2-Methoxyestradiol (2-ME2) 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.

2-Methoxyestradiol（60 mg/kg/day）可使肿瘤降低4倍,若剂量提高10倍则使之降低23倍.2-Methoxyestradiol对9L大鼠胶质瘤模型(9L-V6R)疗效呈剂量依赖性,使HIF-1活性显著降低,且抑制肿瘤生长.

2-Methoxyestradiol（0.5 μM）对TGF-β3诱导胶原(Col)I型(αI)、Col III(αI)、结缔组织生长因子、纤溶酶原激活物抑制剂和α-平滑肌肌动蛋白表达具有阻断作用。 作用于MDA-MB-231细胞时,2-Methoxyestradiol对HIF-1调节的靶基因转录激活有抑制作用,对HIF-1α自身转录无影响。作用于乳腺癌细胞系 MDA-MB-435（IC50：1.38 μM）和卵巢癌细胞系SK-OV-3（IC50：1.79 μM）时,2-Methoxyestradiol抑制细胞增殖。此外, 作用于大鼠主动脉平滑肌A-10细胞时,2-Methoxyestradio可抑制细胞微管解聚（EC50：7.5 μM）。其还减轻TGF-β3诱导的Smad2/3磷酸化和核易位,且对TGF-β3诱导的PI3K/Akt/mTOR通路激活具有抑制作用。2-Methoxyestradiol对MCF-7（IC50：52 μM）和BM（IC50：8 μM）细胞增殖有抑制作用。

Microtubule depolymerizing activity: The effects of 2-Methoxyestradiol on cellular microtubule depolymerization are determined by indirect immunofluorescence techniques in rat aortic smooth muscle A-10 cells. Microtubules are visualized using a β-tubulin antibody. Three viewers determines the percent microtubule loss for each treatment concentration. The data are averaged and plotted as percent microtubule loss versus drug concentration and the EC50s for microtubule depolymerization calculated from the log dose–response curves.

The sulforhodamine B (SRB) assay is used to evaluate the antiproliferative activity of 2-Methoxyestradiol in the MDA-MB-435 and SK-OV-3 cell lines. Cells a plated into 96-well plates and allowed to grow and attach for 24 hours followed by addition of 2-Methoxyestradiol or vehicle controls. The cells are incubated with drugs for 48 hours and then the cellular protein is fixed, stained, and concentration determined by absorbance at 560 nm. Log dose–response curves are constructed for each experiment and the IC50 for inhibition of proliferation determined.(Only for Reference)