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Gilead Sciences therapeutic approaches for sars cov 2
COVID-19 disease course and therapeutic windows of opportunity for DMARDs Schematic depicts the evolution of a severe <t>SARS-CoV-2</t> infection and therapeutic windows of opportunity for the indicated DMARDs according to the timing of the different ongoing immunopathological processes from the initial viral inoculum to multi-organ failure. (A) SARS-CoV-2 binds to the host receptor ACE2 (yellow and green receptors), and viral docking is eased by TRMPSS2 (blue co-receptor) cleaving viral spike protein. (B-C) In the asymptomatic phase, host cell infection, viral diffusion in the human body, and virion production predominate. Mucosal and local innate immunity (natural killer cells, neutrophils and monocyte-macrophages) react to viral replication, causing cytopathic effects and pro-inflammatory mediators release, and the onset of signs and symptoms occurs. (D) Cellular immunity (B cells, CD4 T cells, CD8 T cells) develop locally and systemically, and symptoms and signs increase in severity. (E) An imbalance between effective and hyper-activated immune responses can result in cytokine storm, which deteriorates lung injury, precipitating or determining respiratory insufficiency. (F) At this stage, potentially protective neutralising antibodies could also trigger antibody-dependent enhancement and the activation of the classical pathway of complement system, enhancing viral replication and further proinflammatory cytokine release. (G) The imbalance between inflammation and coagulopathy as well as SARS-CoV-2 infection of endothelial cells and pericytes determine concurrent micro- and macro-thrombotic events enhancing organ damage. (H) These uncontrolled processes trigger reinforcing and self-maintaining pathological loops (dashed arrows) that eventually lead to systemic cellular and organ dysfunction resulting in multi-organ failure. ACE2=angiotensin-converting enzyme 2. DMARD=disease-modifying anti-rheumatic drug. TNF=tumour necrosis factor. TRMPSS2=transmembrane protease serine 2.
Therapeutic Approaches For Sars Cov 2, supplied by Gilead Sciences, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "The role of antirheumatics in patients with COVID-19"

Article Title: The role of antirheumatics in patients with COVID-19

Journal: The Lancet. Rheumatology

doi: 10.1016/S2665-9913(21)00062-X

COVID-19 disease course and therapeutic windows of opportunity for DMARDs Schematic depicts the evolution of a severe SARS-CoV-2 infection and therapeutic windows of opportunity for the indicated DMARDs according to the timing of the different ongoing immunopathological processes from the initial viral inoculum to multi-organ failure. (A) SARS-CoV-2 binds to the host receptor ACE2 (yellow and green receptors), and viral docking is eased by TRMPSS2 (blue co-receptor) cleaving viral spike protein. (B-C) In the asymptomatic phase, host cell infection, viral diffusion in the human body, and virion production predominate. Mucosal and local innate immunity (natural killer cells, neutrophils and monocyte-macrophages) react to viral replication, causing cytopathic effects and pro-inflammatory mediators release, and the onset of signs and symptoms occurs. (D) Cellular immunity (B cells, CD4 T cells, CD8 T cells) develop locally and systemically, and symptoms and signs increase in severity. (E) An imbalance between effective and hyper-activated immune responses can result in cytokine storm, which deteriorates lung injury, precipitating or determining respiratory insufficiency. (F) At this stage, potentially protective neutralising antibodies could also trigger antibody-dependent enhancement and the activation of the classical pathway of complement system, enhancing viral replication and further proinflammatory cytokine release. (G) The imbalance between inflammation and coagulopathy as well as SARS-CoV-2 infection of endothelial cells and pericytes determine concurrent micro- and macro-thrombotic events enhancing organ damage. (H) These uncontrolled processes trigger reinforcing and self-maintaining pathological loops (dashed arrows) that eventually lead to systemic cellular and organ dysfunction resulting in multi-organ failure. ACE2=angiotensin-converting enzyme 2. DMARD=disease-modifying anti-rheumatic drug. TNF=tumour necrosis factor. TRMPSS2=transmembrane protease serine 2.
Figure Legend Snippet: COVID-19 disease course and therapeutic windows of opportunity for DMARDs Schematic depicts the evolution of a severe SARS-CoV-2 infection and therapeutic windows of opportunity for the indicated DMARDs according to the timing of the different ongoing immunopathological processes from the initial viral inoculum to multi-organ failure. (A) SARS-CoV-2 binds to the host receptor ACE2 (yellow and green receptors), and viral docking is eased by TRMPSS2 (blue co-receptor) cleaving viral spike protein. (B-C) In the asymptomatic phase, host cell infection, viral diffusion in the human body, and virion production predominate. Mucosal and local innate immunity (natural killer cells, neutrophils and monocyte-macrophages) react to viral replication, causing cytopathic effects and pro-inflammatory mediators release, and the onset of signs and symptoms occurs. (D) Cellular immunity (B cells, CD4 T cells, CD8 T cells) develop locally and systemically, and symptoms and signs increase in severity. (E) An imbalance between effective and hyper-activated immune responses can result in cytokine storm, which deteriorates lung injury, precipitating or determining respiratory insufficiency. (F) At this stage, potentially protective neutralising antibodies could also trigger antibody-dependent enhancement and the activation of the classical pathway of complement system, enhancing viral replication and further proinflammatory cytokine release. (G) The imbalance between inflammation and coagulopathy as well as SARS-CoV-2 infection of endothelial cells and pericytes determine concurrent micro- and macro-thrombotic events enhancing organ damage. (H) These uncontrolled processes trigger reinforcing and self-maintaining pathological loops (dashed arrows) that eventually lead to systemic cellular and organ dysfunction resulting in multi-organ failure. ACE2=angiotensin-converting enzyme 2. DMARD=disease-modifying anti-rheumatic drug. TNF=tumour necrosis factor. TRMPSS2=transmembrane protease serine 2.

Techniques Used: Infection, Diffusion-based Assay, Activation Assay

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Article Title: Drug repurposing for COVID-19: Approaches, challenges and promising candidates
Article Snippet: One successful repurposing example is recently seen in the FDA approval of remdesivir (Veklury®; Gilead Sciences) for the treatment of COVID-19 ( https://www.fda.gov/drugs/drug-safety-and-availability/fdas-approval-veklury-remdesivir-treatment-covid-19-science-safety-and-effectiveness ), paving the way for many approved and investigational drugs with repurposing potential under clinical trials for COVID-19, such as dexamethasone ( ) and tocilizumab ( ).

Infection:

Article Title: Remdesivir to treat COVID-19: can dosing be optimized?
Article Snippet: .. IntroductionIn November 2020, the first ACTT-1 study results were released showing that the antiviral drug remdesivir (commercial name Veklury) had some efficacy in treating COVID-19, specifically in shortening the time to recovery in adults who were hospitalized with COVID-19 and had evidence of lower respiratory tract infection [ ]. ..

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    Gilead Sciences therapeutic approaches for sars cov 2
    COVID-19 disease course and therapeutic windows of opportunity for DMARDs Schematic depicts the evolution of a severe <t>SARS-CoV-2</t> infection and therapeutic windows of opportunity for the indicated DMARDs according to the timing of the different ongoing immunopathological processes from the initial viral inoculum to multi-organ failure. (A) SARS-CoV-2 binds to the host receptor ACE2 (yellow and green receptors), and viral docking is eased by TRMPSS2 (blue co-receptor) cleaving viral spike protein. (B-C) In the asymptomatic phase, host cell infection, viral diffusion in the human body, and virion production predominate. Mucosal and local innate immunity (natural killer cells, neutrophils and monocyte-macrophages) react to viral replication, causing cytopathic effects and pro-inflammatory mediators release, and the onset of signs and symptoms occurs. (D) Cellular immunity (B cells, CD4 T cells, CD8 T cells) develop locally and systemically, and symptoms and signs increase in severity. (E) An imbalance between effective and hyper-activated immune responses can result in cytokine storm, which deteriorates lung injury, precipitating or determining respiratory insufficiency. (F) At this stage, potentially protective neutralising antibodies could also trigger antibody-dependent enhancement and the activation of the classical pathway of complement system, enhancing viral replication and further proinflammatory cytokine release. (G) The imbalance between inflammation and coagulopathy as well as SARS-CoV-2 infection of endothelial cells and pericytes determine concurrent micro- and macro-thrombotic events enhancing organ damage. (H) These uncontrolled processes trigger reinforcing and self-maintaining pathological loops (dashed arrows) that eventually lead to systemic cellular and organ dysfunction resulting in multi-organ failure. ACE2=angiotensin-converting enzyme 2. DMARD=disease-modifying anti-rheumatic drug. TNF=tumour necrosis factor. TRMPSS2=transmembrane protease serine 2.
    Therapeutic Approaches For Sars Cov 2, supplied by Gilead Sciences, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/therapeutic approaches for sars cov 2/product/Gilead Sciences
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    therapeutic approaches for sars cov 2 - by Bioz Stars, 2021-09
    99/100 stars
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    COVID-19 disease course and therapeutic windows of opportunity for DMARDs Schematic depicts the evolution of a severe SARS-CoV-2 infection and therapeutic windows of opportunity for the indicated DMARDs according to the timing of the different ongoing immunopathological processes from the initial viral inoculum to multi-organ failure. (A) SARS-CoV-2 binds to the host receptor ACE2 (yellow and green receptors), and viral docking is eased by TRMPSS2 (blue co-receptor) cleaving viral spike protein. (B-C) In the asymptomatic phase, host cell infection, viral diffusion in the human body, and virion production predominate. Mucosal and local innate immunity (natural killer cells, neutrophils and monocyte-macrophages) react to viral replication, causing cytopathic effects and pro-inflammatory mediators release, and the onset of signs and symptoms occurs. (D) Cellular immunity (B cells, CD4 T cells, CD8 T cells) develop locally and systemically, and symptoms and signs increase in severity. (E) An imbalance between effective and hyper-activated immune responses can result in cytokine storm, which deteriorates lung injury, precipitating or determining respiratory insufficiency. (F) At this stage, potentially protective neutralising antibodies could also trigger antibody-dependent enhancement and the activation of the classical pathway of complement system, enhancing viral replication and further proinflammatory cytokine release. (G) The imbalance between inflammation and coagulopathy as well as SARS-CoV-2 infection of endothelial cells and pericytes determine concurrent micro- and macro-thrombotic events enhancing organ damage. (H) These uncontrolled processes trigger reinforcing and self-maintaining pathological loops (dashed arrows) that eventually lead to systemic cellular and organ dysfunction resulting in multi-organ failure. ACE2=angiotensin-converting enzyme 2. DMARD=disease-modifying anti-rheumatic drug. TNF=tumour necrosis factor. TRMPSS2=transmembrane protease serine 2.

    Journal: The Lancet. Rheumatology

    Article Title: The role of antirheumatics in patients with COVID-19

    doi: 10.1016/S2665-9913(21)00062-X

    Figure Lengend Snippet: COVID-19 disease course and therapeutic windows of opportunity for DMARDs Schematic depicts the evolution of a severe SARS-CoV-2 infection and therapeutic windows of opportunity for the indicated DMARDs according to the timing of the different ongoing immunopathological processes from the initial viral inoculum to multi-organ failure. (A) SARS-CoV-2 binds to the host receptor ACE2 (yellow and green receptors), and viral docking is eased by TRMPSS2 (blue co-receptor) cleaving viral spike protein. (B-C) In the asymptomatic phase, host cell infection, viral diffusion in the human body, and virion production predominate. Mucosal and local innate immunity (natural killer cells, neutrophils and monocyte-macrophages) react to viral replication, causing cytopathic effects and pro-inflammatory mediators release, and the onset of signs and symptoms occurs. (D) Cellular immunity (B cells, CD4 T cells, CD8 T cells) develop locally and systemically, and symptoms and signs increase in severity. (E) An imbalance between effective and hyper-activated immune responses can result in cytokine storm, which deteriorates lung injury, precipitating or determining respiratory insufficiency. (F) At this stage, potentially protective neutralising antibodies could also trigger antibody-dependent enhancement and the activation of the classical pathway of complement system, enhancing viral replication and further proinflammatory cytokine release. (G) The imbalance between inflammation and coagulopathy as well as SARS-CoV-2 infection of endothelial cells and pericytes determine concurrent micro- and macro-thrombotic events enhancing organ damage. (H) These uncontrolled processes trigger reinforcing and self-maintaining pathological loops (dashed arrows) that eventually lead to systemic cellular and organ dysfunction resulting in multi-organ failure. ACE2=angiotensin-converting enzyme 2. DMARD=disease-modifying anti-rheumatic drug. TNF=tumour necrosis factor. TRMPSS2=transmembrane protease serine 2.

    Article Snippet: Although the first vaccines have been approved and vaccination campaigns are underway, much of the research done this far has focused on early therapeutic approaches for SARS-CoV-2 (eg, lopinavir-ritonavir, remdesivir, azithromycin, interferon, hydroxychloroquine).

    Techniques: Infection, Diffusion-based Assay, Activation Assay