ReviewFrontiers in immunology2020
PI3Kδ Inhibition as a Potential Therapeutic Target in COVID-19.
Review in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 30 citations in OpenAlex.
- Epigenetic ageing during the COVID-19 pandemic: global age acceleration, independent of SARS-CoV-2 infection.Clinical epigenetics · 2026Article
- 3D-QSAR, Molecular Docking, Molecular Dynamics Simulation, and Pharmacokinetic Prediction of 1H-Pyrazolo[3,4-d]pyrimidine Derivatives as PI3Kδ Inhibitors.Current medicinal chemistry · 2026Article
- Identification of effective synthetic molecules against viral-induced cytokine release syndrome using in silico and in vitro approaches.Molecular diversity · 2025Article
- Drug repurposing of cyclin-dependent kinase inhibitors for neutrophilic acute respiratory distress syndrome and psoriasis.Journal of advanced research · 2025Review
- Repurposing clinically available drugs and therapies for pathogenic targets to combat SARS-CoV-2.MedComm · 2023Review
- Severe COVID-19: Drugs and Clinical Trials.Journal of clinical medicine · 2023Review
- Dysregulated Neutrophil Phenotype and Function in Hospitalised Non-ICU COVID-19 Pneumonia.Cells · 2022Article
- Review
- PI3K/Akt/mTOR pathway: a potential target for anti-SARS-CoV-2 therapy.Immunologic research · 2022Review
- Article
- PI3K Signaling in Mechanisms and Treatments of Pulmonary Fibrosis Following Sepsis and Acute Lung Injury.Biomedicines · 2022Review
- The PI3K/Akt/mTOR pathway: A potential pharmacological target in COVID-19.Drug discovery today · 2022Review
- Transcriptional landscape of circulating platelets from patients with COVID-19 reveals key subnetworks and regulators underlying SARS-CoV-2 infection: implications for immunothrombosis.Cell & bioscience · 2022Article
- Targeting the PI3K/Akt/mTOR pathway: A therapeutic strategy in COVID-19 patients.Immunology letters · 2021Review
- Article
- Repurpose but also (nano)-reformulate! The potential role of nanomedicine in the battle against SARS-CoV2.Journal of controlled release : official journal of the Controlled Release Society · 2021Review
- ACE2 correlates with immune infiltrates in colon adenocarcinoma: Implication for COVID-19.International immunopharmacology · 2021Article
- Evaluation of SARS-CoV-2 Spike S1 Protein Response on PI3K-Mediated IL-8 Release.Medical sciences (Basel, Switzerland) · 2021Article
- Analysis of Thrombotic Adverse Reactions of COVID-19 AstraZeneca Vaccine Reported to EudraVigilance Database.Vaccines · 2021Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The spread of the novel human respiratory coronavirus (SARS-CoV-2) is a global public health emergency. There is no known successful treatment as of this time, and there is a need for medical options to mitigate this current epidemic. SARS-CoV-2 uses the angiotensin-converting enzyme 2 (ACE2) receptor and is primarily trophic for the lower and upper respiratory tract. A number of current studies on COVID-19 have demonstrated the substantial increase in pro-inflammatory factors in the lungs during infection. The virus is also documented in the central nervous system and, particularly in the brainstem, which plays a key role in respiratory and cardiovascular function. Currently, there are few antiviral approaches, and several alternative drugs are under investigation. Two of these are Idelalisib and Ebastine, already proposed as preventive strategies in airways and allergic diseases. The interesting and evolving potential of phosphoinositide 3-kinase δ (PI3Kδ) inhibitors, together with Ebastine, lies in their ability to suppress the release of pro-inflammatory cytokines, such as IL-1β, IL-8, IL-6, and TNF-α, by T cells. This may represent an optional therapeutic choice for COVID-19 to reduce inflammatory reactions and mortality, enabling patients to recover faster. This concise communication aims to provide new potential therapeutic targets capable of mitigating and alleviating SARS-CoV-2 pandemic infection.
Indexed as
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.