Salirasib is a potent and competitive prenylated protein methyltransferase (PPMTase) inhibitor with K_i of 2.6 μM, which inhibits Ras methylation. IC50 & Target: Ki: 2.6 μM (PPMTase) In Vitro: Salirasib (12.5-100 μM) inhibits the proliferation of ELT3 cells in a dose-dependent manner with an average IC₅₀ of 58.57±4.59 μM. The effects of Salirasib on the TSC2-null cells are evidently mimicked by DN-Rheb but not by DN-Ras. Salirasib reduces Rheb in TSC2-null cells and TSC2 expression rescues the cells from the inhibitory effect of Salirasib. Salirasib reduces phosphorylation of S6K but not of ERK in the TSC2-null ELT3 cells^[1]. Salirasib (50, 100, 150 μM) induces a dose- and time-dependent decrease of cell growth in HCC cells. Salirasib reduces cell proliferation through modulation of cell cycle effectors and inhibitors. Salirasib induces apoptosis in HepG2 and Hep3B cells. The growth inhibitory effect of salirasib in HCC cell lines is associated with mTOR inhibition independent of ERK or Akt activation^[2]. In Vivo: Salirasib (40, 60 or 80 mg/kg, p.o.) significantly inhibits the tumor growth in a dose dependent manner in vivo^[1]. Salirasib (5 mg/kg, i.p.) significantly decreases Ras expression in the dy^2J/dy^2Jmice, and causes an increase in Ras expression which is by far much lower than the increase observed in the dy^2J/dy^2J mice. Salirasib treatment is associated with significantly inhibition of both MMP-2 and MMP-9 activities in the dy^2J/dy^2J mice^[2]. Salirasib (10 mg/kg, i.p.) inhibits tumour growth in a subcutaneous xenograft mice model without weight loss^[3].