The pharmacological improvements result in substantially enhanced ASO activity in vivo in several tumor xenograft models.26 In one example where we compared pacDNA with AZD4785, a clinical ASO targeting wild-type KRAS mRNA, pacDNA achieved more pronounced tumor suppression levels than AZD4785 at a fraction (2.5%) of the dosage and with greatly reduced dosing frequency in non-small cell lung carcinoma (NSCLC) mouse models.27 In addition, the treatment was free of common deleterious effects such as acute toxicity, inflammation, coagulopathy, and anti-PEG immunity.27 This evidence concerns the gene KRAS and neoplasm.