ArticleInvestigational new drugs2010
B5, a novel pyrrole-substituted indolinone, exerts potent antitumor efficacy through G2/M cell cycle arrest.
Article in Investigational new drugs, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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
2 citing papers in PubMed, 11 citations in OpenAlex.
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
(E)-Ethyl 3,5-dimethyl-4-[(indolin-2-one-3-ylidene)methyl]-1H-pyrrole-2-carboxylate (B5) was one of the novel pyrrole-substituted indolinones synthesized in our research with the initial aim of developing selective epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKIs). However, B5 exhibited weak inhibitory potency against a variety of protein tyrosine kinases including EGFR, but potent kinase inhibition against several members of the cyclin-dependent kinase (CDK) family. The results of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay demonstrated that B5 had approximately 500 times more potent antitumor activity than PD153035, a known standard EGFR-TKI, in a panel of ten epithelial cancer cell lines. B5 did not inhibit the phosphorylation of EGFR induced by EGF in vitro. DNA flow cytometric analysis revealed that B5 induced cell cycle arrest at G2/M phase and western blot analysis indicated that both CDK1 (Cdc2) and cyclin B1 proteins were decreased after B5 treatment. Our findings suggested the potential therapeutic applications of B5 in numerous cancers and a promising new template for further development of antitumor agents.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.