Category: 243984-11-4

Related Products of 243984-11-4In 2021, Chang, Chao;Hu, Liya;Sun, Shanshan;Song, Yanqiu;Liu, Shan;Wang, Jing;Li, Peijun published 《Regulatory role of the TLR4/JNK signaling pathway in sepsis-induced myocardial dysfunction》. 《Molecular Medicine Reports》published the findings. The article contains the following contents:

Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection, and is a leading cause of mortality worldwide. Myocardial dysfunction is associated with poor prognosis in patients with sepsis and contributes to a high risk of mortality. However, the pathophysiol. mechanisms underlying sepsis-induced myocardial dysfunction are not completely understood. The aim of the present study was to investigate the role of toll-like receptor 4 (TLR4)/c-Jun N-terminal kinase (JNK) signaling in pro-inflammatory cytokine expression and cardiac dysfunction during lipopolysaccharide (LPS)-induced sepsis in mice. C57BL/6 mice were pretreated with TAK-242 or saline for 1 h and then subjected to LPS (12 mg/kg, i.p.) treatment. Cardiac function was assessed using an echocardiogram. The morphol. changes of the myocardium were examined by hematoxylin and eosin staining and transmission electron microscopy. The serum protein levels of cardiac troponin I (cTnI) and tumor necrosis factor-α (TNF-α) were determined by an ELISA (ELISA). The TLR4 and JNK mRNA levels were analyzed via reverse transcription-quant. PCR. TLR4, JNK and phosphorylated-JNK protein levels were measured by western blotting. In response to LPS, the activation of TLR4 and JNK in the myocardium was upregulated. There were significant increases in the serum levels of TNF-α and cTnI, as well as histopathol. changes in the myocardium and suppressed cardiac function, following LPS stimulation. Inhibition of TLR4 activation using TAK-242 led to a decrease in the activation of JNK and reduced the protein expression of TNF-α in plasma, and alleviated histol. myocardial injury and improved cardiac function during sepsis in mice. The present data suggested that the TLR4/JNK signaling pathway played a critical role in regulating the production of pro-inflammatory cytokines and myocardial dysfunction induced by LPS. 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) can reduces lesion volume in a mouse model of cerebral cavernous malformations (CCMs).Related Products of 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

Quality Control of (R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate《TAK-242 ameliorates olfactory dysfunction in a mouse model of allergic rhinitis by inhibiting neuroinflammation in the olfactory bulb》 was published in 2021. The authors were Lv, Hao;Liu, Peiqiang;Zhou, Fangwei;Gao, Ziang;Fan, Wenjun;Xu, Yu, and the article was included in《International Immunopharmacology》. The author mentioned the following in the article:

Olfactory dysfunction (OD) is a common symptom of allergic rhinitis (AR) that can seriously affect patient quality of life; however, the associated pathogenesis remains unclear. This study aimed to explore the relationship between OD and damage of the olfactory bulb (OB) in allergic rhinitis (AR). The therapeutic potential of TAK-242, a selective TLR4 inhibitor, was evaluated for OD. An AR mouse model was established with ovalbumin (OVA) to test the olfactory function of AR mice using the buried food pellet test (BFPT). Mice with OD were i.p. injected with TAK-242 or 1% DMSO (vehicle). Immunohistochem. was used to detect microglia and astrocyte activation in the OB. TUNNEL staining was performed to detect apoptosis in the OB. Proteins in the TLR4 signaling pathway were detected by Western blot. The level of proinflammatory factor mRNA in the OB was determined by RT-PCR. Neuroinflammation was observed in the OB of the OD group, as evidenced by glial cell activation and increased proinflammatory factor expression. The number of apoptotic cells was significantly increased in the OB of the OD group. The expression of TLR4, MyD88, and p-NF-κBp65 was significantly up-regulated in the OB of the OD group. TAK-242 treatment significantly reduced the level of IL-1β, IL-6, and TNF-α mRNA expression, as well as activation of microglia and astrocytes in the OB tissues. TAK-242 improve olfactory function in AR mice mainly by reducing neuroinflammation and apoptosis in the OB, which may be related to blocking the TLR4/MyD88/NF-κB signaling 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) can reduces lesion volume in a mouse model of cerebral cavernous malformations (CCMs).Quality Control 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

Grigoryeva, Lubov S.;Cianciotto, Nicholas P. published 《Human macrophages utilize a wide range of pathogen recognition receptors to recognize Legionella pneumophila, including Toll-Like Receptor 4 engaging Legionella lipopolysaccharide and the Toll-like Receptor 3 nucleic-acid sensor》 in 2021. The article was appeared in 《PLoS Pathogens》. They have made some progress in their research.Category: chlorides-buliding-blocks The article mentions the following:

Cytokines made by macrophages play a critical role in determining the course of Legionella pneumophila infection. Prior murine-based modeling indicated that this cytokine response is initiated upon recognition of L. pneumophila by a subset of Toll-like receptors, namely TLR2, TLR5, and TLR9. Through the use of shRNA/siRNA knockdowns and subsequently CRISPR/Cas9 knockouts (KO), we determined that TRIF, an adaptor downstream of endosomal TLR3 and TLR4, is required for full cytokine secretion by human primary and cell-line macrophages. By characterizing a further set of TLR KO’s in human U937 cells, we discerned that, contrary to the viewpoint garnered from murine-based studies, TLR3 and TLR4 (along with TLR2 and TLR5) are in fact vital to the macrophage response in the early stages of L. pneumophila infection. This conclusion was bolstered by showing that (i) chem. inhibitors of TLR3 and TLR4 dampen the cytokine output of primary human macrophages and (ii) transfection of TLR3 and TLR4 into HEK cells conferred an ability to sense L. pneumophila. TLR3- and TLR4-dependent cytokines promoted migration of human HL-60 neutrophils across an epithelial layer, pointing to the biol. importance for the newfound signaling pathway. The response of U937 cells to L. pneumophila LPS was dependent upon TLR4, a further contradiction to murine-based studies, which had concluded that TLR2 is the receptor for Legionella LPS. Given the role of TLR3 in sensing nucleic acid (i.e., dsRNA), we utilized newly-made KO U937 cells to document that DNA-sensing by cGAS-STING and DNA-PK are also needed for the response of human macrophages to L. pneumophila. Given the lack of attention given them in the bacterial field, C-type lectin receptors were similarly examined; but, they were not required. Overall, this study arguably represents the most extensive, single-characterization of Legionella-recognition receptors within human macrophages. 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.Category: chlorides-buliding-blocks 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

Recommanded Product: (R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate《Cutaneous ischemia-reperfusion injury is exacerbated by IL-36 receptor antagonist deficiency》 was published in 2022. The authors were Tanaka, Y.;Iwata, Y.;Saito, K.;Fukushima, H.;Watanabe, S.;Hasegawa, Y.;Akiyama, M.;Sugiura, K., and the article was included in《Journal of the European Academy of Dermatology and Venereology》. The author mentioned the following in the article:

Loss-of-function homozygous or compound heterozygous mutations in IL36RN, which encodes interleukin-36 receptor antagonist (IL-36Ra), has been implicated in the pathogenesis of skin disorders. However, the pathogenic role of IL-36Ra in cutaneous ischemia-reperfusion (I/R) injury remains unclear. We investigated the role of IL36Ra in cutaneous I/R injury. We examined I/R injury in Il36rn^-/- mice. The area of wounds, numbers of infiltrated cells, apoptotic cells and neutrophil extracellular trap (NET) formation were assessed. The expression levels of various genes were analyzed using real-time RT-PCR. The expression of high mobility group box 1 (HMGB1), an endogenous toll-like receptor (TLR) 4 ligand, was confirmed using immunohistol., and serum HMGB1 levels were measured by ELISA. Cytokine production by stimulated cultured J774A.1 and HaCaT cells was examined IL-36Ra deficiency resulted in significantly delayed wound healing and increased neutrophil and macrophage infiltration into the wound tissues. Il36rn-/- mice had increased mRNA expression levels of CXCL1, CXCL2, CCL4, TNF-α, TGF-β, IL-1β, IL-6 and IL-36γ relative to wild-type mice. Apoptosis was identified in keratinocytes by TUNEL assay. HMGB1 expression in the I/R site was decreased in both keratinocytes and adnexal cells, while serum HMGB1 levels were significantly elevated after reperfusion. The mRNA levels of various cytokines, including IL-1β, were elevated in J774A.1 cells through TLR4 signalling by HMGB1 stimulation. In addition, HaCaT cells stimulated with IL-1β showed significantly increased CXCL1, TNF-α, IL-6, IL-36β and IL-36γ mRNA expression. Furthermore, NET formation was increased by IL-36Ra deficiency. Finally, either the blockade of TLR4 signalling by TAK-242 or inhibition of NET formation by Cl-amidine normalized exacerbated I/R injury in Il36rn-/- mice. This study indicated that IL-36Ra deficiency exacerbates cutaneous I/R injury due to excessive inflammatory cell recruitment, NET formation, and excessive cytokine and chemokine production via the TLR4 pathway by HMGB1 released from epidermal apoptotic cells. 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).Recommanded Product: (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

COA of Formula: C15H17ClFNO4SIn 2022, Liu, Litong;Yang, Xu;Yuan, Pengfei;Cai, Shanshan;Bao, Jing;Zhao, Yanan;Aimaier, Alimu;Aipire, Adila;Lu, Jun;Li, Jinyao published 《In Vitro and In Vivo Dendritic Cell Immune Stimulation Effect of Low Molecular Weight Fucoidan from New Zealand Undaria pinnatifida》. 《Marine Drugs》published the findings. The article contains the following contents:

Low mol. weight fucoidan (LMWF) has been reported to have immunomodulation effects through the increase of the activation and function of macrophages. In this study, the regulating effect of LMWF from Undaria pinnatifida grown in New Zealand on dendritic cells (DCs) was investigated. We discovered that LMWF could stimulate DCs’ maturation and migration, as well as CD4+ and CD8+ T cells’ proliferation in vitro. We proved that this immune promoting activity is activated through TLR4 and its downstream MAPK and NF-κB signaling pathways. Further in vivo (mouse model) investigation showed that LMWF has a strong immunol. boosting effect, such as facilitating the proliferation of immune cells and increasing the index of immune organs. These findings suggest that LMWF has a pos. immunomodulatory effect and is a promising candidate to supplement cancer immunotherapy.(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.COA of Formula: 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

Synthetic Route of C15H17ClFNO4S《Astaxanthin protects against early acute kidney injury in severely burned rats by inactivating the TLR4/MyD88/NF-κB axis and upregulating heme oxygenase-1》 was published in 2021. The authors were Guo, Songxue;Guo, Linsen;Fang, Quan;Yu, Meirong;Zhang, Liping;You, Chuangang;Wang, Xingang;Liu, Yong;Han, Chunmao, and the article was included in《Scientific Reports》. The author mentioned the following in the article:

Early acute kidney injury (AKI) contributes to severe morbidity and mortality in critically burned patients. Renal inflammation plays a vital role in the progression of early AKI, acting as a therapeutic target. Astaxanthin (ATX) is a strong antioxidant widely distributed in marine organisms that exerts many biol. effects in trauma and disease. ATX is also suggested to have anti-inflammatory activity. Hence, we attempted to explore the role of ATX in protecting against early postburn AKI via its anti-inflammatory effects and the related mechanisms. A severely burned model was established for histol. and biochem. assessments based on adult male rats. We found that oxidative stress-induced tissue inflammation participated in the development of early AKI after burn injury and that the MyD88-dependent TLR4/NF-κB pathway was activated to regulate renal inflammation. The TLR4 and NF-κB inhibitors TAK242 and PDTC showed similar effects in attenuating burn-induced renal inflammation and early AKI. Upon ATX treatment, the release of inflammatory mediators in the kidneys was downregulated, while the TLR4/MyD88/NF-κB axis was inhibited in a dose-related manner. TAK242 and PDTC could enhance the anti-inflammatory effect of high-dose ATX, whereas lipopolysaccharide (LPS) reversed its action. Furthermore, the expression of heme oxygenase (HO)-1 was upregulated by ATX in a dose-related manner. Collectively, the above data suggest that ATX protects against renal inflammation in a dose-related manner by regulating the TLR4/MyD88/NF-κB axis and HO-1 and ultimately prevents early AKI following severe burns. 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

Calmasini, Fabiano B.;Alexandre, Eduardo C.;Oliveira, Mariana G.;Silva, Fabio H.;Soares, Antonio G.;Costa, Soraia K. P.;Antunes, Edson published 《Lipopolysaccharide reduces urethral smooth muscle contractility via cyclooxygenase activation》 in 2021. The article was appeared in 《Journal of Physiology and Biochemistry》. They have made some progress in their research.Reference of (R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate The article mentions the following:

In the present study, we evaluated the functional and mol. effects of LPS in mouse USM in vitro, focusing on the LPS-induced TLR4-signaling pathway. Male C57BL6/JUnib and TLR4 knockout mice (TLR4 KO) were used. The USM contraction was performed in the presence of LPS (62.5-500μg/mL), indomethacin (10μM), L-NAME (100μM), and TAK 242 (1μM). The RT-PCR assay for the IL-1β, NF-kB, and COX-2 genes was also evaluated in the presence of LPS (125μg/mL) and caspase 1 inhibitor (20μM). Our results showed that LPS reduces mouse USM contraction elicited by phenylephrine and vasopressin. This LPS-induced urethral inhibitory effect was not reversed by the TLR4 inhibition or its absence in the TLR4 KO mice. Conversely, indomethacin (but not L-NAME) reversed the LPS-induced USM hypocontractility. Mol. protocols indicated upregulation of IL-1β, NF-kβ, and COX-2 mRNA upon LPS incubation, which were blunted by caspase 1 inhibition. Our data showed that LPS reduced mouse USM contraction independently of TLR4 activation, involving caspase 1 and IL1β, NF-kB, and COX-2 gene overexpression. Therefore, this alternative pathway might be a valuable target to reduce the LPS-induced urethral dysfunction under infection and inflammatory conditions. 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.Reference 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

Safety of (R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylateIn 2022, Liu, Yanyao;Pu, Xingyu;Qin, Xiaoyan;Gong, Junhua;Huang, Zuotian;Luo, Yunhai;Mou, Tong;Zhou, Baoyong;Shen, Ai;Wu, Zhongjun published 《Neutrophil extracellular traps regulate HMGB1 translocation and kupffer cell M1 polarization during acute liver transplantation rejection》. 《Frontiers in Immunology》published the findings. The article contains the following contents:

Neutrophil extracellular traps (NETs) play important roles in hepatic ischemic reperfusion injury (IRI) and acute rejection (AR)-induced immune responses to inflammation. After liver transplantation, HMGB1, an inflammatory mediator, contributes to the development of AR. Even though studies have found that HMGB1 can promote NET formation, the correlation between NETs and HMGB1 in the development of AR following liver transplantation has not been elucidated. In this study, levels of serum NETs were significantly elevated in patients after liver transplantation. Moreover, we found that circulating levels of NETs were neg. correlated with liver function. In addition, liver transplantation and elevated extracellular HMGB1 promoted NET formation. The HMGB1/ TLR-4/MAPK signaling pathway, which is initiated by HMGB1, participates in NET processes. Moreover, in the liver, Kupffer cells were found to be the main cells secreting HMGB1. NETs induced Kupffer cell M1 polarization and decreased the intracellular translocation of HMGB1 by inhibiting DNase-1. Addnl., co-treatment with TAK-242 (a TLR-4 inhibitor) and rapamycin more effectively alleviated the damaging effects of AR following liver transplantation than either drug alone. 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.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

Reynolds, Kathryn E.;Krasovska, Victoria;Scott, Angela L. published 《Converging purinergic and immune signaling pathways drive IL-6 secretion by Fragile X cortical astrocytes via STAT3》 in 2021. The article was appeared in 《Journal of Neuroimmunology》. 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:

Fragile X syndrome (FXS), the most common heritable form of autism spectrum disorder (ASD), is characterized by an absence of the FMRP protein resulting from expanded and hypermethylated CGG repeats within the Fmr1 gene. FXS are driven in part by abnormal glial-mediated function. FXS astrocytes release elevated levels of immune-related factors interleukin-6 (IL-6) and tenascin C (TNC), and also demonstrate increased purinergic signaling, a pathway linked to signaling factor release. Here, in cortical astrocytes from the Fmr1 knockout (KO) FXS mouse model, purinergic agonism enhanced TNC secretion and STAT3 phosphorylation, two processes linked to elevated IL-6 secretion in FXS, while STAT3 knockdown and TLR4 antagonism normalized Fmr1 KO IL-6 release. Author therefore suggest that purinergic signaling and immune regulatory pathways converge to drive FXS cortical pro-inflammatory responses.(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.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

HPLC of Formula: 243984-11-4In 2022, Oh, Ki-Kwang;Adnan, Md.;Cho, Dong-Ha published 《Drug Investigation to Dampen the Comorbidity of Rheumatoid Arthritis and Osteoporosis via Molecular Docking Test》. 《Current Issues in Molecular Biology》published the findings. The article contains the following contents:

At present, most rheumatoid arthritis (RA) patients are at risk of osteoporosis (OP), which is increased by 1.5 times compared to non-RA individuals. Hence, we investigated overlapping targets related directly to the occurrence and development of RA and OP through public databases (DisGeNET, and OMIM) and literature. A total of 678 overlapping targets were considered as comorbid factors, and 604 out of 678 were correlated with one another. Interleukin 6 (IL-6), with the highest degree of value in terms of protein-protein interaction (PPI), was considered to be a core target against comorbidity. We identified 31 existing small mols. (< 1000 g/mol) as IL-6 inhibitors, and 19 ligands were selected by the 3 primary criteria (Lipinski′s rule, TPSA, and binding energy). We postulated that MD2-TLR4-IN-1 (PubChem ID: 138454798), as confirmed by the three criteria, was the key ligand to alleviate comorbidity between RA and OP. In conclusion, we described a promising active ligand (MD2-TLR4-IN-1), and a potential target (IL-6) against comorbidity of RA and OP, providing scientific evidence for a further clin. trial. 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.HPLC of Formula: 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