Category: 243984-11-4

Peled, Ella;Sosnik, Alejandro published 《Amphiphilic galactomannan nanoparticles trigger the alternative activation of murine macrophages》 in 2021. The article was appeared in 《Journal of Controlled Release》. They have made some progress in their research.Formula: C15H17ClFNO4S The article mentions the following:

Macrophages are highly plastic phagocytic cells that can exist in distinct phenotypes and play key roles in physiol. and pathol. pathways. They can be classically activated to the pro-inflammatory M1 phenotype or alternatively activated to an M2 anti-inflammatory one by various stimuli in the biol. milieu. Different biomaterials polarize macrophages to M1 or M2 phenotypes and emerged as a very promising strategy to modulate their activation and performance. In this work, we investigate the ability of drug-free amphiphilic nanoparticles (hydrodynamic diameter of ∼130 nm) produced by the self-assembly of a graft copolymer of hydrolyzed galactomannan, a natural polysaccharide of galactose and mannose, that was hydrophobized in the side-chain with poly(Me methacrylate) blocks and that can encapsulate hydrophobic drugs, to trigger macrophage polarization. The compatibility and uptake of the nanoparticles are demonstrated in the murine macrophage cell line RAW264.7 by a metabolic assay, confocal laser scanning fluorescence microscopy (CLSFM) and imaging flow cytometry in the absence and the presence of endocytosis inhibitors. Results indicate that they are internalized by both clathrin- and caveolin-mediated endocytosis. The ability of these drug-free nanoparticles to polarize these cells to the M2-like phenotype and to switch an M1 to an M2 phenotype is confirmed by the downregulation of the M1 marker cluster of differentiation 80 (CD80), and upregulation of M2 markers CD163 and CD206, as measured by flow cytometry and CLSFM. In addition, we preliminarily assess the effect of the nanoparticles on wound healing by tracking the closure of an artificial wound of RAW264.7 macrophages in a scratch assay. Findings indicate a faster closure of the wound in the presence of the nanoparticles with respect to untreated cells. Finally, a migration assay utilizing a macrophage/fibroblast co-culture model in vitro demonstrates that M2 polarization increases fibroblast migration by 24-fold with respect to untreated cells. These findings demonstrate the ability of this nanotechnol. platform to interfere and change the macrophages phenotype in vitro and represent robust evidence for the investigation of their therapeutic performance alone or in combination with an encapsulated hydrophobic drug in wound models in vivo. And (R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate (cas: 243984-11-4) was used in the research process.

(R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate(cas:243984-11-4) can reduces lesion volume in a mouse model of cerebral cavernous malformations (CCMs).Formula: C15H17ClFNO4S Also attenuates increased cytokine levels in a mouse sepsis model, when given in combination with ceftazidime. Cell permeable.

Reference:
Chloride – Wikipedia,
Chlorides – an overview | ScienceDirect Topics

Zeng, Qi;Ye, Liu;Ling, Maoyao;Ma, Riliang;Li, Junda;Chen, Haishao;Pan, Linghui published 《TLR4/TRAF6/NOX2 signaling pathway is involved in ventilation-induced lung injury via endoplasmic reticulum stress in murine model》. The research results were published in《International Immunopharmacology》 in 2021.Synthetic Route of C15H17ClFNO4S The article conveys some information:

In ventilation-induced lung injury (VILI), prolonged nonpathogen-mediated inflammation is triggered as a result of alveolar hyperinflation. In our previous study, we suggested that endoplasmic reticulum (ER) stress-mediated inflammation was involved in VILI, but how ER stress is triggered remains unknown. Toll-like receptor 4 (TLR4) activation plays an important role in mech. ventilation (MV)-induced lung inflammation, however, it is unknown whether ER stress is activated by TLR4 to participate in VILI. In this study, C57BL/6 mice were exposed to MV with high tidal volumes (HTV 20 mL/kg). Mice were pretreated with TAK-242 the TLR4 inhibitor, C25-140, the TRAF6 inhibitor, or GSK2795039, the NOX2 inhibitor. Lung tissue and bronchoalveolar lavage fluid (BALF) were collected to measure lung injury, inflammatory responses and mRNA/protein expression associated with ER stress and the TLR4/TRAF6/NOX2 signaling pathway. Our results indicate that MV with HTV caused the TLR4/TRAF6/NOX2 signaling pathway activation and production of large amounts of ROS, which led to ER stress and NF-κB mediated inflammation in VILI. Furthermore, TLR4/TRAF6/NOX2 signaling pathway inhibition attenuated ER stress response and alleviate lung injury in mice. And (R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate (cas: 243984-11-4) was used in the research process.

(R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate(cas:243984-11-4) can reduces lesion volume in a mouse model of cerebral cavernous malformations (CCMs).Synthetic Route of C15H17ClFNO4S Also attenuates increased cytokine levels in a mouse sepsis model, when given in combination with ceftazidime. Cell permeable.

Reference:
Chloride – Wikipedia,
Chlorides – an overview | ScienceDirect Topics

Sasaki, Yumi;Guo, Yong-Mei;Goto, Tatsufumi;Ubukawa, Kumi;Asanuma, Ken;Kobayashi, Isuzu;Sawada, Kenichi;Wakui, Hideki;Takahashi, Naoto published 《IL-6 generated from human hematopoietic stem and progenitor cells through TLR4 signaling promotes emergency granulopoiesis by regulating transcription factor expression》 in 2021. The article was appeared in 《Journal of Immunology》. They have made some progress in their research.HPLC of Formula: 243984-11-4 The article mentions the following:

Emergency granulopoiesis, also known as demand-adapted granulopoiesis, is defined as the response of an organism to systemic bacterial infections, and it results in neutrophil mobilization from reservoir pools and increased myelopoiesis in the bone marrow. Indirect and direct initiating mechanisms of emergency granulopoiesis have been hypothesized. However, the detailed mechanism of hyperactive myelopoiesis in the bone marrow, which leads to granulocyte left shift, remains unknown. In this study, we report that TLR4 is expressed on granulo-monocytic progenitors, as well as mobilized human peripheral blood CD34⁺ cells, which account for 0.2% of monocytes in peripheral blood, and ∼ 10% in bone marrow. LPS, a component of Gram-neg. bacteria that results in a systemic bacterial infection, induces the differentiation of peripheral blood CD34⁺ cells into myelocytes and monocytes in vitro via the TLR4 signaling pathway. Moreover, CD34⁺ cells directly responded to LPS stimulation by activating the MAPK and NF-κB signaling pathways, and they produced IL-6 that promotes emergency granulopoiesis by phosphorylating C/EBPα and C/EBPβ, and this effect was suppressed by the action of an IL-6 receptor inhibitor. This work supports the finding that TLR is expressed on human hematopoietic stem and progenitor cells, and it provides evidence that human hematopoietic stem and progenitor cells can directly sense pathogens and produce cytokines exerting autocrine and/or paracrine effects, thereby promoting differentiation. The experimental procedure involved many compounds, such as (R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate (cas: 243984-11-4) .

(R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate(cas:243984-11-4) can reduces lesion volume in a mouse model of cerebral cavernous malformations (CCMs).HPLC of Formula: 243984-11-4 Also attenuates increased cytokine levels in a mouse sepsis model, when given in combination with ceftazidime. Cell permeable.

Reference:
Chloride – Wikipedia,
Chlorides – an overview | ScienceDirect Topics

Recommanded Product: 243984-11-4In 2021, Izumi, Yukitoshi;Cashikar, Anil G.;Krishnan, Kathiresan;Paul, Steven M.;Covey, Douglas F.;Mennerick, Steven J.;Zorumski, Charles F. published 《A proinflammatory stimulus disrupts hippocampal plasticity and learning via microglial activation and 25- hydroxycholesterol》. 《Journal of Neuroscience》published the findings. The article contains the following contents:

Inflammatory cells, including macrophages and microglia, synthesize and release the oxysterol 25-hydroxycholesterol (25HC), which has antiviral and immunomodulatory properties. Here, we examined the effects of lipopolysaccharide (LPS), an activator of innate immunity, on 25HC production in microglia, and the effects of LPS and 25HC on CA1 hippocampal synaptic plasticity and learning. In primary microglia, LPS markedly increases the expression of cholesterol 25-hydroxylase (Ch25h), the key enzyme involved in 25HC synthesis, and increases the levels of secreted 25HC. Wild-type microglia produced higher levels of 25HC than Ch25h knock-out (KO) microglia with or without LPS. LPS treatment also disrupts long-term potentiation (LTP) in hippocampal slices via induction of a form of NMDA receptor-dependent metaplasticity. The inhibitory effects of LPS on LTP were mimicked by exogenous 25HC, and were not observed in slices from Ch25h KO mice. In vivo, LPS treatment also disrupts LTP and inhibits one-trial learning in wild-type mice, but not Ch25h KO mice. These results demonstrate that the oxysterol 25HC is a key modulator of synaptic plasticity and memory under proinflammatory stimuli.(R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate (cas: 243984-11-4) were involved in the experimental procedure.

(R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate(cas:243984-11-4) is a toll-like receptor 4 (TLR4) signaling inhibitor.Recommanded Product: 243984-11-4 And it can inhibits LPS-induced cytokine production in vitro (IC50 values are 1.3, 1.3 and 3.2 nM for IL-6, TNFα and NO production).

Reference:
Chloride – Wikipedia,
Chlorides – an overview | ScienceDirect Topics

Synthetic Route of C15H17ClFNO4SIn 2021, Wang, Haiyan;Li, Xuehui;Dong, Guanjun;Yan, Fenglian;Zhang, Junfeng;Shi, Hui;Ning, Zhaochen;Gao, Min;Cheng, Dalei;Ma, Qun;Wang, Changying;Zhao, Mingsheng;Dai, Jun;Li, Chunxia;Li, Zhihua;Zhang, Hui;Xiong, Huabao published 《Toll-like Receptor 4 Inhibitor TAK-242 Improves Fulminant Hepatitis by Regulating Accumulation of Myeloid-Derived Suppressor Cell》. 《Inflammation》published the findings. The article contains the following contents:

The purpose of this study was to determine the protective effect of the Toll-like receptor 4 (TLR4) inhibitor TAK-242 on lipopolysaccharide (LPS)/D-galactosamine (D-GalN)-induced explosive hepatitis and explore in vivo and in vitro mechanisms. Mice were pretreated with TAK-242 for 3 h prior to LPS (10μg/kg)/D-GalN (250 mg/kg) administration. Compared to the LPS/D-GalN group, the TAK-242 pretreatment group showed significantly prolonged survival, reduced serum alanine aminotransferase and aspartate aminotransferase levels, relieved oxidative stress, and reduced inflammatory interleukin (IL)-6, IL-12, and tumor necrosis factor-α levels. In addition, TAK-242 increased the accumulation of myeloid-derived suppressor cells (MDSCs). Next, mice were treated with an anti-Gr-1 antibody to deplete MDSCs, and adoptive transfer experiments were performed. We found that TAK-242 protected against FH by regulating MDSCs. In the in vitro studies, TAK-242 regulated the accumulation of MDSCs and promoted the release of immunosuppressive inflammatory cytokines. In addition, TAK-242 inhibited protein expression of nuclear factor-κB and mitogen-activated protein kinases. In summary, TAK-242 had a hepatoprotective effect against LPS/D-GalN-induced explosive hepatitis in mice. Its protective effect may be involved in suppressing inflammation, reducing oxidative stress, and increasing the proportion of MDSCs. To complete the study, the researchers used (R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate (cas: 243984-11-4) .

(R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate(cas:243984-11-4) is a toll-like receptor 4 (TLR4) signaling inhibitor.Synthetic Route of C15H17ClFNO4S And it can inhibits LPS-induced cytokine production in vitro (IC50 values are 1.3, 1.3 and 3.2 nM for IL-6, TNFα and NO production).

Reference:
Chloride – Wikipedia,
Chlorides – an overview | ScienceDirect Topics

HPLC of Formula: 243984-11-4《The role of HMGB1 on TDI-induced NLPR3 inflammasome activation via ROS/NF-κB pathway in HBE cells》 was published in 2021. The authors were Jiao, Bo;Guo, Sumei;Yang, Xiaohan;Sun, Lei;Sai, Linlin;Yu, Gongchang;Bo, Cunxiang;Zhang, Yu;Peng, Cheng;Jia, Qiang;Dai, Yufei, and the article was included in《International Immunopharmacology》. The author mentioned the following in the article:

To explore the potential role of HMGB1 on TDI-induced NLRP3 inflammasome activation, HBE cells were treated with TDI-HSA conjugate to observe the changes of HMGB1, TLR4, NF-κB, Nrf2 and NLRP3 inflammasome related proteins expressions, ROS release and MMP. NAC, TPCA-1 and Resatorvid pre-treatments were applied to explore the effects of ROS, NF-κB and TLR4 on TDI-induced NLRP3 inflammasome activation. The CRISPR/Cas9 system was used to construct HMGB1 gene knockout HBE cell line and then to explore the role of HMGB1 on TDI-HSA induced NLRP3 inflammasome activation. GL pre-treatment was applied to further confirm the role of HMGB1. Results showed that TDI increased HMGB1, TLR4, P-p65, Nrf2 proteins expressions and ROS release, decreased MMP level and activated NLRP3 inflammasome in HBE cells in a dose dependent manner. NAC, TPCA-1 and Resatorvid pre-treatments decreased the expression of P-p65 and inhibited NLRP3 inflammasome activation. Inhibition of HMGB1 decreased Nrf2 expression and ROS release, improved MMP level and reduced NLRP3 inflammasome activation. GL ameliorated NLRP3 inflammasome activation via inhibiting HMGB1 regulated ROS/NF-κB pathway. These results indicated that HMGB1 was involved in TDI-induced NLRP3 inflammasome activation as a pos. regulatory mechanism. The study provided a potential target for early prevention and treatment of TDI-OA. The experimental procedure involved many compounds, such as (R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate (cas: 243984-11-4) .

(R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate(cas:243984-11-4) can reduces lesion volume in a mouse model of cerebral cavernous malformations (CCMs).HPLC of Formula: 243984-11-4 Also attenuates increased cytokine levels in a mouse sepsis model, when given in combination with ceftazidime. Cell permeable.

Reference:
Chloride – Wikipedia,
Chlorides – an overview | ScienceDirect Topics

Wang, Meng;Feng, Li-Rong;Li, Zi-Long;Ma, Kai-Ge;Chang, Ke-Wei;Chen, Xin-Lin;Yang, Peng-Bo;Ji, Sheng-Feng;Ma, Yan-Bing;Han, Hua;Ruganzua, John Bosco;Yang, Wei-Na;Qian, Yi-Hua published 《Thymosin β4 reverses phenotypic polarization of glial cells and cognitive impairment via negative regulation of NF-κB signaling axis in APP/PS1 mice》. The research results were published in《Journal of Neuroinflammation》 in 2021.Synthetic Route of C15H17ClFNO4S The article conveys some information:

Thymosin β4 (Tβ4) is the most abundant member of the β-thymosins and plays an important role in the control of actin polymerization in eukaryotic cells. While its effects in multiple organs and diseases are being widely investigated, the safety profile has been established in animals and humans, currently, little is known about its influence on Alzheimers disease (AD) and the possible mechanisms. Thus, we aimed to evaluate the effects and mechanisms of Tβ4 on glial polarization and cognitive performance in APP/PS1 transgenic mice. Behavior tests were conducted to assess the learning and memory, anxiety and depression in APP/PS1 mice. Thioflavin S staining, Nissl staining, immunohistochem./immunofluorescence, ELISA, qRT-PCR, and immunoblotting were performed to explore Aβ accumulation, phenotypic polarization of glial cells, neuronal loss and function, and TLR4/NF-κB axis in APP/PS1 mice. We demonstrated that Tβ4 protein level elevated in all APP/PS1 mice. Over-expression of Tβ4 alone alleviated AD-like phenotypes of APP/PS1 mice, showed less brain Aβ accumulation and more Insulin-degrading enzyme (IDE), reversed phenotypic polarization of microglia and astrocyte to a healthy state, improved neuronal function and cognitive behavior performance, and accidentally displayed antidepressant-like effect. Besides, Tβ4 could downregulate both TLR4/MyD88/NF-κB p65 and p52-dependent inflammatory pathways in the APP/PS1 mice. While combination drug of TLR4 antagonist TAK242 or NF-κB p65 inhibitor PDTC exerted no further effects. These results suggest that Tβ4 may exert its function by regulating both classical and non-canonical NF-κB signaling and is restoring its function as a potential therapeutic target against AD. And (R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate (cas: 243984-11-4) was used in the research process.

(R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate(cas:243984-11-4) is a toll-like receptor 4 (TLR4) signaling inhibitor.Synthetic Route of C15H17ClFNO4S And it can inhibits LPS-induced cytokine production in vitro (IC50 values are 1.3, 1.3 and 3.2 nM for IL-6, TNFα and NO production).

Reference:
Chloride – Wikipedia,
Chlorides – an overview | ScienceDirect Topics

Rong, Bohan;Wu, Qiong;Reiter, Russel J.;Sun, Chao published 《The Mechanism of Oral Melatonin Ameliorates Intestinal and Adipose Lipid Dysmetabolism Through Reducing Escherichia Coli-Derived Lipopolysaccharide》. The research results were published in《Cellular and Molecular Gastroenterology and Hepatology》 in 2021.Electric Literature of C15H17ClFNO4S The article conveys some information:

Gut microbiota have been reported to be sensitive to circadian rhythms and host lipometabolism, resp. Although melatonin-mediated beneficial efforts on many physiol. sites have been revealed, the regulatory actions of oral melatonin on the communication between gut microbiota and host are still not clear. Angiopoietin-like 4 (ANGPTL4) has been shown to be strongly responsible for the regulation of systemic lipid metabolism Herein, we identified that oral melatonin improved lipid dysmetabolism in ileum and epididymal white adipose tissue (eWAT) via gut microbiota and ileac ANGPTL4. Analyses of jet-lag (JL) mice, JL mice with oral melatonin administration (JL+MT), and the control for mRNA and protein expression regarding lipid uptake and accumulation in ileum and eWAT were made. Gut microbiome sequencing and exptl. validation of target strains were included. Functional anal. of key factors/pathways in the various rodent models, including the depletion of gut microbiota, mono-colonization of Escherichia coli, and other genetic intervention was made. Analyses of transcriptional regulation and effects of melatonin on E coli-derived lipopolysaccharide (LPS) in vitro were made. JL mice have a higher level of ileal lipid uptake, fat accumulation in eWAT, and lower level of circulating ANGPTL4 in comparison with the control mice. JL mice also showed a significantly higher abundance of E coli and LPS than the control mice. Conversely, oral melatonin supplementation remarkably reversed these phenotypes. The test of depletion of gut microbiota further demonstrated that oral melatonin-mediated improvements on lipometabolism in JL mice were dependent on the presence of gut microbiota. By mono-colonization of E coli, LPS has been determined to trigger these changes similar to JL. Furthermore, we found that LPS served as a pivotal link that contributed to activating toll-like receptor 4 (TLR4)/signal transducer and activator of transcription 3 (STAT3_/REV-ERBα) signaling to up-regulate nuclear factor interleukin-3-regulated protein (NFIL3) expression, resulting in increased lipid uptake in ileum. In MODE-K cells, the activation of NFIL3 has further been shown to inhibit ANGPTL4 transcription, which is closely associated with lipid uptake and transport in peripheral tissues. Finally, we confirmed that melatonin inhibited LPS via repressing the expression of LpxC in E coli. Overall, oral melatonin decreased the quantity of E coli-generated LPS, which alleviated NFIL3-induced transcriptional inhibition of ANGPTL4 through TLR4/IL-22/STAT3 signaling in ileum, thereby resulting in the amelioration of ileal lipid intake and lower fat accumulation in eWAT. These results address a novel regulation of oral melatonin originating from gut microbiota to host distal tissues, suggesting that microbe-generated metabolites are potential therapies for melatonin-mediated improvement of circadian rhythm disruption and related metabolic syndrome. The experimental procedure involved many compounds, such as (R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate (cas: 243984-11-4) .

(R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate(cas:243984-11-4) is a toll-like receptor 4 (TLR4) signaling inhibitor.Electric Literature of C15H17ClFNO4S And it can inhibits LPS-induced cytokine production in vitro (IC50 values are 1.3, 1.3 and 3.2 nM for IL-6, TNFα and NO production).

Reference:
Chloride – Wikipedia,
Chlorides – an overview | ScienceDirect Topics

Safety of (R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate《Atorvastatin upregulates microRNA-186 and inhibits the TLR4-mediated MAPKs/NF-κB pathway to relieve steroid-induced avascular necrosis of the femoral head》 was published in 2021. The authors were Zhang, Yusong;Ma, Limin;Lu, Erhai;Huang, Wenhua, and the article was included in《Frontiers in Pharmacology》. The author mentioned the following in the article:

Steroid-induced avascular necrosis of the femoral head (SANFH) is caused by the death of active components of the femoral head owing to hormone overdoses. The use of lipid-lowering drugs to prevent SANFH in animals inspired us to identify the mechanisms involving Atorvastatin (Ato) in SANFH. However, it is still not well understood how and to what extent Ato affects SANFH. This study aimed to figure out the efficacy of Ato in SANFH and the underlying mol. mechanisms. After establishment of the SANFH model, histol. evaluation, lipid metabolism, inflammatory cytokines, oxidative stress, apoptosis, and autophagy of the femoral head were evaluated. The differentially expressed microRNAs (miRs) after Ato treatment were screened out using microarray anal. The downstream gene and pathway of miR-186 were predicted and their involvement in SANFH rats was analyzed. OB-6 cells were selected to simulate SANFH in vitro. Cell viability, cell damage, inflammation responses, apoptosis, and autophagy were assessed. Ato alleviated SANFH, inhibited apoptosis, and promoted autophagy. miR-186 was significantly upregulated after Ato treatment. miR-186 targeted TLR4 and inactivated the MAPKs/NF-κB pathway. Inhibition of miR-186 reversed the protection of Ato on SANFH rats, while inhibition of TLR4 restored the protective effect of Ato. Ato reduced apoptosis and promoted autophagy of OB-6 cells by upregulating miR- 186 and inhibiting the TLR4/MAPKs/NF-κB pathway. In conclusion, Ato reduced apoptosis and promoted autophagy, thus alleviating SANFH via miR-186 and the TLR4-mediated MAPKs/NF-κB pathway. The experimental procedure involved many compounds, such as (R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate (cas: 243984-11-4) .

(R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate(cas:243984-11-4) can reduces lesion volume in a mouse model of cerebral cavernous malformations (CCMs).Safety of (R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate Also attenuates increased cytokine levels in a mouse sepsis model, when given in combination with ceftazidime. Cell permeable.

Reference:
Chloride – Wikipedia,
Chlorides – an overview | ScienceDirect Topics

Liu, Shaoguang;Zhang, Shaotong;Sun, Yulong;Zhou, Wence published 《Transcriptomics Changes in the Peritoneum of Mice with Lipopolysaccharide-Induced Peritonitis》. The research results were published in《International Journal of Molecular Sciences》 in 2021.Safety of (R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate The article conveys some information:

Peritonitis caused by LPS is a severe clin. challenge, which causes organ damage and death. However, the mechanism of LPS-induced peritonitis has not been fully revealed yet. Here, we investigated the transcriptome profile of the peritoneal tissue of LPS-induced peritonitis in mice. A model of LPS-induced peritonitis in mice was established (LPS 10 mg/kg, i.p.), and the influence of TAK 242 (TLR4 inhibitor) on the level of inflammatory cytokines in mouse peritoneal lavage fluid was investigated by using an ELISA test. Next, the peritoneal tissues of the three groups of mice (Control, LPS, and LPS+TAK 242) (n = 6) were isolated and subjected to RNA-seq, followed by a series of bioinformatics analyses, including differentially expressed genes (DEGs), enrichment pathway, protein-protein interaction, and transcription factor pathway. Then, qPCR verified-hub genes that may interact with TAK 242 were obtained. Subsequently, the three-dimensional structure of hub proteins was obtained by using homol. modeling and mol. dynamics optimization (300 ns). Finally, the virtual docking between TAK 242 and hub proteins was analyzed. Our results showed that TAK 242 significantly inhibited the production of inflammatory cytokines in the peritoneal lavage fluid of mice with peritonitis, including IL-6, IFN-γ, IL-1β, NO, and TNF-α. Compared with the Control group, LPS treatment induced 4201 DEGs (2442 down-regulated DEGs and 1759 up-regulated DEGs). Compared with the LPS group, 30 DEGs were affected by TAK 242 (8 down-regulated DEGs and 22 up-regulated DEGs). A total of 10 TAK 242-triggered hub genes were obtained, and the possible docking modes between TAK 242 and hub proteins were acquired. Overall, our data demonstrated that a large number of DEGs were affected in LPS-triggered peritonitis mice. Moreover, the TLR4 inhibitor TAK 242 is capable of suppressing the inflammatory response of LPS-induced peritonitis. Our work provides clues for understanding the pathogenesis of LPS-induced peritonitis in mice. To complete the study, the researchers used (R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate (cas: 243984-11-4) .

(R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate(cas:243984-11-4) is a toll-like receptor 4 (TLR4) signaling inhibitor.Safety of (R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate And it can inhibits LPS-induced cytokine production in vitro (IC50 values are 1.3, 1.3 and 3.2 nM for IL-6, TNFα and NO production).

Reference:
Chloride – Wikipedia,
Chlorides – an overview | ScienceDirect Topics