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Merck
CN

SML2371

Sigma-Aldrich

FC-99 hydrochloride

≥98% (HPLC)

别名:

FC 99 hydrochloride, FC99 hydrochloride, N1-[(4-Methoxyphenyl)methyl]-4-methyl-1,2-benzenediamine hydrochloride

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关于此项目

经验公式(希尔记法):
C15H18N2O · xHCl
CAS Number:
分子量:
242.32 (free base basis)
UNSPSC代码:
12352200
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方案

≥98% (HPLC)

表单

powder

储存条件

desiccated

颜色

white to beige

溶解性

H2O: 2 mg/mL, clear (warmed)

储存温度

2-8°C

SMILES字符串

CC1=CC(N)=C(C=C1)NCC2=CC=C(C=C2)OC

InChI

1S/C15H18N2O/c1-11-3-8-15(14(16)9-11)17-10-12-4-6-13(18-2)7-5-12/h3-9,17H,10,16H2,1-2H3

InChI key

ZPNPYWSZYRMBNP-UHFFFAOYSA-N

生化/生理作用

FC-99 is a benzenediamine derivative that inhibits LPS-induced IRAK4 phosphorylation/activation and downstream signaling events (5-45 μM; murine RAW 264.7 & peritoneal macrophages), including IRAK1 (a TLR3 pathway negative regulator) degradation, p38/ERK/JNK activation, and cytokines production. FC-99 inhibits RSV replication (50 μM; A549) and poly(I:C)-indued IRF3/IFN-α/JAK/STAT1 signalling in cultures (0.5-50 μM; murine peritoneal macrophages), and ameliorates sepsis induction following caecal ligation puncture (CLP) in mice in vivo (100/70/32.5% motality in 7 days with 0/30/100 mg/kg i.p. 2 h prior to CLP).
FC-99 is known to affect the levels of serum immunoglobulin. It might be therapeutically beneficial in systemic lupus erythematosus.
IRAK4 activation and IRAK1 degradation inhibitor that suppresses toll-like receptors (TLRs) cellular signaling and ameliorates sepsis induction in mice in vivo.

储存分类代码

11 - Combustible Solids

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable

法规信息

新产品

历史批次信息供参考:

分析证书(COA)

Lot/Batch Number

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Liu Yang et al.
Life sciences, 144, 129-137 (2015-12-02)
Inflammatory bowel disease (IBD) is an inflammatory disorder, characterized by abnormally increased expression of Toll-like receptors TLR2 and TLR4 in the colon and increased pro-inflammatory cytokine production by macrophages. In the present study, we explored the effect of FC-99, a
Yarong Zhao et al.
Oncotarget, 9(19), 14959-14976 (2018-03-31)
The liver is a vital target for sepsis-related injury, leading to inflammatory pathogenesis, multiple organ dysfunction and high mortality rates. Monocyte-derived macrophage transformations are key events in hepatic inflammation. N1-[(4-methoxy)methyl]-4-methyl-1,2-benzenediamine (FC-99) previously displayed therapeutic potential on experimental sepsis. However, the
A benzenediamine derivate FC-99 attenuates lupus nephritis in MRL/lpr mice via inhibiting myeloid dendritic cell-secreted BAFF
Ji J, et al.
Acta biochimica et biophysica Sinica, 48(5), 411-419 (2016)
Huan Dou et al.
American journal of respiratory cell and molecular biology, 51(2), 191-200 (2014-03-05)
We designed and synthesized a novel benzenediamine derivate, FC-99, that was tested for its ability to protect mice from experimental sepsis. Moreover, we sought to determine whether FC-99 could control a bacterial infection and to clarify the mechanism by which
Jianjian Ji et al.
Acta biochimica et biophysica Sinica, 48(5), 411-419 (2016-04-29)
Myeloid dendritic cells (DCs) can produce B-cell-activating factor (BAFF) that modulates survival and differentiation of B cells and plays a pivotal role in the pathogenesis of systemic lupus erythematosus (SLE). Toll-like receptor 4 (TLR4) signaling has important functions in the

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