103417-86-3

Basic information

• Product Name: 3,5-Pyridinedicarboxylic acid, 1,4-dihydro-2-[2-(1H-imidazol-1-yl)ethyl]-6-methyl-4-(3-nitrophenyl)-, diethyl ester
• CAS NO: 103417-86-3
• Molecular Formula: C23H26N4O6
• Molecular Weight: 454.483
• Mol File: 103417-86-3.mol
• Article Data: 1

Chemical Properties

• CAS DataBase Reference: 3,5-Pyridinedicarboxylic acid, 1,4-dihydro-2-[2-(1H-imidazol-1-yl)ethyl]-6-methyl-4-(3-nitrophenyl)-, diethyl ester(CAS DataBase Reference)
• NIST Chemistry Reference: 3,5-Pyridinedicarboxylic acid, 1,4-dihydro-2-[2-(1H-imidazol-1-yl)ethyl]-6-methyl-4-(3-nitrophenyl)-, diethyl ester(103417-86-3)
• EPA Substance Registry System: 3,5-Pyridinedicarboxylic acid, 1,4-dihydro-2-[2-(1H-imidazol-1-yl)ethyl]-6-methyl-4-(3-nitrophenyl)-, diethyl ester(103417-86-3)

Safety Data

• Hazardous Substances Data: 103417-86-3(Hazardous Substances Data)

Upstream product

• 21829-28-7 2,6-dimethyl-4-(3-nitro-phenyl)-1,4-dihydro-pyridine-3,5-dicarboxylic acid diethyl ester 
• 288-32-4 1H-imidazole 
• 103417-87-4 2-(2-Dimethylamino-ethyl)-6-methyl-4-(3-nitro-phenyl)-1,4-dihydro-pyridine-3,5-dicarboxylic acid diethyl ester 

Relevant articles and documents

Design of an antithrombotic-antihypertensive agent (Wy 27569). Synthesis and evaluation of a series of 2-heteroaryl-substituted dihydropyridines

An approach to the design of potential combined antithrombotic-antihypertensive agents is described. A series of 1,4-dihydropyridines bearing a 1H-imidazol-1-yl or pyrid-3-yl substituted side chain in the 2-position were synthesized and tested for antihypertensive activity in spontaneously hypertensive rats and for inhibition of TXA2 synthetase in rabbit platelets, in vitro. 1,4-Dihydro-2-(1H-imidazol-1-ylmethyl) -6-methyl-4-(3-nitrophenyl)pyridine-3,5-dicarboxylic acid 3-ethyl 5-methyl diester (1) was shown to be similar in potency to nitrendipine as an antihypertensive agent. Compound 1 inhibited TXA2 synthetase in rabbit and human platelets in vitro and reduced plasma TXB2 levels in rats at antihypertensive dose levels. The reductions in thromboxane production observed in vivo and in vitro were accompanied by enhanced levels of 6-KPGF(1α), reflecting diversion of the arachidonic acid cascade toward prostacyclin synthesis.