Solubility | DMSO : 100 mg/mL mother liquor preservation: sub-package and freeze storage to avoid repeated freezing and thawing;-20 ℃,1 month;-80 ℃,6 months (after dilution, the solution temperature is low and storage may precipitate, try to use it now) Cell experiment: Dissolve with DMSO first: dilute with culture medium then, and the dilution process is recommended to be carried out in stages to avoid too fast concentration change leading to compound precipitation. If the compound is precipitated during the dilution process, it can be redissolved by ultrasound. During dilution, ensure that the final concentration of DMSO in the working fluid should be below 0.1% as far as possible, and the maximum should not exceed 0.5%, and set up a DMSO control group with corresponding concentration. Animal experiment: Dissolve with DMSO first: dilute with water or normal saline, etc. The dilution process is recommended to be carried out in sections to avoid excessive concentration changes leading to compound |
In vitro study | SU11274 is 50-fold more selective for Met than Flk and 500-1000-fold more selective for other tyrosine kinases, such as FGFR-1, c-src, PDGF BR, and EGFR. SU11274 inhibits phosphorylation of key regulators of the PI3K pathway, including AKT, FKHR, or GSK3β. In the presence of interleukin-3, SU11274 treatment inhibited the growth of transformed BaF3 cells by TPR-MET in a dose-dependent manner with IC50<3 μm, other oncogenic tyrosine kinase-transformed BaF3 cell growth was not inhibited, including BCR-ABL, TEL-JAK2, TEL-ABL, and TEL-PDGFβR. In addition to inhibition of cell growth, SU11274 treatment also significantly inhibited BaF3.TPR-MET cell migration by 44.8% and 80% for 1 μm and 5 μm treatments, respectively. SU11274 inhibits HGF-dependent Met phosphorylation, and HGF-dependent cell proliferation and activity with an IC50 of 1-1.5 μm. SU11274 inhibited HGF-induced cell growth by acting on H69 and H345 cells with functional Met receptors with IC50 of 3.4 μm and 6.5 μm, respectively. 5 M SU11274 treatment, the cell cycle was stopped at G1 phase, the G1 phase cells increased from 42.4% to 70.6%, and induced caspase dependent apoptosis, according to 1 M treatment, apoptosis of 24%. SU1127 acts on non-small cell lung cancer (NSCLC) cells expressing c-Met, inhibits cell viability with an IC50 of 0.8-4.4 μm, and abrogates liver growth factor-induced phosphorylation of c-Met and its downstream signals. |