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 interactions

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]
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]
To support the above reported involvement of Akt/mTOR pathway in the altered regulation of OPG and cathepsin K, we inhibited Akt activity, using MK2206 and mTOR, using the Rapamycin analog RAD001 that impairs mTORC1 activity (Figure 4). [source, 2015]
To test the efficacy of RAD001 or Mevinolin treatment in terms of inhibition of osteoclastogenesis, we used conditioned media from R527H U2-OS cells to trigger osteoclast differentiation in peripheral blood monocytes from healthy donors. [source, 2015]
These results were in agreement with the observed rescue of Akt/mTOR signaling elicited by RAD001 or Mevinolin treatment. [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]
Mevinolin was from Sigma-Aldrich while MK2206 and RAD001 were purchased from Selleck Chemicals. [source, 2015]
A series of first-generation mTOR inhibitors have been developed including everolimus (Afinitor, Novartis) [29] and temsirolimus (Torisel, Wyeth) [30] as Rapamycin derivatives that inhibit mTOR through allosteric binding to mTORC1. [source, 2015]