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UTL-5g (GBL-5g), an anti-inflammatory TNF-α inhibitor, has chemoprotective and liver radioprotective effects. UTL-5g lowers hepatotoxicity, nephrotoxicity, and myelotoxicity induced by Cisplatin through TNF-α inhibition among other factors[1][2].

RAW 264.7 macrophages are transfected with the respective reporter assay plasmids, pretreated with UTL-5g at 1, 10 or 50 μM for 60 min and then challenged with 100 ng/ml LPS. After a 16 h incubation, transcription factor activity is measured. Transcription factors that shows a UTL-5g dose-dependent decrease in activity in two experiments are categorized as being disrupted by UTL-5g.

UTL-5g (GBL-5g) lowers levels of TGF-β and TNF-α elevated by lung irradiation[1].UTL-5g (60 mg/kg; p.o.; daily for 4 days) shows positive effects in increasing the survival rates and extending the survival times[3]. Animal Model: C57BL/6, male mice (8-10 weeks)[1]

[1]. Stephen Brown, et al. UTL-5g Lowers Levels of TGF-β and TNF-α Elevated by Lung Irradiation [2]. Carruthers NJ, et al. Phosphoproteome and transcription factor activity profiling identify actions of the anti-inflammatory agent UTL-5g in LPS stimulated RAW 264.7 cells including disrupting actin remodeling and STAT-3 activation. Eur J Pharmacol. 2017;811:66-73. [3]. Shaw J, et al. The small-molecule TNF-α inhibitor, UTL-5g, delays deaths and increases survival rates for mice treated with high doses of cisplatin. Cancer Chemother Pharmacol. 2013;72(3):703-707.

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