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363600-92-4

中文名稱 TLR2-IN-C29
CAS 363600-92-4
分子式 C16H15NO4
分子量 285.29
MOL 文件 363600-92-4.mol
更新日期 2024/12/16 10:39:34
363600-92-4 結(jié)構(gòu)式 363600-92-4 結(jié)構(gòu)式

基本信息

中文別名
化合物C29
3-((2-羥基-3-甲氧基亞芐基)氨基)-2-甲基苯甲酸
英文別名
R2-IN-C29
TLR2-IN-C29
C29
C 29
C-29
Benzoic acid, 3-[[(2-hydroxy-3-methoxyphenyl)methylene]amino]-2-methyl-

物理化學(xué)性質(zhì)

沸點(diǎn)505.7±50.0 °C(Predicted)
密度1.21±0.1 g/cm3(Predicted)
儲(chǔ)存條件Inert atmosphere,Store in freezer, under -20°C
酸度系數(shù)(pKa)4.01±0.10(Predicted)

安全數(shù)據(jù)

危險(xiǎn)性符號(hào)(GHS)GHS hazard pictograms
GHS07
警示詞警告
危險(xiǎn)性描述H302-H315-H319-H335
防范說(shuō)明P261-P305+P351+P338
TLR2-IN-C29價(jià)格(試劑級(jí))
報(bào)價(jià)日期產(chǎn)品編號(hào)產(chǎn)品名稱CAS號(hào)包裝價(jià)格
2024/11/08S6597TLR2-IN-C29
TLR2-IN-C29
363600-92-45mg1170元
2024/11/08S6597TLR2-IN-C29363600-92-410mM (1mL in DMSO)1285.83元
2024/11/08S6597TLR2-IN-C29
TLR2-IN-C29
363600-92-425mg3970元

常見(jiàn)問(wèn)題列表

生物活性
TLR2-IN-C29 (C29)是一種 Toll-like receptor 2 (TLR2) 的抑制劑,可抑制TLR2/1和TLR2/6的信號(hào)傳導(dǎo)。
靶點(diǎn)
TargetValue
TLR2
()
體外研究

C29 (10 or 50 μΜ; 1 hour) blocks P3C- and P2C-induced IL-8 mRNA dose-dependently in HEK-TLR2 stable transfectants. C29 (50-200 μM; 1 hour) inhibits P3C- and P2C-induced IL-1β gene expression significantly at both 1 h and 4 h following stimulation in THP-1 cells.
C29 (25 or 50 μΜ; 1 hour) reduces P3C-induced but not P2C-induced TNF-α mRNA and IL-12 p40 protein significantly in primary murine macrophages.
C29 (50 μΜ; 1 hour) blocks TLR2 bacterial agonist-induced proinflammatory gene expression in HEK-TLR2 cells and murine macrophages.

Western Blot Analysis

Cell Line: THP-1 cells
Concentration: 150 μM
Incubation Time: 1 hours
Result: Diminished the interaction between endogenous TLR2 and myeloid differentiation primary response gene 88 (MyD88) at 15 and 30 min poststimulation with P3C.

Western Blot Analysis

Cell Line: Murine peritoneal macrophages
Concentration: 50 μM
Incubation Time: 1 hours
Result: Blocked robust MAPK activation at 30 min and reduced NF-κB activation from 5 to 30 min.
Prevented P3C-induced degradation of IκBα at 15 and 30 min.
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