This compound was found to be initially promising; however Rippin et al. [85] determined by florescence experiments that CP-31398 intercalated into free DNA and remained bound when DNA complexed with p53, but had no detectable binding to the wild-type or R249S p53 core domain with concentrations up to 3 mM and concluded that this drug suppressed tumor cell growth in a p53 independent manner, likely due to its ability to intercalate into DNA [85]. The gene discussed is TP53; the disease is neoplasm.