945397-21-7

Basic information

• Product Name: 3,5-di(morpholino)aniline
• Synonyms: 3,5-di(morpholino)aniline
• CAS NO: 945397-21-7
• Molecular Weight: 263.34
• Mol File: 945397-21-7.mol
• Article Data: 11

Chemical Properties

• CAS DataBase Reference: 3,5-di(morpholino)aniline(CAS DataBase Reference)
• NIST Chemistry Reference: 3,5-di(morpholino)aniline(945397-21-7)
• EPA Substance Registry System: 3,5-di(morpholino)aniline(945397-21-7)

Safety Data

• Hazardous Substances Data: 945397-21-7(Hazardous Substances Data)

Upstream product

• 55086-81-2 4,4'-(5-chloro-m-phenylene)-bis-morpholine 
• 620-81-5 N,N'-Diphenyloxamid 
• 195062-61-4 4-chlorophenylboronic acid pinacol ester 
• 2265-94-3 1,3-difluoro-5-nitrobenzene 
• 1051899-19-4 4-(3-iodo-5-nitrophenyl)-morpholine 
• 3819-88-3 1-fluoro-3-iodo-5-nitrobenzene 
• 6311-60-0 3,5-dibromonitrobenzene 
• 827-94-1 2,6-dibromo-4-nitroaniline 
• 220954-17-6 4,4’-(5-nitro-1,3-phenylene)dimorpholine 

Downstream Products

• 945397-00-2 N-(3,5-dimorpholin-4-ylphenyl)formamide 
• 1051898-83-9 (3-((2-(3,5-dimorpholinophenylamino)pyrimidin-4-yl)(2-methoxyethyl)amino)-4-methylphenyl)methanol 
• 1051899-11-6 1-(3-((2-(3,5-dimorpholinophenylamino)pyrimidin-4-yl)(methyl)amino)-4-methylphenyl)ethanone 
• 1051899-15-0 (2-((2-(3,5-dimorpholinophenylamino)pyrimidin-4-yl)(methyl)amino)-4-methoxyphenyl)methanol 
• 1051899-17-2 (4-chloro-2-((2-(3,5-dimorpholinophenylamino)pyrimidin-4-yl)(methyl)amino)phenyl)methanol 
• 1051896-49-1 [3-[[2-[(3,5-dimorpholin-4-ylphenyl)amino]pyrimidin-4-yl]-methyl-amino]-4-methyl-phenyl]methanol 
• 1104455-09-5 N'-(6-chloropyridin-2-yl)-N-(3,5-dimorpholin-4-ylphenyl)-N'-methylpyrimidine-2,4-diamine 
• 1104455-19-7 N'-(2-chloro-5-methoxypyridin-3-yl)-N-(3,5-dimorpholin-4-ylphenyl)-N'-methylpyrimidine-2,4-diamine 
• 1104455-20-0 (6-((2-(3,5-dimorpholinophenylamino)pyrimidin-4-yl)(methyl)amino)-5-methylpyridin-2-yl)methanol 
• 945397-12-6 N-(3,5-dimorpholin-4-ylphenyl)-N'-[1-[(4-methoxyphenyl)methyl]-3-methyl-indazol-4-yl]-N'-methyl-pyrimidine-2,4-diamine 
• 945396-61-2 N'-benzooxazol-7-yl-N-(3,5-dimorpholin-4-ylphenyl)pyrimidine-2,4-diamine 
• 1312291-11-4 N-[3,5-bis(morpholin-4-yl)phenyl]-7-chloro-quinolin-4-amine 
• 945396-55-4 N²-(3,5-dimorpholinophenyl)-N⁴-(1H-indazol-4-yl)-N⁴-methylpyrimidine-2,4-diamine 
• 945396-58-7 N²-(3,5-dimorpholinophenyl)-N⁴-(1H-indazol-4-yl)pyrimidine-2,4-diamine 

Relevant articles and documents

Structure-based design of highly selective 2,4,5-trisubstituted pyrimidine CDK9 inhibitors as anti-cancer agents

Cyclin-dependent kinases (CDKs) are a family of Ser/Thr kinases involved in cell cycle and transcriptional regulation. CDK9 regulates transcriptional elongation and this unique property has made it a potential target for several diseases. Due to the conserved ATP binding site, designing selective CDK9 inhibitors has been challenging. Here we report our continued efforts in the optimization of 2,4,5-tri-substituted pyrimidine compounds as potent and selective CDK9 inhibitors. The most selective compound 30m was >100-fold selective for CDK9 over CDK1 and CDK2. These compounds showed broad anti-proliferative activities in various solid tumour cell lines and patient-derived chronic lymphocytic leukaemia (CLL) cells. Decreased phosphorylation of the carboxyl terminal domain (CTD) of RNAPII at Ser-2 and down-regulation of anti-apoptotic protein Mcl-1 were confirmed in both the ovarian cancer model A2780 and patient-derived CLL cells.

Discovery and Optimization of a Novel Series of Highly Selective JAK1 Kinase Inhibitors

Janus kinases (JAKs) have been demonstrated to be critical in cytokine signaling and have thus been implicated in both cancer and inflammatory diseases. The JAK family consists of four highly homologous members: JAK1-3 and TYK2. The development of small-m

Chemoproteomics-Aided Medicinal Chemistry for the Discovery of EPHA2 Inhibitors

The receptor tyrosine kinase EPHA2 has gained attention as a therapeutic drug target for cancer and infectious diseases. However, EPHA2 research and EPHA2-based therapies have been hampered by the lack of selective small-molecule inhibitors. Herein we rep