Nonetheless, while effective in cell lines, the use of these chemicals in vivo has been limited by their low potency (IC50s of 41.1 μM and 22.5 μM for 10058-F4 and 10074-G5, respectively, on growth inhibition of HL-60 human promyelocytic leukemia cells that overexpress Myc due to gene amplification) [100], lack of selectivity, and poor pharmacokinetic behavior as they undergo rapid metabolism resulting in low tumoral concentrations that are insufficient to block Myc-Max interactions in vivo, thus restricting their clinical applicability [101,102]. Here, MYC is linked to acute promyelocytic leukemia.