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Cited by 284

The DOI matches its Crossref record; 77 of the 77 references it cites were found in a registry or an index.

An Overview of the Mechanism of Action of the Monoclonal Antibody Vedolizumab

Wyant, Tim, Fedyk, Eric, Abhyankar, Brihad·2016·Journal of Crohn's and Colitis

Abstract

integrin to mucosal addressin cell adhesion molecule-1 expressed on the surface of mucosal endothelial cells is a crucial component of the gut-selective homing mechanism for lymphocytes.In contrast, other monoclonal antibodies approved for the treatment of inflammatory bowel diseases, such as tumour necrosis factor α antagonists and the integrin antagonist natalizumab, act systemically or on multiple targets to reduce inflammation.The unique gut selectivity of vedolizumab may contribute to the favourable benefit-risk profile observed in vedolizumab clinical trials. In this review, we summarise data from the preclinical development of vedolizumab and describe the current understanding of the mechanism of action as it relates to other biological therapies for inflammatory bowel disease.

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Metadata

Authors
Wyant, T., Fedyk, E., & Abhyankar, B.
Venue
Journal of Crohn's and Colitis
Published
2016-06-01
Volume
10
Issue
12
Pages
1437-1444
ISSN
  • 1873-9946 (ISSN-L)
  • 1876-4479
OpenAlex
W2414026316
Cited by
284
References
77
FWCI
12.96
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: An Overview of the Mechanism of Action of the Monoclonal Antibody Vedolizumab. https://app.cochat.ai/papers/10.1093/ecco-jcc/jjw092
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Wyant, T., Fedyk, E., & Abhyankar, B. (2016). An Overview of the Mechanism of Action of the Monoclonal Antibody Vedolizumab. Journal of Crohn's and Colitis. https://doi.org/10.1093/ecco-jcc/jjw092

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.