Coumarin for COVID-19

Coumarin 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 coumarin in detail.
Fadel et al., Targeting asparagine and cysteine in SARS-CoV-2 variants and human pro-inflammatory mediators to alleviate COVID-19 severity; a cross-section and in-silico study, Scientific Reports, doi:10.1038/s41598-025-19359-y
Abstract To date, COVID-19 continues to pose a global health challenge, with substantial morbidity, mortality, and long-term post-COVID-19 complications threatening public health resilience. During the early pandemic, the IL-6 inhibitor (tocilizumab) was the widely used approved immunotherapy for critically ill patients; however, a subset of ICU cases exhibited normal interleukin-6 (IL-6) levels and failed to respond. We hypothesized that interleukin-17 (IL-17), which acts synergistically with IL-6, contributes to cytokine storm progression and severe inflammation. Our study uniquely integrates a clinical cross-sectional analysis with advanced in-silico modelling, directly linking patient-derived biomarker, radiological, and statistical data to molecular-level mechanisms of COVID-19 severity. Serum IL-17 was significantly elevated in critical versus moderate COVID-19 cases, with a threshold of 187.9 ng/mL predicting poor outcomes by ROC analysis. Logistic regression identified age and monocytes as independent predictors of severity, supporting a combined biomarker approach for improving the prognosis and clinical outcomes. Radiological findings, including ground-glass opacities and consolidations, alongside hematological abnormalities, were more frequent in critical cases. Computational docking revealed key amino acid residues—particularly asparagine (Asn) and cysteine (Cys)—as structural determinants shared by SARS-CoV-2 spike protein and human inflammatory mediators (IL-17R, IL-6R, CD41/CD61, CD47/SIRP). Asparaginase (ASNase) targeted critical residues such as the invariant gate residue “Asn343” and Cys213 of spike protein, Asn240 of IL-17R, and Asn136 of IL-6R. Several phytochemicals, including phytic acid and amygdalin, as well as synthetic agents such as candesartan, remdesivir, and enalapril, were found to preferentially bind to cysteine (Cys) residues—and, to a lesser extent, asparagine (Asn) residues—within key binding interfaces, in addition to targeting B-cell epitopes. This conserved residue preference supports the rationale for a dual-action therapeutic strategy in which asparaginase (ASNase) is combined with selected plant-derived ligands to simultaneously disrupt viral entry mechanisms and attenuate the inflammatory signalling. This dual-perspective approach not only identified IL-17 and IL-6 as independent severity predictors but also revealed conserved Asn and Cys motifs as critical therapeutic targets, leading to novel strategies—such as ASNase, synthetic agents and phytochemical combinations—for simultaneously blocking viral entry and modulating hyperinflammatory pathways. These findings warrant rigorous experimental and clinical validation to facilitate translation into effective therapeutic interventions.
Ma et al., Integration of human organoids single‐cell transcriptomic profiles and human genetics repurposes critical cell type‐specific drug targets for severe COVID‐19, Cell Proliferation, doi:10.1111/cpr.13558
AbstractHuman organoids recapitulate the cell type diversity and function of their primary organs holding tremendous potentials for basic and translational research. Advances in single‐cell RNA sequencing (scRNA‐seq) technology and genome‐wide association study (GWAS) have accelerated the biological and therapeutic interpretation of trait‐relevant cell types or states. Here, we constructed a computational framework to integrate atlas‐level organoid scRNA‐seq data, GWAS summary statistics, expression quantitative trait loci, and gene–drug interaction data for distinguishing critical cell populations and drug targets relevant to coronavirus disease 2019 (COVID‐19) severity. We found that 39 cell types across eight kinds of organoids were significantly associated with COVID‐19 outcomes. Notably, subset of lung mesenchymal stem cells increased proximity with fibroblasts predisposed to repair COVID‐19‐damaged lung tissue. Brain endothelial cell subset exhibited significant associations with severe COVID‐19, and this cell subset showed a notable increase in cell‐to‐cell interactions with other brain cell types, including microglia. We repurposed 33 druggable genes, including IFNAR2, TYK2, and VIPR2, and their interacting drugs for COVID‐19 in a cell‐type‐specific manner. Overall, our results showcase that host genetic determinants have cellular‐specific contribution to COVID‐19 severity, and identification of cell type‐specific drug targets may facilitate to develop effective therapeutics for treating severe COVID‐19 and its complications.
Abou Baker et al., An overview on medicinal plants used for combating coronavirus: Current potentials and challenges, Journal of Agriculture and Food Research, doi:10.1016/j.jafr.2023.100632
Bekheit et al., Potential RNA-dependent RNA polymerase inhibitors as prospective drug candidates for SARS-CoV-2, European Journal of Medicinal Chemistry, doi:10.1016/j.ejmech.2023.115292
Qi et al., Discovery of TCMs and Derivatives Against the Main Protease of SARS-CoV-2 via High Throughput Screening, ADMET Analysis, and Inhibition Assay in Vitro, Journal of Molecular Structure, doi:10.1016/j.molstruc.2022.133709