Category: 243984-11-4

Moreno, Carlos;Bybee, Ellie;Tellez Freitas, Claudia M.;Pickett, Brett E.;Weber, K. Scott published 《Meta-Analysis of Two Human RNA-seq Datasets to Determine Periodontitis Diagnostic Biomarkers and Drug Target Candidates》 in 2022. The article was appeared in 《International Journal of Molecular Sciences》. They have made some progress in their research.Formula: C15H17ClFNO4S The article mentions the following:

Periodontitis is a chronic inflammatory oral disease that affects approx. 42% of adults 30 years of age or older in the United States. In response to microbial dysbiosis within the periodontal pockets surrounding teeth, the host immune system generates an inflammatory environment in which soft tissue and alveolar bone destruction occur. The objective of this study was to identify diagnostic biomarkers and the mechanistic drivers of inflammation in periodontitis to identify drugs that may be repurposed to treat chronic inflammation. A meta-anal. comprised of two independent RNA-seq datasets was performed. RNA-seq anal., signal pathway impact anal., protein-protein interaction anal., and drug target anal. were performed to identify the critical pathways and key players that initiate inflammation in periodontitis as well as to predict potential drug targets. Seventy-eight differentially expressed genes, 10 significantly impacted signaling pathways, and 10 hub proteins in periodontal gingival tissue were identified. The top 10 drugs that may be repurposed for treating periodontitis were then predicted from the gene expression and pathway data. The efficacy of these drugs in treating periodontitis has yet to be investigated. However, this anal. indicates that these drugs may serve as potential therapeutics to treat inflammation in gingival tissue affected by periodontitis. 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).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

Qu, Zhehui;Li, Mingzhu;An, Ran;Dai, Haiyue;Yu, Yueyang;Li, Chenfeng;Cao, Chong;Meng, Ye;Wang, Junwei;Gao, Mingchun published 《Self-assembled BPIV3 nanoparticles can induce comprehensive immune responses and protection against BPIV3 challenge by inducing dendritic cell maturation in mice》 in 2022. The article was appeared in 《Veterinary Microbiology》. They have made some progress in their research.Recommanded Product: 243984-11-4 The article mentions the following:

Bovine parainfluenza virus type 3 (BPIV3) is one of the most important viral respiratory pathogens of cattle. No specific therapies are available for BPIV3 infection; vaccination is one of the most effective ways to prevent BPIV3 infection. We therefore prepared the self-assembled BPIV3 nanoparticles by genetically fusing the ectodomain of BPIV3 haemagglutinin-neuraminidase (HN) (HNex) to the NH2 terminus of ferritin (HNex-RFNp) using a baculovirus expression system. It was found that HNex-RFNp-induced bone marrow-derived dendritic cell (BMDC) maturation through the upregulated expression of surface mols. (MHC II, CD80, CD86, and CD40), increased the secretion of inflammatory cytokines (IL-6, IL-12, TNF-α, and IFN-γ), and reduced antigen phagocytosis and T cell activation capacity. HNex-RFNp pos. regulated IκBα and NF-κB (p65) phosphorylation and facilitated NF-κB (p65) translocation into the nuclei of mature BMDCs. Incubating RFNp-treated BMDCs with TLR4 and NF-κB (p65) inhibitors, suppressed surface mol. expression as well as pro-inflammatory cytokine production and IκBα and NF-κB (p65) activities. The BPIV3 HNex protein induced BMDC maturation to some extent but was significantly weaker than HNex-RFNp. We found that HNex-RFNp induced a higher titer of specific antibodie, hemagglutinin inhibition (HI) antibody, and virus neutralisation (VN) antibody, and a comprehensive cellular immune response. We examined protection against BPIV3 challenge in a mouse model. Pathol. changes were not observed in the lungs of HNex-RFNp-vaccinated mice. Levels of BPIV3 RNA and virus titers in the lungs and trachea were significantly lower in the HNex-RFNp, than HNex, inactivated BPIV3, and PBS groups. In summary, HNex-RFNp elicited better immunogenicity than HNex or inactivated BPIV3 and could be developed as an effective vaccine to protect against BPIV3 infection. 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.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

Moraes-Vieira, Pedro M.;Yore, Mark M.;Sontheimer-Phelps, Alexandra;Castoldi, Angela;Norseen, Julie;Aryal, Pratik;Sjodin, Kotryna Simonyte;Kahn, Barbara B. published 《Retinol binding protein 4 primes the NLRP3 inflammasome by signaling through Toll-like receptors 2 and 4》 in 2020. The article was appeared in 《Proceedings of the National Academy of Sciences of the United States of America》. They have made some progress in their research.Application In Synthesis of (R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate The article mentions the following:

Adipose tissue (AT) inflammation contributes to systemic insulin resistance. In obesity and type 2 diabetes (T2D), retinol binding protein 4 (RBP4), the major retinol carrier in serum, is elevated in AT and has proinflammatory effects which are mediated partially through Toll-like receptor 4 (TLR4). We now show that RBP4 primes the NLRP3 inflammasome for interleukin-1β (IL1β) release, in a glucose-dependent manner, through the TLR4/MD2 receptor complex and TLR2. This impairs insulin signaling in adipocytes. IL1β is elevated in perigonadal white AT (PGWAT) of chow-fed RBP4-overexpressing mice and in serum and PGWAT of high-fat diet-fed RBP4-overexpressing mice vs. wild-type mice. Holo- or apo-RBP4 injection in wild-type mice causes insulin resistance and elevates PGWAT inflammatory markers, including IL1β. TLR4 inhibition in RBP4-overexpressing mice reduces PGWAT inflammation, including IL1β levels and improves insulin sensitivity. Thus, the proinflammatory effects of RBP4 require NLRP3-inflammasome priming. These studies may provide approaches to reduce AT inflammation and insulin resistance in obesity and diabetes. 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.Application In Synthesis 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

Alshaghdali, Khalid;Saeed, Mohd;Kamal, Mohammad Amjad;Saeed, Amir published 《Interaction of Ectodomain of Respiratory Syncytial Virus G Protein with TLR2/ TLR6 Heterodimer: An In vitro and In silico Approach to Decipher the Role of RSV G Protein in Pro-inflammatory Response against the Virus》 in 2021. The article was appeared in 《Current Pharmaceutical Design》. They have made some progress in their research.COA of Formula: C15H17ClFNO4S The article mentions the following:

Human respiratory syncytial virus (RSV) has been shown to be linked with various forms of respiratory diseases, such as common cold and lower respiratory tract illnesses like pneumonia and bronchiolitis. TLRs play critical role in generating host immune response against RSV. TLRs are expressed not only on leukocytes but also on many other cell types and can recognize RSV. Previous studies have established that RSV can interact with TLR4 and initiate inflammatory cascade of cytokines. The data from a recent study indicated that TLR2/TLR6 is involved in RSV recognition and subsequent innate immune activation. However, the nature of binding and the envelope protein of RSV involved in this interaction with TLRs are not studied yet. We hypothesized that RSV G protein can bind to TLRs and mediate the inflammatory immune response against the virus infection. Therefore, we investigated whether RSV G protein could activate innate immune response through TLR signaling. Different TLR antagonists were used to assess the effect of the exposure of RSV and RSV G ectodomain in human primary small airway epithelial cells (HSAECs). Various inflammatory cytokines, chemokines and type I IFNs were measured by ELISA along with their mRNA expression by qPCR. In silico interaction of RSV G protein with TLR2/TLR6 was also analyzed. Results of ELISA and qPCR anal. have shown that TLR2/TLR6 signaling is activated in HSAECs upon RSV and RSV G protein exposure which initiates innate immune response against RSV. Moreover, RSV envelope protein G plays a crucial role in binding and activation of TLR2/TLR6 signaling. In summary, our study shows that TLR2/TLR6 play important role in the activation of innate immune response upon RSV recognition which could be helpful in promoting RSV clearance and preventing RSV-induced disease. 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).COA of 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

Su, Xiaonan;Ma, Xiaowen;Xie, Xiaoyu;Wu, Hao;Wang, Le;Feng, Yuemin;Yu, Zhen;Liu, Chenxi;Qi, Jianni;Zhu, Qiang published 《FN-EDA mediates angiogenesis of hepatic fibrosis via integrin-VEGFR2 in a CD63 synergetic manner》. The research results were published in《Cell Death Discovery》 in 2020.Application In Synthesis of (R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate The article conveys some information:

Pathol. angiogenesis is an important component of hepatic fibrosis along with fibrous deposition, but its role is not well understood. Here, we demonstrated that fibronectin containing extra domain A(FN-EDA), a fibronectin splice variant highly expressed in hepatic fibrosis, mediated angiogenesis in disease progression. FN-EDA was pos. correlated with pathol. angiogenesis in hepatic fibrosis, and a reduction in FN-EDA expression was associated with diminished intrahepatic angiogenesis and fibrosis. FN-EDA mostly colocalized with hepatic stellate cells (HSCs) and interference or blockage of FN-EDA attenuated migration and tube formation in co-cultured endothelial cells. Mechanistic studies indicated that FN-EDA was secreted to promote phosphorylation of VEGFR2 with the assistance of integrin and CD63. Targeting FN-EDA-integrin combination postponed the progression of hepatic angiogenesis and fibrosis in vivo. These results indicated that FN-EDA plays an emerging role in angiogenesis in hepatic fibrosis and could be a potential therapeutic intervention for the disease. 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.Application In Synthesis 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

Zhou, Mingxu;Yang, Yang;Wu, Miaomiao;Ma, Fang;Xu, Yue;Deng, Bihua;Zhang, Jinqiu;Zhu, Guoqiang;Lu, Yu published 《Role of long polar fimbriae type 1 and 2 in pathogenesis of mammary pathogenic Escherichia coli》. The research results were published in《Journal of Dairy Science》 in 2021.Related Products of 243984-11-4 The article conveys some information:

Escherichia coli is a leading cause of bovine mastitis worldwide. The bacteria can rapidly grow in milk and elicit a strong lipopolysaccharide (LPS)/toll-like receptor-4 (TLR4)-dependent inflammatory response. Recently, the long polar fimbriae (LPF) were identified as a promising virulence factor candidate widely distributed in mammary pathogenic E. coli (MPEC) strains. Mammary pathogenic E. coli possess 2 lpf loci encoding LPF1 and LPF2, resp. By deleting the major fimbrial subunit gene, lpfA, we found that both LPF1 and LPF2 contribute to MPEC adhesion, invasion, and biofilm formation in vitro. The lpf1A and lpf2A mutants showed reduced cytotoxicity in our in vitro cell infection model. Furthermore, we observed that LPF2 induced a mild TLR4-independent proinflammatory response. The median LD (LD50) of both Δlpf2A and Δlpf1AΔlpf2A mutants to BALB/c mice increased by 0.38 and 0.15 logs, resp., whereas that of wild-type strain MPJS13 was 8.69 logs. In contrast, LPF1 deficiency significantly enhanced the LPS/TLR4-mediated inflammatory response in mammary epithelial cells, and the LD50 of the mutant decreased to 8.18 logs. In conclusion, our data suggested that LPF are important in MPEC colonization of mammary cells and may provide a benefit to bacterial intracellular survival that induces persistent bovine mastitis. 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.Related Products of 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

Geum, Na Gyeong;Yu, Ju-Hyeong;Yeo, Joo Ho;Choi, Min Yeong;Lee, Jae Won;Beak, Jueng Kyu;Jeong, Jin Boo published 《Immunostimulatory activity and anti-obesity activity of Hibiscus manihot leaves in mouse macrophages, RAW264.7 cells and mouse adipocytes, 3T3-L1 cells》 in 2021. The article was appeared in 《Journal of Functional Foods》. They have made some progress in their research.SDS of cas: 243984-11-4 The article mentions the following:

In this study, we investigated whether Hibiscus manihot leaves (HML) exhibits immune-enhancing activity and anti-obesity in RAW264.7 and 3T3-L1 cells. HML increased the production of inflammatory mols., cell viability and phagocytosis in RAW264.7 cells. TLR2 and TLR4 blocked HML-mediated production of inflammatory mols. in RAW264.7 cells. In addition, the inhibition of MAPK signaling pathway reduced HML-mediated production of inflammatory mols. and the activation of MAPK signaling pathway by HML suppressed the inhibition of TLR2/4. HML reduced the lipid accumulation and TG contents in 3T3-L1 cells. HML inhibited the protein expressions such as CEBPα, PPARγ, perilipin-1, adiponectin and FABP4 related to the lipid accumulation of the mature adipocytes. In addition, HML reduced CEBPα and PPARγ during the differentiation process from preadipocytes to mature adipocytes. 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.SDS of cas: 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

Yang, Caixia;Sui, Guanghong;Wang, Lu;Chen, Zheng;Wang, Feng published 《MiR-124 Prevents the Microglial Proinflammatory Response by Inhibiting the Activities of TLR4 and Downstream NLRP3 in Palmitic Acid-Treated BV2 Cells》 in 2022. The article was appeared in 《Journal of Molecular Neuroscience》. They have made some progress in their research.Application In Synthesis of (R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate The article mentions the following:

Neuroinflammation is a mechanism by which obesity or a high-fat diet leads to cognitive impairment. MiR-124, a highly expressed microRNA in the brain, can alleviate neuroinflammation by regulating microglial activation, but its mechanism is unclear. The aim of the study was to explore whether miR-124 exerted this effect through TLR4/MyD88/NF-κB p65/NLRP3 signaling in palmitic acid-treated BV2 cells. Prepared BV2 cells were treated with palmitic acid to establish an in vitro model of a high-fat diet. An miR-124 mimic and inhibitor were adopted to upregulate and downregulate the expression of miR-124, resp. TAK-242 and NLRP3 siRNA were used to downregulate the expression of TLR4 and NLRP3. The expression levels of miR-124, signaling proteins (TLR4, MyD88, and NF-κB p65), inflammasome markers (NLRP3 and IL-1β), and microglial activated markers (CD206, Arg-1, CD86, and iNOS) were measured by qPCR and western blotting. The pyroptosis rate was assessed using flow cytometry. First, palmitic acid upregulated TLR4/MyD88/NF-κB p65 signaling, increased NLRP3 expression, elevated the pyroptosis rate, and promoted the microglial proinflammatory response in BV2 cells. Second, the miR-124 mimic and inhibitor sep. alleviated and aggravated the effect of palmitic acid on microglial activation and NLRP3 expression. The miR-124 mimic also downregulated TLR4/MyD88/NF-κB p65 signaling. Third, TAK-242 did not affect the expression of miR-124 but simulated the protective effect of the miR-124 mimic on microglial activation and NLRP3 expression. Fourth, NLRP3 siRNA also inhibited the microglial proinflammatory response in BV2 cells. MiR-124 prevented the microglial proinflammatory response through TLR4/MyD88/NF-κB p65/NLRP3 signaling in palmitic acid-treated BV2 cells. 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.Application In Synthesis 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

Application In Synthesis of (R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylateIn 2022, Sun, Lihua;Zhu, Hongchao;Zhang, Kui published 《GAB1 alleviates septic lung injury by inhibiting the TLR4/ NF-κB pathway》. 《Clinical and Experimental Pharmacology and Physiology》published the findings. The article contains the following contents:

Sepsis, with its high morbidity and mortality, is a difficult problem in critical care medicine. The purpose of this study is to investigate the involvement of GRB2-associated binding protein 1 (GAB1) in septic lung injury. Lipopolysaccharide (LPS)-induced mouse model and A549 cell model were used to simulate septic lung injury. Haematoxylin and eosin (H&E) staining was used to observe the pathol. changes. The terminal-deoxynucleotidyl transferase/(TdT)-mediated dUTP-biotin nick end labeling (TUNEL) staining and flow cytometry were used to detect apoptosis. The levels of inflammatory factors in the bronchoalveolar lavage fluid (BALF) were determined by ELISA (ELISA). In LPS-induced sepsis mice, GAB1 expression was markedly reduced, and GAB1 overexpression significantly attenuated cell apoptosis and decreased levels of macrophages, neutrophils, and inflammatory factors in the BALF. Our results also demonstrated that GAB1 overexpression significantly reduced LPS-induced apoptosis and inflammation of A549 cells. More importantly, GAB1 overexpression significantly inhibited the Toll-like receptor/ NFkappaB (TLR4/NF-κB) pathway, while silencing GAB1 significantly activated the TLR4/NF-κB pathway and induced apoptosis and increased expression of inflammatory factors. However, the TLR4 inhibitor TAK-242 eliminated the effect of GAB1 silencing on A549. In conclusion, GAB1 is a key regulator of sepsis by inhibiting TLR4/NF-κB mediated apoptosis and inflammation. 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.Application In Synthesis 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

Li, Yuhua;Sun, Yang;Diao, Fanrong;Ruan, Yiming;Chen, Gui’e;Tang, Tianle;Liu, Yongsheng;Zhou, Huiping;Lin, Wenming;Dong, Mingzhi;Liu, Tieming;Mei, Qibing;Cai, De published 《Jiaolong capsule protects SD rats against 2,4,6-trinitrobenzene sulfonic acid induced colitis》 in 2021. The article was appeared in 《Journal of Ethnopharmacology》. They have made some progress in their research.Recommanded Product: (R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate The article mentions the following:

Jiaolong capsule (JLC) was approved for the therapy of gastrointestinal diseases by the State Food and Drug Administration (SFDA) of China. It has a satisfactory curative effect in the treatment of patients with inflammatory bowel disease, however, the mechanism remains to be elucidated. In current study, the effects and possible mechanisms of JLC on 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis were investigated. Sulfasalazine and JLC were administrated orally and initialized 6 h after TNBS enema, once a day for seven consecutive days. The effect of JLC on intestinal microbial populations and LPS/TLR-4/NF-κB pathway was observed and assessed. Thirty female SD rats were distributed into six groups randomly and equally, namely, control, TNBS, TNBS + sulfasalazine (625 mg/kg), and TNBS + three different doses of JLC (25, 50, and 100 mg/kg) groups. The effect of JLC on restoring normal structures of colorectum and repairing colonic damage were superior to that of sulfasalazine. JLC showed a pos. effect in re-balancing intestinal bacteria population of colitis, and suppressed the activation of LPS/TLR-4/NF-κB pathway. The results suggest that JLC demonstrated a beneficial effect on treating colitis in a rat model. The possible mechanisms may be through the regulatory effect of intestinal commensal bacteria and down-regulation of LPS/TLR-4/NF-κB pathway. 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.Recommanded Product: (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