ArticleJournal of biomolecular structure & dynamics2022
Naltrexone a potential therapeutic candidate for COVID-19.
Article in Journal of biomolecular structure & dynamics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
What it found
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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
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Indian contribution toward biomedical research and development in COVID-19: A systematic review.Indian journal of pharmacologyPooled it
- Neurological impairment in long COVID: implications for neurodegenerative disease.Journal of translational medicine · 2026Review
- Low-Dose naltrexone restored TRPM3 ion channel function in natural killer cells from long COVID patients.Frontiers in molecular biosciences · 2025Article
- SARS-CoV-2 Infection and Alpha-Synucleinopathies: Potential Links and Underlying Mechanisms.International journal of molecular sciences · 2024Review
- Angiotensin-Converting Enzyme 2 Posttranslational Modifications and Implications for Hypertension and SARS-CoV-2: 2023 Lewis K. Dahl Memorial Lecture.Hypertension (Dallas, Tex. : 1979) · 2024Review
- Article
- Beyond prediction: unveiling the prognostic power of μ-opioid and cannabinoid receptors, alongside immune mediators, in assessing the severity of SARS-CoV-2 infection.BMC infectious diseases · 2024Article
- Low-dose naltrexone and NAD+ for the treatment of patients with persistent fatigue symptoms after COVID-19.Brain, behavior, & immunity - health · 2024Article
- Long COVID and its association with neurodegenerative diseases: pathogenesis, neuroimaging, and treatment.Frontiers in neurology · 2024Review
- Strategies for the Management of Spike Protein-Related Pathology.Microorganisms · 2023Review
- Article
- The impact of COVID-19 on chronic pain.Frontiers in pain research (Lausanne, Switzerland) · 2023Review
- Computational pharmacology: New avenues for COVID-19 therapeutics search and better preparedness for future pandemic crises.Biophysical chemistry · 2022Article
- Review
- Identification of phytocompounds as newer antiviral drugs against COVID-19 through molecular docking and simulation based study.Journal of molecular graphics & modelling · 2022Article
- Races of small molecule clinical trials for the treatment of COVID-19: An up-to-date comprehensive review.Drug development research · 2022Review
- Therapeutic potential of long-acting opioids and opioid antagonists for SARS-CoV-2 infection.British journal of anaesthesia · 2021Article
- Review
- Immunometabolic Modulatory Role of Naltrexone in BV-2 Microglia Cells.International journal of molecular sciences · 2021Article
- Opioid use disorder and health service utilization among COVID-19 patients in the US: A nationwide cohort from the Cerner Real-World Data.EClinicalMedicine · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is the cause of Coronavirus Disease (COVID-19) that has resulted in a global pandemic. At the time of writing, approximately 16.06 million cases have been reported worldwide. Like other coronaviruses, SARS-CoV-2 relies on the surface Spike glycoprotein to access the host cells, mainly through the interaction of its Receptor Binding Domain (RBD) with the host receptor Angiotensin-Converting Enzyme2 (ACE2). SARS-CoV-2 infection induces a profound downstream pro-inflammatory cytokine storm. This release of the pro-inflammatory cytokines is underpinning lung tissue damage, respiratory failure, and eventually multiple organ failure in COVID-19 patients. The phosphorylation status of ERK1/2 is positively correlated with virus load and ERK1/2 inhibition suppressed viral replication and viral infectivity. Therefore, molecular entities able to interfere with binding of the SARS-CoV-2 Spike protein to ACE2, or damping hyperinflammatory cytokines storm, blocking ERK1/2 phosphorylation have a great potential to inhibit viral entry along with viral infectivity. Herein, we report that the FDA-approved non-peptide opioid antagonist drug, naltrexone suppresses high fat/LPS induced pro-inflammatory cytokine release both from macrophage cells and Adipose Tissue Macrophage. Moreover, Low Dose Naltrexone (LDN) also showed its activity as an ERK1/2 inhibitor. Notably, virtual docking and simulation data also suggest LDN may disrupt the interaction of ACE2 with RBD. LDN may be considered as a target as the treatment and (or) adjuvant therapy for coronavirus infection. Clinical toxicity measurements may not be required for LDN since naltrexone was previously tested and is an approved drug by the FDA.Communicated by Ramaswamy H. Sarma.
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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.