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Aandeel Pharming Group AEX:PHARM.NL, NL0010391025

  • 0,830 28 sep 2021 14:17
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Cytokine Storm in COVID-19

78 Posts
Pagina: «« 1 2 3 4 »» | Laatste | Omlaag ↓
  1. Jesse L. Livermore 25 november 2020 20:57
    De HAE expert Coen Maas, collega van Frank van de Veerdonk op het Radboud UMC maakt melding van het Pharming onderzoek van Osthoff in Basel.

    Met Dank aan Beukie.

    journals.lww.com/hemasphere/Fulltext/...


    quote

    A Pathophysiological Perspective on the SARS-CoV-2 Coagulopathy
    Kusadasi, Nuray1; Sikma, Maaike1,2; Huisman, Albert3; Westerink, Jan4; Maas, Coen3; Schutgens, Roger5

    Considering its role in the bradykinin pathway, FXII is the attractive target in SARS-CoV-2 related pathology.

    From this point of view, blocking FXIIa by its strong inhibitor C1-esterase inhibitor (C1-INH) is of interest and is currently been explored by Osthoff and colleagues at the University Hospital Basel in Switzerland.

    The potential role of plasma kallikrein in case of SARS-CoV-2 infection may be summarized as (1) the activation of FXII with the end-product thrombin (2) the generation of bradykinin with subsequent vascular permeability and leakage, (3) the activation of the renin-angiotensin system through conversion of renin from pre-renin leading to a pro-inflammatory state through increased angiotensin 1 receptor activation and (4) the activation of C5, in part through activation of C1 via FXII and in part through activation of C3 via plasmin. The inhibition of plasma kallikrein might therefore play a central role as target treatment, especially as 2 drugs are already on the market (lanadelumab and ecallantide). The use of these agents, alone or in combination with other agents acting on complement, coagulation and/or renin-angiotensin systems, might be an attractive treatment strategy. At the level of the complement system, the risk of thrombotic complications in patients with paroxysmal nocturnal hemoglobinuria, a rare life threatening disease manifesting with hemolytic anemia, bone marrow failure and thrombosis, has well been established.85 Even more so, treatment with the C5 blocking agent eculizumab decreases these thrombotic risk significantly indicating the inhibition of complement activation as a possible target to reduce the risk of thrombotic complications.86 Finally, the interplay between inflammation and thrombosis has already being stressed. Interfering with anti-inflammatory agents, such as tocilizumab, anti-IL-6, anti-IL-1 and others, could have a beneficial effect on the level of coagulopathy as well. Future research to prevent or treat the SARS-CoV-2 infection related coagulopathy should therefore focus on targets other than regular antithrombotic treatment.


    Conclusion

    The severe critical illness as seen in patients infected with SARS-CoV-2 is characterized by multiple organ failure and a deep hypoxia related to ARDS and pulmonary embolism. Central in the pathogenesis are the activation of the renin-angiotensin, the kallikrein-kinin, the complement and the coagulation system.

    Pharmacological interventions aimed at these mechanisms may alter the clinical course in these patients.


    unquote


    Groeten,


    Jesse Livermore
  2. forum rang 4 Uniek 2 december 2020 10:23
    Brazil

    Study sheds light on immune mechanism that triggers cytokine storm typical of COVID-19
    ...
    Separately, the scientists are testing the use of a drug to inhibit the NLRP3 inflammasome in patients with severe COVID-19. Promising preliminary results have been published on medRxiv.

    "We're looking for other drugs capable of inhibiting the NLRP3 inflammasome for testing in a clinical trial," Zamboni said. "As we discover more about inflammasome activation mechanisms in COVID-19, we can identify drugs that reduce the inflammatory process more effectively."

    medicalxpress.com/news/2020-12-immune...
    - - - -
    Hereditary autoinflammatory diseases are caused by gene mutations of the innate immune pathway, e.g. nucleotide receptor protein 3 (NLRP3).

    sorry...
  3. forum rang 6 Misschien 2 december 2020 10:35
    quote:

    Uniek schreef op 2 december 2020 10:23:


    Brazil

    Study sheds light on immune mechanism that triggers cytokine storm typical of COVID-19
    ...
    Separately, the scientists are testing the use of a drug to inhibit the NLRP3 inflammasome in patients with severe COVID-19. Promising preliminary results have been published on medRxiv.

    "We're looking for other drugs capable of inhibiting the NLRP3 inflammasome for testing in a clinical trial," Zamboni said. "As we discover more about inflammasome activation mechanisms in COVID-19, we can identify drugs that reduce the inflammatory process more effectively."

    medicalxpress.com/news/2020-12-immune...
    - - - -
    Hereditary autoinflammatory diseases are caused by gene mutations of the innate immune pathway, e.g. nucleotide receptor protein 3 (NLRP3).

    sorry...
  4. [verwijderd] 2 december 2020 10:38
    quote:

    Uniek schreef op 2 december 2020 10:23:


    Brazil

    Study sheds light on immune mechanism that triggers cytokine storm typical of COVID-19
    ...
    Separately, the scientists are testing the use of a drug to inhibit the NLRP3 inflammasome in patients with severe COVID-19. Promising preliminary results have been published on medRxiv.

    "We're looking for other drugs capable of inhibiting the NLRP3 inflammasome for testing in a clinical trial," Zamboni said. "As we discover more about inflammasome activation mechanisms in COVID-19, we can identify drugs that reduce the inflammatory process more effectively."

    medicalxpress.com/news/2020-12-immune...
    - - - -
    Hereditary autoinflammatory diseases are caused by gene mutations of the innate immune pathway, e.g. nucleotide receptor protein 3 (NLRP3).

    sorry...


    Bedankt Uniek, het is een verschrikkelijk probleem, zo'n cytokinestorm...Zojuist heb ik gehoord dat iemand in mijn bekenden kring dichtbij hieraan overleden is na 2 weken op z'n buik aan de beademing, 60 jaar, nieren, alles heeft het begeven.
    Dus fingers crossed voor Pharming en andere biotech's om zo snel mogelijk iets te vinden en zoveel mogelijk mensen te helpen.
  5. forum rang 4 Uniek 2 december 2020 10:54
    maar zou Pharming al gereageerd hebben hierop..

    "We're looking for other drugs capable of inhibiting the NLRP3 inflammasome for testing in a clinical trial," Zamboni said. "As we discover more about inflammasome activation mechanisms in COVID-19, we can identify drugs that reduce the inflammatory process more effectively."
  6. forum rang 6 Misschien 2 december 2020 10:56
    quote:

    La Reina schreef op 2 december 2020 10:38:


    [...]

    Bedankt Uniek, het is een verschrikkelijk probleem, zo'n cytokinestorm...Zojuist heb ik gehoord dat iemand in mijn bekenden kring dichtbij hieraan overleden is na 2 weken op z'n buik aan de beademing, 60 jaar, nieren, alles heeft het begeven.
    Dus fingers crossed voor Pharming en andere biotech's om zo snel mogelijk iets te vinden en zoveel mogelijk mensen te helpen.


    Ik een ijzersterke kerel met een grondverzetbedrijf die een grote bekende in heel Noord Holland van net 50!

    Mijn zoon was verbijsterd en altijd op zijn hoede.

    Tini
  7. [verwijderd] 2 december 2020 11:26
    quote:

    Misschien schreef op 2 december 2020 10:56:


    [...]

    Ik een ijzersterke kerel met een grondverzetbedrijf die een grote bekende in heel Noord Holland van net 50!

    Mijn zoon was verbijsterd en altijd op zijn hoede.

    Tini

    Tini, bedoel je nu dat je eigen zoon ook het slachtoffer is geworden van die Kl..ziekte? Hoop het toch niet.

    Hier krijg je nu het afscheidsritueel dat we niet eens mogen bijwonen. En je mag niemand troosten, alleen een beetje appen en videobellen met huilende nog jonge kinderen...dat is wel heel moeilijk.
  8. [verwijderd] 7 december 2020 14:38
    Wel of geen relatie tussen cytokinestorm en covid19:

    onlinelibrary.wiley.com/doi/10.1111/e...

    Conclusion
    Severe COVID-19 is characterized by significantly increased levels of pro-inflammatory cytokines and reduced T lymphocytes. Well-designed and adequately powered prospective studies are needed to amplify the current evidence and provide definitive answers to dilemmas regarding timing and type of anti-COVID-19 therapy particularly in severe patients.


    jamanetwork.com/journals/jamainternal...

    www.ncbi.nlm.nih.gov/pmc/articles/PMC...

    www.ncbi.nlm.nih.gov/pmc/articles/PMC...

    www.frontiersin.org/articles/10.3389/...
  9. forum rang 4 Uniek 12 december 2020 12:42
    3 voordelen die Ruconest heeft voor de behandeling van Covid 19 tov andere Pharma's zijn ,

    1) het dempen van ongecontroleerde complementactivering en collaterale longschade;
    2) capillaire lekkage en daaropvolgend longoedeem verminderen door directe remming van het kallikreïne-kininesysteem;
    3) de vorming van microthrombi verminderen door remming van door MASP-1 geïnduceerde stolselvorming en door factor XII versterkte trombo-ontsteking.

  10. forum rang 4 Uniek 13 december 2020 11:54
    Belangrijkste was ik toch bijna vergeten, hoop nu dat MEER mensen/beleggers nu begrijpen wat Pharmings Ruconest kan betekenen en is dit de aanzet hiervoor (Covid 19)

    There are multiple other protein deficiency disorders that Pharming could apply its technology to, Herrmann added, notably Pompe, Fabry and Gaucher's diseases — all of which are rare diseases known as lysosomal storage disorders, and represent a global market opportunity worth some $5.6 billion in 2017.

    People with HAE are unable to make C1 esterase inhibitor, which is the handbrake of 90% of human inflammatory processes, including most of those that involve fatal cytokine storms, said CFO Robin Wright. As a consequence, sepsis, kidney injury and meningitis are all potential further indications for Ruconest.

    "In a cytokine storm situation — such as is caused by pre-eclampsia, contrast-induced nephropathy, kidney injury, meningitis, sepsis — the pro-inflammatory molecules just swamp any production of C1 that is meaningful," said Wright. "So you have to supply if you want to treat it. The idea is if you supply lots of C1 early on, you can slow that storm down, so that it doesn't cause so much damage and ideally doesn't kill the patient. All of these indications are linked by that fundamental concept."
  11. forum rang 6 pacman 30 december 2020 09:43
    Dit was het "vooronderzoek" hier begon het,

    Relative bradycardia in patients with COVID-19

    We retrospectively reviewed the electronic medical records of
    the first 174 patients with confirmed COVID-19 (detection of severe
    acute respiratory syndrome coronavirus 2 (SARS-CoV-2) by realtime reverse transcriptase PCR from nasopharyngeal swabs)
    admitted to the University Hospital Basel, Switzerland, from 27
    February 2020 to 15 April 2020. During this period, symptomatic
    inpatients without contraindications were routinely treated with
    lopinavir/ritonavir for 5 to 7 days and hydroxychloroquine for 2 dys

    www.clinicalmicrobiologyandinfection....
    - -
    www.pharming.com/nl/node/185

  12. forum rang 6 pacman 4 januari 2021 11:28
    Merck's Recent Acquisition Highlights OWS Funding Flowing Into COVID-19 Therapeutics

    There has been non-stop chatter about the new COVID-19 vaccines, but at the same time, there seems to be a pause as Operation Warp Speed (OWS) tries to fill the void between now and April when the vaccines will be more widely available. The first to break an unprecedented focus on the vaccine was therapeutics maker Merck (MRK). In collaboration with Health and Human Services (HHS) Merck is continuing the development of large-scale manufacturing of their investigational therapeutic MK-7110 to treat hospitalized patients with severe or critical COVID-19. The drug is called SACCOVIDTM, and it is a recombinant fusion protein that blocks pattern recognition receptors that trigger the innate immune response. This molecule was repurposed from Graft versus Host Disease (GvHD) in order to quiet the cytokine storm in severe-to-critical COVID-19 patients.

    cytokine storm ook weer... en zo gaat het Merck krijgt geld om onderzoek te doen ( $356 million ) en nemen OncoImmune over voor $425 million... Big money Rules nog steeds

    seekingalpha.com/article/4397128-merc...

    en kijk ff waartegen Pharmings Ruconest moet vechten..Amerika first Cytodyn

    staat best veel info in .
  13. forum rang 6 pacman 6 januari 2021 10:26
    The emergence of a new cytokine storm during the COVID-19 pandemic: Multisystem inflammatory syndrome in children.
    ...
    The mainstay of treatments in MIS-C was intravenous immunoglobulin (IVIG), aspirin, and corticosteroid. Interleukin-1 inhibitor, interleukin-6 inhibitor, and tumor necrosis factor-a inhibitor have been tried with success in a few patients. The report of IVIG refractory rate was relatively high.4 The overall first-course IVIG resistance rate was 21% in MIS-C, but the IVIG resistance rate was up to 34% in those who fulfilled both criteria of MIS-C and Kawasaki disease. Remdesivir had a role in shortening hospital stay in adults with SARS-CoV-2 infection and lower respiratory tract infection.5 Nevertheless, remdesivir was not effective in treating MIS-C, because MIS-C was a postinfectious outburst of the interferon response, macrophage activation, and cytokine storm, instead of resulting from active viral replication.

    COVID-19 is an emerging infectious disease, which contributes to the emergence of a new cytokine storm disorder, MIS-C.

    onlinelibrary.wiley.com/doi/10.1002/k...


    ps, Ruconest is currently approved in dozens of countries as an on-demand treatment for acute HAE attacks in adults and adolescents. The European Commission has also approved it for use in young children, ages 2 and older.
  14. forum rang 6 pacman 8 januari 2021 16:12
    NEWS RELEASE 4-JAN-2021
    Severe sepsis predicted by common protein

    A sugar-binding protein could fuel terrible inflammation and worsen sepsis, a disease that kills more than 270,000 people every year in the US alone, reports a team of researchers led by UConn Health in the 4 January issue of Nature Immunology.

    Sepsis is caused mostly by bacterial infections. The immune system runs out of controls and triggers a cytokine storm, a condition in which inflammation-causing proteins flood the blood. Organs may break down, and death often follows.

    Other diseases can also cause cytokine storms; medical historians believe cytokine storms were behind the lethality of the 1918-1919 flu epidemic, as well as the Black Death. Cytokine storms are also observed in patients with severe COVID-19 and believed to be involved in death in COVID-19.

    A main trigger for the cytokine storms during sepsis is the overreaction of the body when it detects an infection inside the cells. When a cell detects bacteria or pieces of bacteria inside itself, it immediately activates enzymes that in turn activate a protein that pokes holes on the cell membrane from within, eventually causing the cell to burst open and spill cytokines into the bloodstream. Cytokines are alarm signals, calling in the immune system to fight the bacteria. Cytokines also make other cells more likely to burst open and sound the alarm. Usually, the system damps itself after a while and calms down, but in sepsis it spins out of control, causing more and more cells to burst and die and release even more cytokines into the bloodstream.

    When cells burst open, they release not only cytokines, but also other danger molecules called alarmins that alarm the body of an infection or injury and can amplify the ongoing cytokine storm.
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