Buparlisib Hydrochloride (BKM120 HCl) is a specific and orally bioavailable pan-class I PI3K inhibitor that competitively inhibits PI3K/AKT kinase at the nanomolar level and suppresses cancer cell growth, making it suitable for studying breast cancer, glioblastoma, and solid tumours.

p110α:52 nM, p110α-E545K:99 nM, Vps34:2.4 μM, p110α-H1047R:58 nM, p110γ:262 nM, p110δ:116 nM, mTOR:4.6 μM, p110β:166 nM

MM cell lines were treated with Buparlisib Hydrochloride (10 μM, 24 hours) to observe its effects on cells.
Results: Buparlisib Hydrochloride treatment resulted in growth inhibition and apoptosis of MM cells in a dose- and time-dependent manner. The IC50 values for ARP-1, ARK, and MM.1R were between 1 and 10 μM, the IC50 value for MM.1S was <1 μM, and the IC50 value for U266 was between 10 and 100 μM. Buparlisib Hydrochloride treatment resulted in growth inhibition and apoptosis of MM cells in a dose- and time-dependent manner. [2]

Methods: Abcg2−/−, Abcb1a/b−/−, and Abcb1a/b;Abcg2−/− mice were treated with Buparlisib Hydrochloride (2 mg/kg, intravenously, 1 hour) to investigate whether P-gp and BCRP could attenuate Buparlisib Hydrochloride brain penetration in vivo. Results: P-gp and BCRP did not limit Buparlisib Hydrochloride brain penetration in vivo. Brain-to-plasma ratios were between 1.5 and 2 for all strains, indicating that Buparlisib Hydrochloride exhibited excellent brain penetration. [3]