It has been since discovered that there are other receptors/pathways too for SARS-CoV-2 to enter the cell, but it's still unclear which ones are the main culprits.
I too tried to follow the progress of Apeiron's APN01 which started to get news coverage at the end of February due to a University of British Columbia press release [1]. This pre-existing therapeutic was created out of SARS-CoV-1 research and I expected a SARS-CoV-2 trial to be accelerated. It never happened.
There is a story to be told here. Either a missed opportunity, incompetence, or a complete misunderstanding on my part of what a promising COVID-19 therapeutic looks like.
When the first study started for this in February I was always optimistic this would both work and be cheap and easy to mass produce - it was the method I was hoping for and betting on. I've been disappointed to not see more news about this, I wonder what happened.
I know it's a gross question but who would invest the money to get FDA approval for it? The better angels of our nature don't have a couple hundred million sitting around to throw at the process. Are there grants or funds for getting approval for development of medicines that aren't patentable?
If it is not, it will encounter hurdles at every step, and probably never make it past initial trials. Nobody wants patent-free medicine except the public, and the public doesn't make decisions about drug safety...
AFAIK the way soluble ACE2 therapy works is you flood the body with "dummy" targets for SARS-CoV-2 to bind to instead of real cells, to slow down the virus infecting more and more cells.
As long as the spike of the new mink strains still binds to ACE2, it should provide some benefit.
Yes, this is one reason why an approach using a form of soluble ACE2 is so promising; mutations that would normally cause e.g. monoclonal antibodies to stop working (as detailed with the mink mutation) would in theory not stop the 'decoy receptor' approach.
Despite the fact soluble ACE2 is not looking like it'll be developed in time to impact the pandemic, there is a silver lining:
Interestingly, in this n=1 case report, it looks like the soluble ACE2 is unlikely to have worked as an antiviral; the patient already had a high level of antibodies, as you can see in the Lancet paper above. So /if/ the patient's improvements can be ascribed to the soluble ACE2 treatment, it's likely the improvement was because of the effect the soluble ACE2 had on the person's renin-angiotensin system.
And if this holds, then it's likely many of these same improvements would be possible using a common class of widely-available blood pressure medications called ARBs.
This approach would not neutralize the virus, but instead stop the body from damaging itself. That's the theory, at least.
There are ~20 trials of ARBs for COVID-19 in progress now, though almost all are underdosed.
[+] [-] dharma1|5 years ago|reply
Here's a great breakdown of how it works by the founder of Apeiron, Dr Joseph Penninger, from March. https://www.youtube.com/watch?v=jAW6VBWTiAA
It has been since discovered that there are other receptors/pathways too for SARS-CoV-2 to enter the cell, but it's still unclear which ones are the main culprits.
https://theconversation.com/a-second-pathway-into-cells-for-...
[+] [-] sradman|5 years ago|reply
There is a story to be told here. Either a missed opportunity, incompetence, or a complete misunderstanding on my part of what a promising COVID-19 therapeutic looks like.
[1] https://www.med.ubc.ca/news/pilot-clinical-trial-in-china-to...
[+] [-] unknown|5 years ago|reply
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[+] [-] gfodor|5 years ago|reply
[+] [-] SftwreEngnr|5 years ago|reply
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[+] [-] thro1|5 years ago|reply
https://www.youtube.com/watch?v=EMaKFcpV5wg
https://www.youtube.com/watch?v=VB06uVA97zI
but.. 'linoleic acid is a precursor to arachidonic acid which is involved in inflamation'.
Any news about zinc acetate (losenges) with zinc ionophores as hydroxychloroquine (in small doses, early) or quercetin pythosome (quercenase)?
edit: (to downvoter: would you mind telling me where I'm wrong? https://news.ycombinator.com/item?id=22627167 https://news.ycombinator.com/item?id=22603462 https://news.ycombinator.com/item?id=22631469 , as well quite promising)
[+] [-] CameronNemo|5 years ago|reply
[+] [-] jcims|5 years ago|reply
[+] [-] londons_explore|5 years ago|reply
[+] [-] 1024core|5 years ago|reply
[+] [-] newsbinator|5 years ago|reply
[+] [-] dharma1|5 years ago|reply
As long as the spike of the new mink strains still binds to ACE2, it should provide some benefit.
[+] [-] philipn|5 years ago|reply
Despite the fact soluble ACE2 is not looking like it'll be developed in time to impact the pandemic, there is a silver lining:
If you look at the original paper (https://www.thelancet.com/journals/lanres/article/PIIS2213-2...), you'll note they include details on angiotensin peptide levels in the patient.
Interestingly, in this n=1 case report, it looks like the soluble ACE2 is unlikely to have worked as an antiviral; the patient already had a high level of antibodies, as you can see in the Lancet paper above. So /if/ the patient's improvements can be ascribed to the soluble ACE2 treatment, it's likely the improvement was because of the effect the soluble ACE2 had on the person's renin-angiotensin system.
And if this holds, then it's likely many of these same improvements would be possible using a common class of widely-available blood pressure medications called ARBs.
This approach would not neutralize the virus, but instead stop the body from damaging itself. That's the theory, at least.
There are ~20 trials of ARBs for COVID-19 in progress now, though almost all are underdosed.