GP262

GP262 (0-5 μM, 0-24 h) efficiently reduces PI3K and mTOR Levels and this degradation is attenuated upon 26S proteasome inhibition, can be blocked under high concentration competition (MG132 (HY-13259) and VH032 (HY-120217)) and depends on VHL recruitment in MDA-MB-231 cells^[1].
GP262 (8-1000 nM) significantly inhibits proliferation and induces programmed cell death (apoptosis), reveals dose-dependent growth inhibition with IC₅₀ values of 68.0 nM (in MDA-MB-231), 161.6 nM (in MCF-7), and 124.2 nM (in MDA-MB-361), achieving maximum inhibition (I_max) of 65.4, 83.4, and 97.7% respectively, impairs colony formation in MDA-MB-231 cells at 200 nM, and has a degradation efficacy against mTOR and PI3Kα with IC₅₀ values of 167.6 and 40 nM in MCF-7 cells^[1].
GP262 (8-5000 nM, 24 h) demonstrates concentration-dependent reduction of PI3Kγ protein levels in THP-1 cells and antiproliferative effects in OCI-AML3 (IC₅₀ = 44.3 nM) and THP-1 cells (IC₅₀ = 48.3 nM)^[1].
GP262 (1000 nM, 12 h) increases apoptosis to 32.1% in MDA-MB-231 cells^[1].
GP262 (0.03125-2 μM) reveals dissociation constants with K_d of 0.867 μM for PI3Kα and 0.479 μM for mTOR^[1].
GP262 induces polyubiquitination-dependent proteasomal degradation^[1].
GP262 exhibits excellent kinase selectivity for the PI3K family and mTOR, thereby inducing widespread transcriptomic alterations including multiple differentially expressed genes (DEGs) associated with cell cycle regulation, cancer-related processes, and apoptosis, which collectively demonstrate significant enrichment and profound impact on cell cycle-related pathways in MDA-MB-231 cells^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.