To enhance service speed and avoid tariff delays, we've opened a US warehouse. All US orders ship directly from our US facility.
| Cas No.: | 1224844-38-5 |
| Chemical Name: | Sapanisertib (MLN0128) |
| Synonyms: | INK 128; INK128 |
| SMILES: | CC(C)N1C2=C(C(=N1)C3=CC4=C(C=C3)OC(=N4)N)C(=NC=N2)N |
| Formula: | C15H15N7O |
| M.Wt: | 309.333 |
| Sotrage: | 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO |
| Description: | Sapanisertib (INK-128) is a ATP-dependent mTOR1/2 inhibitor with an IC50 of 1 nM for mTOR kinase. |
| In Vivo: | In a ZR-75-1 breast cancer xenograft model, Sapanisertib (INK-128) shows tumor growth inhibition efficacy at a dose of 0.3 mg/kg/day[1]. 4EBP1 and p70S6K1/2 phosphorylation is completely restored to wild-type levels after treatment with INK128 in PtenL/L mice. Sapanisertib (INK-128) treatment results in a 50% decrease in prostatic intraepithelial neoplasia (PIN) lesions in PtenL/L mice and induces programmed cell death in multiple cancer cell lines in mice[2]. |
| In Vitro: | Sapanisertib (INK-128) exhibits an enzymatic inhibition activity against mTOR and more than 100-fold selectivity to PI3K kinases[1]. Sapanisertib (INK-128) selectively decreases the expression of YB1, MTA1, vimentin and CD44 at the protein but not transcript level in PC3 cells. Sapanisertib (INK-128) decreases the invasive potential of PC3 prostate cancer cells. Furthermore, Sapanisertib (INK-128) inhibits cancer cell migration starting at 6 h of treatment, precisely correlating with when decreases in the expression of pro-invasion genes are evident, but preceding any changes in the cell cycle or overall global protein synthesis[2]. |