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JAK1 inhibition and inflammatory bowel disease

Primary non-response and secondary loss of response remain a significant issue with the currently available treatment options for a significant proportion of patients with inflammatory bowel disease (IBD). There are multiple unmet needs in the IBD treatment algorithm and new treatment options are re...

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Detalles Bibliográficos
Autores principales: Harris, Clare, Cummings, J R Fraser
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8098109/
https://www.ncbi.nlm.nih.gov/pubmed/33950226
http://dx.doi.org/10.1093/rheumatology/keaa896
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author Harris, Clare
Cummings, J R Fraser
author_facet Harris, Clare
Cummings, J R Fraser
author_sort Harris, Clare
collection PubMed
description Primary non-response and secondary loss of response remain a significant issue with the currently available treatment options for a significant proportion of patients with inflammatory bowel disease (IBD). There are multiple unmet needs in the IBD treatment algorithm and new treatment options are required. As our understanding of the pathogenesis of IBD evolves, new therapeutic targets are being identified. The JAK-STAT pathway has been extensively studied. Tofacitinib, a JAK1 inhibitor, is now licensed for use in the induction and maintenance of ulcerative colitis and there are a large number of molecules currently under investigation. These new small molecule drugs (SMDs) will challenge current treatment pathways at a time when clinical therapeutic outcomes are rapidly evolving and becoming more ambitious. This is a review of the current JAK1 inhibitors in IBD including the current evidence from clinical trials.
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spelling pubmed-80981092021-05-10 JAK1 inhibition and inflammatory bowel disease Harris, Clare Cummings, J R Fraser Rheumatology (Oxford) Supplement Papers Primary non-response and secondary loss of response remain a significant issue with the currently available treatment options for a significant proportion of patients with inflammatory bowel disease (IBD). There are multiple unmet needs in the IBD treatment algorithm and new treatment options are required. As our understanding of the pathogenesis of IBD evolves, new therapeutic targets are being identified. The JAK-STAT pathway has been extensively studied. Tofacitinib, a JAK1 inhibitor, is now licensed for use in the induction and maintenance of ulcerative colitis and there are a large number of molecules currently under investigation. These new small molecule drugs (SMDs) will challenge current treatment pathways at a time when clinical therapeutic outcomes are rapidly evolving and becoming more ambitious. This is a review of the current JAK1 inhibitors in IBD including the current evidence from clinical trials. Oxford University Press 2021-05-05 /pmc/articles/PMC8098109/ /pubmed/33950226 http://dx.doi.org/10.1093/rheumatology/keaa896 Text en © The Author(s) 2021. Published by Oxford University Press on behalf of the British Society for Rheumatology. https://creativecommons.org/licenses/by-nc/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/ (https://creativecommons.org/licenses/by-nc/4.0/) ), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com
spellingShingle Supplement Papers
Harris, Clare
Cummings, J R Fraser
JAK1 inhibition and inflammatory bowel disease
title JAK1 inhibition and inflammatory bowel disease
title_full JAK1 inhibition and inflammatory bowel disease
title_fullStr JAK1 inhibition and inflammatory bowel disease
title_full_unstemmed JAK1 inhibition and inflammatory bowel disease
title_short JAK1 inhibition and inflammatory bowel disease
title_sort jak1 inhibition and inflammatory bowel disease
topic Supplement Papers
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8098109/
https://www.ncbi.nlm.nih.gov/pubmed/33950226
http://dx.doi.org/10.1093/rheumatology/keaa896
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