17332-56-8

Basic information

• Product Name: 2-[(4-tert-butylphenyl)amino]benzoic acid
• CAS NO: 17332-56-8
• Molecular Formula: C₁₇H₁₉NO₂
• Molecular Weight: 269.3383
• Mol File: 17332-56-8.mol
• Article Data: 6

Chemical Properties

• Boiling Point: 411.3°C at 760 mmHg
• Flash Point: 202.5°C
• Density: 1.147g/cm³
• Vapor Pressure: 1.68E-07mmHg at 25°C
• Refractive Index: 1.606
• CAS DataBase Reference: 2-[(4-tert-butylphenyl)amino]benzoic acid(CAS DataBase Reference)
• NIST Chemistry Reference: 2-[(4-tert-butylphenyl)amino]benzoic acid(17332-56-8)
• EPA Substance Registry System: 2-[(4-tert-butylphenyl)amino]benzoic acid(17332-56-8)

Safety Data

• Hazardous Substances Data: 17332-56-8(Hazardous Substances Data)

Upstream product

• 769-92-6 4-tert-Butylaniline 
• 118-91-2 ortho-chlorobenzoic acid 
• 3282-56-2 4-tert-butylnitrobenzene 
• 20330-45-4 4-tert-butylacetanilide 
• 88-65-3 2-bromobenzoic-acid 
• 113146-11-5 methyl 2‐[(4‐tert‐butylphenyl)amino]benzoate 
• 17763-70-1 methyl 2-(trifluoromethylsulfonyloxy)benzoate 
• 610-94-6 2-bromobenzoic acid methyl ester 

Downstream Products

• 4496-49-5 4-tert-butyldiphenylamine 

Relevant articles and documents

Development of LM98, a Small-Molecule TEAD Inhibitor Derived from Flufenamic Acid

The YAP-TEAD transcriptional complex is responsible for the expression of genes that regulate cancer cell growth and proliferation. Dysregulation of the Hippo pathway due to overexpression of TEAD has been reported in a wide range of cancers. Inhibition of TEAD represses the expression of associated genes, demonstrating the value of this transcription factor for the development of novel anti-cancer therapies. We report herein the design, synthesis and biological evaluation of LM98, a flufenamic acid analogue. LM98 shows strong affinity to TEAD, inhibits its autopalmitoylation and reduces the YAP-TEAD transcriptional activity. Binding of LM98 to TEAD was supported by 19F-NMR studies while co-crystallization experiments confirmed that LM98 is anchored within the palmitic acid pocket of TEAD. LM98 reduces the expression of CTGF and Cyr61, inhibits MDA-MB-231 breast cancer cell migration and arrests cell cycling in the S phase during cell division.

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.

NOVEL ANTHRANILIC ACID DERIVATIVES AND CHLORIDE CHANNEL BLOCKING AGENT CONTAINING THE SAME

The present invention relates to novel anthranilic acid derivatives represented by Chemical Formula I, and a chloride channel blocking agent containing the anthranilic acid derivative or its pharmacologically acceptable salts as an active ingredient. In another aspect, the present invention relates to a method of accurately and efficiently detecting the intracellular chloride channel inhibition and method of screening a chloride channel blocking agent.