Dasabuvir is an antiviral drug used in the treatment of chronic hepatitis C virus (HCV) infection.
ChEBI: A member of the class of pyrimidone, which is (as the monohydrate of its sodium salt) in combination with ombitasvir, paritaprevir and ritonavir (under the trade name Viekira Pak) for treatment of chronic hepatitis C virus genotype 1 infection as well as c
rrhosis of the liver.
Treatment of chronic hepatitis C infection
Potentially hazardous interactions with other drugs
Antibacterials: avoid concomitant use with
clarithromycin and telithromycin; concentration
possibly reduced by rifampicin - avoid.
Antidepressants: concentration possibly reduced by
St John’s wort - avoid.
Antiepileptics: concentration reduced by
carbamazepine - avoid; concentration possibly
reduced by fosphenytoin, phenobarbital, phenytoin
and primidone - avoid.
Antifungals: concentration of both drugs increased
with ketoconazole and possibly itraconazole and
posaconazole - avoid.
Diuretics: concentration of furosemide increased
(reduce furosemide dose).
Immunosuppressants: increases concentration of
ciclosporin (reduce ciclosporin dose by a fifth);
everolimus (avoid); sirolimus and tacrolimus (reduce
dose and use only if benefit outweighs risk - see
SPC).
Lipid-regulating drugs: avoid with atorvastatin,
gemfibrozil and simvastatin; concentration of
rosuvastatin increased (reduce dose of rosuvastatin).
Oestrogens: avoid concomitant use with
ethinylestradiol.
Dasabuvir is mainly metabolised by CYP2C8 and to
a lesser extent by CYP3A. Seven metabolites were
identified in plasma. The most abundant plasma
metabolite was M1, which represented 21% of drugrelated radioactivity (AUC) in circulation following single
dose; it is formed via oxidative metabolism predominantly
by CYP2C8.
Following a 400 mg 14C-dasabuvir dose, approximately
94% of the radioactivity was recovered in faeces with
limited radioactivity (approximately 2%) in urine.
Unchanged dasabuvir accounted for 26.2% and M1 for
31.5% of the total dose in faeces. M1 is mainly cleared
through direct biliary excretion with the contribution of
UGT-mediated glucuronidation and, to a small extent,
oxidative metabolism.
