21889-32-7Relevant academic research and scientific papers
Synthesis and vasodilator activity of new 1,4-dihyropyridines bearing sulfonylurea, urea and thiourea moieties
Stiti, Mohamed Zakaria,Belghobsi, Mebrouk,Habila, Tahir,Goffin, Eric,de Tullio, Pascal,Pirotte, Bernard,Faury, Gilles,Khelili, Smail
, p. 915 - 928 (2020)
Abstract: Some new 1,4-dihydropyridines bearing sulfonylurea, urea and thiourea moieties were synthesized and pharmacologically evaluated for their vasodilator activity, comparatively to nifedipine and diazoxide. The investigations of the target compounds
Synthesis and pharmacological evaluation of novel homocamptothecin- dihydropyridine derivative conjugates as potent topoisomerase i inhibitors
Zhu, Ling-Jian,Zhuang, Chun-Lin,Lei, Ning,Sheng, Chun-Quan,Guo, Wei,Miao, Zhen-Yuan,Liu, Wen-Feng,Yao, Jian-Zhong,Zhang, Wan-Nian
, p. 1390 - 1396 (2012/02/03)
Homocamptothecins (hCPT) represent a new generation of antitumour agents targeting DNA topoisomerase I. The expanded seven-membered lactone E-ring that characterizes hCPT enhances the plasma stability of the drug and reinforces the inhibition of topoisomerase I (Topo I) compared with conventional six-membered CPT. In an attempt to improve the antitumour activity of hCP, a series of novel hCPT derivatives conjugating with dihydropyridine derivates were designed and synthesized based on a synthetic route that couples 7-formylhomocamptothecin with different dihydropyridine derivates. Most of the synthesized compounds exhibited good cytotoxic activity on tumour cell line A549, MDA-MB-435, and HCT116. Furthermore, this class of compounds showed superior Topo I inhibition activity comparable to or higher than CPT. CSIRO 2011.
Dihydropyridines as inhibitors of capacitative calcium entry in leukemic HL-60 cells
Harper, Jacquie L.,Camerini-Otero, Carol S.,Li, An-Hu,Kim, Soon-Ai,Jacobson, Kenneth A.,Daly, John W.
, p. 329 - 338 (2007/10/03)
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.
