Salubrinal |
| رقم الكتالوجGC17331 |
Salubrinal هو مثبط انتقائي ومنفذ للخلايا من eIF2α نزع الفسفرة
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 405060-95-9
Sample solution is provided at 25 µL, 10mM.
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IC50: A cell-permeable and selective inhibitor of eIF2α dephosphorylation with an IC50 of 15 M.
The eukaryotic translation initiation factor 2 subunit α (eIF2α) is crucial in protein synthesis. eIF2α phosphorylation played an important role in protecting cells from apoptosis. Salubrinal selectively suppresses the phosphatase complexes that dephosphorylate eIF-2α. [1]
In vitro: This agent is reported to protect cells from endoplasmic reticulum (ER) stress-induced apoptosis (EC50 ~15 M) in PC12 cell lines induced with the protein glycosylation inhibitor tunicamycin and brefeldin A, which causes ER stress by blocking ER-to-Golgi vesicle transport. Salubrinal is a potentially useful agent to study mechanisms of ER stress-induced apoptosis. In addition, it was reported that salubrinal at 50 μM prevented cells from the autophagic and apoptotic progresses induced by loss of Bcl-2 function in murine leukemia L1210 cells. [1]
In vivo: Study from male ICR mice showed that salubrinal significantly aggravated the cisplatin-induced nephrotoxicity. In the kidneys of cisplatin-treated mice, the phosphorylation of eIF2α was significantly increased by salubrinal. In addition, the expression of CCAAT/enhancer binding protein, activating transcription factor 4 as well as the cleavage of caspases 3, 9 and 12 were also up-regulated. Moreover, salubrinal also increased the cisplatin-induced oxidative stress. These findings indicated that salubrinal aggravated cisplatin-induced nephrotoxicity via the up-regulation of ER stress-related cell apoptosis and oxidative stress. [2]
Clinical trial: So far, no clinical trial has been conducted.
References:
[1] Kessel D. Protection of Bcl-2 by salubrinal. Biochem Bioph Res Co. 2006; 346: 1320-3.
[2] Wu CT, Sheu ML, Tsai KS, Chiang CK and Liu SH. Salubrinal, an eIF2α dephosphorylation inhibitor, enhances cisplatin-induced oxidative stress and nephrotoxicity in a mouse model. Free Radic Biol Med, 2011; 51(3): 671-680.
Average Rating: 5 (Based on Reviews and 24 reference(s) in Google Scholar.)
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