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Thus, truncation of the C-terminal L585 residue of the GLP-1 fusion containing WT albumin reduces its cellular recycling in vitro and plasma half-life in vivo, which may be compensated for by QMP engineering of albumin, irrespective of the presence of L585
Studies on protein therapeutics consistently show that agitation-induced degradation is one of the primary causes of potency loss
GLP-1 RA-experienced patients switching to once-weekly semaglutide in a real-world setting (EXPERT Study)
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