ARP-100

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Chemical Structure| 704888-90-4 同义名 : CAY10609;MMP-2 Inhibitor III;​Matrix Metalloproteinase-2 Inhibitor III;Compound 10a
CAS号 : 704888-90-4
货号 : A443997
分子式 : C17H20N2O5S
纯度 : 96%
分子量 : 364.42
MDL号 : MFCD09971105
存储条件：

Pure form Keep in dark place,Sealed in dry,2-8°C

In solvent -20°C:3-6个月-80°C:12个月
溶解度 :

DMSO: 105 mg/mL(288.13 mM)，配合低频超声助溶，注意：DMSO长时间开封后，会吸水并导致溶解能力下降，请避免使用长期开封的DMSO
动物实验配方：
生物活性
描述 Matrix metalloproteinases (MMPs) are a family of zinc-dependent proteinases that are associated with the tumorigenic process. MMPs degrade the extracellular matrix, promoting tumor invasion and metastasis[1]. MMPs degrade various protein substrates in ECM including collagen and elastin. MMPs could also influence endothelial cell function as well as VSM cell migration, proliferation, Ca2+ signaling, and contraction. MMPs play a role in vascular tissue remodeling during various biological processes such as angiogenesis, embryogenesis, morphogenesis, and wound repair. Alterations in specific MMPs could influence arterial remodeling and lead to various pathological disorders such as hypertension, preeclampsia, atherosclerosis, aneurysm formation, as well as excessive venous dilation and lower extremity venous disease[2].ARP-100 is a potent and selective matrix metalloproteinase MMP-2 inhibitor (IC50=12 nM). ARP-100 interacts with S1’pocket of MMP-2 and shows anti-invasive properties in an in vitro model of invasion on matrigel. ARP-100 shows the less inhibitory activity towards MMP-1 (>50 μM), MMP-3 (4.5 μM), MMP-7 (>50 μM), and MMP-9 (0.2 μM)[3].Inhibition of MMP activity with ARP-100 significantly improved the recovery of cardiac mechanical function and prevented the increase of a 70 kDa SERCA2a degradation fragment following IR injury, although 110 kDa SERCA2a and phospholamban levels appeared unchanged[4]. Significant increases in CD3, CD68, neutrophils, vascular cell adhesion molecule-1 and MMP-2 in perivascular adipose tissue(PVAT), and TGF-β1 and IMT of the aorta of TNF-α-injected mice were observed. PVAT of TNF-α-injected mice significantly up-regulated TGF-β1 and increased cell proliferation in a dose-dependent manner and was attenuated by SB-431542, batimastat, ARP 100 and TIMP-2[5].
实验方案
1mg 5mg 10mg

1 mM

5 mM

10 mM

2.74mL

0.55mL

0.27mL

13.72mL

2.74mL

1.37mL

27.44mL

5.49mL

2.74mL
参考文献

[1]Nithya Ramnath,et al. Matrix metalloproteinase inhibitors. Curr Oncol Rep. 2004 Mar;6(2):96-102.

[2]Xi Wang,et al. Matrix Metalloproteinases, Vascular Remodeling, and Vascular Disease. Adv Pharmacol. 2018;81:241-330.

[3] Rossello A, et al. New N-arylsulfonyl-N-alkoxyaminoacetohydroxamic acids as selective inhibitors of gelatinase A (MMP-2). Bioorg Med Chem. 2004 May 1;12(9):2441-50.

[4] Andrej Roczkowsky,et al. Myocardial MMP-2 contributes to SERCA2a proteolysis during cardiac ischaemia-reperfusion injury. Cardiovasc Res.2020 Apr 1;116(5):1021-1031.

[5]Kyaw Thu Moe,et al. Tumor necrosis factor-α induces aortic intima-media thickening via perivascular adipose tissue inflammation. J Vasc Res. 2013;50(3):228-37.