Cell adhesion molecules play a pivotal role in chronic inflammation and pathological angiogenesis. In the present study, we investigated the inhibitory effects of clotrimazole (CLT) on tumor necrosis factor (TNF)-$alpha$-induced changes in adhesion molecule expression. CLT dose-dependently inhibited monocyte chemoattractant protein-1 (MCP-1), intercellular cell adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) expressions in TNF-$alpha$-stimulated HT29 colonic epithelial cells. This inhibitory action of CLT correlated with a significant reduction in TNF-$alpha$-induced adhesion of monocytes to HT29 cells, which was comparable to the inhibitory effects of anti-ICAM-1 and VCAM-1 monoclonal antibodies on monocyte-epithelial adhesion. These inhibitory actions of CLT were, at least in part, attributable to the inhibition of redox sensitive NF-${kappa}B$ activation, as CLT inhibited TNF-$alpha$-induced ROS generation as well as NF-${kappa}B$ nuclear translocation and activation in HT29 cells. Furthermore, the inhibition of TNF-$alpha$-induced monocyte adhesion was also mimicked by the specific NF-${kappa}B$ inhibitor, pyrrolidine dithiocarbamate (PDTC). Inflammatory mediators including TNF-$alpha$ have known to promote angiogenesis, which in turn further contributes to inflammatory pathology. Therefore, we additionally evaluated whether CLT modulates TNF-$alpha$-induced angiogenesis using in vivo chick chorioallantoic membrane (CAM) assay. The CAM assay showed that CLT dose-dependently attenuated TNF-$alpha$-induced angiogenesis, and the effect was correlated with decreased inflammation of the CAM tissue. In conclusion, our results suggest that CLT can inhibit TNF-$alpha$-triggered expression of adhesion molecules, ICAM-1 and VCAM-1, and angiogenesis during inflammation.