CDDO-Im

Research use only, not for human use.

CDDO-Im is an activator of Nrf2 and PPAR (Kis: 232/344 nM for PPARα/PPARγ).

CDDO-Im is an activator of Nrf2 and PPAR (Kis: 232/344 nM for PPARα/PPARγ).

CDDO-Im is highly active in suppressing cellular proliferation of human leukemia and breast cancer cell lines (IC50 approximately 10-30 nM). In U937 leukemia cells, CDDO-Im also induces monocytic differentiation as measured by increased cell surface expression of CD11b and CD36. Treatment with CDDO-Im elevates protein levels of Nrf2, a transcription factor previously shown to bind ARE sequences, and increases expression of a number of antioxidant and detoxification genes regulated by Nrf2. CDDO-Im is one of the most potent synthetic triterpenoids shown to induce growth inhibition and apoptosis in various human cancer cells, including multiple myeloma, lung, pancreas and breast cancer. CDDO-Im treatment markedly induces cell cycle arrest at G2/M-phase and apoptosis in the triple-negative breast cancer cell lines, SUM159 and MDA-MB-231. The CD24?/EpCAM+ cells in SUM159 tumorspheres are significantly inhibited by CDDO-Im treatment. CDDO-Im also significantly decreases sphere forming efficiency and tumorsphere size in both primary and secondary sphere cultures.

CDDO-Im is a potent inhibitor of de novo inducible nitric oxide synthase expression in primary mouse macrophages. Moreover, CDDO-Im inhibits growth of B16 murine melanoma and L1210 murine leukemia cells in vivo. Injection of 10 nM (5.4 μg) of CDDO-Im almost completely blocks the ability of IFN-γ to induce iNOS, and treatment with as little as 1 nmol of CDDO-Im (0.54 μg) is partially effective.

RTA-403 | TP-235 | CDDO-Imidazolide

Nuclear Receptor/Transcription Factor

Keap1-Nrf2

Nrf2|PPAR|PPARα|PPARγ

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443104-02-7

541.72

C34H43N3O3

>98% (HPLC)

DMSO:50 mg/mL (92.30 mM; Need ultrasonic);Water:Insoluble

C[C@@]12CC[C@]3(CCC(C[C@H]3[C@H]1C(=O)C=C4[C@]2(CC[C@@H]5[C@@]4(C=C(C(=O)C5(C)C)C#N)C)C)(C)C)C(=O)N6C=CN=C6

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(-20℃)

With Ice Pack

≥ 2 years