Prinomastat hydrochloride

Modify Date: 2024-01-10 19:03:10

Prinomastat hydrochloride structure	Common Name	Prinomastat hydrochloride
	CAS Number	1435779-45-5	Molecular Weight	459.97
	Density	N/A	Boiling Point	N/A
	Molecular Formula	C₁₈H₂₂ClN₃O₅S₂	Melting Point	N/A
	MSDS	N/A	Flash Point	N/A

Use of Prinomastat hydrochloride

Prinomastat hydrochloride (AG3340 hydrochloride) is a broad spectrum, potent, orally active metalloproteinase (MMP) inhibitor with IC50s of 79, 6.3 and 5.0 nM for MMP-1, MMP-3 and MMP-9, respectively. Prinomastat hydrochloride inhibits MMP-2, MMP-3 and MMP-9 with Kis of 0.05 nM, 0.3 nM and 0.26 nM, respectively. Prinomastat hydrochloride can cross blood-brain barrier. Antitumor avtivity[1][2][3][4].

Name	Prinomastat hydrochloride

Description	Prinomastat hydrochloride (AG3340 hydrochloride) is a broad spectrum, potent, orally active metalloproteinase (MMP) inhibitor with IC50s of 79, 6.3 and 5.0 nM for MMP-1, MMP-3 and MMP-9, respectively. Prinomastat hydrochloride inhibits MMP-2, MMP-3 and MMP-9 with Kis of 0.05 nM, 0.3 nM and 0.26 nM, respectively. Prinomastat hydrochloride can cross blood-brain barrier. Antitumor avtivity[1][2][3][4].
Related Catalog	Research Areas >> Cancer Signaling Pathways >> Metabolic Enzyme/Protease >> MMP
Target	MMP-9:5 nM (IC50) MMP-9:0.26 nM (Ki) MMP-2:0.05 nM (Ki) MMP-1:79 nM (IC50) MMP-13:6.3 nM (IC50) MMP-13:0.3 nM (Ki)
In Vitro	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]. Western Blot Analysis[1] 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 Vivo	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 T1/2 of 1.6 hours[1].
References	[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.

Molecular Formula	C₁₈H₂₂ClN₃O₅S₂
Molecular Weight	459.97

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China
Product Name: Prinomastat hydrochloride
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Purity: 98.0%
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Prinomastat hydrochloride

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