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Anilide of 3-aminopyrazinecarboxylic acid is a chemical compound with the molecular formula C11H11N3O2. It is derived from the condensation of 3-aminopyrazinecarboxylic acid with an aniline molecule, resulting in an amide linkage. anilide of 3-aminopyrazinecarboxylic acid is characterized by its aromatic structure, featuring a pyrazine ring fused with an aniline group. It is known for its potential applications in the synthesis of pharmaceuticals and agrochemicals, particularly as an intermediate in the production of various biologically active molecules. The compound's properties, such as its reactivity and stability, make it a valuable component in organic synthesis and medicinal chemistry.

36204-80-5

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36204-80-5 Usage

Check Digit Verification of cas no

The CAS Registry Mumber 36204-80-5 includes 8 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 5 digits, 3,6,2,0 and 4 respectively; the second part has 2 digits, 8 and 0 respectively.
Calculate Digit Verification of CAS Registry Number 36204-80:
(7*3)+(6*6)+(5*2)+(4*0)+(3*4)+(2*8)+(1*0)=95
95 % 10 = 5
So 36204-80-5 is a valid CAS Registry Number.

36204-80-5Downstream Products

36204-80-5Relevant academic research and scientific papers

Derivatives of 3-Aminopyrazine-2-carboxamides: Synthesis, antimicrobial evaluation, and in vitro cytotoxicity

Bouz, Ghada,Semelková, Lucia,Jand’ourek, Ond?ej,Kone?ná, Klára,Paterová, Pavla,Navrátilová, Lucie,Kubí?ek, Vladimír,Kune?, Ji?í,Dole?al, Martin,Zitko, Jan

, (2019/04/05)

We report the design, synthesis, and in vitro antimicrobial activity of a series of N-substituted 3-aminopyrazine-2-carboxamides with free amino groups in position 3 on the pyrazine ring. Based on various substituents on the carboxamidic moiety, the series is subdivided into benzyl, alkyl, and phenyl derivatives. The three-dimensional structures of the title compounds were predicted using energy minimization and low mode molecular dynamics under AMBER10:EHT forcefield. Compounds were evaluated for antimycobacterial, antibacterial, and antifungal activities in vitro. The most active compound against Mycobacterium tuberculosis H37Rv (Mtb) was 3-amino-N-(2,4-dimethoxyphenyl)pyrazine-2-carboxamide (17, MIC = 12.5 μg/mL, 46 μM). Antimycobacterial activity against Mtb and M. kansasii along with antibacterial activity increased among the alkyl derivatives with increasing the length of carbon side chain. Antibacterial activity was observed for phenyl and alkyl derivatives, but not for benzyl derivatives. Antifungal activity was observed in all structural subtypes, mainly against Trichophyton interdigitale and Candida albicans. The four most active compounds (compounds 10, 16, 17, 20) were evaluated for their in vitro cytotoxicity in HepG2 cancer cell line; only compound 20 was found to exert some level of cytotoxicity. Compounds belonging to the current series were compared to previously published, structurally related compounds in terms of antimicrobial activity to draw structure activity relationships conclusions.

Discovery of Potent and Selective Inhibitors of Ataxia Telangiectasia Mutated and Rad3 Related (ATR) Protein Kinase as Potential Anticancer Agents

Charrier, Jean-Damien,Durrant, Steven J.,Golec, Julian M. C.,Kay, David P.,Knegtel, Ronald M. A.,MacCormick, Somhairle,Mortimore, Michael,O'Donnell, Michael E.,Pinder, Joanne L.,Reaper, Philip M.,Rutherford, Alistair P.,Wang, Paul S. H.,Young, Stephen C.,Pollard, John R.

, p. 2320 - 2330 (2011/06/17)

DNA-damaging agents are among the most frequently used anticancer drugs. However, they provide only modest benefit in most cancers. This may be attributed to a genome maintenance network, the DNA damage response (DDR), that recognizes and repairs damaged DNA. ATR is a major regulator of the DDR and an attractive anticancer target. Herein, we describe the discovery of a series of aminopyrazines with potent and selective ATR inhibition. Compound 45 inhibits ATR with a Ki of 6 nM, shows >600-fold selectivity over related kinases ATM or DNA-PK, and blocks ATR signaling in cells with an IC50 of 0.42 μM. Using this compound, we show that ATR inhibition markedly enhances death induced by DNA-damaging agents in certain cancers but not normal cells. This differential response between cancer and normal cells highlights the great potential for ATR inhibition as a novel mechanism to dramatically increase the efficacy of many established drugs and ionizing radiation.

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