Prinomastat (AG3340) is a broad spectrum, potent, orally activemetalloproteinase (MMP)inhibitor withIC₅₀s of 79, 6.3 and 5.0 nM forMMP-1,MMP-3andMMP-9, respectively. Prinomastat inhibitsMMP-2,MMP-3andMMP-9withK_is of 0.05 nM, 0.3 nM and 0.26 nM, respectively. Prinomastat crosses blood-brain barrier. Antitumor avtivity^[1][2][3][4].

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^[1].
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)^[1].
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^[1].

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_1/2of 1.6 hours^[1].

423.51

Solid

C₁₈H₂₁N₃O₅S₂

192329-42-3

普啉司他

Room temperature in continental US; may vary elsewhere.

DMSO :< 1 mg/mL (ultrasonic;warming;heat to 60℃)(insoluble or slightly soluble)