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PX 12
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。
PX 12图片
CAS NO:141400-58-0
规格:98%
分子量:188.31
包装与价格:
包装价格(元)
10mg电议
50mg电议

产品介绍
Trx-1 inhibitor
CAS:141400-58-0
分子式:C7H12N2S2
分子量:188.31
纯度:98%
存储:Store at -20°C

Background:

PX 12 is an inhibitor of thioredoxin-1 [1].


Thioredoxin-1 (Trx-1) is a small redox protein with a conserved catalytic site and plays an important role in cells that includes the regulation of trans-activating activity and the DNA binding of redox-sensitive transcription factors [1].


In HT-29 human colon carcinoma cells and MCF-7 human breast cancer, PX 12 prevented the hypoxia-induced increase in HIF-1 protein. Also, PX 12 decreased inducible nitric oxide synthase, HIF-1-trans-activating activity and VEGF formation [2].


In immunodeficient mice bearing HT-29 human colon xenografts, PX 12 decreased the average tumor blood vessel permeability by 63% within 2 hours and returned to pretreatment values after 48 hours. PX 12 reduced tumor-derived VEGF and tumor after 24 hours. Also, Trx-1 showed a rapid decrease within 2 hours and maintained for 24 hours [1]. In mice bearing MCF-7 tumor xenografts, PX 12 reduced HIF-1ɑ and VEGF protein levels [2]. In cancer patients, PX-12 treatment significantly reduced the levels of Trx-1 and VEGF in plasma [3].


参考文献:
[1].  Jordan BF, Runquist M, Raghunand N, et al. The thioredoxin-1 inhibitor 1-methylpropyl 2-imidazolyl disulfide (PX-12) decreases vascular permeability in tumor xenografts monitored by dynamic contrast enhanced magnetic resonance imaging. Clin Cancer Res, 2005, 11(2 Pt 1): 529-536.
[2].  Welsh SJ, Williams RR, Birmingham A, et al. The thioredoxin redox inhibitors 1-methylpropyl 2-imidazolyl disulfide and pleurotin inhibit hypoxia-induced factor 1alpha and vascular endothelial growth factor formation. Mol Cancer Ther, 2003, 2(3): 235-243.
[3].  Baker AF, Dragovich T, Tate WR, et al. The antitumor thioredoxin-1 inhibitor PX-12 (1-methylpropyl 2-imidazolyl disulfide) decreases thioredoxin-1 and VEGF levels in cancer patient plasma. J Lab Clin Med, 2006, 147(2): 83-90.