SML2371
FC-99 hydrochloride
≥98% (HPLC)
Synonym(s):
FC 99 hydrochloride, FC99 hydrochloride, N1-[(4-Methoxyphenyl)methyl]-4-methyl-1,2-benzenediamine hydrochloride
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About This Item
Empirical Formula (Hill Notation):
C15H18N2O · xHCl
CAS Number:
Molecular Weight:
242.32 (free base basis)
UNSPSC Code:
12352200
NACRES:
NA.21
Assay:
≥98% (HPLC)
Form:
powder
Storage condition:
desiccated
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
SMILES string
CC1=CC(N)=C(C=C1)NCC2=CC=C(C=C2)OC
assay
≥98% (HPLC)
form
powder
storage condition
desiccated
color
white to beige
solubility
H2O: 2 mg/mL, clear (warmed)
storage temp.
2-8°C
Related Categories
Biochem/physiol Actions
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.
Storage Class
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Regulatory Information
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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)
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
Jianjian Ji et al.
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
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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