Category: 329-89-5

COA of Formula: C6H7N3O《LEADS-FRAG: A Benchmark Data Set for Assessment of Fragment Docking Performance》 was published in 2020. The authors were Chachulski, Laura;Windshuegel, Bjoern, and the article was included in《Journal of Chemical Information and Modeling》. The author mentioned the following in the article:

Fragment-based drug design is a popular approach in drug discovery, which makes use of computational methods such as mol. docking. To assess fragment placement performance of mol. docking programs, we constructed LEADS-FRAG, a benchmark data set containing 93 high-quality protein-fragment complexes that were selected from the Protein Data Bank using a rational and unbiased process. The data set contains fully prepared protein and fragment structures and is publicly available. Moreover, we used LEADS-FRAG for evaluating the small-mol. docking programs AutoDock, AutoDock Vina, FlexX, and GOLD for their fragment docking performance. GOLD in combination with the scoring function ChemPLP and AutoDock Vina performed best and generated near-native conformations (root mean square deviation <1.5 Å) for more than 50% of the data set considering the top-ranked docking pose. Taking into account all docking poses, the tested programs generated near-native conformations for up to 86% of the fragments in LEADS-FRAG. By rescoring all docking poses with the GOLD scoring functions and the Protein-Ligand Informatics force field, the number of near-native conformations increased up to 40% with respect to the top-rescored poses. Our results show that conventional small-mol. docking programs achieve a satisfactory fragment docking performance when utilizing rescoring. 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 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,
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SDS of cas: 329-89-5In 2017, Gorgun, Murat F.;Zhuo, Ming;Englander, Ella W. published 《Erratum to: Cisplatin Toxicity in Dorsal Root Ganglion Neurons Is Relieved by Meclizine via Diminution of Mitochondrial Compromise and Improved Clearance of DNA Damage [Erratum to document cited in CA168:230203]》. 《Molecular Neurobiology》published the findings. The article contains the following contents:

In the original publication, At Fig. 3, the image under “cisplatin + meclizine and NF200” is missing on the online published paper both in the pdf and HTML version of this article; the correction is provided here. And 6-Aminonicotinamide (cas: 329-89-5) was used in the research process.

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

Xin, Qi;Yuan, Miaomiao;Li, Huanping;Song, Xiaoxia;Lu, Jun;Jing, Tao published 《In vitro effects of lonidamine and 6-aminonicotinamide against Echinococcus granulosussensu stricto and Echinococcus multilocularis》. The research results were published in《Veterinary Research》 in 2020.Reference of 6-Aminonicotinamide The article conveys some information:

Abstract: Echinococcosis is a zoonotic disease caused by cestode species of the genus Echinococcus, which demonstrates considerable medical and veterinary concerns. The development of novel drugs for echinococcosis treatment is urgently needed. In this study, we demonstrated that lonidamine (LND) and 6-aminonicotinamide (6-AN) exhibited considerable in vitro effects against both larval- and adult-stage of E. granulosussensu stricto (s. s.) and E. multilocularis. The combination of LND and 6-AN exhibited a significantly higher activity than the single drug treatment. These results highlight the therapeutic potential of LND, 6-AN and the combination of LND and 6-AN for the treatment of echinococcosis. 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

Champion, Cody J.;Xu, Jiannong published 《Redox state affects fecundity and insecticide susceptibility in Anopheles gambiae》 in 2018. The article was appeared in 《Scientific Reports》. They have made some progress in their research.Formula: C6H7N3O The article mentions the following:

Redox reactions play a central role in the metabolism of an organism. It is vital to maintain redox homeostasis in response to the fluctuation of redox shift in various biol. contexts. NADPH-dependent reducing capacity is one of the key factors contributing to the redox homeostasis. To understand the redox capacity and its impact on mosquito fecundity and susceptibility to insecticides in Anopheles gambiae, we examined the dynamics of elevated oxidative state via induction by paraquat (PQ) and the inhibition of NADPH regeneration by 6-aminonicotinamide (6AN). In naive conditions, inherent oxidative capacity varies between individuals, as measured by GSSG/GSH ratio. The high GSSG/GSH ratio was neg. correlated with fecundity. Both PQ and 6AN feeding increased GSSG/GSH ratio and elevated protein carbonylation, a marker of oxidative damage. Both pro-oxidants lowered egg production Co-feeding the pro-oxidants with antioxidant lycopene attenuated the adverse effects on fecundity, implying that oxidative stress was the cause of this phenotype. Pre-feeding with 6AN increased insecticide susceptibility in DDT resistant mosquitoes. These results indicate that oxidative state is delicate in mosquitoes, manipulation of NADPH pool may adversely affect fecundity and insecticide detoxification capacity. This knowledge can be exploited to develop novel vector control strategies targeting fecundity and insecticide resistance. To complete the study, the researchers used 6-Aminonicotinamide (cas: 329-89-5) .

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

Synthetic Route of C6H7N3OIn 2015, Gladysz, Rafaela;Adriaenssens, Yves;De Winter, Hans;Joossens, Jurgen;Lambeir, Anne-Marie;Augustyns, Koen;Van der Veken, Pieter published 《Discovery and SAR of Novel and Selective Inhibitors of Urokinase Plasminogen Activator (uPA) with an Imidazo[1,2-a]pyridine Scaffold》. 《Journal of Medicinal Chemistry》published the findings. The article contains the following contents:

Urokinase plasminogen activator (uPA) is a biomarker and therapeutic target for several cancer types. Its inhibition is regarded as a promising, noncytotoxic approach in cancer therapy by blocking growth and/or metastasis of solid tumors. Earlier, the authors reported the modified substrate activity screening (MSAS) approach and applied it for the identification of fragments with affinity for uPA’s S1 pocket. Here, these fragments are transformed into a novel class of uPA inhibitors with an imidazo[1,2-a]pyridine scaffold. The SAR for uPA inhibition around this scaffold is explored, and the best compounds in the series have nanomolar uPA affinity and selectivity with respect to the related trypsin-like serine proteases (thrombin, tPA, FXa, plasmin, plasma kallikrein, trypsin, FVIIa). Finally, the approach followed for translating fragments into small mols. with a decorated scaffold architecture is conceptually straightforward and can be expected to be broadly applicable in fragment-based drug design. To complete the study, the researchers used 6-Aminonicotinamide (cas: 329-89-5) .

6-Aminonicotinamide (cas:329-89-5)Synthetic Route of C6H7N3O 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

Product Details of 329-89-5In 2013, Sugita, Kazunari;Ikenouchi-Sugita, Atsuko;Nakayama, Yasuko;Yoshioka, Haruna;Nomura, Takashi;Sakabe, Jun-Ichi;Nakahigashi, Kyoko;Kuroda, Etsushi;Uematsu, Satoshi;Nakamura, Jun;Akira, Shizuo;Nakamura, Motonobu;Narumiya, Shuh;Miyachi, Yoshiki;Tokura, Yoshiki;Kabashima, Kenji published 《Prostaglandin E₂ is critical for the development of niacin-deficiency-induced photosensitivity via ROS production.》. 《Scientific reports》published the findings. The article contains the following contents:

Pellagra is a photosensitivity syndrome characterized by three “D’s”: diarrhea, dermatitis, and dementia as a result of niacin deficiency. However, the molecular mechanisms of photosensitivity dermatitis, the hallmark abnormality of this syndrome, remain unclear. We prepared niacin deficient mice in order to develop a murine model of pellagra. Niacin deficiency induced photosensitivity and severe diarrhea with weight loss. In addition, niacin deficient mice exhibited elevated expressions of COX-2 and PGE syntheses (Ptges) mRNA. Consistently, photosensitivity was alleviated by a COX inhibitor, deficiency of Ptges, or blockade of EP4 receptor signaling. Moreover, enhanced PGE2 production in niacin deficiency was mediated via ROS production in keratinocytes. In line with the above murine findings, human skin lesions of pellagra patients confirmed the enhanced expression of Ptges. Niacin deficiency-induced photosensitivity was mediated through EP4 signaling in response to increased PGE2 production via induction of ROS formation. And 6-Aminonicotinamide (cas: 329-89-5) was used in the research process.

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

Formula: C6H7N3O《Removal of retained electrospinning solvent prolongs drug release from electrospun PLLA fibers》 was published in 2017. The authors were D’Amato, Anthony R.;Schaub, Nicholas J.;Cardenas, Jesus M.;Fiumara, Andrew S.;Troiano, Paul M.;Fischetti, Andrea;Gilbert, Ryan J., and the article was included in《Polymer》. The author mentioned the following in the article:

A major challenge in developing drug-releasing electrospun nanofibers is obtaining long-term drug release over many weeks with no burst release of drug. Here, we present new methods capable of prolonging the diffusive release of small mol. drugs from electrospun poly-L-lactic acid (PLLA) nanofibers. The methods focus on removal of retained electrospinning solvent through fiber heating, maintaining fibers in a laboratory setting, or a combination of these methods. These post-fabrication methods altered the release characteristics of a model small mol. drug, 6-aminonicotinamide (6AN), from PLLA fibers. Specifically, untreated fibers released 6AN over 9 days, and fibers that underwent a combined treatment of maintenance in a laboratory setting and heating released 6AN over 44 days. The unique and simple method presented here prolongs diffusive release of a small mol. drug from electrospun fibers and has potential to assist in lengthening small mol. drug release from a variety of polymeric nanomaterials. The experimental procedure involved many compounds, such as 6-Aminonicotinamide (cas: 329-89-5) .

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

Mims, Jade;Bansal, Nidhi;Bharadwaj, Manish S.;Chen, Xiaofei;Molina, Anthony J.;Tsang, Allen W.;Furdui, Cristina M. published 《Energy metabolism in a matched model of radiation resistance for head and neck squamous cell cancer》 in 2015. The article was appeared in 《Radiation Research》. They have made some progress in their research.SDS of cas: 329-89-5 The article mentions the following:

While radiation therapy is commonly used for treating cancer, radiation resistance can limit long-term control of the disease. In this study, we investigated the reprogramming of the energy metabolism in radiosensitive and radioresistant head and neck squamous cell carcinomas (HNSCC) using a preclin. matched model of radiation resistance. Our investigation found that radioresistant rSCC-61 cells: 1. They display increased glucose uptake and decreased fatty acid uptake;. 2. They deviate from the classical Warburg effect by diverting the glycolytic flux into the pentose phosphate pathway;. 3.They are more dependent on glucose than glutamine metabolism to support growth;. 4.They have decreased mitochondrial oxidative phosphorylation;. 5.They have enhanced fatty acid biosynthesis by increasing the expression of fatty acid synthase; and 6.They utilize endogenous fatty acids to meet the energy demands for proliferation. Inhibition of fatty acid synthase with orlistat or FASN siRNA resulted in increased cytotoxicity and sensitivity to radiation in rSCC-61 cells. These results demonstrate the potential of combination therapy using radiation and orlistat or other inhibitors of lipid and energy metabolism for treating radiation resistance in HNSCC. And 6-Aminonicotinamide (cas: 329-89-5) was used in the research process.

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

Zamani, Shahrzad;Hoseini, Ahmad Zavaran;Namin, Alireza Mesbah published 《Glucose-6-phosphate dehydrogenase (G6PD) activity can modulate macrophage response to Leishmania major infection》. The research results were published in《International Immunopharmacology》 in 2019.Category: amides-buliding-blocks The article conveys some information:

Glucose-6-phosphate dehydrogenase (G6PDH) ultimately plays a critical role in macrophage functions used against infectious agents. The present study investigated whether changes in G6PDH activity could influence the resistance of infected macrophages against Leishmania major infection. Mouse peritoneal and J774 macrophages were infected, resp., ex vivo and in vitro, with L. major and then exposed to an inhibitor (6-aminonicotinamide) or activator (LPS + melatonin) of G6PDH activity for 24 h. Cell viability [using MTT assay] was measured to assess any direct toxicity from the doses of inhibitor/activator used for the macrophage treatments. Nitric oxide (NO) produced by the cells and released into culture supernatants was measured (Griess method) and cell G6PDH activity was also determined Moreover, the number of amastigotes form Leishmania in macrophages that developed over a 7-d period was evaluated. The results showed that an increase in G6PDH activity after treatment of both types of macrophages with a combination of LPS + melatonin caused significant increases in NO production and cell resistance against L. major amastigote formation/survival. However, exposure to 6-aminonicotinamide led to remarkable suppression of G6PDH activity and NO production, events that were associated with a deterioration in cell resistance against (and an increase in cell levels of) the parasites. The results suggested that activation or suppression of G6PDH activity could affect leishmanicidal function of both mouse peritoneal and J774 macrophages. Thus, regulation of macrophages via modulation of G6PDH activity appears to provide a novel window for those seeking to develop alternative therapies for the treatment of leishmaniasis. 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

Name: 6-Aminonicotinamide《L-Cysteine in vitro can restore cellular glutathione and inhibits the expression of cell adhesion molecules in G6PD-deficient monocytes》 was published in 2018. The authors were Parsanathan, Rajesh;Jain, Sushil K., and the article was included in《Amino Acids》. The author mentioned the following in the article:

L-Cysteine is a precursor of glutathione (GSH), a potent physiol. antioxidant. Excess glucose-6-phosphate dehydrogenase (G6PD) deficiency in African Americans and low levels of L-cysteine diet in Hispanics can contributes to GSH deficiency and oxidative stress. Oxidative stress and monocyte adhesion was considered to be an initial event in the progression of vascular dysfunction and atherosclerosis. However, no previous study has investigated the contribution of GSH/G6PD deficiency to the expression of monocyte adhesion mols. Using human U937 monocytes, this study examined the effect of GSH/G6PD deficiency and L-cysteine supplementation on monocyte adhesion mols. G6PD/GSH deficiency induced by either siRNA or inhibitors (6AN/BSO, resp.) significantly (p < 0.005) increased the levels of cell adhesion mols. (ICAM-1, VCAM-1, SELL, ITGB1 and 2); NADPH oxidase (NOX), reactive oxygen species (ROS) and MCP-1 were upregulated, and decreases in levels of GSH, and nitric oxide were observed The expression of ICAM-1 and VCAM-1 mRNA levels increased in high glucose, MCP-1 or TNF-α-treated G6PD-deficient compared to G6PD-normal cells. L-Cysteine treatment significantly (p < 0.005) increased G6PD activity and levels of GSH, and decreased NOX, ROS, and adhesion mols. Thus, GSH/G6PD deficiency increases susceptibility to monocyte adhesion processes, whereas L-cysteine supplementation can restore cellular GSH/G6PD and attenuates NOX activity and expression of cell adhesion mols. The experimental procedure involved many compounds, such as 6-Aminonicotinamide (cas: 329-89-5) .

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