444241
MMP-2/MMP-9 Inhibitor I
The MMP-2/MMP-9 Inhibitor I, also referenced under CAS 193807-58-8, controls the biological activity of MMP-2/MMP-9. This small molecule/inhibitor is primarily used for Protease Inhibitors applications.
别名:
MMP-2/MMP-9 Inhibitor I, (2R)-2-[(4-Biphenylylsulfonyl)amino]-3-phenylpropionic Acid
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About This Item
质量水平
检测方案
≥95% (HPLC)
形式
solid
制造商/商品名称
Calbiochem®
储存条件
OK to freeze
颜色
white
溶解性
DMSO: 200 mg/mL
运输
ambient
储存温度
−20°C
一般描述
A potent inhibitor of MMP-2 (IC50 = 310 nM) and MMP-9 (IC50 = 240 nM). Orally active in animal models of tumor growth and metastasis.
A potent inhibitor of MMP-2 (gelatinase A; IC50 = 310 nM) and MMP-9 (gelatinase B; IC50 = 240 nM).
生化/生理作用
Cell permeable: no
Primary Target
MMP-2, MMP-9
MMP-2, MMP-9
Product does not compete with ATP.
Reversible: no
Target IC50: 310 nM and 240 nM against MMP-2 and MMP-9
包装
Packaged under inert gas
警告
Toxicity: Standard Handling (A)
重悬
Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 6 months at -20°C.
其他说明
Tamura, Y., et al. 1998. J. Med. Chem.41, 640.
法律信息
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
WGK
WGK 1
闪点(°F)
Not applicable
闪点(°C)
Not applicable
Y Tamura et al.
Journal of medicinal chemistry, 41(4), 640-649 (1998-03-04)
Various N-sulfonylamino acid derivatives were synthesized and evaluated for their in vitro and in vivo activities to inhibit type IV collagenase (MMP-9 and MMP-2). When the amino acid residue and the sulfonamide moiety were modified, their inhibitory activities were greatly
Raina D Ramnath et al.
Kidney international, 97(5), 951-965 (2020-02-11)
The endothelial glycocalyx is a key component of the glomerular filtration barrier. We have shown that matrix metalloproteinase (MMP)-mediated syndecan 4 shedding is a mechanism of glomerular endothelial glycocalyx damage in vitro, resulting in increased albumin permeability. Here we sought to
Michael Roth et al.
Biomedicines, 12(6) (2024-06-27)
Chronic inflammatory lung diseases are characterized by disease-specific extracellular matrix accumulation resulting from an imbalance of matrix metalloproteinases (MMPs) and their inhibitors. Zinc is essential for the function of MMPs, and zinc deficiency has been associated with enhanced tissue remodeling.
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