GSK2586184, a JAK1 selective inhibitor, in two patients with ulcerative colitis

Vries, L C S De; Ludbrook, Valerie J.; Hicks, Kirsty; D’Haens, Geert R.

doi:10.1136/bcr-2017-221078

Cited by 2 publications

(2 citation statements)

References 18 publications

(8 reference statements)

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“…90 Other JAK inhibitors such as tofacitinib and GSK2586184 have been reported as decreasing CRP drugs. 91 Several other drugs that decrease circulating CRP concentrations have been reported. In this context, beta-blockers may affect CRP concentrations.…”

Section: Drugs That Block C-reactive Protein With a Potential Therapeutic Effect On Covid-19mentioning

confidence: 99%

C‐reactive protein as an effector molecule in Covid‐19 pathogenesis

Mosquera-Sulbarán

Pedreáñez

Carrero

et al. 2021

Reviews in Medical Virology

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The current pandemic caused by SARS-CoV-2 virus infection is known as Covid-19 (coronavirus disease 2019). This disease can be asymptomatic or can affect multiple organ systems. Damage induced by the virus is related to dysfunctional activity of the immune system, but the activity of molecules such as C-reactive protein (CRP) as a factor capable of inducing an inflammatory status that may be involved in the severe evolution of the disease, has not been extensively evaluated. A systematic review was performed using the NCBI-PubMed database to find articles related to Covid-19 immunity, inflammatory response, and CRP published from December 2019 to December 2020. High levels of CRP were found in patients with severe evolution of Covid-19 in which several organ systems were affected and in patients who died. CRP activates complement, induces the production of pro-inflammatory cytokines and induces apoptosis which, together with the inflammatory status during the disease, can lead to a severe outcome. Several drugs can decrease the level or block the effect of CRP and might be useful in the treatment of Covid-19.From this review it is reasonable to conclude that CRP is a factor that can contribute to severe evolution of Covid-19 and that the use of drugs able to lower CRP levels or block its activity should be evaluated in randomized controlled clinical trials. K E Y W O R D SC-reactive protein, COVID-19, SARS-CoV-2, severe evolution | INTRODUCTIONSARS-CoV-2 starts its pathogenetic process through reninangiotensin system (RAS) activation, binding to the angiotensin II converting enzyme (ACE2) and originating a series of proinflammatory events that can induce a cytokine storm. 1,2 The C-reactive protein (CRP) is a molecule produced by the interaction of SARS-CoV-2 with ACE2, 3-5 which is not only an indicator of acute phase of inflammation but also has been related to prognosis and severity of Covid-19. [5][6][7] Therefore, CRP can be an important factor in the cellular damage during Covid-19. This review aims to describe the different mechanisms by which SARS-CoV-2 can induce cell

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Section: Drugs That Block C-reactive Protein With a Potential Therapeutic Effect On Covid-19mentioning

confidence: 99%

C‐reactive protein as an effector molecule in Covid‐19 pathogenesis

Mosquera-Sulbarán

Pedreáñez

Carrero

et al. 2021

Reviews in Medical Virology

View full text Add to dashboard Cite

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“…The interplay between the different JAKs may limit the applicability of highly selective JAK-inhibitors [81]. Of note also JAK1, JAK3 and TYK2 selective inhibitors are currently under investigation in clinical trials for different inflammatory diseases [82,83,84,85,86,87,88,89,90,91,92,93].…”

Section: Consequences Of Deregulated Jak2 Signaling In Hematopoiesmentioning

confidence: 99%

Roles of JAK2 in Aging, Inflammation, Hematopoiesis and Malignant Transformation

Perner

Ernst

et al. 2019

Cells

153

108

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Clonal alterations in hematopoietic cells occur during aging and are often associated with the establishment of a subclinical inflammatory environment. Several age-related conditions and diseases may be initiated or promoted by these alterations. JAK2 mutations are among the most frequently mutated genes in blood cells during aging. The most common mutation within the JAK2 gene is JAK2-V617F that leads to constitutive activation of the kinase and thereby aberrant engagement of downstream signaling pathways. JAK2 mutations can act as central drivers of myeloproliferative neoplasia, a pre-leukemic and age-related malignancy. Likewise, hyperactive JAK-signaling is a hallmark of immune diseases and critically influences inflammation, coagulation and thrombosis. In this review we aim to summarize the current knowledge on JAK2 in clonal hematopoiesis during aging, the role of JAK-signaling in inflammation and lymphocyte biology and JAK2 function in age-related diseases and malignant transformation.

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GSK2586184, a JAK1 selective inhibitor, in two patients with ulcerative colitis

Cited by 2 publications

References 18 publications

C‐reactive protein as an effector molecule in Covid‐19 pathogenesis

C‐reactive protein as an effector molecule in Covid‐19 pathogenesis

Roles of JAK2 in Aging, Inflammation, Hematopoiesis and Malignant Transformation

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