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SB-3CT
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
SB-3CT图片
CAS NO:292605-14-2
规格:98%
分子量:306.4
包装与价格:
包装价格(元)
5mg电议
25mg电议
100mg电议

产品介绍
gelatinases inhibitor, potent and selective
CAS:292605-14-2
分子式:C15H14O3S2
分子量:306.4
纯度:98%
存储:Store at -20°C

Background:

SB-3CT is a potent and selective inhibitor of gelatinases with Ki values of 13.9 and 600 nM for MMP-2 and MMP-9, respectively.


Gelatinases A (MMP-2) and B (MMP-9) belong to matrix metalloproteinases family and are involved in tumor metastasis and angiogenesis by hydrolyzing extracellular matrix [1].


SB-3CT is a potent and selective gelatinases inhibitor. SB-3CT was a novel mechanism-based inhibitor that directly bound to the catalytic zinc ion of MMP-2 [1]. SB-3CT inhibited purified mouse MMP-9 with Ki value of 120 nM [2].


In mice bearing T-cell lymphoma L-CI.5s cells, SB-3CT reduced the number of liver metastases in a dose dependent way and reduced the number of tumor colonies by >70% at 50 mg/kg/d. SB-3CT (50 mg/kg/d) also significantly reduced colony size and the number of PCNA positive tumor cells in the livers. These results suggested that SB-3CT effectively inhibited tumor cell extravasation and exhibited an antiproliferative effect. SB-3CT completely inhibited MMP-mediated gelatinolytic activity through the inhibition of both MMP-2 and MMP-9. Also, SB-3CT increased survival [2]. In a transient focal cerebral ischemia mice model, SB-3CT inhibited laminin cleavage mediated by MMP-9 and then rescued neurons from apoptosis [3].


参考文献:
[1].  Kleifeld O, Kotra LP, Gervasi DC, et al. X-ray absorption studies of human matrix metalloproteinase-2 (MMP-2) bound to a highly selective mechanism-based inhibitor. comparison with the latent and active forms of the enzyme. J Biol Chem, 2001, 276(20): 17125-17131.
[2].  Krüger A, Arlt MJ, Gerg M, et al. Antimetastatic activity of a novel mechanism-based gelatinase inhibitor. Cancer Res, 2005, 65(9): 3523-3526.
[3].  Gu Z, Cui J, Brown S, et al. A highly specific inhibitor of matrix metalloproteinase-9 rescues laminin from proteolysis and neurons from apoptosis in transient focal cerebral ischemia. J Neurosci, 2005, 25(27): 6401-6408.