Examples of using Sofosbuvir in English and their translations into Slovenian
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Sofosbuvir(400 mg once daily)/.
Use with ledipasvir and sofosbuvir.
Median sofosbuvir EC50, nM(range).
See also under Use with ledipasvir and sofosbuvir below.
Monotherapy with Sofosbuvir is not recommended;
Each analogue contains in its composition a certain amount of ledipasvir and sofosbuvir.
Ciclosporin(600 mg single dose)/ sofosbuvir(400 mg single dose)f.
Sofosbuvir and GS-331007 AUCs are near dose-proportional over the dose range of 200 mg to 1,200 mg.
Previously treated adults who have failed on sofosbuvir+ ribavirin± PEG-IFN.
Sofosbuvir is a substrate of drug transporter P-gp and breast cancer resistance protein(BCRP) while GS-331007 is not.
The clinical data to support the use of Daklinza and sofosbuvir in patients infected with HCV genotypes 4 and 6 are limited.
Sofosbuvir and GS-331007 AUCs are near dose proportional over the dose range of 200 mg to 400 mg.
The highest documented doses of ledipasvir and sofosbuvir were 120 mg twice daily for 10 days and a single dose of 1,200 mg, respectively.
Sofosbuvir and GS-331007 AUC0-24 and Cmax were similar in healthy adult subjects and patients with HCV infection.
The highest documented doses of Ledipasvir and Sofosbuvir are 120 mg twice per day for 10 days, and a single dose of 1200 mg, respectively.
Sofosbuvir and GS-331007 are not substrates or inhibitors of UGT1A1 or CYP3A4, CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, and CYP2D6 enzymes.
Table 4: Adverse drug reactions identified with sofosbuvir in combination with ribavirin or peginterferon alfa and ribavirin.
The sofosbuvir resistance-associated substitution S282T emerged in only 1 non-SVR12 patient infected with genotype 3.
In clinical studies of Daklinza in combination with sofosbuvir with or without ribavirin, 2% of patients had Grade 3 haemoglobin decreases;
Sofosbuvir and GS-331007 are not inhibitors of P-gp and BCRP and thus are not expected to increase exposures of drugs that are substrates of these transporters.
The AUC0-inf of GS-331007 in patients with ESRD administered with sofosbuvir 1 hour before or 1 hour after haemodialysis was at least 10-fold and 20-fold higher.
Sofosbuvir and GS-331007 are not inhibitors of P-glycoprotein and BCRP, so the effect of drugs that are substrates for these transporters is not expected to increase.
The moderate or high fat meal increased sofosbuvir AUC0-inf by 60% and 78%, respectively, but did not substantially affect the sofosbuvir Cmax.
The sofosbuvir resistance-associated substitution S282T was not detected in the baseline NS5B sequence of any patient in Phase 3 studies by population or deep sequencing.
The antiviral effect of sofosbuvir in vitro against less common genotypes 4, 5 and 6 was similar to that observed in genotypes 1, 2 and 3.
Increase in sofosbuvir exposure observed in the pharmacokinetic substudy is not clinically relevant.
The majority of the sofosbuvir dose recovered in urine was GS-331007(78%) while 3.5% was recovered as sofosbuvir.
GS-461203(active metabolite sofosbuvir) is not an inhibitor of human DNA and RNA polymerase, nor is it an inhibitor of mitochondrial RNA polymerase.
The efficacy of ledipasvir/sofosbuvir inpatients who had previously failed treatment with sofosbuvir+ ribavirin± PEG-IFN is supported by two clinical studies.