Taselisib

1282512-48-4

C24H28N8O2

DMSO : 50 mg/mL (108.57 mM; Need ultrasonic)

PI3K/Akt/mTOR

Taselisib (GDC-0032) is a potent PI3K inhibitor targets PIK3CA mutations, with K_is of 0.12 nM, 0.29 nM, 0.97 nM, and 9.1 nM for PI3Kdelta, PI3Kalpha, PI3Kgamma and PI3Kbeta, respectively. IC50 & Target: Ki: 0.29 nM (PI3Kalpha), 9.1 nM (PI3Kbeta), 0.97 nM (PI3Kgamma), 0.12 nM (PI3Kdelta)^[3] In Vitro: Taselisib (GDC-0032) (100 nM) inhibits AKT/mTOR signaling in PIK3CA mutant cell lines but not in cells with loss or mutation of PTEN; Taselisib (GDC-0032) enhances radiation-induced apoptosis and inhibits growth in head and neck cancer cell lines that are sensitive to its single-agent activiy^[1]. Taselisib (GDC-0032) enhances the effects of MEK1/2 inhibition on both BRAF^V600E/PTEN^Null human melanoma cells autochthonous mouse melanomas^[2]. In Vivo: Taselisib (GDC-0032) (5 mg/kg, p.o.) potently impairs PI3K signaling and enhances the efficacy of fractionated radiotherapy; Taselisib (GDC-0032) and radiation is more effective than either treatment alone in nude mice implanted with subcutaneous Cal-33 xenografts^[1]. The vehicle-treated BRAFV600E/PTENNull melanoma-bearing mice experiencs initial tumor regression after treatment with Taselisib (GDC-0032) (22.5 mg/kg, p.o.)^[2].