Evidence map›Paper›PMID 42634207›Full record

ReviewJournal of cellular and molecular medicine2026

Emetine and Its Derivatives as Anticancer Agents Targeting the PI3K/AKT/mTOR Pathway: A Narrative Review of Mechanisms, Pharmacology, and Clinical Insights.

Mst Ismatara Khatun, Samy Selim, Asif Hassan Malik, Md Sakib Al Hasan, Abul Bashar Ripon Khalipha, Noshin Tasnim Yana, Mohammad Y Alshahrani, Md Arif Hossain, Imam Hossen Rakib, Anike Chakrabarty and 1 more

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of cellular and molecular medicine, 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

11 authors.

Mst Ismatara KhatunDepartment of Pharmacy, Faculty of Biological Science and Technology, Jashore University of Science and Technology, Jashore, Bangladesh.
Samy SelimDepartment of Clinical Laboratory Sciences, College of Applied Medical Sciences, Jouf University, Sakaka, Saudi Arabia.ORCID 0000-0003-4025-8586
Asif Hassan MalikDepartment of Chemistry, York College of The City University of New York (CUNY), Jamaica, New York, USA.
Md Sakib Al HasanDepartment of Pharmacy, Gopalganj Science and Technology University, Gopalganj, Bangladesh.ORCID 0009-0004-7560-4041
Abul Bashar Ripon KhaliphaDepartment of Pharmacy, Gopalganj Science and Technology University, Gopalganj, Bangladesh.
Noshin Tasnim YanaDepartment of Pharmacy, Gopalganj Science and Technology University, Gopalganj, Bangladesh.
Mohammad Y AlshahraniCentral Labs, King Khalid University, Abha, Saudi Arabia.ORCID 0000-0002-7096-0221
Md Arif HossainDepartment of Pharmacy, Gopalganj Science and Technology University, Gopalganj, Bangladesh.
Imam Hossen RakibDepartment of Pharmacy, Gopalganj Science and Technology University, Gopalganj, Bangladesh.ORCID 0009-0003-2552-8952
Anike ChakrabartyDepartment of Biotechnology, Faculty of Engineering and Science, University of Greenwich, Kent, UK.ORCID 0009-0003-2723-3031
Emon MiaDepartment of Pharmacy, Gopalganj Science and Technology University, Gopalganj, Bangladesh.ORCID 0009-0007-7390-056X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Emetine (EMT), a naturally occurring tetrahydroisoquinoline alkaloid, shows diverse biological actions, including anticancer effects. Despite existing studies, the role of EMT derivatives in cancer, particularly in relation to the PI3K/AKT/mTOR signalling pathway, remains largely underexplored. This review explores the potential of EMT in targeting PI3K/AKT/mTOR molecular pathways across different cancer types. Data were collected from reliable and well-established sources, including PubMed, Scopus, Wiley Online, Web of Science, ScienceDirect, and Google Scholar. Findings showed that EMT derivatives suppress PI3K-AKT-mTOR pathway activity in multiple cancers such as liver, gastric, acute myeloid leukaemia (AML), and brain, with IC

Indexed as

Antineoplastic AgentsEmetineNeoplasmsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesAnimalsHumansAntineoplastic AgentsEmetineMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesAnticancerEmetineLiterature reviewPI3K‐AKT‐mTOR pathwaytoxicity

Identifiers

PMID42634207
PMCPMC13500901

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.