The latest Investing Matters Podcast episode featuring Jeremy Skillington, CEO of Poolbeg Pharma has just been released. Listen here.
If what you are saying was the case, the implication would be an increase in viral replication and higher mortality rate in the trial. So far the trial hasn't been stopped as far as we know so I'm thinking it's not making patients worse.
But we do know Sars COV virus from 2003 and Sars cov 2 both use ACE2 receptors to gain cell entry from studies put on here yesterday and we know interferon beta 1a reduced viral replication by over 90% when given less than 24 hours from infection from Sars COV (2003). So my basic understanding from that is that the Ace2 receptors isn't an issue.
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Found him, this was his garden right? How appropriate is it to send a letter showing interest in his trial with an open invite to a phone conversation regarding his trial?? Might not be appropriate...what do you all think?
Looking at the other meds on recovery at Leicester only Dexamethasone looks like it could be delivered by nebulisers (budesonide), I just seems a coincidence that they've reported 100 patients on the trial. I don't there's any rose tinted specs here, just process of elimination.
What makes you think that trek?
Looks like he wasn't in hospital long before he was given it, i.e less than 24 hours from positive test result. And he took it home with him.
can't think of another trial at that time in Leicester that used a nebulizer to deliver their drugs?
This looks like a new trial and says only 24 patients being recruited, the guy in Leicester hospital must have come out of hospital well over a week ago. I'd be surprised if it wasn't sng001 he was on...
Still interesting to know there's another nebulisers trial ongoing for future reference.
https://www.sciencemag.org/news/2020/04/these-drugs-don-t-target-coronavirus-they-target-us#
This is quite a good piece about camostat mesothylate, this blocks the enzyme we are discussing and stops the virus entering. it's already approved in Japan for pancreatitis, but has no patent. It's being trialled in Denmark currently, there are some concerns about how much would reach the lungs as it's taken orally.
Possible competition? They also have similar arguments to us about catching patients who are infected early to get best results.
Lp absolutely no need to call me a moron. All on the same side here, trying to do our bit.
Hold my hands up, I'm wrong. Either way, giving them the best chance of getting as many people on the drug as soon as they are confirmed to have it which should result in positive results.
A good article Trek, puts it in much simpler terms. If what they are implying (that interferons make things worse, by helping the virus) is true in real covid patients then the trials would have stopped by now surely?
Based on my research I feel like ringing Trump right now and telling him to get the entire world on sng001 immediately!!!
If sars COV 2 binds less to ACE2 receptors than sars COV (this seems to be a shared pathway to cell entry) then you should get an even greater than 90% reduction in viral replication if interferon beta1a is given less than 24 hours post infection.
If that is accurate then the problem we have here is quick reliable testing. This could be where it all falls apart. Saying that, I think it also said 70% reduction in viral replication if given within 72 hours of infection.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3322919/
Hopefully think above works, it shows interferon beta 1a does reduce viral replication by more than 90% if given less than 24 hours post infection.
Following Robbie Williams link I've located this section in the article which seems relevant.
'SARS-CoV-2 S protein bound to soluble hACE2 at a level similar to SARS-CoV S protein, although the mean fluorescence intensity (MFI) for SARS-CoV-2 S protein was slightly lower than SARS-CoV S protein. To further investigate if hACE2 is the receptor for SARS-CoV-2, we performed inhibition experiments using soluble hACE2. Soluble hACE2 proteins were pre-incubated with SARS-CoV-2 S pseudovirons on ice for 1?h, then virus-protein mixture was added onto 293/hACE2 cells. Entry of SARS-CoV-2 S pseudovirions was significantly prevented by pre-incubation of soluble hACE2 at both 10?µg/ml and 50? µg/ml (Fig. 2d), further supporting the notion that hACE2 is the receptor and soluble hACE2 might be used as a therapeutic inhibitor against SARS-CoV-2 infection.'
So it would be interesting to see how interferon beta reacted with Sars- COV...as it seems like they rely on similar cell entry.