Prinomastat inhibits MMP-2, MMP-3 and MMP-9 (Kis: 0.05 nM, 0.3 nM and 0.26 nM, respectively). Prinomastat crosses the blood-brain barrier. It also has antitumor activity. Prinomastat is a broad-spectrum, potent, orally active metalloproteinase inhibitor (IC50s of 79, 6.3, and 5.0 nM for MMP-1, MMP-3, and MMP-9, respectively).

In C57MG/Wnt1 cells, the effect of Wnt1 on the cellular distribution of vimentin is reversed by Prinomastat. Prinomastat (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. 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. 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. The effect of Prinomastat on Wnt1-induced migration is then examined using an in vitro wound assay. The migration of C57MG/Wnt1 cells is increased by 1.8-fold when compared with C57MG cells [1].

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 (a short T1/2: 1.6 hours). The mice are treated therapeutically for 14-16 days with 50 mg/kg/day ip daily starting day 3 to 6 after tumor inoculation in a human fibrosarcoma mouse model (HT1080) [1].

192329-42-3

C18H21N3O5S2

423.51

KB-R9896;AG3340;普啉司他

(< 1 mg/ml refers to the product slightly soluble or insoluble )
Powder: -20°C for 3 years
In solvent: -80°C for 2 years