Size: | Price | Quantity | |
---|---|---|---|
10 mg | $55.00 | ||
50 mg | $245.00 |
NGI-1 (790702-57-7) is a cell-permeable inhibitor of oligosaccharyltransferase (OST) – IC50 = 1.1 µM.1 It blocks cell-surface localization and signaling of the epidermal growth factor receptor (EGFR) glycoprotein and selectively arrests proliferation only in cells dependent on EGFR for survival. NGI-1 caused G1 arrest and senescence in RTK-dependent NSCLC cells (PC9, HCC827, H3255,H1581). NGI-1 displays antiviral behavior against various flaviviruses (Dengue, West Nile, Yellow fever and Zika).2 It also was able to overcome resistance to EGFR tyrosine kinase inhibitors in mutant NSCLC cells3 and enhance radiosensitivity and cytotoxic effects of chemotherapy in glioma cells with high levels of RTK activation4.
References/Citations:
1) Lopez-Sambrooks et al. (2016), Oligosaccharyltransferase inhibition induces senescence in RTK-driven tumor cells; Nature Chem. Biol. 12 1023
2) Puschnik et al. (2017), A small molecule oligosaccharyltransferase inhibitor with pan-flaviviral activity; Cell Rep. 21 3032
3) Lopez-Sambrooks et al. (2018), Oligosaccharyltransferase Inhibition Overcomes Therapeutic Resistance to EGFR Tyrosine Kinase Inhibitors; Cancer Res. July 19, 2018 Epub ahead of print
4) Baro et al. (2018), Oligosaccharyltransferase Inhibition Reduces Receptor Tyrosine Kinase Activation and Enhances Glioma Radiosensitivity; Clin. Cancer Res. July 2, 2018 Epub ahead of print
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NGI-1 (790702-57-7) is a cell-permeable inhibitor of oligosaccharyltransferase (OST) – IC50 = 1.1 µM.1 It blocks cell-surface localization and signaling of the epidermal growth factor receptor (EGFR) glycoprotein and selectively arrests proliferation only in cells dependent on EGFR for survival. NGI-1 caused G1 arrest and senescence in RTK-dependent NSCLC cells (PC9, HCC827, H3255,H1581). NGI-1 displays antiviral behavior against various flaviviruses (Dengue, West Nile, Yellow fever and Zika).2 It also was able to overcome resistance to EGFR tyrosine kinase inhibitors in mutant NSCLC cells3 and enhance radiosensitivity and cytotoxic effects of chemotherapy in glioma cells with high levels of RTK activation4.
References/Citations:
1) Lopez-Sambrooks et al. (2016), Oligosaccharyltransferase inhibition induces senescence in RTK-driven tumor cells; Nature Chem. Biol. 12 1023
2) Puschnik et al. (2017), A small molecule oligosaccharyltransferase inhibitor with pan-flaviviral activity; Cell Rep. 21 3032
3) Lopez-Sambrooks et al. (2018), Oligosaccharyltransferase Inhibition Overcomes Therapeutic Resistance to EGFR Tyrosine Kinase Inhibitors; Cancer Res. July 19, 2018 Epub ahead of print
4) Baro et al. (2018), Oligosaccharyltransferase Inhibition Reduces Receptor Tyrosine Kinase Activation and Enhances Glioma Radiosensitivity; Clin. Cancer Res. July 2, 2018 Epub ahead of print
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