The etiology of
inflammatory bowel disease (IBD), of which
ulcerative colitis (UC) and
Crohn's disease (CD) are the two most prevailing entities, is unknown. However, IBD is characterized by an imbalanced synthesis of pro-inflammatory mediators of the inflamed intestine, and for more than a decade
tumor necrosis factor-(TNF) α has been a major target for
monoclonal antibody therapy. However,
TNF inhibitors are not useful for one third of all patients (i.e. "primary failures"), and further one third lose effect over time ("secondary failures"). Therefore, other strategies have in later years been developed including
monoclonal antibodies targeting the
interleukin (IL)-6 family of receptors (the p40 subunit of
IL-12/IL-23) as well as
monoclonal antibodies inhibiting adhesion molecules (the α4β7 heterodimers), which direct leukocytes to the intestinal mucosa. Recently, small molecules, which are inhibitors of
Janus kinases (JAKs), hold promise with a tolerable safety profile and efficacy in UC, and the field of nanomedicine is emerging with siRNAs loaded into polyactide nanoparticles that may silence gene transcripts at sites of intestinal
inflammation. Thus,
drug development for IBD holds great promise, and patients as well as their treating physicians can be hopeful for the future.