Evidence map›Paper›PMID 28205624›Full record

ArticleScientific reports2017

The small molecule AUTEN-99 (autophagy enhancer-99) prevents the progression of neurodegenerative symptoms.

Tibor Kovács, Viktor Billes, Marcell Komlós, Bernadette Hotzi, Anna Manzéger, Anna Tarnóci, Diána Papp, Fanni Szikszai, Janka Szinyákovics, Ákos Rácz and 21 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 7% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Autophagy: A Double-Edged Sword in the Aging ofInternational journal of molecular sciences · 2026
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Autophagy: Regulator of cell death.Cell death & disease · 2023
    Review
  14. Article
  15. Review
  16. The Small-Molecule Enhancers of Autophagy AUTEN-67 and -99 Delay Ageing inInternational journal of molecular sciences · 2023
    Article
  17. Article
  18. The RING finger protein family in health and disease.Signal transduction and targeted therapy · 2022
    Review
  19. Review
  20. Article
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

31 authors at 8 institutions in 3 countries.

Tibor KovácsVelgene Biotechnology Research Ltd., Szeged, H-6726, Hungary.
Viktor BillesVelgene Biotechnology Research Ltd., Szeged, H-6726, Hungary.
Marcell KomlósVelgene Biotechnology Research Ltd., Szeged, H-6726, Hungary.
Bernadette HotziVelgene Biotechnology Research Ltd., Szeged, H-6726, Hungary.
Anna ManzégerDepartment of Genetics, Eötvös Loránd University, Budapest, H-1117, Hungary.
Anna TarnóciVelgene Biotechnology Research Ltd., Szeged, H-6726, Hungary.
Diána PappVelgene Biotechnology Research Ltd., Szeged, H-6726, Hungary.
Fanni SzikszaiDepartment of Genetics, Eötvös Loránd University, Budapest, H-1117, Hungary.
Janka SzinyákovicsDepartment of Genetics, Eötvös Loránd University, Budapest, H-1117, Hungary.
Ákos RáczDepartment of Pharmaceutical Chemistry, Semmelweis University, Budapest, H-1092, Hungary.
Béla NoszálDepartment of Pharmaceutical Chemistry, Semmelweis University, Budapest, H-1092, Hungary.
Szilvia VeszelkaGroup of Biological Barriers, Institute of Biophysics, Biological Research Centre, Hungarian Academy of Sciences, Szeged, H-6726, Hungary.
Fruzsina R WalterGroup of Biological Barriers, Institute of Biophysics, Biological Research Centre, Hungarian Academy of Sciences, Szeged, H-6726, Hungary.
Mária A DeliGroup of Biological Barriers, Institute of Biophysics, Biological Research Centre, Hungarian Academy of Sciences, Szeged, H-6726, Hungary.
Laszlo HacklerAvidin Ltd., Szeged, H-6726, Hungary.
Robert AlfoldiAvidin Ltd., Szeged, H-6726, Hungary.
Orsolya HuzianAvidin Ltd., Szeged, H-6726, Hungary.
Laszlo G PuskasAvidin Ltd., Szeged, H-6726, Hungary.
Hanna LiliomDepartment of Physiology and Neurobiology, Eötvös Loránd University, Budapest, H-1117, Hungary.
Krisztián TárnokDepartment of Physiology and Neurobiology, Eötvös Loránd University, Budapest, H-1117, Hungary.
Katalin SchlettDepartment of Physiology and Neurobiology, Eötvös Loránd University, Budapest, H-1117, Hungary.
Adrienn BorsyInstitute of Enzymology, Research Centre for Natural Sciences, Budapest, H-1117, Hungary.
Ervin WelkerInstitute of Enzymology, Research Centre for Natural Sciences, Budapest, H-1117, Hungary.
Attila L KovácsDepartment of Anatomy, Cell and Developmental Biology, Eötvös Loránd University, Budapest, H-1117, Hungary.
Zsolt PádárVelgene Biotechnology Research Ltd., Szeged, H-6726, Hungary.
Attila ErdősVelgene Biotechnology Research Ltd., Szeged, H-6726, Hungary.
Adam LegradiDepartment of Cell Biology and Molecular Medicine, University of Szeged, Szeged, H-6720, Hungary.
Annamaria BjelikDepartment of Cell Biology and Molecular Medicine, University of Szeged, Szeged, H-6720, Hungary.
Károly GulyaDepartment of Cell Biology and Molecular Medicine, University of Szeged, Szeged, H-6720, Hungary.
Balázs GulyásKarolinska Institute, Department of Clinical Neuroscience, S-171 76 Stockholm, Sweden.
Tibor VellaiVelgene Biotechnology Research Ltd., Szeged, H-6726, Hungary.
Eötvös Loránd University · HUUniversity of Szeged · HUHUN-REN Research Centre for Natural Sciences · HUSemmelweis University · HUHungarian Academy of Sciences · HUHUN-REN Szegedi Biológiai Kutatóközpont · HUInstitute of Biophysics · HUNanyang Technological University · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy functions as a main route for the degradation of superfluous and damaged constituents of the cytoplasm. Defects in autophagy are implicated in the development of various age-dependent degenerative disorders such as cancer, neurodegeneration and tissue atrophy, and in accelerated aging. To promote basal levels of the process in pathological settings, we previously screened a small molecule library for novel autophagy-enhancing factors that inhibit the myotubularin-related phosphatase MTMR14/Jumpy, a negative regulator of autophagic membrane formation. Here we identify AUTEN-99 (autophagy enhancer-99), which activates autophagy in cell cultures and animal models. AUTEN-99 appears to effectively penetrate through the blood-brain barrier, and impedes the progression of neurodegenerative symptoms in Drosophila models of Parkinson's and Huntington's diseases. Furthermore, the molecule increases the survival of isolated neurons under normal and oxidative stress-induced conditions. Thus, AUTEN-99 serves as a potent neuroprotective drug candidate for preventing and treating diverse neurodegenerative pathologies, and may promote healthy aging.

Indexed as

AnimalsAutophagyCells, CulturedCell SurvivalDisease Models, AnimalDrosophilaNeurodegenerative DiseasesNeuronsNeuroprotective AgentsNeuroprotective Agents

Identifiers

PMID28205624
PMCPMC5311965
OpenAlexW2587866198

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.