Month: February 2023

Vinpocetine reduces cisplatin-induced acute kidney injury through inhibition of NF-κB pathway and activation of Nrf2/ARE pathway in rats was written by Song, Wenjing;Yin, Weinan;Ding, Liang;Gao, Yang;Xu, JingJing;Yang, Yan;He, Xin;Gong, Pengju;Wei, Lei;Chen, Wenli;Zhang, Jingwei. And the article was included in International Urology and Nephrology in 2020.SDS of cas: 42971-09-5 This article mentions the following:

Acute kidney injury is a complex clin. disease that is associated with a high incidence of morbidity and mortality. Drug-induced acute kidney injury occurs in approx. 19-33% of hospitalized patients. Cisplatin, one of the most commonly used and effective chemotherapeutic drugs not only exerts anti-tumor effects but also causes renal toxicity damage, affecting its clin. application. Vinpocetine is an anti-inflammatory and antioxidant drug that predominately acts in the nervous system. In this study, we investigated the effects and mechanisms of vinpocetine in an animal model of cisplatin-induced acute renal injury. Rats were randomly divided into three exptl. groups. During a 10-day trial, rats in the control group were administered a physiol. saline solution; rats in the model group received a 5 mg/kg i.p. injection of cisplatin; and rats in the cisplatin + vinpocetine group received a 5 mg/kg i.p. injection of cisplatin as well as a 5 mg/kg dose of vinpocetine via gavage. We observed that following cisplatin administration, the rats exhibited an increase in blood urea and creatinine levels as well as an increase in their inflammation and oxidative stress levels. In renal tissue, cisplatin caused the morphol. changes typical of acute tubular injury. Vinpocetine reduced the cisplatin-induced acute renal function damage and tubular injury. In both in vivo and in vitro experiments, we found that vinpocetine can confer protection of rat renal cells by inhibiting the NF-κB signaling pathway and activating the Nrf2/ARE signaling pathway. Therefore, vinpocetine is a promising therapeutic drug for the treatment of cisplatin-induced acute kidney injury. In the experiment, the researchers used many compounds, for example, (41S,13aS)-Ethyl 13a-ethyl-2,3,41,5,6,13a-hexahydro-1H-indolo[3,2,1-de]pyrido[3,2,1-ij][1,5]naphthyridine-12-carboxylate (cas: 42971-09-5SDS of cas: 42971-09-5).

(41S,13aS)-Ethyl 13a-ethyl-2,3,41,5,6,13a-hexahydro-1H-indolo[3,2,1-de]pyrido[3,2,1-ij][1,5]naphthyridine-12-carboxylate (cas: 42971-09-5) belongs to naphthyridine derivatives. The naphthyridine ring system, being very π-deficient, is highly vulnerable towards nucleophilic attack, and consequently there has been extensive investigation of reactions involving nitrogen nucleophiles. Enoxacin, nalidixic acid, and trovafloxacin are 1,8-naphthyridine derivatives with antibacterial properties related to the fluoroquinolones.SDS of cas: 42971-09-5

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

Casein kinase 2 inhibition sensitizes medulloblastoma to temozolomide was written by Nitta, Ryan T.;Bolin, Sara;Luo, Emily;Solow-Codero, David E.;Samghabadi, Peyman;Purzner, Teresa;Aujla, Parvir S.;Nwagbo, Ginikachi;Cho, Yoon-Jae;Li, Gordon. And the article was included in Oncogene in 2019.Product Details of 1009820-21-6 This article mentions the following:

Medulloblastoma (MB) is the most common malignant pediatric brain tumor. Since surviving patients experience severe neurocognitive disabilities, better and more effective treatments are needed to enhance their quality of life. Casein kinase 2 (CK2) is known to regulate cell growth and survival in multiple cancers; however, the role of CK2 in MB is currently being studied. In this study, we verified the importance of CK2 in MB tumorigenesis and discovered that inhibition of CK2 using the small mol. inhibitor, CX-4945, can sensitize MB cells to a well-known and tolerated chemotherapeutic, temozolomide (TMZ). To study the role of CK2 in MB we modulated CK2 expression in multiple MB cells. Exogenous expression of CK2 enhanced cell growth and tumor growth in mice, while depletion or inhibition of CK2 expression decreased MB tumorigenesis. Treatment with CX-4945 reduced MB growth and increased apoptosis. We conducted a high-throughput screen where 4000 small mol. compounds were analyzed to identify compounds that increased the anti-tumorigenic properties of CX-4945. TMZ was found to work synergistically with CX-4945 to decrease cell survival and increase apoptosis in MB cells. O-6-methylguanine-DNA methyltransferase (MGMT) activity is directly correlated to TMZ sensitivity. We found that loss of CK2 activity reduced β-catenin expression, a known MGMT regulator, which in turn led to a decrease in MGMT expression and an increased sensitivity to TMZ. Our findings show that CK2 is important for MB maintenance and that treatment with CX-4945 can sensitize MB cells to TMZ treatment. 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. 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.Product Details of 1009820-21-6

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

Investigation of COSMO-SAC model for solubility and cocrystal formation of pharmaceutical compounds was written by Mahmoudabadi, Samane Zarei;Pazuki, Gholamreza. And the article was included in Scientific Reports in 2020.Electric Literature of C22H26N2O2 This article mentions the following:

In this study, a predictive model named COSMO-SAC was investigated in solid/liquid equilibrium for pharmaceutical compounds The examined properties were the solubility of drug in the pure and mixed solvents, octanol/water partition coefficient, and cocrystal formation. The results of the original COSMO-SAC model (COSMO-SAC (2002)) was compared with a semi-predictive model named Flory-Huggins model and a revised version of the COSMO-SAC (COSMO-SAC (2010)). The results indicated the acceptable accuracy of the COSMO-SAC (2002) in the considered scope. The results emphasized on the suitability of the COSMO-SAC model for simple mols. containing C, H, and O by covalent and hydrogen bonding interactions. Applicability of the COSMO-SAC for more complicated mols. made of various functional groups such as COO and COOH doubly requires more modification in the COSMO-SAC. In the experiment, the researchers used many compounds, for example, (41S,13aS)-Ethyl 13a-ethyl-2,3,41,5,6,13a-hexahydro-1H-indolo[3,2,1-de]pyrido[3,2,1-ij][1,5]naphthyridine-12-carboxylate (cas: 42971-09-5Electric Literature of C22H26N2O2).

(41S,13aS)-Ethyl 13a-ethyl-2,3,41,5,6,13a-hexahydro-1H-indolo[3,2,1-de]pyrido[3,2,1-ij][1,5]naphthyridine-12-carboxylate (cas: 42971-09-5) 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.Electric Literature of C22H26N2O2

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

Targeting protein kinase CK2 suppresses bladder cancer cell survival via the glucose metabolic pathway. was written by Zhang, Xiaolei;Yang, Xiao;Yang, Chengdi;Li, Peng;Yuan, Wenbo;Deng, Xiaheng;Cheng, Yidong;Li, Pengchao;Yang, Haiwei;Tao, Jun;Lu, Qiang. And the article was included in Oncotarget in 2016.Formula: C19H12ClN3O2 This article mentions the following:

Casein kinase 2 (CK2) is a constitutively active serine/threonine kinase that promotes cell proliferation and resists apoptosis. Elevated CK2 expression has been demonstrated in several solid tumors. The expression of CK2α in bladder cancer was elevated in tumor tissues compared with that in adjacent normal tissues. Amplified expression of CK2α was highly correlated with histological grade in bladder cancer(P = 0.024). Knockdown of CK2α in bladder cancer cell lines resulted in a reduction in tumor aerobic glycolysis, accompanied with lower phosphorylated AKT. Moreover, low CK2α levels suppressed cell growth, and similar results could be reproduced after treatment with CX-4945 with a dose-dependent response. CX-4945 inhibited migration and induced apoptosis. Furthermore, knockdown of CK2α decreased the tumorigenicity of bladder cancer cells in vivo. This study is the first to report that CK2 increases glucose metabolism in human bladder cancer. Blocking CK2 function may provide novel diagnostic and potential therapeutic. In the experiment, the researchers used many compounds, for example, 5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid (cas: 1009820-21-6Formula: C19H12ClN3O2).

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. Enoxacin, nalidixic acid, and trovafloxacin are 1,8-naphthyridine derivatives with antibacterial properties related to the fluoroquinolones.Formula: C19H12ClN3O2

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

A CK2-targeted Pt(IV) prodrug to disrupt DNA damage response was written by Chen, Feihong;Huang, Xiaochao;Wu, Mian;Gou, Shaohua;Hu, Weiwei. And the article was included in Cancer Letters (New York, NY, United States) in 2017.Reference of 1009820-21-6 This article mentions the following:

A Pt(IV) prodrug, Cx-platin, containing CX-4945 (a CK2 inhibitor) as an axial ligand was designed and prepared by targeting CK2 to disrupt DNA damage response. In vitro study indicated that Cx-platin had superior cytotoxicity to cisplatin against a number of cancer cell lines with distinct CK2-expressed levels, caused CK2-overexpressed cancer cells death via suppressing CK2-mediated DNA damage repair and reversed cisplatin resistance. Mechanistic investigation suggested that the potent antitumor activity of Cx-platin resulted from its major suppression of CK2-phosphorylated MDC1 to combine FHA domain of aprataxin to DNA double strand breaks (DSBs) caused by improved cellular uptakes of Pt and ATM deactivation. Further in vivo tests exhibited that Cx-platin displayed high tumor inhibition rates, increased weight gain, and hardly toxicity effects in contrast to cisplatin. In the experiment, the researchers used many compounds, for example, 5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid (cas: 1009820-21-6Reference of 1009820-21-6).

5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid (cas: 1009820-21-6) belongs to naphthyridine derivatives. The naphthyridine ring system, being very π-deficient, is highly vulnerable towards nucleophilic attack, and consequently there has been extensive investigation of reactions involving nitrogen nucleophiles. 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.Reference of 1009820-21-6

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

Vinpocetine attenuates fluoxetine-induced liver damage in rats; Role of Nrf2 and PPAR-γ was written by Mohamed Kamel, Gellan Alaa. And the article was included in Human & Experimental Toxicology in 2021.Product Details of 42971-09-5 This article mentions the following:

Fluoxetine (FLX) has been widely used as first-line treatment in cases of depression and other neuropsychiatric disorders. Although its safety has been approved, the use of FLX was associated with liver injury and chronic liver disease. Vinpocetine (Vinpo), a nootropic drug, possesses antioxidant and anti-inflammatory effects. This study aimed to evaluate the protective effects of Vinpo on FLX-induced liver damage pointing to the role of peroxisome proliferator-activated receptor-gamma (PPAR-γ) and nuclear factor erythroid 2-related factor 2 (Nrf2). Rats were randomized to four groups: control group, Vinpo group (20 mg/kg/day; orally), FLX group (10 mg/kg/day; orally), and Vinpo + FLX group. FLX-induced liver damage was evidenced through elevated liver function biomarkers and induced hepatic histopathol. changes. Concurrent Vinpo treatment resulted in a significant decrease in hepatotoxicity biomarkers and histopathol. alterations. FLX-induced oxidative stress and inflammation were attenuated by Vinpo. In addition, Vinpo attenuated the hepatic NRF2 and HO-1 levels and up-regulated PPAR-γ expression. Moreover, FLX elevated Bcl-2-associated X protein (Bax) mRNA expression and decreased B-cell lymphoma 2 (Bcl2) mRNA expression were markedly reversed by Vinpo. Vinpo possesses ameliorative effects against FLX-induced liver injury in rats. This effect may be due to attenuation of oxidative stress and inflammation, in addition to upregulation of PPAR-γ expression. In the experiment, the researchers used many compounds, for example, (41S,13aS)-Ethyl 13a-ethyl-2,3,41,5,6,13a-hexahydro-1H-indolo[3,2,1-de]pyrido[3,2,1-ij][1,5]naphthyridine-12-carboxylate (cas: 42971-09-5Product Details of 42971-09-5).

(41S,13aS)-Ethyl 13a-ethyl-2,3,41,5,6,13a-hexahydro-1H-indolo[3,2,1-de]pyrido[3,2,1-ij][1,5]naphthyridine-12-carboxylate (cas: 42971-09-5) 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. 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.Product Details of 42971-09-5

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

Comparison of RNA-seq and microarray platforms for splice event detection using a cross-platform algorithm was written by Romero, Juan P.;Ortiz-Estevez, Maria;Muniategui, Ander;Carrancio, Soraya;de Miguel, Fernando J.;Carazo, Fernando;Montuenga, Luis M.;Loos, Remco;Pio, Ruben;Trotter, Matthew W. B.;Rubio, Angel. And the article was included in BMC Genomics in 2018.Reference of 1009820-21-6 This article mentions the following:

RNA-seq is a reference technol. for determining alternative splicing at genome-wide level. Exon arrays remain widely used for the anal. of gene expression, but show poor validation rate with regard to splicing events. Com. arrays that include probes within exon junctions have been developed in order to overcome this problem. We compare the performance of RNA-seq (Illumina HiSeq) and junction arrays (Affymetrix Human Transcriptome array) for the anal. of transcript splicing events. Three different breast cancer cell lines were treated with CX-4945, a drug that severely affects splicing. To enable a direct comparison of the two platforms, we adapted EventPointer, an algorithm that detects and labels alternative splicing events using junction arrays, to work also on RNA-seq data.Common results and discrepancies between the technologies were validated and/or resolved by over 200 PCR experiments As might be expected, RNA-seq appears superior in cases where the technologies disagree and is able to discover novel splicing events beyond the limitations of phys. probe-sets. We observe a high degree of coherence between the two technologies, however, with correlation of EventPointer results over 0.90. Through decimation, the detection power of the junction arrays is equivalent to RNA-seq with up to 60 million reads. Our results suggest, therefore, that exon-junction arrays are a viable alternative to RNA-seq for detection of alternative splicing events when focusing on well-described transcriptional regions. In the experiment, the researchers used many compounds, for example, 5-((3-Chlorophenyl)amino)benzo[c][2,6]naphthyridine-8-carboxylic acid (cas: 1009820-21-6Reference of 1009820-21-6).

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.Reference of 1009820-21-6

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

Synthesis of 2,6-naphthyridine was written by Giacomello, G.;Gualtieri, F.;Riceieri, F. M.;Stein, M. L.. And the article was included in Tetrahedron Letters in 1965.Name: 2,6-Naphthyridine This article mentions the following:

Transformation of 4-carbethoxynicotinic acid via the acid chloride, b_0.1 102°, gave Et β-diazoacetylisonicotinate (I), m. 58-60° (Et₂O). I treated with Ag₂O in absolute alc. with rearrangement and loss of N gave di-Et β-homocinchomeronate (II), b_0.05 116-17°; picrate m. 104-6°. II kept several days with alc. NH₄OH in a sealed tube and heated at 100° gave the diamide, converted by heating above the m.p. at 177-82° to give the imide (III), m. 229-30° (H₂O). III kept several hrs. at 120° in a sealed tube with POCl₃ gave 1,3-dichloro-2,6-naphthyridine (IV), m. 116° (petr. ether), converted to the 1,3-dihydrazine derivative, m. 300°. The dihydrazine in H₂O-AcOH heated with 10% CuSO₄ solution on a steam bath and the mixture made alk. with 5N NaOH, extracted with CH₂Cl₂ and the dried (Na₂SO₄) extract evaporated gave a solid, sublimed at 60°/0.1 mm. to yield 2,6-naphthyridine, m. 114-15°; monopicrate m. 206° (alc.). Attempted hydrogenolysis of IV with H over prereduced PtO₂ gave 5,6,7,8-tetrahydro-1,3-dichloro-2,6-naphthyridine, m. 125-7° (petr. ether). III mixed with Zn dust and heated at 170° in a sealed tube also gave 2,6-naphthyridine in poorer yields. Spectral data are given. In the experiment, the researchers used many compounds, for example, 2,6-Naphthyridine (cas: 253-50-9Name: 2,6-Naphthyridine).

2,6-Naphthyridine (cas: 253-50-9) belongs to naphthyridine derivatives. The naphthyridines and their derivatives exhibit various types of biological activity, and the organic chemistry has been frequently reviewed. Enoxacin, nalidixic acid, and trovafloxacin are 1,8-naphthyridine derivatives with antibacterial properties related to the fluoroquinolones.Name: 2,6-Naphthyridine

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

Click Quantitative Mass Spectrometry Identifies PIWIL3 as a Mechanistic Target of RNA Interference Activator Enoxacin in Cancer Cells was written by Abell, Nathan S.;Mercado, Marvin;Caneque, Tatiana;Rodriguez, Raphael;Xhemalce, Blerta. And the article was included in Journal of the American Chemical Society in 2017.HPLC of Formula: 84294-96-2 This article mentions the following:

Enoxacin is a small mol. that stimulates RNA interference (RNAi) and acts as a growth inhibitor selectively in cancer but not in untransformed cells. Here, we used alkenox, a clickable enoxacin surrogate, coupled with quant. mass spectrometry, to identify PIWIL3 as a mechanistic target of enoxacin. PIWIL3 is an Argonaute protein of the PIWI subfamily that is mainly expressed in the germline and that mediates RNAi through piRNAs. Our results suggest that cancer cells re-express PIWIL3 to repress RNAi through miRNAs and thus open a new opportunity for cancer-specific targeting. In the experiment, the researchers used many compounds, for example, 1-Ethyl-6-fluoro-4-oxo-7-(piperazin-1-yl)-1,4-dihydro-1,8-naphthyridine-3-carboxylic acid sesquihydrate (cas: 84294-96-2HPLC of Formula: 84294-96-2).

1-Ethyl-6-fluoro-4-oxo-7-(piperazin-1-yl)-1,4-dihydro-1,8-naphthyridine-3-carboxylic acid sesquihydrate (cas: 84294-96-2) 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. Halogen atoms attached to the naphthyridine moiety can be easily replaced by other nucleophiles such as alkoxides and amines.HPLC of Formula: 84294-96-2

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

Effectiveness and safety of Ginkgo biloba, vinpocetine and piracetam as a single agent and fixed dose combination in patients with subjective tinnitus was written by Mathai, Paul;Chandran, Anu;Das, Sourav. And the article was included in Journal of Clinical and Diagnostic Research in 2021.COA of Formula: C22H26N2O2 This article mentions the following:

Owing to the lack of any standard treatment, subjective tinnitus can be debilitating, manifesting a varied population response to tinnitus management. There is, therefore, an unmet need to optimize the existing treatment options and generate data to help physicians provide the best possible care for individual patients. To compare the effectiveness and safety of Ginkgo biloba, vinpocetine, and piracetam as a single agent and their Fixed Dose Combination (FDC) in patients with subjective tinnitus. Patients with complaints of subjective tinnitus were enrolled in this longitudinal cohort, single center study which was conducted at Outpatient Clinic of the ENT Department of Justice KS Hegde Charitable Hospital, Karnataka, India. Patients received one of the five treatments, oral route, three times a day, {group 1: Ginkgo biloba (40 mg); group 2: vinpocetine (5 mg); group 3: piracetam (400 mg); group 4: FDC of Ginkgo biloba (60 mg) and piracetam (400 mg); group 5: FDC of Ginkgo biloba (60 mg), piracetam (800 mg) and vinpocetine (5 mg)} and were followed-up for six weeks using a modified version of Tinnitus Handicap Inventory (THI) and Visual Analog Scale (VAS), before and after the treatment. Data for safety were also recorded. The association between each attribute and the presence of tinnitus was assessed through chi-square tests. A total of 130 out of 149 enrolled patients completed the study. All the groups showed significant improvement in the severity of symptoms at the end of six weeks as assessed by the modified THI and VAS scores. The improvement was found to be better in group 5 than in other groups, which was evident from the percentage improvement at the end of the treatment compared to other groups. No adverse drug reactions were associated with any of the treatment groups. Though all the drugs were found to be effective and safe in reducing the intensity of subjective tinnitus, FDC of Ginkgo biloba-piracetam-vinpocetine may be considered a better alternative than Ginkgo biloba-piracetam combination and Ginkgo biloba, piracetam, or vinpocetine as single agents. In the experiment, the researchers used many compounds, for example, (41S,13aS)-Ethyl 13a-ethyl-2,3,41,5,6,13a-hexahydro-1H-indolo[3,2,1-de]pyrido[3,2,1-ij][1,5]naphthyridine-12-carboxylate (cas: 42971-09-5COA of Formula: C22H26N2O2).

(41S,13aS)-Ethyl 13a-ethyl-2,3,41,5,6,13a-hexahydro-1H-indolo[3,2,1-de]pyrido[3,2,1-ij][1,5]naphthyridine-12-carboxylate (cas: 42971-09-5) 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. Halogen atoms attached to the naphthyridine moiety can be easily replaced by other nucleophiles such as alkoxides and amines.COA of Formula: C22H26N2O2

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