ArticleBiochemical pharmacology2003
Dihydropyridines as inhibitors of capacitative calcium entry in leukemic HL-60 cells.
Article in Biochemical pharmacology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 111 citations in OpenAlex.
- A Reappraisal of the Effects of L-type CaFunction (Oxford, England) · 2023Pooled it
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- Orai1 is Required for Osteogenic Differentiation on Nanoparticulate Mineralized Collagen Glycosaminoglycan Materials.Macromolecular bioscience · 2025Article
- Metal Ion Signaling in Biomedicine.Chemical reviews · 2025Review
- Side-by-side comparison of published small molecule inhibitors against thapsigargin-induced store-operated Ca2+ entry in HEK293 cells.PloS one · 2024Article
- Depleted Calcium Stores and Increased Calcium Entry in Rod Photoreceptors of theInternational journal of molecular sciences · 2022Article
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- Oscillatory calcium release and sustained store-operated oscillatory calcium signaling prevents differentiation of human oligodendrocyte progenitor cells.Scientific reports · 2022Article
- Dihydropyridines Potentiate ATP-Induced Currents Mediated by the Full-Length Human P2X5 Receptor.Molecules (Basel, Switzerland) · 2022Article
- Development of Store-Operated Calcium Entry-Targeted Compounds in Cancer.Frontiers in pharmacology · 2021Review
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- Targeting calcium signaling in cancer therapy.Acta pharmaceutica Sinica. B · 2017Review
- UTP - Gated Signaling Pathways of 5-HT Release from BON Cells as a Model of Human Enterochromaffin Cells.Frontiers in pharmacology · 2017Article
- Methylglyoxal induces cell death through endoplasmic reticulum stress-associated ROS production and mitochondrial dysfunction.Journal of cellular and molecular medicine · 2016Article
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- New insights into pharmacological tools to TR(i)P cancer up.British journal of pharmacology · 2014Review
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- A microwave-assisted bismuth nitrate-catalyzed unique route toward 1,4-dihydropyridines.Molecules (Basel, Switzerland) · 2012Article
- Mitochondrial pathway mediates the antileukemic effects of Hemidesmus indicus, a promising botanical drug.PloS one · 2011Article
- Synthesis of new tripodal Hantzsch 1,4-dihydropyridines under solvent-free condition and their conversion to the corresponding tripodal pyridines.Molecular diversity · 2010Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
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 (IP(3))-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 (IC(50) values: 3-6 microM). 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 IP(3)-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 (IC(50) 2.6 microM, MRS 1844) and N-propargylnifrendipine (IC(50) 1.7 microM, MRS 1845) represent possible lead compounds for the development of selective SOC channel inhibitors.
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