CDDO-Me | Nrf2 activator
NMR (Conforms)
Available Options
| Size: | Price | Quantity | |
|---|---|---|---|
| 5 mg | $60.00 | ||
| 25 mg | $198.00 |
CDDO-Me (218600-53-4) is a potent activator of Nrf2 target transcription via interaction with thiol groups of Keap1, an Nrf2 partner, in phase 2 response against oxidative stress.1 Inhibits the NF-κB pathway via inhibition of IKKα activation in vitro2 and reduces expression of proinflammatory cytokines in vivo3. Alters tumor microenvironment causing breast tumor associated macrophages to switch from tumor-promoting to tumor-inhibiting characteristics in vitro.4 Reduces cancer stem cell marker expression in Ec109 and KYSE70 cells.5
References/Citations:
- Dinkova-Kostova et al. (2005) Extremely potent triterpenoid inducers of the phase 2 response: correlations of protection against oxidant and inflammatory stress; Proc. Natl. Acad. Sci. USA 102 4584
- Shishodia et al. (2006) A synthetic triterpenoid, CDDO-Me, inhibits IkappaBalpha kinase and enhances apoptosis induced by TNF and chemotherapeutic agents through down-regulation of expression of nuclear factor kappaB-regulated gene products in human leukemic cells; Clin Cancer Res. 12 1828
- Wang et al. (2015) Therapeutic effects of C-28 methyl ester of 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid (CDDO-Me; bardoxolone methyl) on radiation-induced lung inflammation and fibrosis in mice; Drug Des. Devel. Ther. 9 3163
- Ball et al. (2020) CDDO-Me Alters the Tumor Microenvironment in Estrogen Receptor Negative Breast Cancer; Sci. Rep. 10 6560
- Wang et al. (2015) Bardoxolone methyl induces apoptosis and autophagy and inhibits epithelial-to-mesenchymal transition and stemness in esophageal squamous cancer cells; Drug Des. Devel. Ther. 9 993
NMR (Conforms)
Safety Data Sheet:
Product Data Sheet:
Materials provided by Focus Biomolecules are for laboratory research use only and are not intended for human or veterinary applications. Please note that we do not sell to individuals and that all orders placed by non-research organizations will incur a $20 restocking/refund fee
CDDO-Me (218600-53-4) is a potent activator of Nrf2 target transcription via interaction with thiol groups of Keap1, an Nrf2 partner, in phase 2 response against oxidative stress.1 Inhibits the NF-κB pathway via inhibition of IKKα activation in vitro2 and reduces expression of proinflammatory cytokines in vivo3. Alters tumor microenvironment causing breast tumor associated macrophages to switch from tumor-promoting to tumor-inhibiting characteristics in vitro.4 Reduces cancer stem cell marker expression in Ec109 and KYSE70 cells.5
References/Citations:
- Dinkova-Kostova et al. (2005) Extremely potent triterpenoid inducers of the phase 2 response: correlations of protection against oxidant and inflammatory stress; Proc. Natl. Acad. Sci. USA 102 4584
- Shishodia et al. (2006) A synthetic triterpenoid, CDDO-Me, inhibits IkappaBalpha kinase and enhances apoptosis induced by TNF and chemotherapeutic agents through down-regulation of expression of nuclear factor kappaB-regulated gene products in human leukemic cells; Clin Cancer Res. 12 1828
- Wang et al. (2015) Therapeutic effects of C-28 methyl ester of 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid (CDDO-Me; bardoxolone methyl) on radiation-induced lung inflammation and fibrosis in mice; Drug Des. Devel. Ther. 9 3163
- Ball et al. (2020) CDDO-Me Alters the Tumor Microenvironment in Estrogen Receptor Negative Breast Cancer; Sci. Rep. 10 6560
- Wang et al. (2015) Bardoxolone methyl induces apoptosis and autophagy and inhibits epithelial-to-mesenchymal transition and stemness in esophageal squamous cancer cells; Drug Des. Devel. Ther. 9 993
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