CYC-116 is a novel, ATP-competitive, pyrimidine drug that is taken by mouth as a capsule. The drug is a selective agent that potently inhibits the enzymes Aurora kinases and VEGFR-2 kinase at comparable levels with a range of 19 to 69 nanomolar. Median potency of CYC-116 in cancer cells is approximately 300 nanomolar. CYC-116 has demonstrated a broad spectrum of potent cytotoxic activity against human tumor cell types. Non-clinical efficacy of CYC-116 has been demonstrated by the oral route using mouse leukemia models, in which increased survival was observed, and human solid tumor xenograft models, in which reductions in tumor growth were observed. Cancer cell types that appear to be particularly sensitive to CYC-116 are leukemia, non-small cell lung cancer and pancreatic cancer. CYC-116 works by affecting the cell cycle progression of cancer cells before they enter mitosis or divide to create daughter cancer cells. The mechanism of action of CYC-116 affects cancer cells in several ways. CYC-116-treated cells display delayed entry into mitosis; defective polymerization of tubulins, or proteins that make up microtubules which are the target of the taxane drugs; changes in the function of the centrosome, or the cell's microtubule organizing center; and formation of the mitotic spindle, or the highway along which chromosomes and cellular materials are transported from the mother cell to the daughter cells. After cancer cells are treated with CYC-116, their spindle checkpoint is inactivated resulting in inhibition of cytokinesis or the process by which a mother cell divides. These defects result in the generation of polyploidy or cells with more than two chromosome sets, multinucleated cells or cells with multiple cores and apoptosis or cancer cell death. In a mouse model of leukemia CYC116-treatment induced decreases in tumor cell volume and infiltration of leukemic cells in the bone marrow and resulted in an increase in life span. No significant effects on body weight or normal bone marrow cells were observed at effective doses of CYC-116. Tumor neovascularization, or creation of new blood vessels around a tumor, was significantly reduced in a dose dependent manner. The data confirm that CYC-116 acts as a dual mitotic and angiogenesis inhibitor, a combination of anti-cancer mechanisms which could have therapeutic benefit in the clinic. CYC-116 is currently being studied in a Phase 1 trial in patients with solid tumors at Roswell Park Cancer Institute in Buffalo, New York, and South Texas Accelerated Research Therapeutics (START) in San Antonio. The study is designed to identify the maximum tolerated dose of CYC-116 and evaluate its pharmacokinetic, pharmacodynamic and anti-tumor effects.