CDDO Im
Chemical Name: 1-(2-Cyano-3,12,28-trioxooleana-1,9(11)-dien-28-yl)-1H-imidazole
Purity: ≥98%
Biological Activity
CDDO Im is an Nrf2 signaling activator; increases Nrf2 protein expression and enhances Nrf2-dependent cytoprotective gene expression. CDDO Im inhibits cell growth and induces apoptosis of pancreatic cancer cells in vitro. Also reduces acetaminophen-induced liver injury in mice.Technical Data
The technical data provided above is for guidance only.
For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Background References
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CDDO-Im protects from acetaminophen hepatotoxicity through induction of Nrf2-dependent genes.
Reisman et al.
Toxicol.Appl.Pharmacol., 2009;236:109 -
2-Cyano-3,12-dioxooleana-1,9-dien-28-imidazolide (CDDO-Im) directly targets mitochondrial glutathione to induce apoptosis in pancreatic cancer.
Samudio et al.
J.Biol.Chem., 2005;280:36273 -
Transcriptional regulation of renal cytoprotective genes by Nrf2 and its potential use as a therapeutic target to mitigate cisplatin-induced nephrotoxicity.
Aleksunes et al.
J.Pharmacol.Exp.Ther., 2010;335:2
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Citations for CDDO Im
The citations listed below are publications that use Tocris products. Selected citations for CDDO Im include:
4 Citations: Showing 1 - 4
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Genetic or pharmacologic Nrf2 activation increases proteinuria in chronic kidney disease in mice.
Authors: Thomas W Et al.
Kidney Int 2021;99:102-116
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NRF2 Is an Upstream Regulator of MYC-Mediated Osteoclastogenesis and Pathological Bone Erosion.
Authors: Kyung-Hyun Et al.
Cells 2020;9
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Nrf2-Mediated Fibroblast Reprogramming Drives Cellular Senescence by Targeting the Matrisome.
Authors: Jörn Et al.
Dev Cell 2018;46:145-161.e10
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Nrf2 deletion from adipocytes, but not hepatocytes, potentiates systemic metabolic dysfunction after long-term high-fat diet-induced obesity in mice.
Authors: Chartoumpekis Et al.
Am J Physiol Endocrinol Metab 2018;315:E180
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