Lectifitin-36 for COVID-19
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COVID-19 Treatment Clinical Evidence
COVID-19 involves the interplay of 400+ viral and host proteins and factors, providing many therapeutic targets.
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Only three high-profit early treatments are approved in the US.
In reality, many treatments reduce risk,
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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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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.
Lectifitin-36 may be beneficial for
COVID-19 according to the study 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 Lectifitin-36 in detail.
, Engineered Dual‐Function Antibody‐Like Proteins to Combat SARS‐CoV‐2‐Induced Immune Dysregulation and Inflammation, Advanced Science, doi:10.1002/advs.202504690
AbstractComplement dysregulation and immune hyperactivation are pivotal factors contributing to the mortality associated with SARS‐CoV‐2 infection. Engineered Antibody‐like proteins (ALPs) targeting the SARS‐CoV‐2 spike protein are engineered to address immune dysregulation in COVID‐19. In this study, Lectifitin‐36 and Lectifitin‐41, two such ALPs, are developed using cDNA display technology. These ALPs demonstrate strong binding affinity for the spike protein and effectively inhibit its interaction with ACE2 and several C‐type lectins, including MBL, DC‐SIGN, and L‐SIGN. Both in vitro and in vivo analyses reveal that Lectifitin‐36 and Lectifitin‐41 suppress complement activation via the lectin pathway, reduce neutrophil extracellular trap (NET) formation, and attenuate hyper‐inflammatory responses. In mouse models, Lectifitin‐36 and Lectifitin‐41 significantly mitigate inflammation, NETosis, and lung tissue damage induced by the spike protein. These results suggest that these ALPs hold promise as therapeutic candidates for alleviating SARS‐CoV‐2‐induced immune dysfunction, with the potential to reduce severe COVID‐19 outcomes and long‐term sequelae. This study underscores the therapeutic potential of targeting spike protein‐mediated immune modulation as an innovative approach to combat COVID‐19.