Didesmethylrocaglamide 是一种 Rocaglamide 的衍生物，也是一种有效的真核起始因子 4A (eIF4A) 抑制剂。Didesmethylrocaglamide 具有有效的生长抑制活性，IC₅₀ 为 5 nM。Didesmethylrocaglamide 抑制多种促进生长的信号通路，并诱导肿瘤细胞凋亡 (apoptosis)。抗肿瘤活性。

Didesmethylrocaglamide, a derivative of Rocaglamide, is a potent eukaryotic initiation factor 4A (eIF4A) inhibitor. Didesmethylrocaglamide has potent growth-inhibitory activity with an IC 50 of 5 nM. Didesmethylrocaglamide suppresses multiple growth-promoting signaling pathways and induces apoptosis in tumor cells. Antitumor activity.

Solid

Eukaryotic initiation factor 4A (eIF4A)

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 i

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[1]. Long-Sheng Chang, et al. Targeting Protein Translation by Rocaglamide and Didesmethylrocaglamide to Treat MPNST and Other Sarcomas. Mol Cancer Ther. 2020 Mar;19(3):731-741.
[2]. Long-Sheng Chang, et al. Abstract 1950: The eIF4A inhibitors didesmethylrocaglamide and rocaglamide as effective treatments for pediatric bone and soft-tissue sarcomas. Cancer Res 2020;80(16 Suppl):Abstract nr 1950.

In Vitro: DMSO : 100 mg/mL (209.42 mM; Need ultrasonic)配制储备液