Tag: M.W=400-600

Wang, Juan; Du, Tongde; Lu, Ya; Lv, Yan; Du, Yuxin; Wu, Jianzhong; Ma, Rong; Xu, Chenxin; Feng, Jifeng published the artcile< VLX1570 regulates the proliferation and apoptosis of human lung cancer cells through modulating ER stress and the AKT pathway>, Safety of 9-(6-Aminopyridin-3-yl)-1-(3-(trifluoromethyl)phenyl)benzo[h][1,6]naphthyridin-2(1H)-one, the main research area is AKT endoplasmic reticulum stress human lung cancer proliferation apoptosis; cell proliferation endoplasmic reticulum stress AKT pathway; AKT pathway; ER stress; VLX1570; apoptosis; lung cancer; proliferation.

The ubiquitin-proteasome system (UPS) possesses unique functions in tumorigenesis and has great potential for targeting tumors. The effectiveness of inhibitors targeting UPS in solid tumors remains to be studied. We screened a library of inhibitors targeting the ubiquitination system and found the highly potent, low-concentration inhibitor mol. VLX1570 that specifically killed lung cancer cells. VLX1570 is an inhibitor of deubiquitinating enzyme activity and has also shown potential for preclin. cancer treatment. We found that VLX1570 significantly inhibited lung cancer cells proliferation and colony formation. VLX1570 induced a G2/M cell cycle arrest by downregulating CDK1 and CyclinB1. Moreover, VLX1570 significantly promoted the mitochondrial-associated apoptosis. Mechanistically speaking, VLX1570 activated the PERK/IRE1/ATF6 pathway and induced ER stress in lung cancer cell lines. The inhibition of ER stress by tauroursodeoxycholic acid sodium or 4-phenylbutyric acid enhanced VLX1570-induced apoptosis. In addition, VLX1570 treatment led to the inactivation of Akt signalling and inhibited the proliferation of lung cancer cells by downregulating the Akt pathway. Moreover, combined treatment with VLX1570 and Afatinib or Gefitinib induced synergistic anti-lung cancer activity. Our present study demonstrated a novel therapy using VLX1570, which inhibited the proliferation and increased apoptosis in human lung cancer.

Journal of Cellular and Molecular Medicine published new progress about Activating transcription factor 6α Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 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

Balukoff, Nathan C.; Ho, J. J. David; Theodoridis, Phaedra R.; Wang, Miling; Bokros, Michael; Llanio, Lis M.; Krieger, Jonathan R.; Schatz, Jonathan H.; Lee, Stephen published the artcile< A translational program that suppresses metabolism to shield the genome>, Application of C24H15F3N4O, the main research area is genome metabolism translational program.

Translatome reprogramming is a primary determinant of protein levels during stimuli adaptation. This raises the question: what are the translatome remodelers that reprogram protein output to activate biochem. adaptations. Here, we identify a translational pathway that represses metabolism to safeguard genome integrity. A system-wide MATRIX survey identified the ancient eIF5A as a pH-regulated translation factor that responds to fermentation-induced acidosis. TMT-pulse-SILAC anal. identified several pH-dependent proteins, including the mTORC1 suppressor Tsc2 and the longevity regulator Sirt1. Sirt1 operates as a pH-sensor that deacetylates nuclear eIF5A during anaerobiosis, enabling the cytoplasmic export of eIF5A/Tsc2 mRNA complexes for translational engagement. Tsc2 induction inhibits mTORC1 to suppress cellular metabolism and prevent acidosis-induced DNA damage. Depletion of eIF5A or Tsc2 leads to metabolic re-initiation and proliferation, but at the expense of incurring substantial DNA damage. We suggest that eIF5A operates as a translatome remodeler that suppresses metabolism to shield the genome.

Nature Communications published new progress about Acidosis. 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

Kowalski, Elizabeth; Geng, Shuo; Rathes, Allison; Lu, Ran; Li, Liwu published the artcile< Toll-interacting protein differentially modulates HIF1α and STAT5-mediated genes in fibroblasts>, Safety of 9-(6-Aminopyridin-3-yl)-1-(3-(trifluoromethyl)phenyl)benzo[h][1,6]naphthyridin-2(1H)-one, the main research area is inflammation infection Toll interacting protein HIF1alpha STAT5 gene fibroblast; gene expression profile inflammatory cytokine IL6 IL12 TNFalpha FABP4; fibroblast; gene expression; inflammation; innate immunity; signal transduction.

Toll-interacting protein (Tollip) deficiency has been implicated in complex inflammatory and infectious diseases whose mechanisms are poorly understood. Comparing the gene expression profiles of WT and Tollip-deficient murine embryonic fibroblasts, we observed here that Tollip deficiency selectively reduces the expression of the inflammatory cytokines interleukin 6 (IL-6), IL-12, and tumor necrosis factor α (TNFα) but potentiates the expression of fatty acid-binding protein 4 (FABP4) in these cells. We also observed that expression of hypoxia-inducible factor 1-α (HIF1α) is reduced, whereas that of signal transducer and activator of transcription 5 (STAT5) is elevated, in Tollip-deficient cells, correlating with the decreased expression of inflammatory cytokines and increased expression of FABP4 in these cells. We further found that the coupling of ubiquitin to ER degradation (CUE) domain of Tollip is required for stimulating HIF1α activity, because Tollip CUE-domain mutant cells exhibited reduced levels of HIF1α and selected cytokines. Tollip is known to mediate autophagy and lysosome fusion, and herein we observed that Tollip’s autophagy function is required for modulating STAT5 and FABP4 expression. Bafilomycin A, an inhibitor of lysosome fusion, enhanced STAT5 and FABP4 expression in WT fibroblasts, whereas torin 2, an activator of autophagy, reduced STAT5 and FABP4 expression in Tollip-deficient fibroblasts. Taken together, our study reveals that Tollip differentially modulates HIF1α and STAT5 expression in fibroblasts, potentially explaining the complex and context-dependent contribution of Tollip to disease development.

Journal of Biological Chemistry published new progress about Autophagy (lysosome fusion). 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

Banerjee, Dipanjan; Sinha, Archana; Saikia, Sudeshna; Gogoi, Bhaskarjyoti; Rathore, Arvind K.; Das, Anindhya Sundar; Pal, Durba; Buragohain, Alak K.; Dasgupta, Suman published the artcile< Inflammation-induced mTORC2-Akt-mTORC1 signaling promotes macrophage foam cell formation>, Formula: C24H15F3N4O, the main research area is inflammation mTORC1 2 Akt signal transduction macrophage foam cell; Akt phosphorylation; Inflammation; Macrophage foam cell; TLR4 signaling; mTORC2.

The transformation of macrophages into lipid-loaded foam cells is a critical and early event in the pathogenesis of atherosclerosis. Several recent reports highlighted that induction of TLR4 signaling promotes macrophage foam cell formation; however, the underlying mol. mechanisms have not been clearly elucidated. Here, we found that the TLR4 mediated inflammatory signaling communicated with mTORC2-Akt-mTORC1 metabolic cascade in macrophage and thereby promoting lipid uptake and foam cell formation. Mechanistically, LPS treatment markedly upregulates TLR4 mediated inflammatory pathway which by activating mTORC2 induces Akt phosphorylation at serine 473 and that aggravate mTORC1 dependent scavenger receptors expression and consequent lipid accumulation in THP-1 macrophages. Inhibition of mTORC2 either by silencing Rictor expression or inhibiting its association with mTOR notably prevents LPS induced Akt activation, scavenger receptors expression, and macrophage lipid accumulation. Although suppression of mTORC1 expression by genetic knockdown of Raptor did not produce any significant change in Akt S473 phosphorylation, however, incubation with Akt activator in Rictor silenced cells failed to promote scavenger receptors expression and macrophage foam cell formation. Thus, present research explored the signaling pathway involved in inflammation-induced macrophage foam cells formation and therefore, targeting this pathway might be useful for preventing macrophage foam cell formation.

Biochimie published new progress about Atherosclerosis. 1223001-51-1 belongs to class naphthyridine, and the molecular formula is C24H15F3N4O, Formula: C24H15F3N4O.

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

Miller, William P.; Mihailescu, Maria L.; Yang, Chen; Barber, Alistair J.; Kimball, Scot R.; Jefferson, Leonard S.; Dennis, Michael D. published the artcile< The translational repressor 4E-BP1 contributes to diabetes-induced visual dysfunction>, Quality Control of 1223001-51-1, the main research area is diabetes visual dysfunction 4EBP1.

PURPOSE: The translational repressor 4E-BP1 interacts with the mRNA cap-binding protein eIF4E and thereby promotes cap-independent translation of mRNAs encoding proteins that contribute to diabetic retinopathy. Interaction of 4E-BP1 with eIF4E is enhanced in the retina of diabetic rodents, at least in part, as a result of elevated 4E-BP1 protein expression. In the present study, we examined the role of 4E-BP1 in diabetes-induced visual dysfunction, as well as the mechanism whereby hyperglycemia promotes 4E-BP1 expression. METHODS: Nondiabetic and diabetic wild-type and 4E-BP1/2 knockout mice were evaluated for visual function using a virtual optomotor test (Optomotry). Retinas were harvested from nondiabetic and type 1 diabetic mice and analyzed for protein abundance and posttranslational modifications. Similar analyses were performed on cells in culture exposed to hyperglycemic conditions or an O-GlcNAcase inhibitor (Thiamet G [TMG]). RESULTS: Diabetes-induced visual dysfunction was delayed in mice deficient of 4E-BP1/2 as compared to controls. 4E-BP1 protein expression was enhanced by hyperglycemia in the retina of diabetic rodents and by hyperglycemic conditions in retinal cells in culture. A similar elevation in 4E-BP1 expression was observed with TMG. The rate of 4E-BP1 degradation was significantly prolonged by either hyperglycemic conditions or TMG. A PEST motif in the C-terminus of 4E-BP1 regulated polyubiquitination, turnover, and binding of an E3 ubiquitin ligase complex containing CUL3. CONCLUSIONS: The findings support a model whereby elevated 4E-BP1 expression observed in the retina of diabetic rodents is the result of O-GlcNAcylation of 4E-BP1 within its PEST motif.

Investigative Ophthalmology & Visual Science published new progress about Amino acids Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 1223001-51-1 belongs to class naphthyridine, and the molecular formula is C24H15F3N4O, Quality Control of 1223001-51-1.

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

Wang, Congcong; Zhang, Ruiguo; Tan, Jian; Meng, Zhaowei; Zhang, Yueqian; Li, Ning; Wang, Hanjie; Chang, Jin; Wang, Renfei published the artcile< Effect of mesoporous silica nanoparticles co-loading with 17-AAG and Torin2 on anaplastic thyroid carcinoma by targeting VEGFR2>, Quality Control of 1223001-51-1, the main research area is anaplastic thyroid carcinoma mesoporous silica nanoparticle; anaplastic thyroid carcinoma; vascular endothelial growth factor receptor 2; molecular targeted drugs; drug combination therapy; resistance; nanoparticles.

Anaplastic thyroid carcinoma (ATC) is a highly aggressive tumor with a poor prognosis and a low median survival rate because of insufficient effective therapeutic modalities. Recently, mesoporous silica nanoparticles (MSNs) as a green non-toxic and safe nanomaterial have shown advantages to be a drug carrier and to modify the targeting group to the targeted therapy. To aim of the study was to explore the effects of MSNs co-loading with 17-allylamino-17-demethoxy-geldanamycin (17-AAG; HSP90 inhibitor) and 9-(6-aminopyridin-3-yl)-1-(3-(trifluoromethyl)phenyl)benzo[h][1,6]naphthyridin-2(1H)-one (Torin2; mTOR inhibitor) by targeting vascular endothelial growth factor receptor 2 (VEGFR2) on the viability of human anaplastic thyroid carcinoma FRO cells. The cytotoxicity of 17-AAG and Torin2 were analyzed by MTT assay. The possible synergistic antitumor effects between 17-AAG and Torin2 were evaluated by CompuSyn software. Flow cytometry was performed to assess the VEGFR2 targeting of (17-AAG + Torin2)@MSNs-anti-VEGFR2 ab and uptake by FRO cells. An ATC xenograft mouse model was established to assess the antitumor effect of (17-AAG + Torin2)@MSNs-anti-VEGFR2 ab in vivo. The results revealed that the combination of 17-AAG and Torin2 inhibited the growth of FRO cells more effectively compared with single use of these agents. Addnl., the synergistic antitumor effect appeared when concentration ratio of the two drugs was 1:1 along with total drug concentration greater than 0.52μM. Furthermore, in an ATC animal model, it was revealed that the (17-AAG + Torin2)@MSNs-anti-VEGFR2 ab therapy modality could most effectively prolong the median survival time [39.5 days vs. 33.0 days (non-targeted) or 27.5 days (control)]. Compared to (17-AAG + Torin2)@MSNs, the (17-AAG + Torin2)@MSNs-anti-VEGFR2 ab could not only inhibit ATC cell growth but also prolong the median survival time of tumor-bearing mice in vivo and vitro more effectively, which may provide a new promising therapy for ATC.

Oncology Reports published new progress about Anaplastic thyroid gland carcinoma. 1223001-51-1 belongs to class naphthyridine, and the molecular formula is C24H15F3N4O, Quality Control of 1223001-51-1.

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

Bruning, Ulrike; Morales-Rodriguez, Francisco; Kalucka, Joanna; Goveia, Jermaine; Taverna, Federico; Queiroz, Karla C. S.; Dubois, Charlotte; Cantelmo, Anna Rita; Chen, Rongyuan; Loroch, Stefan; Timmerman, Evy; Caixeta, Vanessa; Bloch, Katarzyna; Conradi, Lena-Christin; Treps, Lucas; Staes, An; Gevaert, Kris; Tee, Andrew; Dewerchin, Mieke; Semenkovich, Clay F.; Impens, Francis; Schilling, Birgit; Verdin, Eric; Swinnen, Johannes V.; Meier, Jordan L.; Kulkarni, Rhushikesh A.; Sickmann, Albert; Ghesquiere, Bart; Schoonjans, Luc; Li, Xuri; Mazzone, Massimiliano; Carmeliet, Peter published the artcile< Impairment of Angiogenesis by Fatty Acid Synthase Inhibition Involves mTOR Malonylation>, Safety of 9-(6-Aminopyridin-3-yl)-1-(3-(trifluoromethyl)phenyl)benzo[h][1,6]naphthyridin-2(1H)-one, the main research area is fatty acid synthase mTOR acetyl CoA malonylation angiogenesis; angiogenesis; endothelial cell; fatty acid synthase; lipids; mTOR; mTORC1; malonyl-CoA; metabolism; post-translational modifications; protein malonylation.

The role of fatty acid synthesis in endothelial cells (ECs) remains incompletely characterized. We report that fatty acid synthase knockdown (FASNKD) in ECs impedes vessel sprouting by reducing proliferation. Endothelial loss of FASN impaired angiogenesis in vivo, while FASN blockade reduced pathol. ocular neovascularization, at >10-fold lower doses than used for anti-cancer treatment. Impaired angiogenesis was not due to energy stress, redox imbalance, or palmitate depletion. Rather, FASNKDelevated malonyl-CoA levels, causing malonylation(a post-translational modification) of mTOR at lysine 1218 (K1218). MTOR K-1218 malonylation impaired mTOR complex 1 (mTORC1) kinase activity, thereby reducing phosphorylation of downstream targets(p70S6K/4EBP1). Silencing acetyl-CoA carboxylase 1 (an enzyme producing malonyl-CoA) normalized malonyl-CoA levels and reactivated mTOR in FASNKD ECs. Mutagenesis unveiled the importance of mTOR K1218 malonylation for angiogenesis. This study unveils a novel role of FASN in metabolite signaling that contributes to explaining the anti-angiogenic effect of FASN blockade.

Cell Metabolism published new progress about Angiogenesis. 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

Kumar, Pavan; Awasthi, Ankita; Nain, Vikrant; Issac, Biju; Puria, Rekha published the artcile< Novel insights into TOR signaling in Saccharomyces cerevisiae through Torin2>, Application In Synthesis of 1223001-51-1, the main research area is gene transcription repression mTOR signaling Saccharomyces Torin2 inhibition; Asymmetric cell division; Budding pattern; Iron toxicity; Saccharomyces; Torin2.

Target of rapamycin (TOR) regulates cellular homeostasis by coordinating cellular growth pathways in response to different environmental signals. Rapamycin, an allosteric TOR complex 1 (TORC1) inhibitor, has proven to be invaluable for elucidating various aspects of the TOR signaling pathway; however, its applications are limited due to its inability to completely suppress TORC2. In the present study, we examined the effects of a newly discovered potent TOR inhibitor, Torin2, which inhibits both TORC1 and TORC2, on Saccharomyces cerevisiae growth. Genome-scale expression profiling of Torin2 treated yeast cells showed an expression profile similar to that of other TOR inhibitors such as rapamycin and caffeine. Distinct inhibition of cell growth by Torin2 treatment is indicated by the fact that a smaller number of transcripts are altered, compared to the changes after rapamycin and caffeine treatments. Our results revealed that Torin2 leads to increased expression of the calcineurin pathway genes favoring a synergistic therapeutic response of Torin2 in combination with calcineurin inhibitors. Further, Torin2 causes defective bud site selection during asym. cell division, indicating a role of TOR signaling in regulation of the budding pattern. Torin2 treated yeast cells exhibit increased expression of metalloreductases which affects iron homeostasis leading to iron toxicity. Notably, the enhanced expression of TOR1 and TOR2 rescue the Torin2 augmented iron toxicity of yeast cell. This study has revealed novel conduits and our results suggest that using Torin2 will enable the dissection of TORC2 mediated functions of the TOR signaling pathway.

Gene published new progress about Asymmetric cell division. 1223001-51-1 belongs to class naphthyridine, and the molecular formula is C24H15F3N4O, Application In Synthesis of 1223001-51-1.

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

Vogel, K. R.; Ainslie, G. R.; McConnell, A.; Roullet, J.-B.; Gibson, K. M. published the artcile< Toxicologic/transport properties of NCS-382, a γ-hydroxybutyrate (GHB) receptor ligand, in neuronal and epithelial cells: Therapeutic implications for SSADH deficiency, a GABA metabolic disorder>, Name: 9-(6-Aminopyridin-3-yl)-1-(3-(trifluoromethyl)phenyl)benzo[h][1,6]naphthyridin-2(1H)-one, the main research area is NCS382 hydroxybutyrate receptor ligand toxicol transport neuron epithelium; GABA metabolism; NCS-382; Neuronal stem cells; SSADH deficiency (SSADHD); Succinic semialdehyde dehydrogenase (SSADH); γ-Hydroxybutyric acid (GHB).

We report the in vitro assessment of pharmacotoxicity for the high-affinity GHB receptor ligand, NCS-382, using neuronal stem cells derived from mice with a targeted deletion of the aldehyde dehydrogenase 5a1 gene (succinic semialdehyde dehydrogenase (SSADH)-deficient mice). These animals represent a phenocopy of the human disorder of GABA metabolism, SSADH deficiency, that metabolically features accumulation of both GABA and the GABA-analog γ-hydroxybutyric acid in conjunction with a nonspecific neurol. phenotype. We demonstrate for the first time using MDCK cells that NCS-382 is actively transported and capable of inhibiting GHB transport. Following these in vitro assays with in vivo studies in aldh5a1-/- mice, we found the ratio of brain/liver GHB to be unaffected by chronic NCS-382 administration (300 mg/kg; 7 consecutive days). Employing a variety of cellular parameters (reactive oxygen and superoxide species, ATP production and decay, mitochondrial and lysosomal number, cellular viability and necrosis), we demonstrate that up to 1 mM NCS-382 shows minimal evidence of pharmacotoxicity. As well, studies at the mol. level indicate that the effects of NCS-382 at 0.5 mM are minimally toxic as evaluated using gene expression assay. The cumulative data provides increasing confidence that NCS-382 could eventually be considered in the therapeutic armament for heritable SSADH deficiency.

Toxicology In Vitro published new progress about Animal gene Role: BSU (Biological Study, Unclassified), BIOL (Biological Study) (aldh5a1). 1223001-51-1 belongs to class naphthyridine, and the molecular formula is C24H15F3N4O, Name: 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

Vogel, Kara R.; Ainslie, Garrett R.; Walters, Dana C.; McConnell, Alice; Dhamne, Sameer C.; Rotenberg, Alexander; Roullet, Jean-Baptiste; Gibson, K. Michael published the artcile< Succinic semialdehyde dehydrogenase deficiency, a disorder of GABA metabolism: an update on pharmacological and enzyme-replacement therapeutic strategies>, Name: 9-(6-Aminopyridin-3-yl)-1-(3-(trifluoromethyl)phenyl)benzo[h][1,6]naphthyridin-2(1H)-one, the main research area is NCS 382 enzyme replacement therapy succinic semialdehyde dehydrogenase deficiency; Enzyme replacement therapy; GABA; Gamma-hydroxybutyric aciduria; Succinic semialdehyde dehydrogenase deficiency; Torin 2; mTOR.

We present an update to the status of research on succinic semialdehyde dehydrogenase (SSADH) deficiency (SSADHD), a rare disorder of GABA metabolism This is an unusual disorder featuring the accumulation of both GABA and its neuromodulatory analog, gamma-hydroxybutyric acid (GHB), and recent studies have advanced the potential clin. application of NCS-382, a putative GHB receptor antagonist. Animal studies have provided proof-of-concept that enzyme replacement therapy could represent a long-term therapeutic option. The characterization of neuronal stem cells (NSCs) derived from aldehyde dehydrogenase 5a1-/- (aldh5a1-/-) mice, the murine model of SSADHD, has highlighted NSC utility as an in vitro system in which to study therapeutics and associated toxicol. properties. Gene expression analyses have revealed that transcripts encoding GABAA receptors are down-regulated and may remain largely immature in aldh5a1-/- brain, characterized by excitatory as opposed to inhibitory outputs, the latter being the expected action in the mature central nervous system. This indicates that agents altering chloride channel activity may be therapeutically relevant in SSADHD. The most recent therapeutic prospects include mTOR (mechanistic target of rapamycin) inhibitors, drugs that have received attention with the elucidation of the effects of elevated GABA on autophagy. The outlook for novel therapeutic trials in SSADHD continues to improve.

Journal of Inherited Metabolic Disease published new progress about Autophagy. 1223001-51-1 belongs to class naphthyridine, and the molecular formula is C24H15F3N4O, Name: 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