Evidence map›Paper›PMID 31143125›Full record

ArticleFrontiers in pharmacology2019

Identification of GLPG/ABBV-2737, a Novel Class of Corrector, Which Exerts Functional Synergy With Other CFTR Modulators.

Gert de Wilde, Maarten Gees, Sara Musch, Katleen Verdonck, Mia Jans, Anne-Sophie Wesse, Ashvani K Singh, Tzyh-Chang Hwang, Thierry Christophe, Mathieu Pizzonero and 6 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2019. 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
3.7field-weighted citation impact, top 6% 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, 39 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Functional Consequences of CFTR Interactions in Cystic Fibrosis.International journal of molecular sciences · 2024
    Review
  11. Structural basis for CFTR inhibition by CFTRProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Novel Correctors and Potentiators Enhance Translational Readthrough in CFTR Nonsense Mutations.American journal of respiratory cell and molecular biology · 2021
    Article
  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

16 authors at 4 institutions in 3 countries.

Gert de WildeGalapagos NV, Mechelen, Belgium.
Maarten GeesGalapagos NV, Mechelen, Belgium.
Sara MuschGalapagos NV, Mechelen, Belgium.
Katleen VerdonckGalapagos NV, Mechelen, Belgium.
Mia JansGalapagos NV, Mechelen, Belgium.
Anne-Sophie WesseGalapagos NV, Mechelen, Belgium.
Ashvani K SinghAbbVie, North Chicago, IL, United States.
Tzyh-Chang HwangDepartment of Medical Pharmacology and Physiology, University of Missouri, Columbia, MO, United States.
Thierry ChristopheGalapagos NV, Mechelen, Belgium.
Mathieu PizzoneroGalapagos SASU, Paris, France.
Steven Van der PlasGalapagos NV, Mechelen, Belgium.
Nicolas DesroyGalapagos SASU, Paris, France.
Marlon CowartAbbVie, North Chicago, IL, United States.
Pieter StoutenGalapagos NV, Mechelen, Belgium.
Luc NellesGalapagos NV, Mechelen, Belgium.
Katja ConrathGalapagos NV, Mechelen, Belgium.
Galapagos (Belgium) · BEAbbVie (United States) · USGalapagos (France) · FRUniversity of Missouri · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The deletion of phenylalanine at position 508 (F508del) in cystic fibrosis transmembrane conductance regulator (CFTR) causes a severe defect in folding and trafficking of the chloride channel resulting in its absence at the plasma membrane of epithelial cells leading to cystic fibrosis. Progress in the understanding of the disease increased over the past decades and led to the awareness that combinations of mechanistically different CFTR modulators are required to obtain meaningful clinical benefit. Today, there remains an unmet need for identification and development of more effective CFTR modulator combinations to improve existing therapies for patients carrying the F508del mutation. Here, we describe the identification of a novel F508del corrector using functional assays. We provide experimental evidence that the clinical candidate GLPG/ABBV-2737 represents a novel class of corrector exerting activity both on its own and in combination with VX809 or GLPG/ABBV-2222.

Indexed as

chloride channelcystic fibrosiscystic fibrosis transmembrane conductance regulator (CFTR)electrophysiologyprotein misfolding

Identifiers

PMID31143125
PMCPMC6521598
OpenAlexW2944120532

What OpenQuestion holds

Textmetadata
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.