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Topic: Narsoplimab, MASP2, Lectin Pathway & COVID

The role of the lectin pathway of the complement system in SARS-CoV-2 lung injury

full article:
https://www.translationalres.com/articl … 0/fulltext

quotes
"The intense activation of the lectin pathway, with particular emphasis on the MBL pathway, together with endothelial dysfunction and a massive proinflammatory cytokines production, possibly lead to a worse outcome in patients infected with SARS-Cov-2 "

Abstract
Although some evidence showed the activation of complement systems in COVID-19 patients, proinflammatory status and lectin pathway remain unclear. Thus, the present study aimed to demonstrate the role of MBL and ficolin-3 in the complement system activation and compared to pandemic Influenza A virus H1N1 subtype infection (H1N1pdm09) and control patients. A total of 27 lungs formalin-fixed paraffin-embedded (FFPE) samples (10 from H1N1 group, 6 from the COVID-19 group, and 11 from the control group) were analyzed by immunohistochemistry using anti-IL-6, TNF-alfa, CD163, MBL e FCN3 antibodies. Genotyping of target polymorphisms in the MBL2 gene was performed by real-time PCR. Proinflammatory cytokines such as IL-6 and TNF-alpha presented higher tissue expression in the COVID-19 group compared to H1N1 and control groups. The same results were observed for ICAM-1 tissue expression. Increased expression of the FCN3 was observed in the COVID-19 group and H1N1 group compared to the control group. The MBL tissue expression was higher in the COVID-19 group compared to H1N1 and control groups. The genotypes AA for rs180040 (G/A), GG for rs1800451 (G/A) and CC for rs5030737 (T/C) showed a higher prevalence in the COVID-19 group. The intense activation of the lectin pathway, with particular emphasis on the MBL pathway, together with endothelial dysfunction and a massive proinflammatory cytokines production, possibly lead to a worse outcome in patients infected with SARS-Cov-2. Moreover, 3 SNPs of our study presented genotypes that might be correlated with high MBL tissue expression in the COVID-19 pulmonary samples.

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

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Re: Narsoplimab, MASP2, Lectin Pathway & COVID

https://www.ncbi.nlm.nih.gov/pmc/articl … 585243.pdf

The Influence of the Lectin Pathway
of Complement Activation on
Infections of the Respiratory System
Anna S. S´ wierzko and Maciej Cedzyn´ ski*
Laboratory of Immunobiology of Infections, Institute of Medical Biology, Polish Academy of Sciences, Ło´ dz´, Poland
Lung diseases are among the leading causes of morbidity and mortality. Complement
activation may prevent a variety of respiratory infections, but on the other hand, could
exacerbate tissue damage or contribute to adverse side effects. In this review, the
associations of factors specific for complement activation via the lectin pathway (LP)
with infections of the respiratory system, from birth to adulthood, are discussed. The most
extensive data concern mannose-binding lectin (MBL) which together with other collectins
(collectin-10, collectin-11) and the ficolins (ficolin-1, ficolin-2, ficolin-3) belong to patternrecognition molecules (PRM) specific for the LP. Those PRM form complexes with MBLassociated serine proteases (MASP-1, MASP-2, MASP-3) and related non-enzymatic
factors (MAp19, MAp44). Beside diseases affecting humanity for centuries like
tuberculosis or neonatal pneumonia, some recently published data concerning COVID19 are summarized.

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

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Re: Narsoplimab, MASP2, Lectin Pathway & COVID

This long article
https://www.theatlantic.com/health/arch … ms/615382/

illustrates the HELL that CV19 Sequelae can make your life, even if you had a mild case. You will find out the already huge and growing population of people who have survived Covid but will now suffer for weeks, months, and years with continuing symptoms long after they no longer have an active case of the virus.

The full article without the links, is here, for your convenience.

So far, the data says that CV19 patients treated with narso do not develop Sequelae.

It appears that treating someone with narso after they recover may also prevent sequelae, and Greg thinks that  narso can treat sequelae because it treats the same kind of thing in TA-TMA patients whoo suffer similar problems due to endothelial inlammation and hyper-clotting.
http://www.trustintelligence.com/viewto … d=265#p265

We

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

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Re: Narsoplimab, MASP2, Lectin Pathway & COVID

60 Minutes apparently had a piece on the Long-Timers, https://www.cbsnews.com/news/covid-long … 020-11-22/

like the article from The Atlantic that I already posted.

And there are more institutions setting up treatment programs for the increasing number of patients I have been warning about for months. Do you recall the piece I did about the 3 Dialysis companies?

Here's an advert: https://www.mountsinai.org/about/covid1 … covid-care

Center for Post-COVID Care
Recovery from COVID-19 is posing a new set of challenges for patients and physicians alike. There is much we don’t know, but the Center for Post-COVID Care at Mount Sinai is bringing together a team from a broad range of specialties to address the issues of COVID-19 aftercare. If you have had COVID-19, the Center will provide you the best care available, based on the latest understanding of the disease.

Leading the Way in COVID-19 Research and Treatment
Mount Sinai has been in the forefront of understanding and treating COVID-19. We were among the first to develop an antibody test to identify individuals who have recovered from COVID-19. We were then able to use plasma from these individuals to help critically ill patients recover. Researchers at the Icahn School of Medicine at Mount Sinai have been helping our frontline physicians treat all the varied aspects of the disease—from thrombosis to the sudden inflammatory response known as a “cytokine storm.” Because COVID-19 behaves so differently in many patients, we have created this multi-disciplinary team working together for your recovery to health.

Experts from Every Specialty, Working for Your Care
The long-term effects of COVID-19 are not clear yet. The virus can affect many different systems within the body—from the lungs to the heart to the kidneys. But by bringing in specialists who have been on the frontlines of the outbreak, you will have the most knowledgeable experts available. Your team and clinical staff may include disciplines such as:

Primary Care
Pulmonary Medicine
Cardiology
Infectious Diseases
Nephrology
Physiatry
Physical and Occupational Therapy
Radiology
Neuropsychiatry
Behavioral Health
Social Workers
Pharmacists
Treating the Whole Person, Not Just the Disease
This time has caused all of us anxiety—and some, more than others. The Center has the resources to help you manage anxiety and depression, PTSD, and other emotional issues. Getting “back to normal” may require physical therapy, occupational therapy, or other types of support—whether in groups or one-on-one. Whatever your needs, the Center is a compassionate, holistic source of care.

You Can Help Us Understand COVID-19
To understand the long-term effects of COVID-19, we are offering patients the opportunity to participate in the Mount Sinai COVID-19 Registry. Participation is voluntary, and you don’t have to register to get care at the Center. However, by being part of the Registry, you will help us understand the effects of COVID-19 on long-term health and well-being. Together, we will overcome COVID-19.

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

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Re: Narsoplimab, MASP2, Lectin Pathway & COVID

In silico and In vitro Studies Reveal Complement System Drives Coagulation Cascade in SARS-CoV-2 Pathogenesis

https://www.sciencedirect.com/science/a … ihub#s0090
https://doi.org/10.1016/j.csbj.2020.11.005

Highlights
• The structural similarity analysis identified 3,735 human proteins (hSARS-CoV-2) similar to the 16 SARS-CoV-2 proteins.

• MAPK1, MAPK3, AKT1, and SRC proteins are the critical drivers of signaling pathways and often overlap with the associated pathways during SARS-CoV-2 infection.

• Several viral proteins interact with MAVS, TRAF6, IRAK1, IRF3, and IRF7 and inhibit IFN-I and ISGs production.

• TP53, TNF, MAPK3 proteins in Cytokines storm and VAMP8, ITGAM, and STOM in Neutrophils degranulation are regulatory proteins associated with the ARDS.

• Proteomics data showed 28 candidates associated with complement and coagulation cascade during SARS-CoV-2 infection.

• Our study suggests that therapeutic targeting of the downstream proteins of the complement system can mitigate SARS-CoV-2 pathogenesis.

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

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Re: Narsoplimab, MASP2, Lectin Pathway & COVID

In today's MRK announcement we have the crux of the Omeros dilemma.

The drug, known as CD24Fc, appeared to reduce the risk of respiratory failure or death in severe Covid-19 patients by 50% in a 203-person Phase III trial, OncoImmune said in September.

Those results floored Merck, Perlmutter told CNBC, but posed a clear problem: OncoImmune, like other small biotechs with promising Covid-19 drugs or vaccines, was in no position to scale the molecule to anywhere near the capacity required to make a dent on the pandemic. Merck will switch over existing manufacturing to produce the drug, an antibody, with the aim of developing sufficient supply by the middle of next year.

OncoImmune (http://www.oncoimmune.com/ ) is a privately help biotech company that cannot adequately serve the potential addressable market because it has not production facilities and cannot ramp up massive production (or pay for it) on its own.

Other than being private, Omeros' situation is very similar. While it has been slowly accumulating small lots it buys from Lonza in Singapore, it cannot hope to treat all the people who need narsoplimab. That's why (IMO) it is looking for Govt. help. Of course, that will come with a price, most likely a reduction in the price charged to patients or the Govt.

The drug MRK is buying is almost surely a complement drug, but neither MRK or OmcoImmune is being free with the information. Here's what MRK said today:

OncoImmune’s lead product is CD24Fc, a first-in-class recombinant fusion protein that targets the innate immune system. Prior to the Phase 3 clinical trial for COVID-19 patients, CD24Fc has been studied for safety in healthy volunteers and in Phase 2 clinical trials for the prevention of graft versus host disease (GVHD) following hematopoietic stem cell transplantation in patients with leukemia. A pivotal Phase 3 clinical trial (NCT04095858) for prophylaxis of GVHD has been initiated nationwide.

CD24Fc regulates DAMPs in the immune system. You can read about it on the company's website, here: http://www.oncoimmune.com/index.php?opt … Itemid=426

CD24Fc has a dual mechanism of action:

CD24Fc binds DAMPs, trapping the inflammatory stimuli to prevent their interaction with TLR receptors
CD24Fc binds Siglec G/10 and regulates host response to tissue injuries Siglec G/10-associated SHP1 inhibitory signaling
Both mechanisms likely act in concert to modulate immune responses.


This is the link to the clinical trial that ended in Sept.: https://clinicaltrials.gov/ct2/show/NCT04317040

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

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Re: Narsoplimab, MASP2, Lectin Pathway & COVID

Rambaldi's group in Italy supporting endothelial damage syndrome as involved in all the respiratory viruses. You can read and/or download it for free at the linK, published in
https://www.nature.com/articles/s41590-020-00832-x

Published: 18 November 2020
Macrophage expression and prognostic significance of the long pentraxin PTX3 in COVID-19
Enrico Brunetta, Marco Folci, […]Alberto Mantovani
Nature Immunology (2020)Cite this article


Abstract
Long pentraxin 3 (PTX3) is an essential component of humoral innate immunity, involved in resistance to selected pathogens and in the regulation of inflammation1,2,3. The present study was designed to assess the presence and significance of PTX3 in Coronavirus Disease 2019 (COVID-19)4,5,6,7. RNA-sequencing analysis of peripheral blood mononuclear cells, single-cell bioinformatics analysis and immunohistochemistry of lung autopsy samples revealed that myelomonocytic cells and endothelial cells express high levels of PTX3 in patients with COVID-19. Increased plasma concentrations of PTX3 were detected in 96 patients with COVID-19. PTX3 emerged as a strong independent predictor of 28-d mortality in multivariable analysis, better than conventional markers of inflammation, in hospitalized patients with COVID-19. The prognostic significance of PTX3 abundance for mortality was confirmed in a second independent cohort (54 patients). Thus, circulating and lung myelomonocytic cells and endothelial cells are a major source of PTX3, and PTX3 plasma concentration can serve as an independent strong prognostic indicator of short-term mortality in COVID-19.

Main
Highly pathogenic betacoronaviruses causing severe acute respiratory syndrome, Middle East respiratory syndrome and the current COVID-19 pandemic, affect the lower respiratory tract leading to critical acute respiratory distress syndrome (ARDS) and fatality in a high percentage of cases4,5,6,7. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is characterized by variable clinical forms, with symptoms including fever, cough and general malaise in mild and moderate cases, which progress to severe pneumonia or ARDS, shock and/or multiple organ failure, requiring admission to intensive care units (ICUs) in more severe cases. The high morbidity and mortality observed in the COVID-19 pandemic are caused by alveolar damage and pneumonia, cardiovascular complications and multi-organ failure.

SARS-CoV-2 interacts with angiotensin-converting enzyme 2 expressed by pneumocytes in the alveolar lining, leading to lung injury. Angiotensin-converting enzyme 2 is also widely expressed on endothelial cells, thus possibly explaining the evidence of direct viral infection of the endothelium, diffuse endothelial inflammation and widespread microvascular dysfunction, leading to organ ischemia, inflammation, edema and a procoagulant state7,8,9,10,11,12. In addition, uncontrolled activation of innate and adaptive immunity in response to the infection results in hyperinflammatory responses, which, by affecting lung tissue and blood vessels, contribute to ARDS pathogenesis, shock and multi-organ failure7,13. Macrophages are central drivers of uncontrolled inflammation and tissue damage associated with COVID-19 (refs. 7,13,14).

PTX3 is a key component of humoral innate immunity, belonging to the family of pentraxins1,2. In contrast with its relative, the short pentraxin C-reactive protein (CRP), essentially produced by the liver in response to interleukin (IL)-6 during the acute-phase response3, PTX3 is rapidly produced by several cell types, including myeloid cells, endothelial cells and respiratory epithelial cells, particularly in response to IL-1, tumor necrosis factor, microbial molecules and tissue damage1,2. PTX3 is an essential component of humoral innate immunity, involved in resistance to selected pathogens and in the regulation of inflammation1,2. The similarity with CRP prompted investigations as to the usefulness of PTX3 as a marker in diverse human conditions of infective or inflammatory origin. The local production by different cell types at inflammatory sites and the release of the preformed protein by neutrophils in response to primary proinflammatory cytokines or microbial recognition accounts for the rapidity of PTX3 increase in these conditions. Increased PTX3 plasma concentrations were described in infections of fungal, bacterial and viral origin15,16, severe inflammatory response syndrome, sepsis17,18,19,20 and cardiovascular diseases21. In different pathological conditions, high PTX3 plasma concentrations were associated with disease severity and mortality17,18,19. Moreover, PTX3 has been shown to serve as a biomarker of disease activity in inflammatory conditions involving the vascular bed, ranging from atherosclerosis to vasculitis21,22,23,24.

Previous findings on the prognostic significance of PTX3 in systemic inflammatory conditions, as well as in vascular pathology17,21, prompted the present investigation, which was designed to investigate the cellular sources and significance of PTX3 in patients with COVID-19.

We conducted an in silico bioinformatic analysis of the expression of PTX3 using public databases25,26,27. SARS-CoV-2 strongly induced or amplified PTX3 transcript expression in two lines representative of respiratory tract epithelial cells, Calu-3 and A549 (Fig. 1a). The same trend was observed in normal human bronchial cells, although it did not reach statistical significance (GSE147507)25. Bulk RNA sequencing (RNA-seq) of purified monocytes (Fig. 1b) and bioinformatic analysis at single-cell level of peripheral blood mononuclear cells (PBMCs) obtained from patients with COVID-19 (Fig. 1c) revealed that PTX3 was selectively expressed by COVID-19 neutrophils and monocytes (GSE150728)26. Moreover, bioinformatic analysis of COVID-19 bronchoalveolar lavage fluid (BALF) cells at single-cell level27 revealed that PTX3 was strongly expressed in neutrophils and monocyte-derived macrophage populations, as identified by molecular signatures (Fig. 1d).

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

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Re: Narsoplimab, MASP2, Lectin Pathway & COVID

This is conversation with K, a OMER shareholder from Belgium, which has high Covid/capita and a current surge. He recently went into quarantine because to of his co-workers got the virus. He has some odd job unload fishing trawlers  a couple of times a week. It's like a part-time job but pays full-time.

k wrote:

At webcast 6 weeks ago Greg said something covid related and very very soon. Can't remember what it was, was it more data? Been 6 weeks, so in biotech terms I think another 4 weeks or 10 weeks total is very very soon. About the time we hopefully granted priority review by fda. Could change real fast real hard somewhere between end December and early 2021.

Alan wrote:

I don't recall Greg saying there would be news on Covid "very very soon". I don't recall even 1 soon. I had hoped he'd have learned his lesson about giving that kind of guidance already...especially about things that he can't completely control. He is still probably looking for a way to not ruin the narso price for non-Covid sales... and the Trump Admin. is a bit preoccupied with other things. I presume he will have a better chance with Biden's group as it is their constituency at risk of dying and sequelae. When Govt. changes progress slows down to give the new guys time to find the bathroom. Unless Trump all of a sudden wants to take credit for narso.... I doubt it, as the turkey reportedly doesn't even care to read the briefing books (which have been condensed into a comic book summary for him).

k wrote:

Yeah, relisten to webcast, he said at 1h03 minutes... we have more to report in the Not so distant future.

Alan wrote:

"in the not so distant future" does not even approach "soon", much less VERY soon or "very very soon".

When I hear guidance, I always ask myself how much control over timing does the company have? Is it a task that requires time and repetition or are they depending on others who they can't control?

I am not holding my breath to hear anything Covid. And I anticipate a decision or announcement that some won't like, when it comes.

Short-term we have CMS Final Rule, possibly next week, BLA acceptance and Priority Review award potential. Either narso milestone may trigger JPM Initiation of Coverage or a BAM upgrade, both of which will be positive.

The most surprising guidance from Greg was for Narso approval in 'early 2021'. I would never have said that, even if I believed it. If it is justified, I think it has to do with FDA wanting narso available, off-label, so with the covid surge happening now, the FDA would want that all the more.  OTOH, I doubt they want to set a precedent for the fastest approval ever.

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

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Re: Narsoplimab, MASP2, Lectin Pathway & COVID

The Novartis approval was 10 weeks I think, so I doubt they would technically set a precedent with Narso.  I’m willing for it to be a tie.

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Re: Narsoplimab, MASP2, Lectin Pathway & COVID

So, a Groundhog Day approval?
tongue lol

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

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Re: Narsoplimab, MASP2, Lectin Pathway & COVID

https://www.cell.com/cell/fulltext/S009 … 20)31311-8
| VOLUME 183, ISSUE 5, P1354-1366.E13, NOVEMBER 25, 2020

Vascular Disease and Thrombosis in SARS-CoV-2-Infected Rhesus Macaques
Highlights

SARS-CoV-2 infection leads to macrophage infiltrates in the lung of infected macaques

SARS-CoV-2 upregulates proinflammatory cytokines and ISGs in macaques

SARS-CoV-2 upregulates complement and coagulation cascade in macaques

SARS-CoV-2 infection leads to endothelial damage and thrombosis in macaques
Summary
The COVID-19 pandemic has led to extensive morbidity and mortality throughout the world. Clinical features that drive SARS-CoV-2 pathogenesis in humans include inflammation and thrombosis, but the mechanistic details underlying these processes remain to be determined. In this study, we demonstrate endothelial disruption and vascular thrombosis in histopathologic sections of lungs from both humans and rhesus macaques infected with SARS-CoV-2. To define key molecular pathways associated with SARS-CoV-2 pathogenesis in macaques, we performed transcriptomic analyses of bronchoalveolar lavage and peripheral blood and proteomic analyses of serum. We observed macrophage infiltrates in lung and upregulation of macrophage, complement, platelet activation, thrombosis, and proinflammatory markers, including C-reactive protein, MX1, IL-6, IL-1, IL-8, TNFα, and NF-κB. These results suggest a model in which critical interactions between inflammatory and thrombosis pathways lead to SARS-CoV-2-induced vascular disease. Our findings suggest potential therapeutic targets for COVID-19.

https://els-jbs-prod-cdn.jbs.elsevierhealth.com/cms/attachment/f70d1da4-24fe-4c99-a82b-317b14d1326d/fx1.jpg

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

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Re: Narsoplimab, MASP2, Lectin Pathway & COVID

NYTimes headlines today, both relevant to potential use of narsoplimab in CV19.
================
Covid Survivors With Long-Term Symptoms Need Urgent Attention, Experts Say

By Pam Belluck

In a two-day meeting sponsored by the N.I.H., officials acknowledged an insufficient understanding of the issues and warned of a growing public health problem.
Doctors Are Skeptical of Pricey Drug Given Emergency Approval for Covid
Doctors Are Skeptical of Pricey Drug Given Emergency Approval for Covid

By Katherine J. Wu

Baricitinib, an arthritis drug made by Eli Lilly, may reduce recovery time by a day, but costs about $1,500 and comes with side effects.

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

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Re: Narsoplimab, MASP2, Lectin Pathway & COVID

Children do get Covid and they seem to have damage that narso could fix.

https://www.studyfinds.org/children-wit … el-damage/

A lot of people could be helped if Greg can find a way to produce more narso and demonstrate its benefits in a clear and unambiguous way.

I just sent this article without comment, to Greg, with the subject: The world needs narso, now, as you know.

I included the picture published with the article
https://www.studyfinds.org/wp-content/uploads/2020/06/AdobeStock_332467270-816x520.jpeg
==========================
Virtually all children infected with COVID-19 show signs of blood vessel damage, study shows
by John Anderer
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PHILADELPHIA, Pa. — The news about coronavirus and children just got a lot worse. A troubling study by researchers at the Children’s Hospital of Philadelphia reports a “high proportion” of children infected with SARS-CoV-2 show elevated levels of a biomarker tied to blood vessel damage. Making matters worse, this sign of cardiovascular damage is being seen in asymptomatic children as well as kids experiencing COVID-19 symptoms.

Additionally, many examined children testing positive for SARS-CoV-2 are being diagnosed with thrombotic microangiopathy (TMA). TMA leads to clots in small blood vessels and has been linked to severe COVID symptoms among adult patients.

“We do not yet know the clinical implications of this elevated biomarker in children with COVID-19 and no symptoms or minimal symptoms,” says co-senior author David T. Teachey, MD, Director of Clinical Research at the Center for Childhood Cancer Research at CHOP, in a media release. “We should continue testing for and monitoring children with SARS-CoV-2 so that we can better understand how the virus affects them in both the short and long term.”

The complex connection between kids and COVID
It’s fairly well established at this point that most children who contract coronavirus experience little to no symptoms. However, a small portion of young patients develop major symptoms or a post-viral inflammatory response to COVID-19 called Multisystem Inflammatory Syndrome in Children (MIS-C).

TMA in adults has a connection to more severe cases of COVID-19. Scientists believe the component of the immune system called “complement cascade” helps to mediate TMA in adults. The complement cascade is supposed to enhance and strengthen immune responses when a threat is present, but it can also backfire and lead to more inflammation. Up until now, the role of complement cascade during childhood TMA hadn’t been investigated.

To research the topic of “complement activation” in kids with SARS-CoV-2, researchers analyzed a group of 50 pediatric COVID-19 patients between April and July 2020. Among the group, 21 showed minimal to no symptoms, 11 experienced severe symptoms, and 18 developed MIS-C.

To search for complement activation and TMA among each patient, researchers used soluble C5b9 (sC5b9) as a biomarker. Scientists have used this substance for quite some time to assess the severity of TMA after stem cell procedures. In brief terms, the higher the level of sC5b9 in a transplant patient, the greater their mortality risk.

No symptoms doesn’t mean there’s no problem
Study authors discovered elevated levels of C5b9 in both patients with severe COVID-19 and MIS-C. While this didn’t surprise researchers, they did get a shock from seeing high levels of C5b9 among even asymptomatic youngsters.

Some of the lab data regarding TMA had to be obtained after the fact. This meant researchers didn’t have a complete dataset to work with for all 50 studied patients. Among 22 patients researchers did have complete data for, 86 percent (19 children) were diagnosed with TMA. Every child had elevated levels of sC5b9, even those without TMA.

“Although most children with COVID-19 do not have severe disease, our study shows that there may be other effects of SARS-CoV-2 that are worthy of investigation,” Dr. Teachey concludes. “Future studies are needed to determine if hospitalized children with SARS-CoV-2 should be screened for TMA, if TMA-directed management is helpful, and if there are any short- or long-term clinical consequences of complement activation and endothelial damage in children with COVID-19 or MIS-C. The most important takeaway from this study is we have more to learn about SARS-CoV-2. We should not make guesses about the short and long-term impact of infection.”

The study is published in Blood Advances.

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

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Re: Narsoplimab, MASP2, Lectin Pathway & COVID

https://mancunion.com/2020/12/10/have-w … -covid-19/

Have we misunderstood COVID-19?
WRITTEN ON 10TH DECEMBER 2020. POSTED IN SCIENCE & TECH

To date, COVID-19 has been around for nearly a year. In 2020, the world seemed to come to a standstill, but some areas of science have been advancing at a faster rate than ever. Scientists have produced promising vaccines in 10 months, rather than 10 years. In addition, thousands of papers have been published, aiming to contribute to our understanding of the underlying mechanisms of the disease.

Initially, the scientific literature focused primarily on two main aspects of SARS-CoV-2, the virus which causes COVID-19. The first was how it binds to ACE2 receptors, which are proteins that allow the virus to hijack human cells. The second was how the infection damages the lungs. These two targets seemed to be the key to treating the disease and reducing its mortality rate. Around 1/3 of patients admitted to hospital developed acute respiratory distress syndrome (ARDS).

ARDS is a complication of several respiratory illnesses, including the flu, pneumonia, and COVID-19. However, as our experience treating COVID-19 increased, scientists noticed that the level of damage to the lungs was disproportionate to the lack of oxygen in the blood and tissues when compared to other ARDS cases. This observation led them to consider other ways that COVID-19 could damage the body.

A study published in The New England Journal of Medicine compared 7 lungs obtained from patients who died of ARDS secondary to COVID-19, with 7 lungs affected by ARDS as a complication of the flu. Alongside these, they looked at 10 uninfected lungs.

Their research showed that COVID-19 ARDS showed the typical features of classical ARDS. This included a layer of cells lining the alveoli that caused fluid to enter the lungs. In turn, this reduces the amount of oxygen getting into the blood. However, they also found features that set it apart from typical ARDS. All of which involved the endothelium, the inner lining of the blood vessels.

These features were: extensive damage to endothelial cells, an exceedingly large number of small blood clots, thickening and weakening of the endothelium, and the formation of new vessels by splitting off existing ones. This splitting is a compensatory mechanism which increases blood supply, in order to supply tissues with enough nutrients and oxygen.

Damage to endothelial cells initiates a series of reactions which leads to the formation of a blood clot. The clot is meant to stop bleeding and initiate wound healing. This damage uncovers areas and molecules, to which platelets, which form the blood clot, can be bound. As platelets continue to bind themselves to one another, they eventually form a platelet plug.

In addition, the damage setts of a coagulation cascade. The result of this process is an insoluble fibrin clot. This surrounds and stabilises the platelet plug. Healthy wound healing depends on the tight regulation of both of these processes with the participation of a vast number of molecules. The platelet plug has to be prevented from growing too big, and it eventually has to be broken down alongside the fibrin clot.

https://mancunion.com/wp-content/uploads/sites/6/Laras-covid-diagram.png
Boglarka Kenedi, created with biorender.com

These findings tie in well with our current understanding of how SARS-CoV-2 binds to ACE2 receptors.

The ACE2 proteins can be found on the cells of the lung, the intestines, the kidney, the heart and the endothelium. Their role is to control the activity of angiotensin II. This is another protein which increases inflammation and damage to the endothelium. They do this by breaking the protein down.

When the virus binds to ACE2 receptors, it prevents them from breaking down angiotensin II. This increases inflammation and endothelial injury. Angiotensin II inhibits the secretion of the fibrinolysis inhibitor, preventing the breakdown of the blood clot.

Since then, several other studies have supported the theory that the endothelial layer plays an important role in the course of the infection. However, whether the differences in the presentation of COVID-19 ARDS is enough for it to be classified as an atypical subtype remains to be seen.

The research raises questions about COVID-19 ARDS. Can it be treated using the same parameters for mechanical ventilation as patients with classical ARDS due to the differences in the targets of damage? At the moment, the recommendation is to stick to the treatment guidelines already in place.

Understanding the underlying mechanisms of COVID-19 is paramount for developing effective treatments. By identifying the cells and molecules involved in the development of the immune response and complications like ARDS, we can target them more easily.

In this case, addressing endothelial dysfunction may lead to better patient outcomes. A study proposed statins, a common class of drugs used to treat high cholesterol, as a potential treatment endothelial dysfunction, as well as to prevent endothelial damage in patients at risk for cardiovascular disease, a risk factor for severe COVID-19.

With the rollout of the vaccine predicted to take months, who knows how many lives this new research could save? It will perhaps be a long time until science once again has the same life-saving impact for this many people. As we reach the end of a year of COVID, we can hopefully learn lessons about how quickly medicine can progress with enough scientists, funding, and determination.

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

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Re: Narsoplimab, MASP2, Lectin Pathway & COVID

Please correct me if I am wrong.  The above article describes a process.  Narsoplimab fights against a process that is deleterious to human health.  My question is, is the above article merely a restate of what OMER has already figured out as to Narsoplimab?  IOW, the authors of the above article are not aware of Narsoplimab.....

16

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

The scientific world mostly never heard of narso or the lectin pathway. Before I owned stock in Omeros, I never heard of "complement" but I was following the development of cancer treatment using the immune system.

Anyway, these people in the article are working from the virus, looking for the causes of the symptoms and finding it is endothelial damage and clotting. This is very good for OMER because Omeros has an obvious bias and they attack by starting from narsoplimab progressing to the virus and its effects.

The more people conclude that the existing treatments are inadequate and endothelial damage is not being addressed, the logic behind using narso (which also inhibits excessive clotting) gets more obviously something to try.

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

17

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

https://www.cell.com/trends/immunology/ … 0283-0.pdf

Journal Pre-proof
Complement factors in COVID-19 therapeutics and vaccines
Liriye Kurtovic, James G. Beeson
PII: S1471-4906(20)30283-0
DOI: https://doi.org/10.1016/j.it.2020.12.002
Reference: TREIMM 1756
To appear in: Trends in Immunology

misspelled narsoplimab

Complement-based therapeutics
Inhibitors targeting the early stages of complement activation have been used in small case
studies to treat COVID-19. These include a case series of a C1-inhibitor in non-critical
COVID-19 patients (conestat alfa, n=5) and a MASP2-inhibitor in severe COVID-19 patients with ARDS (naroplimab, n=6), whereby all patients had recovered and were discharged from
the hospital by days 22 and 91, respectively[47, 48]. The C3 inhibitor, AMY-101, was also
shown to improve clinical outcomes in COVID-19 patients with ARDS (n=4), as indicated by
reduced inflammatory markers (such as CRP and LDH) and improved respiratory
function[49, 50]. There have been several reports of individuals (n=8) already on C5-
inhibitors (eculizumab, ravulizumab) for unrelated conditions, at the time of SARS-CoV-2
infection [51-54]. While most patients had a standard recovery, two were admitted to the
intensive care unit (ICU), one of which did not recover[52, 53]. Other case reports of C5-
inhibitors (eculizumab, LFG316) administered to severe/critical COVID-19 patients (n=22)
also found some promising results [50, 55-57]. Although, two patients acquired bacterial
infections and another two developed mechanical ventilation-associated pneumonia, all four
died [50, 56, 57]. Few control studies have been performed; one of these evaluated a
combination of C5 (eculizumab) and JAK1/2 (ruxolitinib) inhibitors (treatment n=7, control
n=10)in COVID-19 patients [58]. A larger study evaluated the experimental treatment of
severe patients with a C5-inhibitor (eculizumab; treatment n=35, control n=45)[59]. The
treatment group presented enhanced survival at day 28 (p=0.005), although serious adverse
events were 2-fold higher than in controls, and included infectious complications and
ventilator-associated pneumonia[59]. The one randomized control, phase 2 trial
(NCT04333420)i
of a C5-inhibitor administered to severe COVID-19 patients (vilobelimab;
treatment n=15, control n=15) found no improvement in the primary outcome of respiratory
function (PaO2/FiO2)[60], but the authors noted that the study was not sufficiently powered to
detect significant differences between groups[60].
While these studies suggest some promise, it is too early to conclude whether complement
inhibitors have any clinical benefit in treating severe COVID-19. Several clinical trials of
AMY-101 and eculizumab are ongoing, as well as larger clinical studies. We also need to
acknowledge that complement inhibitors may not be suitable for all patients, particularly for
those with mild disease that display serum concentrations of complement proteins within the
normal range[14-16]. Complement may contribute to mounting an effective immune
response, and so, administration of therapeutics to inhibit complement might potentially be
harmful in COVID-19 patients with mild disease who may be mounting an effective immune
response. Furthermore, complement deficiencies are known to increase the risk of bacterial
infections[61], and several participants treated with eculizumab were reported to have
bacterial infections and ventilator-associated pneumonia (some of which did not recover)[50,
56, 57, 59, 60]. Overall, larger, randomized controlled clinical trials are required to formally
evaluate the therapeutic efficacy of complement inhibitors.

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

18 (edited by dorcse 2020-12-15 16:51:49)

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

If anyone is interested in the Narsoplimab HSCT-TMA NTAP presentation to CMS today by Dr. Perales on behalf of Omeros, I've uploaded it to Drive and it's available to view now. 

It's only about 16 minutes long.   Has an interesting question related to COVID and a comment from CMS panelist expressing interest in more data/studies.  Also, a question from CMS panelist about lack of a control group in HSCT-TMA and specifically how representative the treated patients are in HSCT-TMA patient population.  Excellent responses from Dr. Perales in my opinion.  Worth a listen.  His final comment is a killer.

https://drive.google.com/file/d/16IJUfj … sp=sharing

19

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

Was the first Q, your, Ed?

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

20

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

Not me.  Maybe somebody from ST?

21

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

Thanks for making the recording and giving us the link, Ed.

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

22

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

Thanks for the recording, Ed.  Seems like there's a question out there, that Omeros has the answer to.

23

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

Thanks Ed!!!

24

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

Patient admitted for Covid, had kidney TMA treated with usual crap for CV19 like hydroxycrapola, did not respond.

Given Soliris instead of narso:
Died and autopsied.
case:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7276225/

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

25

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

This is a sad story, I hope she did not suffer.  "Earlier diagnosis could perhaps lead to prompt treatment with plasma exchange OR COMPLEMENT PATHWAY INHIBITORS."  So the doctors here seem to be stuck on second base, without a way to get all the way home.  They know what they need, but they didn't get it.  Narsoplimab, right?  I wonder if they have heard of it.....

26

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

This was posted on Stocktwits by EyeMD87 and reports on IV by someone who also posts on IV and has been in OMER quite some time. The comments are his and I agree narso is the obvious answer to the CV19 mortality rate. we keep seeing this in studies of why people are dying from the response to the virus. The article is called:

" Emerging evidence of a COVID-19 thrombotic syndrome has treatment implications"
https://www.nature.com/articles/s41584-020-0474-5
--------------------------------
If you have the time, I would encourage all to read it in its entirety. Here is the first part of the conclusion:

A substantial subset of patients with COVID-19 are dying with a severe TMA, arising in association with viral invasion of endothelial cells and triggering a robust innate immune response with widespread activation of immune cells, cytokines and complement activation. The range of clinical, laboratory and pathological findings reviewed here confirms a diffuse, small-vessel microangiopathy similar to complement-associated TMA syndromes. This COVID-19-associated TMA can be accompanied by full-blown viral sepsis, cytokine storm and/or advanced inflammation in the lungs, which would probably synergistically increase the risk of thrombosis. The COVID-19-associated thrombotic syndrome is a novel condition, which might be described as SARS-CoV-2-incited, complement-mediated TMA with or without cytokine storm. However, patients with this syndrome rarely receive interventions that are known to be effective for dangerous TMA conditions.

Boom!! If this does not point to Narso, at least after it is approved, I don't know what will!!

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

27

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

Yep

28

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

They may never apply for approval for CV19.
Doesn't mean it won't be used.
Not being approved may lead to it costing more money, although will insurance companies in the USA pay for an off-label drug?

I don't know.

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

29

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

The narso restrictions on CUP availability, originally posted on the page below in early April 2020, is no longer there.

https://www.omeros.com/narsoplimab/

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

30

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

CV19 seldom kills children... but can do significant harm. Does the world care about children more than about saving the lives of old people?
The answer is obviously YES.

Narsoplimab is needed for everyone, to avoid the SEQUELAE.
Will the Biden Administration figure this out?

https://medicalxpress.com/news/2020-12- … ssion=true

"Researchers at Children's Hospital of Philadelphia (CHOP) have found elevated levels of a biomarker related to blood vessel damage in children with SARS-CoV-2 infection, even if the children had minimal or no symptoms of COVID-19. They also found that a high proportion of children with SARS-CoV-2 infection met clinical and diagnostic criteria for thrombotic microangiopathy (TMA)"

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

31

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

I read the article in the link.  It seems odd that 21 of 50 patients had minimal covid, yet were hospitalized with acute covid infection.  If the biomarker test is easy (cheap?) they should test many more people, including those who never went to the hospital.

32

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

I can't assert I know the reasons you are alluding to, but the thing about biomarkers is/tends to be that it is their utility to be correlated with something else that makes them useful, not that they are a cause of the thing that needs to be predicted.

Like, for example, Keytruda is approved for use in patients who test positive for some biomarker. That doesn't mean it will work for all the patients with that biomarker. Whereas Opdivo and other Checkpoint inhibitor is approved without any biomarker indication.

Does that throw any light on the situation?

Hope you (& other TIPSters) had a good New Year celebration.

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

33

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

The biomarkers reliability is interesting, as is the statement that many kids met the clinical criteria for TMA, which is more than a biomarker presumably.


While I think they may be making broad generalization based on the description of their 50 person sample, it's pretty clear that kids may not be immune to the longer term health consequences, and the lifetime costs associated with those may be multiples of the costs associated with much older people.

34

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

new article in Nature (prestigious) is difficult to copy.

https://www.nature.com/articles/s41581- … IDmRgf0%3D

"Immunity, endothelial injury and complement-induced coagulopathy in COVID-19"

excerpt:


Coronaviruses are enveloped, single-stranded RNA viruses (Fig. 1a). The Orthocoronavirinae family encom-passes several coronaviruses that can infect mammals and birds. Although such infections usually cause mild respiratory disease, in the past two decades, corona-viruses have caused two epidemic diseases in humans: severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS) in 2003 and 2012, respectively. Severe acute respiratory syndrome coro-navirus 2 (SARS-CoV-2) is a novel coronavirus that was isolated from the respiratory epithelium of patients with unexplained pneumonia in Wuhan, China, in December 2019. As of 17 September 2020, the disease caused by SARS-CoV-2, named coronavirus disease 2019 (COVID-19), has reached pandemic proportions, affect-ing more than 30 million individuals and claiming more than 1 million lives worldwide.Bats are considered to be the most likely natural SARS-CoV-2 reservoir1, although phylogenetic stud-ies have suggested that intermediate animal hosts may have mediated zoonotic transmission to humans2–5. The genome of SARS-CoV-2 is similar to that of a typi-cal betacoronavirus and contains at least ten open reading frames (ORFs; Fig. 1b). The ORF1a and ORF1b encode non-structural proteins (NSPs) that are generated by proteolytic processing1,6. The NSP12 catalytic sub-unit, along with its cofactors NSP7 and NSP8, consti-tutes the SARS-CoV-2 RNA-dependent RNA polymerase(RdRp) complex, which is essential for viral replication7. The near-atomic resolution of the NSP12–NSP7–NSP8 complex revealed a molecular assembly similar to the equivalent complex in SARS-CoV, the virus responsi-ble for SARS8, although biochemical analyses showed that the polymerase activity and thermostability of the SARS-CoV-2 RdRp complex was lower than that of the SARS-CoV RdRp complex, suggesting adap-tation of SARS-CoV-2 towards humans, which have lower body temperatures than bats7. The other ORFs encode the four main structural proteins: the spike, envelope, nucleocapsid and membrane pro-teins, as well as several accessory proteins with unknown functions1,6.Immunity, endothelial injury and complement-induced coagulopathy in COVID-19

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

35

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

Blood clots in the brain linked to Covid, of course.
https://www.medicalnewstoday.com/articl … od-vessels

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

36

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

He's some interesting intel from a guy who is a member of the OMER email group I am part of. It speaks for itself.
==================
About a month ago a friends mother had critical CV19 and I reached out to Dr and Omeros. (Friend from NY helped).  Dr Whitaker reached out and said have her Dr call him directly and they would arrange Narso. Her Dr never called him and I am livid on that. Dr G emailed me for follow up and asked how she was doing and told him she past.   I firmly believe drug is being used in US for CV19 just that reason and Dr’s email to me in around about says it.
=====================
Please don't show to anyone else, lest it get back to the author or his friend.

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

37

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

Covid may not be going away after everyone (who wants it) gets vaccinated. This may provide continuing demand for narso to treat the symptoms and save lives.

The emergence of new Covid variants is leading to more reports of reinfection. It remains to be seen whether vaccines will work for all subsequent mutations, or how long the vaccine protection will last if the original vaccine they were developed for has changed.

from an overview of CV19 on Medscape published Jan. 9th:

https://charts.stocktwits.com/production/original_271882142.png

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

38 (edited by Alan Robert Ross 2021-01-15 08:15:49)

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

from Stat talking about the Biden plan (see Govt. Pandemic Programs):

"The transition also circulated a fact sheet that called for the development and procurement of new Covid-19 therapies, but provided little detail."

Another article says:

"Invest in treatments for COVID-19. Months into this pandemic, we still do not have reliable and accessible treatments. The federal government urgently needs to invest to support development, manufacturing, and purchase of therapies to ensure wide availability and affordability of effective treatments, as well as invest in studies of the long-term health impacts of COVID-19 and potential therapies to address them."
https://www.krwg.org/post/fact-sheet-bi … ndividuals

Most stories covering this topic focus on vaccinations, not taking about treatment.

Nobody talks about cure of the virus OR curing what problems the virus causes (endothelial damage) that leads to death.

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

39

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

Through the grapevine from a European oncologist with a colleague with knowledge of I-SPY (which was ongology originally) indicates first CV19 patient get treated with Narso on or about Feb. 1st. 

I do not know how/if this is public so please keep it to yourselves. I have not checked ST or other Boards for it because I am busy wrapping glass tabletops, coffee tables etc.

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

40

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

If that's true, that's way before we started wondering why we hadn't heard any news re people with Covid getting Narso for treatment.  In hindsight, I suppose Greg kept it quiet because he wanted to wait and see how the drug would work - just to be sure.  Can't fault him for that, it was prudent.

41

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

???
Treating 50 patients starting Feb 1, 2021 in the ISPY trial (they have been treating others in CUP or ??? for months already).

THIS IS CONFIDENTIAL........NOT FOR ANY Circulation.

more later

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

42

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

from ST

Another event to keep an eye on: 90mins of Narsoplimab presentation at EBMT2021 ebmt2021.abstractserver.com...

Industry Symposium
Auditorium 3
Sunday, March 14, 14:30 - 16:00
IS15 Emerging Evidence on the Role of Complement Pathway in the Pathophysiology of HSCT-TMA - Omeros Industry Symposium
Miguel-Angel Perales
IS15-1 From bench to clinics: what evidence do we have about the complement pathway’s role in HSCT-TMA
Jeffrey Laurence (United States)
14:30 – 14:55
25 min
IS15-2 Emerged clinical data (including pivotal trial data review with subgroup analysis)
Alessandro Rambaldi (Italy)
14:55 – 15:25
30 min
IS15-3 Implications to clinical practice (with potential case study)
Miguel-Angel Perales (United States)
15:25 – 15:50
25 min
IS15-4 Q&A

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

43

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

I hear that there are only 5 or 6 drugs being tested ISPY as CV treatments including Narso.

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

44

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

A poster who is not a jerk says that narso for CV19 is entering PHASE 3. He bases it on this chart:
https://charts.stocktwits.com/production/original_274848882.png which shows the arrow at the end of Phase 2, compared to the pipeline programs below.

SO IS IT REALLY A PHASE 3 trial?????

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

45

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

I have just sent an email to Greg entitled:

"A simple confirmation would be appreciated"

Apparently, if I understand correctly, narsoplimab will soon be entering an ISPY trial for the treatment of CV19....

Omeros has divulged that narso for CV19 has completed, or is at the very end of Phase 2:

https://charts.stocktwits.com/production/original_274848882.png

So, am I correct in the logical conclusion that the narsoplimab ISPY trial is a Phase 3 pivotal trial?

I presume also that FDA agrees with your oft-repeated (and data-supported) assessment that the endothelial damage syndrome for HSCT-TMA and CV19 are the same basic MOA with different triggers.

I am very impressed that you have managed to "skip a grade in school" twice.
For the same drug.
Your detractors are blind fools.

Best...
Alan
**************
I wonder whether he will confirm.
He has left sufficient bread crumbs.

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

46

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

He actually replied.
Not exactly about the literal question as much as to the point of the question, which is even better.

To paraphrase, he indicated that the results of the ISPY trial (if they are good and depending on how well narso does, may support actual approve or an Emergency Use Authorization.

Obviously, this is for your eyes and ears only....

This is exactly what I expected because Greg's trademark MOA is to get the most out of the minimum of data and spending. This fits in with narso development from the start.

I have also been in contact with an oncologist with contacts to the ISPY group (which originally was an Oncology group trying to run trials more efficiently). He told me (again... DO NOT PASS THIS ON) that there are 5 drugs already being tested and at the end of the month, Omer will be added with another 4. Patients will be added to the trial, with the BEST-PERFORMING treatments getting the patients, preferentially, so that they will have more data sooner than ones that don't work as well.

They were enrolling 50/week with 5 drugs, so they will probably double that enrollment rate, with the patients distributed as I explained.

His guess is that the first 50 will be treated with narso within about 2-3 months and this will be the first "readout". So potential Narso in CV19 in April.

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

47

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

I think that at long last, Narsoplimab is playing in the Super Bowl.  Will it win?

48

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

More like the tryouts for a Pro team, with aspirants of widely varying abilities and specialties.

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.

49

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

Excellent news Alan.  Thanks for digging into it.  Thanks for all you do.

50

Re: Narsoplimab, MASP2, Lectin Pathway & COVID

Glad to do it, when it turns out well, Ed.

I should stress/reiterate that GD indicated that ISPY-Covid has the POTENTIAL to lead to approval in either or both the 2 way (emergency or regular). He certainly did not say it WOULD or WILL or anything definitive.

He and we know that the drug has to perform in an extraordinary way, like no other drug that has been tried, to save a higher % of the severely infected from death.

Sick people need it and all those suffering from a difficult and disrupted economy need it. Biden will be a hero for getting it approved if it works to lessen the emergency.

Once approved, the biggest problem will be to produce enough to fulfill demand, most likely.

original content ©2020 to 2021 by Alan Robert Ross
Founder, Trust Intelligence
The foregoing is not investment advice.