Ustekinumab: A Review in Moderate to Severe Crohn’s Disease LambYvette DugganSean 2018 <div>Compliance with Ethical Standards</div><div><br></div><div><i>Funding:</i> The preparation of this review was not supported by any external funding.</div><div><br></div><div><i>Conflicts of interest</i>: Yvette Lamb and Sean Duggan are salaried employees of Adis/Springer, are responsible for the article content and declare no relevant conflicts of interest. </div><div><br></div><div>Additional information about this Adis Drug Review can be found <b><a href="http://www.springer.com/gp/adis/products-services/adis-journals-newsletters/adis-drug-reviews">here</a>.</b></div><div><br></div><div>Abstract</div><div><br></div><div>Ustekinumab (Stelara®) has been recently approved in the EU and the USA as intravenous induction and subcutaneous maintenance therapy for adult patients with moderately to severely active Crohn’s disease who have failed or were intolerant to treatment with immunomodulators, corticosteroids or at least one tumour necrosis factor (TNF) antagonist. Ustekinumab, a monoclonal antibody to the shared p40 subunit of the proinflammatory interleukin (IL)-12 and IL-23 cytokines, has a unique mechanism of action distinct from that of TNF antagonists. In pivotal phase III trials, compared with placebo, ustekinumab induction therapy improved clinical response and remission rates in patients who had previously failed or were intolerant to conventional therapies or at least one TNF antagonist. When administered as subcutaneous maintenance therapy, ustekinumab continued to offer benefits over placebo for clinical response and remission in patients who had clinically responded to the induction therapy. Ustekinumab was generally well tolerated as both induction and maintenance therapy; serious infections and malignancies were rare. Thus, ustekinumab presents a promising alternative treatment option in patients with moderately to severely active Crohn’s disease who have failed or are intolerant to treatment with conventional therapies or TNF antagonists. Access to the full article can be found <b><a href="http://dx.doi.org/10.1007/s40265-017-0765-6">here</a>.</b></div><div><br></div><div>© Springer International Publishing AG, part of Springer Nature 2017</div>