I am getting the people in my life to take Serrapeptase/Nattokinase, quercetin, and NAC... all of which help breakdown fibrins or help against dementia.
On NNN I just read about the antidote (E64d, a research drug that prevents the cardiac amyloidosis). So I will look into that, as well.
Aloxistatin (E64d) is an irreversible and membrane-permeable cysteine protease inhibitor with blood platelet aggregation inhibiting activity. The cysteine protease cathepsin L is required for SARS-CoV-2 viral entry, and aloxistatin treatment reduced cellular entry of SARS-CoV-2 pseudovirions by 92.3%.
And here's an article called A Clinical-Stage Cysteine Protease Inhibitor blocks SARS-CoV-2 Infection of Human and Monkey Cells.
Which, for these purposes, if we consider the "vaccine" as what they're referring to as "Covid," especially in terms of spike proteins, then it would be relevant:
However, cleavage of the SARS-CoV-2 spike protein was only carried out by cathepsin L. This cleavage was blocked by K777 and occurred in the S1 domain of the SARS-CoV-2 spike protein, a different site from that previously observed for the SARS-CoV-1 spike protein. These data support the hypothesis that the antiviral activity of K777 is mediated through inhibition of the activity of host cathepsin L and subsequent loss of cathepsin L-mediated viral spike protein processing.
I am getting the people in my life to take Serrapeptase/Nattokinase, quercetin, and NAC... all of which help breakdown fibrins or help against dementia. On NNN I just read about the antidote (E64d, a research drug that prevents the cardiac amyloidosis). So I will look into that, as well.
This guy continues to research https://wmcresearch.substack.com/ Some good info there.
From NNN
Aloxistatin (E64d) is an irreversible and membrane-permeable cysteine protease inhibitor with blood platelet aggregation inhibiting activity. The cysteine protease cathepsin L is required for SARS-CoV-2 viral entry, and aloxistatin treatment reduced cellular entry of SARS-CoV-2 pseudovirions by 92.3%.
And here's an article called A Clinical-Stage Cysteine Protease Inhibitor blocks SARS-CoV-2 Infection of Human and Monkey Cells.
Which, for these purposes, if we consider the "vaccine" as what they're referring to as "Covid," especially in terms of spike proteins, then it would be relevant:
However, cleavage of the SARS-CoV-2 spike protein was only carried out by cathepsin L. This cleavage was blocked by K777 and occurred in the S1 domain of the SARS-CoV-2 spike protein, a different site from that previously observed for the SARS-CoV-1 spike protein. These data support the hypothesis that the antiviral activity of K777 is mediated through inhibition of the activity of host cathepsin L and subsequent loss of cathepsin L-mediated viral spike protein processing.