1435779-45-5
基本信息
(3S)-N-羟基-2,2-二甲基-4-[[4-(4-吡啶氧基)苯基]磺酰基]-3-硫代吗啉甲酰胺盐酸盐
(S)-N-羟基-2,2-二甲基-4-((4-(吡啶-4-基氧基)苯基)磺酰基)硫代吗啉-3-甲酰胺盐酸盐
物理化学性质
| 储存条件 | -20°C储存 |
| 溶解度 | DMSO: 100 mg/mL (217.41 mM) |
| 形态 | Solid |
| 颜色 | White to off-white |
常见问题列表
|
MMP-9 5 nM (IC 50 ) |
MMP-9 0.26 nM (Ki) |
MMP-2 0.05 nM (Ki) |
MMP-1 79 nM (IC 50 ) |
MMP-13 6.3 nM (IC 50 ) |
MMP-13 0.3 nM (Ki) |
Prinomastat (AG3340; 0.1-1 µg/mL; 4 days; C57MG/Wnt1 cells) inhibits Wnt1-induced MMP-3 production. Reversal of Wnt1-induced EMT and β-catenin transcriptional activity by Prinomastat.
Co-culture of L/Wnt3a cells and CT7 cells increases the Topflash activity in CT7 cells, and co-culturing both L/Wnt3a cells and MMP-3 overexpressing C57MG cells with CT7 cells increases the Topflash luciferase activity in CT7 cells beyond the level observed with L/Wnt3a cells, and these effects are all suppressed by Prinomastat (AG3340).
Inhibition of entry of C57MG/Wnt1 cells into S phase by Prinomastat corresponds to a decrease in expression of cyclin D1 and Erk1/2 phosphorylation. The effect of Prinomastat on Wnt1-induced migration is then examined using an in vitro wound assay. As anticipated, the migration of C57MG/Wnt1 cells is increased by 1.8-fold when compared with C57MG cells.The effect of Wnt1 on the cellular distribution of vimentin is reversed by Prinomastat in C57MG/Wnt1 cells.
Western Blot Analysis
| Cell Line: | C57MG/Wnt1 cells |
| Concentration: | 0.1 µg/mL, 1 µg/mL |
| Incubation Time: | 4 days |
| Result: | A significant decrease in MMP-3 promoter activity in C57MG/Wnt1 cells. |
In a human fibrosarcoma mouse model (HT1080), the mice are treated therapeutically for 14-16 days with 50 mg/kg/day ip daily starting day 3 to 6 after tumour inoculation. Prinomastat is well tolerated by the animals, and there are no signs of weight loss or other adverse effects. Prinomastat has good tumour growth inhibition, with a short T 1/2 of 1.6 hours.