ReviewFuture science OA2025
Structure-activity insights and molecular modeling approaches of anti-TNBC agents: a comprehensive systematic review.
Review in Future science OA, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTriple-negative breast cancer (TNBC) is a highly aggressive and treatment-resistant subtype of breast cancer, characterized by the lack of hormone receptor expression. This study aims to comprehensively evaluate the structure-activity relationship (SAR), structural modification, pharmacokinetic profiles, and molecular interaction of bioactive compounds developed for TNBC treatment from 2016 to February 2025. METHODS &
resultsThree identified publications were complemented by a selection of 19 articles, each adhering to predefined criteria. Modification of nitrogen heterocycles, phenolic compounds, β-lactams, and halogenated derivative compounds enhanced cytotoxic potency and selectivity against key targets, including CDK9, EGFR, FOXM1, PARP1, and tubulin.
conclusionStrategic structural modifications significantly enhance the potency, selectivity, and pharmacokinetics of anti-TNBC agents. Future research should emphasize polypharmacology, advanced delivery strategies, and translational validation to address TNBC heterogeneity.
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Registered trials
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