Atraric acid

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].

Research Areas >> Cancer

Signaling Pathways >> Immunology/Inflammation >> NO Synthase

Signaling Pathways >> MAPK/ERK Pathway >> p38 MAPK

Research Areas >> Inflammation/Immunology

Signaling Pathways >> Others >> Androgen Receptor

Androgen receptor, NO synthesis, MAPK-NFκB pathway[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.