PAWI-2 has inhibitory effects on prostate cancer cells and pancreatic cancer stem cells through a novel mechanism of action involving inhibition of tubulin acetylation, BCL-2 and mitochondrial function.  PAWI-2 inhibits cell proliferation of androgen-sensitive and androgen-insensitive prostate cancer cells (LNCaP and PC-3).  Intraperitoneal administration of PAWI-2 in a PC-3 xenograft model resulted in the inhibition of of tumor growth by 49% compared with vehicle treated mice.  PAWI-2 was demonstrated to synergize with the currently used  clinical treatment, enzalutamide, to inhibit PCa cell viability in vitro and resensitized inhibition of PC-3 tumor growth in vivo.  In addition, PAWI-2 was shown to potently inhibit cell viability and the self-renewal capacity of FGb3 cells, a validated cancer stem cell model (CSC).  PAWI-2 inhibited b3-KRAS signalling independent of KRAS which is clinically significant in tumor progression. PAWI-2 overcame erlotinib (an EGFR inhibitor) resistance in FGB3 cells more potently than bortezomib.  PAWI-2 repreasents a new approach to reverse tumor stemness that resensitizes CSC tumors to drug inhibition.