This compound is a customized synthesis product. We have a strong synthesis team with excellent synthesis technology and capabilities. However, due to various objective factors, there is a low probability that the synthesis will not be successful. If you need to learn more, please feel free to consult us, we will serve you wholeheartedly.
This compound is a customized synthesis product. We have a strong synthesis team with excellent synthesis technology and capabilities. However, due to various objective factors, there is a low probability that the synthesis will not be successful. If you need to learn more, please feel free to consult us, we will serve you wholeheartedly.
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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This compound is a customized synthesis product. We have a strong synthesis team with excellent synthesis technology and capabilities. However, due to various objective factors, there is a low probability that the synthesis will not be successful. If you need to learn more, please feel free to consult us, we will serve you wholeheartedly.
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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).
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
Method for preparing DMSO master liquid: mg
drug pre-dissolved in μL DMSO (Master liquid concentration
mg/mL),
Method for preparing in vivo formulation:Take μL
DMSO master liquid, next add μL PEG300, mix and clarify, next add μL
Tween 80,mix and clarify, next add μL ddH2O, mix and clarify.
Method for preparing in vivo formulation:Take μL
DMSO master liquid, next add μL Corn oil,mix and clarify.
Note:
Be sure to add the solvent(s) in order. Physical methods such as vortex, ultrasound or hot water bath can be used to aid dissolving.
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Tech Support
Please see Inhibitor Handling Instructions for more frequently ask questions. Topics include: how to prepare stock solutions, how to store products, and cautions on cell-based assays & animal experiments, etc.