Mifepristone

Catalog No.S2606 Batch:S260605

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Technical Data

Formula

C29H35NO2
Molecular Weight 429.59 CAS No. 84371-65-3
Solubility (25°C)* In vitro DMSO 86 mg/mL (200.19 mM)
Ethanol 43 mg/mL (100.09 mM)
Water Insoluble
* <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 Mifepristone is a remarkably active antagonist of progesterone receptor and glucocorticoid receptor with IC50 of 0.2 nM and 2.6 nM, respectively. Mifepristone promotes cell autophagy and apoptosis, decreases Bcl-2 level and increases Beclin1 level, accompanied by weakened interaction between Bcl-2 and Beclin1.
Targets
Bcl-2 [5] Progesterone receptor [1]
(T47D cells)		 Glucocorticoid receptor [1]
(A549 cells)
0.2 nM 2.6 nM
In vitro

Mifepristone inhibit corticoid-induced transcription from a glucocorticoid response element (GRE)-linked luciferase reporter gene in the human lung carcinoma cell line A549. Moreover, Mifepristone also blocks progesterone induction of alkaline phosphatase activity in the human breast cancer cell line T47D. [1] Mifepristone inhibits ovarian cancer cell growth of SK-OV-3 and OV2008 with IC50 of 6.25 μM and 6.91 μM, respectively. [2] A recent study shows that Mifepristone induces caspase-1 over expression both in differentiated and undifferentiated caspase-1-embryonic stem cells. [3]
In vivo

Mifepristone can impair the growth of SK-OV-3 tumors in immunosuppressed mice at 0.5 mg/day and 1 mg/day. [2] Mifepristone inhibits the prostate weight significantly in the highest doses in vivo, and inhibits growth of the prostate gland produced by dihydrotestosterone (DHT) to a greater extent than the induction of atrophy and cell death in rats. [4]
Features Mifepristone is the first approved medication for patients with endogenous cushing

Protocol (from reference)

Kinase Assay:

[1]
  • Glucocorticoid receptor (GR) antagonist activity, Progesterone receptor (PR) antagonist activity

    T47D alkaline phosphatase assay: T47D human breast cancer cells are plated in 96-well tissue culture plates at 104 cells per well in assay medium [RPMI medium without phenol red containing 5% (v/v) charcoal-treated FBS and 1% (v/v) penicillin–streptomycin]. Two days later, the medium is decanted and Mifepristone or control is added at a final concentration of 0.1% (v/v) dimethylsulfoxide in fresh assay medium. Twenty-four hours later, an alkaline phosphatase assay is performed using a SEAP kit. The medium is decanted and the cells are fixed for 30 minutes at room temperature with 5% (v/v) formalin. The cells are washed once at room temperature with Hanks
Cell Assay:

[2]
  • Cell lines

    OV2008 and SK-OV-3 cells

  • Concentrations

    0-20 μM

  • Incubation Time

    24 hours

  • Method

    Cell growth is evaluated in various ovarian cancer cell lines that are subjected to dose-response or time course treatments. Media containing each of the doses of fresh steroids is replaced every 24 hours. Control groups of cells are treated with vehicle ethanol at a final concentration of less than 0.05%. Number of viable cells is evaluated by trypsinization and counting in a hemocytometer chamber using trypan blue dye exclusion. Experiments are conducted in media without phenol red and supplemented with charcoal extracted fetal bovine serum, or media containing unextracted serum and having phenol red. Similar results are obtained with both media preparations; therefore, after performing the growth curves, all subsequent experiments are conducted using media with unextracted serum and in the presence of phenol red. When indicated, the proliferation IC50s are calculated using software designed to study drug interaction.
Animal Study:

[2]
  • Animal Models

    SK-OV-3 ovarian cancer cells are injected into immunosuppressed mice.

  • Dosages

    0.5 or 1 mg/day

  • Administration

    Implanted s.c. with pellets

Customer Product Validation

Data from [Data independently produced by PLoS One, 2014, 9(8), e105528]

Selleck's Mifepristone has been cited by 30 publications

Human cortical neurogenesis is altered via glucocorticoid-mediated regulation of ZBTB16 expression [ Neuron, 2024, S0896-6273(24)00089-8] PubMed: 38442714
Glucocorticoid activates STAT3 and NF-κB synergistically with inflammatory cytokines to enhance the anti-inflammatory factor TSG6 expression in mesenchymal stem/stromal cells [ Cell Death Dis, 2024, 15(1):70] PubMed: 38238297
Glucocorticoid stress hormones stimulate vesicle-free Tau secretion and spreading in the brain [ Cell Death Dis, 2024, 15(1):73] PubMed: 38238309
Glucocorticoid treatment influences prostate cancer cell growth and the tumor microenvironment via altered glucocorticoid receptor signaling in prostate fibroblasts [ Oncogene, 2024, 43(4):235-247] PubMed: 38017134
Glucocorticoids modulate neural activity via a rapid non-genomic effect on Kv2.2 channels in the central nervous system [ Neurobiol Stress, 2024, 28:100593] PubMed: 38075025
New hormone receptor-positive breast cancer mouse cell line mimicking the immune microenvironment of anti-PD-1 resistant mammary carcinoma [ J Immunother Cancer, 2023, 11(6)e007117] PubMed: 37344100
Genetically engineered human pituitary corticotroph tumor organoids exhibit divergent responses to glucocorticoid receptor modulators [ Transl Res, 2023, S1931-5244(23)00002-6] PubMed: 36640905
PRMT5 triggers glucocorticoid-induced cell migration in triple-negative breast cancer [ Life Sci Alliance, 2023, 6(10)e202302009] PubMed: 37536978
PRMT5 triggers glucocorticoid-induced cell migration in triple-negative breast cancer [ Life Sci Alliance, 2023, 6(10)e202302009] PubMed: 37536978
Glucocorticoid induced group 2 innate lymphoid cell overactivation exacerbates experimental colitis [ Front Immunol, 2022, 13:863034] PubMed: 36032134

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