Atraric acid (Methyl atrarate) 是一种特异的雄激素受体 (androgen receptor) 拮抗剂,具有抗炎和抗癌作用。Atraric acid 抑制 LNCaP 和 C4-2 细胞中内源性前列腺特异性抗原基因的表达。Atraric acid 还能抑制 NO 和细胞因子的合成,抑制 MAPK-NFκB 信号通路。Atraric acid 可用于前列腺疾病和炎症性疾病的研究。
Cas No. | 4707-47-5 |
别名 | Methyl atrarate |
分子式 | C10H12O4 |
分子量 | 196.2 |
储存条件 | 4°C, stored under nitrogen |
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while. |
Shipping Condition | Evaluation sample solution : ship with blue ice All other available size: ship with RT , or blue ice upon request |
产品描述 | Atraric acid (Methyl atrarate) is a specificandrogen receptor (AR)antagonist with anti-inflammatory and anticancer effects. Atraric acid represses the expression of the endogenous prostate specific antigen gene in both LNCaP and C4-2 cells. Atraric acid can also inhibit the synthesis ofNOand cytokine, and suppress theMAPK-NFκBsignaling pathway. Atraric acid can be used to research prostate diseases and inflammatory diseases[1][2]. Atraric acid (10 μM; CV1 cells) represses the transactivation function mediated by Dihydrotestosterone-induced human AR[1]. Atraric acid (10 μM; PCa cells) inhibits the expression of the PSA gene in both androgen-dependent and androgen-independent PCa cells[1]. Atraric acid (1-300 μM; 24 h) dose-dependently inhibits pro-inflammatory cytokine, nitric oxide, prostaglandin E2 in LPS-stimulated RAW264.7 cells, but does not influence the cell viability[2]. Atraric acid (100 and 300 μM; 18 h or 4 h) downregulates the expression of phosphorylated IκB, extracellular signal-regulated kinases (ERK) and nuclear factor kappa B (NFκB) signaling pathway to exhibit anti-inflammatory effects in LPS-stimulated RAW264.7 cells[2]. Cell Viability Assay[2] Cell Line: | RAW264.7 cells | Concentration: | 1-300 μM | Incubation Time: | 24 h | Result: | Did not influence the cell viability. |
Western Blot Analysis[2] Cell Line: | RAW264.7 cells | Concentration: | 100 and 300 μM | Incubation Time: | 18 h or 4 h | Result: | Inhibited LPS-Induced expression of iNOS and COX-2 in a dose-dependent manner. Suppressed LPS-stimulated phosphorylation of the Nfκb signaling pathway. |
Atraric acid (10, 30 mg/kg; i.p.; single dosage) inhibits the production of pro-inflammatory cytokines and reduces pathological damages in LPS-induced endotoxin shock mice[2]. Animal Model: | Female BALB/c mice (7 weeks old, 17-20 g; LPS-induced endotoxin shock)[2] | Dosage: | 10, 30 mg/kg | Administration: | i.p.; single dosage | Result: | Inhibited the production of pro-inflammatory cytokines. Reduced pathological damages such as vasodilation and bleeding. |
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