EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #100-0564_C
孕酮和糖皮质激素受体拮抗剂
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总览
米非司酮是一种孕激素和糖皮质激素受体拮抗剂（Ki 值分别为 0.64 nM 和 0.1 nM；Attardi et al.; Song et al.; von Geldern et al.）。据报道，米非司酮可用于治疗子宫肌瘤、子宫内膜异位症、乳腺癌和脑膜瘤（Mahajan et al.）。
癌症研究
· 抑制细胞周期蛋白依赖性激酶 1 (CDK1) 和细胞周期蛋白依赖性激酶 2 (CDK2) 的表达，导致子宫腺肌症中子宫内膜上皮细胞和间质细胞的细胞周期阻滞和凋亡（Che et al.）。
· 在体外诱导抗雌激素耐药乳腺癌细胞的细胞周期阻滞和凋亡（Gaddy et al.）。
别名
RU-486
细胞类型
癌细胞及细胞系
研究领域
癌症
CAS 编号
84371-65-3
化学式
C29H35NO2
分子量
429.6 g/mol
纯度
≥98%
靶点
CDK1，CDK2，糖皮质激素受体
Protocols and Documentation
Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.
Resources and Publications
Educational Materials (2)
Publications (5)
A new trick for an old dog: The application of mifepristone in the treatment of adenomyosis. Journal of cellular and molecular medicine 2020 jan
Abstract
Adenomyosis is also called internal endometriosis and affects about 20{\%} of reproductive-aged women. It seriously reduces life quality of patients because current drug therapies face with numerous challenges. Long-term clinical application of mifepristone exhibits wonderful therapeutic effects with mild side-effects in many disorders since 1982. Since adenomyosis is a refractory disease, we investigate whether mifepristone can be applied in the treatment of adenomyosis. In this study, we investigated the direct effects of mifepristone on human primary eutopic endometrial epithelial cells and stromal cells in adenomyosis. We found that mifepristone causes cell cycle arrest through inhibiting CDK1 and CDK2 expressions and induces cell apoptosis via the mitochondria-dependent signalling pathway in endometrial epithelial cells and stromal cells of adenomyosis. Furthermore, mifepristone inhibits the migration of endometrial epithelial cells and stromal cells through decreasing CXCR4 expression and restricts the invasion of endometrial epithelial cells via suppression of epithelial-mesenchymal transition in adenomyosis. We also found that mifepristone treatment decreases the uterine volume, CA125 concentration and increases the haemoglobin concentration in serum for adenomyosis patients. Therefore, we demonstrate that mifepristone could serve as a novel therapeutic drug in the treatment of adenomyosis, and therefore, the old dog can do a new trick.
Peptidylarginine deiminase inhibition is immunomodulatory and vasculoprotective in murine lupus. The Journal of clinical investigation 2013 jul
Abstract
Recent evidence suggests that enhanced neutrophil extracellular trap (NET) formation activates plasmacytoid dendritic cells and serves as a source of autoantigens in SLE. We propose that aberrant NET formation is also linked to organ damage and to the premature vascular disease characteristic of human SLE. Here, we demonstrate enhanced NET formation in the New Zealand mixed 2328 (NZM) model of murine lupus. NZM mice also developed autoantibodies to NETs as well as the ortholog of human cathelicidin/LL37 (CRAMP), a molecule externalized in the NETs. NZM mice were treated with Cl-amidine, an inhibitor of peptidylarginine deiminases (PAD), to block NET formation and were evaluated for lupus-like disease activity, endothelial function, and prothrombotic phenotype. Cl-amidine treatment inhibited NZM NET formation in vivo and significantly altered circulating autoantibody profiles and complement levels while reducing glomerular IgG deposition. Further, Cl-amidine increased the differentiation capacity of bone marrow endothelial progenitor cells, improved endothelium-dependent vasorelaxation, and markedly delayed time to arterial thrombosis induced by photochemical injury. Overall, these findings suggest that PAD inhibition can modulate phenotypes crucial for lupus pathogenesis and disease activity and may represent an important strategy for mitigating cardiovascular risk in lupus patients.
Antiandrogen effects of mifepristone on coactivator and corepressor interactions with the androgen receptor. Molecular endocrinology (Baltimore, Md.) 2004 jan
Abstract
Mifepristone is a potent antagonist of steroid hormone receptors such as glucocorticoid and progesterone receptors. We investigated the potential for mifepristone to act as an antiandrogen and compared it with partial androgen receptor (AR) agonists and antagonists, in particular bicalutamide. Mifepristone was an effective antiandrogen in vitro that inhibited transcription from three androgen-responsive promoters and blocked the agonist R1881 in a dose-dependent manner. Like bicalutamide, mifepristone also antagonized the action of androgen receptor with a (T877A) mutation. Mifepristone competed effectively with R1881 with a relative binding affinity comparable to that of cyproterone acetate, and much higher than that of hydroxyflutamide and bicalutamide in a binding assay. Mifepristone could effectively induce the binding of the herpes simplex viral protein 16/AR fusion protein to the hormone response elements in the murine mammary tumor virus-luciferase reporter. With either wild-type or T877A mutant AR, mifepristone alone was unable to induce any detectable interaction with coactivators transcriptional intermediary factor-2 or beta-catenin but could inhibit the R1881-induced binding of AR to transcriptional intermediary factor-2 and beta-catenin. Similarly, mifepristone could inhibit the R1881-induced N/C-terminal interaction in a dose-dependent manner even though mifepristone alone has no effect on the N/C-terminal interaction of AR. We found that mifepristone could induce a strong interaction between AR and corepressors nuclear receptor corepressor and silencing mediator for retinoid and thyroid hormone receptors in both transactivation and two-hybrid assays to a greater degree than hydroxyflutamide, cyproterone acetate, and bicalutamide. The AR-corepressor interaction was also seen in coimmunoprecipitation assays. Finally, mifepristone at high concentrations induced a low level of prostate-specific antigen expression in LNCaP and antagonized prostate-specific antigen expression induced by R1881. Mifepristone also antagonized R1881 action on the growth of LNCaP prostate cancer cells.
更多信息
| Molecular Weight | 429.6 g/mol |
|---|---|
| Alternative Names | RU-486 |
| Cas Number | 84371-65-3 |
| Chemical Formula | C29H35NO2 |
| 纯度 | ≥ 98% |
| Target | CDK1, CDK2, Glucocorticoid Receptor |
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