Evidence map›Paper›PMID 30224383›Full record

Trial reportEMBO molecular medicine2018

The BACE-1 inhibitor CNP520 for prevention trials in Alzheimer's disease.

Ulf Neumann, Mike Ufer, Laura H Jacobson, Marie-Laure Rouzade-Dominguez, Gunilla Huledal, Carine Kolly, Rainer M Lüönd, Rainer Machauer, Siem J Veenstra, Konstanze Hurth and 22 more

Open access · goldAbstract readRandomized Controlled Trial
In one paragraph

Trial report in EMBO molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
9.2field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

82 citing papers in PubMed, 169 citations in OpenAlex.

  1. Regional effects of gantenerumab on neuroimaging biomarkers in the DIAN-TU-001 trial.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
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  7. Toxic mechanisms of amyloid oligomers and therapeutic strategies.Protein science : a publication of the Protein Society · 2026
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22 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

32 authors at 1 institution in 1 country.

Ulf NeumannNeuroscience, Novartis Institute for BioMedical Research, Basel, Switzerland ulf.neumann@novartis.com cristina.lopez_lopez@novartis.com.ORCID 0000-0001-6680-9177
Mike UferTranslational Medicine, Novartis Institute for BioMedical Research, Basel, Switzerland.
Laura H JacobsonNeuroscience, Novartis Institute for BioMedical Research, Basel, Switzerland.
Marie-Laure Rouzade-DominguezTranslational Medicine, Novartis Institute for BioMedical Research, Basel, Switzerland.
Gunilla HuledalPK Sciences, Novartis Institute for BioMedical Research, Basel, Switzerland.
Carine KollyPreclinical Safety, Novartis Institute for BioMedical Research, Basel, Switzerland.
Rainer M LüöndGlobal Discovery Chemistry, Novartis Institute for BioMedical Research, Basel, Switzerland.
Rainer MachauerGlobal Discovery Chemistry, Novartis Institute for BioMedical Research, Basel, Switzerland.
Siem J VeenstraGlobal Discovery Chemistry, Novartis Institute for BioMedical Research, Basel, Switzerland.
Konstanze HurthGlobal Discovery Chemistry, Novartis Institute for BioMedical Research, Basel, Switzerland.
Heinrich RueegerGlobal Discovery Chemistry, Novartis Institute for BioMedical Research, Basel, Switzerland.
Marina Tintelnot-BlomleyGlobal Discovery Chemistry, Novartis Institute for BioMedical Research, Basel, Switzerland.
Matthias StaufenbielNeuroscience, Novartis Institute for BioMedical Research, Basel, Switzerland.
Derya R ShimshekNeuroscience, Novartis Institute for BioMedical Research, Basel, Switzerland.
Ludovic PerrotNeuroscience, Novartis Institute for BioMedical Research, Basel, Switzerland.
Wilfried FrieauffPreclinical Safety, Novartis Institute for BioMedical Research, Basel, Switzerland.
Valerie DubostPreclinical Safety, Novartis Institute for BioMedical Research, Basel, Switzerland.
Hilmar SchillerPK Sciences, Novartis Institute for BioMedical Research, Basel, Switzerland.
Barbara VoggPK Sciences, Novartis Institute for BioMedical Research, Basel, Switzerland.
Karen BeltzPK Sciences, Novartis Institute for BioMedical Research, Basel, Switzerland.
Alexandre AvrameasBiomarker Discovery, Novartis Institute for BioMedical Research, Basel, Switzerland.
Sandrine KretzBiomarker Discovery, Novartis Institute for BioMedical Research, Basel, Switzerland.
Nicole PezousTranslational Medicine, Novartis Institute for BioMedical Research, Basel, Switzerland.
Jean-Michel RondeauChemical Biology and Therapeutics, Novartis Institute for BioMedical Research, Basel, Switzerland.
Nicolau BeckmannMusculoskeletal Diseases, Novartis Institute for BioMedical Research, Basel, Switzerland.
Andreas HartmannPreclinical Safety, Novartis Institute for BioMedical Research, Basel, Switzerland.
Stefan VormfeldeTranslational Medicine, Novartis Institute for BioMedical Research, Basel, Switzerland.
Olivier J DavidGlobal Drug Development, Novartis, Basel, Switzerland.
Bruno GalliGlobal Drug Development, Novartis, Basel, Switzerland.
Rita RamosGlobal Drug Development, Novartis, Basel, Switzerland.
Ana GrafGlobal Drug Development, Novartis, Basel, Switzerland.
Cristina Lopez LopezGlobal Drug Development, Novartis, Basel, Switzerland ulf.neumann@novartis.com cristina.lopez_lopez@novartis.com.ORCID 0000-0003-4954-3754
Novartis (Switzerland) · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The beta-site amyloid precursor protein cleaving enzyme-1 (BACE-1) initiates the generation of amyloid-β (Aβ), and the amyloid cascade leading to amyloid plaque deposition, neurodegeneration, and dementia in Alzheimer's disease (AD). Clinical failures of anti-Aβ therapies in dementia stages suggest that treatment has to start in the early, asymptomatic disease states. The BACE-1 inhibitor CNP520 has a selectivity, pharmacodynamics, and distribution profile suitable for AD prevention studies. CNP520 reduced brain and cerebrospinal fluid (CSF) Aβ in rats and dogs, and Aβ plaque deposition in APP-transgenic mice. Animal toxicology studies of CNP520 demonstrated sufficient safety margins, with no signs of hair depigmentation, retina degeneration, liver toxicity, or cardiovascular effects. In healthy adults ≥ 60 years old, treatment with CNP520 was safe and well tolerated and resulted in robust and dose-dependent Aβ reduction in the cerebrospinal fluid. Thus, long-term, pivotal studies with CNP520 have been initiated in the Generation Program.

Indexed as

Alzheimer DiseaseAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesAnimalsAspartic Acid EndopeptidasesAstrocytesBrainCathepsin DCerebral HemorrhageFemaleHominidaeHumansInflammationMaleMice, Inbred C57BLMice, TransgenicAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesAspartic Acid EndopeptidasesBACE1 protein, humanBace1 protein, mouseCathepsin DOxazinesUmibecestatAlzheimer's diseaseBACE‐1 inhibitordrug discoverypreventionβ‐amyloid

Identifiers

PMID30224383
PMCPMC6220303
OpenAlexW2890206141

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.