Evidence map›Paper›PMID 31019997›Full record

ArticleAnnals of clinical and translational neurology2019

Repurposing the KCa3.1 inhibitor senicapoc for Alzheimer's disease.

Lee-Way Jin, Jacopo Di Lucente, Hai M Nguyen, Vikrant Singh, Latika Singh, Monique Chavez, Trevor Bushong, Heike Wulff, Izumi Maezawa

Abstract read
In one paragraph

Article in Annals of clinical and translational neurology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
–field-weighted citation impact
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

40 citing papers in PubMed.

  1. KArchiv der Pharmazie · 2026
    Article
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  5. Article
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  7. Design and structural basis of selective 1,4-dihydropyridine inhibitors of the calcium-activated potassium channel KProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  8. Article
  9. Article
  10. Administration of the KFrontiers in pharmacology · 2025
    Article
  11. Article
  12. Repurposing the KTranslational stroke research · 2024
    Article
  13. Review
  14. Article
  15. Review
  16. Targeting KCell death discovery · 2024
    Article
  17. Review
  18. Review
  19. Review
  20. Review
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

9 authors.

Lee-Way JinDepartment of Pathology and Laboratory Medicine University of California Davis Medical Center Sacramento California.
Jacopo Di LucenteDepartment of Pathology and Laboratory Medicine University of California Davis Medical Center Sacramento California.
Hai M NguyenDepartment of Pharmacology University of California Davis Davis California.
Vikrant SinghDepartment of Pharmacology University of California Davis Davis California.
Latika SinghDepartment of Pharmacology University of California Davis Davis California.
Monique ChavezDepartment of Pathology and Laboratory Medicine University of California Davis Medical Center Sacramento California.
Trevor BushongDepartment of Pathology and Laboratory Medicine University of California Davis Medical Center Sacramento California.
Heike WulffDepartment of Pharmacology University of California Davis Davis California.ORCID https://orcid.org/0000-0003-4437-5763
Izumi MaezawaDepartment of Pathology and Laboratory Medicine University of California Davis Medical Center Sacramento California.

Funding

UC Davis Alzheimer's Disease Core CenterP30AG010129 · NIA · UNIVERSITY OF CALIFORNIA DAVIS · PI DECARLI, CHARLES · 1991 to 2020
$28.3M
The Role of KCa3.1 in Neuroinflammation in Alzheimer DiseaseR01AG043788 · NIA · UNIVERSITY OF CALIFORNIA AT DAVIS · PI MAEZAWA, IZUMI · 2013 to 2017
$1.6M
Microglial K+ Channels in Ischemic StrokeR01NS100294 · NINDS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI WULFF, HEIKE · 2017 to 2020
$1.3M
NIA NIH HHS P30 AG010129NIA NIH HHS R01 AG043788NINDS NIH HHS R01 NS100294
6 · The paper itself

Abstract

objectiveMicroglia play a pivotal role in the initiation and progression of Alzheimer's disease (AD). We here tested the therapeutic hypothesis that the Ca

methodsTo determine if KCa3.1 is relevant to AD, we tested if treating cultured microglia or hippocampal slices with A

resultsWe found markedly enhanced microglial KCa3.1 expression/activity in brains of both 5xFAD mice and AD patients. In hippocampal slices, microglial KCa3.1 expression/activity was increased by A

interpretationOur results prompt us to propose repurposing senicapoc for AD clinical trials, as senicapoc has excellent pharmacological properties and was safe and well-tolerated in a prior phase-3 clinical trial for sickle cell anemia. Such repurposing has the potential to expedite the urgently needed new drug discovery for AD.

Indexed as

AcetamidesAlzheimer DiseaseAmyloid beta-PeptidesAnimalsBrainDrug RepositioningHumansIntermediate-Conductance Calcium-Activated Potassium ChannelsMice, TransgenicMicrogliaTriphenylmethyl CompoundsAcetamidesAmyloid beta-PeptidesIntermediate-Conductance Calcium-Activated Potassium ChannelssenicapocTriphenylmethyl Compounds

Identifiers

PMID31019997
PMCPMC6469250

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.