The most common manageable adverse events are rash, pruritus, fatigue and headache. Tofacitinib Citrate JAK Neutropenia, anemia, thrombocytopenia, elevations of liver enzymes, cardiac toxicity, namely QT prolongation, fluid retention, edema, and weight gain are among the less common side effects[19]. TK inhibitors affect several key components in the pathogenesis of IBD, including TNF alpha, PDGFR, and NO synthesis. In this study, we evaluated the efficacy of nilotinib on weight, macroscopic and microscopic pathological scores, TNF alpha and PDGFR levels, and the apoptotic index in rat models with TNBS-induced colitis. There are no previous reports in the literature evaluating the efficacy of nilotinib in either a rat model of colitis or in human colitis. In the present study, the weights of the control and experimental rats were monitored daily.

At the end of 14 d, rats in the nilotinib group had lost significantly less weight than rats in the TNBS group (P = 0.047). These results are similar to those obtained in the study by Cuzzocrea et al[16], in which weight loss was significantly reduced by 7 d of treatment with the TK inhibitor tyrphostin AG126 in a DNBS-induced colitis animal model. The TK inhibitor used in the study by Cuzzocrea et al[16] is different from that used in our study. However, our study indicates that nilotinib does have a positive effect on weight in animal models with colitis. The first therapeutic target in drug studies for the treatment of IBD was the regression of disease-related symptoms. The most important reason for this was that the agents used in the treatment of IBD were not disease-modifying drugs.

In more recent studies, however, the primary endpoint in evaluating the therapeutic efficacy of drugs used to treat IBD has been ��mucosal healing��[20]. With mucosal healing as the therapeutic target, continuous clinical remission and survival without surgery can be achieved[21]. The mucosal healing rates of anti-TNF agents have been reported at approximately 60% in the active ulcerative colitis trials (ACT)-1 and ACT-2 studies[7,10]. In the present study, the effects of nilotinib on mucosal healing and pathological macroscopic and microscopic scores yielded quite remarkable results. The macroscopic and microscopic pathological scores of intestinal tissue from the nilotinib group were similar to those of the control group (P > 0.

05) but significantly lower than those of the TNBS group (P = 0.009; P = 0.030, respectively). In our study, the similar microscopic and macroscopic scores of the nilotinib and control groups constituted the most important evidence of the mucosal healing effect of nilotinib. Indeed, in the study conducted by Cuzzocrea et al[16], the rats treated Batimastat with the TK inhibitor showed significant histological improvements after treatment compared with the control rats. This result parallels the results of our study.