NOVEL MECHANISM FOR THE SUSTAINED DURABILITY OF PROPROTEIN CONVERTASE SUBTILISIN-KEXIN TYPE 9 MONOCLONAL ANTIBODY LY3015014

NOVEL MECHANISM FOR THE SUSTAINED DURABILITY OF PROPROTEIN CONVERTASE SUBTILISIN-KEXIN TYPE 9 MONOCLONAL ANTIBODY LY3015014

LY did not cause an accumulation of intact PCSK9 in serum, which was seen preclinically and in humans treated with other PCSK9 Mabs. Because the LY epitope excludes the furin cleavage site in PCSK9, we asked if furin-mediated degradation proceeds when LY is bound but is blocked by other Mabs.

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Veröffentlicht in:Journal of the American College of Cardiology 2015-03, Vol.65 (10), p.A1577-A1577
Hauptverfasser: Eacho, Patrick, Schroeder, Krista, Beyer, Thomas, Hansen, Ryan, Wroblewski, Victor, Han, Bomie, Pickard, Richard, Kowala, Mark
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Sprache:eng
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Cardiology
Cardiovascular
Cholesterol
Internal Medicine
Medical research
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container_end_page A1577
container_issue 10
container_start_page A1577
container_title Journal of the American College of Cardiology
container_volume 65
creator Eacho, Patrick
Schroeder, Krista
Beyer, Thomas
Hansen, Ryan
Wroblewski, Victor
Han, Bomie
Pickard, Richard
Kowala, Mark
description LY did not cause an accumulation of intact PCSK9 in serum, which was seen preclinically and in humans treated with other PCSK9 Mabs. Because the LY epitope excludes the furin cleavage site in PCSK9, we asked if furin-mediated degradation proceeds when LY is bound but is blocked by other Mabs.
doi_str_mv 10.1016/S0735-1097(15)61577-7
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source Elsevier ScienceDirect Journals Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection
subjects Cardiology
Cardiovascular
Cholesterol
Internal Medicine
Medical research
title NOVEL MECHANISM FOR THE SUSTAINED DURABILITY OF PROPROTEIN CONVERTASE SUBTILISIN-KEXIN TYPE 9 MONOCLONAL ANTIBODY LY3015014
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