Day: November 22, 2022

KDM6B epigenetically regulated-interleukin-6 expression in the dorsal root ganglia and spinal dorsal horn contributes to the development and maintenance of neuropathic pain following peripheral nerve injury in male rats was written by Li, Liren;Bai, Liying;Yang, Kangli;Zhang, Jian;Gao, Yan;Jiang, Mingjun;Yang, Yin;Zhang, Xuan;Wang, Li;Wang, Xueli;Qiao, Yiming;Xu, Ji-Tian. And the article was included in Brain, Behavior, and Immunity in 2021.Category: pyrimidines The following contents are mentioned in the article:

The lysine specific demethylase 6B (KDM6B) has been implicated as a coregulator in the expression of proinflammatory mediators, and in the pathogenesis of inflammatory and arthritic pain. However, the role of KDM6B in neuropathic pain has yet to be studied. In the current study, the neuropathic pain was determined by assessing the paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) following lumbar 5 spinal nerve ligation (SNL) in male rats. Immunohistochem., Western blotting, qRT-PCR, and chromatin immunoprecipitation (ChIP)-PCR assays were performed to investigate the underlying mechanisms. Our results showed that SNL led to a significant increase in KDM6B mRNA and protein in the ipsilateral L4/5 dorsal root ganglia (DRG) and spinal dorsal horn; and this increase correlated a markedly reduction in the level of H3K27me3 methylation in the same tissue. Double immunofluorescence staining revealed that the KDM6B expressed in myelinated A- and unmyelinated C-fibers in the DRG; and located in neuronal cells, astrocytes, and microglia in the dorsal horn. Behavioral data showed that SNL-induced mech. allodynia and thermal hyperalgesia were impaired by the treatment of prior to i.t. injection of GSK-J4, a specific inhibitor of KDM6B, or KDM6B siRNA. Both microinjection of AAV2-EGFP-KDM6B shRNA in the lumbar 5 dorsal horn and sciatic nerve, sep., alleviated the neuropathic pain following SNL. The established neuropathic pain was also partially attenuated by repeat i.t. injections of GSK-J4 or KDM6B siRNA, started on day 7 after SNL. SNL also resulted in a remarkable increased expression of interleukin-6 (IL-6) in the DRG and dorsal horn. But this increase was dramatically inhibited by i.t. injection of GSK-J4 and KDM6B siRNA; and suppressed by prior to microinjection of AAV2-EGFP-KDM6B shRNA in the dorsal horn and sciatic nerve. Of ChIP-PCR assay showed that SNL-induced enhanced binding of STAT3 with IL-6 promoter was inhibited by prior to i.t. injection of GSK-J4. Meanwhile, the level of H3K27me3 methylation was also decreased by the treatment. Together, our results indicate that SNL-induced upregulation of KDM6B via demethylating H3K27me3 facilitates the binding of STAT3 with IL-6 promoter, and subsequently mediated-increase in the expression of IL-6 in the DRG and dorsal horn contributes to the development and maintenance of neuropathic pain. Targeting KDM6B might a promising therapeutic strategy to treatment of chronic pain. This study involved multiple reactions and reactants, such as Ethyl 3-((6-(4,5-dihydro-1H-benzo[d]azepin-3(2H)-yl)-2-(pyridin-2-yl)pyrimidin-4-yl)amino)propanoate (cas: 1373423-53-0Category: pyrimidines).

Ethyl 3-((6-(4,5-dihydro-1H-benzo[d]azepin-3(2H)-yl)-2-(pyridin-2-yl)pyrimidin-4-yl)amino)propanoate (cas: 1373423-53-0) belongs to pyrimidine derivatives. The pyrimidine nitrogenous bases are derived from the organic compound pyrimidine through the addition of various functional groups. Therapy for fungal infections is based mainly on four classes of antifungals: azoles, echinocandins, polyenes, and pyrimidine analogs.Category: pyrimidines

Referemce:
Pyrimidine | C4H4N2 – PubChem,
Pyrimidine – Wikipedia

The antischistosomal potential of GSK-J4, an H3K27 demethylase inhibitor: insights from molecular modeling, transcriptomics and in vitro assays was written by Lobo-Silva, Jessica;Cabral, Fernanda J.;Amaral, Murilo S.;Miyasato, Patricia A.;de Freitas, Rafaela Paula;Pereira, Adriana S. A.;Khouri, Mariana I.;Barbosa, Mayra M. F.;Ramos, Pablo I. P.;Leite, Luciana C. C.;Asojo, Oluwatoyin A.;Nakano, Eliana;Verjovski-Almeida, Sergio;Farias, Leonardo P.. And the article was included in Parasites & Vectors in 2020.Name: Ethyl 3-((6-(4,5-dihydro-1H-benzo[d]azepin-3(2H)-yl)-2-(pyridin-2-yl)pyrimidin-4-yl)amino)propanoate The following contents are mentioned in the article:

Abstract: Background: Schistosomiasis chemotherapy is largely based on praziquantel (PZQ). Although PZQ is very safe and tolerable, it does not prevent reinfection and emerging resistance is a primary concern. Recent studies have shown that the targeting of epigenetic machinery in Schistosoma mansoni may result in severe alterations in parasite development, leading to death. This new route for drug discovery in schistosomiasis has focused on classes of histone deacetylases (HDACs) and histone acetyltransferases (HATs) as epigenetic drug targets. Schistosoma histone demethylases also seem to be important in the transition of cercariae into schistosomula, as well as sexual differentiation in adult worms. Methods: The Target-Pathogen database and mol. docking assays were used to prioritize the druggability of S. mansoni histone demethylases. The transcription profile of Smp_03400 was re-analyzed using available databases. The effect of GSK-J4 inhibitor in schistosomula and adult worms’ motility/viability/oviposition was assessed by in vitro assays. Ultrastructural anal. was performed on adult worms exposed to GSK-J4 by SEM, while internal structures and muscle fiber integrity was investigated by confocal microscopy after Langeron’s carmine or phalloidin staining. Results: The present evaluation of the potential druggability of 14 annotated S. mansoni demethylase enzymes identified the S. mansoni ortholog of human KDM6A/UTX (Smp_034000) as the most suitable druggable target. In silico anal. and mol. modeling indicated the potential for cofactor displacement by the chem. probe GSK-J4. Our re-anal. of transcriptomic data revealed that Smp_034000 expression peaks at 24 h in newly transformed schistosomula and 5-wk-old adult worms. Moreover, this gene was highly expressed in the testes of mature male worms compared to the rest of the parasite body. In in vitro schistosome cultures, treatment with GSK-J4 produced striking effects on schistosomula mortality and adult worm motility and mortality, as well as egg oviposition, in a dose- and time-dependent manner. Unexpectedly, western blot assays did not demonstrate overall modulation of H3K27me3 levels in response to GSK-J4. Confocal and SEM revealed the loss of original features in muscle fibers and alterations in cell-cell contact following GSK-J4 treatment. Conclusions: GSK-J4 presents promising potential for antischistosomal control; however, the underlying mechanisms warrant further investigation.[graphic not available: see fulltext]. This study involved multiple reactions and reactants, such as Ethyl 3-((6-(4,5-dihydro-1H-benzo[d]azepin-3(2H)-yl)-2-(pyridin-2-yl)pyrimidin-4-yl)amino)propanoate (cas: 1373423-53-0Name: Ethyl 3-((6-(4,5-dihydro-1H-benzo[d]azepin-3(2H)-yl)-2-(pyridin-2-yl)pyrimidin-4-yl)amino)propanoate).

Ethyl 3-((6-(4,5-dihydro-1H-benzo[d]azepin-3(2H)-yl)-2-(pyridin-2-yl)pyrimidin-4-yl)amino)propanoate (cas: 1373423-53-0) belongs to pyrimidine derivatives. The aromatic compound pyrimidine, and its derivatives, are ubiquitous in nature. They are found in nucleic acids, vitamins, amino acids, antibiotics, alkaloids, and a variety of toxins. For example, the neurotoxin tetrodotoxin is a pyrimidine derivative. It is found in a number of species including the Japanese puffer fish, the blue-ringed octopus, and the orange-bellied newt. Tetrodotoxin prevents the transmission of nerve signals and can result in paralysis and death.Name: Ethyl 3-((6-(4,5-dihydro-1H-benzo[d]azepin-3(2H)-yl)-2-(pyridin-2-yl)pyrimidin-4-yl)amino)propanoate

Referemce:
Pyrimidine | C4H4N2 – PubChem,
Pyrimidine – Wikipedia

Relation between goitrogenic effect and chemical constitution was written by Jensen, K. A.;Kjerulf-Jensen, K.. And the article was included in Acta Pharmacologica et Toxicologica in 1945.Name: 5-Ethyl-6-methyl-2-thioxo-2,3-dihydropyrimidin-4(1H)-one The following contents are mentioned in the article:

In young rats, benzenesulfonic acid, phenyl p-toluenesulfonate, p-toluenesulfonamide, taurine, N⁴-(o-carboxybenzoyl)sulfathiazole, Na salt of N⁴-(1-sulfoethyl)sulfathiazole, p-tolyl isothiocyanate, ethylene dithiocyanate, mercaptoacetic acid, cysteine, mercaptosuccinic acid, p-toluenethiol, o-mercaptobenzoic acid, dibenzyl sulfide, bis(2-carboxyethyl) sulfide, α,α’-(thiocarbonyldithio)bis[glycolic acid], thioacetamide, thiobenzamide, xanthogenamide (H₂NC(:S)OEt), Et thionocarbanilate, N-allyl-N’-(m-carboxyphenyl)thiourea, selenourea, 2-methyl-2-thiopseudourea sulfate, thiosemicarbazide, 4-allylthiosemicarbazide, hydrazodithiodicarboxamide, 1,3-oxalylthiourea (thioparabanic acid), 1,3-ethylenethiocarbamide (2-thioxoimidazolidine), 2(3)-benzimidazolethione, 2-imino-4-thiazolidone-5-acetic acid, 5-imino-3-thioxo-1,2,4-dithiazolidine, 2-aminothiazole, thioammeline, 2-amino-4-methyl-6-mercaptopyrimidine, 6-methyl-4-thiouracil, 5-methyl-2-thiouracil (thiothymine), 6-methyluracil, 6-amino-2-thiouracil, 2-amino-4-hydroxy-6-methylpyrimidine, 2-mercapto-4-methyl-6-aminopyrimidine, 2-mercapto-4,6-dimethylpyrimidine, 2-methylmercapto-4-mercapto-6-methylpyrimidine, 2-mercapto-4-phenyl-6-methylpyrimidine, compound (1:1) of NH₃ and 6-imino-5-isonitroso-2-thiouracil, 2-thio-5-aminobarbituric acid (thiouramil), 2-thio-5-ethylbarbituric acid, 2-thioxanthine, 2-thiopseudouric acid, dithiohydurilic acid, 2,4-dioxothiazolidine, 1,4-dithiane, s-trithiane, phenothiazine, biuret, biguanide, dicyandiamidine, thiodicyandiamidine, 1-phenylsemicarbazide, benzoylacetone, salicylaldehyde oxime, β-isatin oxime, dimethylglyoxime, 5-isonitrosobarbituric (violuric) acid, 1-phenyl-3-methyl-4-isonitroso-5-pyrazolone, salicylaldehyde phenylhydrazone, glyoxal osazone, 8-hydroxyquinoline, triphenylphosphine, triphenylarsine, K xanthate, Na diethyldithiocarbamate, KCN, Na₂S, and Na₂S₂O₃ had no goitrogenic action. Sulfaguanidine, sulfonal, dithioöxamide, thiourea, allylthiourea, 1,3-diphenylthiourea, 2-thiohydantoin, 4-oxo-2-thioxo-1,2,3,4-tetrahydroquinazoline, 1,3-(1,8-naphthylene)thiourea, thioantipyrine, and p-aminobenzoic acid were weakly goitrogenic or of doubtful effect. Methylthiourea, trimethylthiourea, tetramethylthiourea, dithizone, 6-methyl-2-thiouracil, 6-methyl-5-ethyl-2-thiouracil, 6-methyl-5-butyl-2-thiouracil (m. 189°, preparation described), 6-methyl-5-isoamyl-2-thiouracil (m. 222-3°, preparation given), and 4-phenyl-2-thiouracil were strongly goitrogenic. This study involved multiple reactions and reactants, such as 5-Ethyl-6-methyl-2-thioxo-2,3-dihydropyrimidin-4(1H)-one (cas: 39083-15-3Name: 5-Ethyl-6-methyl-2-thioxo-2,3-dihydropyrimidin-4(1H)-one).

5-Ethyl-6-methyl-2-thioxo-2,3-dihydropyrimidin-4(1H)-one (cas: 39083-15-3) belongs to pyrimidine derivatives. Pyrimidines are isomeric with two other forms of diazines: pyridazine, with the nitrogen atoms in the 1 and 2 positions; and pyrazine, with the nitrogen atoms in the 1 and 4 positions. Pyrimidine derivatives have been used in a wide variety of pharmaceuticals including general anesthetics, anti-epilepsy medication, anti-malaria medication, drugs for treating high blood pressure, and HIV medication.Name: 5-Ethyl-6-methyl-2-thioxo-2,3-dihydropyrimidin-4(1H)-one

Referemce:
Pyrimidine | C4H4N2 – PubChem,
Pyrimidine – Wikipedia

Cross-suppression of EGFR ligands amphiregulin and epiregulin and de-repression of FGFR3 signalling contribute to cetuximab resistance in wild-type KRAS tumour cells was written by Oliveras-Ferraros, C.;Cufi, S.;Queralt, B.;Vazquez-Martin, A.;Martin-Castillo, B.;de Llorens, R.;Bosch-Barrera, J.;Brunet, J.;Menendez, J. A.. And the article was included in British Journal of Cancer in 2012.Name: 1-(tert-Butyl)-3-(2-((4-(diethylamino)butyl)amino)-6-(3,5-dimethoxyphenyl)pyrido[2,3-d]pyrimidin-7-yl)urea The following contents are mentioned in the article:

BACKGROUND: In addition to the mutational status of KRAS, the epidermal growth factor receptor (EGFR) ligands amphiregulin (AREG) and epiregulin (EREG) might function as bona fide biomarkers of cetuximab (Ctx) sensitivity for most EGFR-driven carcinomas. METHODS: Lentivirus-delivered small hairpin RNAs were employed to specifically reduce AREG or EREG gene expression in wild-type KRAS A431 squamous cell carcinoma cells. Colony-forming assays were used to monitor the impact of AREG and EREG knockdown on Ctx efficacy. Amphiregulin and EREG protein expression levels were assessed by quant. ELISA in parental A431 cells and in pooled populations of A431 cells adapted to grow in the presence of Ctx. A phosphoproteomic platform was used to measure the relative level of phosphorylation of 42 distinct receptor tyrosine kinases before and after the acquisition of resistance to Ctx. RESULTS: Stable gene silencing of either ligand was found to notably reduce the expression of the other ligand. Parental A431 cells with normal expression levels of AREG/EREG exhibited significantly increased growth inhibition in response to Ctx, compared with derivatives that are engineered to produce minimal AREG/EREG. The parental A431 cells acutely treated with Ctx exhibited reduced basal expression levels of AREG/EREG. Pooled populations of Ctx-resistant A431 cells expressed significantly lower levels of AREG/EREG and were insensitive to the downregulatory effects of Ctx. Phosphoproteomic screen identified a remarkable hyperactivation of FGFR3 in Ctx-resistant A431 cells, which gained sensitivity to the cytotoxic and apoptotic effects of the FGFR3 TK inhibitor PD173074. The A431 parental cells acutely treated with Ctx rapidly activated FGFR3 and their concomitant exposure to Ctx and PD173074 resulted in synergistic apoptosis. CONCLUSION: Cross-suppression of AREG/EREG expression may explain the tight co-expression of AREG and EREG, as well as their tendency to be more highly expressed than other EGFR ligands to determine Ctx efficacy. The pos. selection for Ctx-resistant tumor cells exhibiting AREG/EREG cross-suppression may have an important role in the emergence of Ctx resistance. As de-repression of FGFR3 activity rapidly replaces the loss of EGFR-ligand signalling in terms of cell proliferation and survival, combinations of Ctx and FGFR3-targeted drugs may be a valuable strategy to enhance the efficacy of single Ctx while preventing or delaying acquired resistance to Ctx. British Journal of Cancer (2012) 106, 1406-1414. doi:10.1038/bjc.2012.103 www.bjcancer.com. This study involved multiple reactions and reactants, such as 1-(tert-Butyl)-3-(2-((4-(diethylamino)butyl)amino)-6-(3,5-dimethoxyphenyl)pyrido[2,3-d]pyrimidin-7-yl)urea (cas: 219580-11-7Name: 1-(tert-Butyl)-3-(2-((4-(diethylamino)butyl)amino)-6-(3,5-dimethoxyphenyl)pyrido[2,3-d]pyrimidin-7-yl)urea).

1-(tert-Butyl)-3-(2-((4-(diethylamino)butyl)amino)-6-(3,5-dimethoxyphenyl)pyrido[2,3-d]pyrimidin-7-yl)urea (cas: 219580-11-7) belongs to pyrimidine derivatives. Pyrimidine is an aromatic heterocyclic organic compound similar to pyridine. We all know its importance to life – pyrimidine and purine bases are included in the structure of DNA and RNA.Name: 1-(tert-Butyl)-3-(2-((4-(diethylamino)butyl)amino)-6-(3,5-dimethoxyphenyl)pyrido[2,3-d]pyrimidin-7-yl)urea

Referemce:
Pyrimidine | C4H4N2 – PubChem,
Pyrimidine – Wikipedia

Gadolinium chloride inhibition of rat hepatic microsomal epoxide hydrolase and glutathione S-transferase gene expression was written by Kim, Sang Geon;Choi, Sung Hee. And the article was included in Drug Metabolism and Disposition in 1997.Reference of 39083-15-3 The following contents are mentioned in the article:

The effects of gadolinium chloride, a Kupffer cell toxicant, on the constitutive and inducible expression of hepatic microsomal epoxide hydrolase (mEH) and glutathione S-transferase (GST) genes were examined in rats. Northern blot anal. showed that treatment of rats with GdCl₃ caused suppression of mEH and GST gene expression. MEH mRNA levels were decreased in a time-dependent manner after a single injected dose of GdCl₃ (10 mg/kg, i.v.), resulting in 95, 55, 17, 36, and 69% of the levels in untreated animals at 6, 12, 18, 24, and 48 h after treatment, resp. A maximal reduction in GST Ya, Yb1/2, and Yc1 mRNA levels was also noted at 18 h after treatment with GdCl₃, followed by a gradual return to levels in untreated rats at later time points. Whereas treatment of rats with thiazole, allyl disulfide, Pr sulfide, oltipraz, or clotrimazole caused 2-13-fold increases in mEH mRNA levels at 18 h after treatment, concomitant GdCl₃ treatment caused 30-70% reductions in the increases in mEH mRNA levels. The chem.-inducible mRNA levels for GST Ya, Yb1/2, and Yc1 were also significantly inhibited by GdCl₃ at 18 h after treatment. Rats treated with GdCl₃ (10 mg/kg/day, i.v.) for 3-5 consecutive days exhibited 40-90% decreases in mEH, GST Ya, and GST Yb1/2 mRNA levels, relative to control, whereas the Yc1 mRNA level was suppressed at early times and returned to levels in untreated animals at day 5 after treatment. The mRNA levels for mEH and GST Ya in rats treated daily with both allyl disulfide (25 mg/kg, po) and GdCl₃ for 3 consecutive days were 20-30% of those in rats treated with allyl disulfide alone. Western immunoblotting showed that mEH and GST Ya protein expression was decreased at 1-3 days after consecutive daily treatment with GdCl₃. Whereas treatment of rats with GdCl₃ at a dose of 1 mg/kg suppressed constitutive hepatic mEH gene expression by 85% at 18 h, rats treated with CaCl₂ (10 mg/kg, i.v.) in combination with GdCl₃ (1 mg/kg, i.v.) showed 45% suppression of the mEH mRNA level, compared with untreated animals. GdCl₃-induced suppression was also significantly reversed for GST Ya mRNA by excessive CaCl₂ administration. These results demonstrate that GdCl₃ effectively inhibits constitutive and inducible mEH and GST expression, with decreases in their mRNA levels. GdCl₃ suppression of detoxifying enzyme expression may be associated with its blocking of intracellular Ca²⁺ influx, which affects signaling pathways for the expression of the genes. This study involved multiple reactions and reactants, such as 5-Ethyl-6-methyl-2-thioxo-2,3-dihydropyrimidin-4(1H)-one (cas: 39083-15-3Reference of 39083-15-3).

5-Ethyl-6-methyl-2-thioxo-2,3-dihydropyrimidin-4(1H)-one (cas: 39083-15-3) belongs to pyrimidine derivatives. The pyrimidine nitrogenous bases are derived from the organic compound pyrimidine through the addition of various functional groups. For example, the neurotoxin tetrodotoxin is a pyrimidine derivative. It is found in a number of species including the Japanese puffer fish, the blue-ringed octopus, and the orange-bellied newt. Tetrodotoxin prevents the transmission of nerve signals and can result in paralysis and death.Reference of 39083-15-3

Referemce:
Pyrimidine | C4H4N2 – PubChem,
Pyrimidine – Wikipedia

[(N-aryl)piperazinyl]butylpyrimidine derivatives with neurotropic and actoprotective properties was written by Andronati, S. A.;Soboleva, S. G.;Zamkovat, A. V.;Karasyova, T. L.;Rakipov, I. M.;Tsymbal, D. I.. And the article was included in Zhurnal Organichnoi ta Farmatsevtichnoi Khimii in 2016.Quality Control of 5-Ethyl-6-methyl-2-thioxo-2,3-dihydropyrimidin-4(1H)-one The following contents are mentioned in the article:

In this study the potential ligands of 5-HT1A receptors – arylpiperazines containing the residues of tetrahydropyrimidine as terminal fragments, compounds I·HCl [R¹ = Pr-i, R² = H, Me-2, Me-3, X = S; R¹ = Pr-n, R² = Me-3, X = O; R¹ = Et, R² = Me-2, X = S] and II·HCl, and dihydropyrimidine III·2HCl have been synthesized. The structures of I·HCl [R¹ = Pr-i, R² = H, Me-2, Me-3 X = S; R¹ = Pr-n, R² = Me-3 X = O;], II·HCl and III·2HCl have been confirmed by IR-spectroscopy, mass spectrometry and 1H-NMR-spectroscopy. Substances I [R¹ = Pr-i, R² = Me-2, Me-3, X = S; R¹ = Pr-n, R² = Me-3, X = O;] and III·2HCl inhibit the specific binding of the radioligand [³H]8-OH-DPAT with 5-HT1A receptors; it has been found that they have a pronounced affinity for these receptors. In the conflict situation test compounds of I·HCl [R¹ = Pr-i, R² = H, Me-2, Me-3, X = S; R¹ = Pr-n, R² = Me-3, X = O; R¹ = Et, R² = Me-2, X = S] and III·2HCl showed anxiolytic properties, whereas phenylpiperazinil- and o-tolylpiperazinilbutyl-4-methyl-5-isopropyl-1,2,3,-6-tetrahydropyrimidine-2-thio-6-ones (I·HCl; R¹ = Pr-i, R² = H, Me-2) exceeded the known drug buspirone by the level of the anxiolytic activity. The absence of this activity in compound II·HCl is probably due to the differences of substituents at N1 atom of the pyrimidine nucleus of compound II·HCl and other compounds of this series. It has been shown that on the model of hyperthermia all of these compounds in the dose range of 0.04-0.1 mg/kg possessed a high actoprotective activity increased the rat capacity work by 1.4-2.5 times compared to the control. The most active compound, I·HCl [R¹ = Pr-i, R² = Me-3, X = S;], in the ED50 dose of 0.04 mg/kg increased the duration of swimming in rats by 2.2 times (122%) compared to bemithylum. Some of the compounds (15 mg/kg) showed antihypoxic activity on the models of hemic [compounds I (R¹ = Pr-i, R² = Me-2, Me-3, S = S; R¹ = Pr-n, R² = Me-3, X = O;) and III·2HCl] and normobaric hypoxia [compounds I·HCl (R¹ = Pr-i, R² = H, Me-2, X = S) and II·HCl] and exceeded bemithylym (33.5 mg/kg) by their activity. The compounds synthesized are low toxic with the LD50 value of 150-250 mg/kg. This study involved multiple reactions and reactants, such as 5-Ethyl-6-methyl-2-thioxo-2,3-dihydropyrimidin-4(1H)-one (cas: 39083-15-3Quality Control of 5-Ethyl-6-methyl-2-thioxo-2,3-dihydropyrimidin-4(1H)-one).

5-Ethyl-6-methyl-2-thioxo-2,3-dihydropyrimidin-4(1H)-one (cas: 39083-15-3) belongs to pyrimidine derivatives. Heterocyclic compounds bearing the pyrimidine core are of tremendous interest as they constitute an important class of natural and synthetic compounds exhibiting diverse useful biological activities that hold attractive potential for clinical translation as therapeutic agents in alleviation of a myriad of diseases. As nucleotides in DNA and RNA, pyrimidine nucleotide derivatives have a wide range of biological applications. For example, pyrimidine derivatives are useful in DNA repair studies involving cancer and epigenetics.Quality Control of 5-Ethyl-6-methyl-2-thioxo-2,3-dihydropyrimidin-4(1H)-one

Referemce:
Pyrimidine | C4H4N2 – PubChem,
Pyrimidine – Wikipedia

Synthesis of pyrimidine-5-carboxaldehydes by the Reimer-Tiemann reaction was written by Wiley, Richard H.;Yamamoto, Yuzuru. And the article was included in Journal of Organic Chemistry in 1960.Application of 14160-85-1 The following contents are mentioned in the article:

Substituted pyrimidines, N:CR.N:CR¹.CX:CR² (I, X = H, R = OH. Me, OH, SH, SMe, OH, Me, H, H, OH, R¹ = OH, OH, OH, OH, OH, Me, OH, OH, OH, OH, R² = H, OH, Me, Me, Me, Me, Me, Me, H, OH) (II-XI) were submitted to the Reimer-Tiemann reaction by treatment 1 h. in dilute alc. with KOH and CHCl₃ at 80° and neutralization of the precipitate K salts with AcOH to give the corresponding 5-carboxaldehydes I (X = CHO) (XII). The monohydroxylated pyrimidines V, VI, VII, and VIII did not precipitate the K salt and were isolated through a suitable derivative Data were tabulated for the isolated XII [pyrimidine, % yield of XII, and m.p. (solvent) given)]: XI, 42, 330° (H₂O); II, 18, 304° (MeOH, H₂O); III, 29, 300° (AcOH); IV, 14, -; V, 17, 300° (H₂O); VI, 14, 300° (dilute alc.); VII, 26, -; VIII, 13, -. IX gave only 1.5% non-characterized derivative and no aldehyde or derivative was obtained from X. The data were consistent with the established difference in reactivity between IX and VIII, the less reactive nature of the pyrimidine nucleus than that of benzene, and the mechanism of the Reimer-Tiemann reaction. Various derivatives of XII were prepared and m.p. data listed [aldehyde, m.p. (solvent) of phenylhydrazone, dinitrophenylhydrazone, dimethylhydrazone, bis(2-hydroxyethyl)hydrazone, oxime, and semicarbazone of the corresponding XII given]: XI, 271-3° (AcOH), 301-2° (HCONMe₂-alc.), 283-4° (MeOH), -, 250° (H₂O),-; II, 298-300° (HCONMe₂), 270-2° (MeOH), -, above 330° (MeOH), 260° (HCONMe₂), 240° (reprecipitated from alk. solution); III, 240° (reprecipitated), above 330° (HCONMe₂-H₂O), 200° (EtOAc), -, -, 205° (reprecipitated); IV, -, -, 258-9° (MeOH), 320° (MeOH), 260° (MeOH),-; V, 276-7° (MeOH), -, 232-3° (MeOH), -, -, -; VI, 250-1° (MeOH), 283-4° (HCONMe₂), 168-70° (MeOH), -, 228-9° (MeOH), 263° (reprecipitated); VII, 229-31° (MeOH), -, -, -, -, -; VIII, 277-9° (MeOH), 305° (HCONMe₂), 192-3° (MeOH), -, 238-40° (MeOH), 265-6° (reprecipitated from alk. solution). CHCl₃ (24 mL.) and 56 g. KOH in 60 mL. H₂O added in 20 min. with stirring to 22.4 g. II and 11.2 g. KOH in 180 mL. 5:4 H₂O-alc. at 80°, the mixture refluxed 1 h., the cooled mixture filtered from KCl, kept 10 h. at 20°, the precipitated K salt suspended in H₂O, and neutralized with AcOH gave 8.6% XII (R = R¹ = OH, R² = H). The filtrate with PhNHNH₂ gave 9.4% phenylhydrazone. XII (R = R¹ = OH, R² = Me) oxime (XIII) (0.5 g.) and 10 mL. Ac₂O refluxed 30 min. and the hot filtered solution cooled to 20° gave 0.15 g. I (R = R¹ = OH, R² = Me, X = CN), m. above 330°, λ 273 mμ, also obtained (56%) by refluxing 0.5 g. XIII with 4.5 mL. POCl₃, pouring the mixture onto ice, and recrystallizing from alc. XIII (0.7 g.) in 6 mL. POCl₃ treated slowly with cooling with 3 mL. PhNMe₂, the mixture refluxed 30 min., cooled, poured onto ice, extracted with Et₂O, and the product recrystallized from ligroine (b. 60-80°) yielded 57% I (R = R¹ = OH, R² = Me, X = CN), m. 93-4°, converted by recrystallization from EtOH to I [R = Cl(EtO), R¹ = EtO(Cl), R² = Me, X = CN], m. 134-6°. The ease with which XIII was dehydrated suggested that the HO group and H atom were in the trans configuration. This study involved multiple reactions and reactants, such as 4,6-Dihydroxy-2-methylpyrimidine-5-carbaldehyde (cas: 14160-85-1Application of 14160-85-1).

4,6-Dihydroxy-2-methylpyrimidine-5-carbaldehyde (cas: 14160-85-1) belongs to pyrimidine derivatives. Pyrimidines are isomeric with two other forms of diazines: pyridazine, with the nitrogen atoms in the 1 and 2 positions; and pyrazine, with the nitrogen atoms in the 1 and 4 positions. As nucleotides in DNA and RNA, pyrimidine nucleotide derivatives have a wide range of biological applications. For example, pyrimidine derivatives are useful in DNA repair studies involving cancer and epigenetics.Application of 14160-85-1

Referemce:
Pyrimidine | C4H4N2 – PubChem,
Pyrimidine – Wikipedia

Chemotherapy. X. Antithyroid compounds. Synthesis of 5- and 6-substituted 2-thiouracils from β-oxo esters and thiourea was written by Anderson, George W.;Halverstadt, I. F.;Miller, Wilbur H.;Roblin, Richard O. Jr.. And the article was included in Journal of the American Chemical Society in 1945.Reference of 39083-15-3 The following contents are mentioned in the article:

5- and 6-Substituted 2-thiouracils have been prepared by condensing CS(NH₂)₂ with β-keto esters. The latter were prepared by one of several methods. As an example of the first, 0.84 mol of AcCHNaCO₂Et in 500 mL. ether was treated with 0.84 mol of PrCOCl during 3 h., allowed to stand overnight, treated with 200 cc. H₂O, extracted with 600 cc. ether, and treated with 40 g. NH₃ gas at 0-25°, giving 39% of Et β-ketocaproate; similarly prepared were Et γ-methyl-β-ketovalerate (41%), Et β-ketoenanthate (40%), Et β-ketocyclohexanepropionate (40%), and Et β-keto-γ-phenylbutyrate (31%). In the 2nd method the reactions involved were: RCOCl + EtOMgCH(CO₂Et)CO₂CMe₃ → RCOCH(CO₂Et)CO₂CMe₃ → RCOCH₂CO₂Et + CH₂:CMe₂ + CO₂; this method gives the best results when only small quantities are required; the limiting factor is the relative unavailability of tert-BuCH(CO₂Et)₂; prepared by this method were: Et β-ketovalerate (I) (60%), Et γ-methyl-β-ketocaproate (49%), Et β-(4-chlorophenyl)-β-ketopropionate (82%), and Et β-keto-δ-phenylvalerate (61%). The 3rd method involved the reaction of RAc with NaNH₂, followed by Et₂CO₃; Et γ-methyl-β-ketocaproate (68%), Et γ-γ-dimethyl-β-ketovalerate (43%), Et β-ketocaprylate (57%), and Et β-ketopelargonate (61%) were prepared by this method. The 4th method consisted in the reaction of RCOCH₂CO₂Et with R’X; AcCHMeCO₂Et (45%), AcCHEtCO₂Et (58%), and Et α-ethyl-β-ketovalerate, b₈ 83-5° (75%), were prepared by this method. The 5th method involved the reaction of RCO₂Et and R’CH₂CO₂Et with EtONa or Na; prepared by this method were Et α-methyl-β-ketovalerate (26%) and 2-carbethoxycyclopentanone (71%). Details are given of the reaction of EtMgBr and NCCH₂CO₂Et, which yields 58% of I. In the preparation of the uracils, 0.1 g.-atom of Na in 50 cc. anhydrous EtOH, 0.07 mol of CS(NH₂)₂, and 0.05 mol of the keto ester were heated on the steam bath for 6-7 h. and allowed to stand overnight; the solution was evaporated at 40-50°, the residue taken up in 50 cc. H₂O, and the product precipitated by addition of 7 cc. concentrated HCl and then AcOH to pH 4; the compounds were crystallized from boiling H₂O or AcOH. The m. ps. (corrected), yield (from the ester), and antithyroid activity (thiouracil = 1) are given. 6-Substituted 2-thiouracils: Me, m. above 300°, 63%, 1.0; Et, m. 228.5-30.5°, 78%, 8; Pr, m. 218-19°, 70%, 11; iso-Pr, m. 179-80°, 45%, 9; Bu, m. 207.5-9°, 31%, 3; iso-Bu, m. 220.5-1.5°, 36%, 5; sec-Bu, m. 222-4%, 55%, 6; tert-Bu, m. 178-80°, 43%, 9; Am, m. 153-4.5° and 163-4°, 33%, 1.3; hexyl, m. 144.5-5.5°, 27%, 0.18; cyclohexyl, m. 282-5°, 69%, 1.2; Ph, m. 263-4.5%, 45%, 1; p-chlorophenyl, m. 289-91°, 21%, less than 0.01; benzyl, m. 223-4°, 71%, 10; phenethyl, m. 223.5-5.5°, 41%, 1.2. 5,6-Dimethyl-2-thiouracil, m. 283-5°, 42%, 1.2; 5-methyl-6-Et homolog, m. 223-4°, 48%, 3.5; 5-ethyl-6-Me isomer, m. 216-18°, 53%, 0.9; 5,6-di-Et homolog, m. 214.5-15.5°, 41%, 2.0; trimethylene homolog, m. 336-7° (decomposition), 10%, 0.3; 5-(2-hydroxyethyl)-6-Me compound, m. 265-7, 13%, less than 0.01. BuCO₂Et (II) (28.6 g.) and 28.4 g. HCO₂Et, added during 4 h. to 4.85 g. Na in 100 cc. ether, the mixture allowed to stand overnight, evaporated in vacuo, treated with 0.75 g. CS(NH₂)₂ and 85 cc. absolute EtOH, and refluxed 7 h., give 3.4 g. (based on II) of 5-propyl-2-thiouracil, m. 161-3°, 2; 5-iso-Pr isomer, m. 242-4°, 6%, 2.5; 5-Bu homolog, m. 151.5-3.5°, 6%, 0.6; 5-Et homolog, m. 190-2°, 4%, 3.5. Et α-cyano-β-ethoxyacrylate (30 g.), added slowly to 4.22 g. Na in 200 cc. absolute EtOH and 13.5 g. CS(NH₂)₂, the mixture refluxed 1 h. and allowed to stand overnight, the solution concentrated to 75 cc., diluted with 400 cc. H₂O, neutralized to pH 7, the precipitate taken up in 350 cc. H₂O and acidified to pH 3, gives 18.9 g. of the Et ester, m. 277° (decomposition), of 2-mercapto-4-amino-5-pyrimidinecarboxylic acid, m. 276-9° (decomposition); the filtrate yields 14% of 5-cyano-2-thiouracil, m. 282-3° (decomposition), activity less than 0.01. The maximum antithyroid activity appears when the alkyl group contains 3 or 4 C atoms. The benzyl derivative was the most active of the aralkyl compounds This study involved multiple reactions and reactants, such as 5-Ethyl-6-methyl-2-thioxo-2,3-dihydropyrimidin-4(1H)-one (cas: 39083-15-3Reference of 39083-15-3).

5-Ethyl-6-methyl-2-thioxo-2,3-dihydropyrimidin-4(1H)-one (cas: 39083-15-3) belongs to pyrimidine derivatives. The pyrimidine derivatives can easily interact with enzymes, genetic materials, and bio components within the cell. A Cu-catalyzed and 4-HO-TEMPO-mediated [3 + 3] annulation of commercially available amidines with saturated ketones enables an efficient and facile synthesis of structurally important pyrimidines via a cascade reaction of oxidative dehydrogenation/annulation/oxidative aromatization.Reference of 39083-15-3

Referemce:
Pyrimidine | C4H4N2 – PubChem,
Pyrimidine – Wikipedia

Some thiopyrimidine derivatives was written by Monti, Lydia;Pacini, Carlo. And the article was included in Gazzetta Chimica Italiana in 1948.Product Details of 39083-15-3 The following contents are mentioned in the article:

By the reaction of HCHO (I), in the presence of H₂SO₄, on thiopyrimidines of the HN.CO.CH:CR.NH.CS ⇄ N:C(OH).CH:CR.N:CSH (II) and HN.CO.CR’:CMe.NH.CS ⇄ N:C(OH).CR’:CMe.N:CSH (III) types, 2 series of new derivatives were obtained. They are essentially different from those prepared by Kircher (C.A. 6, 857) and Poetsch and Behrend (C.A. 20, 2681) by the action of I on HN.CO.CH:CMe.NH.CO and HN.CO.CH:CMe.NH.CS, resp., in acid medium. With II the reactions involve the initial reaction of I with enolic II in the 5-position, following which another I mol. reacts with the newly formed OH group and the original OH group in the 6-position, with final formation of compounds of the C:CR.N:C(SH).N:C.O.CH₂.O.CH₂ (IV) type. With III, in which the H in the 5-position is replaced by an alkyl group, the formation of analogous compounds is difficult to explain, for no intermediate products could be isolated. Perhaps I reacts with III in the ketone-imide form with formation of SC.N.CO.CR’:CMe.N.CH₂.O.CH₂ compounds If so, 1,3-dimethylol compounds would be intermediate products, but none was isolated. Possibly the NH group in the 1-position (between CS and CO) is more reactive than that in the 3-position, and SC.N.CH₂.O.CH₂.O.C:CR’.CMe:N or S.CH₂.O.CH₂.N.CO.CR’:CMe.N:C compounds are formed. Or III compounds may react in a tautomeric form N:C(OH).CHR’.CMe:N.CS, with formation of N:C.O.CH₂.O.CH₂.CR’.CMe:N.CS compounds Comparative physiol. tests of these doubtful compounds and of II, III, and IV now in progress may help solve this problem. (H₂N)₂CS (2.5 g.), 6 g. AcAmCHCO₂Et, and alc. NaOEt (from 1.5 g. Na in a min. of EtOH), refluxed 30-40 min., evaporated, the residue taken up in AcOH (60 cc. AcOH + 40 cc. water), filtered, and the product purified by water, yield 60% of 4-methyl-5-amyl-2-thiouracil (V), m. 217-19°, soluble in dilute aqueous alkalies, and decomposed by boiling concentrated aqueous alkalies (evolution of H₂S and NH₃). It behaves like a weak monobasic acid. With aqueous AgNO₃, its boiling concentrated aqueous solutions deposit the Ag salt, C₁₀H₁₅ON₂SAg. The Cu and Hg salts were prepared similarly. 4-Phenyl-2-thiouracil (IV) (2 g.) in 15 cc. hot 10% aqueous NaOH, allowed to stand 24 hrs. with 4 cc. 40% I, diluted, neutralized with dilute HCl, and the precipitate purified by EtOH, yields 86% 5-(hydroxymethyl)-4-phenyl-2-thiouracil (VII), m. 250-1°, evolves I when heated; its solutions in concentrated H₂SO₄ are intensely yellow. 4-Methyl-2-thiouracil (2 g.), 16 cc. dilute H₂SO₄ (4 volumes concentrated H₂SO₄ + 1 volume water), and 3 cc. 40% I, allowed to stand 24 hrs. (with frequent agitation), diluted with 100 cc. water, neutralized with NH₄OH, filtered, and the residue purified by boiling water and CCl₄, yield the methylenic ether of 2-thio-4-methyl-6-hydroxy-5-pyrimidinemethanol (VIII), does not form an Ac derivative; its concentrated H₂SO₄ solution with a trace of gallic acid gives the green-to-blue Labat reaction; when heated with a dilute alkali, it evolves H₂S and NH₃. VII and I in dilute H₂SO₄, also under the same conditions, form VIII. VI or VII (3 g.) and 4 cc. 40% I in 16 cc. dilute H₂SO₄ (4 volumes concentrated H₂SO₄ + 1 volume water), treated as above, yield 95% of methylenic ether of 2-thio-4-phenyl-6-hydroxy-5-pyrimidinemethanol, m. 151-2°, yellow when crystallized from EtOH but colorless from CCl₄. It gives a pos. Labat reaction, and is decomposed, with evolution of H₂S and NH₃, by hot dilute alkalies. Prepared under similar conditions from 4,5-dimethyl-2-thiouracil (IX) and I in 73% yield and purified by boiling water, the methylenic ether (X) of IX m. 133-5°, does not give an Ac derivative, gives a pos. Labat reaction, and is decomposed by hot aqueous alkalies with evolution of H₂S and NH₃. 4-Methyl-5-ethyl-2-thiouracil and I give 82-3% of the methylenic ether (XI), m. 163-4°, with chem. properties similar to those of X. V (2 g.) in 22 cc. dilute H₂SO₄ (same concentration as before) and 3 cc. 40% I, allowed to stand 24 hrs., diluted, neutralized with NH₄OH, concentrated, and the product purified by boiling water, yield 41% of the methylenic ether, m. 122-5°, with chem. properties like those of X and XI. This study involved multiple reactions and reactants, such as 5-Ethyl-6-methyl-2-thioxo-2,3-dihydropyrimidin-4(1H)-one (cas: 39083-15-3Product Details of 39083-15-3).

5-Ethyl-6-methyl-2-thioxo-2,3-dihydropyrimidin-4(1H)-one (cas: 39083-15-3) belongs to pyrimidine derivatives. The pyrimidine derivatives can easily interact with enzymes, genetic materials, and bio components within the cell. Pyrimidine derivatives also play an important role in drug development, either in concert with other compounds or on their own.Product Details of 39083-15-3

Referemce:
Pyrimidine | C4H4N2 – PubChem,
Pyrimidine – Wikipedia

The synthesis of 5-carbethoxyuracils was written by Whitehead, Calvert W.. And the article was included in Journal of the American Chemical Society in 1952.Formula: C9H12N2O4 The following contents are mentioned in the article:

To NaOEt from 2.3 g. Na in 150 cc. EtOH was added 6.0 g. urea, then 21.6 g. EtOCH:CH(CO₂Et)₂, the mixture let stand 7 days at room temperature, the EtOH removed in vacuo, the residue dissolved in 50 cc. cold H₂O, and the solution acidified with dilute HCl to give 6 g. (21.8%) H₂NCONHCH: C(CO₂Et)₂ (I), m. 207-9° (from EtOH). I (23 g.) in 200 cc. absolute EtOH containing 0.1 mol. NaOEt let stand 12 hrs. at room temperature, refluxed 5 hrs., the EtOH removed in vacuo, and the residue in 50 cc. acidified yielded 13 g. (72%) 5-carbethoxyuracil, m. 232° (from EtOH). CO(NHMe)₂ (44 g.) and 108 g. I heated 24 hrs. at 120°, and the product recrystallized with charcoal from EtOAc gave 66 g. (62%) 1,3-dimethyl-5-carbethoxyuracil, m. 112° (from EtOH). H₂NCONHMe (14.8 g.) and 43.2 g. I gave 16 g. (41%) 3-methyl-5-carbethoxyuracil (II), m. 221° (from EtOH). II (10 g.) and 50 cc. 10% aqueous NaOH heated 2 hrs. on a steam bath, and the mixture acidified with dilute HCl gave 8.5 g. (98%) 3-methyl-5-carboxyuracil (III), m. 242° (from EtOH). III (2 g.) heated 10 min. at 225° yielded 90% 3-methyluracil, m. 174-5° (from EtOH). H₂NCONHPr (10.2 g.) and 21.6 g. I heated 12 hrs. at 110° yielded 50% PrNHCONHCH: C(CO₂Et)₂ (IV), b₁ 165-70°. IV (14.5 g.) and 2.88 g. NaOMe in 50 cc. MeOH let stand 48 hrs. at room temperature and then heated 6 hrs. at 80° gave 6 g. (56.5%) 3-propyl-5-carbomethoxyuracil, m. 205° (from EtOH). AmNHCONH₂ (13.0 g.) and 21.6 g. I heated 24 hrs. at 120°, the resulting sirup added to 200 cc. absolute EtOH containing 0.1 mol. NaOEt, the mixture let stand 24 hrs. at room temperature, the EtOH removed in vacuo, and the residue taken up in 100 cc. H₂O and 100 g. ice and acidified with dilute HCl yielded 6.2 g. (24%) 3-amyl-5-carbethoxyuracil, m. 152° (from aqueous EtOH). Similarly were prepared the following compounds (V), where R = H, R’ = Bu (VI), 53%, m. 152°, and R = H, R’ = C₆H₁₃, 50%, m. 140°. HOCH₂CHEtNHCONH₂ (11.6 g.) in 200 cc. absolute EtOH containing 0.1 mol. NaOEt and 21.6 g. I let stand 48 hrs. at room temperature and the mixture worked up as above yielded 21.0 g. (82%) 3-(1-hydroxymethylpropyl)-5-carbethoxyuracil, m. 161° (from EtOAc). Similarly were obtained the following V, where R = H (R’ given): Et, 82%, m. 219°; HO(CH₂)₂, 79%, m. 175-6°; CH₂:CHCH₂, 80%, m. 174°; iso-Bu, 62%, m. 167°; cyclohexyl, 49%, m. 282°; p-ClC₆H₄, 88%, m. 265°; p-MeOC₆H₄, 90%, m. 185-94°; p-MeC₆H₄, 97%, m. 235°; PhCH₂, 90%, m. 215°; C₇H₁₅, 49%, m. 133°; PhCHMe, 77%, m. 130°; Ph(CH₂)₂, 84%, m. 228°; and C₈H₁₇, 48%, m. 130°. PhNHCONH₂ (27.2 g.) and 43.2 g. I in 250 cc. absolute EtOH containing 0.2 mol. NaOEt let stand 3 days at room temperature, and the mixture worked up as usual yielded 46 g. (88%) 3-phenyl-5-carbethoxyuracil (VIII), m. 230-1° (from EtOH). VIII (5.2 g.) refluxed 2 hrs. with 100 cc. 5% aqueous NaOH, and the mixture cooled, filtered, and acidified yielded 2.5 g. 3-phenyl-5-carboxyuracil (IX), m. 243° (decomposition). IX (1.0 g.) heated 15 min. at 243° gave 0.6 g. 3-phenyluracil, m. 242-6° (from H₂O). VI (20 g.) stirred vigorously at 40° with 3.4 g. NaOH in 150 cc. H₂O and 12.9 g. Et₂SO₄ added dropwise during 1 hr., the mixture stirred another hr., the H₂O removed in vacuo, and the residue extracted gave 14.5 g. (65%) 1-ethyl-3-butyl-5-carbethoxyuracil, m. 41-3°. Similarly were prepared from the corresponding monoalkyl derivatives of V the following V (R and R’ given): Me, Et, 76%, m. 116°; Me, iso-Pr, 78%, m. 98°; Me, Bu, < 50%, m. 60°; Me, iso-Bu, 72%, m. 119°; Et, iso-Bu, 65%, m. 90-90.5°; Me, p-ClC₆H₄, – , m. 141°; and Me, PhCH₂, 76%, m. 79°. The above V heated 24-48 hrs. with 10% excess of an amine, the mixture cooled, and the product recrystallized from hot EtOAc gave the following 5-carbamyluracils (X) (R, R’, and Y given): Me, Me, NHMe, 100%, m. 196°; Me, Me, NHEt(XI), 95%, m. 158°; H, Pr, NHCONH₂, (50%), m. 234°; H, HO(CH₂)₂, NHEt, 75%, m. 222° Me, Me, NH(CH₂)₂OH (XII), 100%, m. 151°; H, HO(CH₂)₂, NH(CH₂)₂OH, 60%, m. 185°; Me, Et, NH(CH₂)₂OH, 57%, m. 179°; Et, Me, NH(CH₂)₂OH, 70%, m. 123°; Me, Me, NHBu, 100%, m. 125°; Me, Me, NHCH₂CHMe₂ (XIII), 100%, m. 150.5°; Me, iso-Pr, NH(CH₂)₂OH (XIV), 93%, m. 114°; Me, Me, N(CH₂CH₂OH)₂ (XV), 45%, m. 122°; Me, Me, NHAm, 100%, m. 115.5°; Me, iso-Bu, NH(CH₂)₂OH, 49%, m. 142°; Me, Me, NH(CH₂₃N Me₂, 86%, m. 89°; H, cyclohexyl, NH(CH₂)₂OH, 89%, m. 232°; Me, Me, NHC₆H₁₃, 79%, m. 121°; Me, Me, NH(CH₂)₃NEt₂, 66%, m. 69.5°; and Me, Me, NHC₇H₁₅, 87%, m. 107°. Alk. hydrolysis of the above V with refluxing 5% aqueous NaOH gave the following XVI (R and R’ given): Me, Me (XVII), 90%, m. 183°; H, Et, 70%, m. 179°; H, Pr, 90%, m. 172-3°; Me, Et, 70%, m. 172°; H, iso-Pr, 69%, m. 192°; Me, CH₂:CHCH₂, 70%, m. 161-2°; H, iso-Bu, 80%, m. 211°; H, HOCH₂CHEt, 90%, m. 166°; Me, Bu, 80%, m. 148°; Et, Bu, 95%, m. 107°; Me, Am, 74%, m. 152° H, p-ClC₆H₄, 98%, m. 255° (decomposition); H, p-MeC₆H₄, 90%, m. 240° (decomposition); and Me, C₆H₁₃, 66%, m. 151°. XII and XVII showed moderate diuresis in dogs with oral doses of 0.5-1 g.; XI, XIII, and XIV with intravenous doses of 5-10 mg.; XII caused marked diuresis with oral doses of 0.5-1 g.; and XII and XV with intravenous doses of 5-10 mg./kg. This study involved multiple reactions and reactants, such as Ethyl 1,3-dimethyl-2,4-dioxo-1,2,3,4-tetrahydropyrimidine-5-carboxylate (cas: 39513-47-8Formula: C9H12N2O4).

Ethyl 1,3-dimethyl-2,4-dioxo-1,2,3,4-tetrahydropyrimidine-5-carboxylate (cas: 39513-47-8) belongs to pyrimidine derivatives. The pyrimidine nitrogenous bases are derived from the organic compound pyrimidine through the addition of various functional groups. As nucleotides in DNA and RNA, pyrimidine nucleotide derivatives have a wide range of biological applications. For example, pyrimidine derivatives are useful in DNA repair studies involving cancer and epigenetics.Formula: C9H12N2O4

Referemce:
Pyrimidine | C4H4N2 – PubChem,
Pyrimidine – Wikipedia