The desired mechanism for treatment of cancer is to cause significant amounts of DNA damage, that ultimately leads the to cell apoptosis. Unfortunately many cells have the ability to detect this damage and initiate repair. This is the basis by which many treatments fail long term. Sensitising agents to inhibit this repair have proven successful, although there means of action is not entirely understood. The purpose of this study was to examine the mechanisms of action for radio and chemo sensitising agents belonging to the benzoaxine family of compounds. The compounds were developed, like similar sensitises to inhibit the action of DNA-PK, an important protein in the initiation of DNA repair. To understand the interactions of benzoxazine with DNA-PK, computational docking analysis was conducted and identified positions and chemical additions that were required for DNA-PK inhibition. Several compounds were developed and found not to be toxic to various cancer cell lines and several were found to enhance the effects of various chemotherapy treatments and at various radiation dosages. One of the benzoaxines, LTU27, was found to work by inhibiting not only DNA-PK, but AKT a similar acting protein, and thus contributing to a more potent sensitising effect. Another benzoaxine, LTUSI54, was found to enhance the effect of Etoposide by increasing cell cycle arrest of HeLa cells. Another aspect of cancer that the benzoaxines can inhibit is by reducing angiogenesis, the formation of new blood vessels. LTUSI122, has shown to inhibit proliferation, migration and tube formation of HUVECs in vitro. It is interesting to observe the many effects of benzoaxines in vitro, sensitising cancers cells to the effects of chemo and radiation treatments, and reducing blood supply. The ramifications of molecules that effect multiply pathways leading to apoptosis of cancer cells has many clinical possibilities.