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147030-01-1

中文名稱 喹夫拉朋鈉
英文名稱 sodium 3-[1-[(4-chlorophenyl)methyl]-5-(quinolin-2-ylmethoxy)-3-tert-butylsulfanyl-indol-2-yl]-2,2-dimethyl-propanoate
CAS 147030-01-1
分子式 C34H34ClN2NaO3S
MOL 文件 147030-01-1.mol
147030-01-1 結(jié)構(gòu)式 147030-01-1 結(jié)構(gòu)式

基本信息

中文別名
喹夫拉朋鈉
英文別名
MK 591
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
所屬類別
生物:小分子化合物

物理化學(xué)性質(zhì)

儲存條件-20°C
溶解度DMSO : 50 mg/mL (82.08 mM; Need ultrasonic)H2O : < 0.1 mg/mL (insoluble)
形態(tài)粉末
顏色White to off-white
喹夫拉朋鈉價格(試劑級)
報價日期產(chǎn)品編號產(chǎn)品名稱CAS號包裝價格
2026/06/05HY-50714喹夫拉朋鈉
Quiflapon sodium
147030-01-11 mg465元
2026/06/05HY-50714R喹夫拉朋鈉
Quiflapon sodium (Standard)
147030-01-15 mg2850元
2026/06/05HY-50714喹夫拉朋鈉
Quiflapon sodium
147030-01-15mg950元

常見問題列表

生物活性
Quiflapon sodium (MK-591 sodium) 是選擇性的,特異性的 FLAP 抑制劑。Quiflapon sodium 是一種有效的,具有口服活性的白三烯生物合成 (leukotriene biosynthesis) 抑制劑。誘導(dǎo)細(xì)胞凋亡 (apoptosis)。
體外研究

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.

體內(nèi)研究

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.

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