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fingolimod omdannes hos mennesker ved en reversibel, stereoselektiv fosforylering til den farmakologisk aktive (s)-enantiomer fingolimodphosphat.
fingolimod is transformed in humans by reversible stereoselective phosphorylation to the pharmacologically active (s)-enantiomer of fingolimod phosphate.
in vitro hæmmer lamivudin den intracellulære fosforylering af cladribin, hvilket kan medføre en potentiel risiko for manglende effekt af cladribin, hvis kombinationen anvendes klinisk.
in vitro lamivudine inhibits the intracellular phosphorylation of cladribine leading to a potential risk of cladribine loss of efficacy in case of combination in the clinical setting.
crizotinib udviste koncentrationsafhængig hæmning af kinaseaktivitet af alk, ros1 og c-met i biokemiske test og hæmmede fosforylering og modulerede kinaseafhængige fænotyper i cellebaserede test.
crizotinib demonstrated concentration-dependent inhibition of the kinase activity of alk, ros1, and c-met in biochemical assays and inhibited phosphorylation and modulated kinase-dependent phenotypes in cell-based assays.
da interaktion med lægemidler, som gennemgår intracellulær fosforylering, som fx antivirale stoffer, eller med hæmmere af adenosinoptagelse kan forventes, tilrådes samtidig brug af disse og cladribine ikke.
since interactions with drugs undergoing intracellular phosphorylation, such as antiviral agents, or with inhibitors of adenosine uptake may be expected, their concomitant use with cladribine is not recommended.
zidovudin og stavudin fosforyleres ved det cellulære enzym (thymidin kinase), som fortrinsvis fosforylerer zidovudin og dermed øger fosforyleringen af stavudin til dets aktive trifosfat form.
zidovudine and stavudine are phosphorylated by the cellular enzyme (thymidine kinase), which preferentially phosphorylates zidovudine, thereby decreasing the phosphorylation of stavudine to its active triphosphate form.