Ketotifen for COVID-19
c19early.org
COVID-19 Treatment Clinical Evidence
COVID-19 involves the interplay of 400+ viral and host proteins and factors, providing many therapeutic targets.
c19early analyzes 6,000+ studies for 210+ treatments—over 17 million hours of research.
Only three high-profit early treatments are approved in the US.
In reality, many treatments reduce risk,
with 25 low-cost treatments approved across 163 countries.
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Naso/
oropharyngeal treatment Effective Treatment directly to the primary source of initial infection. -
Healthy lifestyles Protective Exercise, sunlight, a healthy diet, and good sleep all reduce risk.
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Immune support Effective Vitamins A, C, D, and zinc show reduced risk, as with other viruses.
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Thermotherapy Effective Methods for increasing internal body temperature, enhancing immune system function.
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Systemic agents Effective Many systemic agents reduce risk, and may be required when infection progresses.
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High-profit systemic agents Conditional Effective, but with greater access and cost barriers.
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Monoclonal antibodies Limited Utility Effective but rarely used—high cost, variant dependence, IV/SC admin.
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Acetaminophen Harmful Increased risk of severe outcomes and mortality.
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Remdesivir Harmful Increased mortality with longer followup. Increased kidney and liver injury, cardiac disorders.
Ketotifen may be beneficial for
COVID-19 according to the studies below.
COVID-19 involves the interplay of 400+ viral and host proteins and factors providing many therapeutic targets.
Scientists have proposed 11,000+ potential treatments.
c19early.org analyzes
210+ treatments.
We have not reviewed ketotifen in detail.
, Mast cells and histamine receptor-targeted adjunctive treatments for COVID-19: A literature review, Innovative Medicines & Omics, doi:10.36922/IMO025440058
With the rollout of multiple COVID-19 vaccines, adjunctive treatments for COVID-19 have received less attention. Breakthrough infections post-vaccination (including boosters) underscore the need to continue evaluating repurposed drugs and nutraceuticals as candidate adjunctive treatments. Early clinical studies of antihistamines hypothesized that targeting mast cells (and/or histamine receptors) might benefit COVID-19 patients. In cultured human coronary artery endothelial cells, histamine potentiated spike-mediated angiotensin-converting enzyme 2 internalization; this effect can be blocked by the antihistamine famotidine. This literature review focuses on clinical studies of antihistamines, mast cell stabilizers, and leukotriene receptor antagonists for COVID-19 patients. Several antihistamines and mast cell-targeting agents, including fluvoxamine, cyproheptadine, hydroxyzine, and antihistamines used alone or with azithromycin (dexchlorpheniramine, cetirizine, loratadine, and ebastine), as well as azelastine, famotidine (standard or high-dose), high-dose famotidine with celecoxib, and the flavonoid mast cell stabilizer quercetin, have been reported to be associated with clinical benefits in COVID-19 patients. Multiple studies have reported mixed results for aspirin, montelukast, and normal-dose famotidine; patients taking aspirin often have associated COVID-19 risk factors. In the context of current standard-of-care treatments, clinical studies evaluating candidate adjunctive treatments should carefully consider and avoid known drug–drug interactions, such as those involving celecoxib and dexamethasone. Further clinical studies of the identified treatments targeting mast cells and/or histamine receptors in COVID-19 patients associated with clinical benefits are therefore strongly recommended.
, Virion-Independent Extracellular Vesicle (EV)-Dependent Transmission of SARS-CoV-2 as a Potential New Mechanism of Viral RNA Spread in Human Cells, Viruses, doi:10.3390/v18010145
The concentration of extracellular vesicles (EVs) in the peripheral blood of COVID-19 patients is increased. Nevertheless, their potential role in the transmission of infection remains unclear. This study was performed to determine whether EVs produced by the sub-genomic replicon system developed in Baby Hamster Kidney (BHK-21) cells could transfer SARS-CoV-2 replicon RNA, leading to the establishment of a viral replication system in human cells. Purified EVs from the SARS-CoV-2 sub-genomic replicon cell line BHK-21 were cultured with a naive human cell line. The success of EV-mediated transfer of SARS-CoV-2 replicon RNA and its productive replication was assessed using G-418 selection, a luciferase assay, immunostaining, and Western blot. We found that the A549 cell line cultured with EVs isolated from SARS-CoV-2 BHK-21 replicon cells developed G-418-resistant cell colonies. SARS-COV-2 RNA replication in A549 cells was confirmed by nano luciferase, Nsp1 protein. SARS-CoV-2 RNA replication causes massive morphological changes. Treatment of cells with the FDA-approved Paxlovid demonstrated a dose-dependent inhibition of viral replication. We isolated two human epithelial cell lines (gastrointestinal and neuroblastoma) and one vascular endothelial cell line that stably support high-level replication of SARS-CoV-2 sub-genomic RNA. Viral elimination did not revert the abnormal cellular shape, vesicle accumulation, syncytia formation, or EV release. Our study’s findings highlight the potential implications of EV-mediated transfer of replicon RNA to permissive cells. The replicon model is a valuable tool for studying virus-induced reversible and irreversible cellular reprogramming, as well as for testing novel therapeutic strategies for SARS-CoV-2.
, Novel receptor, mutation, vaccine, and establishment of coping mode for SARS-CoV-2: current status and future, Frontiers in Microbiology, doi:10.3389/fmicb.2023.1232453
Since the outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and its resultant pneumonia in December 2019, the cumulative number of infected people worldwide has exceeded 670 million, with over 6.8 million deaths. Despite the marketing of multiple series of vaccines and the implementation of strict prevention and control measures in many countries, the spread and prevalence of SARS-CoV-2 have not been completely and effectively controlled. The latest research shows that in addition to angiotensin converting enzyme II (ACE2), dozens of protein molecules, including AXL, can act as host receptors for SARS-CoV-2 infecting human cells, and virus mutation and immune evasion never seem to stop. To sum up, this review summarizes and organizes the latest relevant literature, comprehensively reviews the genome characteristics of SARS-CoV-2 as well as receptor-based pathogenesis (including ACE2 and other new receptors), mutation and immune evasion, vaccine development and other aspects, and proposes a series of prevention and treatment opinions. It is expected to provide a theoretical basis for an in-depth understanding of the pathogenic mechanism of SARS-CoV-2 along with a research basis and new ideas for the diagnosis and classification, of COVID-19-related disease and for drug and vaccine research and development.