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Prinomastat

Catalog No. T12539L   CAS 192329-42-3
Synonyms: KB-R9896, AG3340

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).

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Prinomastat Chemical Structure
Prinomastat, CAS 192329-42-3
Pack Size Availability Price/USD Quantity
1 mg 4-5 weeks $ 75.00
5 mg 4-5 weeks $ 315.00
10 mg 4-5 weeks $ 593.00
25 mg 4-5 weeks $ 1,200.00
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Biological Description
Chemical Properties
Storage & Solubility Information
Description 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).
Targets&IC50 MMP1:79 nM, MMP2:0.05 nM (ki), MMP9:0.26 nM (ki), MMP9:5 nM, MMP3:0.3 nM (ki), MMP3:6..3 nM
In vitro 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].
In vivo 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].
Synonyms KB-R9896, AG3340
Molecular Weight 423.51
Formula C18H21N3O5S2
CAS No. 192329-42-3

Storage

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

TargetMolReferences and Literature

1. Sørensen MD, et al. Cyclic phosphinamides and phosphonamides, novel series of potent matrix metalloproteinase inhibitors with antitumour activity. Bioorg Med Chem. 2003 Dec 1;11(24):5461-84. 2. Blavier L, et al. Stromelysin-1 (MMP-3) is a target and a regulator of Wnt1-induced epithelial-mesenchymal transition (EMT). Cancer Biol Ther. 2010 Jul 15;10(2):198-208. 3. Shalinsky DR, et al. Broad antitumor and antiangiogenic activities of AG3340, a potent and selective MMP inhibitor undergoing advanced oncology clinical trials. Ann N Y Acad Sci. 1999 Jun 30;878:236-70. 4. Ozerdem U, et al. The effect of prinomastat (AG3340), a potent inhibitor of matrix metalloproteinases, on a subacute model of proliferative vitreoretinopathy. Curr Eye Res. 2000 Jun;20(6):447-53.

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Keywords

Prinomastat 192329-42-3 Proteases/Proteasome MMP KB-R9896 AG-3340 KB-R 9896 AG3340 AG 3340 KB-R-9896 inhibitor inhibit

 

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