Oncogenic variants of K-Ras, a member of the Ras GTPase superfamily, are present in over 90% of pancreatic and 50% of colorectal cancers. K-Ras is linked to numerous aspects of morphologic and growth transformation, such as an increase in cell proliferation and metastasis and resistance to suspension-induced cell death, or anoikis.  The ruthenium-based drug NAMI-A (Imidazolium trans-imidazoledimethylsufoxidetetrachlororuthenate) demonstrates selective chemotherapeutic properties against the metastasis of some tumor cell lines at a lower level of cytotoxicity than clinically used metallopharmaceuticals, such as cisplatin. However, the hydrolysis mechanism, effects on neoplastic transformation, and specific molecular target(s) remain unclear. Thus, this study investigated the intrinsic activity of NAMI-A as well as the effect of NAMI-A on oncogenic K-Ras-mediated transformation of intestinal epithelial cells. Kinetic studies of NAMI-A dissolved in phosphate buffer or cell culture growth medium indicated that the rate of hydrolysis increased in the presence of growth medium. At 37°C one chloride ligand of NAMI-A was hydrolyzed after eight min and NAMI-A was converted to a different species after 100 min.  Furthermore, addition of NAMI-A to K-Ras-transformed cells slowed proliferation and reverted several phenotypes of transformation. Specifically, NAMI-A-treated cells showed a decrease in anchorage-independent cell proliferation, and preliminary data suggest an increased sensitivity to anoikis. Together, these results suggest that NAMI-A is a potent anti-cancer agent, reverting various aspects of oncogenic transformation previously unstudied in relation to NAMI-A and that the molecular target(s) of NAMI-A may lie with K-Ras or within its signaling pathway.