CAS NO: | 932730-51-3 |
规格: | 98% |
分子量: | 518.73 |
包装 | 价格(元) |
200mg | 电议 |
500mg | 电议 |
2mg | 电议 |
5mg | 电议 |
10mg | 电议 |
50mg | 电议 |
100mg | 电议 |
Background:
CDDO-EA is an NF-E2 related factor 2/antioxidant response element (Nrf2/ARE) activator. Nrf2/ARE[1]
CDDO-EA potently activates Nrf2/ARE in a cell culture model of ALS and in the G93A SOD1 mouse model of ALS[1]. CDDO-EA is a potent inducer of apoptosis in A549 lung cancer cells, as shown both by PARP cleavage and Annexin staining. CDDO-EA is more potent than CDDO itself as inducers of heme oxygenase-1 (HO-1). In RAW264.7 macrophage-like cells, CDDO-EA is 7-fold more potent than CDDO as suppressors of the ability of IFN-γ to induce iNOS[2].
The survival analysis shows that G93A mice treated with CDDO-EA, compared to G93A littermate controls, lives significantly longer. CDDO-EA treatment increases the life-span by 20.6 days from 124.05±3.7 days to 144.72±8.1 days (16.6%) (p<0.001). In CDDO-EA-treated G93A mice, the age of death is 141.4±5.2 days and the duration from the age of onset to the age of death is 57.6±7.6 days, which means that the age of death from onset is prolonged by 17.5 days (43%)[1].
[1]. Neymotin A, et al. Neuroprotective effect of Nrf2/ARE activators, CDDO ethylamide and CDDO trifluoroethylamide, in a mouse model of amyotrophic lateral sclerosis. Free Radic Biol Med. 2011 Jul 1;51(1):88-96. [2]. Liby K, et al. The synthetic triterpenoids CDDO-methyl ester and CDDO-ethyl amide prevent lung cancer induced by vinyl carbamate in A/J mice. Cancer Res. 2007 Mar 15;67(6):2414-9.