121866-26-0

Basic information

• Product Name: 3-heptylbenzenaMine
• Synonyms: 3-heptylbenzenaMine
• CAS NO: 121866-26-0
• Molecular Formula: C₁₃H₂₁N
• Molecular Weight: 191.31254
• Mol File: 121866-26-0.mol
• Article Data: 4

Chemical Properties

• Appearance: /
• CAS DataBase Reference: 3-heptylbenzenaMine(CAS DataBase Reference)
• NIST Chemistry Reference: 3-heptylbenzenaMine(121866-26-0)
• EPA Substance Registry System: 3-heptylbenzenaMine(121866-26-0)

Safety Data

• Hazardous Substances Data: 121866-26-0(Hazardous Substances Data)

Upstream product

• 923027-30-9 1-(hept-1-yn-1-yl)-3-nitrobenzene 
• 5411-50-7 3,4-dibromonitrobenzene 
• 608-22-0 3-amino-1,2-dibromobenzene 
• 615-55-4 3,4-dibromoaniline 
• 628-71-7 1-Heptyne 
• 645-00-1 m-iodonitrobenzene 
• 121866-24-8 1-(2-bromo-5-aminophenyl)heptyne 
• 121866-29-3 1-(2-bromo-3-aminophenyl)heptyne 

Downstream Products

• 925706-76-9 (R)-[3-tert-butoxycarbonylamino-3-(3-heptylphenylcarbamoyl)propyl]phosphonic acid diethyl ester 
• 121866-27-1 m-n-heptylacetanilide 

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.

N-Phenyl-N′-(2-chloroethyl)ureas (CEU) as potential antineoplastic agents. Part 2: Role of ω-hydroxyl group in the covalent binding to β-tubulin

Tubulin is the target of many anticancer drugs, including N-phenyl-N′-(2-chloroethyl)urea (CEU). Unlike most anti-β-tubulin agents, CEUs are protein monoalkylating agents binding through their N′-(2-chloroethyl)urea moiety to an amino acid nearby the colchicine-binding site on β-tubulin isoform-2. Following the previously synthesized and attractive N-(3-ω-hydroxyalkylphenyl)-N′-(2-chloroethyl)urea that exhibited growth inhibitory activity at the nanomolar level, we investigated the importance of lower alkyl and alkoxy groups to evaluate the effect of hydroxylated group and chain length on both cell growth inhibition and the mechanism of action of CEU. Here, we describe the preparation of two new series of CEU and show that the most potent CEU derivatives beside the ω-hydroxylated 1f were 2f and 3e, respectively. We have confirmed that the pentyl substituted CEUs 1f, 2f, and 3e are still covalently binding to β-tubulin and still arrest cell division in G2/M phase. Crown Copyright