Crohn's disease (CD) is a chronic inflammatory disorder that primarily affects small intestine and colon and causes tissue damage. The aetiology of CD is unknown, but a large body of evidence suggests that the pathological process is driven by excessive immune response, which is direct against components of the luminal flora and sustained by defects in counter-regulatory mechanisms. CD is a transmural progressive and destructive disease leading to irreversible bowel damage characterized by stenosis of the intestinal lumen and penetrating lesions such as fistulas and abscesses. The goals of medical therapy in CD are to: 1) induce symptomatic remission; 2) maintain steroid-free remission; 3) enhance quality of life; 4) prevent/treat complications of disease; 5) avoid short and long term toxicity of therapy. Achieving these goals requires a sophisticated approach that tailors therapy to each patient, involving attempts to risk stratify the patient, optimizing each therapy, and monitoring for objective evidence of resolution of inflammation. Although the number of medications available to treat CD has increased in the last 15 years, with the important addition of biologic therapies, including anti-TNF antibodies such as infliximab, adalimumab, and certolizumab pegol, and more recently, vedolizumab, an anti-α4β7 integrin antibody, the number of agents remains relatively small.