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.

Latest findings

For example, an inhibitor named RAD001 or everolimus could significantly inhibit the growth of bladder tumor both in vitro and in vivo [18]. [source, 2016]
Patel et al45 found that Rapamycin and the rapalog RAD001 diminished lymphangiogenesis in the primary tumors and prevented the dissemination of HNSCC cells to the cervical lymph nodes, thereby prolonging NOD/SCID mice survival, suggesting that mTOR was a potential target of HNSCC. [source, 2016]
Everolimus (RAD001) is an oral mTOR inhibitor. [source, 2016]
Two Rapamycin derivatives – RAD001 and CCI-779 – have demonstrated promising antitumor activity with relatively minor toxicity in early clinical trials in advanced cancer patients. [source, 2016]
Recent trials have indicated that adding Afinitor (everolimus) to Exemestane therapy against advanced breast cancer can significantly improve progression-free survival compared with Exemestane therapy alone. [source, 2016]
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]
Furthermore, high levels of phosphorylated AKT, GSK3β, and TSC2 have also been demonstrated to correlate with increased sensitivity to RAD001 (everolimus).149 [source, 2016]
These results were in agreement with the observed rescue of Akt/mTOR signaling elicited by RAD001 or Mevinolin treatment. [source, 2015]
For in vitro experiments, cells were seeded on the appropriated plates overnight and treated with HCQ (75 or 100 μM, Acro Chemicals), RAD001 (10 μM, LC Laboratories), bafilomycin A1 (50 nM, Sigma), or spautin-1 (10 μM, Sigma) for 48 hours. [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]