Furthermore, CDDO-Im acts as a strong suppressor of inducible nitric oxide synthase (iNOS) expression in primary mouse macrophages and impedes the growth of B16 murine melanoma and L1210 murine leukemia cells in vivo. The injection of 10 nM (5.4 μg) CDDO-Im nearly abolishes IFN-γ's ability to induce iNOS expression, and even a minimal dose of 1 nmol (0.54 μg) CDDO-Im partially achieves this effect^[1].

CDDO-Im has a high inhibitory effect on cell proliferation in human leukemia and breast cancer cell lines (IC50 of about 10-30 nM). In U937 leukemia cells, CDDO-Im can also induce monocyte differentiation by increasing the expression of CD11b and CD36 on the cell surface ^[1].

Otherwise, CDDO-Im improves protein levels of Nrf2, a transcription factor known to bind to antioxidant response element (ARE) sequences, and amplifies the expression of several antioxidant and detoxification genes regulated by Nrf2^[2].

Among synthetic triterpenoids, CDDO-Im stands out for its potent ability to inhibit growth and induce apoptosis across various human cancer types, including multiple myeloma, lung, pancreas, and breast cancers. Notably, in triple-negative breast cancer cell lines SUM159 and MDA-MB-231, CDDO-Im significantly causes cell cycle arrest in the G2/M phase and prompts apoptosis. It also effectively reduces the population of CD24−/EpCAM+ cells in SUM159 tumorspheres, decreasing both the sphere forming efficiency and the size of tumorspheres in primary and secondary cultures^[3].