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Merck
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444264

Sigma-Aldrich

MMP Inhibitor III

The MMP Inhibitor III, also referenced under CAS 927827-98-3, controls the biological activity of MMP. This small molecule/inhibitor is primarily used for Protease Inhibitors applications.

别名:

MMP Inhibitor III

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About This Item

经验公式(希尔记法):
C19H29N3O4
分子量:
363.45
分類程式碼代碼:
12352200
NACRES:
NA.77

品質等級

化驗

≥90% (TLC)

形狀

lyophilized solid

製造商/商標名

Calbiochem®

儲存條件

OK to freeze
desiccated

顏色

off-white

溶解度

DMSO: 5 mg/mL

運輸包裝

ambient

儲存溫度

−20°C

一般說明

A homophenylalanine-hydroxamic acid based broad-spectrum cell-permeable, reversible inhibitor of matrix metalloproteinases (supplied as a racemic mixture). Inhibits MMP-1 (IC50 = 7.4 nM), MMP-2 (IC50 = 2.3 nM), MMP-3 (IC50 = 135 nM), MMP-7 (IC50 = 10-100 nM), and MMP-13 (IC50 = 1-10 nM).

生化/生理作用

Cell permeable: yes
Primary Target
MMP-1
Product does not compete with ATP.
Reversible: yes
Target IC50: 7.4 nM, 2.3 nM, 135 nM, 10-100 nM, 1-10 nM, against MMP-1, MMP-2, MMP-3, MMP-7, and MMP-13, respectively

警告

Toxicity: Standard Handling (A)

重構

Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 6 months (-20°C).

其他說明

Covington, M.D., et al. 2006, Am. J. Physiol. Renal. Physiol.290, F43.

法律資訊

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

儲存類別代碼

11 - Combustible Solids

水污染物質分類(WGK)

WGK 1

閃點(°F)

Not applicable

閃點(°C)

Not applicable


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Søren B van Witteloostuijn et al.
Journal of peptide science : an official publication of the European Peptide Society, 23(12), 845-854 (2017-10-24)
Bariatric surgery is currently the most effective treatment of obesity, which has spurred an interest in developing pharmaceutical mimetics. It is thought that the marked body weight-lowering effects of bariatric surgery involve stimulated secretion of appetite-regulating gut hormones, including glucagon-like
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Oncogene, 42(49), 3633-3647 (2023-10-21)
Cutaneous squamous cell carcinoma (cSCC) is the most common metastatic skin cancer. The prognosis of patients with metastatic cSCC is poor emphasizing the need for new therapies. We have previously reported that the activation of Ras/MEK/ERK1/2 and transforming growth factor

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