Atraric acid (Synonyms: Methyl atrarate) |
| カタログ番号GC66207 |
アトラリン酸 (メチル アトラレート) は、抗炎症作用と抗がん作用を持つ特定のアンドロゲン受容体 (AR) 拮抗薬です。アトラリン酸は、LNCaP 細胞と C4-2 細胞の両方で内因性前立腺特異抗原遺伝子の発現を抑制します。アトラリン酸は、NO とサイトカインの合成も阻害し、MAPK-NFκB シグナル伝達経路を抑制します。アトラリン酸は、前立腺疾患や炎症性疾患の研究に使用できます。
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 4707-47-5
Sample solution is provided at 25 µL, 10mM.
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Atraric acid (Methyl atrarate) is a specific androgen 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 of NO and cytokine, and suppress the MAPK-NFκB signaling 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. |
Average Rating: 5 (Based on Reviews and 30 reference(s) in Google Scholar.)
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