产品
编 号：F212072
分子式：C27H27NO7
分子量：477.51
分子式：C27H27NO7
分子量：477.51
产品类型
规格
价格
是否有货
10mM*1mL in DMSO
询价
询价
1mg
询价
询价
5mg
询价
询价
10mg
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询价
结构图
CAS No: 177262-30-5
产品详情
生物活性：
Didesmethylrocaglamide, a derivative of Rocaglamide, is a potent eukaryotic initiation factor 4A (eIF4A) inhibitor. Didesmethylrocaglamide has potent growth-inhibitory activity with an IC50 of 5 nM. Didesmethylrocaglamide suppresses multiple growth-promoting signaling pathways and induces apoptosis in tumor cells. Antitumor activity.
体外研究：
Didesmethylrocaglamide (5 nM, and 10 nM; 72 hours; MPNST cells) treatment arrests MPNST cells at G2-M, increases the sub-G1 population, induces cleavage of caspases and PARP, and elevates the levels of the DNA-damage response marker γH2A.X, while decreasing the expression of AKT and ERK1/2.Didesmethylrocaglamide inhibits MPNST cell proliferation by inducing cell cycle arrest at G2/M and subsequently, cell death. Didesmethylrocaglamide-treated 697-R cells exhibits IC50 values is very similar to those of parental 697 cells (4 vs 3nM of IC50, respectively).Didesmethylrocaglamide induces apoptosis in both neurofibromatosis type 1 (NF1)-expressing and NF1-deficient MPNST cells, possibly subsequent to the activation of the DNA damage response. Didesmethylrocaglamide-treated sarcoma cells show decreased levels of multiple oncogenic kinases, including insulin-like growth factor-1 receptor.
Didesmethylrocaglamide, a derivative of Rocaglamide, is a potent eukaryotic initiation factor 4A (eIF4A) inhibitor. Didesmethylrocaglamide has potent growth-inhibitory activity with an IC50 of 5 nM. Didesmethylrocaglamide suppresses multiple growth-promoting signaling pathways and induces apoptosis in tumor cells. Antitumor activity.
体外研究：
Didesmethylrocaglamide (5 nM, and 10 nM; 72 hours; MPNST cells) treatment arrests MPNST cells at G2-M, increases the sub-G1 population, induces cleavage of caspases and PARP, and elevates the levels of the DNA-damage response marker γH2A.X, while decreasing the expression of AKT and ERK1/2.Didesmethylrocaglamide inhibits MPNST cell proliferation by inducing cell cycle arrest at G2/M and subsequently, cell death. Didesmethylrocaglamide-treated 697-R cells exhibits IC50 values is very similar to those of parental 697 cells (4 vs 3nM of IC50, respectively).Didesmethylrocaglamide induces apoptosis in both neurofibromatosis type 1 (NF1)-expressing and NF1-deficient MPNST cells, possibly subsequent to the activation of the DNA damage response. Didesmethylrocaglamide-treated sarcoma cells show decreased levels of multiple oncogenic kinases, including insulin-like growth factor-1 receptor.
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