Fulvestrant

Catalog No.S1191 Batch:S119121

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Technical Data

Formula

C32H47F5O3S
Molecular Weight 606.77 CAS No. 129453-61-8
Solubility (25°C)* In vitro DMSO 100 mg/mL (164.8 mM)
Ethanol 100 mg/mL (164.8 mM)
Water Insoluble
In vivo (Add solvents to the product individually and in order)
Homogeneous suspension
CMC-NA
≥5mg/ml Taking the 1 mL working solution as an example, add 5 mg of this product to 1 ml of CMC-Na solution, mix evenly to obtain a homogeneous suspension with a final concentration of 5 mg/ml.
Clear solution
2%DMSO 30%PEG300 2%Tween80 66%ddH2O

Validated by Selleck labs. Should you need adjustments to this formulation, contact our sales team for custom testing.

 0.400mg/ml (0.66mM) Taking the 1 mL working solution as an example, add 20 μL of clarified DMSO stock solution of 20 mg/ml to 300 μL of PEG300, mix evenly to clarify it; add 20 μL of Tween80 to the above system, mix evenly to clarify it; then continue to add 660 μL of ddH2O to adjust the volume to 1 mL. The mixed solution should be used immediately for optimal results. 
* <1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
* Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

Preparing Stock Solutions

Biological Activity

Description Fulvestrant is an estrogen receptor (ER) antagonist with IC50 of 0.94 nM in a cell-free assay. Fulvestrant also induces autophagy and apoptosis and has antitumor activity.
Targets
ER [1]
(Cell-free assay)
0.94 nM
In vitro Fulvestrant is an effective inhibitor of the growth of ER-positive MCF-7 (with IC50 of 0.29 nM) but with no effect on the growth of ER-negative BT-20 human breast cancer cells. Fulvestrant causes accumulation of cells in G0/G1 and also reduces the proportion of cells capable of continued DNA synthesis. [1] Fulvestrant competitively inhibits binding of oestradiol to the estrogen receptor. Fulvestrant blocks nuclear localization of the ER through impairing receptor dimerisation, and energy-dependent nucleo-cytoplasmic shuttling. Because of the instability of fulvestrant-ER complex, the binding of Fulvestrant with ER finally results in accelerated degradation of the ER protein. [2] Fulvestrant (10 nM) not only decreases IGF-IR mRNA levels but also decreases the half-life. [3] Treatment with 100 μM Fulvestrant leads to a time dependent increase of TNFR1 and TRADD steady-state mRNA levels in MCF-7 cells. [4] Fulvestrant is capable of down-regulating androgen receptor expression and diminishes androgenic responses in LNCaP human prostate cancer cells. Fulvestrant also significantly attenuates R1881-stimulated growth by 70%. [5] Fulvestrant is able to modulate mitosis and cell death in immature cerebellar neurons via rapid activation of MAPK. [6]
In vivo Fulvestrant is devoid of uterotropic activity, and when co-administered with estradiol, it effectively blocks the uterotropic action of estradiol with ED50 of 0.06 mg/kg/day s.c. in immature female rats. A single s.c. injection of 5 mg of Fulvestrant suspension blocks completely the growth of MCF-7 xenografts. The growth of transplants of the BrlO human breast tumor is also suppressed effectively by 10 μM Fulvestrant. [1] Fulvestrant (10 mg/rat, s.c.) reduces the androgen receptor expression, ERK1/2 phosphorylation and cell proliferation in the rat ventral prostate. [7] Fulvestrant also displays anti-angiogenesis in the chick egg chorioallantoic membrane. [8]

Protocol (from reference)

Cell Assay:[1]
  • Cell lines

    MCF-7 breast cancer cells

  • Concentrations

    2.9 nM

  • Incubation Time

    5 days

  • Method

    MCF-7 cells are cultured in multiwell plates (24-well, seeding density 4 × 104) in minimal essential medium containing phenol red, insulin (10 μg/mL), and 5% charcoal-stripped fetal calf serum without additional estradiol. Fulvestrant and/or estradiol are added in fresh medium 2 days after seeding. Cultures are maintained for 5 days with one further medium change and growth is assessed by measurement of total cell protein at the beginning and end of treatment and compared with that of controls treated with ethanol (0.1%) alone.
Animal Study:[6]
  • Animal Models

    The human breast cancer xenografts MCF-7 in nude mice

  • Dosages

    5 mg/mouse

  • Administration

    s.c. injection

References

  • https://pubmed.ncbi.nlm.nih.gov/1855205/
  • https://pubmed.ncbi.nlm.nih.gov/15094757/
  • https://pubmed.ncbi.nlm.nih.gov/9816164/
  • https://pubmed.ncbi.nlm.nih.gov/11110059/
  • https://pubmed.ncbi.nlm.nih.gov/16818513/
  • https://pubmed.ncbi.nlm.nih.gov/12832521/
  • https://pubmed.ncbi.nlm.nih.gov/20874728/
  • https://pubmed.ncbi.nlm.nih.gov/7678775/

Customer Product Validation

PTPH1 confers breast cancer cell sensitivity to fulvestrant. E and F, PTPH1 overexpression increases the growth inhibition by fulvestrant. PTPH1 was overexpressed by a Tet-on system or a stable transfection, and resultant cells were incubated with fulvestrant as indicated for about 2 weeks. Colony formed was stained and counted. Results shown are normalized to its own solvent control of Vector and PTPH1-overexpressed cells, respectively (means ± SD; n = 3–5) with insets showing PTPH1 overexpression. *, versus vector or no Tet cells for E and F.

Data from [ Mol Cancer Ther , 2014 , 13(1), 230-8 ]

<p> </p><div>Fulvestrant resistance induced by 6 different ZF-TFs. (A) Drug sensitivity of fulvestrant-selected MCF7 ZF-TF-transduced cells. MCF7 cells transduced with one of six different ZF-TF-expressing retroviruses selected first in puromycin (the transduction selection marker) and then in fulvestrant for 1 month were grown in the absence of fulvestrant for 7 days and then challenged with 100 nM fulvestrant or vehicle (0.1% ethanol) for 21 days followed by crystal violet staining and visualization. Data are representative of triplicate experiments.</div>

Data from [ PLoS One , 2011 , 6, e21112 ]

<p>Fulvestrant resistance induced by 6 different ZF-TFs. (B and C) Growth curves of MCF7 and T47D cells in the presence and absence of fulvestrant. Comparison of cell growth rates (cell number, mean +/2 SEM, n = 8; time in days as indicated) of MCF7 and T47D cells stably transduced with control retrovirus or one of six different ZF-TF-expressing retroviruses (7, 19, 64, 70, 83 and 115) in the presence (blue line) or absence (pink line) of fulvestrant.</p>

Data from [ PLoS One , 2011 , 6, e21112 ]

<p>CDK4/6 inhibitor resistance promotes diminished ER expression and activity. (a and b) Proliferation of MCF-7 and MR cells in the presence of different concentrations of ICI (a) or 4-hydroxytamoxifen (4-OHT) (b) was measured by the alamarBlue assay and plotted as % inhibition of proliferation against log concentration of inhibitor. Each data point represents the average value±s.d. of six replicates obtained in three independent experiments. (c) MCF-7 and MR cells were treated with different concentrations of ICI, collected after 24 h and then immunoblotted with the indicated antibodies.</p>

, , Oncogene, 2017, 36(16):2255-2264

Selleck's Fulvestrant has been cited by 195 publications

Dual targeting CDK4/6 and CDK7 augments tumor response and anti-tumor immunity in breast cancer models [ J Clin Invest, 2025, e188839] PubMed: 40794455
Combined inhibition of KAT6A/B and Menin reverses estrogen receptor-driven gene expression programs in breast cancer [ Cell Rep Med, 2025, 6(7):102192] PubMed: 40516531
A bedside-to-bench translational analysis of NF1 alterations and CDK4/6 inhibitor resistance in hormone receptor-positive metastatic breast cancer [ EBioMedicine, 2025, 118:105828] PubMed: 40578027
Blocking cancer-fibroblast mutualism inhibits proliferation of endocrine therapy resistant breast cancer [ Mol Syst Biol, 2025, 10.1038/s44320-025-00104-6] PubMed: 40341770
Selective degradation of FGFR1/2 overcomes antiestrogen resistance in ER+ breast cancer with FGFR1/2 alterations [ Cancer Lett, 2025, 619:217668] PubMed: 40127812
Targeting estrogen-regulated system xc- promotes ferroptosis and endocrine sensitivity of ER+ breast cancer [ Cell Death Dis, 2025, 16(1):30] PubMed: 39833180
Oestrogen Receptor Alpha in Myocyte Maintains Muscle Regeneration in Duchenne Muscular Dystrophy [ J Cachexia Sarcopenia Muscle, 2025, 16(2):e13807] PubMed: 40258782
Annotation-free deep learning algorithm trained on hematoxylin & eosin images predicts epithelial-to-mesenchymal transition phenotype and endocrine response in estrogen receptor-positive breast cancer [ Breast Cancer Res, 2025, 27(1):6] PubMed: 39800743
Progranulin deficiency associates with postmenopausal osteoporosis via increasing ubiquitination of estrogen receptor α [ Genes Dis, 2025, 12(1):101221] PubMed: 39559258
Co-targeting of metabolism using dietary and pharmacologic approaches reduces breast cancer metastatic burden [ NPJ Breast Cancer, 2025, 11(1):3] PubMed: 39809806

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