AZD8055 is a potent, selective, and orally bioavailable ATP-competitive mammalian target of rapamycin kinase inhibitor with in vitro and in vivo antitumor activity.

By C. Chresta, B. Davies, Ian D. Hickson, Tom Harding, S. Cosulich, S. Critchlow, J. Vincent, Rebecca P A Ellston, Darren R. Jones, P. Sini and 14 more. Cancer Research, 2010

799 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/148731ccfb7be50dec395eed9fe7efc67f5c12a2

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Citations in the corpus

Targeting PI3K/Akt signal transduction for cancer therapy (2021, background): “AZD8055, one of the most recent and potent ATP-competitive mTOR inhibitors, functions by inhibiting the phosphorylation of Akt and its downstream proteins and has been shown to induce autophagy in cancer cells and inhibit tumor growth in vivo.(220) In conclusion, inhibitors targeting the PI3K/Akt pa”
mTOR: from growth signal integration to cancer, diabetes and ageing (2010, background): “Recently, independent groups generated a series of synthetic small molecules that function as ATP-competitive inhibitors and block all known mTORC1 and mTORC2 action”
The Role of Autophagy in Cancer: Therapeutic Implications (2011, background): “Colorectal cancer In vitro, in vivo CQ þ bortezomib (63) CQ þ vorinostat (56) Phase II HCQ þ XELOX þ bevacizumab Gastrointestinal stromal tumor In vitro, in vivo CQ þ imatinib (75) Prostate cancer In vitro, in vivo CQ þ Src kinase inhibitors (57) Vulvar cancer In vitro CQ þ cetuximab (34) Chronic my”
Lysosomal metabolomics reveals V-ATPase- and mTOR-dependent regulation of amino acid efflux from lysosomes (2017, background): “Importantly, other chemically distinct ATP-competitive inhibitors of mTOR, including AZD8055 and WYE-132 (21, 22), also increased the concentration of these 7 amino acids (Fig.”
mTOR: a pharmacologic target for autophagy regulation. (2015, neutral): “Additionally, another mTOR-KI, AZD8055, potently induces autophagy and inhibits proliferation in a broad range of cancer cell lines (108).”
Inferring causal molecular networks: empirical assessment through a community-based effort (2016, background): “In addition, data suggest that the mTOR inhibitor used here is reasonably specific 37 .”
mTOR signaling in growth control and disease (2012, positive): “groups have developed small molecules that directly inhibit mTOR kinase activity (Chresta et al., 2010; Feldman et al., 2009; Garcı́a-Martı́nez et al., 2009; Thoreen et al., 2009; Yu et al., 2009).”
Reciprocal feedback regulation of PI3K and androgen receptor signaling in PTEN-deficient prostate cancer. (2011, background): “This question can be addressed using selective TORC1/2 inhibitors (Chresta et al., 2010; Thoreen et al., 2009).”
Small molecule inhibition of the autophagy kinase ULK1 and identification of ULK1 substrates (2015, methodology): “To activate endogenous ULK1, we treated MEFs with either amino acid starvationmedia (Earle’s balanced salt solution [EBSS]) or themTORATP-competitive inhibitors INK128 or AZD8055 (Chresta et al., 2010; Hsieh et al., 2012).”