There is reasonably solid evidence that ivermectin docks to the spike protein itself to prevent binding to the ACE2 receptor which is the primary pathology causing the tissue damage and clots related to SARS-CoV-2. Therefore, this is also an implication that this ability of ivermectin to disable the binding of the Spike protein including the vaccine-produced spike proteins.
This binding of ivermectin to disable the spike protein is also preserved even with the newer spike protein mutations, but its activity against the original Wuhan spike protein,(the one vaccines were designed to produce) is fairly well studied at this point.
Background/Aim: Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). One drug that has attracted interest is the antiparasitic compound ivermectin, a macrocyclic lactone derived from the bacterium Streptomyces avermitilis. We carried out a docking study to determine if ivermectin might be able to attach to the SARS-CoV-2 spike receptor-binding domain bound with ACE2. Materials and Methods: We used the program AutoDock Vina Extended to perform the docking study. Results: Ivermectin docked in the region of leucine 91 of the spike and histidine 378 of the ACE2 receptor. The binding energy of ivermectin to the spike-ACE2 complex was -18 kcal/mol and binding constant was 5.8 e-08. Conclusion: The ivermectin docking we identified may interfere with the attachment of the spike to the human cell membrane. Clinical trials now underway should determine whether ivermectin is an effective treatment for SARS-Cov2 infection.
The following video explains the multiple mechanisms of the activity of Ivermectin including the ability of the body to maintain its basic defense of the cell nucleus in preserving the body’s ability to produce antiviral proteins, inhibition of RNA dependant RNA polymerase which inhibits the replication of viral RNA (possibly including that from the mRNA vaccine package), the stat 3 human signaling pathway which inhibits the production of blood clots also possibly mitigating some of the vaccines most dangerous side effects. Also discussed is the inhibition of the CD147 pathway by ivermectin which again may clock the clumping of platelets due to spike protein either from the virus or possibly the vaccines.
The following video explains the computational modeling of how ivermectin is theorized to directly impact the spike protein. Ivermectin appears to have the ability to bind to the spike protein, binds with more affinity than the spike protein active site that binds to the human ACE2 site, and binds with stability.
These factors seem to indicate that ivermectin, in essence, seems to neutralize the interaction of the spike protein with body tissues, possibly inactivating the damaging effects from the spike protein, including the spike proteins produced by current vaccines.
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