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TL, wishful thinking! Matt will be touring the studios about supporting this fantastic British treatment (with the odd free research session during a trial)

Sorry theboyg, my first paragraph should have read hospital trial, not home trial

HT ambiguous!

Sorry theboyg, my first paragraph should have read hospital trial, not home trial

HT ambiguous!

Theboyg - the dusting off comment was to do with the original hospital trial and dusting off the protocol to ask for amendments. That will allow them to ask the original HT survivors about their recovery at 12 months (about now).

Not to be confused with the 90 day (originally planned) symptoms for the HT. It is possible that they will not break the randomisation code until this is in. THat's why I was asking if anyone has the HT protocol - often hard to find the document from the outside. It will certainly say in there when the data read starts. Quite possible no data available until 90 days after last patient enrolled.

Does anyone have the trial protocol for HT please? I'd love to read the unblinding bit in detail. Thanks

Doc, I support what you have said and even IF HT is not dramatic due to its small size and probably smaller signal effect it can still be very useful. It can prove telemedicine works for a therapeutic in COVID, a first. It can add to the number of patients ever treated without significant side effects. It may show some data in the right direction that with ACTIV-2 data added shortly, gets us over the hurdle for a move to ACTIV-3. And all that without breathtaking results in this small study alone. It can still be useful and science being science and I genuinely don't think RM had seen the unblinded data when that interview taken, maybe he was just commenting on the company research strategy for COVID being such that they thought it was a little early for where it has seen fires being put out in Asthma and COPD. Nothing more?

Invst, recorded a month ago behind a paywall

Mact - totally agree about long covid, this is very positive and he is clearly interested in this further data about to be harvested

"Our drug seems to want to have a fire to put out. In asthma and COPD, the poorlier the patient, the stronger the result is the general theme. It might be so for COVID in the home setting, the patients aren’t poorly enough to generate a big signal. Nevertheless you don’t need much of an effect when the world is broken and straining and hospitals are filled up with patients, any effect you can have in the home environment is priceless"

This looks like he's managing expectations. As I said earlier, not so on hospital P3, sounds solid.

I know it is a month ago but very interesting to see RM discuss the company research strategy development over time. They picked the more diseased end of the spectrum initially (those sick enough to be in hospital) for their first dalliance into C19 as their work on other respiratory diseases showed a stronger effect if the patient was sicker at the start of treatment. He therefore seemed less confident (albeit a month ago) about the strength of reading that the HT will have. This makes sense as it is a small study and many of the patients, even though they are at higher risk (older or with co-pathology) who get placebo will just get better. That's common with any age group that simply have a positive SARS-CoV2 PCR swab. He is still hopeful clearly, that's why they have done the study. But the nature of science is exactly what they are doing, try all eventualities and find the sweet spot for the timing of treatment.

He sounds a LOT more confident (albeit a month ago) about the P3 hospital trial, indeed I hadn't realised they have "dusted off" the original P2 ethics/protocol and asked for an amendment to approach the patients at a year post randomisation to look for a different rate of long COVID. This is an excellent strategy and could be gold-dust. I think he said they finished recruitment about a year ago so that is now another RNS we should be excitedly awaiting. Seriously for me, this it the golden nugget in RMs panel contributions published today.

GLA!

Sachs interview about to start

https://www.youtube.com/watch?v=-6UUKBD62gk

And SP in the solid blue too

Awww, Doc and Oak, that's the spirit!

Now the cork is out the bottle with the Polar RNS, let’s hope there are more RNSs ASAP!!

Thanks Spin

Very interesting read. If I am picking up the drift correctly, we may end up being exactly what the Doctor ordered for those with SARS CoV2 PCR +ve but IFN1 low levels on swabs. The dataset was too small for this group to answer this question and more work would be done later once we have EUA/license but interesting that worthy authors are now putting in some sentences at the start explaining that it is now accepted that those with autoantibodies to Type 1 IFN are at higher risk of severe disease.

"The general paradigm for early antiviral host defence is dominated by induction of type 1 IFNs. Attenuated responses as a result of autoantibodies to type 1 IFNs, and genetic polymorphisms associated with reduced expression of a type 1 IFN receptor subunit or with reduced expression of the IFN-inducible oligoadenylate synthetase (OAS) gene cluster have all been associated with severe disease9,10. These provide strong evidence that type 1 IFN responses contribute to effective protection against SARS-CoV-2 infection."

More support for type 1 IFN being at the centre of the (commonly successful) human defence to COVID. Alongside T cell response in the same paper. Very helpful and reassuring paper IMHO

This article shows that by the stage the patients are in ICU with COVID, those with a high expression of endogenous IFN beta-1 mRNA (called transcript level) do worse than those with low transcript of IFN beta-1. It is statistically significant in a multitude of parameters that matter.

I take heart that we seem to have the exact Interferon that is at the root of disease severity expression. On the face of it, we could be worried that it is the wrong finding - more endogenous IFNB1 transcript being clearly a bad thing a that stage but we are never planning to use it after admission to ICU. We are using it either for hospitalised but not yet ICU admitted patients (P2 -> P3, Sprinter trial), or earlier yet in home setting for vulnerable individuals).

We have data that P2 supported the use in hospitalised and hope HT may soon show similar for pre-hospital patients. It being therapeutic, rather than endogenous and importantly to be used before the cytokine storm. The findings in this paper, despite seemingly opposite to expectations, in my view emphasise the importance of this particular interferon. Timing and source will hopefully be supported by our awaited trials.

I agree with others that the use of SNG001 may become more "individualised medicine" later as tests like the one in this paper may indicate if it is likely to help each individual. IMO

Holding strong for the data flows to come!

Peel

Thanks Rich, that completely explains the findings. And it will be mauled at peer review with the current text, I agree.

Thanks for posting Matml.

Sorry for the following, I am having a weak scientific/research moment and if anyone can help I'd be grateful. This has been bugging me all day. From my reading this paper I can't be sure exactly what it is saying as it doesn't specify. It seems from the ******-Mayer curve that IFNB1+ stay in ICU for statistically significantly longer than IFNB1-

But it doesn't define what IFNB1+ or IFNB1- are precisely. Is this above or below a certain amount of IFNB1 in the nasal swab. Does IFNB1 refer to "InterFeron Beta 1" or is IFNB1 the name of a gene that it is calling + if it is expressed.

Lastly what it suggests if it is above or below a level is that having more IFNB1 is leading to longer in ICU (independent of viral load). Is this simply a demonstration that if the cytokine storm includes a lot of endogenous IFNB1 this late in the disease, you are really sick? Because otherwise it tends to suggest IFNB may be unhelpful by the stage of ICU, which doesn't make sense as P2 showed SNG001 is useful at keeping people out of hospital - admittedly it is from an exogenous source, which may make a difference.

Lastly, the Hazard ratio is 0.30, which might mean there is less chance of illness with IFNB+ but I can't see that from the curve

Again sorry for being so weak at reading this (VERY) important paper. Thanks in advance of any help!

Peel

My take on this is that we have learnt something new. There were 13 UK centres recruiting, not 9. Although over a longer timeframe since last update of text, it might mean that the P3 is also expanding into some of these other sites. Only 8 on the last update on the same US site for SG018 at last update. Fingers crossed.

Top effort finding that gggg. It is so hard to get info on progress and reassuring to see recruitment is proceeding.

Please note

https://clinicaltrials.gov/ct2/show/NCT04732949

Various things are explicit on this page and you can see from the "history of changes" hyperlink in the "more information" bit at the bottom, what the latest position was on 2/3/21

We can say for sure that on 2/3/21, there were 8 UK centres recruiting and zero actually recruiting elsewhere in the world. The 8 centres in the UK are

Hull Royal Infirmary Recruiting
Hull, North Humberside, East Riding Of Yorkshire, United Kingdom, HU3 2RW
Royal Victoria Infirmary, Newcastle Recruiting
Newcastle, England, United Kingdom, NE2 4HH
Southampton General Hospital Recruiting
Southampton, Hampshire, United Kingdom, SO16 6YD
Queen Elizabeth Hospital Birmingham Recruiting
Birmingham, United Kingdom, B15 2TH
The Royal Bournemouth & Christ Recruiting
Bournemouth, United Kingdom, BH7 7DP
Glenfield Hospital Recruiting
Leicester, United Kingdom, LE3 9QP
Plymouth Hospitals NHS Trust Recruiting
Plymouth, United Kingdom, PL6 8DH
Morriston Hospital Swansea NHS Recruiting
Swansea, United Kingdom, SA6 6NL

Only one other centre is mentioned in the world and it is in Texas but not actually recruiting as of 2/3/21

United States, Texas
PharmaTex Research, LLC Not yet recruiting
Amarillo, Texas, United States, 79109

Must admit I am gutted to see that there were so few activated recruiting sites by 7 weeks after the first recruit on 13/1/21 but that is the publicly available situation by 2/3/21 for what it's worth. I am unaware of any way of knowing numbers recruited in any site

GLA