Примери за използване на Ribociclib на Английски и техните преводи на Български
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Ribociclib 600 mg N=248.
Time(months) Ribociclib Placebo.
Ribociclib is primarily metabolised by CYP3A4.
The absolute bioavailability of ribociclib is not known.
Ribociclib has not been evaluated in male fertility studies.
Drug-drug interaction between ribociclib and letrozole.
Ribociclib was the major circulating drug-derived entity in plasma.
Censoring times Ribociclib(N=334) Placebo(N=334).
Ribociclib has no potential for time-dependent inhibition of CYP1A2, CYP2C9, and CYP2D6.
Substances that may increase ribociclib plasma concentrations.
Ribociclib is not a substrate for hepatic uptake transporters OATP1B1, OATP1B3 or OCT-1 in vitro.
In vitro data are not sufficient to exclude a potential of ribociclib to induce CYP2B6 via CAR.
The exposure to ribociclib was higher in milk than in plasma.
These are known to inhibit cytochrome CYP3A4 enzymes andmay increase the exposure to ribociclib.
The effect of a moderate CYP3A4 inducer on ribociclib exposure has not been studied.
Ribociclib has not been studied in breast cancer patients with moderate or severe hepatic impairment.
Examples used for breast cancer include lapatinib,palbociclib, ribociclib, and everolimus(see below).
The efficacy and safety of ribociclib have not been studied in patients with critical visceral disease.
Therefore, medicinal products that can influence CYP3A4 enzyme activity may alter the pharmacokinetics of ribociclib.
Each film-coated tablet contains ribociclib succinate equivalent to 200 mg ribociclib.
Ribociclib showed foetotoxicity and teratogenicity at doses which did not show maternal toxicity in the rats or rabbits.
In vitro andin vivo studies indicated ribociclib is eliminated primarily via hepatic metabolism mainly via CYP3A4 in humans.
There are two other drugs in this class that are approvedfor certain patients with breast cancer,palbociclib approved in February 2015 and ribociclib approved in March 2017.
The pharmacokinetics of ribociclib in breast cancer patients with severe renal impairment have not been studied.
Data in subjects with ESRD are limited(n=3) but indicate a similar orsomewhat larger increase in ribociclib exposure compared to subjects with severe renal impairment.
No dose adjustments of ribociclib are required at initiation of treatment with mild or moderate CYP3A4 inhibitors.
Physiologically-based pharmacokinetic simulations suggested that a moderate CYP3A4 inducer(efavirenz)may decrease steady-state ribociclib Cmax and AUC by 51% and 70%, respectively.
Based on animal studies, ribociclib may impair fertility in males of reproductive potential(see section 5.3).
Data from a clinical study in patients with breast cancer indicated no clinically relevant effects of fulvestrant on ribociclib exposure following co-administration of these medicinal products.
Phase II conjugates of ribociclib phase I metabolites involved N-acetylation, sulfation, cysteine conjugation, glycosylation and glucuronidation.