Category: 243984-11-4

Jing, Na;Fang, Bo;Li, Zhe;Tian, Ayong published 《Exogenous activation of cannabinoid-2 receptor modulates TLR4/MMP9 expression in a spinal cord ischemia reperfusion rat model》 in 2020. The article was appeared in 《Journal of Neuroinflammation》. They have made some progress in their research.HPLC of Formula: 243984-11-4 The article mentions the following:

Background: Cannabinoid-2 receptor (CB2R) plays an important role in the cascading inflammation following ischemic injury. The toll-like receptors 4 (TLR4)/matrix metalloproteinase 9 (MMP9) signal pathway is involved in blood-brain barrier dysfunction induced by ischemia stroke. The aim of this study is to investigate the roles of exogenous activation of CB2R on attenuating neurol. deficit and blood-spinal cord barrier (BSCB) disruption during rat spinal cord ischemia reperfusion (I/R) injury, through modulation of the TLR4/MMP9 axis. Methods: Animals were i.p. pretreated with TLR4 inhibitor TAK-242, CB2R agonist JWH-133 with or without CB2R antagonist AM630, or equivalent volume of vehicle 1 h before undergoing 14-min occlusion of descending aorta or sham operation. One, two, three, and 7 days after reperfusion, hindlimb locomotor function was evaluated with Basso, Beattie, and Bresnahan (BBB) Locomotor Scale, BSCB integrity was detected by measurement of Evans blue (EB) extravasation and spinal cord edema. The protein expression levels of CB2R, tight junction protein Zonula occluden-1 (ZO-1), TLR4, MMP9, MyD88, NF-κB p65, and NF-κB p-p65 were determined by western blot. The MMP9 activity was analyzed by gelatin zymog. Double immunofluorescence staining was used to identify the perivascular localization of CB2R, TLR4, MMP9, and reactive astrocytes, as well as the colocalization of CB2R, TLR4, and MMP9 with reactive astrocytes. Results: JWH-133 pretreatment attenuated hindlimb motor functional deficit and BSCB leakage, along with preventing downregulation of ZO-1 and upregulation of TLR4/MMP9, similar to the effects of TAK-242 preconditioning. JWH-133 or TAK-242 pretreatment reduced the perivascular expression of TLR4/MMP9 and reactive astrocytes following injury. JWH-133 pretreatment also downregulated MyD88/NF-κB level, MMP9 activity, and the astrocytic TLR4/MMP9 after I/R injury. Conclusions: Exogenous activation of CB2R by JWH-133 attenuated neurol. deficit and BSCB disruption after spinal cord I/R injury via inhibition of TLR4/MMP9 expression. 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.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

Category: chlorides-buliding-blocks《Toll-like receptor 4 inhibition ameliorates mesencephalic substantia nigra injury in neonatal rats exposed to lipopolysaccharide via regulation of neuro-immunity》 was published in 2020. The authors were He, Wei;Jiang, Mei;Mao, Ping;Yan, Fang, and the article was included in《Brain Research Bulletin》. The author mentioned the following in the article:

Toll-like receptor 4 (TLR4) is a transmembrane protein which is widely distributed in nerve cells. Its activation will activate the innate immune system through increasing an intracellular signaling pathway NF-κB and inflammatory cytokine production Here, One-day-old rats were exposed to lipopolysaccharide (LPS, 1 mg/kg) as a sepsis model. We pre-treat neonatal rats with TAK-242, a TLR4 inhibitor, 1 day and 1 h before LPS injection to observe the neuroprotective effects on dopaminergic neurons of inhibition TLR4 in septic neonatal rats. The number of dopaminergic neurons in the mesencephalic substantia nigra in septic brain was significantly reduced. Meanwhile, the number of activated microglia was increased. The total number of lattice in the open field test of septic rats was less than that of control rats at the age of postnatal day 80 (PND80), the total time of septic rats to catch the rope in the grip traction test was less than the control rats at the age of PND80, and the septic rats were easier to slide down in the slopes experiment However, TAK-242 administration significantly ameliorated LPS-induced dopaminergic neurons loss, prevented microglia activation, and improved behavioral test results of septic rats. We also found that TLR4 inhibition decreased the LPS-induced high expressions of NF-κB p65 and IL-1β of microglia. In conclusion, TLR4 inhibition showed neuroprotective effects on septic neonatal rats via regulation of neuro-immunity.(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) can reduces lesion volume in a mouse model of cerebral cavernous malformations (CCMs).Category: chlorides-buliding-blocks 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 2022, Zaniani, Nosaibeh Riahi;Roohbakhsh, Ali;Moghimi, Ali;Mehri, Soghra published 《Protective effect of Toll-like receptor 4 antagonist on inflammation, EEG, and memory changes following febrile seizure in Wistar rats》. 《Behavioural Brain Research》published the findings. The article contains the following contents:

Neuroinflammation and fever are the main triggers in febrile seizures (FS). Focusing on inflammatory pathways and anti-inflammatory drugs could compensate for the limitations of existing medications. The aim of this study is to evaluate the neuroprotective effect of specific antagonizing Toll-like receptor 4 (TLR4), as a prominent inflammatory axis, on the consequences of FS and adulthood using animal models. Complex FS was induced on 9-11 day old male rat pups using a heated chamber. TAK-242, as a specific TLR4 inhibitor, was injected i.p. before seizure induction. Seizure threshold, duration, and spike number were measured by electrocorticog. The levels of inflammatory cytokines, TLR4 protein expression, and oxidative stress markers were detected by ELISA, western blotting, malondialdehyde (MDA), catalase (CAT), and superoxide dismutase (SOD) assessments in the cortex and hippocampus. Also, spatial and non-spatial memory were evaluated using the novel object recognition test (NORT) and double Y-maze test during adulthood. The results revealed that provoked inflammatory responses in neonate rats, after FS, were associated with the increase of the tumor necrosis factor alpha, interleukin-1β, and enhanced TLR4 protein expression. Meanwhile, based on performed behavioral tests, the inflammatory process was also involved in adulthood memory deficit. Pretreatment with TAK-242 reduced the inflammatory cytokines and TLR4 protein expression in the cortex and hippocampus of neonate rats and improvement in memory deficit in NORT and double Y-maze tasks. Also, pretreatment with TAK-242 elevated seizure threshold, SOD, and CAT activities, and decreased seizure duration and MDA level with no significant change in spike number TAK-242 possibly controlled FS via inhibiting 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) can reduces lesion volume in a mouse model of cerebral cavernous malformations (CCMs).Recommanded Product: 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

Product Details of 243984-11-4In 2021, Baakhlagh, Sedigheh;Kashani, Bahareh;Zandi, Zahra;Bashash, Davood;Moradkhani, Malihe;Nasrollahzadeh, Ali;Yaghmaei, Marjan;Mousavi, Seyed A.;Ghaffari, Seyed H. published 《Toll-like receptor 4 signalling pathway is correlated with pathophysiological characteristics of AML patients and its inhibition using TAK-242 suppresses AML cell proliferation》. 《International Immunopharmacology》published the findings. The article contains the following contents:

Acute myeloid leukemia (AML) is one of the most severe blood cancers. Many studies have revealed that inflammation has an essential role in the progression of hematopoietic malignancies. Since the toll-like receptor 4 (TLR4) pathway, an important pathway involved in inflammation induction, has previously been associated with solid tumors, we hypothesized that it would be correlated with the pathophysiol. characteristics of AML patients and could be considered as an anticancer target. We evaluated the mRNA expression of TLR4, MyD88, RelB, and NF-B using qRT-PCR in bone-marrow samples of 40 AML patients categorized into four groups according to prognosis, cell type, age, and drug response. Next, we explored the expression of these genes in three AML cell lines (NB4, U937, and KG-1) and used TAK-242, a specific inhibitor of TLR4, to investigate whether this inhibition could suppress AML cell proliferation using cell-cycle anal. The effect of TAK-242 on arsenic trioxide (ATO) cytotoxicity was also assessed. The results of qRT-PCR showed that most genes had higher expression in patients with poor prognosis or drug-resistant statues. They were also overexpressed in patients with less-differentiated cells. Moreover, TAK-242 inhibited cell proliferation of all the cell lines and altered their cell cycle distribution. It could also intensify the cytotoxicity of ATO in combination therapy. In sum, the TLR4 pathway was related to pathophysiol. characteristics of AML and its inhibition using TAK-242 could be considered as a promising treatment strategy in the TLR4 expressing AML cells, individually or in combination with ATO. 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).Product Details 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

Formula: C15H17ClFNO4SIn 2021, Huck, Nolan A.;Siliezar-Doyle, Janelle;Haight, Elena S.;Ishida, Ryosuke;Forman, Thomas E.;Wu, Shaogen;Shen, Huaishuang;Takemura, Yoshinori;Clark, J. David;Tawfik, Vivianne L. published 《Temporal contribution of myeloid-lineage TLR4 to the transition to chronic pain: a focus on sex differences》. 《Journal of Neuroscience》published the findings. The article contains the following contents:

Complex regional pain syndrome (CRPS) is a chronic pain disorder with a clear acute-to-chronic transition. Preclin. studies demonstrate that toll-like receptor 4 (TLR4), expressed by myeloid-lineage cells, astrocytes, and neurons, mediates a sex-dependent transition to chronic pain; however, evidence is lacking on which exact TLR4-expressing cells are responsible. We used complementary pharmacol. and transgenic approaches in mice to more specifically manipulate myeloid-lineage TLR4 and outline its contribution to the transition from acute-to-chronic CRPS based on three key variables: location (peripheral vs central), timing (prevention vs treatment), and sex (male vs female). We demonstrate that systemic TLR4 antagonism is more effective at improving chronic allodynia trajectory when administered at the time of injury (early) in the tibial fracture model of CRPS in both sexes. In order to clarify the contribution of myeloid-lineage cells peripherally (macrophages) or centrally (microglia), we rigorously characterize a novel spatiotemporal transgenic mouse line, Cx3CR1-Cre^ERT2-eYFP;TLR4^fl/fl (TLR4 cKO) to specifically knock out TLR4 only in microglia and no other myeloid-lineage cells. Using this transgenic mouse, we find that early TLR4 cKO results in profound improvement in chronic, but not acute, allodynia in males, with a significant but less robust effect in females. In contrast, late TLR4 cKO results in partial improvement in allodynia in both sexes, suggesting that downstream cellular or mol. TLR4-independent events may have already been triggered. Overall, we find that the contribution of TLR4 is time- and microglia-dependent in both sexes; however, females also rely on peripheral myeloid-lineage (or other TLR4 expressing) cells to trigger chronic pain. 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.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

Chen, Xiangwa;Deng, Tao;Huo, Tingting;Dong, Faqin;Deng, Jianjun published 《MiR-140-5p/TLR4 /NF-kappa B signaling pathway: Crucial role in inflammatory response in 16HBE cells induced by dust fall PM2.5》. The research results were published in《Ecotoxicology and Environmental Safety》 in 2021.Quality Control of (R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate The article conveys some information:

Fine atm. particles with a diameter of 2.5μm or less (PM2.5) have a large sp. surface area, and carry a variety of organic matter, heavy metals, minerals and bacteria. They are an important risk factor in human non-communicable disease. To explore the mol. regulatory mechanism of the airway inflammation caused by PM2.5, an in vitro human bronchial epithelial (16HBE) cells poisoning model was deployed. Results showed that PM2.5 had a strong inhibitory effect on cells viability, and induced cells to secrete high levels of IL-6 and CXCL 8. These two biomarkers of inflammation were significantly reduced in the presence of TAK 242. TLR4, MyD88, IKK, and p-p65 proteins were highly expressed on exposure to PM2.5. Pretreatment with TAK 242 interfered with the activation of the TLR4 signaling pathway. By detecting the presence of lipopolysaccharides (LPS) in PM2.5 which had been autoclaved, it was speculated that the activation of the TLR4/NF-κB signaling pathway may be mediated by LPS. It was demonstrated using gain- and loss- function experiments that miR-140-5p neg. regulated TLR4 to mediate inflammation in 16HBE cells. The dual-luciferase reporter assay confirmed that miR-140-5p directly binds to the 3′ untranslated region (3′ UTR) of TLR4 to initiate biol. activity. In conclusion, this study revealed a new mechanism by which the miR-140-5p/TLR4 signaling pathway mediated the inflammatory response of 16HBE cells induced by PM2.5. Differential expression of miRNA, and the activation of the TLR4/NF-kappa B signaling pathway induced by PM2.5 implicates PM2.5 in the pathogenesis of airway inflammation.(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) 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

Reference of (R)-Ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-enecarboxylate《Toll-like receptors in the mechanism of tributyltin-induced production of pro-inflammatory cytokines, IL-1β and IL-6》 was published in 2022. The authors were Alcala, Aliyah;Osborne, Brooke;Allen, Blake;Seaton-Terry, Aleshia;Kirkland, Toran;Whalen, Margaret, and the article was included in《Toxicology》. The author mentioned the following in the article:

Tributyltin (TBT) is an environmental contaminant due to its use in a variety of applications as a biocide, including in marine anti-fouling paints. It has been detected in a number of human tissues including blood. Previous studies have shown that exposure to TBT increases the cellular production (secretion plus intracellular levels) of the pro-inflammatory cytokines IL-1β and IL-6 by peripheral blood mononuclear cells (PMBCs) and this increase requires MAPK activation. Toll-like receptors (TLR) activate immune cells to produce pro-inflammatory cytokines in response to pathogen associated mol. patterns (PAMPs) and damage associated mol. patterns (DAMPs) leading to activation of MAPKs as well as other intracellular components that regulate cytokine production The current study shows that selective inhibition of TLRs 4,1/2, and 8 diminishes the ability of TBT to stimulate IL-1β and IL-6 production However, selective inhibition of TLR3 enhanced the TBT-induced production of IL-1β. This indicates that TBT may be either directly or indirectly interacting with certain TLR receptors as part of its mechanism of stimulating pro-inflammatory cytokine production These results provide an important advance in understanding TBT stimulation of IL-1β and IL-6, which has the potential to cause chronic inflammation and its attendant pathologies. 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).Reference 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

Product Details of 243984-11-4《P53 affects epigenetic signature on SOCS1 promoter in response to TLR4 inhibition》 was published in 2021. The authors were Sheikh, Touseef;Sen, Ellora, and the article was included in《Cytokine+》. The author mentioned the following in the article:

Suppressor of cytokine signaling (SOCS1) functions as a neg. regulator of toll-like receptor (TLR) induced inflammatory signaling. As silencing of SOCS1 is concomitant with elevated TLR4 levels in glioblastoma, we investigated the effect of TLR4 inhibition on SOCS1 expression. Pharmacol. inhibition of TLR4 signaling by TAK242 or its siRNA-mediated knockdown in p53 mutant or wild-type glioma cells resulted in either increased or decreased SOCS1 expression and promoter activity, resp. Genetic manipulation of p53 indicated that SOCS1 expression upon TLR4 inhibition is dependent on p53 mutational status. Increased SOCS1 level was concomitant with diminished nucleosomal occupancy around p53-binding site on SOCS1 promoter. This altered nucleosomal landscape was accompanied by (i) diminished nuclear H3K9me3 and (ii) increased JMJD2A and Brg1 levels. JMJD2A inhibition or ectopic expression of ATPase-deficient BRG1 prevented TAK242 mediated increase in SOCS1 expression. Recruitment of Brg1-p53-JMJD2A complex on p53 binding sites of SOCS1 promoter upon TLR4 inhibition was concomitant with increased SOCS1 expression in p53-mutant cells. The Cancer Genome Atlas (TCGA) dataset indicated an inverse correlation between TLR4 and SOCS1 levels in p53 mutant but not in p53WT GBM. Taken together, p53 mutational status regulates transcriptional plasticity of SOCS1 promoter through differential recruitment of chromatin remodelers and epigenetic regulators in response to TLR4 inhibition.(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) can reduces lesion volume in a mouse model of cerebral cavernous malformations (CCMs).Product Details 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

Fang, Bin;Wen, Shujuan;Li, Yan;Bai, Facheng;Wei, Yuanyuan;Xiong, Yuhua;Huang, Quanfang;Lin, Xing published 《Prediction and verification of target of helenalin against hepatic stellate cell activation based on miR-200a-mediated PI3K/Akt and NF-κB pathways》 in 2021. The article was appeared in 《International Immunopharmacology》. They have made some progress in their research.Related Products of 243984-11-4 The article mentions the following:

Hepatic stellate cell (HSC) activation is a crucial event in the progress of liver fibrosis. In this study, the target of helenalin was firstly predicted by bioinformatics anal., and then the prediction was verified by various experiments The HSC-T6 cells were activated by interleukin-1 beta (IL-1β) and then treated with helenalin. Moreover, HSC-T6 cells were transfected with miR-200a mimic or inhibitor, and the effect of helenalin on the miR-200a-mediated PI3K/Akt and NF-κB signaling pathways was investigated. The bioinformatics anal. indicated that miR-200a might regulate the PI3K/Akt pathway, NF-κB activation, Bcl-2 family and Caspases, ultimately affecting cell survival and apoptosis. Interestingly, the mol. docking demonstrated that the target of helenalin might be miR-200a-mediated the PI3K/Akt and NF-κB pathways. Moreover, the experiments showed that helenalin administration led to the inactivation of HSC-T6 cells, as evidenced by the inhibition of cell proliferation, α-SMA expression and collagen production The mechanism studies showed that helenalin reduced collagen accumulation by restoring the balance of MMPs/TIMPs. Moreover, helenalin markedly suppressed HSC activation by inhibiting the PI3K/Akt pathway and alleviated inflammatory response by blocking the NF-κB signal transduction. Further study indicated that helenalin up-regulated miR-200a expression, thus leading to the inhibition of the PI3K/Akt and NF-κB signaling pathways. In conclusion, helenalin inhibits HSC activation via inhibiting the miR-200a-mediated PI3K/Akt and NF-κB pathways, and it may be developed as a potential medicine for the treatment of liver fibrosis. 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

Synthetic Route of C15H17ClFNO4SIn 2022, Tao, Yuheng;Ma, Junmei;Huang, Caoxing;Lai, Chenhuan;Ling, Zhe;Yong, Qiang published 《The immunomodulatory activity of degradation products of Sesbania cannabina galactomannan with different molecular weights》. 《International Journal of Biological Macromolecules》published the findings. The article contains the following contents:

Galactomannan (GM) is widely recognized as an immune enhancer; however, the underlying mol. mechanism is still unknown. Herein, four products with mol. weights in descending order, namely GM40, GM50, GM65, and GMOS, were separated from incomplete degradation products of Sesbania cannabina GM by ethanol precipitation, followed by their immunomodulatory activity. Through FTIR and XPS spectra, the amount of free hydroxyl groups was shown to decrease in the following order: GM > GM50 > GMOS > GM40 > GM65. Moreover, the immunomodulatory activity of different products decreased in abovementioned order. The TNF-α, IL-6 and TLR4 content in RAW 264.7 cells treated with different GM products in the presence or absence of TAK-242 (TLR4 inhibitor) suggested that the immunomodulatory activity of GM and its degradation products is TLR4-dependent. Overall, the preliminary relationship indicated here between the hydroxyl groups or the possible deeper structural changes of GM and the immunomodulatory activity need to be further investigated. 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).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