Evidence map›Paper›PMID 30136756›Full record

ArticleClinical and translational science2018

Evaluation of Pharmacokinetics and Pharmacodynamics of BI 425809, a Novel GlyT1 Inhibitor: Translational Studies.

Holger Rosenbrock, Michael Desch, Oliver Kleiner, Cornelia Dorner-Ciossek, Bernhard Schmid, Sascha Keller, Christina Schlecker, Viktoria Moschetti, Sophia Goetz, Karl-Heinz Liesenfeld and 5 more

Open access · goldAbstract readClinical Trial, Phase I
In one paragraph

Article in Clinical and translational science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

25 citing papers in PubMed, 43 citations in OpenAlex.

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  4. GlyT1 (SLC6A9) inhibition in neurological and psychiatric disorders.Naunyn-Schmiedeberg's archives of pharmacology · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 3 institutions in 3 countries.

Holger RosenbrockBoehringer Ingelheim International GmbH, Biberach an der Riss, Germany.
Michael DeschBoehringer Ingelheim International GmbH, Biberach an der Riss, Germany.
Oliver KleinerBoehringer Ingelheim International GmbH, Biberach an der Riss, Germany.
Cornelia Dorner-CiossekBoehringer Ingelheim International GmbH, Biberach an der Riss, Germany.
Bernhard SchmidBoehringer Ingelheim International GmbH, Biberach an der Riss, Germany.
Sascha KellerBoehringer Ingelheim International GmbH, Biberach an der Riss, Germany.
Christina SchleckerBoehringer Ingelheim International GmbH, Ingelheim am Rhein, Germany.
Viktoria MoschettiBoehringer Ingelheim International GmbH, Ingelheim am Rhein, Germany.
Sophia GoetzBoehringer Ingelheim International GmbH, Biberach an der Riss, Germany.
Karl-Heinz LiesenfeldBoehringer Ingelheim International GmbH, Biberach an der Riss, Germany.
Gwenaelle FillonBoehringer Ingelheim International GmbH, Biberach an der Riss, Germany.
Riccardo GiovanniniBoehringer Ingelheim International GmbH, Biberach an der Riss, Germany.
Steven RamaelSGS, Antwerpen, Belgium.
Glen WunderlichBoehringer Ingelheim (Canada) Ltd, Burlington, Ontario, Canada.
Sven WindBoehringer Ingelheim International GmbH, Biberach an der Riss, Germany.
Boehringer Ingelheim (Germany) · DEBoehringer Ingelheim (Canada) · CAProvince of Antwerp · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BI 425809 is a potent and selective glycine transporter 1 (GlyT1) inhibitor being developed for the treatment of cognitive impairment in Alzheimer disease and schizophrenia. Translational studies evaluated the effects of BI 425809 on glycine levels in rat and human cerebrospinal fluid (CSF). Oral administration of BI 425809 in rats induced a dose-dependent increase of glycine CSF levels from 30% (0.2 mg/kg, not significant) to 78% (2 mg/kg, P < 0.01), relative to vehicle. Similarly, oral administration of BI 425809 in healthy volunteers resulted in a dose-dependent increase in glycine CSF levels at steady state, with a mean 50% increase at doses as low as 10 mg. The peak plasma concentration (C

Indexed as

Administration, OralAdultAlzheimer DiseaseAnimalsArea Under CurveCell LineDose-Response Relationship, DrugGlycineGlycine Plasma Membrane Transport ProteinsHealthy VolunteersHumansMaleMiddle AgedNeuronsNootropic AgentsOrganic ChemicalsBI 425809GlycineGlycine Plasma Membrane Transport ProteinsNootropic AgentsOrganic ChemicalsSLC6A9 protein, humanSlc6a9 protein, rat

Identifiers

PMID30136756
PMCPMC6226115
OpenAlexW2888273825

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.