Heterocyclic Building Blocks-Naphthyridine

Vogel, Kara R.; Ainslie, Garrett R.; Gibson, K. Michael published the artcile< mTOR inhibitors rescue premature lethality and attenuate dysregulation of GABAergic/glutamatergic transcription in murine succinate semialdehyde dehydrogenase deficiency (SSADHD), a disorder of GABA metabolism>, Recommanded Product: 9-(6-Aminopyridin-3-yl)-1-(3-(trifluoromethyl)phenyl)benzo[h][1,6]naphthyridin-2(1H)-one, the main research area is rapamycin mTOR inhibitor GABA glutamate succinate semialdehyde dehydrogenase deficiency.

Recent studies have identified a role for supraphysiol. gamma-aminobutyric acid (GABA) in the regulation of mechanistic target of rapamycin (mTOR), a protein kinase with pleiotropic roles in cellular development and homeostasis, including integration of growth factors and nutrient sensing and synaptic input in neurons (Lakhani et al. 2014; Vogel et al. 2015). Aldehyde dehydrogenase 5a1-deficient (aldh5a1-/-) mice, the murine orthologue of human succinic semialdehyde dehydrogenase deficiency (SSADHD), manifest increased GABA that disrupts mitophagy and increases mitochondria number with enhanced oxidant stress. Treatment with the mTOR inhibitor, rapamycin, significantly attenuates these GABA-related anomalies. We extend those studies through characterization of addnl. rapamycin analog (rapalog) agents including temsirolimus, dual mTOR inhibitors [Torin 1 and 2 (Tor 1/ Tor 2), Ku-0063794, and XL-765], as well as mTOR-independent autophagy inducers [trehalose, tat-Beclin 1, tacrolimus (FK-506), and NF-449) in aldh5a1-/- mice. Rapamycin, Tor 1, and Tor 2 rescued these mice from premature lethality associated with status epilepticus. XL-765 extended lifespan significantly and induced weight gain in aldh5a1-/- mice; untreated aldh5a1-/- mice failed to increase body mass. Expression profiling of animals rescued with Tor 1/Tor 2 and XL-765 revealed multiple instances of pharmacol. compensation and/or correction of GABAergic and glutamatergic receptors, GABA/glutamate transporters, and GABA/glutamate-associated proteins, with Tor 2 and XL-765 showing optimal outcomes. Our studies lay the groundwork for further evaluation of mTOR inhibitors in aldh5a1-/- mice, with therapeutic ramifications for heritable disorders of GABA and glutamate neurotransmission.

Journal of Inherited Metabolic Disease published new progress about Adenosine A2A receptors Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 1223001-51-1 belongs to class naphthyridine, and the molecular formula is C24H15F3N4O, Recommanded Product: 9-(6-Aminopyridin-3-yl)-1-(3-(trifluoromethyl)phenyl)benzo[h][1,6]naphthyridin-2(1H)-one.

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

Amin, Anubhav G.; Jeong, Seung Won; Gillick, John L.; Sursal, Tolga; Murali, Raj; Gandhi, Chirag D.; Jhanwar-Uniyal, Meena published the artcile< Targeting the mTOR pathway using novel ATP-competitive inhibitors, Torin1, Torin2 and XL388, in the treatment of glioblastoma>, Electric Literature of 1223001-51-1, the main research area is mTOR Torin1 Torin2 XL388 glioblastoma; PRAS40; Torin1; Torin2; glioblastoma; mTOR; mTOR inhibitors.

Mechanistic target of rapamycin (mTOR), which functions via two multiprotein complexes termed mTORC1 and mTORC2, is positioned in the canonical phosphoinositide 3-kinase-related kinase (PI3K)/AKT (PI3K/AKT) pathways. These complexes exert their actions by regulating other important kinases, such as 40S ribosomal S6 kinases (S6K), eukaryotic translation initiation factor 4E (elF4E)-binding protein 1 (4E-BP1) and AKT, to control cell growth, proliferation, migration and survival in response to nutrients and growth factors. Glioblastoma (GB) is a devastating form of brain cancer, where the mTOR pathway is deregulated due to frequent upregulation of the Receptor Tyrosine Kinase/PI3K pathways and loss of the tumor suppressor phosphatase and tensin homolog (PTEN). Rapamycin and its analogs were less successful in clin. trials for patients with GB due to their incomplete inhibition of mTORC1 and the activation of mitogenic pathways via neg. feedback loops. Here, the effects of selective ATP-competitive dual inhibitors of mTORC1 and mTORC2, Torin1, Torin2 and XL388, are reported. Torin2 exhibited concentration-dependent pharmacodynamic effects on inhibition of phosphorylation of the mTORC1 substrates S6KSer235/236 and 4E-BP1Thr37/46 as well as the mTORC2 substrate AKTSer473 resulting in suppression of tumor cell migration, proliferation and S-phase entry. Torin1 demonstrated similar effects, but only at higher doses. XL388 suppressed cell proliferation at a higher dose, but failed to inhibit cell migration. Treatment with Torin1 suppressed phosphorylation of proline rich AKT substrate of 40 kDa (PRAS40) at Threonine 246 (PRAS40Thr246) whereas Torin2 completely abolished it. XL388 treatment suppressed the phosphorylation of PRAS40Thr246 only at higher doses. Drug resistance anal. revealed that treatment of GB cells with XL388 rendered partial drug resistance, which was also seen to a lesser extent with rapamycin and Torin1 treatments. However, treatment with Torin2 completely eradicated the tumor cell population. These results strongly suggest that Torin2, compared to Torin1 or XL388, is more effective in suppressing mTORC1 and mTORC2, and therefore in the inhibition of the GB cell proliferation, dissemination and in overcoming resistance to therapy. These findings underscore the significance of Torin2 in the treatment of GB.

International Journal of Oncology published new progress about Antitumor agents. 1223001-51-1 belongs to class naphthyridine, and the molecular formula is C24H15F3N4O, Electric Literature of 1223001-51-1.

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

Mosaddeghi, Pouria; Eslami, Mahboobeh; Farahmandnejad, Mitra; Akhavein, Mahshad; Ranjbarfarrokhi, Ratin; Khorraminejad-Shirazi, Mohammadhossein; Shahabinezhad, Farbod; Taghipour, Mohammadjavad; Dorvash, Mohammadreza; Sakhteman, Amirhossein; Zarshenas, Mohammad M.; Nezafat, Navid; Mobasheri, Meysam; Ghasemi, Younes published the artcile< A systems pharmacology approach to identify the autophagy-inducing effects of Traditional Persian medicinal plants>, HPLC of Formula: 1223001-51-1, the main research area is autophagy systems pharmacol medicinal plant Persia.

Abstract: Identifying the nature of this correlation and treatment of age-related diseases has been a major subject of both modern and traditional medicine. Traditional Persian Medicine (TPM) embodies many prescriptions for the treatment of ARDs. Given that autophagy plays a critical role in antiaging processes, the present study aimed to examine whether the documented effect of plants used in TPM might be relevant to the induction of autophagy. To this end, the TPM-based medicinal herbs used in the treatment of the ARDs were identified from modern and traditional references The known phytochems. of these plants were then examined against literature for evidence of having autophagy inducing effects. As a result, several plants were identified to have multiple active ingredients, which indeed regulate the autophagy or its upstream pathways. In addition, gene set enrichment anal. of the identified targets confirmed the collective contribution of the identified targets in autophagy regulating processes. Also, the protein-protein interaction (PPI) network of the targets was reconstructed. Network centrality anal. of the PPI network identified mTOR as the key network hub. Given the well-documented role of mTOR in inhibiting autophagy, our results hence support the hypothesis that the antiaging mechanism of TPM-based medicines might involve autophagy induction.

Scientific Reports published new progress about Acute respiratory distress syndrome. 1223001-51-1 belongs to class naphthyridine, and the molecular formula is C24H15F3N4O, HPLC of Formula: 1223001-51-1.

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

ur Rashid, Haroon; Rasool, Shagufta; Ali, Yousaf; Khan, Kamin; Martines, Marco Antonio Utrera published the artcile< Anti-cancer potential of sophoridine and its derivatives: Recent progress and future perspectives>, Recommanded Product: (41S,7aR,13aR,13bR)-Dodecahydro-1H-dipyrido[2,1-f:3′,2′,1′-ij][1,6]naphthyridin-10(41H)-one, the main research area is review antitumor cancer sophoridine derivative; Alkaloid; Cancer; Phytochemical; Sophoridine; Topoisomerase I.

A review. Cancer is the second leading cause of mortality and has resulted in about 9.6 million deaths around the world in 2018. Cancer-caused deaths are expected to be 11.5 million by 2030 all over the world. Because of the fatal nature of cancer, substantial efforts are made all over the world to combat it. Phytoconstituents such as certain alkaloids, saponins, tannins, polyphenols, and terpenoids exhibit anticancer effects. Sophoridine is a tetracyclic quinolizidine alkaloid isolated from the stem and leaves of medicinal plants Sophora alopecuroides L., and Euchresta japonica Benth, and roots of Sophora alopecuroides Ait. Chinese Food and Drug Administration (CFDA) approved sophoridine as an antitumor agent in 2005. This review covers the antitumor activities of sophoridine and its derivatives The efficacy of sophoridine analogs is expressed with respect to their half-maximal inhibitory concentration (IC50 values). Structure-activity relationship (SAR) study for most of the sophoridine derivatives has been explained. Moreover, the current market of anticancer drugs and its expected growth are discussed. Prospects provide suggestions and clues for novel sophoridine-based anticancer agents with enhanced expected efficacy and min. toxicity.

Bioorganic Chemistry published new progress about Antitumor agents. 6882-68-4 belongs to class naphthyridine, and the molecular formula is C15H24N2O, Recommanded Product: (41S,7aR,13aR,13bR)-Dodecahydro-1H-dipyrido[2,1-f:3′,2′,1′-ij][1,6]naphthyridin-10(41H)-one.

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

Yin, Liqing; Zhang, Yongzhu; Azi, Fidelis; Tekliye, Mekonen; Zhou, Jianzhong; Liu, Xiaoli; Dong, Mingsheng; Xia, Xiudong published the artcile< Neuroprotective Potency of Tofu Bio-Processed Using Actinomucorelegans against Hypoxic Injury Induced by Cobalt Chloride in PC12 Cells>, Recommanded Product: 9-(6-Aminopyridin-3-yl)-1-(3-(trifluoromethyl)phenyl)benzo[h][1,6]naphthyridin-2(1H)-one, the main research area is cobalt chloride actinomucorelegan hypoxic injury Tofu bioprocessed neuroprotective potency; autophagy; cell apoptosis; cell arrest; oxidative stress; soybean products.

Fermented soybean products have attracted great attention due to their health benefits. In the present study, the hypoxia-injured PC12 cells induced by cobalt chloride (CoCl2) were used to evaluate the neuroprotective potency of tofu fermented by Actinomucor elegans (FT). Results indicated that FT exhibited higher phenolic content and antioxidant activity than tofu. Moreover, most soybean isoflavone glycosides were hydrolyzed into their corresponding aglycons during fermentation FT demonstrated a significant protective effect on PC12 cells against hypoxic injury by maintaining cell viability, reducing lactic dehydrogenase leakage, and inhibiting oxidative stress. The cell apoptosis was significantly attenuated by the FT through down-regulation of caspase-3, caspases-8, caspase-9, and Bax, and up-regulation of Bcl-2 and Bcl-xL. S-phase cell arrest was significantly inhibited by the FT through increasing cyclin A and decreasing the p21 protein level. Furthermore, treatment with the FT activated autophagy, indicating that autophagy possibly acted as a survival mechanism against CoCl2-induced injury. Overall, FT offered a potential protective effect on nerve cells in vitro against hypoxic damage.

Molecules published new progress about Actinomucor elegans. 1223001-51-1 belongs to class naphthyridine, and the molecular formula is C24H15F3N4O, Recommanded Product: 9-(6-Aminopyridin-3-yl)-1-(3-(trifluoromethyl)phenyl)benzo[h][1,6]naphthyridin-2(1H)-one.

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

Zhao, Yi-Shu; Qian, Xing-Kai; Guan, Xiao-Qing; Song, Pei-Fang; Song, Yun-Qing; He, Rong-Jing; Sun, Meng-Ru; Wang, Xiu-Yang; Zou, Li-Wei; Ge, Guang-Bo published the artcile< Discovery of natural alkaloids as potent and selective inhibitors against human carboxylesterase 2>, Name: (41S,7aR,13aR,13bR)-Dodecahydro-1H-dipyrido[2,1-f:3′,2′,1′-ij][1,6]naphthyridin-10(41H)-one, the main research area is natural alkaloid screening carboxylesterase inhibitor structure; Alkaloids; Human carboxylesterase 2A (hCES2A); Inhibitor; Reserpine.

Human Carboxylesterase 2A (hCES2A), one of the most important serine hydrolases, plays crucial roles in the hydrolysis and the metabolic activation of a wide range of esters and amides. Increasing evidence has indicated that potent inhibition on intestinal hCES2A may reduce the excessive accumulation of SN-38 (the hydrolytic metabolite of irinotecan with potent cytotoxicity) in the intestinal tract and thereby alleviate the intestinal toxicity triggered by irinotecan. In this study, more than sixty natural alkaloids have been collected and their inhibitory effects against hCES2A are assayed using a fluorescence-based biochem. assay. Following preliminary screening, seventeen alkaloids are found with strong to moderate hCES2A inhibition activity. Primary structure-activity relationships (SAR) anal. of natural isoquinoline alkaloids reveal that the benzo-1,3-dioxole group and the aromatic pyridine structure are beneficial for hCES2A inhibition. Further investigations demonstrate that a steroidal alkaloid reserpine exhibits strong hCES2A inhibition activity (IC50 = 0.94μM) and high selectivity over other human serine hydrolases including hCES1A, dipeptidyl peptidase IV (DPP-IV), butyrylcholinesterase (BChE) and thrombin. Inhibition kinetic analyses demonstrated that reserpine acts as a non-competitive inhibitor against hCES2A-mediated FD hydrolysis. Mol. docking simulations demonstrated that the potent inhibition of hCES2A by reserpine could partially be attributed to its strong σ-π and S-π interactions between reserpine and hCES2A. Collectively, our findings suggest that reserpine is a potent and highly selective inhibitor of hCES2A, which can be served as a promising lead compound for the development of more efficacious and selective alkaloids-type hCES2A inhibitors for biomedical applications.

Bioorganic Chemistry published new progress about Alkaloids Role: PAC (Pharmacological Activity), THU (Therapeutic Use), BIOL (Biological Study), USES (Uses). 6882-68-4 belongs to class naphthyridine, and the molecular formula is C15H24N2O, Name: (41S,7aR,13aR,13bR)-Dodecahydro-1H-dipyrido[2,1-f:3′,2′,1′-ij][1,6]naphthyridin-10(41H)-one.

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

Liu, Zhichao; Chen, Xi; Roberts, Ruth; Huang, Ruili; Mikailov, Mike; Tong, Weida published the artcile< Unraveling gene fusions for drug repositioning in high-risk neuroblastoma>, Safety of 9-(6-Aminopyridin-3-yl)-1-(3-(trifluoromethyl)phenyl)benzo[h][1,6]naphthyridin-2(1H)-one, the main research area is neuroblastoma gene fusion drug repositioning; drug repositioning; gene fusions; neuroblastoma; next-generation sequencing; precision medicine 3; structural variants.

High-risk neuroblastoma (NB) remains a significant therapeutic challenge facing current pediatric oncol. patients. Structural variants such as gene fusions have shown an initial promise in enhancing mechanistic understanding of NB and improving survival rates. In this study, we performed a comprehensive in silico investigation on the translational ability of gene fusions for patient stratification and treatment development for high-risk NB patients. Specifically, three state-of-the-art gene fusion detection algorithms, including ChimeraScan, SOAPfuse, and TopHat-Fusion, were employed to identify the fusion transcripts in a RNA-seq data set of 498 neuroblastoma patients. Then, the 176 high-risk patients were further stratified into four different subgroups based on gene fusion profiles. Furthermore, Kaplan-Meier survival anal. was performed, and differentially expressed genes (DEGs) for the redefined high-risk group were extracted and functionally analyzed. Finally, repositioning candidates were enriched in each patient subgroup with drug transcriptomic profiles from the LINCS L1000 Connectivity Map. We found the number of identified gene fusions was increased from clin. the low-risk stage to the high-risk stage. Although the tech. concordance of fusion detection algorithms was suboptimal, they have a similar biol. relevance concerning perturbed pathways and regulated DEGs. The gene fusion profiles could be utilized to redefine high-risk patient subgroups with significant onset age of NB, which yielded the improved survival curves (Log-rank p value le 0.05). Out of 48 enriched repositioning candidates, 45 (93.8%) have antitumor potency, and 24 (50%) were confirmed with either on-going clin. trials or literature reports. The gene fusion profiles have a discrimination power for redefining patient subgroups in high-risk NB and facilitate precision medicine-based drug repositioning implementation.

Frontiers in Pharmacology published new progress about Antitumor agents. 1223001-51-1 belongs to class naphthyridine, and the molecular formula is C24H15F3N4O, Safety of 9-(6-Aminopyridin-3-yl)-1-(3-(trifluoromethyl)phenyl)benzo[h][1,6]naphthyridin-2(1H)-one.

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

Wang, Han; Xu, Xiuli; Wang, Xiujuan; Guo, Wei; Jia, Wei; Zhang, Feng published the artcile< An analytical strategy for discovering structural analogues of alkaloids in plant food using characteristic structural fragments extraction by high resolution orbitrap mass spectrometry>, Recommanded Product: (41S,7aR,13aR,13bR)-Dodecahydro-1H-dipyrido[2,1-f:3′,2′,1′-ij][1,6]naphthyridin-10(41H)-one, the main research area is alkaloid plant food fragment extraction mass spectrometry.

Structural analogs of alkaloids are a huge risk for food safety. However, the discovery of potentially homolog-type alkaloids remains a challenge. A new strategy for discovering structural analogs of alkaloids using high resolution mass spectrometry under data independent acquisition was established using extracted characteristic ions chromatograms and mass spectrometry fragmentations pathway, and successfully developed for discovering and identificating multiple classes of alkaloids in plant food. In this work, we selected 24 alkaloids (pyrrolizidine alkaloids, solanine-type alkaloids, matrine-type alkaloids) as target compounds The data acquisition was based on a non-target approach of data independent acquisition. The general workflow of structural analogs of alkaloids confirming strategy can be split into four major stages: (i) the pathway of fragmentation clarifying, (ii) characteristic structural fragments filtering and confirming, (iii) structural analogs of alkaloids discovery method establishing, (iv) real sample anal. This scheme provided an efficient confirming method for discovering structural analogs of alkaloids in plant food.

LWT–Food Science and Technology published new progress about Alkaloids Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 6882-68-4 belongs to class naphthyridine, and the molecular formula is C15H24N2O, Recommanded Product: (41S,7aR,13aR,13bR)-Dodecahydro-1H-dipyrido[2,1-f:3′,2′,1′-ij][1,6]naphthyridin-10(41H)-one.

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

Phan, Trong-Nhat; Baek, Kyung-Hwa; Lee, Nakyung; Byun, Soo Young; Shum, David; No, Joo Hwan published the artcile< In vitro and in vivo activity of mTOR kinase and PI3K inhibitors against Leishmania donovani and Trypanosoma brucei>, Application of C24H15F3N4O, the main research area is Leishmania Trypanosoma acute monocytic leukemia dactolisib Torin2 PI3K mTOR; Leishmania; Trypanosoma; inhibitors; mammalian target of rapamycin; phosphoinositide 3-kinase.

Kinetoplastid parasites, including Leishmania and Trypanosoma spp., are life threatening pathogens with a worldwide distribution. Next-generation therapeutics for treatment are needed as current treatments have limitations, such as toxicity and drug resistance. In this study, we examined the activities of established mammalian target of rapamycin (mTOR)/phosphoinositide 3-kinase (PI3K) inhibitors against these tropical diseases. High-throughput screening of a library of 1742 bioactive compounds against intracellular L. donovani was performed, and seven mTOR/PI3K inhibitors were identified. Dose-dilution assays revealed that these inhibitors had half maximal effective concentration (EC50) values ranging from 0.14 to 13.44 muM for L. donovani amastigotes and from 0.00005 to 8.16 muM for T. brucei. The results of a visceral leishmaniasis mouse model indicated that treatment with Torin2, dactolisib, or NVP-BGT226 resulted in reductions of 35%, 53%, and 54%, resp., in the numbers of liver parasites. In an acute T. brucei mouse model using NVP-BGT226 parasite numbers were reduced to under the limits of detection by five consecutive days of treatment. Multiple sequence and structural alignment results indicated high similarities between mTOR and kinetoplastid TORs; the inhibitors are predicted to bind in a similar manner. Taken together, these results indicated that the TOR pathways of parasites have potential for the discovery of novel targets and new potent inhibitors.

Molecules published new progress about Acute monocytic leukemia. 1223001-51-1 belongs to class naphthyridine, and the molecular formula is C24H15F3N4O, Application of C24H15F3N4O.

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

Lin, Beibei; Xu, Dingqiao; Wu, Sanqiao; Qi, Shanshan; Xu, Youmei; Liu, Xiang; Zhang, Xiaoying; Chen, Chen published the artcile< Antioxidant effects of Sophora davidi (Franch.) Skeels on D-galactose-induced aging model in mice via activating the SIRT1/p53 pathway>, COA of Formula: C15H24N2O, the main research area is Sophora aging SIRT1 p53 antioxidant; D-galactose; SIRT1; Sophora davidi (franch.) skeels fruits extract; anti-aging; p53.

This study investigated the protective effect of Sophora davidi (Franch.) Skeels fruits extract (SDE) on D-galactose-induced acute aging in mice. Ultra performance liquid chromatog. coupled with tine-of-flight mass spectrometry (UPLC-Q-TOF/MS) was performed to identify the composition of compounds in SDE. KM mice were divided stochastically into the normal control group (NC, saline), D-galactose (D-gal) model group, vitamin C (Vc) group (pos. control), low-, medium-and high-dose SDE treat groups. After 28 days administration and fasting overnight, the serum, liver, and brain samples of mice were collected. The levels of inducible nitric oxide synthase (iNOS), acetylcholinesterase (AChE) activity in the brain, malondialdehyde (MDA) and reduced glutathione (GSH) content, superoxide dismutase (SOD) and total antioxidant capacity (T-AOC) activity in the liver and brain were measured. Immunohistochem. was applied to detect silent information regulator 1 (SIRT1) and p53 protein expression in the liver and brain, and quant. real-time polymerase chain reaction (qRT-PCR) was used to detect the expression of nuclear factor κB (NF-κB), tumor necrosis factor (TNF-α), interleukin-6 (IL-6), interleukin-1β (IL-1β), and anti-aging factor Klotho in the liver and brain. The results showed that UPLC-Q-TOF/MS identified 78 compounds in SDE. SDE could reduce the iNOS activity in serum and AChE activity in the brain, upregulate the levels of SOD, T-AOC and GSH in liver and brain, and debase the MDA content in liver and brain. SDE could downregulate the mRNA expressions of TNF-α, NF-κB, IL-1β, and IL-6 in the liver and brain, and elevate the mRNA expression of Klotho. SDE improved the pathol. changes of the liver and brain induced by D-gal, increased the expression of SIRT1 protein in the liver and brain, and inhibited the expression of p53 protein induced by D-gal. To summarize, SDE demonstrated clear anti-aging effect, and its mechanism may be relevant to the activation of the SIRT1/p53 signal pathway.

Frontiers in Pharmacology published new progress about Aging, animal. 6882-68-4 belongs to class naphthyridine, and the molecular formula is C15H24N2O, COA of Formula: C15H24N2O.

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