Alpelisib

1217486-61-7

C19H22F3N5O2S

DMSO : >= 100 mg/mL (226.52 mM)

PI3K/Akt/mTOR

Alpelisib (BYL-719) is a potent and selective PI3Kalpha inhibitor with IC₅₀s of 5 nM, 250 nM, 290 nM and 1200 nM for p110alpha, p110gamma, p110delta, and p110beta, respectively^[1]. IC50 & Target: IC50: 5 nM (p110alpha), 250 nM (p110gamma), 290 nM (p110delta), 1200 nM (p110beta)^[1] In Vitro: Alpelisib (BYL-719) potently inhibits the 2 most common PIK3CA somatic mutations (H1047R, E545K; IC₅₀sca.4 nM). Alpelisib potently inhibits Akt phosphorylation in cells transformed with PI3Kalpha (IC₅₀=74+/-15 nM) and shows significant reduced inhibitory activity in PI3Kbeta or PI3Kdelta isoforms transformed cells (>=15-fold compared with PI3Kalpha)^[2].
Alpelisib (BYL-719, 0-50 uM; 72 hours) inhibits the cell growth of osteosarcoma cell lines MG63, HOS, POS-1 and MOS-J in a dose-dependent manner^[3].
Alpelisib (BYL-719) significantly alters the distribution of cell cycle phases. Alpelisib (BYL-719, 25 uM; 18 hours) induces a cell cycle arrest in the G0/G1 phase of human and murine osteosarcoma cell lines^[3].
In Vivo: Alpelisib (BYL-719) (12.5 mg/kg and 50 mg/kg for C57Bl/6J mice; 50 mg/kg for female Rj:NMRI-nude mice; oral administration; daily) significantly reduces tumor volumes and deposition of ectopic bone matrix^[3].
Alpelisib has moderate terminal elimination half-life (t_1/2=2.9+/-0.2 h) for rat (1 mg/kg, iv) ^[1].