Vedolizumab in the Treatment of Ulcerative Colitis: An Evidence-Based Review of Safety, Efficacy, and Place of Therapy.
efficacy
inflammatory bowel disease
integrin antagonist
safety
ulcerative colitis
vedolizumab
Journal
Core evidence
ISSN: 1555-1741
Titre abrégé: Core Evid
Pays: New Zealand
ID NLM: 101256593
Informations de publication
Date de publication:
2020
2020
Historique:
received:
01
09
2019
accepted:
08
03
2020
entrez:
14
4
2020
pubmed:
14
4
2020
medline:
14
4
2020
Statut:
epublish
Résumé
Selective blockade of the integrins and mucosal adhesion molecules is a promising therapeutic strategy for ulcerative colitis (UC). Vedolizumab (VDZ), a humanized IgG1 monoclonal antibody against α4β7 integrin, selectively blocks the trafficking of the leukocytes into the gastrointestinal tract through its binding with the α4β7 integrin. In this review, we provide an overview of the unique mechanism of VDZ, along with its efficacy, safety, and pharmacokinetic and pharmacodynamic data obtained from clinical trials, observational studies, and meta-analyses. A positive exposure-efficacy relationship with regard to clinical remission and clinical response was apparent in VDZ induction therapy. No drug-specific safety signals are currently available. VDZ has been shown to be effective as first- or second-line induction and maintenance therapy in UC. VDZ is a safe and effective treatment option for patients with UC. Prolonged VDZ induction therapy may contribute to improved outcomes in patients with UC, particularly those previously treated with tumor necrosis factor-α. Prospective head-to-head study of VDZ and other biologics would alter the positioning of VDZ much more clearly.
Identifiants
pubmed: 32280316
doi: 10.2147/CE.S179053
pii: 179053
pmc: PMC7131995
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
7-20Informations de copyright
© 2020 Takatsu et al.
Déclaration de conflit d'intérêts
Toshiyuki Matsui has received honoraria from EA Pharma Co. Ltd., Abbvie GK, Eisai Co. Ltd., Kyorin Pharmaceutical Co. Ltd., Zeria Pharmaceutical Co. Ltd., Takeda Pharmaceutical Co. Ltd., Mitsubishi Tanabe Pharma Corporation and Janssen Pharmaceutical K.K.; has received research grants from Takeda Pharmaceutical Co. Ltd., Mitsubishi Tanabe Pharma Corporation and Otsuka Pharmaceutical Co. Ltd.; has received scholarship grants from EA Pharma Co. Ltd., Otsuka Pharmaceutical Co. Ltd., JIMRO Co. Ltd. and Nippon Kayaku Co. Ltd.; and was a recipient of endowed chairs funded by AbbVie GK, Asahi Kasei Medical Co. Ltd., Ajinomoto Seiyaku, Inflammatory Bowel Disease Advanced Clinical Treatment endowed chair, Regional/Emergency Medical Management endowed chair (Fukuoka). The authors report no other conflicts of interest in this work.
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