59875-58-0

Usage

Uses

Used in Pharmaceutical Applications:
2-(N-benzyl-N-methylamino)ethyl methyl 2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridinedicarboxylate is used as an active pharmaceutical ingredient (API) for the development of drugs targeting cardiovascular conditions. Its role as a metabolite of Nicardipine indicates its potential in antianginal and antihypertensive therapies, helping to manage and treat conditions such as angina and hypertension.
Used in Neuroprotective Applications:
In the field of neuroresearch, 2-(N-benzyl-N-methylamino)ethyl methyl 2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridinedicarboxylate is used as a neuroprotective agent. It contributes to the development of therapies aimed at protecting the nervous system and preserving brain function, which can be beneficial in treating various neurological disorders and conditions.
Used in Phototodegradation Studies:
As a phototodegradation product of Nicardipine, 2-(N-benzyl-N-methylamino)ethyl methyl 2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridinedicarboxylate is also utilized in research studies to understand the degradation processes of pharmaceuticals under light exposure. This knowledge can be crucial in optimizing drug stability and shelf life, as well as in the development of new drugs with improved photostability.
Used in Chemical Research:
2-(N-benzyl-N-methylamino)ethyl methyl 2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridinedicarboxylate serves as a valuable compound in chemical research, particularly in the synthesis of new molecules and the study of reaction mechanisms involving pyridine and nitrophenyl groups. Its unique structure makes it a useful building block for the development of novel chemical entities with potential applications in various industries.

InChI:InChI=1/C26H27N3O6/c1-17-22(25(30)34-4)24(20-11-8-12-21(15-20)29(32)33)23(18(2)27-17)26(31)35-14-13-28(3)16-19-9-6-5-7-10-19/h5-12,15H,13-14,16H2,1-4H3

Upstream product

• 55985-32-5 Nicardipine 

Downstream Products

• 59875-60-4 methyl 2-(N-methylamino)ethyl 4-(m-aminophenyl)-2,6-dimethylpyridine-3,5-dicarboxylate 

Relevant academic research and scientific papers

Intramolecular electron transfer in the photochemistry of some nitrophenyldihydropyridines

4-Phenyl-1,4-dihydropyridine-3,5-dicarboxylates contain two π chromophores separated by an sp3 carbon. The lowest singlet is localized on the dihydropyridine moiety (1PyH2-Ph) and emits a blue fluorescence (with close to unitary efficiency in glass at 77 K). In 3-nitrophenyl derivatives (PyH2-PhNO2, some of which are photolabile drugs) the fluorescence is completely quenched. Reasonably, this is due to intramolecular electron transfer between the close-lying donor and acceptor moieties to give the charge-separated species (PyH2 .+-PhNO2.-). In EPA glass at 77 K, back-electron transfer gives the dihydropyridine-localized triplet ( 3PyH2-PhNO2), which emits a yellow phosphorescence. In solution, deprotonation from the radical cation on the dihydropyridine moiety initiates rearomatization, finally giving Py-PhNO 2 with low quantum yield (5 × 10-4 to 5 × 10-3, increasing up to 0.013 by irradiation at 254 nm, where direct excitation of the nitrophenyl chromophore contributes). In the presence of triethylamine, the reaction changes to neat reduction of the nitro group. When a tethered alkylamino group is present, oxidative degradation of that moiety occurs, again via an electron-transfer intramolecular process. This has been found with the drug nicardipine, where photodegration is more efficient (Φ 0.02 to 0.1). Donor-acceptor dyads of this type, easily available through the Hantzsch synthesis, may be useful for building new photoinduced electron-transfer systems.

Structural effects on the reactivity 1,4-dihydropyridines with alkylperoxyl radicals and ABTS radical cation

A series of eight commercial C-4 substituted 1,4-dihydropyridines and other synthesized related compounds were tested for direct potential scavenger effect towards alkylperoxyl radicals and ABTS radical cation in aqueous Britton-Robinson buffer pH7.4. A direct quenching radical species was established. The tested 1,4-dihydropyridines were 8.3-fold more reactive towards alkylperoxyl radicals than ABTS cation radical, expressed by their corresponding kinetic rate constants. Furthermore, NPD a photolyte of nifedipine and the C-4 unsubstituted 1,4-DHP were the most reactive derivatives towards alkylperoxyl radicals. The pyridine derivative was confirmed by GC/MS technique as the final product of reaction. In consequence, the reduction of alkylperoxyl and ABTS radicals by 1,4-dihydropyridines involved an electron transfer process. Also, the participation of the hydrogen of the 1-position appears as relevant on the reactivity. Results of reactivity were compared with Trolox.

Pyridyl compounds and pharmaceutical compositions containing them

The present invention is concerned with new pyridine double esters of formula (I), their acids, and pharmaceutically acceptable salts. These compounds can be obtained by oxydation of the corresponding 1,4-dihydropyridines, and they are useful as cardioprotective agents in pharmaceutical compositions.

Oxidation of dihydropyridine calcium channel blockers and analogues by human liver cytochrome P-450 IIIA4

A series of 21 different 4-substituted 2,6-dimethyl-3-(alkoxycarbonyl)-1,4-dihydropyridines was considered with regard to oxidation to pyridine derivatives by human liver microsomal cytochrome P-450 (P-450). Antibodies raised against P-450 IIIA4 inhibited the microsomal oxidation of nifedipine and felodipine to the same extent, as did cimetidine and the mechanism-based inactivator gestodene. Gestodene was ~ 103 times more effective an inhibitor than cimetidine, on a molar basis. When rates of oxidation of the 1,4-dihydropyridines were compared to each other in different human liver microsomal preparations, all were highly correlated with each other with the exceptions of a derivative devoid of a substituent at the 4-position and an N1-CH3 derivative. A P-450 IIIA4 cDNA clone was expressed in yeast and the partially purified protein was used in reconstituted systems containing NADPH-cytochrome P-450 reductase and cytochrome b5. This system catalyzed the oxidation of all of the 1,4-dihydropyridines except the two for which poor correlation was seen in the liver microsomes. Principal component analysis supported the view that most of these reactions were catalyzed by the same enzyme in the yeast P-450 IIIA4 preparation and in the different human liver microsomal preparations, or by a closely related enzyme showing nearly identical properties of catalytic specificity and regulation. The results indicate that the enzyme P-450 IIIA4 is probably the major human catalyst involved in the formal dehydrogenation of most but not all 1,4-dihydropyridine drugs.