CDDO-Me
Nrf2 activator / 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
Biochemicals & reagents
218600-53-4
Bardoxolone methyl; RTA 402; TP-155; CDDO-Methyl ester
1 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 2 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 3 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 4 Ball et al. (2020) CDDO-Me Alters the Tumor Microenvironment in Estrogen Receptor Negative Breast Cancer; Sci. Rep. 10 6560 5 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
-20°C
TARGET: Transcription factor; Kinase -- PATHWAY: NFKappaB; Transcription; Cytokine; Apoptosis inducer; Cell cycle -- RESEARCH AREA: Cell death; Oxidative stress; Cancer stem cells -- DISEASE AREA: Inflammation; DiabetesKidney disease; Cancer