Molecular Formula | C21H16FN7O |
Molar Mass | 401.4 |
Density | 1.50±0.1 g/cm3(Predicted) |
Boling Point | 733.7±70.0 °C(Predicted) |
Solubility | DMSO: ≥ 29 mg/mL |
pKa | 10.01±0.10(Predicted) |
Storage Condition | -20℃ |
In vitro study | Acalisib (GS-9820) is more selective for PI3Kδ (IC 50 =12.7 nM) relative to other PI3K class I enzymes (IC 50 : PI3Kα, 5,441 nM; PI3Kβ, 3,377 nM; PI3Kγ, 1,389 nM). Acalisib is also 10 3 -fold more selective against PI3Kδ than against related kinases, such as PI3KCIIβ (IC 50 >10 nM), hVPS34 (IC 50 =12.7 μM), DNA-PK (IC 50 =18.7 μM), and mTOR (IC 50 >10 nM). In fibroblasts, the PDGF receptor signals through PI3Kα and the GPCR for lysophosphatidic acid (LPA) signals through PI3Kβ. Acalisib reduces PDGF-induced pAkt by only 50% at 11,585 nM, and LPA-induced pAkt by 50% at 2,069 nM. |
In vivo study | To dissect the relative contribution of PI3Kα and PI3Kδ inhibition in the reduction of obesity, obese hyperphagic ob/ob mice are treated with a selective PI3Kα inhibitor, BYL-719, or with a selective PI3Kδ inhibitor, Acalisib (GS-9820). Remarkably, BYL-719 reduces body weight after 15 days of treatment to a similar extent as CNIO-PI3Ki, whereas Acalisib has no significant effect at the same doses as BYL-719. It should be noted that 10 mg/kg of Acalisib is sufficient to reduce the growth of multiple myeloma xenografts in mice. |
1mg | 5mg | 10mg | |
---|---|---|---|
1 mM | 2.491 ml | 12.457 ml | 24.913 ml |
5 mM | 0.498 ml | 2.491 ml | 4.983 ml |
10 mM | 0.249 ml | 1.246 ml | 2.491 ml |
5 mM | 0.05 ml | 0.249 ml | 0.498 ml |