Cancer is a progression of mutations. Uncontrolled cancer cell growth can be initiated by a mutation in any one of several hundred genes involved in the control of normal cell growth. In turn, this uncontrolled cancer cell growth triggers turning on the p53 gene that produces the p53 tumor suppressor protein. This protein initiates a cascade of cellular events that result in the self-destruction and eradication of these cancer cells. In other words, for cancer cells to survive and multiply the function of the p53 tumor suppressor protein must be inactivated by a second mutation.
Since more than half of the mutations that inactivate p53 function are in the p53 gene itself, drug induced reactivation of an inactive mutant p53 tumor suppressor protein is an attractive therapeutic approach to the cure of more than half of all human cancers. Realization of this seemingly insurmountable goal is enabled by an innovative Actavalon computational method supported by high throughput genetic information. This novel method has allowed Actavalon scientists to rapidly develop a pipeline of highly efficient broad spectrum mutant p53 tumor suppressor protein reactivation drugs with promising pharmacological properties.