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.
相关材料与文献
技术资料 (2)
文献 (5)
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.
Liver-selective glucocorticoid antagonists: a novel treatment for type 2 diabetes.
Journal of medicinal chemistry 2004 aug
Abstract
Hepatic blockade of glucocorticoid receptors (GR) suppresses glucose production and thus decreases circulating glucose levels,but systemic glucocorticoid antagonism can produce adrenal insufficiency and other undesirable side effects. These hepatic and systemic responses might be dissected,leading to liver-selective pharmacology,when a GR antagonist is linked to a bile acid in an appropriate manner. Bile acid conjugation can be accomplished with a minimal loss of binding affinity for GR. The resultant conjugates remain potent in cell-based functional assays. A novel in vivo assay has been developed to simultaneously evaluate both hepatic and systemic GR blockade; this assay has been used to optimize the nature and site of the linker functionality,as well as the choice of the GR antagonist and the bile acid. This optimization led to the identification of A-348441,which reduces glucose levels and improves lipid profiles in an animal model of diabetes.
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.
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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