Our research demonstrates that activation of the receptor via sphinganine 1 phosphate protects against hepatic damage and liver IR induced AKI via, ERK, Aurora Kinase Inhibitor Gi/o and Akt mediated mechanisms and the protection is in addition to the pathway. On the other hand, activation of S1P3 receptors attenuated the hepatic protecting effects of exogenous S1P after liver IR. We propose that sphinganine 1 phosphate via selective S1P1 receptor activation without impacting the S1P3 receptors is better than S1P in attenuating hepatic IR damage and might be a promising pharmacological agent for protecting both kidney and liver function after hepatic IR. Purchase of mesenchymal phenotype by epithelial cells by means of epithelial mesenchymal transition is considered as an early event in the multi step process of tumor metastasis. Therefore, inhibition of EMT might be a rational technique to prevent metastasis. Methods?Utilizing the global gene expression profile from Skin infection the cell culture style of TGF T caused EMT, we revealed potential EMT inhibitors. We used a publicly available database containing gene expression profiles obtained from multiple different cell lines in response to various drugs to uncover adverse correlations to EMT gene expression profile using Connectivity Map, a pattern matching tool. ?Experimental consent of the identified substances confirmed rapamycin as a novel inhibitor of TGF T signaling along with 17 AAG, an identified modulator of TGF B pathway. These two compounds entirely blocked EMT and the related migratory and invasive phenotype. Another identified element, LY294002, demonstrated a selective inhibition of mesenchymal markers, cell migration and invasion, without affecting the loss of E cadherin phrase or Smad phosphorylation. Metastasis is BIX01294 the major cause of mortality in cancer related deaths. Targeting and thus identifying specific molecular mechanisms of metastasis is important for a successful reduction strategy. Throughout metastasis, cancer cells get the capability to invade surrounding tissue with subsequent distribution to secondary organs. The acquisition of migratory and invasive potential by normally stationary epithelial cells is associated with gain of mesenchymal traits and concomitant lack of epithelial phenotype, a phenomenon called epithelial?mesenchymal transition. EMT also confers resistance to anoikis, evasion of immune surveillance, and in particular cases is associated with stem cell like qualities of the resulting mesenchymal cells, which might be needed for a cancer cell to successfully metastasize. Consequently, inhibition of EMT might be a reasonable strategy to prevent metastasis. The cytokine Transforming Growth Factor B plays a paradoxical role in cancer biology, where it acts as a tumor suppressor in early stages and as a tumor promoter in late stages of tumor progression. The tumefaction promoting functions of TGF W include induction of EMT in cancer cells.