Evidence map›Paper›PMID 39506445›Full record

ArticleCurrent pharmaceutical design2025

Design, Synthesis, and Molecular Docking of Quinazolines Bearing Caffeoyl Moiety for Targeting of PGK1/PKM2/STAT3 Signaling Pathway in the Human Breast Cancer.

Rita M Borik, Mohammed A Hussein

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Article in Current pharmaceutical design, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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0cells of the map it votes in
2citing papers in PubMed
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1 · What the graph read from it

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.

2 · The registry

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

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4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Rita M BorikDepartment of Physical Sciences, Chemistry Division, College of Science, Jazan University, P.O. Box. 114, Jazan 45142, Kingdom of Saudi Arabia.
Mohammed A HusseinBiotechnology Department, Faculty of Applied Health Science Technology, October 6 University, Giza 28125, Egypt.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPGK1 and PKM2 are glycolytic enzymes, and their expression is upregulated in cancer cells. STAT3 is a transcription factor implicated in breast cancer progression and chemoresistance. Researchers worldwide continue to explore how targeting genes might lead to more effective anti-breast cancer therapies. The present study aims to synthesize quinazolines containing caffeoyl moiety for developing innovative anticancer agents against the human breast cancer cell line (MCF-7).

methodsA new quinazoline 2 was synthesized by reacting caffeic acid with 5-amino-phenylpyrazole carboxylate 1 in the presence of PCl3. Compound 2 reacted with NH

resultsThe viability of MCF-7 cells was reduced to 22.42% and 45.86% after incubation with compounds 2 and 3 for 48 hours, respectively. The IC

conclusionThe results show that compounds 2 and 3 induce apoptotic activity by blocking the PGK1- PKM2-STAT3 signaling pathway. The present investigation opens exciting possibilities for developing innovative new anticancer quinazolines bearing caffeoyl moiety.

Indexed as

Antineoplastic AgentsBreast NeoplasmsCaffeic AcidsDrug DesignMembrane ProteinsMolecular Docking SimulationPhosphoglycerate KinaseQuinazolinesSTAT3 Transcription FactorThyroid HormonesApoptosisCell ProliferationDose-Response Relationship, DrugDrug Screening Assays, AntitumorFemaleHumansAntineoplastic AgentsCaffeic AcidsMembrane ProteinsPGK1 protein, humanPhosphoglycerate KinaseQuinazolinesSTAT3 protein, humanSTAT3 Transcription FactorThyroid Hormone-Binding ProteinsThyroid Hormonesbreast cancercaffeic acidmolecular dockingPGK1 and PKM2 enzymesQuinazolinessignaling pathway.

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Registered trials

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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.