Buparlisib
PI3-kinase inhibitor / Potent pan-Class I PI3-kinase inhibitor (IC50’s: p110α = 52 nM, p110ß = 166 nM, p110δ = 116 nM. P110g = 262 nM).1,2 It inhibited microtubule dynamics at in vitro concentrations >1µM and doses above 50mg/kg in mice.3 Buparlisib lead to a precipitous drop in DNA synthesis in a mouse model of BRCA1-linked triple-negative breast cancer with less affect in normal tissue.4
Biochemicals & reagents
944396-07-0
NVP-BKM120; BKM-120
Burger et al. (2011), Identification of NVP-BKM120 as a Potent, Selective, Orally Bioavailable Class I PI3 Kinase Inhibitor for Treating Cancer; ACS Med. Chem. Lett. 2 774 Maira et al. (2012), Identification and Characterization of NVP-BKM120, an Orally Available Pan-Class I PI3-Kinase Inhibitor; Mol. Cancer Ther. 11 317 Brachmann et al. (2012), Characterization of the mechanism of action of the pan class I PI3K inhibitor NVP-BKM120 across a broad range of concentrations; Mol. Cancer Ther. 11 1747 Juvekar et al. (2016), Phosphoinositide 3-kinase inhibitors induce DNA damage through nucleoside depletion; Proc. Natl. Acad. Sci USA. 113 E4338
-20°C
TARGET: Kinase; Cytoskeleton -- PATHWAY: AKT; PI3K; Proliferation; DNA synthesis; Cell cycle; Cell migration -- RESEARCH AREA: Cell death -- DISEASE AREA: Cancer