Coadministration has not been studied but based on metabolism and clearance a clinically significant pharmacokinetic interaction is unlikely as abacavir is metabolised by UGTs. No dose adjustment of daclatasvir or abacavir is required.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Abiraterone has multiple metabolic pathways and is an inhibitor of CYP2D6. Daclatasvir is not involved with this pathway.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Acalabrutinib is a CYP3A4 and P-gp substrate but these are not affect by daclatasvir.

Coadministration has not been studied but based on metabolism and clearance, a clinically significant interaction is unlikely as acamprosate does not undergo significant metabolism.

Coadministration has not been studied, but based on metabolism and clearance a clinically significant 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.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Aceclofenac is metabolised by CYP2C9 which is not affected by daclatasvir.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely as acenocoumarol is predominantly metabolised via CYP2C9 and daclatasvir does not affect this enzyme. However, close monitoring of INR is recommended as this may change as a result of improved liver function.

Coadministration has not been studied. Activated charcoal absorbs substances in the stomach and intestines and may decrease absorption of orally administered medications. If coadministration is required, administration of activated charcoal and daclatasvir should be separated by 4 hours. [Note: this interaction is not specific for daclatasvir, but for any medication taken with activated charcoal.]

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Daclatasvir is metabolised by CYP3A4. The potential for hepatically metabolised interactions with adefovir is low. Adefovir is eliminated renally via glomerular filtration and active renal secretion by OAT1. No dose adjustment of daclatasvir or adefovir is required.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Agomelatine is metabolised predominantly by CYP1A2 and daclatasvir does not affect this enzyme. [Note, agomelatine is contraindicated in hepatic impairment as increases in exposure of up to 140-times have been seen in cirrhotic patients.]

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as alemtuzumab is a protein for which the expected metabolic pathway is degradation to small peptides and individual amino acids by widely distributed proteolytic enzymes.

Coadministration has not been studied but alendronate can be administered with daclatasvir and no dose alteration is required. Alendronate is not metabolised and is cleared from the plasma by uptake into bone and elimination via renal excretion. Although no pharmacokinetic interaction is expected, note that alendronate should be separated from food or other medicinal products and therefore should be separated from daclatasvir administration. [Note: this interaction is not specific for daclatasvir, but for any medication taken with alendronic acid.]

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely as allopurinol is metabolised by xanthine oxidase and aldehyde oxidase. [Note, the European SPC and US Prescribing Information for allopurinol recommend a reduced dose in hepatic impairment.]

Coadministration has not been studied but based on metabolism and clearance, a clinically significant interaction is unlikely. Aloe vera is only a weak inhibitor of CYPs in vitro and therefore is unlikely to cause clinically significant interactions. It does not inhibit P-gp and there is no evidence to suggest it impacts UGTs.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Alogliptin does not undergo extensive metabolism and is excreted mainly unchanged in the urine and metabolism by CYPs is minimal. No transporter interactions have been described.

Coadministration has not been studied but no clinically relevant effect on alprazolam concentrations is expected. Alprazolam and daclatasvir are substrates of CYP3A4 and daclatasvir is a mild inducer of this enzyme, but a pharmacokinetic interaction is unlikely at clinically relevant concentrations. No dose adjustment of alprazolam is required.

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 limited understanding of metabolism and clearance a clinically significant interaction is unlikely. However as alverine citrate affects gastric motility, an effect on the absorption of daclatasvir cannot be ruled out. Doses of daclatasvir and alverine should be separated by 4 hours if possible. [Note: this interaction is not specific for daclatasvir, but for any medication taken with alverine citrate.]

Coadministration has not been studied. Ambrisentan is glucuronidated by several UGT isoenzymes and is metabolised to a lesser extent by CYP3A4. Ambrisentan is also a substrate of P-gp and OATP1B1. Coadministration with ciclosporin resulted in a 2-fold increase in ambrisentan exposure (possibly due to OATP1B1 inhibition). A similar effect may occur due to inhibition of OATP1B1 by daclatasvir. Advise patient to be aware of the potential for increased side effects during coadministration.

Coadministration has not been studied and is not recommended due to the potential for serious and/or life-threatening adverse events such as cardiac arrhythmias.

Coadministration has not been studied but may increase daclatasvir concentrations due to inhibition of CYP3A4 by amlodipine. Use with caution.

Coadministration has not been studied and is not recommended. Amobarbital induces CYP3A4 and P-gp and could decrease concentrations of daclatasvir. This may result in loss of efficacy and potential virological failure.

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

Coadministration has not been studied. Apixaban is metabolized mainly by CYP3A4/5 (with minor contributions from CYPs 1A2, 2C8, 2C9, 2C19, and 2J2) and is a substrate of P-gp and BCRP. Daclatasvir is a mild inhibitor of P-gp but has no clinically relevant effect on CYP3A4. Concentrations of apixaban may increase to a limited extent but this is unlikely to be clinically significant. Patients should be reminded to promptly report any signs of bleeding or bruising as with anyone who is prescribed DOACs. [Note: product labels state that apixaban is contraindicated in patients with hepatic disease associated with coagulopathy and clinically relevant bleeding risk. It is not recommended in severe hepatic impairment and should be used with caution in patients with mild or moderate hepatic impairment.]

Coadministration has not been studied. Aprepitant is metabolised by CYP3A4 but daclatasvir is only a mild inducer of CYP3A4 and no clinically significant effect on aprepitant concentrations is expected. Aprepitant is a moderate inhibitor of CYP3A4 and may increase daclatasvir concentrations. Monitoring may be required as clinically indicated.

Coadministration has not been studied. Artemisinins undergo rapid metabolism via several CYP450 (CYPs 3A4, 2A6, 2B6). The active metabolite (dihydroartemisinin, which has greater potency than the parent drug) is further metabolized via UGTs 1A9 and 2B7 and has been shown to induce CYP3A4. Dihydroartemisinin may potentially decrease daclatasvir concentrations although the clinical significance of this is uncertain. Caution is advised with close monitoring for therapeutic effect.

Coadministration has not been studied. Dihydroartemisinin (the active metabolite of artesunate) is further metabolised via UGTs 1A9 and 2B7 and has been shown to induce CYP3A4. Dihydroartemisinin may potentially decrease daclatasvir concentrations although the clinical significance of this is uncertain. Caution is advised and with close monitoring for therapeutic effect.

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 (mainly CYP1A2, with minor contributions from CYP3A4 and CYP2D6). As asenapine is metabolised by multiple pathways, a clinically significant effect is unlikely.

Coadministration with atazanavir alone has not been studied. Coadministration of atazanavir/ritonavir (300/100 mg once daily) and daclatasvir (20 mg once daily) increased daclatasvir AUC, Cmax and Cmin by 110%, 35% and 265%, respectively (results dose-normalised to 60 mg dose). The dose of daclatasvir should be reduced to 30 mg once daily when coadministered with atazanavir/ritonavir or atazanavir/cobicistat. However, no dose reduction is required with unboosted atazanavir.

The pharmacokinetics of daclatasvir were determined following coadministration of atazanavir/cobicistat (300/150 mg) and daclatasvir (30 mg) and compared to those of atazanavir/ritonavir (300/100 mg) and daclatasvir (30 mg). Atazanavir/cobicistat and atazanavir/ritonavir were shown to have a similar influence on the pharmacokinetic of daclatasvir in healthy volunteers. Therefore the recommended 30 mg once daily dose of daclatasvir with atazanavir/ritonavir, applies also for cobicistat-boosted atazanavir.

Coadministration of atazanavir/ritonavir (300/100 mg once daily) and daclatasvir (20 mg once daily) increased daclatasvir AUC, Cmax and Cmin by 110%, 35% and 265%, respectively (results dose-normalised to 60 mg dose). The dose of daclatasvir should be reduced to 30 mg once daily when coadministered with atazanavir/ritonavir.

Coadministration has not been studied but atorvastatin concentrations are expected to increase due to inhibition of OATP1B1 and BCRP by daclatasvir. Use with caution. Monitor for atorvastatin-associated adverse events such as myopathy.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Avelumab is primarily metabolised through catabolic pathways and drug-drug interactions are not expected.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Axitinib is metabolised by CYP3A4 but daclatasvir is only a mild inducer of CYP3A4 and no clinically significant interaction is expected.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Azilsartan is predominantly metabolised by CYP2C9 which is not affected by daclatasvir.

Coadministration has not been studied. Azithromycin may be transported by P-gp and as daclatasvir has been shown to be a mild P-gp inhibitor, theoretically concentrations of azithromycin may be increased, however no a priori dose adjustment of daclatasvir or azithromycin is required.

Coadministration has not been studied but based on metabolism and clearance a clinically significant drug interaction is unlikely. Aztreonam is only minimally metabolised and is eliminated mainly unchanged in the urine.

Coadministration has not been studied. Bedaquiline is metabolized by CYP3A4 but daclatasvir is only a mild inducer of CYP3A4 and no clinically significant interaction is expected. Coadministration of bedaquiline (400 mg single dose) and nevirapine (a CYP 3A4 inducer) had no clinically relevant effect on bedaquiline exposure (AUC increased by 3%, Cmax decreased by 20%). No dose adjustment of daclatasvir or bedaquiline is required.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as benazepril is glucuronidated and renally cleared.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bendroflumethiazide is mainly eliminated by hepatic metabolism, although the exact pathway is not known. It is unlikely that CYP enzymes are involved in this process and no transporter interactions have been described.

Coadministration has not been studied but based on metabolism and clearance, a clinically significant interaction is unlikely. Benralizumab is a humanised IgG1 monoclonal antibody that is degraded by proteolytic enzymes widely distributed in the body and not restricted to hepatic tissue.

Coadministration has not been studied but based on metabolism and clearance, a clinically significant interaction is unlikely. Benztropine is primarily metabolised by CYP2D6 which is not affected by daclatasvir.

Coadministration has not been studied but based on metabolism and clearance a clinically significant pharmacokinetic interaction is unlikely. Betahistine undergoes nearly complete metabolism by monoamine oxidase. Based on in-vitro data, no inhibition of cytochrome P450 enzymes by betahistine is expected.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bevacizumab biotransformation involves proteolytic catabolism throughout the body, including endothelial cells, and does not rely primarily on elimination through the kidneys and liver.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bezafibrate is metabolised by hydroxylation, glucuronidation and renal elimination (~50%). Due to the involvement of multiple metabolic pathways and renal elimination, a clinically significant interaction is not expected. [Note, the European SmPC for bezafibrate contraindicates its use in significant hepatic disease.]

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.

Coadministration has not been studied but concentrations of bilastine may be increased due to inhibition of P-gp and OATP by daclatasvir. Caution is advised. Close monitoring for signs and symptoms of increased bilastine exposure is recommended.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. No interactions are anticipated since although the drug is metabolised, the systemic concentrations of bimatoprost are extremely low (less than 0.2 ng/ml) following ocular dosing with bimatoprost.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Although limited human data suggest biperiden undergoes hydroxylation in the liver there are no known or documented interactions with other drugs that have an effect on metabolism or transport. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant pharmacokinetic interaction is unlikely. Absorption of bisacodyl from the GI tract is minimal and the small amount absorbed is excreted in the urine as the glucuronide. However, bisacodyl increases colonic mass movements and may affect absorption of daclatasvir. The potential interaction can be resolved by giving bisacodyl at least 4 hours after daclatasvir. [Note: this interaction is not specific for daclatasvir, but for any medication taken with bisacodyl.]

Coadministration has not been studied. Bisoprolol is metabolised by CYP3A4 and CYP2D6. Daclatasvir has no effect on CYP2D6 and is only a mild inducer of CYP3A4 so a pharmacokinetic interaction is unlikely at clinically relevant concentrations. [Note, the European SPC for bisoprolol recommends a maximum of 10 mg in severe hepatic impairment and the US Prescribing Information for bisoprolol recommends an initial 2.5 mg in hepatic impairment with caution in further dose titration.]

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Black cohosh does not appear to be involved in drug metabolism to a clinically significant effect. Standardized black cohosh supplements, when taken at recommended doses, pose little risk for herb-drug interactions.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. An indirect effect of blinatumomab on CYPs may occur due to transient release of cytokines during the first days of therapy which can inhibit CYP450 metabolism however, a clinically relevant interaction is unlikely. The metabolic pathway of blinatumomab has not been characterised. Like other protein therapeutics, blinatumomab is expected to be degraded into small peptides and amino acids via catabolic pathways.

Coadministration has not been studied. Bosentan is an inducer of CYP2C9 and CYP3A4 and may decrease daclatasvir concentrations. Daclatasvir may increase bosentan concentrations due to inhibition of OATP1B1. Avoid coadministration if possible. Caution and virological monitoring for efficacy is recommended if coadministered.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bosutinib is metabolised principally by CYP3A4 but daclatasvir is only a mild inducer of CYP3A4 and no clinically significant interaction is expected.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Brentuximab vedotin releases the active species MMAE within the tumour cell; MMAE is a substrate of CYP3A4 and possibly CYP2D6 and a weak inhibitor of CYP3A4. Daclatasvir is only a mild inducer of CYP3A4 and no clinically significant effect on MMAE is expected. Daclatasvir is primarily metabolised by CYP3A4 and concentrations may increase slightly due to weak inhibition of CYP3A4 by MMAE, but this is unlikely to be clinically relevant.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Brinozolamide is metabolised by CYP3A4 but daclatasvir is only a mild inducer of CYP3A4 and no clinically significant interaction is expected.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Brodalumab is degraded into small peptides. Brodalumab may modulate serum levels of some cytokines and may modestly increase the exposure of CYP450 substrates such as daclatasvir. However, based on data with midazolam (AUC increased by 24%), this is unlikely to be clinically significant.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Daclatasvir is an inhibitor of P-gp and OATP and mild inducer of CYP3A4, but these transporters/enzymes are not involved in the metabolism of bromazepam.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Bromperidol is metabolised by CYP3A4 but daclatasvir is only a mild inducer of CYP3A4 and no clinically significant interaction is expected.

Coadministration of buprenorphine/naloxone (8/2 to 24/6 mg once daily, individualised dose) and daclatasvir (60 mg once daily) was evaluated in opioid-dependent adults on stable buprenorphine/naloxone maintenance therapy. There was no clinically relevant effect on concentrations of buprenorphine (AUC, Cmax and Cmin increased by 31%, 30% and 20%, respectively) or norbuprenorphine (AUC, Cmax and Cmin increased by 62%, 65% and 46%, respectively). When compared to historical data, there was no clinically relevant effect on daclatasvir concentrations. No dose adjustment of daclatasvir or buprenorphine is required.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Calcium carbimide is a prodrug requiring catalase and hydrogen peroxide to generate the active metabolite. Calcium carbimide is an inhibitor of ALDH but this enzyme is not involved in the metabolism of daclatasvir.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Canagliflozin is primarily metabolised by UGTs 1A9 and 2B4 which are not affected by daclatasvir. Canagliflozin and daclatasvir are substrates and inhibitors of P-gp and concentrations of both drugs may increase, but this is unlikely to be of clinical significance.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as captopril is largely excreted in the urine (40-50% as unchanged drug, the rest as disulfide and other metabolites). It is transported by renal transporter OAT1 which is not affect by daclatasvir.

Coadministration is contraindicated. Induction of CYP3A4 and/or P-gp by carbamazepine may significantly decrease plasma concentrations of daclatasvir; this may lead to reduced therapeutic effect and potential virological failure. Note – a published case series of 6 patients who remained on an inducing antiepileptic with sofosbuvir 400 mg daily and daclatasvir 60 mg twice daily (n=2) or 60 mg three times daily (n=4) reported all patients achieved a sustained virologic response with no serious adverse events reported. Therapeutic drug monitoring was carried out in these patients to guide dose adjustment and in 1 patient who started on daclatasvir 60 mg BID increased to 60 mg TID due to low exposure. Although every effort to prevent concomitant use of daclatasvir and potent inducers should be made, these cases have demonstrated that clinical cure may still be achieved with an increased dose of daclatasvir (guided by TDM) in patients where coadministration cannot be avoided.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Carbimazole is a pro-drug which undergoes rapid and virtually complete metabolism to the active metabolite, thiamazole (also known as methimazole). Despite this potential hepatic metabolism very few data exist on carbimazole drug interactions and an interaction with daclatasvir is not expected. Thiamazole has been shown to have inhibitory effects on CYP3A4 in vitro, however, a clinically relevant effect is not anticipated.

Coadministration has not been studied. Carvediol and daclatasvir are substrates and inhibitors of P-gp and concentrations of both drugs may increase. Carvedilol can also commonly cause anaemia. Close monitoring is recommended for increased side effects and toxicities including dizziness, bradycardia and GI disturbances for carvedilol. [Note, the US Prescribing Information contraindicates carvedilol in patients with severe liver impairment and the European SmPC contraindicates it in patients with hepatic dysfunction.]

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

Coadministration has not been studied. Cat’s claw is a strong inhibitor of CYP3A4 in vitro and increased concentrations of daclatasvir may be expected. Coadministration should be avoided. If coadministration is absolutely necessary, consider dosing daclatasvir at 30mg.

Coadministration has not been studied but based on metabolism and clearance a clinically significant drug interaction is unlikely. Cefaclor is predominantly eliminated unchanged by the kidneys.

Coadministration has not been studied but based on metabolism and clearance a clinically significant drug interaction is unlikely. Cefadroxil is not metabolised and is predominantly eliminated unchanged by the kidneys.

Coadministration has not been studied but based on metabolism and clearance a clinically significant drug interaction is unlikely. Cefradine is not metabolised and is predominantly eliminated unchanged by the kidneys.

Coadministration has not been studied but based on metabolism and clearance a clinically significant drug interaction is unlikely. Ceftaroline is not metabolised by CYP enzymes and is primarily eliminated by the kidneys.

Coadministration has not been studied but based on metabolism and clearance, a clinically significant interaction is unlikely. Celecoxib is mainly metabolised by CYP2C9 and daclatasvir does not affect this enzyme. [Note, use in patients with severe liver impairment is contraindicated in the European SmPC and not recommended in the US Prescribing Information. In patients with moderate liver impairment (serum albumin 25-35 g/L, Child-Pugh Class B), celecoxib treatment should be started at half the recommended dose.]

Coadministration has not been studied. Cetirizine is metabolised only to a limited extent and is eliminated unchanged in the urine by glomerular filtration and tubular secretion. However cetirizine is also transported by P-gp and since daclatasvir is an inhibitor of this transporter there is the possibility of increased cetirizine exposure due to increased bioavailability. Monitoring may be required as clinically indicated.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Like other protein therapeutics, cetuximab is expected to be degraded into small peptides and amino acids via catabolic pathways.

Coadministration has not been studied but a clinically significant interaction is considered unlikely. Very little has been described about chlorambucil metabolism in humans but CYP450 enzymes are not involved.

Coadministration has not been studied but concentrations of daclatasvir may increase with systemic chloramphenicol due to inhibition of CYP3A4. When used topically in the eye, the concentrations achieved through systemic absorption are unlikely to cause a clinically significant interaction.

Coadministration has not been studied but a clinically significant interaction is unlikely. Chloroquine is metabolised by CYP2C8 and CYP3A4/5. Daclatasvir has no effect on CYP2C8 and is only a mild inducer of CYP3A4 so a pharmacokinetic interaction is unlikely at clinically relevant concentrations. Note, the European SPC and US Prescribing Information for chloroquine both recommend caution in impaired hepatic function.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Chlorpromazine is a substrate of CYPs 2D6 (major), 1A2, and 3A4 in vitro. Daclatasvir does not affect these enzymes. [Note, the European SmPC for chlorpromazine advises that its use should be avoided in patients with hepatic dysfunction.]

Co-administration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Chlorprothixene is metabolised by CYP2D6 which is not affected by daclatasvir. [Note, although no interaction is anticipated, ECG monitoring is mandatory prior to treatment with chlorprothixene.]

Coadministration of ciclosporin (400 mg single dose) and daclatasvir (60 mg once daily) had no clinically relevant effect on daclatasvir (AUC, Cmax and Cmin increased by 40%, 4% and 56%, respectively) or ciclosporin (AUC increased by 3%, Cmax decreased by 4%). No dose adjustment of ciclosporin or daclatasvir is required. However, clearance of HCV infection with DAAs may lead to changes in hepatic function, which may impact the safety and efficacy of sensitive comedications. Dose adjustments may be necessary.

Coadministration has not been studied, but based on metabolism and clearance a clinically significant pharmacokinetic interaction is unlikely. Cilazapril is rapidly converted to the active form, cilazaprilat, which is excreted unchanged in the urine. [Note, in patients with cirrhosis, a maximum dose of 0.5 mg/day is recommended as significant hypotension may occur.]

Coadministration has not been studied but may increase daclatasvir concentrations due to inhibition of CYP3A4 by cimetidine. The clinical significance of this is unknown. No a priori dose modification is recommended but monitoring may be required as clinically indicated. Cimetidine is also an inhibitor of the transporter OAT3 although daclatasvir concentrations are unlikely to be altered by this route.

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). No dose adjustment of daclatasvir or ciprofloxacin is required.

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 (Hofmann elimination).

Coadministration has not been studied but is expected to increase daclatasvir concentrations due to inhibition of CYP3A4 by clarithromycin. The dose of daclatasvir should be reduced to 30 mg once daily when coadministered with clarithromycin.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Clevidipine is rapidly metabolised by hydrolysis of the ester linkage and does not undergo CYP metabolism.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Clobazam is metabolised primarily by CYP3A4 and to a lesser extent by CYP2C19. Daclatasvir has no effect on CYP2C19 and is only a mild inducer of CYP3A4 so a pharmacokinetic interaction is unlikely at clinically relevant concentrations. Clobazam is a weak CYP3A4 inducer and could potentially decrease daclatsavir exposure to a very limited extent. However, this is unlikely to be clinically relevant.

Coadministration has not been studied but based on metabolism and clearance a pharmacokinetic interaction is unlikely. Clodronate is not metabolised and is primarily excreted unchanged by the kidney. However, if administered orally, clodronate should be taken more than two hours after and one hour before any other oral drugs. [Note: this interaction is not specific for daclatasvir, but for any medication taken with clodronate.]

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 by CYPs 2C19, 3A4, 2B6, and 1A2. Daclatasvir has no effect on CYPs 2C19, 2B6 or 1A2 and is only a mild inducer of CYP3A4 so a pharmacokinetic interaction is unlikely at clinically relevant concentrations. [Note, the European SmPC for clopidogrel contraindicates clopidogrel in severe hepatic impairment but the US Prescribing Information states no dose alteration.]

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. The metabolism of clotiapine has not been well characterised but is likely to involve CYP450 enzymes. Daclatasvir does not inhibit CYP450 enzymes and is only a mild inducer of CYP3A4.

Coadministration has not been studied but a clinically significant interaction is unlikely as colecalciferol undergoes extensive metabolism by multiple pathways, none of which is significantly affected by daclatasvir.

Coadministration has not been studied. Colestyramine may delay or reduce the absorption of drugs. Administration of other drugs should be at least 1 hour before or 4-6 hours after colestyramine. [Note: this interaction is not specific for daclatasvir, but for any medication taken with colestyramine.]

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Cyanocobalamin undergoes enterohepatic recycling and is excreted almost entirely in the urine.

Co-administration has not been studied but based on limited data for the metabolism and clearance of cyclizine, a clinically significant interaction is unlikely. Cyclizine undergoes hepatic metabolism which may include CYP2D6.

Coadministration has not been studied but is expected to increased dabigatran concentrations due to inhibition of P-gp by daclatasvir. Close monitoring is recommended when initiating treatment with daclatasvir in patients receiving dabigatran.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Danaparoid is renally excreted and no hepatic involvement was shown in animal studies.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dantron is absorbed from the small intestine and acts at the large intestine. 

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as dapagliflozin is metabolised by UGT1A9.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Like other protein therapeutics, daratumumab is expected to be degraded into small peptides and amino acids via catabolic pathways and is not anticipated to alter drug-metabolising enzymes.

Coadministration with darunavir/cobicistat has not been studied. Coadministration of daclatasvir and darunavir/ritonavir (800/100 mg once daily) decreased darunavir AUC, Cmax and Cmin by 10%, 3% and 2%; daclatasvir AUC increased by 41% and Cmax decreased by 23%. No dose adjustment is required with daclatasvir 60 mg once daily and darunavir/ritonavir (800/100 mg once daily or 600/100 mg twice daily). Similarly, no dose adjustment is required with darunavir/cobicistat.

Coadministration with Symtuza has not been studied. Coadministration of daclatasvir and darunavir/ritonavir (800/100 mg once daily) decreased darunavir AUC, Cmax and Cmin by 10%, 3% and 2%; daclatasvir AUC increased by 41% and Cmax decreased by 23%. No dose adjustment is required with daclatasvir 60 mg once daily and darunavir/ritonavir (800/100 mg once daily or 600/100 mg twice daily). Similarly, no dose adjustment is required with darunavir/cobicistat. Emtricitabine and tenofovir alafenamide do not interact with this metabolic pathway.

Coadministration of daclatasvir and darunavir/ritonavir (800/100 mg once daily) decreased darunavir AUC, Cmax and Cmin by 10%, 3% and 2%; daclatasvir AUC increased by 41% and Cmax decreased by 23%. No dose adjustment of daclatasvir 60 mg once daily or darunavir/ritonavir (800/100 mg once daily or 600/100 mg twice daily) is required.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Deferiprone is glucuronidated by UGT1A6 which is not affected by daclatasvir.

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. Daclatasvir is a weak inducer of CYP3A4. As no clinically relevant reduction in delamanid exposure was observed with efavirenz (an inducer of CYP3A4), a clinically significant interaction with daclatasvir is unlikely. [Note, delamanid is not recommended in patients with moderate to severe hepatic impairment.]

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Denosumab is not eliminated via hepatic metabolism but follows the immunoglobulin clearance pathway resulting in degradation to small peptides and individual amino acids.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Desvenlafaxine and daclatasvir are substrates of CYP3A4 and daclatasvir is a mild inducer of this enzyme, but a pharmacokinetic interaction is unlikely at clinically relevant concentrations.

Coadministration has not been studied. Dexamethasone is a substrate and moderate inducer of CYP3A4 at doses above 16 mg. Daclatasvir concentrations may decrease due to moderate induction of CYP3A4 by dexamethasone and may lead to the loss of efficacy of daclatasvir. The European SmPC says that coadministration with systemic dexamethasone is contraindicated. However, the US Prescribing Information advises to increase daclatasvir dose to 90 mg once daily  to counteract moderate CYP3A4 induction.

Coadministration has not been studied but based on limited data for metabolism and clearance a clinically significant interaction is unlikely. Note, the role of CYP450 in the metabolism of dexamfetamine has not been fully described.

Coadministration has not been studied but based on the metabolism and clearance a clinically significant interaction is unlikely. Dexketoprofen is mainly glucuronidated, with CYP mediated metabolism (CYP2C8/9) playing only a minor role. Daclatasvir is not expected to induce or inhibit UGTs or CYP2C8/2C9. [Note, use in patients with severe hepatic impairment (Child Pugh class C) is contraindicated in the European product label for dexketoprofen.]

Coadministration has not been studied but, based on metabolism and clearance, a clinically significant interaction is unlikely. Diazepam is metabolised to nordiazepam by CYPs 3A4 and 2C19 and then to temazepam predominantly by CYP3A4. Daclatasvir has no effect on CYP2C19 and is only a mild inducer of CYP3A4 so a pharmacokinetic interaction is unlikely at clinically relevant concentrations.

Coadministration has not been studied but based on metabolism and clearance a clinically significant pharmacokinetic interaction is unlikely. No dose adjustment of daclatasvir or didanosine is required.

Coadministration of digoxin (0.125 mg once daily) and daclatasvir (60 mg once daily) increase digoxin AUC, Cmax and Cmin by 27%, 65% and 18%, respectively, due to inhibition of P-gp by daclatasvir. Digoxin should be used with caution and the lowest dose of digoxin should be initially prescribed. Serum digoxin concentrations should be monitored and used for dose titration to obtain the desired clinical effect.

Coadministration has not been studied. A clinically significant effect on dihydroartemisinin is unlikely as it is metabolised by UGTs 1A9 and 2B7. However, dihydroartemisinin may induce CYP3A4 and could potentially decrease daclatasvir concentrations. The clinical significance of this potential interaction is unknown and close monitoring for decreased clinical response is recommended.

Coadministration has not been studied but may increase daclatasvir concentrations due to inhibition of CYP3A4 by diltiazem. Use with caution.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Diosmin is a naturally occurring flavonoid. Diosmin-containing products are available as dietary supplements or on prescription (in certain countries). Interaction studies suggest that diosmin may be a weak inhibitor of CYP3A4 and P-gp, but any effect on daclatasvir is unlikely to be clinically relevant.

Coadministration has not been studied but, based on metabolism and clearance, a clinically significant interaction is unlikely as diphenhydramine is metabolised by CYP2D6 and daclatasvir does not affect this enzyme. [Note, diphenhydramine should be used with caution in patients with moderate to severe hepatic impairment.]

Coadministration has not been studied but, based on metabolism and clearance, a clinically significant interaction is unlikely. Disopyramide and daclatasvir are substrates of CYP3A4 and daclatasvir is a mild inducer of this enzyme, but a pharmacokinetic interaction is unlikely at clinically relevant concentrations.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dofetilide is eliminated in the kidney by cationic secretion and is metabolized to a small extent by CYP3A4. Daclatasvir does not undergo significant renal clearance and is only a very weak inducer of CYP3A4.

Coadministration of dolutegravir (50 mg once daily) and daclatasvir (60 mg once daily) had no significant effect on daclatasvir AUC (2% decrease), Cmax (3% increase) or Cmin (6% increase). Dolutegravir AUC, Cmax and Cmin increased by 33%, 29% and 45%, respectively. No dose adjustment of daclatasvir or dolutegravir is required.

Coadministration with dolutegravir/rilpivirine has not been studied. Coadministration of dolutegravir (50 mg once daily) and daclatasvir (60 mg once daily) had no significant effect on daclatasvir AUC (2% decrease), Cmax (3% increase) or Cmin (6% increase). There was no clinically relevant change in dolutegravir exposure (AUC, Cmax and Cmin increased by 33%, 29% and 45%, respectively). No dose adjustment of daclatasvir or dolutegravir is required. Rilpivirine at a dose of 25 mg once daily is unlikely to have a clinically relevant effect on the exposure of medicinal products metabolised by CYP enzymes.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Donepezil is metabolised by CYP3A4 and CYP2D6 (minor) but daclatasvir is only a mild inducer of CYP3A4 and no clinically significant interaction is expected.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as daclatasvir is partly metabolized by CYP3A4 and mainly eliminated unchanged in bile.

Coadministration has not been studied but based on the metabolism and clearance a clinically significant interaction is unlikely. Daclatasvir is partly metabolized by CYP3A4 and mainly eliminated unchanged in bile. No interaction is expected with doravirine or lamivudine. Coadministration of tenofovir-DF (300 mg once daily) and daclatasvir (60 mg once daily) had no clinically relevant effect on daclatasvir AUC, Cmax or Cmin (increases of 10%, 6% and 15%, respectively). There was no clinically relevant effect on tenofovir AUC (10% increase), Cmax (5% decrease) or Cmin (17% increase).

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dosulepin is extensively metabolised in the liver, likely by CYP2D6 (major) and CYP3A4, but daclatasvir is only a weak inducer of CYP3A4 and no clinically significant interaction is expected. [Note: Dosulepin should be used with caution in mild to moderate hepatic impairment and avoided in severe hepatic impairment.]

Coadministration has not been studied but, based on metabolism and clearance, a clinically significant interaction is unlikely. Doxazosin is extensively metabolised by CYP3A4 and to a lesser extent 2D6 and 2C19. Daclatasvir has no effect on CYPs 2D6 or 2C19, and is only a mild inducer of CYP3A4 so a pharmacokinetic interaction is unlikely at clinically relevant concentrations. [Note, the European SmPC does not recommend doxazosin in severe hepatic impairment; the US Prescribing Information has a caution for use in hepatic impairment.]

Coadministration has not been studied but, based on metabolism and clearance, a clinically significant interaction is unlikely as doxepin is metabolised by CYPs 2C19, 2D6, 1A2 and 2C9 and daclatasvir does not affect these enzymes. [Note, the European and US product labels for doxepin advise caution and monitoring in patients with hepatic impairment as a dosage reduction may be required.]

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Doxylamine is metabolized primarily by CYP2D6, CYP1A2, and CYP2C9. Daclatasvir does not interact with these pathways.

Coadministration has not been studied. Droperidol is metabolized by CYP3A4 and CYP1A2 but daclatasvir is only a mild inducer of CYP3A4 and no clinically significant interaction is expected.

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 but interaction studies showed no clinically significant effect on the absorption of concomitantly administered oral medicinal products and no dose adjustment of comedications is recommended.

Coadministration has not been studied, but based on metabolism and clearance a clinically significant pharmacokinetic interaction is unlikely as duloxetine is metabolised by CYP1A2 and CYP2D6. [Note, duloxetine is contraindicated in patients with hepatic impairment as concentrations may increase due to decreased clearance of duloxetine.]

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Dupilimab is a protein and degrades to small peptides and individual amino acids. 

Coadministration has not been studied but, based on metabolism and clearance, a clinically significant interaction is unlikely. Dutasteride and daclatasvir are substrates of CYP3A4 and daclatasvir is a mild inducer of this enzyme, but a pharmacokinetic interaction is unlikely at clinically relevant concentrations. [Note, the European SmPC (but not the US Prescribing Information) cautions against dutasteride use in mild to moderate hepatic impairment and contraindicates it in severe hepatic impairment.]

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Ebastine is metabolised by CYP450 but daclatasvir is only a mild inducer of CYP3A4 and no clinically significant interaction is expected.

Coadministration has not been studied. Edoxaban is a substrate of P-gp and its active metabolite is a substrate of OATP1B1. Concentrations of edoxaban (and its active metabolite) may increase due to inhibition of P-gp and OATP1B1 by daclatasvir although the clinical relevance is unknown. Patients should be reminded to promptly report any signs of bleeding or bruising as with anyone who is prescribed DOACs. [Note: product labels state that rivaroxaban is contraindicated in patients with hepatic disease associated with coagulopathy and clinically relevant bleeding risk, including cirrhotic patients with Child Pugh B and C.] 

Coadministration of efavirenz (600 mg once daily) and daclatasvir (60 or 120 mg once daily) decreased daclatasvir AUC, Cmax and Cmin by 32%, 17% and 59%, respectively (results dose-normalised to 60 mg dose). The dose of daclatasvir should be increased to 90 mg once daily when coadministered with efavirenz.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Eliglustat is metabolised primarily by CYP2D6 and to a lesser extent by CYP3A4. Daclatasvir is only a mild inducer of CYP3A4 and no clinically significant interaction is expected.

Coadministration has not been studied but concentrations of both drugs may increase as both drugs are substrates and inhibitors of the transporter OATP1B1. Caution and close monitoring is required.

Coadministration has not been studied but is expected to increase daclatasvir concentrations due to inhibition of CYP3A4 by cobicistat. The dose of daclatasvir should be reduced to 30 mg once daily when coadministered with cobicistat. Elvitegravir, emtricitabine and tenofovir alafenamide are unlikely to significantly interact with daclatasvir.

Coadministration has not been studied but is expected to increase daclatasvir concentrations due to inhibition of CYP3A4 by cobicistat. The dose of daclatasvir should be reduced to 30 mg once daily when coadministered with cobicistat.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Empagliflozin is metabolised by UGTs and is a substrate of P-gp, BCRP, OAT3 and OATP1B1/1B3. Although daclatasvir is an inhibitor of P-gp and OATP, data with verapamil (a P-gp inhibitor) and rifampicin (a OATP1B1/1B3 inhibitor) suggest a clinically relevant effect on empagliflozin is unlikely.

Coadministration has not been studied but based on metabolism and clearance a clinically significant pharmacokinetic interaction is unlikely. No dose adjustment of daclatasvir or emtricitabine is required.

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. 

Coadministration with emtricitabine/tenofovir-DF has not been studied. Based on metabolism and clearance a clinically significant interaction with emtricitabine is unlikely. Coadministration of tenofovir-DF (300 mg once daily) and daclatasvir (60 mg once daily) had no clinically relevant effect on daclatasvir AUC, Cmax or Cmin (increases of 10%, 6% and 15%, respectively). There was no clinically relevant effect on tenofovir AUC (10% increase), Cmax (5% decrease) or Cmin (17% increase). No dose adjustment of daclatasvir or emtricitabine/tenofovir-DF is required.

Coadministration has not been studied, but based on metabolism and clearance a clinically significant pharmacokinetic interaction is unlikely. Enalapril is a prodrug and is hydrolysed in the liver to enalaprilat.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Daclatasvir is metabolised by CYP3A4. Entecavir is not hepatically metabolised and the potential for interactions via this route is low. Entecavir is eliminated primarily in the urine by glomerular filtration and tubular secretion by OAT1. No dose adjustment of daclatasvir or entecavir is required.

Coadministration has not been studied but based on metabolism and clearance, a clinically significant interaction is unlikely. Epoprostenol is rapidly hydrolysed; there does not appear to be any involvement with CYP isoenzymes or transporter proteins.

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.

Coadministration has not been studied but, based on metabolism and clearance, a clinically significant interaction is unlikely. Ergometrine and daclatasvir are substrates of CYP3A4 and daclatasvir is a mild inducer of this enzyme, but a pharmacokinetic interaction is unlikely at clinically relevant concentrations.

Coadministration has not been studied. Erlotinib is a substrate for CYP3A4 and P-gp. Daclatasvir is only a mild inducer of CYP3A4 and no effect on erlotinib is expected by this pathway. However, concentrations may increase due to inhibition of P-gp by daclatasvir. Use with caution and with close monitoring for erlotinib mediated toxicity. A dose reduction may be required for erlotinib, particularly if toxicity is observed.

Coadministration has not been studied but modest increases in concentrations of daclatasvir are expected due to inhibition of CYP3A4 by erythromycin. No clinically relevant effect on erythromycin concentrations is expected. No dose adjustment of daclatasvir or erythromycin is required.

Coadministration of escitalopram (10 mg once daily) and daclatasvir (60 mg once daily) had no clinically relevant effect on concentrations of daclatasvir (AUC, Cmax and Cmin increased by 12%, 14% and 23%, respectively) or escitalopram (AUC and Cmin increased by 5% and 10%, no change in Cmax). No dose adjustment of daclatasvir or escitalopram is required.

Coadministration has not been studied. Modest to moderate inducers of CYP3A4 (such as eslicarbazepine) are expected to decrease daclatasvir concentrations and may lead to the loss of efficacy of daclatasvir. Consider if there is a suitable alternative anticonvulsant therapy to avoid potential interaction. If coadministration is necessary, the dose of daclatasvir should be increased to 90 mg once daily when coadministered with moderate inducers of CYP3A4.

Coadministration has not been studied but no clinically relevant interaction is expected with proton pump inhibitors. A study with omeprazole and daclatasvir showed no dose adjustment of daclatasvir is required.

Coadministration has not been studied but based on metabolism and clearance, a clinically significant interaction is unlikely. Estazolam and daclatasvir are substrates of CYP3A4 and daclatasvir is a mild inducer of this enzyme, but a pharmacokinetic interaction is unlikely at clinically relevant concentrations.

Coadministration has not been studied but based on metabolism and clearance, a clinically significant interaction is unlikely. Estramustine is dephosphorylated and minimal data show it not to undergo any form of CYP metabolism.

Coadministration has not been studied but based on metabolism and clearance a clinically significant pharmacokinetic interaction is unlikely. [Note, there is a concern of hepatotoxic adverse events in patients with HCV receiving anti-TNF agents. Use with caution and monitor liver enzymes and HCV viral load.]

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. In vitro data suggest etelcalcetide is not metabolised by CYP450 nor transported by common transporter proteins.

Coadministration daclatasvir (60 mg once daily) and a once daily triphasic oral contraceptive containing ethinylestradiol (35 µg) and norgestimate (0.180/0.215/0.250 mg for 7/7/7 days) was studied. There was no clinically relevant effect on the concentrations of ethinylestradiol (AUC and Cmax increased by 1% and 11%), norelgestromin (AUC and Cmax increased by 12% and 6%) or norgestrel (AUC and Cmax increased by 12% and 7%). An oral contraceptive containing ethinylestradiol 35 μg and norgestimate 0.180/0.215/0.250 mg is recommended with daclatasvir. Other oral contraceptives have not been studied.

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. Daclatasvir is a mild inducer of this enzyme, but a pharmacokinetic interaction is unlikely at clinically relevant concentrations.

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 and is coformulated in the CVR with ethinylestradiol which is released at a dose of 0.015 mg/day. Ethinylestradiol is mainly metabolized by hydroxylation. Daclatasvir is a mild CYP3A4 inducer, but a pharmacokinetic interaction is unlikely at clinically relevant concentrations. Coadministration of daclatasvir with ethinylestradiol (in combination with another oral progestogen norgestimate) resulted in no clinically relevant effects on exposure of ethinylestradiol, norelgestromin or norgestrel.  

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Etoposide is mainly metabolised by CYP3A4 and UGT1A1, but daclatasvir is only a mild inducer of CYP3A4 and no clinically significant interaction is expected.

Coadministration has not been studied but is expected to decrease daclatasvir concentrations due induction of CYP3A4 by etravirine. The European SmPC says that coadministration is not recommended due to lack of data, but the US Prescribing information says that daclatasvir can be increased to 90 mg once daily.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Eucalyptus is a mild to moderate inhibitor of CYP3A4, however, a clinically relevant effect is unlikely at doses used for supplementation.

Coadministration has not been studied but may increase everolimus concentrations due to P-gp inhibition by daclatasvir. Concentration of daclatasvir may also increase due to inhibition of CYP3A4 by everolimus. If coadministration cannot be avoided, therapeutic drug monitoring of everolimus should be performed along with close monitoring for daclatasvir related side effects and toxicities.

Coadministration has not been studied but based on metabolism and clearance, a clinically significant interaction is unlikely. Exemestane is metabolised by CYP3A4 but coadministration with ketoconazole (a potent CYP3A4 inhibitor) showed no clinically significant effects and no effect is expected as daclatasvir is only a mild inducer of CYP3A4.

Coadministration with exenatide has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as exenatide is eliminated via glomerular filtration. However, as exenatide slows gastric emptying it is advisable to take daclatasvir at least 1 hour before immediate-release exenatide injection. [Note: this interaction is not specific for daclatasvir, but for any medication taken with exenatide.]

Coadministration has not been studied, but based on metabolism and clearance a clinically significant interaction is unlikely as ezetimibe is primarily metabolized in the small intestine and liver via glucuronidation. [Note, use of ezetemibe is not recommended in moderate to severe hepatic dysfunction.]

Coadministration of famotidine (40 mg single dose) and daclatasvir (60 mg single dose) had no clinically relevant effect on daclatasvir (AUC, Cmax and Cmin decreased by 18%, 44% and 11%, respectively). No dose adjustment of daclatasvir is required.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Febuxostat is extensively metabolised by multiple P450 (CYPs 1A1, CYP1A2, CYP2C8 and CYP2C9) and UGT enzymes (UGTs 1A1, 1A8, and 1A9). A clinically significant interaction is unlikely as febuxostat is metabolised by multiple pathways.

Coadministration has not been studied but may increase felodipine concentrations due to inhibition of P-gp by daclatasvir. Caution is warranted and close monitoring of blood pressure and heart rate is recommended. Although felodipine is a substrate of CYP3A4, as daclatasvir is only a mild inducer of CYP3A4 a pharmacokinetic interaction by this mechanism is unlikely at clinically relevant concentrations.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely as fenofibrate is metabolised by multiple enzyme pathways (esterases, UGT2B7 and UGT1A1). [Note, fenofibrate is contraindicated in severe hepatic disease in its European SmPC, and its US Prescribing Information contraindicates it in active liver disease.]

Coadministration has not been studied. Fexofenadine is a substrate of P-gp and OATP and concentrations may increase due to inhibition of P-gp and OATP1B1 by daclatasvir. The clinical significance of this is unknown. Close monitoring is recommended for adverse effects.

Coadministration has not been studied but, based on metabolism and clearance, a clinically significant interaction is unlikely. Flecainide and daclatasvir are substrates of CYP3A4 and daclatasvir is a mild inducer of this enzyme, but a pharmacokinetic interaction is unlikely at clinically relevant concentrations.

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. Daclatasvir is only a mild inducer of CYP3A4 and no clinically significant interaction is expected.

Coadministration has not been studied. Flucloxacillin is mainly eliminated renally, partly by glomerular filtration and partly by active secretion via OAT1. Daclatasvir is metabolized by CYP3A4. Flucloxacillin is thought to be a weak inducer of CYP3A4, particularly at higher doses (>2-3 g daily). A modest reduction in plasma concentrations of daclatasvir may be observed but this is unlikely to be clinically relevant unless flucloxacillin is prescribed at higher doses for a prolonged course (>10-14 days).

Coadministration has not been studied but modest increases in concentrations of daclatasvir are expected due to inhibition of CYP3A4 by fluconazole. No clinically relevant effect on fluconazole concentrations is expected. No dose adjustment of daclatasvir or fluconazole is required.

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

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Fluinidone is metabolised by CYP2C9 (major) and CYP1A2 (minor) which are not affected by daclatasvir.

Coadministration has not been studied but based on metabolism and clearance, a clinically significant interaction is unlikely as fluoxetine is mainly metabolised by CYP2D6 and daclatasvir does not affect this enzyme. Note, a lower or less frequent dose should be considered in cases of hepatic insufficiency.

Coadministration has not been studied but, based on metabolism and clearance, a clinically significant interaction is unlikely. Flurazepam and daclatasvir are substrates of CYP3A4 and daclatasvir is a mild inducer of this enzyme, but a pharmacokinetic interaction is unlikely at clinically relevant concentrations. No dose adjustment of benzodiazepines is required when coadministered with daclatasvir.

Coadministration has not been studied but is expected to increase fluvastatin concentrations due to inhibition of OATP1B1 and BCRP by daclatasvir. Use with caution. Monitor for fluvastatin-associated adverse events such as myopathy. Note, the use of fluvastatin in active liver disease is contraindicated.

Coadministration has not been studied but based on metabolism and clearance, a clinically significant interaction is unlikely. Fluvoxamine is metabolised mainly by CYP2D6 and to a lesser extent by CYP1A2 and daclatasvir does not affect these enzymes. Fluvoxamine is an inhibitor of CYP3A4, but any increase in daclatasvir concentrations is unlikely to be of clinical significance.

Coadministration has not been studied but is expected to increase daclatasvir concentrations due to inhibition of CYP3A4 by fosamprenavir/ritonavir. The dose of daclatasvir should be reduced to 30 mg once daily.

Coadministration has not been studied but based on metabolism and clearance a clinically significant pharmacokinetic interaction is unlikely. Fosinopril is a prodrug metabolised in the liver by a non-CYP mechanism to the active metabolite.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Gefitinib is metabolised by CYP3A4 but daclatasvir is only a mild inducer of CYP3A4 and no clinically significant interaction is expected.

Coadministration has not been studied, but based on metabolism and clearance a clinically significant pharmacokinetic interaction is unlikely. Gemfibrozil is metabolised by UGT2B7 and daclatasvir does not affect this enzyme. [Note, use of gemfibrozil in hepatic impairment is contraindicated.]

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Although in vitro data show gingerols moderately inhibit CYP3A4, a clinically relevant effect on DAA exposure is unlikely at standard dietary/supplement dosage.

Co-administration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely with standard doses (up to 240 mg) of Ginkgo biloba.

Glecaprevir/pibrentasvir is a complete regimen. There are no data to support the coadministration with another NS5A agent such as daclatasvir.

Coadministration has not been studied. Glibenclamide is metabolized by CYP3A4 but daclatasvir is only a mild inducer of CYP3A4 and no clinically significant interaction is expected.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Gliclazide is metabolized by CYPs 2C19 and 2C9 which are not affected by daclatasvir.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Glimepiride is metabolised by CYP2C9 and daclatasvir does not affect this enzyme.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Glipizide is mainly metabolised by CYP2C9 and daclatasvir does not affect this enzyme.

Coadministration has not been studied. Glycerol phenylbutyrate is metabolised by pancreatic lipases, beta-oxidation, and glutamine conjugation, then eliminated in the urine. Glycerol phenylbutyrate has been shown to be a weak inducer of CYP3A4. This is unlikely to be clinically significant but should be considered in the event of a suboptimal response to HCV treatment. 

Coadministration has not been studied. Concentrations of daclatasvir may increase due to CYP3A4 inhibition by goldenseal. No a priori dose change is required but monitor for increased daclatasvir concentrations and use with caution.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. There is minimal metabolism of goserelin acetate and no clinically relevant accumulation with higher doses of the implant. Goserelin acetate is renally cleared with no dose alteration required in renal or hepatic impairment.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Granisetron is metabolised by CYP3A4 but daclatasvir is only a mild inducer of CYP3A4 and no clinically significant interaction is expected.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Studies have shown that CYP3A4 inhibition by grape seed extract is mild, indicating a clinically relevant effect is unlikely.

Coadministration has not been studied but based on metabolism and clearance a clinically significant interaction is unlikely. Studies have shown variable CYP involvement with green tea metabolism but the overall effect is likely negligible. However, based on some conflicting data indicating possible CYP3A4 inhibition, consider monitoring for additional side effects of daclatasvir at high dose repeated use of green tea.