147030-01-1
基本信息
Quiflapon SodiuM
QUIFLAPON SODIUM
MK-591
MK 591
sodium 3-[1-[(4-chlorophenyl)methyl]-5-(quinolin-2-ylmethoxy)-3-tert-butylsulfanyl-indol-2-yl]-2,2-dimethyl-propanoate
1-[(4-Chlorophenyl)Methyl]-3-[(1,1-diMethylethyl)thio]-α,α-diMethyl-5-(2-quinolinylMethoxy)-1H-Indole-2-propanoic Acid SodiuM Salt
物理化學(xué)性質(zhì)
常見問題列表
Quiflapon sodium (MK591) and SB203580 are able to block SEB-induced human PBMC cell proliferation. Quiflapon sodium (MK591) down regulates three genes [for cathepsin L, IL-17 and guanylate binding protein (GBP)-2] that are up regulated by SEB. Quiflapon sodium (MK591) undergoes apoptosis within hours of treatment. Quiflapon sodium also induces rapid activation of the stress kinase, c-Jun N-terminal kinase (JNK), which plays an important role in the apoptosis process. Quiflapon sodium triggers apoptosis in prostate cancer cells without inhibition of PI3K-Akt, or ERK. Moreover, Quiflapon sodium and LY294002 exert synergistic effect in inducing apoptosis in prostate cancer cells. Quiflapon sodium (MK591) influences cAMP response element-binding protein but not Sp1.
Hyperoxia groups of mice treated with Quiflapon sodium (MK591) (20, 40 mg/kg) show alveolarization that resembles that of room air controls while untreated hyperoxia groups show definite evidence of aberrant alveolarization but no inflammation. Comparison of the Aβ-immunopositive areas between the placebo and Quiflapon sodium (MK591) (320 mg/kg)-treated group reveals a statistically significant reduction of the amyloid burden in the treated mice. Quiflapon sodium also has a significant reduction in brain levels of IL-1β. Mice treated with Quiflapon sodium show a statistically significant decrease in the steady-state levels of total CREB and its phosphorylated form at Ser133.