Tag: 100-200

Luo, Yin;Tang, Haishuang;Zhang, Zhaolong;Zhao, Rui;Wang, Chuanchuan;Hou, Wenguang;Huang, Qinghai;Liu, Jianmin published 《Pharmacological inhibition of epidermal growth factor receptor attenuates intracranial aneurysm formation by modulating the phenotype of vascular smooth muscle cells》 in 2022. The article was appeared in 《CNS Neuroscience & Therapeutics》. They have made some progress in their research.Name: N,2-Dihydroxybenzamide The article mentions the following:

To study the effect of pharmacol. inhibition of epidermal growth factor receptor (EGFR) on intracranial aneurysm (IA) initiation. Human IA samples were analyzed for the expression of p-EGFR and alpha smooth muscle actin (α-SMA) by immunofluorescence (IF). Rat models of IA were established to evaluate the ability of the EGFR inhibitor, erlotinib, to attenuate the incidence of IA. We analyzed anterior cerebral artery tissues by pathol. and proteomic detection for the expression of p-EGFR and relevant proteins, and vessel casting was used to evaluate the incidence of aneurysms in each group. Rat vascular smooth muscle cells (VSMCs) and endothelial cells were extracted and used to establish an in vitro co-culture model in a flow chamber with or without erlotinib treatment. We determined p-EGFR and relevant protein expression in VSMCs by immunoblotting anal. Epidermal growth factor receptor activation was found in human IA vessel walls and rat anterior cerebral artery walls. Treatment with erlotinib markedly attenuated the incidence of IA by inhibiting vascular remodeling and pro-inflammatory transformation of VSMC in rat IA vessel walls. Activation of EGFR in rat VSMCs and phenotypic modulation of rat VSMCs were correlated with the strength of shear stress in vitro, and treatment with erlotinib reduced phenotypic modulation of rat VSMCs. In vitro experiments also revealed that EGFR activation could be induced by TNF-α in human brain VSMCs. These results suggest that EGFR plays a critical role in the initiation of IA and that the EGFR inhibitor erlotinib protects rats from IA initiation by regulating phenotypic modulation of VSMCs. The experimental procedure involved many compounds, such as N,2-Dihydroxybenzamide (cas: 89-73-6) .

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.Name: N,2-Dihydroxybenzamide

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

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

Rauguth, Andreas;Kredel, Alexander;Carrella, Luca M.;Rentschler, Eva published 《3d/4f Sandwich Complex Based on Metallacrowns》. The research results were published in《Inorganic Chemistry》 in 2021.COA of Formula: C7H7NO3 The article conveys some information:

A novel lanthanide double-decker complex with nickel metallacrowns (MCs) as coordinating ligands has been synthesized. In the 3d/4f metallacrown complex Tb^III[12-MC_Ni^IIN(shi)-4]₂, the central lanthanide ion is sandwiched between two [12-MC-4] units, forming an almost ideal square-antiprismatic coordination sphere. The resulting zenithal angles at the central lanthanide ion are smaller than those for previously reported sandwich compounds Magnetic measurements reveal an energy barrier of 346 K under zero field and up to 585 K under 3200 Oe, the highest reported for metallacrowns with D_4d symmetry. And N,2-Dihydroxybenzamide (cas: 89-73-6) was used in the research process.

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. COA of Formula: C7H7NO3 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

Ding, Lingzhi;Zhou, Jiamin;Ye, Lisa;Sun, Yechao;Jiang, Zhenglin;Gan, Deqiang;Xu, Lihua;Luo, Qianqian;Wang, Guohua published 《PPAR-γ Is Critical for HDAC3-Mediated Control of Oligodendrocyte Progenitor Cell Proliferation and Differentiation after Focal Demyelination》. The research results were published in《Molecular Neurobiology》 in 2020.Formula: C7H7NO3 The article conveys some information:

Disruption of remyelination contributes to neurodegeneration and cognitive impairment in chronically disabled patients. Valproic acid (VPA) inhibits histone deacetylase (HDAC) function and probably promotes oligodendrocyte progenitor cell (OPC) proliferation and differentiation; however, the relevant mol. mechanisms remain unknown. Here, focal demyelinating lesions (FDLs) were generated in mice by two-point stereotactic injection of lysophosphatidylcholine (LPC) into the corpus callosum. Cognitive functions, sensorimotor abilities and histopathol. changes were assessed for up to 28 days post-injury with or without VPA treatment. Primary OPCs were harvested and used to study the effect of VPA on OPC differentiation under inflammatory conditions. VPA dose-dependently attenuated learning and memory deficits and robustly protected white matter after FDL induction, as demonstrated by reductions in SMI-32 and increases in myelin basic protein staining. VPA also promoted OPC proliferation and differentiation and increased subsequent remyelination efficiency by day 28 post-FDL induction. VPA treatment did not affect HDAC1, HDAC2 or HDAC8 expression but reduced HDAC3 protein levels. In vitro, VPA improved the survival of mouse OPCs and promoted their differentiation into oligodendrocytes following lipopolysaccharide (LPS) stimulation. LPS caused OPCs to overexpress HDAC3, which translocated from the cytoplasm into the nucleus, where it directly interacted with the nuclear transcription factor PPAR-γ and neg. regulated PPAR-γ expression. VPA decreased the expression of HDAC3 and promoted remyelination and functional neurol. recovery after FDL. These findings may support the use of strategies modulating HDAC3-mediated regulation of protein acetylation for the treatment of demyelination-related cognitive dysfunction. The experimental procedure involved many compounds, such as N,2-Dihydroxybenzamide (cas: 89-73-6) .

N,2-Dihydroxybenzamide(cas: 89-73-6) is widely used for a variety of roles in biology and medicine as a chelating therapy.Formula: C7H7NO3It inhibits bacterial or fungi growth by interfering with iron uptake. It is also active as a inhibitor of enzyme involved in tumour growths.

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

Wang, Yuanyuan;Jin, Tianlin;Wang, Xue;Liang, Dacheng published 《Phytosterol alterations responding to ROS inhibitors by GC-MS in Arabidopsis》. The research results were published in《Pakistan Journal of Botany》 in 2022.Computed Properties of C7H7NO3 The article conveys some information:

Phytosterols, essential components of cellular membrane integrity, play an important role in plant growth, development, and responses to various types of stressors. Emerging studies have proposed that phytosterols are a result of adaptation to the aerobic environment during evolution. We reasoned that phytosterols could dramatically respond to changes in external reactive oxygen species (ROS) levels. The levels of five phytosterols were measured by gas chromatog.-mass spectrometry (GC-MS) after Arabidopsis plants were treated with the ROS-altering drugs 2′-3′-dideoxycytidine (DDC), H2O2, Catalase (CAT), diphenyleneiodonium (DPI), and salicylhydroxamic acid (SHAM) and auxin transport inhibitors 2,3,5-triiodobenzoic acid (TIBA) and 1-N-naphthylphthalamic acid (NPA). We found that all redox-altering agents can dramatically reduce sterol levels, whereas CAT and NPA can partly increase them. Our results establish a link between redox balance and sterol level alteration. The experimental procedure involved many compounds, such as N,2-Dihydroxybenzamide (cas: 89-73-6) .

N,2-Dihydroxybenzamide(cas: 89-73-6) is widely used for a variety of roles in biology and medicine as a chelating therapy.Computed Properties of C7H7NO3It inhibits bacterial or fungi growth by interfering with iron uptake. It is also active as a inhibitor of enzyme involved in tumour growths.

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 89-73-6《Accurate calculation of equilibrium constants using potentiometric titrations》 was published in 2022. The authors were Phansi, Piyawan;Ferreira, Sergio L. C.;Cerda, Victor, and the article was included in《TrAC, Trends in Analytical Chemistry》. The author mentioned the following in the article:

The aim of this work is to revise some programs, which are used to obtain accurate equilibrium constants using several chained programs. For this purpose, the AutoAnal. software is very useful to perform the exptl. work, including potentiometric titrations The POTENtit program allows detecting some problems in the data obtained with AutoAnal. along the exptl. work, like the presence of metals in the sample and the carbonation of the titrant. This program also allows obtaining the standard potential of the working electrode, and the ionic product of the solvent under the used exptl. ionic strength. Finally the MINIPOT program allows refining the results obtained, both for the calibration of the electrodes (E0, jH, JOH, pKs, and g) and for the constants equilibrium (HqLp or MqLp). These three mentioned programs have been updated in order to run under the Windows 10 environment.N,2-Dihydroxybenzamide (cas: 89-73-6) were involved in the experimental procedure.

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. Product Details 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

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

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