Month: October 2022

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

Yeung, Chi-Tung;Chan, Wesley Ting Kwok;Lo, Wai-Sum;Law, Ga-Lai;Wong, Wing-Tak published 《Synthesis of a conformationally stable atropisomeric pair of biphenyl scaffold containing additional stereogenic centers》 in 2019. The article was appeared in 《Molecules》. They have made some progress in their research.Synthetic Route of C10H13ClO3 The article mentions the following:

The synthesis of a new CF₃-containing stereogenic atropisomeric pair of ortho-disubstituted biphenyl scaffolds I and II is presented. The atropisomers are surprisingly conformationally stable for isolation. X-ray structures show that their stability comes from an intramol. hydrogen bond formation from their two hydroxyl groups and renders the spatial arrangement of their peripheral CF₃ and CH₃ groups very different. The synthesized stereogenic scaffolds proved to be effective in catalyzing the asym. N-nitroso aldol reaction of enamines III [X = O, C, Y = (CH₂)_n, n = 1; X = C, Y = (CH₂)_n, n = 0] and nitrosobenzene. Compared to similar scaffolds without CF₃ groups, one of the atropisomers exhibits an increase in enantioselectivity in this reaction.(1S)-4,7,7-Trimethyl-3-oxo-2-oxabicyclo[2.2.1]heptane-1-carbonyl chloride(Chunks or pellets) (cas: 39637-74-6) were involved in the experimental procedure.

(1S)-4,7,7-Trimethyl-3-oxo-2-oxabicyclo[2.2.1]heptane-1-carbonyl chloride(Chunks or pellets) (cas: 39637-74-6 Synthetic Route of C10H13ClO3) is used as a resolving agent for alcohols as the diastereomeric esters by crystallization or chromatography and as a chiral derivatization reagent for determination of enantiomeric excess of alcohols and amines.

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