Increased conc of P-gp (eg, digoxin, dabigatran etexilate), BCRP (eg, rosuvastatin), OATP1B1 & OATP1B3 substrates. Decreased plasma conc w/ strong P-gp &/or strong CYP2B6, CYP2C8, or CYP3A4 inducers (eg, carbamazepine, phenobarb, phenytoin, rifampicin, rifabutin, St. John's wort); moderate P-gp &/or moderate CYP inducers (eg, efavirenz, modafinil, oxcarbazepine, rifapentine). Increased plasma conc w/ P-gp or BCRP inhibitors. Increased velpatasvir plasma conc w/ OATP, CYP2B6, CYP2C8, or CYP3A4 inhibitors. Close monitoring of INR is recommended in patients treated w/ vit K antagonists. Altered pharmacokinetics of drugs metabolized by the liver [eg, immunosuppressive agents (eg, ciclosporin & tacrolimus)]. Decreased velpatasvir conc w/ acid reducing agents including antacids (Al or Mg hydroxide, Ca carbonate), H2
-receptor antagonists (famotidine, cimetidine, nizatidine, ranitidine), proton pump inhibitors (omeprazole, lansoprazole, rabeprazole, pantoprazole, esomeprazole). May result in serious symptomatic bradycardia when sofosbuvir is co-administered w/ amiodarone. Increased exposure of tenofovir disoproxil fumarate. Potential increased conc of statins other than atorvastatin & pravastatin.