Ivermectin ameliorates acute myocarditis via the inhibition of importin-mediated nuclear translocation of NF-κB/p65
et al., International Immunopharmacology, doi:10.1016/j.intimp.2024.112073, Apr 2024
Ivermectin for COVID-19
4th treatment shown to reduce risk in
August 2020, now with p < 0.00000000001 from 106 studies, recognized in 24 countries.
No treatment is 100% effective. Protocols
combine treatments.
6,600+ studies for
220+ treatments. c19early.org
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Mouse study showing that ivermectin improves cardiac function and reduces inflammation in models of viral and autoimmune myocarditis. Authors found that ivermectin inhibited the nuclear translocation of NF-κB/p65 in macrophages by targeting importin β, thereby reducing levels of pro-inflammatory cytokines IL-1β, IL-6, and TNF-α. These effects were confirmed in both Coxsackie B3 virus (CVB3)-induced myocarditis and experimental autoimmune myocarditis (EAM) in BALB/c mice, as well as in CVB3-infected RAW264.7 macrophages treated with ivermectin or a selective NF-κB/p65 nuclear translocation inhibitor, cTN50. While not directly tested against SARS-CoV-2, these findings suggest that ivermectin's ability to suppress NF-κB/p65-mediated inflammation in macrophages may be beneficial in the context of COVID-19-associated myocarditis and cytokine storm.
77 preclinical studies support the efficacy of ivermectin for COVID-19:
Ivermectin, better known for antiparasitic activity, is a broad spectrum antiviral with activity against many viruses including H7N774, Dengue39,75,76 , HIV-176, Simian virus 4077, Zika39,78,79 , West Nile79, Yellow Fever80,81, Japanese encephalitis80, Chikungunya81, Semliki Forest virus81, Human papillomavirus59, Epstein-Barr59, BK Polyomavirus82, and Sindbis virus81.
Ivermectin inhibits importin-α/β-dependent nuclear import of viral proteins74,76,77,83 , shows spike-ACE2 disruption at 1nM with microfluidic diffusional sizing40, binds to glycan sites on the SARS-CoV-2 spike protein preventing interaction with blood and epithelial cells and inhibiting hemagglutination43,84, shows dose-dependent inhibition of wildtype and omicron variants38, exhibits dose-dependent inhibition of lung injury64,69, may inhibit SARS-CoV-2 via IMPase inhibition39, may inhibit SARS-CoV-2 induced formation of fibrin clots resistant to degradation10, inhibits SARS-CoV-2 3CLpro56, may inhibit SARS-CoV-2 RdRp activity1,29, may minimize viral myocarditis by inhibiting NF-κB/p65-mediated inflammation in macrophages63, may be beneficial for COVID-19 ARDS by blocking GSDMD and NET formation85, may interfere with SARS-CoV-2's immune evasion via ORF8 binding5, may inhibit SARS-CoV-2 by disrupting CD147 interaction86-89, may inhibit SARS-CoV-2 attachment to lipid rafts via spike NTD binding3, shows protection against inflammation, cytokine storm, and mortality in an LPS mouse model sharing key pathological features of severe COVID-1961,90, may be beneficial in severe COVID-19 by binding IGF1 to inhibit the promotion of inflammation, fibrosis, and cell proliferation that leads to lung damage9, significantly mitigates bleomycin-induced pulmonary fibrosis by reducing collagen accumulation and inflammatory cell infiltration62, improves oxidative stress markers while suppressing myofibroblast proliferation62, may minimize SARS-CoV-2 induced cardiac damage42,50, may counter immune evasion by inhibiting NSP15-TBK1/KPNA1 interaction and restoring IRF3 activation91, may disrupt SARS-CoV-2 N and ORF6 protein nuclear transport and their suppression of host interferon responses2, reduces TAZ/YAP nuclear import, relieving SARS-CoV-2-driven suppression of IRF3 and NF-κB antiviral pathways37, increases Bifidobacteria which play a key role in the immune system92, has immunomodulatory53 and anti-inflammatory73,93 properties, and has an extensive and very positive safety profile94.
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Gao et al., 17 Apr 2024, peer-reviewed, 6 authors.
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