Evidence map›Paper›PMID 41904818›Full record

ArticleDrug development research2026

Synthesis, Characterization, and Biological Evaluation of Aliphatic-Substituted Benzimidazole Derivatives: Induction of Apoptosis, Cell Cycle Arrest, and Molecular Docking in Breast Cancer Cells.

Murat Keser, Çisil Çamlı Pulat, Harika Atmaca, Hakan Akgün, Canan Albay, Emre Menteşe, Hakan Bektaş, Suleyman Ilhan

Abstract read
In one paragraph

Article in Drug development research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

The trial behind it

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.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

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

8 authors.

Murat KeserDepartment of Medical Oncology, Medicana International İzmir Hospital, İzmir, Türkiye.
Çisil Çamlı PulatApplied Science Research Center, Manisa Celal Bayar University, Manisa, Türkiye.
Harika AtmacaDepartment of Biology, Faculty of Engineering and Natural Sciences, Manisa Celal Bayar University, Manisa, Türkiye.
Hakan AkgünDepartment of Chemistry, Faculty of Science and Art, Giresun University, Giresun, Türkiye.
Canan AlbayDepartment of Chemistry, Faculty of Science and Art, Giresun University, Giresun, Türkiye.
Emre MenteşeDepartment of Chemistry, Faculty of Science and Art, Recep Tayyip Erdogan University, Rize, Türkiye.ORCID https://orcid.org/0000-0002-3408-8202
Hakan BektaşDepartment of Chemistry, Faculty of Science and Art, Giresun University, Giresun, Türkiye.
Suleyman IlhanDepartment of Biology, Faculty of Engineering and Natural Sciences, Manisa Celal Bayar University, Manisa, Türkiye.ORCID https://orcid.org/0000-0002-6584-3979

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A new series of aliphatic-substituted benzimidazole derivatives was synthesized and structurally characterized to evaluate their potential anticancer activity. Among the synthesized compounds, compound 4 exhibited the most potent cytotoxic effects against MCF-7 and MDA-MB-231 breast cancer cell lines, with IC₅₀ values comparable to those of cisplatin, while displaying lower toxicity toward normal breast epithelial cells (MCF-10A). Flow cytometric analysis revealed that treatment with compound 4 resulted in significant accumulation of cells in the S phase, indicating inhibition of DNA synthesis and replication. Furthermore, Annexin V/PI double-staining analysis demonstrated a marked increase in both early and late apoptotic cell populations, confirming the activation of apoptotic pathways. Molecular docking studies supported these experimental findings by revealing strong interactions of compound 4 with key regulatory proteins involved in apoptosis and cell cycle progression, including Bcl-2, Bcl-xL, CDK2, and Cyclin E. The compound exhibited the highest binding affinity toward CDK2 (-164.055 kcal/mol), forming hydrogen bonds with critical residues (LEU134, ASP145, GLN131, and LYS33) within the ATP-binding pocket, suggesting potential inhibition of kinase activity. Interactions with Bcl-2 and Bcl-xL occurred within the BH3-binding grooves, which may impair their anti-apoptotic functions and promote mitochondrial-mediated apoptosis. Collectively, the in vitro and in silico results indicate that this newly synthesized benzimidazole derivative exerts its anticancer effects through a dual mechanism involving cell cycle arrest and apoptosis induction. The selective cytotoxicity and multitarget interaction profile of compound 4 highlight its potential as a promising lead compound for the development of novel therapeutic agents against breast cancer.

Indexed as

Antineoplastic AgentsApoptosisBenzimidazolesBreast NeoplasmsCell Cycle Checkpointsbcl-X ProteinCell Line, TumorCyclin-Dependent Kinase 2Cyclin EFemaleHumansMCF-7 CellsMDA-MB-231 CellsMolecular Docking SimulationProto-Oncogene Proteins c-bcl-2Structure-Activity RelationshipAntineoplastic Agentsbcl-X ProteinBenzimidazolesCDK2 protein, humanCyclin-Dependent Kinase 2Cyclin EProto-Oncogene Proteins c-bcl-2aliphatic‐substituted benzimidazoleapoptosisBcl‐2Bcl‐xLbreast cancerCDK2cell cycle arrestcytotoxicitymolecular dockingmultitarget anticancer agent

Identifiers

PMID41904818
PMCPMC13033344

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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.