I've been waiting to learn more about the highly touted Merck Covid drug, Molnupiravir. It's not that it sounds too good to be true--in fact, it doesn't sound as effective as HCQ or Ivermectin. It's that you know that it will be pushed hard by the medical-scientific establishment and their media proxies. My initial assumption was that it would turn out to be another Ivermectin clone, like Pfizermectin. However, that appears to not be the case.
Mutagenicity was my first question upon hearing how this thing works. A compound that causes replication errors like this in RNA in general. I was not aware that the replication interference was achieved by messing with cytosine, one of the four base pairs used by not just RNA, but DNA as well.
I've been more cautious about characterizing the mRNA viruses as unworthy of use--I think they have potential, but they were rushed out without full long term safety studies. But this new drug being an analog of cytosine--well, this is insane to use. It takes no imagination at all to guess how this compound could mess with you.
I also wondered--if we use a drug that mangles the virus's RNA, we better be damned sure it messes with RNA in a 100% terminal way. Because if one in a million times it just mutates the virus, you're introducing a powerful evolutionary selective pressure.
There has been so little information like what you have provided here Mark--thank you for digging this up for us.
"I can't, somebody said something wrong on the internet...."
I don't get paid to fix the internet, but I can't resist commenting when someone wanders into my wheelhouse.
Molnupiravir is a nucleoside analog. It's a polymerase inhibitor. There is nothing new about this class of enzyme inhibitor drug. Aids patients have been taking them for years, and so have herpes patients.
Some nucleoside analogs are toxic, and some aren't. They can inhibit viral polymerases and human polymerases. The distinction is a matter of specificity, binding constants, and rate constants. In addition to being incorporated into DNA during transcription, they can be excised by polymerase proof reading mechanisms.
Some analogs target viral polymerases with high specificity, and some don't. They can have high or low specificity for human polymerases. The ratio of viral/human specificity, in addition to variable proof reading against viral and human DNA sequences, will determine their toxicity.
I could go on, but, as I said, I don't get paid to do this. In short, Molnupiravir might be useful or it might not, and it might be highly toxic or it might not.
See this publication and similar ones for the real science:
There's another drug in the EUA pipeline that heals lungs that have been damaged by COVID. It's called Zyesami, it's quite safe, and is now approaching 120 days of FDA "expedited review."
I believe it will ultimately be approved for many lung health indications, but in the near term it suffers two fatal problems: First, it won't make any money for Big Pharma. Second, it might reduce the pressure people are under to get jabbed.
Mutagenicity was my first question upon hearing how this thing works. A compound that causes replication errors like this in RNA in general. I was not aware that the replication interference was achieved by messing with cytosine, one of the four base pairs used by not just RNA, but DNA as well.
I've been more cautious about characterizing the mRNA viruses as unworthy of use--I think they have potential, but they were rushed out without full long term safety studies. But this new drug being an analog of cytosine--well, this is insane to use. It takes no imagination at all to guess how this compound could mess with you.
I also wondered--if we use a drug that mangles the virus's RNA, we better be damned sure it messes with RNA in a 100% terminal way. Because if one in a million times it just mutates the virus, you're introducing a powerful evolutionary selective pressure.
There has been so little information like what you have provided here Mark--thank you for digging this up for us.
"Honey, please come to bed!"
"I can't, somebody said something wrong on the internet...."
I don't get paid to fix the internet, but I can't resist commenting when someone wanders into my wheelhouse.
Molnupiravir is a nucleoside analog. It's a polymerase inhibitor. There is nothing new about this class of enzyme inhibitor drug. Aids patients have been taking them for years, and so have herpes patients.
Some nucleoside analogs are toxic, and some aren't. They can inhibit viral polymerases and human polymerases. The distinction is a matter of specificity, binding constants, and rate constants. In addition to being incorporated into DNA during transcription, they can be excised by polymerase proof reading mechanisms.
Some analogs target viral polymerases with high specificity, and some don't. They can have high or low specificity for human polymerases. The ratio of viral/human specificity, in addition to variable proof reading against viral and human DNA sequences, will determine their toxicity.
I could go on, but, as I said, I don't get paid to do this. In short, Molnupiravir might be useful or it might not, and it might be highly toxic or it might not.
See this publication and similar ones for the real science:
https://pubmed.ncbi.nlm.nih.gov/11328813/
Don't know if you saw this but someone posted this yt vid later in KD's comments.
https://www.youtube.com/watch?v=ZwR7natWqLk
My question, has no one else done these basic tests?
about 16 min.
There's another drug in the EUA pipeline that heals lungs that have been damaged by COVID. It's called Zyesami, it's quite safe, and is now approaching 120 days of FDA "expedited review."
I believe it will ultimately be approved for many lung health indications, but in the near term it suffers two fatal problems: First, it won't make any money for Big Pharma. Second, it might reduce the pressure people are under to get jabbed.