Fulvestrant (ZM 182780) is an estrogen receptor (ER) antagonist (IC50=9.4 nM) and an agonist of GPR30. Fulvestrant has antitumor activity, inhibiting cell proliferation and inducing apoptosis and autophagy.

ERR:9.4 nM (cell free)

方法：ER 阳性 MCF-7 和 ER 阴性 MDA-MB-231 细胞用 Fulvestrant (0.01-10000 nM) 处理 6 天，使用 crystal violet staining 检测细胞生长速率。
结果：Fulvestrant 抑制 MCF-7 细胞的生长，IC50 为 0.8 nM。Fulvestrant 不抑制 MDA-MB-231 细胞的生长，IC50 大于 1 µM。[1]
方法：人乳腺癌细胞 MCF-7 用 Fulvestrant (100 nM) 处理 0.25-6 h，使用 Western Blot 检测靶点蛋白表达水平。
结果：当 MCF-7 细胞暴露于 Fulvestrant 时，ERα 蛋白的表达以时间依赖的方式减少。[2]

方法：为检测体内抗肿瘤活性，将 Fulvestrant (25-200 mg/kg，5% DMSO/95% corn oil) 皮下注射给携带 tamoxifen-resistant (TamR) 肿瘤的 Nu/J 小鼠，每周四次，持续四周。
结果：所有剂量的 Fulvestrant 对肿瘤生长的显著抑制，并且在剂量之间没有检测到显著差异。[3]
方法：为检测体内抗肿瘤活性，将 Fulvestrant (5 mg/mouse) 皮下注射给原位建立 ER+ 乳腺癌的裸鼠，每周两次，持续二十四天。
结果：Fulvestrant 治疗导致肿瘤生长显著降低。[4]

In brief, hippocampi were dissected from the brains of embryonic day 18 Sprague-Dawley rat fetuses, treated with 0.02% trypsin in Hanks' balanced salt solution (137 mM NaCl, 5.4 mM KCl, 0.4 mM KH2PO4, 0.34 mM Na2HPO4·7H2O, 10.0 mM glucose, and 10.0 mM HEPES) at 37°C for 5 min and dissociated by repeated passage through a series of fire-polished constricted Pasteur pipettes. For intracellular Ca2+ imaging analyses, approximately 10^4 cells were seeded onto poly-D-lysine (10 μg/ml)-coated 22-mm coverslips in covered 35-mm Petri dishes. For neuroprotection and Western immunoblotting analyses, approximately 10^6 cells/ml were seeded onto poly-D-lysine-coated solid black and clear bottom 96-well culture plates and 60-mm Petri dishes, respectively. Cells were grown in phenol-red free neurobasal medium supplemented with B27, 5 U/ml penicillin, 5 μg/ml streptomycin, 0.5 mM glutamine, and 25 μM glutamate at 37°C in 10% CO2 for the first 3 days and NBM without glutamate afterward. Cultures grown in serum-free NBM yields approximately 99.5% neurons and 0.5% glial cells [2].

MCF-7 cells were suspended in culture medium (no serum) and inoculated s.c. into the flank of adult female nude mice (0.1 ml/approximately 5 x 10^6 cells). Mice were maintained in a clean environment and were given sterile food and water. Estrogen supplementation was provided by ethynyl estradiol at 1 μg/ml in the water. Antiestrogen treatment was initiated when tumor diameter attained a minimum of 0.5 cm. The Br10 tumor at passage 49 was established by implantation of 1-2-mm^3 tumor fragments into the flank of anesthetized intact adult female nude mice. After 3 passages a reproducible pattern of growth was established without additional estrogen supplementation. Approximately two-thirds of animals established progressively growing tumors which attained measurable size (area, ≥70 mm2) after 6-7 weeks. Antiestrogen treatment was initiated at the time of transplantation. Tamoxifen was administered once daily p.o. at a dose of 10 mg/kg (1 ml/100 g body weight of aqueous dispersion in 0.5% Tween 80) and ICI 182,780 as a single s.c. injection of 5 mg/mouse (50 mg/ml in arachis oil). Tumor size was assessed weekly as the product of caliper measurements of the largest diameter and the axis perpendicular to it [1].