| [ Summary ] |
For treatment of Crohn's disease, it has been suggested that overexpression of SMAD7, which is a negative feedback molecule associated with TGFβ signaling, may block immunosuppressive TGFβ signals and may cause overproduction of proinflammatory cytokines. In mouse based colitis models, oral administration of SMAD7 antisense oligonucleotide produced an anti-inflammatory effect. Based on these results, clinical trials were conducted in patients with Crohn's disease. The safety of this treatment was confirmed in a phase 1 trial. Efficacy was suggested in a phase 2 trial. However, an interim report on a phase 3 trial did not exhibit any degree of efficacy compared to a placebo group and was discontinued. |