Category: 329-89-5

De Abrew, K. Nadira;Shan, Yuqing K.;Wang, Xiaohong;Krailler, Jesse M.;Kainkaryam, Raghunandan M.;Lester, Cathy C.;Settivari, Raja S.;LeBaron, Matthew J.;Naciff, Jorge M.;Daston, George P. published 《Use of connectivity mapping to support read across: A deeper dive using data from 186 chemicals, 19 cell lines and 2 case studies》 in 2019. The article was appeared in 《Toxicology》. They have made some progress in their research.Product Details of 329-89-5 The article mentions the following:

The authors previously demonstrated that the Connectivity Map (CMap) (Lamb et al., 2006) concept can be successfully applied to a predictive toxicol. paradigm to generate meaningful MoA-based connections between chems. (De Abrew et al., 2016). Here the authors expand both the chem. and biol. (cell lines) domain for the method and demonstrate two applications, both in the area of read across. In the first application the authors demonstrate CMap’s utility as a tool for testing biol. relevance of source chems. (analogs) during a chem. led read across exercise. In the second application CMap can be used to identify functionally relevant source chems. (analogs) for a structure of interest (SOI)/target chem. with minimal knowledge of chem. structure. Finally, the authors highlight four factors: promiscuity of chem., dose, cell line and timepoint as having significant impact on the output. The authors discuss the biol. relevance of these four factors and incorporate them into a work flow.6-Aminonicotinamide (cas: 329-89-5) were involved in the experimental procedure.

6-Aminonicotinamide (cas:329-89-5)Product Details of 329-89-5 induces apoptosis in tumor cells. It is clinically used in disseminated neoplastic disease. It also acts as 6-phosphogluconate dehydrogenase inhibitor. It aids in the treatment of psoriasis. It is used as cancer chemotherapeutic drug in animals.

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

Wen, Jing;Wang, Guo-Liang;Yuan, Hong-Jie;Zhang, Jie;Xie, Hong-Li;Gong, Shuai;Han, Xiao;Tan, Jing-He published 《Effects of glucose metabolism pathways on nuclear and cytoplasmic maturation of pig oocytes》 in 2020. 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:

The developmental competence of IVM porcine oocytes is still low compared with that in their in vivo counterparts. Although many studies reported effects of glucose metabolism (GM) on oocyte nuclear maturation, few reported on cytoplasmic maturation. Previous studies could not differentiate whether GM of cumulus cells (CCs) or that of cumulus-denuded oocytes (DOs) supported oocyte maturation. Furthermore, species differences in oocyte GM are largely unknown. Our aim was to address these issues by using enzyme activity inhibitors, RNAi gene silencing and special media that could support nuclear but not cytoplasmic maturation when GM was inhibited. The results showed that GM in CCs promoted pig oocyte maturation by releasing metabolites from both pentose phosphate pathway and glycolysis. Both pyruvate and lactate were transferred into pig DOs by monocarboxylate transporter and pyruvate was further delivered into mitochondria by mitochondrial pyruvate carrier in both pig DOs and CCs. In both pig DOs and CCs, pyruvate and lactate were utilized through mitochondrial electron transport and LDH-catalyzed oxidation to pyruvate, resp. Pig and mouse DOs differed in their CC dependency for glucose, pyruvate and lactate utilization. While mouse DOs could not, pig DOs could use the lactate-derived pyruvate. The experimental procedure involved many compounds, such as 6-Aminonicotinamide (cas: 329-89-5) .

6-Aminonicotinamide (cas:329-89-5)Application of 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

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

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

Application of 329-89-5《Glucose-6-phosphate dehydrogenase inhibition attenuates acute lung injury through reduction in NADPH oxidase-derived reactive oxygen species》 was published in 2018. The authors were Nadeem, A.;Al-Harbi, N. O.;Ahmad, S. F.;Ibrahim, K. E.;Siddiqui, N.;Al-Harbi, M. M., and the article was included in《Clinical & Experimental Immunology》. The author mentioned the following in the article:

Summary : Acute lung injury (ALI) is a heterogeneous disease with the hallmarks of alveolar capillary membrane injury, increased pulmonary edema and pulmonary inflammation. The most common direct etiol. factor for ALI is usually parenchymal lung infection or hemorrhage. Reactive oxygen species (ROS) generated by NADP (NADPH) oxidase (NOX2) are thought to play an important role in the pathophysiol. of ALI. Glucose-6-phosphate dehydrogenase (G6PD) plays an important role both in production of ROS as well as their removal through the supply of NADPH. However, how G6PD modulation affects NOX2-mediated ROS in the airway epithelial cells (AECs) during acute lung injury has not been explored previously. Therefore, we investigated the effect of G6PD inhibitor, 6-aminonicotinamide on G6PD activity, NOX2 expression, ROS production and enzymic anti-oxidants in AECs in a mouse model of ALI induced by lipopolysaccharide (LPS). ALI led to increased G6PD activity in the AECs with concomitant elevation of NOX2, ROS, SOD1 and nitrotyrosine. G6PD inhibitor led to reduction of LPS-induced airway inflammation, bronchoalveolar lavage fluid protein concentration as well as NOX2-derived ROS and subsequent oxidative stress. Conversely, ALI led to decreased glutathione reductase activity in AECs, which was normalized by G6PD inhibitor. These data show that activation of G6PD is associated with enhancement of oxidative inflammation in during ALI. Therefore, inhibition of G6PD might be a beneficial strategy during ALI to limit oxidative damage and ameliorate airway inflammation. And 6-Aminonicotinamide (cas: 329-89-5) was used in the research process.

6-Aminonicotinamide (cas:329-89-5)Application of 329-89-5 is a well-established inhibitor of the NADP+-dependent enzyme, 6-phosphogluconate dehydrogenase (Ki = 0.46 μM). 6-Aminonicotinamide also reduces cardiovascular oxidative injury following ischemia/reperfusion.

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

Nakajima, Yutaka;Aoyama, Naohiro;Takahashi, Fumie;Sasaki, Hiroshi;Hatanaka, Keiko;Moritomo, Ayako;Inami, Masamichi;Ito, Misato;Nakamura, Koji;Nakamori, Fumihiro;Inoue, Takayuki;Shirakami, Shohei published 《Design, synthesis, and evaluation of 4,6-diaminonicotinamide derivatives as novel and potent immunomodulators targeting JAK3》. The research results were published in《Bioorganic & Medicinal Chemistry》 in 2016.Category: amides-buliding-blocks The article conveys some information:

In organ transplantation, T cell-mediated immune responses play a key role in the rejection of allografts. Janus kinase 3 (JAK3) is specifically expressed in hematopoietic cells and associated with regulation of T cell development via interleukin-2 signaling pathway. Here, we designed novel 4,6-diaminonicotinamide derivatives as immunomodulators targeting JAK3 for prevention of transplant rejection. Our optimization of C4- and C6-substituents and docking calculations to JAK3 protein confirmed that the 4,6-diaminonicotinamide scaffold resulted in potent inhibition of JAK3. We also investigated avoidance of human ether-a-go-go related gene (hERG) inhibitory activity. Selected compound 28 in combination with tacrolimus prevented allograft rejection in a rat heterotopic cardiac transplantation model. To complete the study, the researchers used 6-Aminonicotinamide (cas: 329-89-5) .

6-Aminonicotinamide (cas:329-89-5)Category: amides-buliding-blocks is a well-established inhibitor of the NADP+-dependent enzyme, 6-phosphogluconate dehydrogenase (Ki = 0.46 μM). 6-Aminonicotinamide also reduces cardiovascular oxidative injury following ischemia/reperfusion.

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

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

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

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