CDDO-Im (TP-235) is an activator of Nrf2 and PPAR (Kis: 232/344 nM for PPARα/PPARγ).

PPARα:232 nM (Ki), PPARγ:344 nM (Ki)

CDDO-Im在抑制人类白血病和乳腺癌细胞系的细胞增殖方面具有高活性（IC50约为10-30 nM）。在U937白血病细胞中，通过增加CD11b和CD36细胞表面表达来衡量，CDDO-Im还诱导单核细胞分化[1]。CDDO-Im处理在三阴性乳腺癌细胞系SUM159和MDA-MB-231中明显诱导细胞周期在G2/M期停滞和凋亡。在SUM159肿瘤球中的CD24^-/EpCAM^+细胞显著被CDDO-Im处理抑制。CDDO-Im还显著降低了初级和二级球体培养中的球体形成效率和肿瘤球大小[2]。用CDDO-Im处理能提高Nrf2蛋白水平，Nrf2是一种先前显示能结合ARE序列并增加Nrf2调控的多种抗氧化和解毒基因表达的转录因子[3]。

CDDO-Im 对初级小鼠巨噬细胞中新生可诱导型一氧化氮合酶(iNOS)表达具有显著的抑制作用。此外，CDDO-Im 在体内抑制B16小鼠黑色素瘤和L1210小鼠白血病细胞的生长。CDDO-Im 10 nM（5.4 μg）的注射几乎完全阻止了IFN-γ诱导iNOS的能力，而使用少至1 nmol的CDDO-Im（0.54 μg）治疗也具有部分效果[1]。

CDDO-Im is dissolved in DMSO. SUM159 and MDA-MB-231 cells are seeded into each well of 96-well plates (1,000 cell/well) and treated the next day with vehicle control or CDDO-Im (1, 10, 50, 100 and 200 nM) for given incubation time. The absorbance is measured with a spectrophotometer to determine the cell proliferation rate [2].

Mice are injected i.p. with thioglycollate, and the resulting resident peritoneal macrophages are activated 3 days later with an i.p. injection of IFN-γ. CDDO and CDDO-Im are injected i.p. 30 min after IFN-γ. Macrophages are harvested 10 h later, cultured for 12 h, and then assayed for expression of iNOS protein and production of nitric oxide (NO) [1].