Ridaforolimus, was formerly known as Deforolimus, it is an inhibitor of mammalian target of rapamycin.

Ridaforolimus used to treat HT-1080 cells induces a dose-dependent inhibition of both S6 and 4E-BP1 phosphorylation, with IC₅₀ of 0.2 nM and 5.6 nM, respectively, and leads to a decrease in cell size, an increase in the proportion of cells in the G1 phase of the cell cycle, and inhibition of glucose uptake. Ridaforolimus shows antiproliferative activity a variety of cell lines with EC₅₀ of 0.2-2.3 nM. Ridaforolimus is a potent and selective inhibitor of VEGF production in a dose-dependent manner. Ridaforolimus treatment causes growth suppression in human NSCLC cell lines with IC30 values of 2.45-8.83 nM, with the exception of H157 with IC₃₀ of >20 nM. Ridaforolimus treatment causes dephosphorylation of p70S6KThr389 in A549, H1703 and H157 cells, except H1666 that may express a resistant variant of mTORC1, and causes increased phosphorylation of pAKTser473 and pAKTThr308 in A549 and H1703 cells. Ridaforolimus, when combined with the MEK inhibitors CI-1040 or PD0325901, exhibits dose-dependent synergism in lung cancer cell lines, which is associated with the suppression of proliferation rather than enhancement of cell death, involving the inhibition of ribosomal biogenesis by 40% within 24 hours and a decreased polysome/monosome ratio.

Ridaforolimus may act as a regulator of protein synthesis, cell proliferation, cell cycle progression and cell survival.