FLI-06 - CAS 313967-18-9
Catalog number: 313967-18-9
Category: Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
Molecular Weight:
Amyloid-β | Notch
FLI-06 , a Notch inhibitor that disrupts Notch trafficking and processing, disrupts the Golgi by mechanisms different from BFA or GCA. It Reduces amyloid β secretion.
Brife Description:
Inhibits Notch signaling (EC50 = 2.3 μM); Reduces amyloid β secretion
White solid powder
cyclohexyl 2,7,7-trimethyl-4-(4-nitrophenyl)-5-oxo-1,4,6,8-tetrahydroquinoline-3-carboxylate; FLI-06; 313967-18-9; cyclohexyl 2,7,7-trimethyl-4-(4-nitrophenyl)-5-oxo-1,4,5,6,7,8-hexahydroquinoline-3-carboxylate; STK368879; AC1MIXAW; BAS 00380830; Oprea1_143746; Oprea1_499413; FLI 06; SCHEMBL15536952; AOB2707; SYN5099; 2412AH; AKOS000650664; AKOS021985195; CS-2407; MCULE-5112819342; BC600549; HY-15860; ST50001800; S7399,313967-18-9; 4-(4-Nitrophenyl)-5-oxo-2,7,7-trimethyl-1,4,5,6,7,8-hexahydroquinoline-3-carboxylic acid cyclohexyl ester; cyclohexyl 2,7,7-trimethyl-4-(4-nitrophenyl)-5-oxo-1,4,6,7,8-pentahydroquinoli ne-3-carboxylate; FLI 06|Cyclohexyl 1,4,5,6,7,8-hexahydro-2,7,7-trimethyl-4-(4-nitrophenyl)-5-oxo-3-quinolinecarboxylate;
Soluble to 100 mM in DMSO and to 20 mM in ethanol
Store in a cool and dry place and at 0 - 4℃ for short term (days to weeks) or -43℃ for long term (months to years).
1.25±0.1 g/cm3
Canonical SMILES:
1.Inhibition effect of blunting Notch signaling on food allergy through improving T
Jiang S;Han S;Chen J;Li X;Che H Ann Allergy Asthma Immunol. 2017 Jan;118(1):94-102. doi: 10.1016/j.anai.2016.10.024.
BACKGROUND: ;Notch signaling regulates proliferation, differentiation, and function of dendritic cells, T cells, and mast cells, as well as many other immune cells, which act as important parts in food allergy, Notch signaling may play an important role in food allergy.;OBJECTIVE: ;To investigate the role of Notch signaling in IgE-mediated food allergy.;METHODS: ;An ovalbumin-induced food allergy mouse model was built (cholera toxin as adjuvant) and Notch signaling was blunted by FLI-06 and MW167, which inhibited Notch receptor-expressing phase and the γ-secretase-affecting phase, respectively. Then food allergy indicators, including levels of serum antibodies, cytokines, and degranulation, were examined. Meanwhile, clinical features, such as vascular permeability changes, intestinal permeability changes, body temperature changes, and symptoms, were also observed.;RESULTS: ;After blunting Notch signaling, the levels of serum ovalbumin specific IgE and IgG;1; were decreased significantly, suggesting that blunting Notch signaling inhibited antibody responses. The levels of T;H;1 cytokines (interferon-γ) were increased significantly, whereas the levels of T;H;2 cytokines (interleukin-4, -5, and -13) were decreased significantly, suggesting T;H;2 polarization was suppressed after blunting Notch signaling.
2.Dynamic secretome of
Štáfková J;Rada P;Meloni D;Žárský V;Smutná T;Zimmann N;Harant K;Pompach P;Hrdý I;Tachezy J Mol Cell Proteomics. 2018 Feb;17(2):304-320. doi: 10.1074/mcp.RA117.000434. Epub 2017 Dec 12.
The secretion of virulence factors by parasitic protists into the host environment plays a fundamental role in multifactorial host-parasite interactions. Several effector proteins are known to be secreted by ;Trichomonas vaginalis;, a human parasite of the urogenital tract. However, a comprehensive profiling of the ;T. vaginalis; secretome remains elusive, as do the mechanisms of protein secretion. In this study, we used high-resolution label-free quantitative MS to analyze the ;T. vaginalis; secretome, considering that secretion is a time- and temperature-dependent process, to define the cutoff for secreted proteins. In total, we identified 2 072 extracellular proteins, 89 of which displayed significant quantitative increases over time at 37 °C. These 89 ;bona fide; secreted proteins were sorted into 13 functional categories. Approximately half of the secreted proteins were predicted to possess transmembrane helixes. These proteins mainly include putative adhesins and leishmaniolysin-like metallopeptidases. The other half of the soluble proteins include several novel potential virulence factors, such as DNaseII, pore-forming proteins, and β-amylases. Interestingly, current bioinformatic tools predicted the secretory signal in only 18% of the identified ;T.
3.MicroRNA‑381/Hes1 is a potential therapeutic target for spinal cord injury.
Ruan W;Ning G;Feng S;Gao S;Hao Y Int J Mol Med. 2018 Aug;42(2):1008-1017. doi: 10.3892/ijmm.2018.3658. Epub 2018 May 8.
The aim of the present study was to investigate whether microRNA‑381 is a potential therapeutic target for spinal cord injury (SCI) and its possible mechanism. Reverse transcription quantitative polymerase chain reaction (qPCR) for mRNA expression was used to analyze the changes of microRNA-381 expression. Cell viability and cell apoptosis were measured using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry. Caspase‑3 activity was measured using caspase‑3 activity kit, and western blot analysis was used to measure the protein expression of neurogenic locus notch homolog protein 1 (Notch1), notch 1 intracellular domain (NICD) and transcription factor HES-1 (Hes1). The data showed that microRNA‑381 expression of model SCI rats was downregulated compared with that of control rats. Overexpression of microRNA‑381 promoted cell proliferation, and inhibited apoptosis and caspase‑3 and apoptosis regulator BAX (Bax) protein expression in neurocytes. Overexpression of microRNA‑381 also increased Wnt and β‑catenin protein expression, and suppressed the protein expression of Notch1, NICD and Hes1 in neurocytes. Wnt inhibitor, Wnt‑C59 (1 µmol/l), inhibited cell proliferation, promoted apoptosis and caspase‑3 and Bax protein expression, suppressed β‑catenin protein expression and induced Hes1 protein expression in neurocytes following microRNA‑381 overexpression.
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CAS 313967-18-9 FLI-06

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