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phosphorylation
phosphorilering

oxidative phosphorylation
oxydativ fosforylering

kinase profile of nilotinib (phosphorylation ic50 nm)
nilotinibskinaseprofil (fosforylation ic50 nm)

erlotinib potently inhibits the intracellular phosphorylation of egfr.
erlotinib hæmmer effektivt den intracellulære phosphorylering af egfr.

table 4 kinase profile of nilotinib (phosphorylation ic50 nm)
tabel 4 nilotinibs kinaseprofil (fosforylation ic50 nm)

lamivudine may inhibit the intracellular phosphorylation of zalcitabine when the two medicinal products are used concurrently.
lamivudin kan hæmme den intracellulære fosforylering af zalcitabin, når de to lægemidler bruges samtidigt.

possible interaction between lamivudine and cladribine due to inhibition of intracellular phosphorylation of cladribine by lamivudine.
mulig interaktion mellem lamivudin og cladribin på grund af hæmning af lamivudins intracellulære fosforylering af cladribin.

stavudine’s influence on the phosphorylation kinetics of nucleoside analogues other than zidovudine has not been investigated.
stavudins påvirkning af nukleosidanalogers fosforyleringskinetik, bortset fra zidovudin, er ikke undersøgt.

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.
in vitro hæmmer lamivudin den intracellulære fosforylering af cladribin, hvilket kan medføre en potentiel risiko for manglende effekt af cladribin, hvis kombinationen anvendes klinisk.

fingolimod is transformed in humans by reversible stereoselective phosphorylation to the pharmacologically active (s)-enantiomer of fingolimod phosphate.
fingolimod omdannes hos mennesker ved en reversibel, stereoselektiv fosforylering til den farmakologisk aktive (s)-enantiomer fingolimodphosphat.

intracellular hydrolytic prodrug cleavage catalysed by enzymes including carboxylesterase 1 and sequential phosphorylation steps catalysed by nucleotide kinases result in formation of the pharmacologically active uridine nucleoside analogue triphosphate.
intracellulær hydrolytisk prodrug- kløvning katalyseret af enzymer, herunder carboxylesterase 1 og sekventiel fosforyleringstrinkatalyseret af nukleotidkinaser fører til dannelsen af det farmakologisk aktive uridin- nukleosidanalog-triphosphat.

tenofovir is then converted to the active metabolite, tenofovir diphosphate, by constitutively expressed cellular enzymes through two phosphorylation reactions in both resting and activated t cells.
tenofovir omdannes så til den aktive metabolit, tenofovirdiphosphat, af konstitutivt eksprimerede celleenzymer via to phosphoryleringsreaktioner i såvel hvilende som aktiverede t-celler.

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.
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.

1) a reversible phosphorylation pathway; 2) a degradative pathway involving deribosylation and amide hydrolysis to yield a triazole carboxyacid metabolite.
1) en reversibel phosphorylering; 2) en nedbrydning, der involverer deribosylation og amidhydrolyse til at danne en triazolcarboxylsyremetabolit.

the metabolic activation pathway involves sequential hydrolysis of the carboxyl ester moiety catalysed by human cathepsin a or carboxylesterase 1 and phosphoramidate cleavage by histidine triad nucleotide-binding protein 1 followed by phosphorylation by the pyrimidine nucleotide biosynthesis pathway.
den metaboliske aktiveringsvej omfatter sekventiel hydrolyse af carboxylesterdelen, hvilket katalyseres af humant cathepsin a eller carboxylesterase 1 og phosphoramidat-kløvning af histidin-triad nukleotid-bindende protein 1, efterfulgt af phosphorylering af pyrimidin-nukleotid-biosyntesevejen.

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.
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.

in vivo, pazopanib inhibited vegf-induced vegfr-2 phosphorylation in mouse lungs, angiogenesis in various animal models, and the growth of multiple human tumour xenografts in mice.
in vivo hæmmede pazopanib vegf-induceret fosforylering af vegfr-2 i muselunger, angiogenese i forskellige dyremodeller og vækst af flere humane tumor xenografter hos mus.

by day 14, combined plasma concentrations of sunitinib and is active metabolite are 62.9 - 101 ng/ ml which are target concentrations predicted from preclinical data to inhibit receptor phosphorylation in vitro and result in tumour stasis/ growth reduction in vivo.
på dag 14 er den kombinerede plasmakoncentration af sunitinib og dets aktive hovemetabolit 62, 9- 101 ng/ ml dette er målkoncentrationen fra de prækliniske data for at kunne hæmme receptorfosforylering in vitro, hvilket resulterer i tumorstase/ vækstreduktion in vivo.