ArticleExpert review of clinical pharmacology2010
Therapeutic potential of KCa3.1 blockers: recent advances and promising trends.
Article in Expert review of clinical pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers.
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.
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.
Who cites it
123 citing papers in PubMed, 201 citations in OpenAlex.
- Senicapoc treatment in COVID-19 patients with severe respiratory insufficiency-A randomized, open-label, phase II trial.Acta anaesthesiologica Scandinavica · 2022Trial
- Senicapoc in Patients with Idiopathic Pulmonary Fibrosis or Other Progressive Fibrotic Interstitial Lung Diseases: Protocol for a Randomised, Double-Blind, Placebo-Controlled, Multicentre Phase II Trial.Diagnostics (Basel, Switzerland) · 2026Article
- The KCa3.1 KCells · 2026Review
- Involvement of Nitric Oxide in TRPV4-Induced Relaxations of Mouse and Human Pulmonary Arteries.Biology · 2026Article
- Visualization of KACS pharmacology & translational science · 2025Article
- Two-pore domain potassium channel TREK-1 contributes to arachidonic acid-induced CaBiochemistry and biophysics reports · 2025Article
- Cell Settling, Migration, and Stochastic Cancer Gene Expression Suggest Potassium Membrane Flux May Initiate pH Reversal.Biomolecules · 2025Article
- 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 · 2025Article
- KCNN4 as a genomic determinant of cytosolic delivery by the attenuated cationic lytic peptide L17E.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Fluorescent Probes to Image the KPharmaceutics · 2025Article
- Integrating endothelium-derived hyperpolarization, nitric oxide, and prostacyclin pathways: the multimodal potential of human tissue kallikrein-1.Vascular biology (Bristol, England) · 2025Review
- Barium and psoriasis: a mini-review and hypothesis linking environmental exposures to ion channel modulation.Frontiers in medicine · 2025Review
- The role and mechanism of vascular wall cell ion channels in vascular fibrosis remodeling.Channels (Austin, Tex.) · 2024Review
- Redox Regulation of KAntioxidants & redox signaling · 2024Review
- Challenges in the Therapeutic Targeting of KCa Channels: From Basic Physiology to Clinical Applications.International journal of molecular sciences · 2024Review
- Targeting KCell death discovery · 2024Article
- Effects of Natural Products through Inhibiting Endoplasmic Reticulum Stress on Attenuation of Idiopathic Pulmonary Fibrosis.Drug design, development and therapy · 2024Review
- Effect of THz Waves of Different Orientations on KInternational journal of molecular sciences · 2023Article
- IK Channel-Independent Effects of Clotrimazole and Senicapoc on Cancer Cells Viability and Migration.International journal of molecular sciences · 2023Article
- Potassium channels as novel molecular targets in hepatocellular carcinoma (Review).Oncology reports · 2023Review
63 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The Ca(2+)-activated K(+) channel K(Ca)3.1 regulates membrane potential and calcium signaling in erythrocytes, activated T and B cells, macrophages, microglia, vascular endothelium, epithelia, and proliferating vascular smooth muscle cells and fibroblasts. K(Ca)3.1 has therefore been suggested as a potential therapeutic target for diseases such as sickle cell anemia, asthma, coronary restenosis after angioplasty, atherosclerosis, kidney fibrosis and autoimmunity, where activation and excessive proliferation of one or more of these cell types is involved in the pathology. This article will review the physiology and pharmacology of K(Ca)3.1 and critically examine the available preclinical and clinical data validating K(Ca)3.1 as a therapeutic target.
Identifiers
What OpenQuestion holds
Registered trials
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.