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“Proven track Record”
Who do we know who’s organised a multi million dollar deal with Astra
Who do we know who’s organised successful P2 COVid trials for in and outpatients.
Who do we know who’s organised a trial with the largest government body on the planet under Activ-2
Who do we know who’s organised working with a leading University and one the worlds biggest Pharma on a patient study.
WHO is this other person who guarantees every single trial will be 100% successful that we could hire!
Oh but we have Mani the expert head hunter to save us
Just wondering if out of these trials particularly around the “Viral persistence”
Are we seeing the possibility of a new patent for the treatment of a condition not previously indicated for sng001’s current applications?
I’m guessing we, or most of us, are invested here because we follow the science, realise the potential value etc.
It would seem from some posts that people didn’t realise the pitfalls or the timeframes involved in delivery / commercialisation of a drug. Particularly after the pandemic eased and funds dried up and timeframes were no longer critically urgent to governments or regulators.
It’s sad that many tried to jump on Sprinter failure losing so much, and I feel for those people.
Personally I’m with Doc83 and a number of others on this board who’ve waited patiently and will wait to the end.
It’s either going to be:
A flop
A commercial success
Stolen from underneath us.
Can’t do a lot about 1 or 3 but I’m in for number 2 to the very end !!
I’m sure a consortium would love to convince shareholders to sell now cheaply. Then continue with the companies plans which if successful would allow them to sell to BP at a large profit.
I wonder if such a consortium would place someone on a public chat forum to promote the idea to unsuspecting investors.
As everyone I assume knows how to read a thread by clicking on it to open it. I’m not sure it’s even possible to bury a thread.
As no one has seriously commented on it today. It seems less buried than almost deceased on life support.
Maybe interferon therapy could save it!
But if it makes you happy Mani keep bumping it all day long.
Personally I’m interested in why the company are trialling “viral persistence” in their P2’s and the underlying science behind it.
Https://err.ersjournals.com/content/errev/32/169/230036.full.pdf
NK cell involvement in respiratory viral infections
Infants who died of IAV infection have almost no detectable NK cells in their lungs but exhibit large quantities of viral antigen, suggesting that NK cells are necessary to clear up the infection
SARS-CoV-2 infection was suggested to impair NK The exact functions of NK cells in SARS-CoV-2 infection have yet to be uncovered, although their dysfunction appears to be linked with disease severity.
Natural killer cells in antiviral immunity
https://www.nature.com/articles/s41577-021-00558-3
NK cell activity is modulated by cytokines, including, but not limited to, the activating cytokines IL-2, IL-12, IL-15, IL-18 and type I interferons.
https://www.nature.com/articles/ni1102-1006
The importance of NK cell defense against these viruses is highlighted by the susceptibility of mice depleted of NK cells to experimental infection and by the invasive or disseminated viral disease that is associated with naturally occurring NK cell deficiencies in humans8,9,10,11. Many of these pathogens have effective means of avoiding the adaptive immune response.
Synairgen’s interim RNS
They will be looking at patients with an inability to clear the virus “viral persistence”
Increasing research may have led Synairgen to change their minds on the benefits of SNG001 as a wider therapeutic.
https://www.nature.com/articles/s41590-023-01661-4
SARS-CoV-2 viral persistence in lung alveolar macrophages is controlled by IFN-γ and NK cells
https://www.pasteur.fr/en/press-area/press-documents/covid-19-persistence-sars-cov-2-lungs-and-role-innate-immunity#:~:text=%22Yet%20it%20has%20long%20been
The study has therefore shed light on a mechanism that may explain the presence of ‘viral reservoirs’: while individuals with little or no long-term virus had adaptive NK cell production, individuals with higher levels of virus had not only an absence of adaptive NK cells, but also a reduction in NK cell activity. Innate immunity therefore appears to play a role in the control of persistent SARS-CoV-2 viruses.
"We will be embarking on a study of a cohort infected with SARS-CoV-2 at the start of the pandemic to find out whether the viral reservoirs and mechanisms identified are related to cases of long COVID.
But the results here already represent an important step in understanding the nature of viral reservoirs and the mechanisms that regulate viral persistence
Https://elifesciences.org/articles/86015
RECOVER: Researching COVID to Enhance Recovery, has sought to understand the basis of long COVID in a large cohort. Given the range of symptoms that occur in long COVID, the mechanisms that may underlie these diverse symptoms may also be diverse. In this review, we focus on the emerging literature supporting the role(s) that viral persistence or reactivation of viruses may play in PASC. Persistence of SARS-CoV-2 RNA or antigens is reported in some organs
https://www.thelancet.com/journals/lanres/article/PIIS2213-2600(23)00142-X/fulltext#:~:text=In%20another%20study%2C%20the%20circulating,as%20shown%20by%20ddPCR%20and
In another study, the circulating SARS-CoV-2 components, spike protein, and viral RNA fragments persisted for up to 1 year or longer after SARS-CoV-2 acute infection in patients with long COVID, whereas these viral components decreased or were totally absent in convalescent patients with COVID-19, as shown by ddPCR and spike protein ELISA techniques.15
These findings provide further evidence that there might be a correlation between the length of time the virus stays in the body and the risk of long COVID
Long COVID is a developing science.
There are many aspects to the symptoms and potentially many underlying causes.
A year ago I would have said SNG001 plays a role in reduction of symptoms post infection as demonstrated by the data presented at IDWeek22 and NO role as a therapeutic for patients suffering LC.
However science is not a static concept and knowledge evolves. The French study is well researched and from a renowned institution. It points to new knowledge on how NK cells might play a part in viral persistence. Their belief is that this could be one of the underlying causes of LC in some patients.
We also know from scientific studies that interferon treatment directly impacts the activity of these cells and has been shown to impact viral persistence in HIV.
We therefore have a potential method of action that could produce results in some LC patients.
It’s interesting that one of the studies in the new trials specifically talks about treating patients with viral persistence, so clearly Synairgen believe their drug could benefit these patients.
If the French study is correct and viral persistence is one of the causes of LC we have a drug in our trials that may show efficacy against LC patients who’s underlying issues are due to this problem.
Looking at the information released by the board about the future trials. We may be pushing at an open door with the points in this thread as it ties into the French study of viral reservoirs and patients unable to clear the virus
Conducting non-interventional preparatory work to expand hospitalised patient populations for potential treatment with SNG001, which are likely to include: ventilated patients with confirmed viral pneumonia;
“and patients who are unable to clear virus and become persistent viral shedders”
…….trials are anticipated to start in H1 2024.
My view is simply Long Covid has a level of continued focus. Covid focus has diminished.
If we’re taking blood samples in P2 why not look at spike proteins pre-treatment and post treatment and compare placebo to drug patients. Nothing lost in gathering that data comparing NK cell activation etc linking it to a French study from a very well respected source.
Whether they did this in P2 or just gathered the samples and ran a retrospective analysis later adds a level of interest in the science community around “Long Covid”.
That might be carried forward in a P3 or open doors to a LC platform trial. If the samples are there make use and advertise the work !
Good article goes the foundation of icu care
https://insight.jci.org/articles/view/140329
Severe immunosuppression and not a cytokine storm characterizes COVID-19 infections
The purpose of this study was to determine whether critically ill COVID-19 patients have an exaggerated proinflammatory cytokine storm versus an immunosuppressive immunological endotype, and determine whether there are changes in immune function during disease progression.
Although several key proinflammatory cytokines, including IL-1β, IFN-ɣ, and TNF-α, were modestly increased in COVID-19 patients compared with healthy control participants, the increases were near the lower limit of detection of the assay
Currently, the prevailing paradigm that guides the therapeutic approach to COVID-19 is that patients are dying from the effects of cytokine storm–mediated inflammation with resultant lung and other organ injury (6, 7, 40–43). Based on this theory of unbridled inflammation, COVID-19 patients are currently being treated with a variety of drugs that block proinflammatory cytokines or inhibit the inflammatory signaling cascade. The results from the present study strongly suggest that the primary endotype of COVID-19 is one of immunosuppression rather than hyperinflammation
Brand
8 Feb 2024 23:03
Posts: 1,143
Price: 5.405
Oh there was this too
" Then there remains the enigma of the post-viral syndrome (Long COVID or post-acute sequelae of SARS-CoV-2 [PASC]) affecting 3% of the UK population with a range of debilitating symptoms, both organ-specific and less specific. The latter symptoms, which include persistent fatigue, myalgias and arthralgias, post-exertion malaise (PEM), cognitive problems (e.g. "brain fog"), headaches, disrupted sleep and orthostatic intolerance are similar, if not identical to, those experienced in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS),3 a greatly misunderstood multi-system post-viral disorder effecting at least 250,000 adults and children in the UK and 17 million worldwide. Hopefully, understanding the mechanisms behind PASC (including PEM4) will also provide insights into those of ME/CFS, and enable effective therapeutic interventions to be developed for both disorders."
https://onlinelibrary.wiley.com/doi/full/10.1111/resp.14661
Another section from Brands French study article
“ The study has therefore shed light on a mechanism that may explain the presence of ‘viral reservoirs’: while individuals with little or no long-term virus had adaptive NK cell production, individuals with higher levels of virus had not only an absence of adaptive NK cells, but also a reduction in NK cell activity. Innate immunity therefore appears to play a role in the control of persistent SARS-CoV-2 viruses”
Studies have show interferon directly impacts NK cell activity and in HIV studies where the virus persists in viral reservoirs, treatment with interferon has been shown to reduce viral reservoirs.
New scientific evidence through this French study may now be showing sng001 could have a role to play not only in reducing symptoms of long covid after covid infection. But possibly treating some forms of long covid due to viral persistence
Https://www.medicalnewstoday.com/articles/long-covid-viral-reservoir-of-spike-protein-may-explain-long-term-symptoms
Researchers investigated the antigens of SARS-CoV-2—the virus that causes COVID-19—present in blood plasma samples collected from individuals with long COVID and typical COVID-19 infection.
They found that one particular SARS-CoV-2 antigen—the spike protein—was present in the blood of a majority of long COVID patients, up to a year after they were first diagnosed with COVID-19.
In patients with typical COVID-19 infection, however, the spike protein was not detected.
This finding provides evidence for the hypothesis that SARS-CoV-2 can persist in the body through viral reservoirs, where it continues to release spike protein and trigger inflammation.
Worth it’s own thread….Thanks to Brand for the find
Brand
Posts: 1,143
The question is could sng001 "cure" long covid.
https://www.pasteur.fr/en/press-area/press-documents/covid-19-persistence-sars-cov-2-lungs-and-role-innate-immunity#:~:text=%22Yet%20it%20has%20long%20been,adaptive%20NK%20cells)%20and%20destroy
One to two weeks after contracting COVID, the SARS-CoV-2 virus generally becomes undetectable in the upper respiratory tract. But does that mean that it is no longer present in the body? To find out, a team from the Institut Pasteur specialized in HIV, in collaboration with a French public research institute, the Alternative Energies and Atomic Energy Commission (CEA), conducted a study on lung cells in an animal model. The results show not only that SARS-CoV-2 is found in the lungs of certain individuals for up to 18 months after infection, but also that its persistence appears to be linked to a failure of innate immunity (the first line of defense against pathogens). This research was published in the journal Nature Immunology on November 2, 2023.