Evidence map›Paper›PMID 37088858›Full record

ArticleTranslational stroke research2024

Repurposing the K

Ruth D Lee, Yi-Je Chen, Hai M Nguyen, Latika Singh, Connor J Dietrich, Benjamin R Pyles, Yanjun Cui, Jonathan R Weinstein, Heike Wulff

Open access · hybridAbstract read
In one paragraph

Article in Translational stroke research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. 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
  5. Article
  6. 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

9 authors at 3 institutions in 1 country.

Ruth D Lee *Department of Pharmacology, School of Medicine, University of California, Davis, CA, 95616, USA.
Yi-Je Chen *Department of Pharmacology, School of Medicine, University of California, Davis, CA, 95616, USA.
Hai M NguyenDepartment of Pharmacology, School of Medicine, University of California, Davis, CA, 95616, USA.
Latika SinghDepartment of Pharmacology, School of Medicine, University of California, Davis, CA, 95616, USA.
Connor J DietrichDepartment of Pharmacology, School of Medicine, University of California, Davis, CA, 95616, USA.
Benjamin R PylesDepartment of Pharmacology, School of Medicine, University of California, Davis, CA, 95616, USA.
Yanjun CuiDepartment of Pharmacology, School of Medicine, University of California, Davis, CA, 95616, USA.
Jonathan R WeinsteinDepartment of Neurology, School of Medicine, University of Washington, Seattle, WA, 98195, USA.
Heike WulffDepartment of Pharmacology, School of Medicine, University of California, Davis, CA, 95616, USA. hwulff@ucdavis.edu.
University of California, Davis · USUniversity of California System · USUniversity of Washington · US

Funding

Microglial K+ Channels in Ischemic StrokeR01NS100294 · NINDS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI WULFF, HEIKE · 2017 to 2020
$1.3M
Repurposing of KCa3.1 Inhibitor Senicapoc for Stroke: A Pre-clinical StudyR61NS123195 · NINDS · UNIVERSITY OF WASHINGTON · PI WEINSTEIN, JONATHAN R · 2021 to 2022
$802k
NINDS NIH HHS NS100294NINDS NIH HHS R01 NS100294NINDS NIH HHS R61 NS123195NINDS NIH HHS R61NS123195
6 · The paper itself

Abstract

Senicapoc, a small molecule inhibitor of the calcium-activated potassium channel KCa3.1, was safe and well-tolerated in clinical trials for sickle cell anemia. We previously reported proof-of-concept data suggesting that both pharmacological inhibition and genetic deletion of KCa3.1 reduces infarction and improves neurologic recovery in rodents by attenuating neuroinflammation. Here we evaluated the potential of repurposing senicapoc for ischemic stroke. In cultured microglia, senicapoc inhibited KCa3.1 currents with an IC

Indexed as

Intermediate-Conductance Calcium-Activated Potassium ChannelsIschemic StrokeMice, Inbred C57BLAcetamidesAnimalsDrug RepositioningInfarction, Middle Cerebral ArteryMaleMiceMicrogliaPotassium Channel BlockersTriphenylmethyl CompoundsAcetamidesIntermediate-Conductance Calcium-Activated Potassium ChannelsKcnn4 protein, mousePotassium Channel BlockerssenicapocTriphenylmethyl CompoundsIschemic strokeKCa3.1Microglia activationMiddle cerebral artery occlusionNeuroinflammationSenicapoc

Identifiers

PMID37088858
PMCPMC11106165
OpenAlexW4366819560

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.