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antibodies are cleared principally by catabolism.
antikorpi jiġu mneħħija prinċipalment minn kataboliżmu.

allopurinol and other xanthine oxidase inhibitors decrease the rate of catabolism of
allopurinol u inibituri oħra ta’ xanthine oxidase jnaqqsu r-rata ta’ kataboliżmu ta’ 6–mercaptopurine.

empliciti is an igg1 monoclonal antibody, which is principally cleared by catabolism.
empliciti huwa antikorp monoklonali igg1, li jitneħħa prinċipalment permezz tal-kataboliżmu.

antibody fragments are known to be eliminated mainly by proteolytic catabolism in the kidney.
frammenti ta' antikorpi huma magħrufin li jiġu eliminati prinċipalment b'kataboliżmu proteolitiku fil-kliewi.

dulaglutide is presumed to be degraded into its component amino acids by general protein catabolism pathways.
wieħed jassumi li dulaglutide jiddiżintegra f’komponenti ta’ amino acids li huwa magħmul minnhom permezz ta’ rotot ġenerali ta’ kataboliżmu tal-proteini.

as with other large proteins elimination of rilonacept is expected to be via proteolytic catabolism and target mediated clearance.
bħal fil-każ ta’ proteini kbar oħrajn, l-eliminazzjoni ta’ rilonacept hi mistennija li tkun permezz ta’ kataboliżmu proteolitiku u tneħħija medjata mill-mira li trid tintlaħaq.

no direct effect of hepatic function on the pharmacokinetics of reslizumab is expected because antibodies are principally cleared by catabolism.
l-ebda effett dirett tal-funzjoni tal- fwied mhu mistenni fuq il-farmakokinetika ta’ reslizumab, minħabba li l-antikorpi jitneħħew l-aktar permezz ta’ kataboliżmu.

the majority of igg elimination occurs via intracellular catabolism, following fluid-phase or receptor mediated endocytosis.
il-biċċa l-kbira tal-eliminazzjoni igg sseħħ permezz ta’ kataboliżmu intraċellulari, wara endoċitożi permezz ta’ fażi fluwida jew riċettur.

as an igg1 monoclonal antibody, daclizumab is expected to undergo catabolism to peptides and amino acids in the same manner as endogenous igg.
bħala antikorp monoklonali igg1, daclizumab hu mistenni li jgħaddi minn kataboliżmu għal peptides u amino acids bl-istess mod bħal igg endoġenu.

mucopolysaccharide storage disorders are caused by the deficiency of specific lysosomal enzymes required for the catabolism of glycosaminoglycans (gags).
problemi tal-ħażna tal-mucopolysaccharide huma kkawżati mid-defiċjenza ta’ enzimi lisosomali speċifiċi li huma meħtieġa għall-kataboliżmu ta’ glycosaminoglycans (gags).

by inhibiting the normal catabolism of tyrosine in patients with ht-1, nitisinone prevents the accumulation of the toxic intermediates maleylacetoacetate and fumarylacetoacetate.
billi jinibixxi l-kataboliżmu normali ta’ tyrosine f’pazjenti b’ht-1, nitisinone jevita l-akkumulazzjoni tal-intermedji tossiċi maleylacetoacetate u fumarylacetoacetate.

during treatment, a diet low in simple sugars and high in protein should be followed due to the hyperglycaemic effect of corticosteroids and their stimulation of protein catabolism with a negative nitrogen balance.
matul il-kura, għandha tiġi segwita dieta baxxa fiz-zokkor sempliċi u għolja fil-proteini minħabba l-effett ipergliċemiku tal-kortikosterojdi u l-istimulazzjoni li jagħmlu tal-kataboliżmu tal-proteini b’bilanċ negattiv tan- nitroġenu.

biotransformation: as a peptide, enfuvirtide is expected to undergo catabolism to its constituent amino acids, with subsequent recycling of the amino acids in the body pool.
bijotrasformazzjoni: bħala peptide, enfuvirtide huwa mistenni li jgħaddi minn kataboliżmu għal l- aċidi amminiċi li minnhom huwa magħmul, biex imbagħad l-aċidi aminiċi jiġu rriċiklati ġol-ġisem.

as with other large proteins, both free and bound aflibercept, are expected to be cleared, more slowly, by other biological mechanisms, such as proteolytic catabolism.
bħal proteini kbar oħra, kemm l-aflibercept ħielsa u kemm dak marbut, huma mistennija li jitneħħew aktar bil-mod, permezz ta’ mekkaniżmi bijoloġiċi oħra, bħall- kataboliżmu proteolitiku.

this results in an increase in the number of ldl-receptors on cell surfaces and enhanced receptor-mediated catabolism and clearance of circulating ldl-cholesterol.
dan jirriżulta f’żieda fin-numru ta’ riċetturi ta’ ldl fuq l-uċuħ taċ-ċelloli u titjib fil- kataboliżmu u t-tneħħija medjati mir-riċetturi, tal-kolesterol ldl li jiċċirkola.

the metabolism and elimination of bevacizumab is similar to endogenous igg i.e. primarily via proteolytic catabolism throughout the body, including endothelial cells, and does not rely primarily on elimination through the kidneys and liver.
il-metaboliżmu u l-eliminazzjoni ta’ bevacizumab huma simili għal igg endoġenu i.e. primarjament permezz ta’ kataboliżmu proteolitiku mal-ġisem kollu, inkluż ċelluli ta’ l-endotilju, u ma jiddependix primarjament minn eliminazzjoni mill-kliewi u l-fwied.

renal elimination of intact ixekizumab, an igg mab, is expected to be low and of minor importance; similarly, igg mabs are mainly eliminated via intracellular catabolism and hepatic impairment is not expected to influence clearance of ixekizumab.
it-tneħħija mill-kliewi ta’ ixekizumab, li huwa igg mab, mhux mibdul, hija mistennija li tkun ftit u ta’ importanza żgħira; b’mod simili, igg mabs il- biċċa l-kbira jitneħħew permezz ta’ kataboliżmu intraċellulari u indeboliment tal-fwied mhuwiex mistenni li jaffettwa t-tneħħija ta’ ixekizumab.

mannose-6-phosphate (m6p) residues on the oligosaccharide chains allow specific binding of the enzyme to the m6p receptors on the cell surface, leading to cellular internalization of the enzyme, targeting to intracellular lysosomes and subsequent catabolism of accumulated gag.
residwi ta’ mannose-6-phosphate (m6p) fuq il-ktajjen ta’ oligosaccharide iħallu rbit speċifiku ta’ l-enzima ma’ riċetturi m6p fuq il-wiċċ taċ-ċellola, li jwassal għal internalizzazzjoni ċellolari ta’ l-enzima, immirata għal liżożomi ċellolari u kataboliżmu sussegwenti ta’ gag akkumulati.