Evidence map›Paper›PMID 42001524›Full record

ArticleChemMedChem2026

Discovery of [1,2,4]triazolo[1,5-a]pyrimidine-Imatinib Hybrids With Selective Cytotoxic Activity: A Mechanistically Divergent Series From Direct BCR-ABL1 Inhibition.

Stefany Castro Bazan Moura, Andressa Paula de Oliveira, Joao de Mello Rezende Neto, Rafael Ferreira Dantas, Floriano Paes Silva-Jr, Luiz Claudio Pimentel, Mayara Salles do Nascimento Carvalho, Debora Inacio Leite, Daiane Vitoria da Silva, Monica Macedo Bastos and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in ChemMedChem, 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.

Stefany Castro Bazan MouraLaboratorio de Sintese de Farmacos, Instituto de Tecnologia em Farmacos-Farmanguinhos, Rio de Janeiro, Brazil.
Andressa Paula de OliveiraLaboratorio de Sintese de Farmacos, Instituto de Tecnologia em Farmacos-Farmanguinhos, Rio de Janeiro, Brazil.
Joao de Mello Rezende NetoLaboratorio de Bioquimica Experimental e Computacional de Farmacos, Instituto Oswaldo Cruz, Rio de Janeiro, Brazil.
Rafael Ferreira DantasLaboratorio de Bioquimica Experimental e Computacional de Farmacos, Instituto Oswaldo Cruz, Rio de Janeiro, Brazil.
Floriano Paes Silva-JrPrograma de Pos-graduação em Farmacologia e Quimica Medicinal, Instituto de Ciencias Biomedicas, Centro de Ciencias da Saude, Rio de Janeiro, Brazil.
Luiz Claudio PimentelLaboratorio de Sintese de Farmacos, Instituto de Tecnologia em Farmacos-Farmanguinhos, Rio de Janeiro, Brazil.
Mayara Salles do Nascimento CarvalhoLaboratorio de Sintese de Farmacos, Instituto de Tecnologia em Farmacos-Farmanguinhos, Rio de Janeiro, Brazil.
Debora Inacio LeiteLaboratorio de Sintese de Farmacos, Instituto de Tecnologia em Farmacos-Farmanguinhos, Rio de Janeiro, Brazil.
Daiane Vitoria da SilvaLaboratorio de Sintese de Farmacos, Instituto de Tecnologia em Farmacos-Farmanguinhos, Rio de Janeiro, Brazil.
Monica Macedo BastosLaboratorio de Sintese de Farmacos, Instituto de Tecnologia em Farmacos-Farmanguinhos, Rio de Janeiro, Brazil.
Nubia BoechatLaboratorio de Sintese de Farmacos, Instituto de Tecnologia em Farmacos-Farmanguinhos, Rio de Janeiro, Brazil.ORCID https://orcid.org/0000-0003-0146-2218

Funding

FAPERJ E-26.200.861.2021, E-26/204.033/2024
6 · The paper itself

Abstract

Chronic myeloid leukemia treatment faces the challenge of resistance to BCR-ABL1 tyrosine kinase inhibitors. To address this, we rationally designed six new imatinib-derived compounds 2(a-f) by replacing the quinoline moiety with a [1,2,4]triazolo[1,5-a]pyrimidine scaffold via classical bioisosterism. The compounds were efficiently synthesized and characterized. Biological evaluation revealed that compound 2a exhibited cytotoxic activity in BCR-ABL1-positive K562 cells (47% viability inhibition at 10 µM, IC

Indexed as

Antineoplastic AgentsDrug DiscoveryFusion Proteins, bcr-ablImatinib MesylateProtein Kinase InhibitorsPyrimidinesTriazolesCell Line, TumorCell ProliferationCell SurvivalDose-Response Relationship, DrugDrug Screening Assays, AntitumorHumansK562 CellsMolecular StructureStructure-Activity RelationshipAntineoplastic AgentsFusion Proteins, bcr-ablImatinib MesylateProtein Kinase InhibitorsPyrimidinesTriazolestriazolo(1,5-a)pyrimidineBCR‐ABL1chronic myeloid leukemiadrug discoveryenzymesmedicinal chemistry

Identifiers

PMID42001524
PMCPMC13092336

What OpenQuestion holds

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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.