Tag: 100-200

Electric Literature of C6H7N3O《Identification and characterization of teratogenic chemicals using embryonic stem cells isolated from a wnt/β-catenin-reporter transgenic mouse line》 was published in 2016. The authors were Kugler, Josephine;Kemler, Rolf;Luch, Andreas;Oelgeschlaeger, Michael, and the article was included in《Toxicological Sciences》. The author mentioned the following in the article:

Embryonic stem cells (ESCs) are commonly used for the anal. of gene function in embryonic development and provide valuable models for human diseases. In recent years, ESCs have also become an attractive tool for toxicol. testing, in particular for the identification of teratogenic compounds The authors have recently described a Bmp-reporter ESC line as a new tool to identify teratogenic compounds and to characterize the mol. mechanisms mediating embryonic toxicity. Here the authors describe the use of a Wnt/β-Catenin-reporter ESC line isolated from a previously described mouse line that carries the LacZ reporter gene under the control of a β-Catenin responsive promoter. The reporter ESC line stably differentiates into cardiomyocytes within 12 days. The reporter was endogenously induced between day 3-5 of differentiation reminiscent of its expression in vivo, in which strong LacZ activity is detected around gastrulation. Subsequently its expression becomes restricted to mesodermal cells and cells undergoing an epithelial to mesenchymal transition. The Wnt/β-Catenin-dependent expression of the reporter protein allowed quantification of dose- and time-dependent effects of teratogenic chems. In particular, valproic acid reduced reporter activity on day 7, whereas retinoic acid induced reporter activity on day 5 at concentrations comparable to the ones inhibiting the formation of functional cardiomyocytes, the classical read-out of the embryonic stem cell test (EST). In addition, the authors were also able to show distinct effects of teratogenic chems. on the Wnt/β-Catenin-reporter compared with the previously described Bmp-reporter ESCs. Thus, different reporter cell lines provide complementary tools for the identification and anal. of potentially teratogenic compounds The experimental procedure involved many compounds, such as 6-Aminonicotinamide (cas: 329-89-5) .

6-Aminonicotinamide (cas:329-89-5)Electric Literature of C6H7N3O is an aminopyridine, which is a specific pentose inhibitor and thus inhibits the NADP production.It can be used as a reactant for the synthesis of 6-substituted imidazo[1,2-a]pyridines with potential application as chemotherapeutic drugs.

Reference:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

Zhang, Qiao;Yang, Zhe;Ni, Yueli;Bai, Honggang;Han, Qiaoqiao;Yi, Zihan;Yi, Xiaojia;Agbana, Yannick Luther;Kuang, Yingmin;Zhu, Yuechun published 《NF-κB and pSTAT3 synergistically drive G6PD overexpression and facilitate sensitivity to G6PD inhibition in ccRCC》. The research results were published in《Cancer Cell International》 in 2020.Formula: C6H7N3O The article conveys some information:

Glucose 6-phosphate dehydrogenase (G6PD) serves key roles in cancer cell metabolic reprogramming, and has been reported to be involved in certain carcinogenesis. Previous results from our laboratory demonstrated that overexpressed G6PD was a potential prognostic biomarker in clear cell renal cell carcinoma (ccRCC), the most common subtype of kidney cancer. G6PD could stimulate ccRCC growth and invasion through facilitating reactive oxygen species (ROS)-phosphorylated signal transducer and activator of transcription 3 (pSTAT3) activation and ROS-MAPK-MMP2 axis pathway, resp. However, the reasons for ectopic G6PD overexpression and the proliferation repressive effect of G6PD inhibition in ccRCC are still unclear. The impact of ROS accumulation on NF-κB signaling pathway and G6PD expression was determined by real-time RT-PCR and Western blot in ccRCC cells following treatment with ROS stimulator or scavenger. The regulatory function of NF-κB signaling pathway in G6PD transcription was analyzed by real-time RT-PCR, Western blot, luciferase and ChIP assay in ccRCC cells following treatment with NF-κB signaling activator/inhibitor or lentivirus infection. ChIP and Co-IP assay was performed to demonstrate protein-DNA and protein-protein interaction of NF-κB and pSTAT3, resp. MTS assay, human tissue detection and xenograft model were conducted to characterize the association between NF-κB, pSTAT3, G6PD expression level and proliferation functions. ROS-stimulated NF-κB and pSTAT3 signaling over-activation could activate each other, and exhibit cross-talks in G6PD aberrant transcriptional regulation. The underlying mechanism was that NF-κB signaling pathway facilitated G6PD transcription via direct DNA-protein interaction with p65 instead of p50. p65 and pSTAT3 formed a p65/pSTAT3 complex, occupied the pSTAT3-binding site on G6PD promoter, and contributed to ccRCC proliferation following facilitated G6PD overexpression. G6PD, pSTAT3, and p65 were highly expressed and pos. correlated with each other in ccRCC tissues, confirming that NF-κB and pSTAT3 synergistically promote G6PD overexpression. Moreover, G6PD inhibitor exhibited tumor-suppressor activities in ccRCC and attenuated the growth of ccRCC cells both in vitro and in vivo. ROS-stimulated aberrations of NF-κB and pSTAT3 signaling pathway synergistically drive G6PD transcription through forming a p65/pSTAT3 complex. Moreover, G6PD activity inhibition may be a promising therapeutic strategy for ccRCC treatment. To complete the study, the researchers used 6-Aminonicotinamide (cas: 329-89-5) .

6-Aminonicotinamide (cas:329-89-5)Formula: C6H7N3O is a monocarboxylic acid amide resulting from the formal condensation of the carboxy group of 6-aminonicotinic acid with ammonia. An inhibitor of the NADP(+)-dependent enzyme,6-phosphogluconate dehydrogenase, it interferes with glycolysis.

Reference:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

Li, Mingyang;Lian, De;Zhao, Fugang;Tong, Xiong;Wu, Chaoyang;Gao, Xiangpeng published 《Structure-activity of chelating depressants for chalcopyrite/pyrite separation: DFT study and flotation experiment》. The research results were published in《Physicochemical Problems of Mineral Processing》 in 2021.Category: amides-buliding-blocks The article conveys some information:

Three types of chelating depressants were studied for chalcopyrite/pyrite separation, including S-S, S-O, and O-O types, via d. functional theory calculations and microflotation. The calculation results indicate that the depressant’s chelating atoms have large coefficient and great activity according to the mol. frontier orbital (HOMO and LUMO) and the orbital coefficients For S-S type of depressant, S atom in both keto or enol forms won’t affect their HOMO and LUMO patterns and the orbital contributions. For S-O type, the presence of N atom in the ring structure of a mol. will increase the reactivity of O-Cu while weak S-Cu. For O-O type, the electron supply capacity of benzene ring is higher than strain chain, and atom N in strain chain increased their electron supply capacity. The microflotation results basically confirmed the prediction based on the calculation The simulation results demonstrate that the interaction of a depressant with metals and minerals are affected obviously by the spatial structure and electronic structure of an atom in its mol.N,2-Dihydroxybenzamide (cas: 89-73-6) were involved in the experimental procedure.

N,2-Dihydroxybenzamide(cas: 89-73-6) can be used:To prepare phenylboronic acid-based bioconjugates for chromatographic applications;As a ligand to synthesize Fe(III), Cu(II), Ni(II) and Zn(II) complexes.Category: amides-buliding-blocks

Reference:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

Ren, Fang;Yang, Xiao;Hu, Zhong-Wen;Wong, Vincent Kam Wai;Xu, Hong-Yan;Ren, Ji-Hua;Zhong, Shan;Jia, Xiao-Jiong;Jiang, Hui;Hu, Jie-Li;Cai, Xue-Fei;Zhang, Wen-Lu;Yao, Fang-Long;Yu, Hai-Bo;Cheng, Sheng-Tao;Zhou, Hong-Zhong;Huang, Ai-Long;Law, Betty Yuen Kwan;Chen, Juan published 《Niacin analogue, 6-Aminonicotinamide, a novel inhibitor of hepatitis B virus replication and HBsAg production.》. The research results were published in《EBioMedicine》 in 2019.SDS of cas: 329-89-5 The article conveys some information:

BACKGROUND: Hepatitis B surface antigen (HBsAg) is one of the important clinical indexes for hepatitis B virus (HBV) infection diagnosis and sustained seroconversion of HBsAg is an indicator for functional cure. However, the level of HBsAg could not be reduced by interferons and nucleoside analogs effectively. Therefore, identification of a new drug targeting HBsAg is urgently needed. METHODS: In this study, 6-AN was screened out from 1500 compounds due to its low cytotoxicity and high antiviral activity. The effect of 6-AN on HBV was examined in HepAD38, HepG2-NTCP and PHHs cells. In addition, the antivirus effect of 6-AN was also identified in mouse model. FINDINGS: 6-AN treatment resulted in a significant decrease of HBsAg and other viral markers both in vitro and in vivo. Furthermore, we found that 6-AN inhibited the activities of HBV SpI, SpII and core promoter by decreasing transcription factor PPARα, subsequently reduced HBV RNAs transcription and HBsAg production. INTERPRETATION: We have identified a novel small molecule to inhibit HBV core DNA, HBV RNAs, HBsAg production, as well as cccDNA to a minor degree both in vitro and in vivo. This study may shed light on the development of a novel class of anti-HBV agent. To complete the study, the researchers used 6-Aminonicotinamide (cas: 329-89-5) .

6-Aminonicotinamide (cas:329-89-5)SDS of cas: 329-89-5 is an aminopyridine, which is a specific pentose inhibitor and thus inhibits the NADP production.It can be used as a reactant for the synthesis of 6-substituted imidazo[1,2-a]pyridines with potential application as chemotherapeutic drugs.

Reference:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

Related Products of 89-73-6《Synthesis and crystal structure of a heterobimetallic nickel-manganese 12-metallacrown-4 methanol disolvate monohydrate compound》 was published in 2020. The authors were Hall, Abigail J.;Zeller, Matthias;Zaleski, Curtis M., and the article was included in《Acta Crystallographica, Section E: Crystallographic Communications》. The author mentioned the following in the article:

The synthesis and crystal structure of the title compound [systematic name: di-μ-acetato-tetrakis(μ₄-N,2-dioxidobenzene-1-carboximidato)hexamethanoltetramanganese(III)nickel(II) methanol disolvate monohydrate], [Mn₄Ni(C₇H₄NO₃)₄(C₂H₃O₂)₂(CH₄O)₆]·₂CH₄O·H₂O or Ni(OAc)₂[12-MC_{Mn(III)N(shi)}-4](CH₃OH)₆·2CH₃OH·H₂O, where MC is metallacrown,^–OAc is acetate, and shi^3-is salicylhydroximate, are reported. The macrocyclic metallacrown is positioned on an inversion center located on the Ni^II ion that resides in the central MC cavity. The macrocycle consists of an Mn^III-N-O repeat unit that recurs four times to generate an overall square-shaped mol. Both the NiII and Mn^III ions are six-coordinate with an octahedral geometry. In addition, the Mn^III ions possess an elongated Jahn-Teller distortion along the z-axis of the coordination environment. The interstitial water mol. is slightly offset from and disordered about an inversion center. And N,2-Dihydroxybenzamide (cas: 89-73-6) was used in the research process.

N,2-Dihydroxybenzamide(cas: 89-73-6) has also been shown to be active against wild-type strains of Candida glabrata, but not against resistant mutants. Related Products of 89-73-6 This drug may have therapeutic potential for bone cancer and metabolic disorders such as obesity.

Reference:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

Rawson, Frankie J.;Downard, Alison J.;Baronian, Keith H. published 《Electrochemical detection of intracellular and cell membrane redox systems in Saccharomyces cerevisiae》 in 2014. The article was appeared in 《Scientific Reports》. They have made some progress in their research.Application of 329-89-5 The article mentions the following:

Redox mediators can interact with eukaryote cells at a number of different cell locations. While cell membrane redox centers are easily accessible, the redox centers of catabolism are situated within the cytoplasm and mitochondria and can be difficult to access. We have systematically investigated the interaction of thirteen commonly used lipophilic and hydrophilic mediators with the yeast Saccharomyces cerevisiae. A double mediator system is used in which ferricyanide is the final electron acceptor (the reporter mediator). After incubation of cells with mediators, steady state voltammetry of the ferri/ferrocyanide redox couple allows quantitation of the amount of mediator reduced by the cells. The plateau current at 425 mV vs Ag/AgCl gives the anal. signal. The results show that five of the mediators interact with at least three different trans Plasma Membrane Electron Transport systems (tPMETs), and that four mediators cross the plasma membrane to interact with cytoplasmic and mitochondrial redox mols. Four of the mediators inhibit electron transfer from S. cerevisiae. Catabolic inhibitors were used to locate the cellular source of electrons for three of the mediators. To complete the study, the researchers used 6-Aminonicotinamide (cas: 329-89-5) .

6-Aminonicotinamide (cas:329-89-5)Application of 329-89-5 is an inhibitor of the NADP+-dependent enzyme, PGD (6-phosphogluconate dehydrogenase). Studies have also shown that 6-aminonicotinamide induces apoptosis in tumor cells and causes glial cell degeneration.

Reference:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

Takahashi, Bitoku;Funami, Hideaki;Shibata, Makoto;Maruoka, Hiroshi;Koyama, Makoto;Kanki, Satomi;Muto, Tsuyoshi published 《Structural optimization of ghrelin receptor inverse agonists to improve lipophilicity and avoid mechanism-based CYP3A4 inactivation》 in 2015. The article was appeared in 《Chemical & Pharmaceutical Bulletin》. They have made some progress in their research.COA of Formula: C6H7N3O The article mentions the following:

Structural optimization of 2-aminonicotinamide derivatives as ghrelin receptor inverse agonists is reported. So as to avoid mechanism-based inactivation (MBI) of CYP3A4, 1,3-benzodioxol ring of the lead compound was modified. Improvement of the main activity and lipophilicity was achieved simultaneously, leading to compound 18a, which showed high lipophilic ligand efficiency (LLE) and low MBI activity. To complete the study, the researchers used 6-Aminonicotinamide (cas: 329-89-5) .

6-Aminonicotinamide (cas:329-89-5)COA of Formula: C6H7N3O is an inhibitor of the NADP+-dependent enzyme, PGD (6-phosphogluconate dehydrogenase). Studies have also shown that 6-aminonicotinamide induces apoptosis in tumor cells and causes glial cell degeneration.

Reference:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

Recommanded Product: N,2-DihydroxybenzamideIn 2020, Li, Yu-Ting;Liu, Mei-Jun;Li, Ying;Liu, Peng;Zhao, Shi-Jie;Gao, Hui-Yuan;Zhang, Zi-Shan published 《Photoprotection by mitochondrial alternative pathway is enhanced at heat but disabled at chilling》. 《Plant Journal》published the findings. The article contains the following contents:

SUMMARY : The mitochondrial alternative pathway (AP) represents an important photoprotective mechanism for the chloroplast, but the temperature sensitivity of its photoprotective role is unknown. In this study, using the aox1a Arabidopsis mutant, the photoprotective role of the AP was verified under various temperatures, and the mechanism underlying the temperature sensitivity of the AP’s photoprotective role was clarified. It was observed that the photoprotective role of the AP increased with rising temperature but was absent at low temperature The photoprotective role of the AP was severely reduced under non-photorespiratory conditions. Disturbance of the AP inhibited the conversion of glycine to serine in mitochondria, which may restrain upstream photorespiratory metabolism and aggravate photoinhibition. With rising temperatures, photorespiration accelerated and the restraint of photorespiration caused by disturbance of the AP also increased, determining the temperature sensitivity of the AP’s photoprotective role. We also verified that not only the AP but also the cytochrome pathway in mitochondria contributes to photoprotection by maintaining photorespiration.N,2-Dihydroxybenzamide (cas: 89-73-6) were involved in the experimental procedure.

N,2-Dihydroxybenzamide(cas: 89-73-6) is a hydroxamic acid that inhibits the activity of p-hydroxybenzoic acid (PHBA) reductase, an enzyme involved in the conversion of PHBA to benzoic acid. Recommanded Product: N,2-Dihydroxybenzamide The compound has been shown to inhibit mitochondrial membrane potential and mitochondrial functions, leading to cell death.

Reference:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

Xiao, Wen-jing;Ma, Ting;Ge, Chun;Xia, Wen-juan;Mao, Yong;Sun, Run-bin;Yu, Xiao-yi;Aa, Ji-ye;Wang, Guang-ji published 《Modulation of the pentose phosphate pathway alters phase I metabolism of testosterone and dextromethorphan in HepG2 cells》. The research results were published in《Acta Pharmacologica Sinica》 in 2015.SDS of cas: 329-89-5 The article conveys some information:

Aim: The pentose phosphate pathway (PPP) is involved in the activity of glucose-6-phosphate dehydrogenase (G6PD) and generation of NADPH, which plays a key role in drug metabolism The aim of this study was to investigate the effects of modulation of the PPP on drug metabolism capacity in vitro. Methods: A pair of hepatic cell lines, ie, the cancerous HepG2 cells and normal L02 cells, was used. The expression of CYP450 enzymes, p53 and G6PD in the cells were analyzed. The metabolism of testosterone (TEST, 10 μmol/L) and dextromethorphan (DEM, 1 μmol/L), the two typical substrates for CYP3A4 and CYP2D6, in the cells was examined in the presence of different agents. Results: Both the expression and metabolic activities of CYP3A4 and CYP2D6 were considerably higher in HepG2 cells than in L02 cells. The metabolism of TEST and DEM in HepG2 cells was dose-dependently inhibited by the specific CYP3A4 inhibitor ketoconazole and CYP2D6 inhibitor quinidine. Addition of the p53 inhibitor cyclic PFT-α (5, 25 μmol/L) in HepG2 cells dose-dependently enhanced the metabolism of DEM and TEST, whereas addition of the p53 activator NSC 66811 (3, 10, 25 μmol/L) dose-dependently inhibited the metabolism Furthermore, addition of the G6PD inhibitor 6-aminonicotinamide (5, 15 μmol/L) in HepG2 cells dose-dependently inhibited the metabolism of DEM and TEST, whereas addition of the PPP activity stimulator menadione (1, 5, 15 μmol/L) dose-dependently enhanced the metabolism Conclusion: Modulation of p53 and the PPP alters the metabolism of DEM and TEST, suggesting that the metabolic flux pattern of PPP may be closely involved in drug metabolism and the individual variance. To complete the study, the researchers used 6-Aminonicotinamide (cas: 329-89-5) .

6-Aminonicotinamide (cas:329-89-5)SDS of cas: 329-89-5 is an aminopyridine, which is a specific pentose inhibitor and thus inhibits the NADP production.It can be used as a reactant for the synthesis of 6-substituted imidazo[1,2-a]pyridines with potential application as chemotherapeutic drugs.

Reference:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

Chen, Xiaoyi;Xu, Zhijie;Zhu, Zhijian;Chen, Anqi;Fu, Guanghou;Wang, Yimin;Pan, Hao;Jin, Baiye published 《Modulation of G6PD affects bladder cancer via ROS accumulation and the AKT pathway in vitro》. The research results were published in《International Journal of Oncology》 in 2018.Reference of 6-Aminonicotinamide The article conveys some information:

Glucose-6-phosphate dehydrogenase (G6PD) is a rate-limiting enzyme of the pentose phosphate pathway. Multiple studies have previously revealed that elevated G6PD levels promote cancer progression in numerous tumor types; however, the underlying mechanism remains unclear. In the present study, it was demonstrated that high G6PD expression is a poor prognostic factor in bladder cancer, and the levels of G6PD expression increase with increasing tumor stage. Patients with bladder cancer with high G6PD expression had worse survival rates compared with those with lower G6PD expression in resected tumors. In vitro experiments revealed that knockdown of G6PD suppressed cell viability and growth in Cell Counting Kit-8 and colony formation assays, and increased apoptosis in bladder cancer cell lines compared with normal cells. Further experiments indicated that the weakening of the survival ability in G6PD-knockdown bladder cancer cells may be explained by intracellular reactive oxygen species accumulation and protein kinase B pathway suppression. Furthermore, it was addnl. revealed that 6-aminonicotinamide (6-AN), a competitive G6PD inhibitor, may be a potential therapy for bladder cancer, particularly in cases with high G6PD expression, and that the combination of cisplatin and 6-AN may optimize the clin. dose or minimize the side effects of cisplatin. The experimental procedure involved many compounds, such as 6-Aminonicotinamide (cas: 329-89-5) .

6-Aminonicotinamide (cas:329-89-5)Reference of 6-Aminonicotinamide is a monocarboxylic acid amide resulting from the formal condensation of the carboxy group of 6-aminonicotinic acid with ammonia. An inhibitor of the NADP(+)-dependent enzyme,6-phosphogluconate dehydrogenase, it interferes with glycolysis.

Reference:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics