23118-50-5

Upstream product

• 101340-05-0 (1R,13R)-9,11-Dimethyl-4-trifluoromethyl-8-thia-10-aza-tricyclo[7.3.1.0^2,7]trideca-2⁽⁷⁾,3,5,11-tetraene-12,13-dicarboxylic acid diethyl ester 
• 454-89-7 3-Trifluoromethylbenzaldehyde 
• 141-97-9 ethyl acetoacetate 
• 626-34-6 ethyl aminocrotonate 

Downstream Products

• 85825-46-3 2-Methyl-5-oxo-4-(3-trifluoromethyl-phenyl)-1,4,5,7-tetrahydro-furo[3,4-b]pyridine-3-carboxylic acid ethyl ester 

Relevant academic research and scientific papers

Synthesis of 2,3-dihydropyrroles by photo rearrangement of Hantzsch 1,4-dihydropyridines with high diastereoselectivity

The Hantzsch 1,4-dihydropyridines were found to be transforming to the 2,3-dihydropyrroles by photo rearrangement with air under irradiation of LED light (410?nm) with high diastereoselectivity (dr?>?20:1). This reaction includes tandem photo oxidation/rearrangement. The 2,3-dihydropyrroles were obtained in moderate yields with successfully one-pot process starting from aldehydes, ammonium acetate and ethyl acetoacetate.

Dihydropyridines as inhibitors of capacitative calcium entry in leukemic HL-60 cells

A series of 1,4-dihydropyridines (DHPs) were investigated as inhibitors of capacitative calcium influx through store-operated calcium (SOC) channels. Such channels activate after ATP-elicited release of inositol trisphosphate (IP3)-sensitive calcium stores in leukemia HL-60 cells. The most potent DHPs were those containing a 4-phenyl group with an electron-withdrawing substituent, such as m- or p-nitro- or m-trifluoromethyl (IC50 values: 3-6μM). Benzyl esters, corresponding to the usual ethyl/methyl esters of the DHPs developed as L-type calcium channel blockers, retained potency at SOC channels, as did N-substituted DHPs. N-Methylation reduced by orders of magnitude the potency at L-type channels resulting in DHPs nearly equipotent at SOC and L-type channels. DHPs with N-ethyl, N-allyl, and N-propargyl groups also had similar potencies at SOC and L-type channels. Replacement of the usual 6-methyl group of DHPs with larger groups, such as cyclobutyl or phenyl, eliminated activity at the SOC channels; such DHPs instead elicited formation of inositol phosphates and release of IP3-sensitive calcium stores. Other DHPs also caused a release of calcium stores, but usually at significantly higher concentrations than those required for the inhibition of capacitative calcium influx. Certain DHPs appeared to cause an incomplete blockade of SOC channel-dependent elevations of calcium, suggesting the presence of more than one class of such channels in HL-60 cells. N-Methylnitrendipine (IC50 2.6μM, MRS 1844) and N-propargylnifrendipine (IC50 1.7μM, MRS 1845) represent possible lead compounds for the development of selective SOC channel inhibitors.

HANTZSCH 1,2,3,4-TETRAHYDROPYRIDINES RELATED TO CALCIUM ANTAGONISTS. TWO SYNTHETIC APPROACHES.

Two stereoselective routes to tetrahydropyridines related to calcium entry antagonists are described.