Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Abacavir is metabolized by alcohol dehydrogenase and UGTs. Remdesivir does not interfere with abacavir’s metabolic pathway.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Albuvirtide is a peptide which is eliminated by catabolism to its constituent amino acids. 

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Alfuzosin is metabolized by CYP3A4. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4, it is unlikely to have a significant effect on alfuzosin. However, both drugs have possible risks of QT prolongation and/or TdP on the CredibleMeds.org website.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Allopurinol is converted to oxipurinol by xanthine oxidase and aldehyde oxidase. Remdesivir is unlikely to affect these enzymes and is a prodrug predominantly metabolized by hydrolase activity.

Coadministration has not been assessed in clinical studies, but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Amiodarone is metabolized by CYPs 3A4 and 2C8 and inhibits intestinal P-gp. Remdesivir does not affect CYP2C8 and due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on amiodarone. However, caution should be exercised as both drugs have risks of QT prolongation and/or TdP on the CredibleMeds.org website (possible risk for remdesivir; known risk for amiodarone). In addition, hepatotoxicity has been reported in one patient receiving remdesivir and amiodarone treatment. It was hypothesized that this adverse effect could arise from an interaction between amiodarone and remdesivir, however, more data are needed to verify this hypothesis as other factors (i.e., effects of COVID-19 on hepatocytes or secondary effect of immune-mediated inflammation or hypoxia) could have led to this adverse effect.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Amlodipine is metabolized by CYP3A4. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on amlodipine. However, amlodipine can prolong the PR interval and remdesivir has a possible risk of QT prolongation and/or TdP on the CredibleMeds.org website.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Remdesivir is a substrate of CYP2C8, CY2D6, CYP3A4, OATP1B1 and P-gp. Anakinra, per se, has no inhibitory or inducing effects on cytochromes. Patients infected with COVID-19 may experience an elevation of IL-1 which has been shown to suppress expression/activity of CYP3A4, CYP2C19, CYP2C9 and CYP1A2. Anakinra will normalize cytochrome activity (via inhibition of IL-1) but no significant effect on remdesivir is expected and no a priori dose adjustment is required.

Coadministration has not been studied. Apalutamide is metabolised by CYP2C8 and CYP3A4. Remdesivir does not affect CYP2C8 and due to its rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on apalutamide. Remdesivir is a prodrug predominantly metabolised by hydrolase, with some involvement (in vitro) of CYPs 2C8, 2D6 and 3A4. Remdesivir has a moderate-high hepatic extraction ratio and based on these pharmacological properties, apalutamide, a strong inducer, is expected to reduce remdesivir to a limited extent (~15-30%). No a priori dose adjustment of remdesivir is needed when administering with strong inducers. However, both drugs have possible risks of QT prolongation and/or TdP on the CredibleMeds.org website.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Apomorphine is metabolized by several pathways that include mainly glucuronidation and sulfation and to a lesser extent N-demethylation. Remdesivir is a prodrug predominantly metabolised by hydrolase, with some involvement (in vitro) of CYPs 2C8, 2D6 and 3A4. Apomorphine neither induces nor inhibits CYPs. However, both drugs have possible risks of QT prolongation and/or TdP on the CredibleMeds.org website.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Aprepitant is mainly metabolized by CYP3A4 and to a lesser extent by CYPs 1A2 and 2C19. Remdesivir is a prodrug predominantly metabolised by hydrolase, with some involvement (in vitro) of CYPs 2C8, 2D6 and 3A4. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on aprepitant. Remdesivir has no effect on CYP2C19, and although it induces CYP1A2 in vitro, no effect is expected at clinically relevant concentrations. Aprepitant is unlikely to affect remdesivir metabolism.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Aripiprazole is metabolized by CYP3A4 and CYP2D6. Remdesivir does not affect CYP2D6 and due to its rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on aripiprazole. However, both drugs have possible risks of QT prolongation and/or TdP on the CredibleMeds.org website.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Artesunate is rapidly converted to dihydroartemisinin, an active metabolite which has greater potency than the parent drug and which is further metabolised via UGTs 1A9 and 2B7. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect. Remdesivir is a prodrug predominantly metabolised by hydrolase, with some involvement (in vitro) of CYPs 2C8, 2D6 and 3A4. Dihydroartemisinin is a weak inducer of CYP3A4 but are unlikely to have a clinically significant effect on remdesivir as remdesivir has a moderate-high hepatic extraction ratio and is used for a short duration in the treatment of COVID-19.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Remdesivir is a substrate of CYP2C8, CY2D6, CYP3A4, OATP1B1 and P-gp. Interactions with aspirin and substrates, inducers, or inhibitors of CYP enzymes are unlikely. Aspirin (acetylsalicylic acid) is rapidly metabolised to salicylic acid, which is further glucuronidated by several UGTs (major UGT1A6). Salicylic acid and its metabolites are predominantly excreted via the kidneys. Aspirin and salicylic acid are extensively bound to plasma proteins, primarily albumin. Remdesivir does not affect UGTs.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Atazanavir/ritonavir is metabolised by CYP3A4 and is an inhibitor of CYP3A4 and UGT1A1, and is a strong inhibitor of OATP1B1. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on atazanavir/ritonavir. Remdesivir is a substrate of CYP2C8, CYP2D6, CYP3A4, OATP1B1 and P-gp. Inhibition of CYP3A4 and OATP1B1 by atazanavir/ritonavir is unlikely to have a significant effect on remdesivir. Note, both drugs have risks of QT prolongation and/or TdP on the CredibleMeds.org website (possible risk for remdesivir; conditional risk for atazanavir). The product label for atazanavir advises caution when prescribing atazanavir with medicinal products which have the potential to increase the QT interval.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Atazanavir is metabolised by CYP3A4 and is an inhibitor of CYP3A4 and UGT1A1, and is a strong inhibitor of OATP1B1. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on atazanavir. Remdesivir is a substrate of CYP2C8, CYP2D6, CYP3A4, OATP1B1 and P-gp. Inhibition of CYP3A4 and OATP1B1 by atazanavir is unlikely to have a significant effect on remdesivir. Note, both drugs have risks of QT prolongation and/or TdP on the CredibleMeds.org website (possible risk for remdesivir; conditional risk for atazanavir). The product label for atazanavir advises caution when prescribing atazanavir with medicinal products which have the potential to increase the QT interval.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Atazanavir/cobicistat is metabolised by CYP3A4 and is an inhibitor of CYP3A4 and UGT1A1, and is a strong inhibitor of OATP1B1. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on atazanavir/cobicistat. Remdesivir is a substrate of CYP2C8, CYP2D6, CYP3A4, OATP1B1 and P-gp. Inhibition of CYP3A4 and OATP1B1 by atazanavir/cobicistat is unlikely to have a significant effect on remdesivir. Note, both drugs have risks of QT prolongation and/or TdP on the CredibleMeds.org website (possible risk for remdesivir; conditional risk for atazanavir). The product label for atazanavir advises caution when prescribing atazanavir with medicinal products which have the potential to increase the QT interval.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Atomoxetine is metabolized by CYP2D6. Remdesivir is a prodrug predominantly metabolised by hydrolase, with some involvement (in vitro) of CYPs 2C8, 2D6 and 3A4. Atomoxetine neither induces nor inhibits CYPs. However, both drugs have possible risks of QT prolongation and/or TdP on the CredibleMeds.org website.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Avapritinib is predominantly mediated by CYP3A4 and to a minor extent by CYP2C9. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect. Remdesivir is a prodrug predominantly metabolised by hydrolase, with some involvement (in vitro) of CYPs 2C8, 2D6 and 3A4. Avapritinib was shown to inhibit and induce CYP3A4 in vitro but is unlikely to have a clinically significant effect on remdesivir as remdesivir has a moderate-high hepatic extraction ratio and is used for a short duration in the treatment of COVID-19. However, avapritinib can potentially prolong the QT interval and remdesivir has a possible risk of QT prolongation and/or TdP on the CredibleMeds.org website.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Azithromycin is mainly eliminated via biliary excretion and animal data suggest this may occur via P-glycoprotein and MRP2. Remdesivir is a substrate of CYP2C8, CY2D6, CYP3A4, OATP1B1 and P-gp. Azithromycin is not expected to have a clinically relevant effect on CYP enzymes or OATP1B1. Although azithromycin inhibits P-gp, no significant effect on remdesivir is expected. However, caution should be exercised as both drugs have risks of QT prolongation and/or TdP on the CredibleMeds.org website (possible risk for remdesivir; known risk for azithromycin).

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Remdesivir is a substrate of CYP2C8, CY2D6, CYP3A4, OATP1B1 and P-gp. Baricitinib is not expected to have a clinically relevant effect on CYP enzymes or OATP1B1. Baricitinib is mainly eliminated renally, with CYP3A4 contributing to less than 10% of its overall metabolism.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Bedaquiline is metabolised by CYP3A4 and mainly eliminated in faeces. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on bedaquiline. However, both drugs have possible risks of QT prolongation and/or TdP on the CredibleMeds.org website.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Bepridil is metabolized by CYP2D6 (major) and CYP3A4. Remdesivir does not affect CYP2D6 and due to its rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on bepridil. However, caution should be exercised as both drugs have risks of QT prolongation and/or TdP on the CredibleMeds.org website (possible risk for remdesivir; known risk for bepridil).

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Betamethasone is metabolized by CYP3A4 and is a moderate inducer of CYP3A4. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on betamethasone. Remdesivir is a prodrug predominantly metabolised by hydrolase, with some involvement (in vitro) of CYPs 2C8, 2D6 and 3A4. Betamethasone is a moderate inducer of CYP3A4 but is unlikely to have a clinically significant effect on remdesivir as remdesivir has a moderate-high hepatic extraction ratio and is used for a short duration in the treatment of COVID-19.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Betrixaban is largely eliminated unchanged through biliary secretion via P-gp. However, both drugs have possible risks of QT prolongation and/or TdP on the CredibleMeds.org website.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bictegravir is metabolised by CYP3A4 and UGT1A1 whereas emtricitabine and tenofovir alafenamide are eliminated renally. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on bictegravir. Remdesivir is a substrate of CYP2C8, CYP2D6, CYP3A4, OATP1B1 and P-gp, however, bictegravir has no significant inhibitory or inducing effects on these enzymes and transporters. No interaction is expected with emtricitabine and tenofovir alafenamide.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Bortezomib is mainly metabolized by CYP3A4 and CYP2C19 and to a lesser extent by CYPs 1A2, 2D6 and 2C9. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect. Remdesivir is a prodrug predominantly metabolised by hydrolase, with some involvement (in vitro) of CYPs 2C8, 2D6 and 3A4. However, both drugs have possible risks of QT prolongation and/or TdP on the CredibleMeds.org website.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bosentan is a substrate of CYP3A4 and CYP2C9. No effect on bosentan is expected as remdesivir does not affect CYP2C9 and due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect. Remdesivir is a prodrug predominantly metabolised by hydrolase, with some involvement (in vitro) of CYPs 2C8, 2D6 and 3A4. Bosentan is a moderate inducer of CYP3A4 but is unlikely to have a clinically significant effect on remdesivir as remdesivir has a moderate-high hepatic extraction ratio and is used for a short duration in the treatment of COVID-19.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Bosutinib is metabolised by CYP3A4. Remdesivir is a prodrug predominantly metabolised by hydrolase, with some involvement (in vitro) of CYPs 2C8, 2D6 and 3A4. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on bosutinib. However, both drugs have possible risks of QT prolongation and/or TdP on the CredibleMeds.org website.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Buprenorphine is mainly metabolized by CYP3A4 to form the active metabolite norbuprenorphine, but is also glucuronidated by UGT2B7 and UGT1A1. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on buprenorphine. Remdesivir does not affect UGTs. However, both drugs have possible risks of QT prolongation and/or TdP on the CredibleMeds.org website.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bupropion is primarily metabolized by CYP2B6. Remdesivir does not affect CYP2B6.

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

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Cabotegravir is mainly metabolized by UGT1A1 and to a lesser extent by UGT1A9. Rilpivirine is primarily metabolized by CYP3A4. Remdesivir does not affect UGTs. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on rilpivirine. Remdesivir is a substrate of CYP2C8, CYP2D6, CYP3A4, OATP1B1 and P-gp, however, cabotegravir and rilpivirine have no significant inhibitory or inducing effects on these enzymes and transporters at clinically relevant concentrations. Note, both remdesivir and rilpivirine have possible risks of QT prolongation and/or TdP on the CredibleMeds.org website. The product labels for rilpivirine indicate that rilpivirine should be used with caution in combination with drugs with a known risk of Torsade de Pointes.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Canakinumab is an IL-1 receptor antagonist and is eliminated via intracellular catabolism. Remdesivir is a substrate of CYP2C8, CY2D6, CYP3A4, OATP1B1 and P-gp. Canakinumab, per se, has no inhibitory or inducing effects on cytochromes. Patients infected with COVID-19 may experience an elevation of IL-1 which has been shown to suppress expression/activity of CYP3A4, CYP2C19, CYP2C9 and CYP1A2. Canakinumab will normalize cytochrome activity (via inhibition of IL-1) but no significant effect on remdesivir is expected and no a priori dose adjustment is required. 

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Capecitabine is activated by sequential enzyme reactions to fluorouracil. Remdesivir is a prodrug predominantly metabolised by hydrolase, with some involvement (in vitro) of CYPs 2C8, 2D6 and 3A4. However, both drugs have possible risks of QT prolongation and/or TdP on the CredibleMeds.org website.

Coadministration has not been studied. Carbamazepine is metabolised by CYP3A4 and UGT2B7. Remdesivir does not affect UGTs and due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on carbamazepine. Remdesivir is predominantly metabolised by carboxylesterase, with some involvement of CYP3A4 and cathepsin A. Furthermore, remdesivir has a moderate-high hepatic extraction ratio. Based on these pharmacological properties, strong inducers such as carbamazepine are expected to reduce remdesivir to a limited extent (~15-30%). No a priori dose adjustment of remdesivir is needed when administering with strong inducers.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Remdesivir is a substrate of CYP2C8, CY2D6, CYP3A4, OATP1B1 and P-gp. Casirivimab and imdevimab are IgG1 monoclonal antibodies and are likely to be eliminated via intracellular catabolism, similarly to endogenous IgG. Casirivimab and imdevimab are not metabolized by CYP enzymes. Interactions with concomitant medications that are substrates, inducers, or inhibitors of CYP enzymes are unlikely.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Ceritinib is metabolized by CYP3A4. Remdesivir is a prodrug predominantly metabolised by hydrolase, with some involvement (in vitro) of CYPs 2C8, 2D6 and 3A4. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on ceritinib. However, both drugs have possible risks of QT prolongation and/or TdP on the CredibleMeds.org website.

Coadministration of remdesivir and chloroquine has not been studied and is not recommended as it may result in reduced antiviral activity of remdesivir. In vitro studies show that chloroquine reduced the formation of the virally active remdesivir triphosphate in normal human bronchial epithelial cells. Due to the long elimination half life of chloroquine, this effect is expected to persist even if chloroquine is stopped prior to the initiation of remdesivir (washout period 180 days). No significant effect on chloroquine is expected. In addition, caution should be exercised as both drugs have risks of QT prolongation and/or TdP on the CredibleMeds.org website (possible risk for remdesivir; known risk for chloroquine).

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Cilostazol is extensively metabolised by CYP3A4 and CYP2C19 and to a lesser extent CYP1A2. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on cilostazol. Remdesivir induces CYP1A2 in vitro but no effect is expected at clinically relevant concentrations. Remdesivir is a prodrug predominantly metabolised by hydrolase, with some involvement (in vitro) of CYPs 2C8, 2D6 and 3A4. Cilostazol is unlikely to affect drugs metabolised by CYP3A4. However, caution should be exercised as both drugs have risks of QT prolongation and/or TdP on the CredibleMeds.org website (possible risk for remdesivir; known risk for cilostazol).

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Ciprofloxacin is primarily eliminated unchanged through the kidneys (by glomerular filtration and tubular secretion via OAT3). However, caution should be exercised as both drugs have risks of QT prolongation and/or TdP on the CredibleMeds.org website (possible risk for remdesivir; known risk for ciprofloxacin).

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Cisapride is metabolized by CYP3A4. However, caution should be exercised as both drugs have risks of QT prolongation and/or TdP on the CredibleMeds.org website (possible risk for remdesivir; known risk for cisapride).

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Citalopram is metabolized by CYPs 2C19 (38%), 2D6 (31%) and 3A4 (31%). Remdesivir has no effect on CYP2C19 or CYPD6, and due to its rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on citalopram. However, caution should be exercised as both drugs have risks of QT prolongation and/or TdP on the CredibleMeds.org website (possible risk for remdesivir; known risk for citalopram).

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Clarithromycin is metabolised by CYP3A4 and is a strong inhibitor of CYP3A4. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on clarithromycin. Inhibition of CYP3A4 by clarithromycin is unlikely to have a significant effect on remdesivir. However, caution should be exercised as both drugs have risks of QT prolongation and/or TdP on the CredibleMeds.org website (possible risk for remdesivir; known risk for clarithromycin).

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. Remdesivir has no effect on CYP2B6 and CYP2C19 and due to its rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on clobazam. Clobazam is a weak inducer but no significant effect on remdesivir is expected.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Clopidogrel is a prodrug that is converted to its active metabolites via CYPs 3A4, 2B6, 2C19 and 1A2. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on clopidogrel. Although remdesivir induces CYP1A2 in vitro, no effect is expected at clinically relevant concentrations. Remdesivir does not affect CYP2B6 and CYP2C19.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Clozapine is metabolized by CYPs 1A2, 2C19, 3A4, and to a lesser extent by CYPs 2C9 and 2D6. Remdesivir has no effect on CYPs 2C19, 2C9 or 2D6, and although it induces CYP1A2 in vitro, no effect is expected at clinically relevant concentrations. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on clozapine. However, both drugs have possible risks of QT prolongation and/or TdP on the CredibleMeds.org website.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Cobimetinib is mainly metabolized by CYP3A and UGT2B7. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect. Remdesivir is a prodrug predominantly metabolised by hydrolase, with some involvement (in vitro) of CYPs 2C8, 2D6 and 3A4. Cobimetinib does not affect CYP3A4 or CYP2D6. However, both drugs have possible risks of QT prolongation and/or TdP on the CredibleMeds.org website.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Cocaine is metabolised by several pathways with metabolism to norcocaine by CYP3A4 being less than 10% of the overall metabolic clearance. Remdesivir is a prodrug predominantly metabolised by hydrolase, with some involvement (in vitro) of CYPs 2C8, 2D6 and 3A4. However, caution should be exercised as both drugs have risks of QT prolongation and/or TdP on the CredibleMeds.org website (possible risk for remdesivir; known risk for cocaine).

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Crizotinib is mainly metabolized by CYP3A4. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect. Remdesivir is a prodrug predominantly metabolised by hydrolase, with some involvement (in vitro) of CYPs 2C8, 2D6 and 3A4. Crizotinib is a moderate inhibitor of CYP3A4 but is unlikely to have a clinically significant effect on remdesivir. However, both drugs have possible risks of QT prolongation and/or TdP on the CredibleMeds.org website.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. The metabolism of cyclizine has not been fully described but may involve CYP2D6. Remdesivir has no effect on CYP2D6 and is a prodrug predominantly metabolized by hydrolase activity.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Dabrafenib is metabolized by CYP3A4 and CYP2C8 and the active metabolites are metabolized by CYP3A4. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect. Remdesivir is a prodrug predominantly metabolised by hydrolase, with some involvement (in vitro) of CYPs 2C8, 2D6 and 3A4. Dabrafenib is a moderate to strong inducer of CYP3A4 but is unlikely to have a clinically significant effect on remdesivir as remdesivir has a moderate-high hepatic extraction ratio. Strong inducers are expected to reduce remdesivir to a limited extent (~15-30%). Thus no a priori dose adjustment of remdesivir is needed when coadministered with moderate to strong inducers like dabrafenib. However, both drugs have possible risks of QT prolongation and/or TdP on the CredibleMeds.org website.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Remdesivir is a substrate of CYP2C8, CY2D6, CYP3A4, OATP1B1 and P-gp. Dalteparin is excreted largely unchanged by the kidneys and does not induce or inhibit CYPs or P-gp.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Darunavir/ritonavir is metabolised by CYP3A4 and is an inhibitor of CYP3A4 as well as OATP1B1. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on darunavir/ritonavir. Remdesivir is a substrate of CYP2C8, CYP2D6, CYP3A4, OATP1B1 and P-gp. Inhibition of CYP3A4 and OATP1B1 by darunavir/ritonavir is unlikely to have a significant effect on remdesivir.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Darunavir/cobicistat is metabolised by CYP3A4 and is an inhibitor of CYP3A4 as well as OATP1B1. Emtricitabine and tenofovir alafenamide are eliminated renally. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on darunavir/cobicistat. Remdesivir is a substrate of CYP2C8, CYP2D6, CYP3A4, OATP1B1 and P-gp. Inhibition of CYP3A4 and OATP1B1 by darunavir/cobicistat is unlikely to have a significant effect on remdesivir. No interaction is expected with emtricitabine and tenofovir alafenamide.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Darunavir/cobicistat is metabolised by CYP3A4 and is an inhibitor of CYP3A4 as well as OATP1B1. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on darunavir/cobicistat. Remdesivir is a substrate of CYP2C8, CYP2D6, CYP3A4, OATP1B1 and P-gp. Inhibition of CYP3A4 and OATP1B1 by darunavir/cobicistat is unlikely to have a significant effect on remdesivir.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Dasatinib is metabolised by CYP3A4. Remdesivir is a prodrug predominantly metabolised by hydrolase, with some involvement (in vitro) of CYPs 2C8, 2D6 and 3A4. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on dasatinib. However, both drugs have possible risks of QT prolongation and/or TdP on the CredibleMeds.org website.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic 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. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on delamanid. However, both drugs have possible risks of QT prolongation and/or TdP on the CredibleMeds.org website.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Desipramine is metabolized by CYP2D6 which is not affected by remdesivir. However, both drugs have possible risks of QT prolongation and/or TdP on the CredibleMeds.org website.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Remdesivir is a prodrug predominantly metabolised by hydrolase, with some involvement (in vitro) of CYPs 2C8, 2D6 and 3A4, and is transported by P-gp. Dexamethasone is a dose-dependent inducer of CYP3A4 and is a moderate CYP3A4 inducer at doses above 16 mg. Dexamethasone is unlikely to have a clinically significant effect on remdesivir as remdesivir has a moderate-high hepatic extraction ratio, and is used for a short duration in the treatment of COVID-19. Dexamethasone is a substrate of CYP3A4 and although remdesivir inhibits CYP3A4, due to remdesivir's rapid clearance after i.v. administration, remdesivir is unlikely to have a significant effect on dexamethasone exposure.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Remdesivir is a prodrug predominantly metabolised by hydrolase, with some involvement (in vitro) of CYPs 2C8, 2D6 and 3A4, and is transported by P-gp. Dexamethasone is a weak inducer of CYP3A4 and P-gp at a low dose. Induction is dose-dependent and occurs after multiple doses. Dexamethasone is unlikely to have a clinically significant effect on remdesivir as remdesivir has a moderate-high hepatic extraction ratio, and is used for a short duration in the treatment of COVID-19. Dexamethasone is a substrate of CYP3A4 and although remdesivir inhibits CYP3A4, due to remdesivir's rapid clearance after i.v. administration, remdesivir is unlikely to have a significant effect on dexamethasone exposure.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Dexmedetomidine undergoes extensive hepatic metabolism through direct glucuronidation (mainly via UGTs 1A4 and 2B10) and cytochrome P450 (mainly CYP2A6) which are not affected by remdesivir. However, both drugs have possible risks of QT prolongation and/or TdP on the CredibleMeds.org website.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Disopyramide is metabolized by CYP3A4 (25%) whereas 50% of the drug is eliminated unchanged in the urine (possibly via OCT2). Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on disopyramide. However, caution should be exercised as both drugs have risks of QT prolongation and/or TdP on the CredibleMeds.org website (possible risk for remdesivir; known risk for disopyramide).

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Dofetilide is metabolized to a small degree by CYP3A4 and is mainly excreted unchanged in urine. Renal elimination involves both glomerular filtration and active tubular secretion (via cation transport system). Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on dofetilide. However, caution should be exercised as both drugs have risks of QT prolongation and/or TdP on the CredibleMeds.org website (possible risk for remdesivir; known risk for disopyramide).

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic 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%). Remdesivir does not affect CYP2D6 and due to its rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on dolasetron. However, caution should be exercised as both drugs have risks of QT prolongation and/or TdP on the CredibleMeds.org website (possible risk for remdesivir; known risk for dolasetron).

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dolutegravir is primarily metabolized by UGT1A1, with some contribution from CYP3A. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on dolutegravir. Remdesivir is a substrate of CYP2C8, CYP2D6, CYP3A4, OATP1B1 and P-gp, however, dolutegravir has no significant inhibitory or inducing effects on these enzymes and transporters.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dolutegravir is primarily metabolized by UGT1A1, with some contribution from CYP3A whereas lamivudine is eliminated renally. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on dolutegravir. Remdesivir is a substrate of CYP2C8, CYP2D6, CYP3A4, OATP1B1 and P-gp, however, dolutegravir has no significant inhibitory or inducing effects on these enzymes and transporters. No interaction is expected with lamivudine.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Dolutegravir is primarily metabolized by UGT1A1, with some contribution from CYP3A whereas rilpivirine is metabolized by CYP3A. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on dolutegravir and rilpivirine. Remdesivir is a substrate of CYP2C8, CYP2D6, CYP3A4, OATP1B1 and P-gp, however, dolutegravir and rilpivirine have no significant inhibitory or inducing effects on these enzymes and transporters. Note, both remdesivir and rilpivirine have possible risks of QT prolongation and/or TdP on the CredibleMeds.org website. The product labels for rilpivirine indicate that rilpivirine should be used with caution in combination with drugs with a known risk of Torsade de Pointes.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dolutegravir is primarily metabolized by UGT1A1, with some contribution from CYP3A, abacavir is metabolized by alcohol dehydrogenase and UGTs whereas lamivudine is eliminated renally. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on dolutegravir. Remdesivir is a substrate of CYP2C8, CYP2D6, CYP3A4, OATP1B1 and P-gp, however, dolutegravir has no significant inhibitory or inducing effects on these enzymes and transporters. No interaction is expected with lamivudine and abacavir.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Donepezil is metabolized by CYP3A4 and CYP2D6 (minor). Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on donepezil. However, caution should be exercised as both drugs have risks of QT prolongation and/or TdP on the CredibleMeds.org website (possible risk for remdesivir; known risk for donepezil).

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Doravirine is primarily metabolized by CYP3A4. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on doravirine. Remdesivir is a substrate of CYP2C8, CYP2D6, CYP3A4, OATP1B1 and P-gp, however, doravirine has no significant inhibitory or inducing effects on these enzymes and transporters.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Doravirine is primarily metabolized by CYP3A4. Lamivudine and tenofovir disoproxil fumarate are eliminated renally. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on doravirine. Remdesivir is a substrate of CYP2C8, CYP2D6, CYP3A4, OATP1B1 and P-gp, however, doravirine has no significant inhibitory or inducing effects on these enzymes and transporters. No interaction is expected with lamivudine and tenofovir-DF.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Doxylamine is metabolised primarily by CYP2D6, CYP1A2 and CYP2C9. Remdesivir is a prodrug predominantly metabolised by hydrolase, with some involvement (in vitro) of CYPs 2C8, 2D6 and 3A4. Doxylamine is unlikely to affect remdesivir metabolism. Although remdesivir induces CYP1A2 in vitro, no effect is expected at clinically relevant concentrations.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Dronedarone is primarily metabolized by CYP3A4. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on dronedarone. A PBPK model predicted that remdesivir would increase the exposure of the sensitive CY3A4 substrate midazolam AUC by <10%. However, caution should be exercised as both drugs have risks of QT prolongation and/or TdP on the CredibleMeds.org website (possible risk for remdesivir; known risk for dronedarone).

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Efavirenz is primarily metabolized by CYP2B6 and CYP3A4. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on efavirenz. Remdesivir is a prodrug predominantly metabolised by hydrolase, with some involvement (in vitro) of CYPs 2C8, 2D6 and 3A4. Efavirenz is a moderate inducer but is unlikely to have a clinically significant effect on remdesivir as remdesivir has a moderate-high hepatic extraction ratio and is used for a short duration in the treatment of COVID-19. Remdesivir has a possible risk of QT prolongation and/or TdP on the CredibleMeds.org website. Efavirenz was shown to prolong the QT interval above the regulatory threshold of concern in homozygous carriers of the CYP2B6*6/*6 allele (i.e. 516T variant in the gene encoding CYP2B6). The European product label for efavirenz contraindicates coadministration with a drug with a known risk of Torsade de Pointes whereas the American product label for efavirenz recommends that alternatives should be considered. As the potential risk of a QT interval prolongation relates specifically to homozygous carriers of CYP2B6*6/*6 and given the accumulated years of safety data with efavirenz and such drugs, the contraindication is not reflected in the colour coding of this interaction summary.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Elvitegravir/cobicistat is metabolised by CYP3A4 and is an inhibitor of CYP3A4 as well as OATP1B1. Emtricitabine and tenofovir alafenamide are eliminated renally. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on elvitegravir/cobicistat. Remdesivir is a substrate of CYP2C8, CYP2D6, CYP3A4, OATP1B1 and P-gp. Inhibition of CYP3A4 and OATP1B1 by elvitegravir/cobicistat is unlikely to have a significant effect on remdesivir. No interaction is expected with emtricitabine and tenofovir alafenamide.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Elvitegravir/cobicistat is metabolised by CYP3A4 and is an inhibitor of CYP3A4 as well as OATP1B1. Emtricitabine and tenofovir disoproxil fumarate are eliminated renally. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on elvitegravir/cobicistat. Remdesivir is a substrate of CYP2C8, CYP2D6, CYP3A4, OATP1B1 and P-gp. Inhibition of CYP3A4 and OATP1B1 by elvitegravir/cobicistat is unlikely to have a significant effect on remdesivir. No interaction is expected with emtricitabine and tenofovir-DF.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Emtricitabine is eliminated renally. Remdesivir does not interfere with emtricitabine’s renal elimination.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Emtricitabine and tenofovir alafenamide are eliminated renally. Remdesivir does not interfere with emtricitabine and tenofovir alafenamide’s renal elimination.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Emtricitabine and tenofovir disoproxil fumarate are eliminated renally. Remdesivir does not interfere with emtricitabine and tenofovir-DF’s renal elimination.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Encorafenib is mainly metabolized by CYP3A4. Remdesivir is a prodrug predominantly metabolised by hydrolase, with some involvement (in vitro) of CYPs 2C8, 2D6 and 3A4. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on encorafenib. However, both drugs have possible risks of QT prolongation and/or TdP on the CredibleMeds.org website.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Remdesivir is a substrate of CYP2C8, CY2D6, CYP3A4, OATP1B1 and P-gp. Enoxaparin does not undergo cytochrome metabolism but is desulphated and depolymerised in the liver and is excreted predominantly renally. Enoxaparin does not induce or inhibit CYPs or P-gp.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Entrectinib is predominantly metabolized by CYP3A4. Due to remdesivir’s rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on entrectinib. Remdesivir is a prodrug predominantly metabolised by hydrolase, with some involvement (in vitro) of CYPs 2C8, 2D6 and 3A4. However, both drugs have possible risks of QT prolongation and/or TdP on the CredibleMeds.org website.

Coadministration has not been studied. Enzalutamide is primarily metabolized by CYP2C8 and to a lesser extent by CYP3A4. Remdesivir does not affect CYP2C8 and due to its rapid clearance, although remdesivir inhibits CYP3A4 it is unlikely to have a significant effect on enzalutamide. Remdesivir is a prodrug predominantly metabolised by hydrolase, with some involvement (in vitro) of CYPs 2C8, 2D6 and 3A4. Remdesivir has a moderate-high hepatic extraction ratio and based on these pharmacological properties, strong inducers such as enzalutamide are expected to reduce remdesivir to a limited extent (~15-30%). No a priori dose adjustment of remdesivir is needed when administering with strong inducers. Note, remdesivir has a possible risk of QT prolongation and/or TdP on the CredibleMeds.org website and androgen deprivation therapy may prolong the QT interval.