NVP-BEZ235 | PI3-K and mTOR inhibitor
NMR (Conforms)
Available Options
| Size : | Price | Quantity | |
|---|---|---|---|
| 10 mg | $40.00 | ||
| 50 mg | $90.00 |
NVP-BEZ235 (915019-65-7) is a dual PI3K and mTOR kinase inhibitor.1 It inhibits VEGF-induced proliferation and angiogenesis.2 Reverses lapatinib resistance.3 It induces G1 arrest and reduces cyclin D1 expression in melanoma cells with negligible apoptosis.4 NVP-BEZ235 inhibits the growth of cancer cells with activating PI3K mutations.5 The ability of NVP-BEZ235 to inhibit PI3K has come into question. This study also shows it to be a potent inhibitor of PRKDC (IC50 = 29 nM), ATM (IC50 = 13 nM), and ATR (IC50 = 8 nM).6 Active in vivo.
References/Citations:
1) Maira et al. (2008), Identification and characterization of NVP-BEZ235, a new orally available dual phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibitor with potent in vivo antitumor activity; Mol. Cancer Ther., 7 1851
2) Schnell et al. (2008), Effects of the dual phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibitor NVP-BEZ235 on the tumor vasculature: implications for clinical imaging; Cancer Res., 68 6598
3) Eichhorn et al. (2008), Phosphatidylinositol 3-kinase hyperactivation results in lapatinib resistance that is reversed by the mTOR/Phosphatidylinositol 3-kinase inhibitor NVP-BEZ235; Cancer Res., 68 9221
4) Marone et al. (2009), Targeting melanoma with dual phosphoinositide 3-kinase/mammalian target of rapamycin inhibitors; Mol. Cancer Res., 7 601
5) Serra et al. (2008), NVP-BEZ235, a dual PI3K/mTOR inhibitor, prevents PI3K signaling and inhibits the growth of cancer cells with activating PI3K mutations; Cancer Res., 68 8022
6) Reinecke et al. (2019), Chemoproteomic selectivity profiling of PIKK and PI3K kinase inhibitors; ACS Chem.Biol., 14 655
NMR (Conforms)
Safety Data Sheet:
Product Data Sheet:
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NVP-BEZ235 (915019-65-7) is a dual PI3K and mTOR kinase inhibitor.1 It inhibits VEGF-induced proliferation and angiogenesis.2 Reverses lapatinib resistance.3 It induces G1 arrest and reduces cyclin D1 expression in melanoma cells with negligible apoptosis.4 NVP-BEZ235 inhibits the growth of cancer cells with activating PI3K mutations.5 The ability of NVP-BEZ235 to inhibit PI3K has come into question. This study also shows it to be a potent inhibitor of PRKDC (IC50 = 29 nM), ATM (IC50 = 13 nM), and ATR (IC50 = 8 nM).6 Active in vivo.
References/Citations:
1) Maira et al. (2008), Identification and characterization of NVP-BEZ235, a new orally available dual phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibitor with potent in vivo antitumor activity; Mol. Cancer Ther., 7 1851
2) Schnell et al. (2008), Effects of the dual phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibitor NVP-BEZ235 on the tumor vasculature: implications for clinical imaging; Cancer Res., 68 6598
3) Eichhorn et al. (2008), Phosphatidylinositol 3-kinase hyperactivation results in lapatinib resistance that is reversed by the mTOR/Phosphatidylinositol 3-kinase inhibitor NVP-BEZ235; Cancer Res., 68 9221
4) Marone et al. (2009), Targeting melanoma with dual phosphoinositide 3-kinase/mammalian target of rapamycin inhibitors; Mol. Cancer Res., 7 601
5) Serra et al. (2008), NVP-BEZ235, a dual PI3K/mTOR inhibitor, prevents PI3K signaling and inhibits the growth of cancer cells with activating PI3K mutations; Cancer Res., 68 8022
6) Reinecke et al. (2019), Chemoproteomic selectivity profiling of PIKK and PI3K kinase inhibitors; ACS Chem.Biol., 14 655
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