PI-103 Hydrochloride is a dual PI3K/Akt and mTOR inhibitor exhibiting nM-level inhibition of p110α, p110β, p110δ, p110γ, DNA-PK, mTORC1, and mTORC2. PI-103 induces autophagy, mitochondrial apoptosis, and cell cycle arrest, making it suitable for leukaemia research.

mTORC1:20 nM, DNA-PK:23 nM, mTORC2:83 nM, p110γ:15 nM, p110α:2 nM, p110δ:3 nM, p110β:3 nM

PI-103 Hydrochloride exhibits anti-proliferative properties in a panel of Homo sapiens cancer cell lines (including prostate cancer, ovarian cancer, glioblastoma, and oropharyngeal squamous cell carcinoma) as well as in Homo sapiens umbilical vein endothelial cells [1].
PI-103 Hydrochloride demonstrates dose-dependent inhibition of proliferation in 37-31E and 37-31E-F3 cells. For 37-31E cells, proliferation growth can be inhibited by 50% when the PI-103 Hydrochloride concentration exceeds 100 nM, whereas the concentration required to achieve 50% inhibition in 37-31E-F3 cells is 40±2 nM. In the 37-31E-F3 cell line, the inhibitory effects of PI-103 Hydrochloride at concentrations of 50 nM and 100 nM are comparable to those achieved with 500 nM PI-103 Hydrochloride in the 37-31E cell line [4].

An orthotopic xenograft model was established by subcutaneously injecting 37-31E-F3 melanoma cells into immunocompetent FVB/N wild-type mice. Subsequent drug administration to the mice showed the following results: PI-103 Hydrochloride (10 mg/kg) significantly promoted in vivo tumor growth, while sorafenib (50 mg/kg) inhibited tumor growth. Compared with sorafenib monotherapy, the combined treatment with the two drugs did not exhibit additional benefits in terms of tumor inhibitory effect; furthermore, the tumor volume in the combined treatment group was even slightly larger than that in the sorafenib monotherapy group [4].

DMSO: 3 mg/mL (7.8 mM), Sonication and heating are recommended.

H2O: < 1 mg/mL (insoluble)