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.[1]
IRAK4 activation and IRAK1 degradation inhibitor that suppresses toll-like receptors (TLRs) cellular signaling and ameliorates sepsis induction in mice in vivo.
Storage Class
11 - Combustible Solids
wgk_germany
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
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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
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
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
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
Acta biochimica et biophysica Sinica, 46(10), 829-836 (2014-09-05)
Increased IL-17-producing helper T (Th17) cells have been observed in patients with rheumatoid arthritis (RA). The retinoic-acid-related orphan nuclear receptor (RORγt) is the master regulator of Th17 cells. Our previous research showed that FC99 possesses anti-inflammation activity. However, to date
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