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The two major forms of IBD, Crohn's disease (CD) and UC, are chronic inflammatory disorders, the pathogenesis of which involves a complex interplay of multiple factors.1 ,2 The introduction of biological agents has substantially expanded and improved the therapeutic options for IBD, but a large proportion of patients still do not respond or achieve remission in the short term or long term. Thus, there is still a considerable need to improve the treatment of IBD, and significant research efforts are underway to address this unmet need.
During the last two decades, the period of time over which the biologics as well as other new drugs for IBD have entered the market, the number of therapies that have failed is remarkably high. This is significant, and understanding the reasons for such failure should lead to a better drug development process and pave the way for alternate and more efficient drug development strategies.
Traditionally, the drug development process initially involves target discovery and selection, and then biological confirmation in cellular and animal models. This is followed by phase I testing in healthy volunteers to check for safety and pharmacokinetics, then phase II testing in patient volunteers to obtain preliminary safety, clinical efficacy and dosing data, and finally phase III clinical studies in patients to obtain a more comprehensive characterisation of the safety and efficacy profile of a drug. This traditional pathway of drug development has had relatively limited success in generating new forms of treatment for IBD. Results have been impacted by predictable high clinical response rates in the placebo groups, a lack of objective end points, trial design with arbitrary definitions of induction and maintenance phases and outcomes, and not taking into account key components of IBD pathogenesis.3 Moreover, a lack of strict criteria to ensure the presence …
Contributors SD, CF and JP participated in the conception, literature review and writing of the manuscript.
Funding This work has been in part supported by grants from Fondazione Humanitas per la Ricerca and FIRMAD to SD, and grant SAF 2012-33560, from Ministerio de Economía y Competitividad, Spain, to JP.
Competing interests SD has received consulting fees from and has served as a speaker, a consultant and an advisory board member for Schering-Plough, Abbott Laboratories, Merck & Co, UCB Pharma, Ferring, Cellerix, Millenium Takeda, Nycomed, Pharmacosmos, Actelion, Alphawasserman, Genentech, Grunenthal, Pfizer, Astra Zeneca, Novo Nordisk, Salix, Cosmo Pharmaceuticals, Vifor and Johnson and Johnson. JP has received consulting fees from Abbvie, Boehringer Ingelheim, Galapagos, Genentech-Roche, Ferring, Janssen, MSD, Novo-Nordisk, Pfizer, Takeda and Tigenix.
Provenance and peer review Not commissioned; externally peer reviewed.