2-Methoxyestradiol is an orally bioavailable estradiol metabolite with potential antineoplastic activity. 2-Methoxyestradiol inhibits angiogenesis by reducing endothelial cell proliferation and inducing endothelial cell apoptosis. This agent also inhibits tumor cell growth by binding to tubulin, resulting in antimitotic activity, and by inducing caspase activation, resulting in cell cycle arrest in the G2 phase, DNA fragmentation, and apoptosis.

＞98%

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

2-甲氧基雌二醇；2-ME2；NSC-659853

白色或类白色结晶性粉末

DMSO : 15.1 mg/mL (50 mM)

HIF-2α ,Microtubule Associated ,HIF-1α

2-Methoxyestradiol exhibits the inhibitory activity of cellular proliferation in a breast carcinoma cell line MDA-MB-435 and an ovarian carcinoma cell line SK-OV-3 with IC50 of 1.38 μM and 1.79 μM, respectively. Furthermore, 2-Methoxyestradiol also inhibits cellular microtubule depolymerization in rat aortic smooth muscle A-10 cells with EC50 of 7.5 μM. 2-Methoxyestradiol inhibits proliferation of MCF-7 and BM cells with IC50 of 52 μM and 8 μM. In MDA-MB-231 cells, 2-Methoxyestradiol inhibits HIF-1-mediated transcriptional activation of target genes without affecting the transcription of HIF-1α itself. A recent study shows that 2-Methoxyestradiol (0.5 μM), blocks TGF-β3-induced expression of collagen (Col) type I(αI), Col III(αI), plasminogen activator inhibitor (PAI) 1, connective tissue growth factor (CTGF), and α-smooth muscle actin (α-SMA). Moreover, 2-Methoxyestradiol ameliorates TGF-β3-induced Smad2/3 phosphorylation and nuclear translocation, and inhibits TGF-β3-induced activation of the PI3K/Akt/mTOR pathway.

In a 9L rat glioma (9L-V6R) rat model, 2-Methoxyestradiol significantly decreases HIF-1 activity and inhibits the tumor growth in a dose-dependent manner by 4-fold reduction for 60 mg/kg/day, and 23-fold reduction for 600 mg/kg/day, respectively.

[1] Rao PN, et al. Steroids. 2002, 67(13-14), 1079-1089.
[2] Shimada et al (2003) Roles of p38 and c-jun NH2-terminal kinase-mediated pathways in 2-methoxyestradiol-induced p53 induction and apoptosis. Carcinogenesis 24 1067.
[3] LaVallee et al (2002) 2-Methoxyestradiol inhibits proliferation and induces apoptosis independently of estrogen receptors α and β. Cancer Res. 62 3691.
[4] LaVallee et al (2003) 2-Methoxyestradiol up-regulates death receptor 5 and induces apoptosis through activation of the extrinsic pathway. Cancer Res. 63 468.
[5] D’Amato et al (1994) 2-Methoxyestradiol, an endogenous mammalian metabolite, inhibits tubulin polymerization by interacting at the colchicine site. Proc.Natl.Acad.Sci.U.S.A. 91 3964.