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@ARTICLE{Tschirner:284027,
author = {Tschirner, Sarah K and Schmidt, Andree and Ito, Mana and
Hyakkoku, Kana and Yoshimura, Akimasa and Müller, Stephan A
and Horiguchi, Naotaka and Lichtenthaler, Stefan F},
title = {{E}lenbecestat and {C}ompound 89 {P}otently {I}nhibit
{BACE}1 but {N}ot {BACE}2 {W}hen {S}ubchronically {D}osed in
{N}on-{H}uman {P}rimates.},
journal = {Proteomics},
volume = {26},
number = {1},
issn = {1615-9853},
address = {Weinheim},
publisher = {Wiley VCH},
reportid = {DZNE-2026-00070},
pages = {100 - 107},
year = {2026},
abstract = {The β-secretase BACE1 (β-site amyloid precursor (APP)
cleaving enzyme 1) is a major drug target for Alzheimer's
disease (AD), as it catalyzes the first step in amyloid β
(Aβ) generation, but has additional substrates and
functions, in particular in the brain. Several advanced
clinical trials with BACE1 inhibitors were stopped because
of an adverse event, a mild cognitive worsening. The
underlying mechanism is not yet known but may result from
co-inhibition of the BACE1-homolog BACE2. While a
cerebrospinal fluid (CSF) biomarker for measuring BACE2
activity is not yet established, VCAM-1 has been suggested
as such a biomarker, but has not yet been tested upon
prolonged dosing in vivo. Using CSF pharmacoproteomics and a
subchronic dosing paradigm in non-human primates, we
demonstrate that compound 89, a BACE inhibitor not yet
tested in humans, and the clinically tested drug
elenbecestat inhibit BACE1 in vivo, with little or no effect
on BACE2, as seen with a reduction of substrates of BACE1,
but not of the BACE2 substrate VCAM-1. As a control,
verubecestat, which inhibits both BACE2 and BACE1, reduced
CSF abundance of BACE1 substrates as well as of VCAM-1. This
study demonstrates the suitability of VCAM-1 as a
pharmacodynamic biomarker for measuring BACE2 target
engagement in CSF.},
keywords = {Amyloid Precursor Protein Secretases: antagonists $\&$
inhibitors / Amyloid Precursor Protein Secretases:
cerebrospinal fluid / Animals / Aspartic Acid
Endopeptidases: antagonists $\&$ inhibitors / Aspartic Acid
Endopeptidases: cerebrospinal fluid / Male / Humans /
Biomarkers: cerebrospinal fluid / Vascular Cell Adhesion
Molecule-1: cerebrospinal fluid / Macaca fascicularis /
Amyloid Precursor Protein Secretases (NLM Chemicals) /
Aspartic Acid Endopeptidases (NLM Chemicals) / BACE1
protein, human (NLM Chemicals) / Biomarkers (NLM Chemicals)
/ Vascular Cell Adhesion Molecule-1 (NLM Chemicals)},
cin = {AG Lichtenthaler},
ddc = {540},
cid = {I:(DE-2719)1110006},
pnm = {352 - Disease Mechanisms (POF4-352)},
pid = {G:(DE-HGF)POF4-352},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:41310967},
pmc = {pmc:PMC12809003},
doi = {10.1002/pmic.70082},
url = {https://pub.dzne.de/record/284027},
}