Category: 329-89-5

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

Quality Control of 6-Aminonicotinamide《SGK1 signaling promotes glucose metabolism and survival in extracellular matrix detached cells》 was published in 2021. The authors were Mason, Joshua A.;Cockfield, Jordan A.;Pape, Daniel J.;Meissner, Hannah;Sokolowski, Michael T.;White, Taylor C.;Valentin Lopez, Jose C.;Liu, Juan;Liu, Xiaojing;Martinez-Reyes, Inmaculada;Chandel, Navdeep S.;Locasale, Jason W.;Schafer, Zachary T., and the article was included in《Cell Reports》. The author mentioned the following in the article:

Loss of integrin-mediated attachment to extracellular matrix (ECM) proteins can trigger a variety of cellular changes that affect cell viability. Foremost among these is the activation of anoikis, caspase-mediated cell death induced by ECM detachment. In addition, loss of ECM attachment causes profound alterations in cellular metabolism, which can lead to anoikis-independent cell death. Here, we describe a surprising role for serum and glucocorticoid kinase-1 (SGK1) in the promotion of energy production when cells are detached. Our data demonstrate that SGK1 activation is necessary and sufficient for ATP generation during ECM detachment and anchorage-independent growth. More specifically, SGK1 promotes a substantial elevation in glucose uptake because of elevated GLUT1 transcription. In addition, carbon flux into the pentose phosphate pathway (PPP) is necessary to accommodate elevated glucose uptake and PPP-mediated glyceraldehyde-3-phosphate (G3P) is necessary for ATP production Thus, our data show SGK1 as master regulator of glucose metabolism and cell survival during ECM-detached conditions. To complete the study, the researchers used 6-Aminonicotinamide (cas: 329-89-5) .

6-Aminonicotinamide (cas:329-89-5)Quality Control 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

Gorgun, Murat F.;Zhuo, Ming;Englander, Ella W. published 《Cisplatin Toxicity in Dorsal Root Ganglion Neurons Is Relieved by Meclizine via Diminution of Mitochondrial Compromise and Improved Clearance of DNA Damage》 in 2017. The article was appeared in 《Molecular Neurobiology》. They have made some progress in their research.Application of 329-89-5 The article mentions the following:

Chemotherapy-induced neurotoxicity of peripheral nervous system (PNS) hinders efficacy of cancer treatments. Mechanisms initiating PNS injury by anticancer drugs are incompletely understood delaying development of effective management strategies. To understand events triggered in PNS by cancer drugs, we exposed dorsal root ganglion (DRG) neurons to cisplatin, a drug from platinum-based class of chemotherapeutics frequently implicated in peripheral neuropathies. While cisplatin enters cancer cells and forms cisplatin/DNA crosslinks that block cell proliferation, circulating cisplatin can also reach the PNS and produce crosslinks that impede critical DNA transactions in postmitotic neurons. Cisplatin forms crosslinks with both, nuclear and mitochondrial DNA (mtDNA). Crosslinks are repairable primarily via the nucleotide excision repair (NER) pathway, which is present in nuclei but absent from mitochondrial compartment. Hence, high mitochondrial content and limited shielding by blood nerve barrier make DRG neurons particularly vulnerable to mitochondrial injury by cisplatin. We report that in DRG neurons, cisplatin elevates reactive oxygen species, depletes mtDNA, and impairs mitochondrial respiration, whereas concomitant meclizine supplementation preserves redox balance, attenuates mitochondrial compromise, and augments DNA repair. Meclizine is an antihistamine drug recently implicated in neuroprotection via modulation of energy metabolism Our data demonstrate that in the mitochondria-rich DRG neurons, meclizine mitigates cisplatin-induced mitochondrial compromise via enhancement of pentose phosphate pathway and repletion of NADP (NADPH) and glutathione stores. The findings suggest that meclizine-mediated preservation of redox balance sustains mitochondrial respiration and supports execution of cellular processes, including timely removal of cisplatin crosslinks from nuclear DNA, thereby attenuating cisplatin toxicity in DRG neurons. Collectively, the findings reveal potential for pharmacol. modulation of dorsal root ganglion neurons metabolism for protection against toxicity of chemotherapeutic drugs. 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 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

Zhelev, Zhivko;Ivanova, Donika;Bakalova, Rumiana;Aoki, Ichio;Higashi, Tatsuya published 《Inhibition of the pentose-phosphate pathway selectively sensitizes leukemia lymphocytes to chemotherapeutics by ROS-independent mechanism》. The research results were published in《Anticancer Research》 in 2016.Synthetic Route of C6H7N3O The article conveys some information:

The aim of the present study was to investigate: (i) the possibility of sensitizing leukemia lymphocytes to anticancer drugs by inhibiting pentose-phosphate pathway using 6-aminonicotinamide (6-ANA); (ii) to find combinations with synergistic cytotoxic effect on leukemia lymphocytes and to investigate their cytotoxicity towards normal lymphocytes; (iii) and to clarify the role of reactive oxygen species (ROS) in the induction of apoptosis by those combinations. The study covers 15 anticancer drugs – conventional and new-generation. The experiments were performed on Jurkat leukemia cell line and normal lymphocytes, isolated from clin. healthy blood donors. Four parameters were analyzed simultaneously in both cell suspensions treated by drug or 6-ANA (sep., and in combination): cell viability, induction of apoptosis, level of ROS, and level of protein-carbonyl products. Most combinations of drug plus 6-ANA were characterized by synergistic cytotoxic effects on Jurkat cells. The synergism increased with increasing incubation time. Upon combination of 6-ANA with conventional chemotherapeutic (e.g. doxorubicin), synergistic cytotoxic effects were also detected in normal lymphocytes. In both cell types, the cytotoxicity of the combination of doxorubicin plus 6-ANA was accompanied by increased induction of apoptosis, but by a slight reduction of ROS and protein-carbonyl products compared to cells treated with doxorubicin only. Upon combination of 6-ANA with new-generation anticancer drugs (e.g. everolimus or barasertib), the synergistic cytotoxic effect on leukemia lymphocytes was also accompanied by very strong induction of apoptosis through ROS-independent mechanism(s). Neither of these combinations exhibited any cytotoxicity towards normal lymphocytes. The data suggest that 6-ANA could be used as a supplementary component in anticancer chemotherapy, and would allows therapeutic doses of anticancer drugs to be reduced, thereby minimizing their side-effects. The experimental procedure involved many compounds, such as 6-Aminonicotinamide (cas: 329-89-5) .

6-Aminonicotinamide (cas:329-89-5)Synthetic Route 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

Candelario, Kate M.;Shuttleworth, C. William;Cunningham, Lee Anna published 《Neural stem/progenitor cells display a low requirement for oxidative metabolism independent of hypoxia inducible factor-1alpha expression》 in 2013. The article was appeared in 《Journal of Neurochemistry》. They have made some progress in their research.Product Details of 329-89-5 The article mentions the following:

Neural stem/progenitor cells (NSPCs) are multipotent cells within the embryonic and adult brain that give rise to both neuronal and glial cell lineages. The maintenance of NSPC multipotency is promoted by low O₂ tension, although the metabolic underpinnings of this trait have not been described. Here, the authors investigated the metabolic state of undifferentiated NSPCs in culture, and tested their relative reliance on oxidative vs. glycolytic metabolism for survival, as well as their dependence on hypoxia inducible factor-1α (HIF-1α) expression for maintenance of metabolic phenotype. Unlike primary neurons, NSPCs from embryonic and adult mice survived prolonged hypoxia in culture. In addition, NSPCs displayed greater susceptibility to glycolytic inhibition compared with primary neurons, even in the presence of alternative mitochondrial TCA substrates. NSPCs were also more resistant than neurons to mitochondrial CN^– toxicity, less capable of utilizing galactose as an alternative substrate to glucose, and more susceptible to pharmacol. inhibition of the pentose phosphate pathway by 6-aminonicotinamide. Inducible deletion of exon 1 of the Hif1a gene improved the ability of NSPCs to utilize pyruvate during glycolytic inhibition, but did not alter other parameters of metabolism, including their ability to withstand prolonged hypoxia. Taken together, these data indicate that NSPCs have a relatively low requirement for oxidative metabolism for their survival and that hypoxic resistance is not dependent upon HIF-1α signaling.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 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

Quality Control of 6-AminonicotinamideIn 2016, Forte, Nicola;Medrihan, Lucian;Cappetti, Beatrice;Baldelli, Pietro;Benfenati, Fabio published 《2-Deoxy-D-glucose enhances tonic inhibition through the neurosteroid-mediated activation of extrasynaptic GABA_A receptors》. 《Epilepsia》published the findings. The article contains the following contents:

Summary : Objective : The inhibition of glycolysis exerts potent antiseizure effects, as demonstrated by the efficacy of ketogenic and low-glucose/nonketogenic diets in the treatment of drug-resistant epilepsy. ATP-sensitive potassium (K_ATP) channels have been initially identified as the main determinant of the reduction of neuronal hyperexcitability. However, a plethora of other mechanisms have been proposed. Herein, we report the ability of 2-deoxy-D-glucose (2-DG), a glucose analog that inhibits glycolytic enzymes, of potentiating γ-aminobutyric acid (GABA)ergic tonic inhibition via neurosteroid-mediated activation of extrasynaptic GABA_A receptors. Methods : Acute effects of 2-DG on the ATP-sensitive potassium currents, GABAergic tonic inhibition, firing activity, and interictal events were assessed in hippocampal slices by whole-cell patch-clamp and local field potential recordings of dentate gyrus granule cells. Results : Acute application of 2-DG activates two distinct outward conductances: a K_ATP channel-mediated current and a bicuculline-sensitive tonic current. The effect of 2-DG on such GABAergic tonic currents was fully prevented by either finasteride or PK11195, which are specific inhibitors of the neurosteroidogenesis pathway acting via different mechanisms. Moreover, the oxidized form of vitamin C, dehydroascorbic acid, known for its ability to induce neurosteroidogenesis, also activated a bicuculline-sensitive tonic current in a manner indistinguishable from that of 2-DG. Finally, we found that the enhancement of K_ATP current by 2-DG primarily regulates intrinsic firing rate of granule cells, whereas the increase of the GABAergic tonic current plays a key role in reducing the frequency of interictal events evoked by treatment of hippocampal slices with the convulsive agent 4-aminopyridine. Significance : We demonstrated, for the first time, that 2-DG potentiates the extrasynaptic tonic GABAergic current through activation of neurosteroidogenesis. Such tonic inhibition represents the main conductance responsible for the antiseizure action of this glycolytic inhibitor.6-Aminonicotinamide (cas: 329-89-5) were involved in the experimental procedure.

6-Aminonicotinamide (cas:329-89-5)Quality Control 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

Vimercati, Claudio;Qanud, Khaled;Mitacchione, Gianfranco;Sosnowska, Danuta;Ungvari, Zoltan;Sarnari, Roberto;Mania, Daniella;Patel, Neel;Hintze, Thomas H.;Gupte, Sachin A.;Stanley, William C.;Recchia, Fabio A. published 《Beneficial effects of acute inhibition of the oxidative pentose phosphate pathway in the failing heart》 in 2014. The article was appeared in 《American Journal of Physiology》. They have made some progress in their research.Name: 6-Aminonicotinamide The article mentions the following:

In vitro studies suggested that glucose metabolism through the oxidative pentose phosphate pathway (oxPPP) can paradoxically feed superoxide-generating enzymes in failing hearts. We therefore tested the hypothesis that acute inhibition of the oxPPP reduces oxidative stress and enhances function and metabolism of the failing heart, in vivo. In 10 chronically instrumented dogs, congestive heart failure (HF) was induced by high-frequency cardiac pacing. Myocardial glucose consumption was enhanced by raising arterial glycemia to levels mimicking postprandial peaks, before and after i.v. administration of the oxPPP inhibitor 6-aminonicotinamide (80 mg/kg). Myocardial energy substrate metabolism was measured with radiolabeled glucose and oleic acid, and cardiac 8-isoprostane output was used as an index of oxidative stress. A group of five chronically instrumented, normal dogs served as control. In HF, raising glycemic levels from ∼80 to ∼170 mg/dL increased cardiac isoprostane output by approx. twofold, whereas oxPPP inhibition normalized oxidative stress and enhanced cardiac oxygen consumption, glucose oxidation, and stroke work. In normal hearts glucose infusion did not induce significant changes in cardiac oxidative stress. Myocardial tissue concentration of 6P-gluconate, an intermediate metabolite of the oxPPP, was significantly reduced by ∼50% in treated vs. nontreated failing hearts, supporting the inhibitory effect of 6-aminonicotinamide. Our study indicates an important contribution of the oxPPP activity to cardiac oxidative stress in HF, which is particularly pronounced during common physiol. changes such as postprandial glycemic peaks. To complete the study, the researchers used 6-Aminonicotinamide (cas: 329-89-5) .

6-Aminonicotinamide (cas:329-89-5)Name: 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

Huang, He;Yuan, Min;Seitzer, Phillip;Ludwigsen, Susan;Asara, John M. published 《IsoSearch: an untargeted and unbiased metaboliteand lipid isotopomer tracing strategy fromHR-LC-MS/MS datasets》. The research results were published in《Methods and Protocols》 in 2020.Recommanded Product: 6-Aminonicotinamide The article conveys some information:

Stable isotopic tracer anal. is a technique used to determine carbon or nitrogen atom incorporation into biol. systems. A number of mass spectrometry based approaches have been developed for this purpose, including high-resolution tandem mass spectrometry (HR-LC-MS/MS), selected reaction monitoring (SRM) and parallel reaction monitoring (PRM). We have developed an approach for analyzing untargeted metabolomic and lipidomic datasets using high-resolution mass spectrometry with polarity switching and implemented our approach in the open-source R script IsoSearch and in Scaffold Elements software. Using our strategy, which requires an unlabeled reference dataset and isotope labeled datasets across various biol. conditions, we traced metabolic isotopomer alterations in breast cancer cells (MCF-7) treated with the metabolic drugs 2-deoxy-glucose, 6-aminonicotinamide, compound 968, and rapamycin. Metabolites and lipids were first identified by the com. software Scaffold Elements and LipidSearch, then IsoSearch successfully profiled the 13C-isotopomers extracted metabolites and lipids from 13C-glucose labeled MCF-7 cells. The results interpreted known models, such as glycolysis and pentose phosphate pathway inhibition, but also helped to discover new metabolic/lipid flux patterns, including a reactive oxygen species (ROS) defense mechanism induced by 6AN and triglyceride accumulation in rapamycin treated cells. The results suggest the IsoSearch/Scaffold Elements platform is effective for studying metabolic tracer anal. in diseases, drug metabolism, and metabolic engineering for both polar metabolites and non-polar lipids. The experimental procedure involved many compounds, such as 6-Aminonicotinamide (cas: 329-89-5) .

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

Nagahori, Hirohisa;Suzuki, Noriyuki;Le Coz, Florian;Omori, Takashi;Saito, Koichi published 《Prediction of in vivo developmental toxicity by combination of Hand1-Luc embryonic stem cell test and metabolic stability test with clarification of metabolically inapplicable candidates》. The research results were published in《Toxicology Letters》 in 2016.Recommanded Product: 329-89-5 The article conveys some information:

Hand1-Luc Embryonic Stem Cell Test (Hand1-Luc EST) is a promising alternative method for evaluation of developmental toxicity. However, the problems of predictivity have remained due to appropriateness of the solubility, metabolic system, and prediction model. Therefore, we assessed the usefulness of rat liver S9 metabolic stability test using LC-MS/MS to develop new prediction model. A total of 71 chems. were analyzed by measuring cytotoxicity and differentiation toxicity, and highly reproducible (CV = 20%) results were obtained. The first prediction model was developed by discriminant anal. performed on a full dataset using Hand1-Luc EST, and 66.2% of the chems. were correctly classified by the cross-validated classification. A second model was developed with addnl. descriptors obtained from the metabolic stability test to calculate hepatic availability, and an accuracy of 83.3% was obtained with applicability domain of 50.7% (=36/71) after exclusion of 22 metabolically inapplicable candidates, which potentially have a metabolic activation property. A step-wise prediction scheme with combination of Hand1-Luc EST and metabolic stability test was therefore proposed. The current results provide a promising in vitro test method for accurately predicting in vivo developmental toxicity. And 6-Aminonicotinamide (cas: 329-89-5) was used in the research process.

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

Zhou, Yanhong;Xia, Xiaojian;Yu, Gaobo;Wang, Jitao;Wu, Jingxue;Wang, Mengmeng;Yang, Youxin;Shi, Kai;Yu, Yunlong;Chen, Zhixiang;Gan, Jay;Yu, Jingquan published 《Brassinosteroids play a critical role in the regulation of pesticide metabolism in crop plants》 in 2015. The article was appeared in 《Scientific Reports》. They have made some progress in their research.Recommanded Product: 329-89-5 The article mentions the following:

Pesticide residues in agricultural produce pose a threat to human health worldwide. Although the detoxification mechanisms for xenobiotics have been extensively studied in mammalian cells, information about the regulation network in plants remains elusive. Here we show that brassinosteroids (BRs), a class of natural plant hormones, decreased residues of common organophosphorus, organochlorine and carbamate pesticides by 30-70% on tomato, rice, tea, broccoli, cucumber, strawberry, and other plants when treated externally. Genome-wide microarray anal. showed that fungicide chlorothalonil (CHT) and BR co-upregulated 301 genes, including a set of detoxifying genes encoding cytochrome P 450, oxidoreductase, hydrolase and transferase in tomato plants. The level of BRs was closely related to the respiratory burst oxidase 1 (RBOH1)-encoded NADPH oxides-dependent H₂O₂ production, glutathione biosynthesis and the redox homeostasis, and the activity of glutathione S-transferase (GST). Gene silencing treatments showed that BRs decreased pesticide residues in plants likely by promoting their metabolism through a signaling pathway involving BRs-induced H₂O₂ production and cellular redox change. Our study provided a novel approach for minimizing pesticide residues in crops by exploiting plants’ own detoxification mechanisms. The experimental procedure involved many compounds, such as 6-Aminonicotinamide (cas: 329-89-5) .

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