ArticleScientific reports2025
Quantum and molecular modelling of abrocitinib as a potential disruptor of cell polarity in colorectal cancer.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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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.
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Who cites it
2 citing papers in PubMed.
- Pharmacophore-based virtual screening, molecular docking, MD simulation, MM-GBSA energy calculation and DFT analysis for theRSC advances · 2026Article
- Comparison of In Vitro Multiple Physiological Activities of Cys-Tyr-Gly-Ser-Arg (CYGSR) Linear and Cyclic Peptides and Analysis Based on Molecular Docking.Biomolecules · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colorectal cancer (CRC) remains a major global health challenge, with chronic inflammation and disruption of epithelial polarity identified as key drivers of tumor progression. Polarity complexes such as Scribble-Mutated in Colorectal Cancer (MCC) are central to maintaining epithelial homeostasis, and their dysregulation has been linked to oncogenic transformation. Drug repurposing offers a promising strategy to accelerate therapeutic discovery by identifying new applications for clinically approved agents. In this study, we investigated abrocitinib (ABR), a selective JAK1 inhibitor, as a candidate for repurposing in CRC. Density functional theory (DFT) calculations at the PBE0-D3/6-31G(d) level were used to examine its electronic properties, including geometry optimization, natural bond orbital (NBO) analysis, molecular electrostatic potential (MESP) mapping, and Fukui function analysis. ABR exhibited a moderate HOMO-LUMO gap (1.827 eV) and an electrophilicity index of 3.492 eV, consistent with favorable reactivity and stability. Molecular docking with the Scribble PDZ1 domain (PDB ID: 6MTV) predicted a strong binding affinity (MolDock score - 78.66 kcal/mol; rerank score - 55.69 kcal/mol), supported by electrostatic and hydrophobic interactions. Importantly, comparative docking with fluorouracil and capecitabine demonstrated that ABR achieved more favorable binding energies and greater interaction stability than these reference CRC drugs, highlighting its superior potential to disrupt Scribble-MCC interactions. Monte Carlo simulations and normal mode analysis further confirmed the dynamic stability of the ABR-PDZ1 complex. Collectively, these findings provide preliminary evidence that abrocitinib may act as a promising modulator of polarity-regulating protein-protein interactions in CRC. While experimental validation remains necessary, this study establishes a computational framework that supports further biochemical and cellular investigations into abrocitinib's potential as a repurposed therapeutic candidate.
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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 Socratic graph.