Category: 329-89-5

Islas-Flores, Hariz;Perez-Alvarez, Itzayana;Gomez-Olivan, Leobardo M. published 《Evaluation of teratogenicity of pharmaceuticals using FETAX》 in 2018. The article was appeared in 《Methods in Molecular Biology (New York, NY, United States)》. They have made some progress in their research.Reference of 6-Aminonicotinamide The article mentions the following:

A review. Pharmaceuticals are chem.compounds which are used to preserve human and animal health. Once administered, these compoundsare metabolized or can remain unaltered until excreted. Therefore, a mixtureof pharmaceuticals and their metabolites enters municipal sewers and wastewater treatment plants where, depending on their polarity, water solubility, and persistence, they cannot be completely removed or transformed during the treatment process, so that unaltered pharmaceuticals and/or their metabolites can enter surface water. As a result, in recent years concern has grown about trace concentrations and the risk they pose to ecosystems, considering the annual increase in pharmaceutical productionand use at world level. This chapter reviews the frog embryo teratogenesis assay-Xenopus (FETAX). Originally developed during the mid-1980s as a test for detecting the developmental toxicity of pure chem. products and complex mixturesin the laboratory, in recent years it has been used to evaluate the mechanisms of action, biotransformation, and detoxification of xenobiotics as well as in ecotoxicol. studies using alternative species and in situ monitoring. And 6-Aminonicotinamide (cas: 329-89-5) was used in the research process.

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

Sun, Y.;Gu, X.;Zhang, E.;Park, M-A.;Pereira, A. M.;Wang, S.;Morrison, T.;Li, C.;Blenis, J.;Gerbaudo, V. H.;Henske, E. P.;Yu, J. J. published 《Estradiol promotes pentose phosphate pathway addiction and cell survival via reactivation of Akt in mTORC1 hyperactive cells》 in 2014. The article was appeared in 《Cell Death & Disease》. They have made some progress in their research.Category: amides-buliding-blocks The article mentions the following:

Lymphangioleiomyomatosis (LAM) is a female-predominant interstitial lung disease that can lead to respiratory failure. LAM cells typically have inactivating TSC2 mutations, leading to mTORC1 activation. The gender specificity of LAM suggests that estradiol contributes to disease development, yet the underlying pathogenic mechanisms are not completely understood. Using metabolomic profiling, we identified an estradiol-enhanced pentose phosphate pathway signature in Tsc2-deficient cells. Estradiol increased levels of cellular NADPH, decreased levels of reactive oxygen species, and enhanced cell survival under oxidative stress. Mechanistically, estradiol reactivated Akt in TSC2-deficient cells in vitro and in vivo, induced membrane translocation of glucose transporters (GLUT1 or GLUT4), and increased glucose uptake in an Akt-dependent manner. ¹⁸F-FDG-PET imaging demonstrated enhanced glucose uptake in xenograft tumors of Tsc2-deficient cells from estradiol-treated mice. Expression array study identified estradiol-enhanced transcript levels of glucose-6-phosphate dehydrogenase (G6PD), the rate-limiting enzyme of the pentose phosphate pathway. Consistent with this, G6PD was abundant in xenograft tumors and lung metastatic lesions of Tsc2-deficient cells from estradiol-treated mice. Mol. depletion of G6PD attenuated estradiol-enhanced survival in vitro, and treatment with 6-aminonicotinamide, a competitive inhibitor of G6PD, reduced lung colonization of Tsc2-deficient cells. Collectively, these data indicate that estradiol promotes glucose metabolism in mTORC1 hyperactive cells through the pentose phosphate pathway via Akt reactivation and G6PD upregulation, thereby enhancing cell survival under oxidative stress. Interestingly, a strong correlation between estrogen exposure and G6PD was also found in breast cancer cells. Targeting the pentose phosphate pathway may have therapeutic benefit for LAM and possibly other hormonally dependent neoplasms. And 6-Aminonicotinamide (cas: 329-89-5) was used in the research process.

6-Aminonicotinamide (cas:329-89-5)Category: amides-buliding-blocks 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

Safety of 6-Aminonicotinamide《Inhibition of glycogen catabolism induces intrinsic apoptosis and augments multikinase inhibitors in hepatocellular carcinoma cells》 was published in 2019. The authors were Barot, Shrikant;Abo-Ali, Ehab M.;Zhou, Daisy L.;Palaguachi, Christian;Dukhande, Vikas V., and the article was included in《Experimental Cell Research》. The author mentioned the following in the article:

Hepatocellular carcinoma (HCC) is one of the leading cancers in the world in incidence and mortality. Current pharmacotherapy of HCC is limited in the number and efficacy of anticancer agents. Metabolic reprogramming is a prominent feature of many cancers and has rekindled interest in targeting metabolic proteins for cancer therapy. Glycogen is a storage form of glucose, and the levels of glycogen have been found to correlate with biol. processes in reprogrammed cancer cells. However, the contribution of glycogen metabolism to carcinogenesis, cancer cell growth, metastasis, and chemoresistance is poorly understood. Thus, we studied the processes involved in the inhibition of glycogen metabolism in HCC cells. Pharmacol. inhibition of glycogen phosphorylase (GP), a rate-limiting enzyme in glycogen catabolism, by CP-91149 led to a decrease in HCC cell viability. GP inhibition induced cancer cell death through the intrinsic apoptotic pathway. Mitochondrial dysfunction and autophagic adaptations accompanied this apoptosis process whereas endoplasmic reticulum stress, necrosis, and necroptosis were not major components of the cell death. In addition, GP inhibition potentiated the effects of multikinase inhibitors sorafenib and regorafenib, which are key drugs in advanced-stage HCC therapy. Our study provides mechanistic insights into cell death by perturbation of glycogen metabolism and identifies GP inhibition as a potential HCC pharmacotherapy target. And 6-Aminonicotinamide (cas: 329-89-5) was used in the research process.

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

Product Details of 329-89-5《Real-time quantification of subcellular H₂O₂ and glutathione redox potential in living cardiovascular tissues》 was published in 2017. The authors were Panieri, Emiliano;Millia, Carlo;Santoro, Massimo M., and the article was included in《Free Radical Biology & Medicine》. The author mentioned the following in the article:

Detecting and measuring the dynamic redox events that occur in vivo is a prerequisite for understanding the impact of oxidants and redox events in normal and pathol. conditions. These aspects are particularly relevant in cardiovascular tissues wherein alterations of the redox balance are associated with stroke, aging, and pharmacol. intervention. An ambiguous aspect of redox biol. is how redox events occur in subcellular organelles including mitochondria, and nuclei. Genetically-encoded Rogfp2 fluorescent probes have become powerful tools for real-time detection of redox events. These probes detect hydrogen peroxide (H₂O₂) levels and glutathione redox potential (E_GSH), both with high spatiotemporal resolution By generating novel transgenic (Tg) zebrafish lines that express compartment-specific Rogfp2-Orp1 and Grx1-Rogfp2 sensors we analyzed cytosolic, mitochondrial, and the nuclear redox state of endothelial cells and cardiomyocytes of living zebrafish embryos. We provide evidence for the usefulness of these Tg lines for pharmacol. compounds screening by addressing the blocking of pentose phosphate pathways (PPP) and glutathione synthesis, thus altering subcellular redox state in vivo. Rogfp2-based transgenic zebrafish lines represent valuable tools to characterize the impact of redox changes in living tissues and offer new opportunities for studying metabolic driven antioxidant response in biomedical research.6-Aminonicotinamide (cas: 329-89-5) were involved in the experimental procedure.

6-Aminonicotinamide (cas:329-89-5)Product Details 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

Recommanded Product: 6-AminonicotinamideIn 2016, Arts, Rob J. W.;Novakovic, Boris;ter Horst, Rob;Carvalho, Agostinho;Bekkering, Siroon;Lachmandas, Ekta;Rodrigues, Fernando;Silvestre, Ricardo;Cheng, Shih-Chin;Wang, Shuang-Yin;Habibi, Ehsan;Goncalves, Luis G.;Mesquita, Ines;Cunha, Cristina;van Laarhoven, Arjan;van de Veerdonk, Frank L.;Williams, David L.;van der Meer, Jos W. M.;Logie, Colin;O’Neill, Luke A.;Dinarello, Charles A.;Riksen, Niels P.;van Crevel, Reinout;Clish, Clary;Notebaart, Richard A.;Joosten, Leo A. B.;Stunnenberg, Hendrik G.;Xavier, Ramnik J.;Netea, Mihai G. published 《Glutaminolysis and Fumarate Accumulation Integrate Immunometabolic and Epigenetic Programs in Trained Immunity》. 《Cell Metabolism》published the findings. The article contains the following contents:

Induction of trained immunity (innate immune memory) is mediated by activation of immune and metabolic pathways that result in epigenetic rewiring of cellular functional programs. Through network-level integration of transcriptomics and metabolomics data, we identify glycolysis, glutaminolysis, and the cholesterol synthesis pathway as indispensable for the induction of trained immunity by β-glucan in monocytes. Accumulation of fumarate, due to glutamine replenishment of the TCA cycle, integrates immune and metabolic circuits to induce monocyte epigenetic reprogramming by inhibiting KDM5 histone demethylases. Furthermore, fumarate itself induced an epigenetic program similar to β-glucan-induced trained immunity. In line with this, inhibition of glutaminolysis and cholesterol synthesis in mice reduced the induction of trained immunity by β-glucan. Identification of the metabolic pathways leading to induction of trained immunity contributes to our understanding of innate immune memory and opens new therapeutic avenues.6-Aminonicotinamide (cas: 329-89-5) were involved in the experimental procedure.

6-Aminonicotinamide (cas:329-89-5)Recommanded Product: 6-Aminonicotinamide 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

Parkhitko, Andrey A.;Priolo, Carmen;Coloff, Jonathan L.;Yun, Jihye;Wu, Julia J.;Mizumura, Kenji;Xu, Wenping;Malinowska, Izabela A.;Yu, Jane;Kwiatkowski, David J.;Locasale, Jason W.;Asara, John M.;Choi, Augustine M. K.;Finkel, Toren;Henske, Elizabeth P. published 《Autophagy-Dependent Metabolic Reprogramming Sensitizes TSC2-Deficient Cells to the Antimetabolite 6-Aminonicotinamide》. The research results were published in《Molecular Cancer Research》 in 2014.COA of Formula: C6H7N3O The article conveys some information:

The mammalian target of rapamycin complex 1 (mTORC1) is hyperactive in many human cancers and in tuberous sclerosis complex (TSC). Autophagy, a key mTORC1-targeted process, is a critical determinant of metabolic homeostasis. Metabolomic profiling was performed to elucidate the cellular consequences of autophagy dysregulation under conditions of hyperactive mTORC1. It was discovered that TSC2-null cells have distinctive autophagy-dependent pentose phosphate pathway (PPP) alterations. This was accompanied by enhanced glucose uptake and utilization, decreased mitochondrial oxygen consumption, and increased mitochondrial reactive oxygen species (ROS) production Importantly, these findings revealed that the PPP is a key autophagy-dependent compensatory metabolic mechanism. Furthermore, PPP inhibition with 6-aminonicotinamide (6-AN) in combination with autophagy inhibition suppressed proliferation and prompted the activation of NF-κB and CASP1 in TSC2-deficient, but not TSC2-proficient cells. These data demonstrate that TSC2-deficient cells can be therapeutically targeted, without mTORC1 inhibitors, by focusing on their metabolic vulnerabilities. Implications: This study provides proof-of-concept that therapeutic targeting of diseases with hyperactive mTORC1 can be achieved without the application of mTORC1 inhibitors. Mol Cancer Res; 12(1); 48-57. ©2013 AACR. The experimental procedure involved many compounds, such as 6-Aminonicotinamide (cas: 329-89-5) .

6-Aminonicotinamide (cas:329-89-5)COA of Formula: C6H7N3O 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

Chen, Huihui;Hao, Shilai;Chen, Zheng;O-Thong, Sompong;Fan, Jiajun;Clark, James;Luo, Gang;Zhang, Shicheng published 《Mesophilic and thermophilic anaerobic digestion of aqueous phase generated from hydrothermal liquefaction of cornstalk: Molecular and metabolic insights》. The research results were published in《Water Research》 in 2020.Recommanded Product: 6-Aminonicotinamide The article conveys some information:

The critical challenge of hydrothermal liquefaction (HTL) for bio-oil production from biomass is the production of large amounts of aqueous products (HTL-AP) with high organic contents. The present study investigated the anaerobic digestion (AD) performances of HTL-AP under both thermophilic and mesophilic conditions, and mol. and metabolic anal. were conducted to provide insights into the different performances. The results showed that thermophilic AD had lower COD removal efficiency compared to mesophilic AD (45.0% vs. 61.6%). Liquid chromatog. coupled with organic carbon detection and organic nitrogen (LC-OCD-OND) anal. showed that both high mol. weight (HMW) and low mol. weight (LMW) compounds were degraded to some extent and more LMW acids (LMWA) and recalcitrant aromatic compounds were degraded in the mesophilic reactor, which was the main reason of higher COD removal efficiency. Ph compounds (e.g. phenol and 2 methoxyphenol), furans and pyrazines were the recalcitrant chems. detected through GC-MS anal. Fourier transform ion cyclone resonance mass spectrometry (FT-ICR-MS) anal. demonstrated the complexity of HTL-AP and the proportions of phenolic or condensed aromatic compounds increased especially in the thermophilic effluents. Metabolites anal. showed that the reasons contributing to the differences of mesophilic and thermophilic AD were not only related to the degradation of organic compounds (e.g. benzoate degradation via CoA ligation) in HTL-AP but also related to the microbial autogenesis (e.g. fatty acid biosynthesis) as well as the environmental information processing. In addition, the enrichment of Mesotoga, responsible for the high degradation efficiency of LMWA, and Pelolinea, involved in the degradation of Ph compounds, were found in mesophilic reactor, which was consistent with higher removal of corresponding organics To complete the study, the researchers used 6-Aminonicotinamide (cas: 329-89-5) .

6-Aminonicotinamide (cas:329-89-5)Recommanded Product: 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

Electric Literature of C6H7N3O《Metabolic interaction of hydrogen peroxide and hypoxia in zebrafish fibroblasts》 was published in 2020. The authors were Dikova, Valentina;Vorhauser, Julia;Geng, Anne;Pelster, Bernd;Sandbichler, Adolf Michael, and the article was included in《Free Radical Biology & Medicine》. The author mentioned the following in the article:

Cells require oxygen for aerobic metabolism, which may also result in the production of reactive oxygen species (ROS) as a byproduct. Under low oxygen conditions, ROS formation has been reported to either increase or decrease. We addressed this physiol. response for the first time in zebrafish embryonic fibroblasts (Z3) and used a hydrogen peroxide (H₂O₂)-specific fluorescent protein (roGFP2-Orp1) either targeted to the mitochondria or expressed in the cytosol. Microfluidic live-cell imaging measurements showed that oxygen deprivation in Z3 cells results in decreased or stable H₂O₂ levels within the mitochondria or the cytosol, resp., and that the reductive shift recorded in the mitochondrial matrix is directly dependent on oxygen concentration The response was accompanied by a transient increase in extracellular acidification rate (ECAR) and a lower cellular reducing potential as assessed by the viability stain alamarBlue. Complex I and III inhibition with Rotenone and Antimycin A led to H₂O₂ production under normoxia but these inhibitors were not able to avert the reductive shift under hypoxia. Only by system-wide inhibition of flavin-containing oxidases with Diphenyleneiodonium (DPI) were we able to decrease the reductive shift, while selective inhibition of NADPH oxidases with the inhibitor Apocynin had no effect on the hypoxia response. Since DPI also led to a strong increase in ECAR we found that, in order to keep the cytosolic H₂O₂ levels stable, glycolytic metabolism was of fundamental importance. According to our experiments with the glucose-6-phosphate dehydrogenase inhibitor 6-Aminonicotinamide, this was attributable to the pentose phosphate pathway producing reducing equivalent required for ROS degradation 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

Le Coz, Florian;Suzuki, Noriyuki;Nagahori, Hirohisa;Omori, Takashi;Saito, Koichi published 《Hand1-Luc embryonic stem cell test (Hand1-Luc EST): a novel rapid and highly reproduciblein vitro test for embryotoxicity by measuring cytotoxicity and differentiation toxicity using engineered mouse ES cells》 in 2015. The article was appeared in 《Journal of Toxicological Sciences》. They have made some progress in their research.Application In Synthesis of 6-Aminonicotinamide The article mentions the following:

The embryonic stem cell test (EST) is a promising alternative method for evaluating embryotoxicity of test chems. by measuring cytotoxicity and differentiation toxicity using mouse ES cells. Differentiation toxicity is analyzed by microscopically counting the beating of embryonic bodies after 10 days of culture. However, improvements are necessary to reduce the laborious manipulations involved and the time required to obtain results. We have previously reported the successful stable transfection of ES cells (ES-D3) with the heart and neural crest derivatives expressed transcript 1 (Hand1) gene and the establishment of a 96-well multi-plate-based new EST with luciferase reporter assay 6 days after treatment with test chems. Now, we propose an even more rapid and easier EST, named Hand1-Luc EST. We established another cell line to monitor the Hand1 gene expression via a luciferase reporter gene. By mRNA anal. and luciferase assay, we examined in detail the luciferase activity during cell differentiation, which allowed us to reduce the time of measurement from day 6 to day 5 (120 h). Furthermore, the protocol was improved, with, among others, the measurement of cytotoxicity and differentiation toxicity taking place in the same 96-well round bottom plate instead of two different plates. With the pos. control, 5-fluorouracil (5-FU), and 9 test chems., data with high reproducibility and very low variation (CV < 50%) in the relevant endpoints were obtained. This study shows that the Hand1-Luc EST could provide an accurate and sensitive short-term test for prediction of embryotoxicants by measuring cytotoxicity and differentiation toxicity from the same sample. The experimental procedure involved many compounds, such as 6-Aminonicotinamide (cas: 329-89-5) .

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

Oburoglu, Leal;Tardito, Saverio;Fritz, Vanessa;de Barros, Stephanie C.;Merida, Peggy;Craveiro, Marco;Mamede, Joao;Cretenet, Gaspard;Mongellaz, Cedric;An, Xiuli;Klysz, Dorota;Touhami, Jawida;Boyer-Clavel, Myriam;Battini, Jean-Luc;Dardalhon, Valerie;Zimmermann, Valerie S.;Mohandas, Narla;Gottlieb, Eyal;Sitbon, Marc;Kinet, Sandrina;Taylor, Naomi published 《Glucose and Glutamine Metabolism Regulate Human Hematopoietic Stem Cell Lineage Specification》. The research results were published in《Cell Stem Cell》 in 2014.Related Products of 329-89-5 The article conveys some information:

The metabolic state of quiescent hematopoietic stem cells (HSCs) is an important regulator of self-renewal, but it is unclear whether or how metabolic parameters contribute to HSC lineage specification and commitment. Here, we show that the commitment of human and murine HSCs to the erythroid lineage is dependent upon glutamine metabolism HSCs require the ASCT2 glutamine transporter and active glutamine metabolism for erythroid specification. Blocking this pathway diverts EPO-stimulated HSCs to differentiate into myelomonocytic fates, altering in vivo HSC responses and erythroid commitment under stress conditions such as hemolytic anemia. Mechanistically, erythroid specification of HSCs requires glutamine-dependent de novo nucleotide biosynthesis. Exogenous nucleosides rescue erythroid commitment of human HSCs under conditions of limited glutamine catabolism, and glucose-stimulated nucleotide biosynthesis further enhances erythroid specification. Thus, the availability of glutamine and glucose to provide fuel for nucleotide biosynthesis regulates HSC lineage commitment under conditions of metabolic stress. To complete the study, the researchers used 6-Aminonicotinamide (cas: 329-89-5) .

6-Aminonicotinamide (cas:329-89-5)Related Products 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