CAS: 1232410-49-9; 3-Amino-6-(4-(Methylsulfonyl)Phenyl)-N-Phenylpyrazine-2-Carboxamide

上下游产品

3-amino-6-(4-(methylsulfonyl)phenyl)pyrazine-2-carboxylic acid aniline Methyl 3-amino-2-pyrazinecarboxylate methyl 3-amino-6-bromopyrazine-2-carboxylate 3-hydroxy-6-(4-(methylsulfonyl)phenyl)-N-phenylpyrazine-2-carboxamide 3-bromo-6-(4-(methylsulfonyl)phenyl)-N-phenylpyrazine-2-carboxamide 3-methyl-6-(4-(methylsulfonyl)phenyl)-N-phenylpyrazine-2-carboxamide

📜3-氨基吡嗪-2-羧酸甲酯置于4-二甲氨基吡啶,N-溴代丁二酰亚胺(Nbs),Sodium Carbonate,N,N-二异丙基乙胺,N,N'-羰基二咪唑,Lithium Hydroxide体系中,用 甲醇,水,二甲基亚砜,N,N-二甲基甲酰胺,乙腈 用作溶剂,化学反应 56.5H,反应生成3-氨基-6-[4-(甲基磺酰基)苯基]-N-苯基-2-吡嗪甲酰胺
参考文献:Discovery Of Potent And Selective Inhibitors Of Ataxia Telangiectasia Mutated And Rad3 Related (Atr) Protein Kinase As Potential Anticancer Agents
标题:Discovery Of Potent And Selective Inhibitors Of Ataxia Telangiectasia Mutated And Rad3 Related (Atr) Protein Kinase As Potential Anticancer Agents
摘要: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 K-I 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 Mu M. 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.
Doi:10.1021/jm101488Z

专利信息

专利号:US-2025034520-A1
优先权日:2022-04-08
标 题:Increasing developmental potential of human preimplantation embryos by reducing genetic instability, aneuploidies and chromosomal mosaicism
发明人：EGLI DIETRICH
权利人:UNIV COLUMBIA
摘要:Disclosed herein are agents, compositions and methods for increasing the developmental potential of human preimplantation embryos. n Disclosed herein are methods of reducing or decreasing replication abnormalities and/or aneuploidies in an embryo as well as increasing genome stability and/or developmental potential of an embryo by activating kinases and/or their signaling pathway in an oocyte including but not limited to ATR, WEE1, and CHK1. n Also disclosed herein are methods of reducing or decreasing replication abnormalities and/or aneuploidies in an embryo as well as increasing genome stability and/or developmental potential of an embryo using polynucleotides, polypeptides and/or agents which increase efficiency of the “fork reversion and repair†pathway and/or decrease detrimental outcomes such as fork collapse, translesion synthesis and/or gap formation. n Lastly disclosed herein are methods of reducing or decreasing replication abnormalities and/or aneuploidies in an embryo as well as increasing genome stability and/or developmental potential of an embryo using one or more polynucleotides or polypeptides including but not limited to CHEK1, WEE1, ETAA1, ATRX, BLM, BRCA2, CHD4, DNA2 (DNA2L), EXO1, FANCC, FANCG, FBH1 (FBX018), HLTF (SMARCA3), MCM9, MSH6, POLD3, POLK, RAD51, RAD52, RAD54L, RB1, RECQL, REV3L, RIF1, RNF8, SETD1A, SHPRH, SMARCAL1, TDRD3, TOPBP1, TP53BP1, WRNIP1, XRCC2, WRN, BRCAI, ZRANB3, CDC6, CDT1, POLH, POLI, FANCD2, INO80, FANCB, ASH2L, FAM35A, XRCC3, BRIP1, and NF168.

专利号:CN-113166767-B
优先权日:2018-09-05
标 题 :Method for engineering synthesis of cis-regulatory DNA

专利号:US-11285169-B2
优先权日:2013-03-13
标题 :Methods for modulating chemotherapeutic cytotoxicity
发明人：ROBERTS DAVID D; SOTO PANTOJA DAVID R
权利人:US HEALTH
摘要:Methods of reducing cytotoxicity of a chemotherapeutic agent to non-cancer cells by administering to a subject with cancer an effective amount of an agent that inhibits CD47 signaling and a DNA damaging agent, such as an anthracycline, topoisomerase inhibitor, or nucleotide synthesis inhibitor, are provided. Example disclosed methods reduce cardiotoxicity. In one example, the methods include administering to a subject with cancer an effective amount of a CD47 antisense morpholino oligonucleotide and an anthracycline such as doxorubicin. Methods of increasing cytotoxicity of a chemotherapeutic agent in cancer cells by administering to a subject with a tumor an effective amount of an agent that inhibits CD47 signaling and a DNA damaging agent such as an anthracycline, topoisomerase inhibitor, or nucleotide synthesis inhibitor, are also provided. In some embodiments, the inhibitor of CD47 signaling is administered to the subject before, during, or after the administration of the DNA damaging agent.