143702-29-8

Basic information

• Product Name: 2-Propenoic acid, 2-azido-3-(4-methoxyphenyl)-, methyl ester, (Z)-
• CAS NO: 143702-29-8
• Molecular Formula: C11H11N3O3
• Molecular Weight: 233.227
• Mol File: 143702-29-8.mol
• Article Data: 11

Chemical Properties

• CAS DataBase Reference: 2-Propenoic acid, 2-azido-3-(4-methoxyphenyl)-, methyl ester, (Z)-(CAS DataBase Reference)
• NIST Chemistry Reference: 2-Propenoic acid, 2-azido-3-(4-methoxyphenyl)-, methyl ester, (Z)-(143702-29-8)
• EPA Substance Registry System: 2-Propenoic acid, 2-azido-3-(4-methoxyphenyl)-, methyl ester, (Z)-(143702-29-8)

Safety Data

• Hazardous Substances Data: 143702-29-8(Hazardous Substances Data)

Upstream product

• 1816-92-8 Methyl azidoacetate 
• 124-41-4 sodium methylate 
• 123-11-5 4-methoxy-benzaldehyde 

Downstream Products

• 1279721-93-5 (Z)-isopropyl 2-azido-3-(4-methoxyphenyl)acrylate 
• 1968-13-4 2-methyl-6-methoxy-1H-indole 
• 143702-33-4 (3R,6S)-3-<1-(benzenesulfonyl-6-methoxy)-3-indoyl>methyl-3,6-dihydro-6-isopropyl-2,5-diethoxypyrazine 
• 143702-34-5 1-benzenesulfonyl-6-methoxy-D(+)-tryptophan ethyl ester 
• 143702-31-2 1-benzenesulfonyl-3-hydroxymethyl-6-methoxyindole 
• 143702-30-1 6-methoxy-1-(phenylsulfonyl)-1H-indole-3-carbaldehyde 
• 143702-32-3 1-benzenesulfonyl-3-bromomethyl-6-methoxyindole 
• 812653-08-0 18-[6-methoxy-1-(4-methoxy-benzenesulfonyl)-1H-indol-3-yl]-octadecan-1-ol 
• 812653-07-9 16-[6-methoxy-1-(4-methoxy-benzenesulfonyl)-1H-indol-3-yl]-hexadecan-1-ol 
• 812653-06-8 14-[6-methoxy-1-(4-methoxy-benzenesulfonyl)-1H-indol-3-yl]-tetradecan-1-ol 
• 651331-76-9 12-[6-methoxy-1-(4-methoxybenzsulfonyl)-1H-indole-3-yl]-dodecane-1-ol 

Relevant articles and documents

Application of 1,4-Oxazinone Precursors to the Construction of Pyridine Derivatives by Tandem Intermolecular Cycloaddition/Cycloreversion

This study reveals a new method for the preparation of 1,4-oxazinone derivatives by Staudinger reductive cyclization of functionalized vinyl azide precursors. The resulting oxazinone derivatives prepared in this manner were intercepted with terminal alkyne substrates through an intermolecular cycloaddition/cycloreversion sequence to afford polysubstituted pyridine products. Alkyne substrates bearing propargyl oxygen substitution showed good regioselectivity in the cycloaddition operation selectively affording 2,4,6-substituted pyridines. Application of this chemistry to the synthesis of an ErbB4 receptor inhibitor is also described.

Cu-Catalyzed Oxidation of C2 and C3 Alkyl-Substituted Indole via Acyl Nitroso Reagents

The selective oxidation of C2-alkyl-substituted indoles to 3-oxindole and the selective C-H oxygenation or amination of C2,C3-dialkyl-substituted indoles at C2 are reported under mild conditions. The position of the alkyl substitution on the indole directs the reaction to different pathways under similar conditions.

Optimization of chemical functionalities of indole-2-carboxamides to improve allosteric parameters for the cannabinoid receptor 1 (CB1)

5-Chloro-3-ethyl-N-(4-(piperidin-1-yl)phenethyl)-1H-indole-2-carboxamide (1; ORG27569) is a prototypical allosteric modulator for the cannabinoid type 1 receptor (CB1). Here, we reveal key structural requirements of indole-2-carboxamides for allosteric modulation of CB1: a critical chain length at the C3-position, an electron withdrawing group at the C5-position, the length of the linker between the amide bond and the phenyl ring B, and the amino substituent on the phenyl ring B these significantly impact the binding affinity (KB) and the binding cooperativity (α). A potent CB1 allosteric modulator 5-chloro-N-(4-(dimethylamino)phenethyl)-3-propyl-1H-indole- 2-carboxamide (12d) was identified. It exhibited a KB of 259.3 nM with a strikingly high binding α of 24.5. We also identified 5-chloro-N-(4-(dimethylamino)phenethyl)-3-hexyl-1H-indole-2-carboxamide (12f) with a KB of 89.1 nM, which is among the lowest KB values obtained for any allosteric modulator of CB1 these positive allosteric modulators of orthosteric agonist binding nonetheless antagonized the agonist-induced G-protein coupling to the CB1 receptor, yet induced β-arrestin mediated ERK1/2 phosphorylation.