产品
编 号：F359497
分子式：C34H43N3O3
分子量：541.72
分子式：C34H43N3O3
分子量：541.72
产品类型
规格
价格
是否有货
10mM*1mL in DMSO
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1mg
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5mg
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10mg
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25mg
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50mg
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100mg
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结构图
CAS No: 443104-02-7
产品详情
生物活性：
CDDO-Im (RTA-403) is an activator of Nrf2 and PPAR, with Kis of 232 and 344 nM for PPARα and PPARγ.
体内研究：
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.
体外研究：
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 (RTA-403) is an activator of Nrf2 and PPAR, with Kis of 232 and 344 nM for PPARα and PPARγ.
体内研究：
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.
体外研究：
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.
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