricitabine and tenofovir alafenamide do not interact with these metabolic pathways. Dose Descovy according to the concomitant antiretroviral.

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. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. In addition, no interaction is expected with estradiol or estrogens administered as part of HRT. Dose Descovy according to the concomitant antiretroviral.

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. Duloxetine is metabolized by CYP2D6 and CYP1A2. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dutasteride is mainly metabolized by CYP3A4. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

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). Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. In addition, no interaction is expected with estradiol or estrogens administered as part of HRT. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on the metabolism and clearance a clinically significant interaction is unlikely. MDMA is metabolized mainly by CYP2D6. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

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.

Coadministration of efavirenz (600 mg once daily) and emtricitabine/tenofovir alafenamide (200/40 mg once daily decreased tenofovir alafenamide AUC and Cmax by 14% and 22%; tenofovir AUC and Cmax decreased by 20% and 24% (n=11). The recommended dose of Descovy for HIV-1 treatment is 200/25 mg once daily.

Coadministration has not been studied. Eflornithine is predominantly eliminated unchanged via the kidneys. As there are no available data determining whether excretion is via active tubular secretion or glomerular filtration, there is potential for competition with emtricitabine for active renal transport mechanisms, which may lead to increased levels of either drug. This mechanism of interaction is unlikely to be problematic for tenofovir alafenamide which results in 90% lower systemic levels of tenofovir compared to tenofovir-DF. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on the metabolism and clearance a clinically significant interaction is unlikely. Dose Descovy according to the concomitant antiretroviral. 

Coadministration has not been studied but based on metabolism and clearance, a clinically significant interaction is unlikely. Eltrombopag is metabolised by cleavage conjugation (via UGT1A1, UGT1A3) and oxidation (via CYP1A2 and CYP2C8). Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Genvoya (elvitegravir, cobicistat, emtricitabine, tenofovir alafenamide) is indicated for use as a complete regimen for the treatment of HIV 1 infection and must not be administered with other antiretroviral products. Furthermore, it must not be administered with other products containing emtricitabine and tenofovir alafenamide.

Stribild (elvitegravir, cobicistat, emtricitabine, tenofovir-DF) is indicated for use as a complete regimen for the treatment of HIV 1 infection and must not be administered with other antiretroviral products. Furthermore, Stribild contains tenofovir-DF and emtricitabine and should not be administered with tenofovir alafenamide or additional emtricitabine.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Empagliflozin is mainly glucuronidated by UGTs 1A3, 1A8, 1A9 and 2B7. It is a substrate of P-gp and BCRP, and also a substrate of the renal transporter OAT3 and the hepatic transporters OATP1B1 and OATP1B3. Although an increased risk for bone fractures and decreased bone mineral density has been reported for other sodium glucose cotransporter 2 inhibitors, coadministration with tenofovir alafenamide is unlikely to be problematic in terms of additive bone toxicity as tenofovir alafenamide results in 90% lower systemic exposure of tenofovir compared to tenofovir disoproxil.

Descovy contains emtricitabine and therefore should not be administered with additional emtricitabine.

Emtricitabine/tenofovir-DF should not be administered with additional emtricitabine or with tenofovir alafenamide.

Coadministration has not been studied but based on metabolism and clearance a clinically significant pharmacokinetic interaction is unlikely. Enalapril is hydrolysed to enalaprilat which is eliminated renally (possibly via OATs). Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Enflurane is predominantly metabolized by CYP2E1. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied, but based on metabolism and clearance a clinically significant pharmacokinetic interaction is unlikely. Enoxaparin does not undergo cytochrome metabolism but is desulphated and depolymerised in the liver, and is excreted predominantly renally. Dose Descovy according to the concomitant antiretroviral.

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. Emtricitabine and tenofovir alafenamide are unlikely to significantly interact with entecavir. Dose Descovy according to the concomitant antiretroviral. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ephedrine is predominantly eliminated unchanged via the kidneys possibly via the renal transporter OCT2. Emtricitabine and tenofovir derived from tenofovir alafenamide are unlikely to interact as they are not transported by OCTs. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Epirubicin is glucuronidated by UGT2B7. Emtricitabine and tenofovir alafenamide do not interfere with this pathway.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Epoprostenol is rapidly hydrolyzed in the blood.

Coadministration has not been studied but based on metabolism and clearance a clinically significant pharmacokinetic interaction is unlikely as eprosartan is largely excreted in bile and urine as unchanged drug. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as ergometrine is metabolized by CYP3A4. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as ergotamine is metabolized by CYP3A4. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Erlotinib is mainly metabolized by CYP3A4. Emtricitabine and tenofovir alafenamide do not interfere with this pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ertapenem is mainly eliminated through the kidneys by glomerular filtration with tubular secretion playing a minor component. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Erythromycin is extensively metabolized in the liver. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Escitalopram is metabolized by CYPs 2C19 (37%), 2D6 (28%) and 3A4 (35%) to form N-desmethylescitalopram. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Eslicarbazepine is partly eliminated unchanged renally and partly glucuronidated by UGT2B4. Eslicarbazepine is a weak/moderate inducer of CYP3A4 but shown to have no clinically significant effect on digoxin (a P-glycoprotein substrate) therefore no significant effect is expected on tenofovir alafenamide. No interaction is expected with emtricitabine.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as esomeprazole is mainly metabolized by CYP2C19. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on the metabolism and clearance a clinically significant interaction is unlikely. Estazolam is metabolized to its major metabolite 4-hydroxyestazolam via CYP3A4. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral. 

Coadministration with estradiol as hormone replacement therapy (HRT) and emtricitabine/tenofovir alafenamide as antiviral therapy has not been studied but no significant interaction was observed when estradiol was administered as feminizing hormone therapy with emtricitabine/tenofovir alafenamide as PrEP. Coadministration of emtricitabine/tenofovir alafenamide and estradiol valerate (2 mg used as feminizing hormone therapy) was studied in 20 transgender women. Coadministration modestly decreased estradiol AUC by 20% and increased Cmax by 11%, these changes were considered to be non-clinically relevant. Estradiol was shown to minimally impact emtricitabine, tenofovir alafenamide and tenofovir AUC and Cmax. Finally, no significant changes in testosterone, FSH and LH were observed. In addition, a study in 10 transgender women showed intracellular tenofovir-DP and emtricitabine-TP concentrations in rectal tissue were comparable when emtricitabine/tenofovir alafenamide PrEP was administered with and without feminizing hormone therapy. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance, a clinically significant interaction is unlikely. Estramustine phosphate undergoes rapid dephosphorylation to estramustine which is then oxidized by 17beta-hydroxysteroid dehydrogenases to estromustine. Estramustine and estromustine are subsequently hydrolyzed to estradiol and estrone, respectively. Estradiol is then hydroxylated by CYPs 1A1, 1A2 and 3A4. Emtricitabine and tenofovir alafenamide do not interfere with this pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ethambutol is partly metabolized by alcohol dehydrogenase (20%) and partly eliminated unchanged in the faeces (20%) and in the urine (50%). Dose Descovy according to the concomitant antiretroviral.

Coadministration of an oral contraceptive containing ethinylestradiol (0.025 mg once daily) and norgestimate (0.180/0.215/0.250 mg once daily) with emtricitabine/tenofovir alafenamide (200/25 mg once daily) had no effect on the AUC, Cmin or Cmax of ethinylestradiol, norelgestromin or norgestrel. Dose Descovy according to the concomitant antiretroviral. Note, use of ethinylestradiol as part of gender affirming treatment is not recommended due to thrombotic risks.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ethionamide is extensively metabolized in the liver and animal studies suggest involvement of flavin-containing monooxygenases. Emtricitabine and tenofovir alafenamide do not interfere with this pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as ethosuximide is mainly oxidized by CYP3A4. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

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

Coadministration with an etonogestrel-containing progestogen-only implant has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Etonogestrel is metabolized by CYP3A4. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration with etonogestrel as a combined vaginal ring (CVR) has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Etonogestrel is metabolized by CYP3A4. Ethinylestradiol is mainly metabolized by hydroxylation. Emtricitabine and tenofovir alafenamide do not interact with these metabolic pathways. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Etoposide is partly metabolized by CYP3A4 to reactive catechol metabolites. Conversion to reactive metabolites can also be mediated by prostaglandin synthase or myeloperoxidase. Furthermore, etoposide is partly glucuronidated by UGT1A1. Emtricitabine and tenofovir alafenamide do not interact with this etoposide metabolism. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. The recommended dose of Descovy is 200/25 mg once daily.

Coadministration has not been studied but based on metabolism and clearance, a clinically significant interaction is unlikely. There is no evidence to suggest that eucalyptus impacts UGTs or P-gp.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Everolimus is metabolized by CYP3A4. Emtricitabine and tenofovir alafenamide do not interfere with this pathway. Dose Descovy according to the concomitant antiretroviral.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Exemestane is metabolized by CYP3A4 and aldoketoreductase. Emtricitabine and tenofovir alafenamide do not interfere with this pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically relevant drug interaction is unlikely as exenatide is cleared mainly by glomerular filtration. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ezetimibe is glucuronidated by UGTs 1A1 and 1A3 and to a lesser extent by UGTs 2B15 and 2B7. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on the metabolism and clearance a clinically significant interaction is unlikely. Famciclovir is converted to penciclovir by aldehyde oxydase. Penciclovir is secreted in the urine possibly by OAT1. No significant interactions were observed when emtricitabine (200 mg single dose) and famciclovir (500 mg single dose) was studied in 12 HIV-negative subjects as there was no change in the AUC or Cmax values for emtricitabine or famciclovir. Tenofovir alafenamide is unlikely to compete with famciclovir for renal transporters as tenofovir alafenamide results in 90% lower systemic levels of tenofovir compared to tenofovir-DF. Dose Descovy according to the concomitant antiretroviral. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Famotidine is eliminated by renal excretion via OAT3 (65-70%) and by metabolic routes (30-35%). Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Felodipine is metabolized by CYP3A4. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fenofibrate is hydrolyzed to an active metabolite, fenofibric acid. In vitro data suggest that fenofibric acid inhibits OAT3 but this is unlikely to impact emtricitabine or tenofovir derived from tenofovir alafenamide as they are eliminated by other renal transporters. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fentanyl undergoes extensive CYP3A4 metabolism. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fesoterodine is rapidly hydrolysed to its active metabolite which is subsequently metabolized by CYP2D6 and CYP3A4.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fexofenadine undergoes negligible metabolism and is mainly eliminated unchanged in the faeces. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Finasteride is metabolised by CYP3A4. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Flecainide is metabolized mainly via CYP2D6, with a proportion (approximately 30%) of the parent drug also eliminated unchanged renally. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Flibanserin is primarily metabolized by CYP3A4 and to a lesser extent by CYP2C19. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Flucloxacillin is mainly eliminated renally partly by glomerular filtration and partly by active secretion via OAT1. Emtricitabine and tenofovir alafenamide are unlikely to compete with flucloxacillin for renal transporters as emtricitabine is eliminated by different renal transporters and tenofovir alafenamide results in 90% lower systemic levels of tenofovir compared to tenofovir-DF. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied. Coadministration of fluconazole may increase plasma concentrations of tenofovir alafenamide. However it is recommended to dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied. Flucytosine is metabolised to 5-flurouracil which is further metabolised by dihydropyrimidine dehydrogenase. This enzyme is also involved in the catabolic pathway of pyrimidine analogs and competition could potentially increase haematological toxicity. This mechanism of interaction is unlikely to be problematic for tenofovir alafenamide which results in 90% lower systemic levels of tenofovir compared to tenofovir-DF but could be relevant for emtricitabine. Monitor haematological parameters and consider dose reduction if required. Dose Descovy according to the concomitant antiretroviral. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fludarabine phosphate is rapidly hydrolyzed to 2F-ara-A, the principal metabolite (non CYP mediated metabolism) which is then eliminated renally. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fludrocortisone is metabolized in the liver to inactive metabolites, possibly via CYP3A. Emtricitabine and tenofovir alafenamide are unlikely to interact with fludrocortisone. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Flunisolide undergoes CYP3A4-mediated metabolism.

Coadministration has not been studied but based on the metabolism and clearance a clinically significant interaction is unlikely. Flunitrazepam is metabolized mainly via CYPs 3A4 and 2C19. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral. 

Coadministration has not been studied but based on metabolism and clearance a clinically relevant drug interaction is unlikely with the topical use of fluocinolone.

Coadministration has not been studied. Fluorouracil is metabolised via the same mechanisms as endogenous uracil, including via dihydropyrimidine dehydrogenase. An interaction is unlikely with tenofovir alafenamide as it results in 90% lower systemic levels of tenofovir compared to tenofovir-DF. However, emtricitabine may compete for this metabolic pathway. The clinical relevance of this interaction is unknown. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fluoxetine is metabolized by CYP2D6 and 2C9 and to a lesser extent by 2C19 and 3A4 to form norfluoxetine. Emtricitabine and tenofovir do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fluphenazine is metabolised by CYP2D6. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral. 

Coadministration has not been studied but based on the metabolism and clearance a clinically significant interaction is unlikely. The metabolism of flurazepam is most likely CYP-mediated. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fluticasone is metabolized by CYP3A4. Emtricitabine and tenofovir alafenamide are unlikely to interact with fluticasone. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as fluvastatin is mainly metabolized by CYP2C9. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fluvoxamine is metabolized mainly by CYP2D6 and to a lesser extent by CYP1A2. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Folic acid is metabolized to dihydrofolic acid and tetrahydrofolic acid with the aid of reduced diphosphopyridine nucleotide and folate reductases. Significant interactions are not expected with emtricitabine and tenofovir alafenamide. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely when folic acid is administered in a multivitamin preparation. Folic acid is metabolized to dihydrofolic acid and tetrahydrofolic acid with the aid of reduced diphosphopyridine nucleotide and folate reductases. Significant interactions are not expected with emtricitabine and tenofovir alafenamide. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fondaparinux does not undergo cytochrome metabolism but is eliminated predominantly renally.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Formestane undergoes reductive metabolism by hepatic hydroxysteroid dehydrogenase and glucuronidation. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Formoterol is eliminated primarily by direct glucuronidation, with O-demethylation (CYPs 2D6, 2C19, 2C9, and 2A6) followed by further glucuronidation being another pathway. Emtricitabine and tenofovir alafenamide do not interact with formoterol metabolic pathway. Dose Descovy according to the concomitant antiretroviral. 

Coadministration has not been studied but based on the metabolism and clearance a clinically significant interaction is unlikely as foscarnet is cleared mainly by glomerular filtration. Coadministration with nephrotoxic agents is unlikely to be of concern for tenofovir alafenamide which results in 90% lower systemic levels of tenofovir compared to tenofovir-DF. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fosinopril is hydrolysed by esterases in the GI mucosa and liver.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Furosemide is glucuronidated mainly in the kidney (UGT1A9) and to a lesser extent in the liver (UGT1A1). A large proportion of furosemide is also eliminated unchanged renally (via OATs). In vitro data indicate that furosemide is an inhibitor of the renal transporters OAT1/OAT3 but this is unlikely to significantly impact tenofovir concentration as tenofovir alafenamide results in 90% lower systemic levels of tenofovir compared to tenofovir-DF. Emtricitabine is unlikely to interact as it is eliminated by different renal transporters. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as gabapentin is cleared mainly by glomerular filtration. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ganciclovir is primarily eliminated by the kidney and in vitro data suggest that it is a substrate of the renal transporter OAT1. Emtricitabine and tenofovir alafenamide are unlikely to compete with ganciclovir for renal transporters as emtricitabine is eliminated by different renal transporters and tenofovir alafenamide results in 90% lower systemic levels of tenofovir compared to tenofovir-DF. Dose Descovy according to the concomitant antiretroviral. 

Coadministration has not been studied. Garlic supplements have been shown to decrease unboosted saquinavir AUC by 50% in a clinical trial and there is a case report of treatment failure due to garlic cloves (six garlic cloves three times weekly) decreasing ritonavir-boosted atazanavir trough concentrations by ~70%. This effect has been attributed to the induction of intestinal CYP3A4 and/or P-gp by garlic. Tenofovir alafenamide (the prodrug of tenofovir) is a substrate of P-gp and its absorption could decrease due to induction of intestinal P-gp by garlic. Patients should be advised against the use of garlic supplements.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Gefitinib is metabolized by CYP3A4 and CYP2D6 and emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Gemcitabine is metabolized in the liver by cytidine deaminase to an inactive metabolite. Emtricitabine and tenofovir alafenamide do not interfere with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Gemfibrozil is metabolised by UGT2B7. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Gentamicin is eliminated unchanged predominantly via glomerular filtration. No interaction is expected with emtricitabine. There is little potential for interaction with tenofovir alafenamide via competition for active renal transport mechanisms. Coadministration with nephrotoxic agents is unlikely to be of concern for tenofovir alafenamide which results in 90% lower systemic levels of tenofovir compared to tenofovir-DF.

Coadministration with a gestodene-containing combined oral contraceptive (COC) has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Gestodene is metabolized by CYP3A4 and to a lesser extent by CYP2C9 and CYP2C19. Ethinylestradiol is mainly metabolized by hydroxylation. Emtricitabine and tenofovir alafenamide do not interact with these metabolic pathways. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Gamma-hydroxybutyrate undergoes first pass metabolism. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance, a clinically significant interaction is unlikely. No effect on absorption of tenofovir alafenamide is expected as gingerols are unlikely to cause clinically significant inhibition of P-gp.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dose Descovy according to the concomitant antiretroviral.

Studies performed with emtricitabine or tenofovir alafenamide showed no clinically significant interactions with glecaprevir/pibrentasvir. No dose adjustment is required when glecaprevir/pibrentasvir is co administered with emtricitabine and tenofovir alafenamide. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Glibenclamide is mainly metabolized by CYP3A4 and to a lesser extent by CYP2C9. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Gliclazide is metabolized mainly by CYP2C9 and to a lesser extent by CYP2C19. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically relevant drug interaction is unlikely. Glimepiride is mainly metabolized by CYP2C9. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Glipizide is mainly metabolized by CYP2C9. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Glyceryl trinitrate is metabolised by aldehyde dehydrogenase-2. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Glycopyrronium bromide is mainly eliminated renally (active secretion via organic cation transporter) and is also partly hydroxylated via multiple CYPs. Inhibition or induction of its metabolism is unlikely to result in a significant change in exposure.

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

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Granisetron is metabolized by CYP3A4. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Less than 1% of a griseofulvin dose is excreted unchanged via the kidneys, emtricitabine and tenofovir derived from tenofovir alafenamide are unlikely to interact. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Halofantrine is extensively metabolized by CYP3A4. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Haloperidol has a complex metabolism as it undergoes glucuronidation (UGT2B7>1A4, 1A9), carbonyl reduction as well as oxidative metabolism (CYP3A4, 2D6). Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Halothane undergoes both oxidative and reductive metabolism by cytochromes. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Heparin is thought to be eliminated via the reticuloendothelial system. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on the metabolism and clearance a clinically significant interaction is unlikely. When used illicitly, heroin is mainly injected or inhaled through the nose and goes directly in the bloodstream. Heroin is then rapidly deacetylated to 6-monoacetylmorphine (6-MAM) and subsequently to morphine by plasma and liver esterases, respectively. Morphine is mainly glucuronidated to morphine-3-glucuronide (UGT2B7>UGT1A1) and, to a lesser extent, to the pharmacologically active morphine-6-glucuronide (UGT2B7>UGT1A1). Emtricitabine and tenofovir alafenamide do not interact with heroin metabolism. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied. In vitro data indicate that extracts of hops activate PXR and induce expression of CYP3A4, CYP2B6 and MDR1 genes to a degree similar to that of St John's wort. However, a pharmacokinetic study with a standardised hop extract showed no clinically relevant effect on CYPs 2C9, 1A2, and 2D6 and suggested only minor induction of CYP3A4/5 (AUC of alprazolam, a CYP3A4/5 substrate, decreased by ~8%). No effect on emtricitabine exposure is expected. However, hops could potentially decrease tenofovir alafenamide absorption via induction of P-gp.

Coadministration has not been studied but based on metabolism and clearance a clinically significant pharmacokinetic interaction is unlikely. Hydralazine is metabolised via primary oxidative metabolism and acetylation and therefore there is little potential for a pharmacokinetic interaction. Hydralazine has some nephrotoxic potential but tenofovir alafenamide is unlikely to be problematic as it results in 90% lower systemic levels of tenofovir compared to tenofovir-DF. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant pharmacokinetic interaction is unlikely. Hydrochlorothiazide is not metabolized and is cleared by the kidneys via OAT1. In vitro data indicate that hydrochlorothiazide is unlikely to inhibit OAT1 in the range of clinically relevant drug concentrations and therefore is unlikely to affect the renal elimination of tenofovir derived from tenofovir alafenamide. Significant interactions are not expected with emtricitabine. Dose Descovy according to the concomitant antiretroviral.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Hydrocodone is metabolised by CYP2D6 to hydromorphone and by CYP3A4 to norhydrocodone, both of which have analgesic effects. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway. Dose Descovy according to the concomitant antiretroviral.