Enalapril 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.
Enalapril 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 enalapril in detail.
, 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.
, 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.
, Real-world evidence with a retrospective cohort of 15,968 Andalusian COVID-19 hospitalized patients suggests 21 new effective treatments and one drug that increases death risk., medRxiv, doi:10.1101/2022.08.14.22278751
Despite the extensive vaccination campaigns in many countries, COVID-19 is still a major worldwide health problem because of its associated morbidity and mortality. Therefore, finding efficient treatments as fast as possible is a pressing need. Drug repurposing constitutes a convenient alternative when the need for new drugs in an unexpected medical scenario is urgent, as is the case with COVID-19. Using data from a central registry of electronic health records (the Andalusian Population Health Database, BPS), the effect of prior consumption of drugs for other indications previous to the hospitalization with respect to patient survival was studied on a retrospective cohort of 15,968 individuals, comprising all COVID-19 patients hospitalized in Andalusia between January and November 2020. Covariate-adjusted hazard ratios and analysis of lymphocyte progression curves support a significant association between consumption of 21 different drugs and better patient survival. Contrarily, one drug, furosemide, displayed a significant increase in patient mortality.