ArticleIn silico pharmacology2023
Molecular docking appraisal of
Article in In silico pharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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
5 citing papers in PubMed, 6 citations in OpenAlex.
- Article
- In silico screening and molecular analyses identify apigenin from Scutellaria barbata as a potent AKT1 inhibitor in breast cancer.PloS one · 2026Article
- Exploring Natural Compounds as Potential CDK4 Inhibitors for Therapeutic Intervention in Neurodegenerative Diseases through Computational Analysis.Molecular biotechnology · 2025Article
- Ameliorative role of naringenin in MPTP- induced Parkinsonism: Insights fromToxicology reports · 2025Article
- Atomistic simulations suggest dietary flavonoids from Beta vulgaris (beet) as promising inhibitors of human angiotensin-converting enzyme and 2-alpha-adrenergic receptors in hypertension.Bioinformatics advances · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple-negative breast cancer (TNBC) is a lethal and aggressive breast cancer subtype. It is characterized by the deficient expression of the three main receptors implicated in breast cancers, making it unresponsive to hormone therapy. Hence, an existing need to develop a targeted molecular therapy for TNBC. The PI3K/AKT/mTOR signaling pathway mediates critical cellular processes, including cell proliferation, survival, and angiogenesis. It is activated in approximately 10-21% of TNBCs, emphasizing the importance of this intracellular target in TNBC treatment. AKT is a prominent driver of the PI3K/AKT/mTOR pathway, validating it as a promising therapeutic target. Graphical Abstract: A structure-based virtual screening and simulation of
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.