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Nrf2 signaling activator; increases Nrf2 protein expression and enhances Nrf2-dependent cytoprotective gene expression. Inhibits cell growth and induces apoptosis of pancreatic cancer cells in vitro. Also reduces acetaminophen-induced liver injury in mice.
|Storage||Store at RT|
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.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 541.72. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||1.85 mL||9.23 mL||18.46 mL|
|5 mM||0.37 mL||1.85 mL||3.69 mL|
|10 mM||0.18 mL||0.92 mL||1.85 mL|
|50 mM||0.04 mL||0.18 mL||0.37 mL|
References are publications that support the biological activity of the product.
Reisman et al (2009) CDDO-Im protects from acetaminophen hepatotoxicity through induction of Nrf2-dependent genes. Toxicol.Appl.Pharmacol. 236 109 PMID: 19371629
Samudio et al (2005) 2-Cyano-3,12-dioxooleana-1,9-dien-28-imidazolide (CDDO-Im) directly targets mitochondrial glutathione to induce apoptosis in pancreatic cancer. J.Biol.Chem. 280 36273 PMID: 16118208
Aleksunes et al (2010) Transcriptional regulation of renal cytoprotective genes by Nrf2 and its potential use as a therapeutic target to mitigate cisplatin-induced nephrotoxicity. J.Pharmacol.Exp.Ther. 335 2 PMID: 20605904
If you know of a relevant reference for CDDO Im, please let us know.
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Keywords: CDDO Im, CDDO Im supplier, CDDOIm, Nrf2, activators, NFE2L2, erythroid-derived, nuclear, factor, 4737, Tocris Bioscience
1 Citation for CDDO Im
Citations are publications that use Tocris products. Selected citations for CDDO Im include:
Chartoumpekis et al (2018) Nrf2 deletion from adipocytes, but not hepatocytes, potentiates systemic metabolic dysfunction after long-term high-fat diet-induced obesity in mice. Am J Physiol Endocrinol Metab 315 E180 PMID: 29486138
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Literature in this Area
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