AZD8055 is a potent, selective, and orally bioavailable ATP-competitive mammalian target of rapamycin kinase inhibitor with in vitro and in vivo antitumor activity
What this study shows
AZD8055, an ATP-competitive mTOR kinase inhibitor, blocks both mTORC1 and mTORC2 (rapamycin-resistant outputs).
At a glance
| Evidence type | M Molecular — cells, biochemistry, structure Marked M because it is molecular or in-vitro work (model: Cancer cells; xenograft) rather than a whole-organism health-outcome study. That is often exactly where causal biology gets established -- the code says which system the finding was shown in, and nothing about how good the work is. |
| Study type | 5 - Mechanistic / In Vitro |
| Model system | Cancer cells; xenograft |
| Journal | Cancer research |
| Year | 2009 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1158/0008-5472.CAN-09-1751 · PMID 20028854 |
Extracted findings
These fields were extracted from the paper with AI assistance and have not been checked against the source. Read them as a pointer into the paper, not as curated claims; where they disagree with the curated summary above, the curated summary stands.
| Intervention | AZD8055 (ATP-competitive mTOR inhibitor) |
| Target | mTORC1 & mTORC2 |
| Model | Cancer cells; xenograft |
| Effect | AZD8055 is a potent, selective, orally bioavailable ATP-competitive mTOR inhibitor with antitumor activity |
In the Atlas
Related topics
Links in the pathway map
More studies on this topic
- Active-site inhibitors of mTOR target rapamycin-resistant outputs of mTORC1 and mTORC2 (2009)
- Ku-0063794 is a specific inhibitor of the mammalian target of rapamycin (mTOR) (2009)
- Effective and selective targeting of leukemia cells using a TORC1/2 kinase inhibitor (2010)
- mTOR kinase inhibition causes feedback-dependent biphasic regulation of AKT signaling (2011)
Was this page useful?
Thank you. Your answer was counted anonymously.