56739-54-9

Basic information

• Product Name: N-(3-nitrophenyl)anthranilic acid methyl ester
• Synonyms: N-(3-nitrophenyl)anthranilic acid methyl ester
• CAS NO: 56739-54-9
• Molecular Weight: 272.26
• Mol File: 56739-54-9.mol

Chemical Properties

• CAS DataBase Reference: N-(3-nitrophenyl)anthranilic acid methyl ester(CAS DataBase Reference)
• NIST Chemistry Reference: N-(3-nitrophenyl)anthranilic acid methyl ester(56739-54-9)
• EPA Substance Registry System: N-(3-nitrophenyl)anthranilic acid methyl ester(56739-54-9)

Safety Data

• Hazardous Substances Data: 56739-54-9(Hazardous Substances Data)

Upstream product

• 610-97-9 o-iodo-methyl-benzoic acid 
• 99-09-2 3-nitro-aniline 
• 88-67-5 2-Iodobenzoic acid 
• 17763-70-1 methyl 2-(trifluoromethylsulfonyloxy)benzoate 
• 67-56-1 methanol 
• 27693-70-5 N-(3-nitrophenyl)anthranilic acid 

Downstream Products

• 56739-22-1 1-(3-nitro-phenyl)-3-propyl-1H-quinazoline-2,4-dione 
• 27693-70-5 N-(3-nitrophenyl)anthranilic acid 
• 17431-90-2 1-nitro-9-chloroacridine 
• 1744-91-8 9-chloro-3-nitroacridine 
• 6237-24-7 N,N-dimethyl-N'-(3-nitro-9-acridinyl)-1,3-propanediamine 
• 1744-92-9 3-nitro-9,10-dihydroacridin-9-one 

Relevant articles and documents

NOVEL NUCLEIC ACID MODIFIERS

The present inventions generally relate to site-specific delivery of nucleic acid modifiers and includes novel DNA-binding proteins and effectors that can be rapidly programmed to make site-specific DNA modifications. The present inventions also provide a synthetic all-in-one genome editor (SAGE) systems comprising designer DNA sequence readers and a set of small molecules that induce double-strand breaks, enhance cellular permeability, inhibit NHEJ and activate HDR, as well as methods of using and delivering such systems.

Development of potent and selective inhibitors of aldo-keto reductase 1C3 (type 5 17β-hydroxysteroid dehydrogenase) based on N -phenyl-aminobenzoates and their structure-activity relationships

Aldo-keto reductase 1C3 (AKR1C3; type 5 17β-hydroxysteroid dehydrogenase) is overexpressed in castration resistant prostate cancer (CRPC) and is implicated in the intratumoral biosynthesis of testosterone and 5α-dihydrotestosterone. Selective AKR1C3 inhibitors are required because compounds should not inhibit the highly related AKR1C1 and AKR1C2 isoforms which are involved in the inactivation of 5α-dihydrotestosterone. NSAIDs, N-phenylanthranilates in particular, are potent but nonselective AKR1C3 inhibitors. Using flufenamic acid, 2-{[3-(trifluoromethyl)phenyl]amino}benzoic acid, as lead compound, five classes of structural analogues were synthesized and evaluated for AKR1C3 inhibitory potency and selectivity. Structure-activity relationship (SAR) studies revealed that a meta-carboxylic acid group relative to the amine conferred pronounced AKR1C3 selectivity without loss of potency, while electron withdrawing groups on the phenylamino B-ring were optimal for AKR1C3 inhibition. Lead compounds did not inhibit COX-1 or COX-2 but blocked the AKR1C3 mediated production of testosterone in LNCaP-AKR1C3 cells. These compounds offer promising leads toward new therapeutics for CRPC.