Category: 1009820-21-6

Combined Casein Kinase II inhibition and epigenetic modulation in acute B-lymphoblastic leukemia. was written by Richter, Anna;Roolf, Catrin;Hamed, Mohamed;Gladbach, Yvonne Saara;Sender, Sina;Konkolefski, Christoph;Knübel, Gudrun;Sekora, Anett;Fuellen, Georg;Vollmar, Brigitte;Murua Escobar, Hugo;Junghanss, Christian. And the article was included in BMC cancer in 2019.Name: 5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid This article mentions the following:

BACKGROUND: The tumor suppressor protein phosphatase and tensin homolog (PTEN) is a key regulator of the PI3K/AKT pathway which is frequently altered in a variety of tumors including a subset of acute B-lymphoblastic leukemias (B-ALL). While PTEN mutations and deletions are rare in B-ALL, promoter hypermethylation and posttranslational modifications are the main pathways of PTEN inactivation. Casein Kinase II (CK2) is often upregulated in B-ALL and phosphorylates both PTEN and DNA methyltransferase 3A, resulting in increased PI3K/AKT signaling and offering a potential mechanism for further regulation of tumor-related pathways. METHODS: Here, we evaluated the effects of CK2 inhibitor CX-4945 alone and in combination with hypomethylating agent decitabine on B-ALL proliferation and PI3K/AKT pathway activation. We further investigated if CX-4945 intensified decitabine-induced hypomethylation and identified aberrantly methylated biological processes after CK2 inhibition. In vivo tumor cell proliferation in cell line and patient derived xenografts was assessed by longitudinal full body bioluminescence imaging and peripheral blood flow cytometry of NSG mice. RESULTS: CX-4945 incubation resulted in CK2 inhibition and PI3K pathway downregulation thereby inducing apoptosis and anti-proliferative effects. CX-4945 further affected methylation patterns of tumor-related transcription factors and regulators of cellular metabolism. No overlap with decitabine-affected genes or processes was detected. Decitabine alone revealed only modest anti-proliferative effects on B-ALL cell lines, however, if combined with CX-4945 a synergistic inhibition was observed. In vivo assessment of CX-4945 in B-ALL cell line xenografts resulted in delayed proliferation of B-ALL cells. Combination with DEC further decelerated B-ALL expansion significantly and decreased infiltration in bone marrow and spleen. Effects in patient-derived xenografts all harboring a t(4;11) translocation were heterogeneous. CONCLUSIONS: We herein demonstrate the anti-leukemic potential of CX-4945 in synergy with decitabine in vitro as well as in vivo identifying CK2 as a potentially targetable kinase in B-ALL. In the experiment, the researchers used many compounds, for example, 5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid (cas: 1009820-21-6Name: 5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid).

5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid (cas: 1009820-21-6) belongs to naphthyridine derivatives. Six naphthyridine isomers exist, based on the positions of the nitrogen atoms; they can be in the 1,5, 1,6, 1,7, 1,8, 2,6, or 2,7 positions. 1,6-Naphthyridine and some of its derivatives have been reported to have medicinal, electronic, and catalytic properties. But none of these investigations has yet resulted in any practical applications. Very few metal complexes of naphthyridines other than 1,8-naphthyridine have been described.Name: 5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid

Referemce:
1,8-Naphthyridine – Wikipedia,
1,8-Naphthyridine | C8H6N2 – PubChem

Exploring the pivotal role of the CK2 hinge region sub-pocket in binding with tricyclic quinolone analogues by computational analysis was written by Zhou, Yue;Zhang, Na;Tang, Shan;Qi, Xiaoqian;Zhao, Lijiao;Zhong, Rugang;Peng, Yongzhen. And the article was included in Molecules in 2017.Product Details of 1009820-21-6 This article mentions the following:

Protein kinase CK2 has been considered as an attractive therapeutic target of cancer therapy. The tricyclic quinoline compound CX-4945 is the first representative of CK2 inhibitors used in human clin. trials. The binding of non-2,6-naphtyridine substituted compounds 27e (IC₅₀ > 500 nM) and 27h (IC₅₀ > 1000 nM) to CK2 is abolished. However, the unbinding mechanisms due to the key pharmacophore group replacement of compounds 27e and 27h are unveiled. In the present work, combined computational anal. was performed to investigate the underlying structural basis of the low-affinity of two systems. As indicated in the results, the loss of hydrogen bonds between the non-2,6-naphtyridine and the hinge region destroyed the proper recognition of the two complexes. Besides, the allosteric mechanisms between the deviated ligands and the changed regions (G-loop, C-loop and β4/β5 loop) are proposed. Furthermore, energetic anal. was evaluated by detailed energy calculation and residue-based energy decomposition More importantly, the summary of known polar pharmacophore groups elucidates the pivotal roles of hinge region sub-pocket in the binding of CK2 inhibitors. These results provide rational clues to the fragment-based design of more potent CK2 inhibitors. In the experiment, the researchers used many compounds, for example, 5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid (cas: 1009820-21-6Product Details of 1009820-21-6).

5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid (cas: 1009820-21-6) belongs to naphthyridine derivatives. Functionalized naphthyridines and their benzo/heterofused analogs are present in numerous marine products and reported to possess wide-ranging activities such as antiproliferative, antiaggressive, and HIV-1 integrase inhibition in addition to their use as anti-HCV agents. 1,6-Naphthyridine and some of its derivatives have been reported to have medicinal, electronic, and catalytic properties. But none of these investigations has yet resulted in any practical applications. Very few metal complexes of naphthyridines other than 1,8-naphthyridine have been described.Product Details of 1009820-21-6

Referemce:
1,8-Naphthyridine – Wikipedia,
1,8-Naphthyridine | C8H6N2 – PubChem

Mechanistic insights of key host proteins and potential repurposed inhibitors regulating SARS-CoV-2 pathway was written by Pramanik, Debabrata;Pawar, Aiswarya B.;Roy, Sudip;Singh, Jayant Kumar. And the article was included in Journal of Computational Chemistry in 2022.Electric Literature of C19H12ClN3O2 This article mentions the following:

The emergence of pandemic situations originated from severe acute respiratory syndrome (SARS)-CoV-2 and its new variants created worldwide medical emergencies. Due to the non-availability of efficient drugs and vaccines at these emergency hours, repurposing existing drugs can effectively treat patients critically infected by SARS-CoV-2. Finding a suitable repurposing drug with inhibitory efficacy to a host-protein is challenging. A detailed mechanistic understanding of the kinetics, (dis)association pathways, key protein residues facilitating the entry-exit of the drugs with targets are fundamental in selecting these repurposed drugs. Keeping this target as the goal of the paper, the potential repurposing drugs, Nafamostat, Camostat, Silmitasertib, Valproic acid, and Zotatifin with host-proteins HDAC2, CSK22, and eIF4E2 are studied to elucidate energetics, kinetics, and dissociation pathways. From an ensemble of independent simulations, we observed the presence of single or multiple dissociation pathways with varying host-proteins-drug systems and quant. estimated the probability of unbinding through these specific pathways. We also explored the crucial gateway residues facilitating these dissociation mechanisms. Interestingly, the residues we obtained for HDAC2 and CSK22 are also involved in the catalytic activity. Our results demonstrate how these potential drugs interact with the host machinery and the specific target residues, showing involvement in the mechanism. Most of these drugs are in the preclin. phase, and some are already being used to treat severe COVID-19 patients. Hence, the mechanistic insight presented in this study is envisaged to support further findings of clin. studies and eventually develop efficient inhibitors to treat SARS-CoV-2. In the experiment, the researchers used many compounds, for example, 5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid (cas: 1009820-21-6Electric Literature of C19H12ClN3O2).

5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid (cas: 1009820-21-6) belongs to naphthyridine derivatives. Six naphthyridine isomers are white solids with a surprisingly wide span of melting points: 1,6-Naphthyridine’s is the lowest at <40 ºC; 2,6-naphthyridine’s is the highest at 114–115 ºC. Halogen atoms attached to the naphthyridine moiety can be easily replaced by other nucleophiles such as alkoxides and amines.Electric Literature of C19H12ClN3O2

Referemce:
1,8-Naphthyridine – Wikipedia,
1,8-Naphthyridine | C8H6N2 – PubChem

Protein Kinase CK2 Acts as a Molecular Brake to Control NADPH Oxidase 1 Activation and Colon Inflammation was written by Liu, Dan;Marie, Jean-Claude;Pelletier, Anne-Laure;Song, Zhuoyao;Ben-Khemis, Marwa;Boudiaf, Kaouthar;Pintard, Coralie;Leger, Thibaut;Terrier, Samuel;Chevreux, Guillaume;El-Benna, Jamel;Dang, Pham My-Chan. And the article was included in Cellular and Molecular Gastroenterology and Hepatology in 2022.Synthetic Route of C19H12ClN3O2 This article mentions the following:

NADPH oxidase 1 (NOX1) has emerged as a prime regulator of intestinal mucosa immunity and homeostasis. Dysregulation of NOX1 may cause inflammatory bowel disease (IBD). It is not clear how NOX1 is regulated in vivo under inflammatory conditions. We studied the role of CK2 in this process. The NOX1 organizer subunit, NADPH oxidase organizer 1 (NOXO1), was immunoprecipitated from cytokine-treated colon epithelial cells, and bound proteins were identified by mass spectrometry anal. Sites on NOXO1 phosphorylated by CK2 were identified by nanoscale liquid chromatog. coupled to tandem mass spectrometry. NOX1 activity was determined in colon epithelial cells and colonoids in the presence or absence of CX-4945, a CK2 specific inhibitor. Acute colitis was induced by administration of trinitrobenzenesulfonic acid in mice treated or not with CX-4945. Colon tissues were analyzed by histol. examination, quant. polymerase chain reaction, and Western blots. CK2 activity, markers of inflammation, and oxidative stress were assessed. We identified CK2 as a major partner of NOXO1 in colon epithelial cells under inflammatory conditions. CK2 directly binds NOXO1 at the C-terminus containing the Phox homol. domain and phosphorylates NOXO1 on several sites. CX-4945 increased ROS generation by NOX1 in human colon epithelial cells and organoids. Strikingly, CK2 activity was reduced in trinitrobenzenesulfonic acid-induced acute colitis, and CX-4945 exacerbated colitis inflammation as shown by increased levels of CXCL1, ROS generation, lipid peroxidation, and colon damage. The ubiquitous protein kinase CK2 limits NOX1 activity via NOXO1 binding and phosphorylation in colonic epithelial cells and lessens exptl. colitis. Loss of CK2 activity during acute colitis results in excessive ROS production, contributing to the pathogenesis. Strategies to activate CK2 could be an effective novel therapeutic approach in IBD. In the experiment, the researchers used many compounds, for example, 5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid (cas: 1009820-21-6Synthetic Route of C19H12ClN3O2).

5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid (cas: 1009820-21-6) belongs to naphthyridine derivatives. Six naphthyridine isomers are white solids with a surprisingly wide span of melting points: 1,6-Naphthyridine’s is the lowest at <40 ºC; 2,6-naphthyridine’s is the highest at 114–115 ºC. Halogen atoms attached to the naphthyridine moiety can be easily replaced by other nucleophiles such as alkoxides and amines.Synthetic Route of C19H12ClN3O2

Referemce:
1,8-Naphthyridine – Wikipedia,
1,8-Naphthyridine | C8H6N2 – PubChem

Multistep virtual screening based identification of homeodomain-interacting protein kinase 2 inhibitors: An opportunity for treating Chronic Kidney Disease was written by Cao, Yuanyuan;Le, Xiangyang;Shi, Xiaomei;Hao, Chao;Ma, Binghao;Chen, Zhuo;Hu, Gaoyun;Cao, Dongsheng;Li, Qianbin. And the article was included in Chemometrics and Intelligent Laboratory Systems in 2021.Safety of 5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid This article mentions the following:

Homeodomain-Interacting Protein Kinase 2 (HIPK2) is a critical regulator of multiple pathways upstream of Chronic Kidney Disease (CKD). With the purpose of seeking HIPK2 inhibitors with novel scaffolds, a multistep virtual screening from the SPECS library was conducted. The screening process generally included similarity screening, random forest modeling, docking and ADMET prediction. Ten compounds were finally purchased and evaluated in biol. activity test. The activity results demonstrated that the compound 1 (SPECS ID AG-401/37408043) can inhibit enzymic activity and cell viability of high-glucose-induced rat normal renal interstitial fibroblast cells (NRK49F) with moderate activity. Its binding modes with the HIPK2 ATP binding site were analyzed. Overall, the compound 1 with a rather new scaffold might be used as the lead for the future structural optimization to seek potent HIPK2 inhibitors. In the experiment, the researchers used many compounds, for example, 5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid (cas: 1009820-21-6Safety of 5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid).

5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid (cas: 1009820-21-6) belongs to naphthyridine derivatives. The naphthyridines and their derivatives exhibit various types of biological activity, and the organic chemistry has been frequently reviewed. Very few metal complexes of naphthyridines other than 1,8-naphthyridine have been described.Safety of 5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid

Referemce:
1,8-Naphthyridine – Wikipedia,
1,8-Naphthyridine | C8H6N2 – PubChem

Targeting CK2 in cancer: a valuable strategy or a waste of time? was written by Salvi, Mauro;Borgo, Christian;Pinna, Lorenzo A.;Ruzzene, Maria. And the article was included in Cell Death Discovery in 2021.Computed Properties of C19H12ClN3O2 This article mentions the following:

CK2 is a protein kinase involved in several human diseases (ranging from neurol. and cardiovascular diseases to autoimmune disorders, diabetes, and infections, including COVID-19), but its best-known implications are in cancer, where it is considered a pharmacol. target. Several CK2 inhibitors are available and clin. trials are underway in different cancer types. Recently, the suitability of CK2 as a broad anticancer target has been questioned by the finding that a newly developed compound, named SGC-CK2-1, which is more selective than any other known CK2 inhibitor, is poorly effective in reducing cell growth in different cancer lines, prompting the conclusion that the anticancer efficacy of CX-4945, the commonly used clin.-grade CK2 inhibitor, is to be attributed to its off-target effects. Here we perform a detailed scrutiny of published studies on CK2 targeting and a more in-depth anal. of the available data on SGC-CK2-1 vs. CX-4945 efficacy, providing a different perspective about the actual reliance of cancer cells on CK2. Collectively taken, our arguments would indicate that the pretended dispensability of CK2 in cancer is far from having been proved and warn against premature conclusions, which could discourage ongoing investigations on a potentially valuable drug target. In the experiment, the researchers used many compounds, for example, 5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid (cas: 1009820-21-6Computed Properties of C19H12ClN3O2).

5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid (cas: 1009820-21-6) belongs to naphthyridine derivatives. The naphthyridines and their derivatives exhibit various types of biological activity, and the organic chemistry has been frequently reviewed. Transition metal complexes of 1,5-naphthyridine (1,5-napy) seems to form one-dimensional coordination polymers with the ligand acting as bidentate in a “stepped” bridging fashion.Computed Properties of C19H12ClN3O2

Referemce:
1,8-Naphthyridine – Wikipedia,
1,8-Naphthyridine | C8H6N2 – PubChem

Casein kinase 2 inhibition impairs spontaneous and oxytocin-induced contractions in late pregnant mouse uterus was written by Suhas, K. S.;Parida, Subhashree;Gokul, Chandrasekaran;Srivastava, Vivek;Prakash, E.;Chauhan, Sakshi;Singh, Thakur Uttam;Panigrahi, Manjit;Telang, Avinash G.;Mishra, Santosh K.. And the article was included in Experimental Physiology in 2018.Recommanded Product: 5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid This article mentions the following:

The protein kinase casein kinase 2 (CK2) is a ubiquitously expressed serine or threonine kinase known to phosphorylate a number of substrates. The aim of this study was to assess the effect of CK2 inhibition on spontaneous and oxytocin-induced uterine contractions in 19 day pregnant mice. The CK2 inhibitor CX-4945 elicited a concentration-dependent relaxation in late pregnant mouse uterus. CX-4945 and another selective CK2 inhibitor, apigenin, also inhibited the oxytocin-induced contractile response in late pregnant uterine tissue. Apigenin also blunted the prostaglandin F_2a response, but CX-4945 did not. Casein kinase 2 was located in the lipid raft fractions of the cell membrane, and disruption of lipid rafts was found to reverse its effect. The results of the present study suggest that CK2, located in lipid rafts of the cell membrane, is an active regulator of spontaneous and oxytocin-induced uterine contractions in the late pregnant mouse. In the experiment, the researchers used many compounds, for example, 5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid (cas: 1009820-21-6Recommanded Product: 5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid).

5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid (cas: 1009820-21-6) belongs to naphthyridine derivatives. Functionalized naphthyridines and their benzo/heterofused analogs are present in numerous marine products and reported to possess wide-ranging activities such as antiproliferative, antiaggressive, and HIV-1 integrase inhibition in addition to their use as anti-HCV agents. Imidazonaphthyridines have been prepared through a ‘one-pot’ three-component ‘domino’ reaction between the keto-ester, acrolein, and ethylenediamine in presence of 4 Å molecular sieves.Recommanded Product: 5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid

Referemce:
1,8-Naphthyridine – Wikipedia,
1,8-Naphthyridine | C8H6N2 – PubChem

Anti-Growth, Anti-Angiogenic, and Pro-Apoptotic Effects by CX-4945, an Inhibitor of Casein Kinase 2, on HuCCT-1 Human Cholangiocarcinoma Cells via Control of Caspase-9/3, DR-4, STAT-3/STAT-5, Mcl-1, eIF-2α, and HIF-1α was written by Wang, Saini;Yadav, Anil Kumar;Han, Jin-Yi;Ahn, Keun Soo;Jang, Byeong-Churl. And the article was included in International Journal of Molecular Sciences in 2022.Quality Control of 5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid This article mentions the following:

Overexpression of casein kinase 2 (CK2) has an oncogenic and pro-survival role in many cancers. CX-4945 (Silmitasertib) is a CK2 inhibitor with anti-cancerous and anti-angiogenic effects. Up to date, the anti-cancer effect and mechanism of CX-4945 on human cholangiocarcinoma (CCA) remain unclear. This study investigated whether CX-4945 inhibits growth and induces apoptosis of HuCCT-1 cells, a human CCA cell line. Of note, treatment with CX-4945 at 20μM markedly reduced survival and induced apoptosis of HuCCT-1 cells, as evidenced by nuclear DNA fragmentation, PARP cleavage, activation of caspase-9/3, and up-regulation of DR-4. Although CX-4945 did not affect the phosphorylation and expression of CK2, it vastly inhibited the phosphorylation of CK2 substrates, supporting the drug’s efficacy in inhibiting CK2 and its downstream pathway. Importantly, knockdown of CK2 that partially suppressed the phosphorylation of CK2 substrates resulted in a significant reduction of HuCCT-1 cell survival. In addition, CX-4945 reduced the phosphorylation and expression of STAT-3 and STAT-5 in HuCCT-1 cells, and pharmacol. inhibition or resp. knockdown of these proteins resulted in significant growth suppression of HuCCT-1 cells. CX-4945 also had abilities to decrease Mcl-1 expression while increasing eIF-2α phosphorylation in HuCCT-1 cells. Furthermore, there was a time-differential neg. regulation of HIF-1α expression by CX-4945 in HuCCT-1 cells, and knockdown of HIF-1α caused a significant reduction of the cell survival. In summary, these results demonstrated that CX-4945 has anti-growth, anti-angiogenic, and pro-apoptotic effects on HuCCT-1 cells, which are mediated through control of CK2, caspase-9/3, DR-4, STAT-3/5, Mcl-1, eIF-2α, and HIF-1α. In the experiment, the researchers used many compounds, for example, 5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid (cas: 1009820-21-6Quality Control of 5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid).

5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid (cas: 1009820-21-6) belongs to naphthyridine derivatives. Heterocyclic nitrogen compounds, including fused 1,5-naphthyridines, have versatile applications in synthetic organic chemistry and play an important role in the field of medicinal chemistry, as many of them have a wide range of biological activities. Transition metal complexes of 1,5-naphthyridine (1,5-napy) seems to form one-dimensional coordination polymers with the ligand acting as bidentate in a “stepped” bridging fashion.Quality Control of 5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid

Referemce:
1,8-Naphthyridine – Wikipedia,
1,8-Naphthyridine | C8H6N2 – PubChem

The Global Phosphorylation Landscape of SARS-CoV-2 Infection was written by Bouhaddou, Mehdi;Memon, Danish;Meyer, Bjoern;White, Kris M.;Rezelj, Veronica V.;Correa Marrero, Miguel;Polacco, Benjamin J.;Melnyk, James E.;Ulferts, Svenja;Kaake, Robyn M.;Batra, Jyoti;Richards, Alicia L.;Stevenson, Erica;Gordon, David E.;Rojc, Ajda;Obernier, Kirsten;Fabius, Jacqueline M.;Soucheray, Margaret;Miorin, Lisa;Moreno, Elena;Koh, Cassandra;Tran, Quang Dinh;Hardy, Alexandra;Robinot, Remy;Vallet, Thomas;Nilsson-Payant, Benjamin E.;Hernandez-Armenta, Claudia;Dunham, Alistair;Weigang, Sebastian;Knerr, Julian;Modak, Maya;Quintero, Diego;Zhou, Yuan;Dugourd, Aurelien;Valdeolivas, Alberto;Patil, Trupti;Li, Qiongyu;Huttenhain, Ruth;Cakir, Merve;Muralidharan, Monita;Kim, Minkyu;Jang, Gwendolyn;Tutuncuoglu, Beril;Hiatt, Joseph;Guo, Jeffrey Z.;Xu, Jiewei;Bouhaddou, Sophia;Mathy, Christopher J. P.;Gaulton, Anna;Manners, Emma J.;Felix, Eloy;Shi, Ying;Goff, Marisa;Lim, Jean K.;McBride, Timothy;O’Neal, Michael C.;Cai, Yiming;Chang, Jason C. J.;Broadhurst, David J.;Klippsten, Saker;De wit, Emmie;Leach, Andrew R.;Kortemme, Tanja;Shoichet, Brian;Ott, Melanie;Saez-Rodriguez, Julio;tenOever, Benjamin R.;Mullins, R. Dyche;Fischer, Elizabeth R.;Kochs, Georg;Grosse, Robert;Garcia-Sastre, Adolfo;Vignuzzi, Marco;Johnson, Jeffery R.;Shokat, Kevan M.;Swaney, Danielle L.;Beltrao, Pedro;Krogan, Nevan J.. And the article was included in Cell (Cambridge, MA, United States) in 2020.Synthetic Route of C19H12ClN3O2 This article mentions the following:

The causative agent of the coronavirus disease 2019 (COVID-19) pandemic, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has infected millions and killed hundreds of thousands of people worldwide, highlighting an urgent need to develop antiviral therapies. Here, we present a quant. mass spectrometry-based phosphoproteomics survey of SARS-CoV-2 infection in Vero E6 cells, revealing dramatic rewiring of phosphorylation on host and viral proteins. SARS-CoV-2 infection promoted casein kinase II (CK2) and p38 MAPK activation, production of diverse cytokines, and shutdown of mitotic kinases, resulting in cell cycle arrest. Infection also stimulated a marked induction of CK2-containing filopodial protrusions possessing budding viral particles. Eighty-seven drugs and compounds were identified by mapping global phosphorylation profiles to dysregulated kinases and pathways. We found pharmacol. inhibition of the p38, CK2, CDK, AXL, and PIKFYVE kinases to possess antiviral efficacy, representing potential COVID-19 therapies. In the experiment, the researchers used many compounds, for example, 5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid (cas: 1009820-21-6Synthetic Route of C19H12ClN3O2).

5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid (cas: 1009820-21-6) belongs to naphthyridine derivatives. The naphthyridines have 10 delocalized π-electrons located in five molecular orbitals, each of which is distorted by the presence of the nitrogen atoms causing an electron drift in that direction. Transition metal complexes of 1,5-naphthyridine (1,5-napy) seems to form one-dimensional coordination polymers with the ligand acting as bidentate in a “stepped” bridging fashion.Synthetic Route of C19H12ClN3O2

Referemce:
1,8-Naphthyridine – Wikipedia,
1,8-Naphthyridine | C8H6N2 – PubChem

Proteomic investigation reveals dominant alterations of neutrophil degranulation and mRNA translation pathways in patients with COVID-19 was written by Bankar, Renuka;Suvarna, Kruthi;Ghantasala, Saicharan;Banerjee, Arghya;Biswas, Deeptarup;Choudhury, Manisha;Palanivel, Viswanthram;Salkar, Akanksha;Verma, Ayushi;Singh, Avinash;Mukherjee, Amrita;Pai, Medha Gayathri J.;Roy, Jyotirmoy;Srivastava, Alisha;Badaya, Apoorva;Agrawal, Sachee;Shrivastav, Om;Shastri, Jayanthi;Srivastava, Sanjeeva. And the article was included in iScience in 2021.Application In Synthesis of 5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid This article mentions the following:

The altered mol. proteins and pathways in response to COVID-19 infection are still unclear. Here, we performed a comprehensive proteomics-based investigation of nasopharyngeal swab samples from patients with COVID-19 to study the host response by employing simple extraction strategies. Few of the host proteins such as interleukin-6, L-lactate dehydrogenase, C-reactive protein, Ferritin, and aspartate aminotransferase were found to be upregulated only in COVID-19-pos. patients using targeted multiple reaction monitoring studies. The most important pathways identified by enrichment anal. were neutrophil degranulation, interleukin-12 signaling pathways, and mRNA translation of proteins thus providing the detailed investigation of host response in COVID-19 infection. Thus, we conclude that mass spectrometry-detected host proteins have a potential for disease severity progression; however, suitable validation strategies should be deployed for the clin. translation. Furthermore, the in silico docking of potential drugs with host proteins involved in the interleukin-12 signaling pathway might aid in COVID-19 therapeutic interventions. In the experiment, the researchers used many compounds, for example, 5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid (cas: 1009820-21-6Application In Synthesis of 5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid).

5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid (cas: 1009820-21-6) belongs to naphthyridine derivatives. Six naphthyridine isomers exist, based on the positions of the nitrogen atoms; they can be in the 1,5, 1,6, 1,7, 1,8, 2,6, or 2,7 positions. Transition metal complexes of 1,5-naphthyridine (1,5-napy) seems to form one-dimensional coordination polymers with the ligand acting as bidentate in a “stepped” bridging fashion.Application In Synthesis of 5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid

Referemce:
1,8-Naphthyridine – Wikipedia,
1,8-Naphthyridine | C8H6N2 – PubChem