Latest research on RAD001

Everolimus is a derivative of Rapamycin (sirolimus), and works similarly to Rapamycin as an mTOR (mammalian target of rapamycin) inhibitor. It is currently used as an immunosuppressant to prevent rejection of organ transplants. In a similar fashion to other mTOR inhibitors Everolimus' effect is solely on the mTORC1 protein and not on the mTORC2 protein.

RAD001 indications

One example is everolimus (RAD001), an oral inhibitor of mammalian target of Rapamycin acting downstream of the PI3K/AKT pathway, which was shown to have effective inhibitory effects on cancer stem cells in vitro and in vivo, and combination treatment with RAD001 and Docetaxel or trastuzumab has been reported to be effective in refractory metastatic BC [81]. [source, 2016]
Our data demonstrate that TGFbeta 2 increase in R527H cells is associated with activation of the Akt/mTOR pathway and this effect is reversed by TGFbeta 2 neutralizing antibody, statins and the mTOR inhibitor RAD001, which also avoid the aberrant osteoclastogenesis triggered by laminopathic culture media. [source, 2015]
It should be noted that both RAD001 and Mevinolin had been removed from medium after U2-OS treatment, so that we can rule out direct drug effects on osteoclast differentiation. [source, 2015]
Surprisingly, we also found that HCQ altered the levels of the mTORC1 activation marker phospho-S6 and that this effect was mediated by a different mechanism than that observed for the mTOR inhibitor RAD001. [source, 2015]
We also compared the effects of HCQ, the mTOR inhibitor RAD001, and the combination of both drugs on cell growth (Fig 1B). [source, 2015]
We next compared the effect of HCQ and RAD001 on the mTORC1 pathway. [source, 2015]
We also examined the effects of combining Atg7 depletion with HCQ, RAD001, or both together. [source, 2015]
Control reactions included leaving out ATP, which is required for S6 phosphorylation, and the addition of RAD001, which had no effect. [source, 2015]
We found that bortezomib treatment had no effect on the levels of phospho-S6 in untreated and RAD001 treated cells, but resulted in a large increase in phospho-S6 levels in HCQ treated cells (Fig 6). [source, 2015]
This was in contrast to the effects of RAD001, bafilomycin A1, and spautin-1 on these same cells, which inhibited phosphorylation of all three molecules. [source, 2015]