Not All Ivermectin Is Created Equal: Comparing The Quality of 11 Different Ivermectin Sources

Williams, T., Do Your Own Research, Jun 2022
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
In vitro analysis of ivermectin from 11 different sources showing highly variable antiparasitic efficacy. Multiple sources and brands were more effective than the US mass produced Edenbridge brand.
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.
Williams et al., 14 Jun 2022, preprint, 1 author.
In vitro studies are an important part of preclinical research, however results may be very different in vivo.
Please send us corrections, updates, or comments. c19early involves the extraction of 200,000+ datapoints from thousands of papers. Community updates help ensure high accuracy. Treatments and other interventions are complementary. All practical, effective, and safe means should be used based on risk/benefit analysis. No treatment or intervention is 100% available and effective for all current and future variants. We do not provide medical advice. Before taking any medication, consult a qualified physician who can provide personalized advice and details of risks and benefits based on your medical history and situation. IMA and WCH provide treatment protocols.
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