ArticleMolecular diversity2026
Canthaxanthin downregulates EGFR in NSCLC: network pharmacology, molecular docking, dynamics simulations, ADMET, and in-vitro analysis.
Article in Molecular diversity, 2026. 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.
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.
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Who cites it
2 citing papers in PubMed.
- Canthaxanthin downregulates EGFR in NSCLC: network pharmacology, molecular docking, dynamics simulations, ADMET, and in-vitro analysis.Molecular diversity · 2026Article
- Network Pharmacology-Driven Sustainability: AI and Multi-Omics Synergy for Drug Discovery in Traditional Chinese Medicine.Pharmaceuticals (Basel, Switzerland) · 2025Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-small cell lung cancer (NSCLC) remains a leading cause of cancer-related mortality, with current therapies often limited by toxicity and resistance. Natural compounds like canthaxanthin, a carotenoid with demonstrated anticancer properties, offer a promising alternative. This study investigates canthaxanthin's therapeutic potential in NSCLC through an integrated computational and experimental approach. Network pharmacology identified 34 shared targets between canthaxanthin and NSCLC, with EGFR, SRC, and CASP3 emerging as key hubs. Molecular docking revealed strong binding affinities (- 9.0, - 7.6, and - 8.0 kcal/mol, respectively), supported by 200-ns molecular dynamics simulations demonstrating complex stability. ADMET analysis predicted favourable pharmacokinetics and low toxicity (Class 6). In-vitro validation via MTT assay showed selective cytotoxicity against A549 cells (IC₅₀ = 23.66 µg/mL) compared to normal lung cells (HEL 299; IC₅₀ = 57.77 µg/mL), outperforming 5-fluorouracil in selectivity (SI = 2.64 vs. 2.23). Pathway enrichment implicated cancer-related signaling (PI3K-AKT, MAPK) and apoptosis. Canthaxanthin's multi-target action-inhibiting EGFR proliferation, SRC migration, and activating CASP3-mediated apoptosis-suggests a polypharmacological advantage. Computational predictions aligned with experimental results, confirming dose-dependent cytotoxicity and minimal mutagenic risk. Canthaxanthin exhibits potent, selective anti-NSCLC activity through multi-target modulation, supported by robust binding stability and low toxicity. These findings highlight its potential as an adjunct or alternative therapy, particularly for resistant NSCLC. Future studies should explore in-vivo efficacy, combination regimens, and clinical translation.
Indexed as
Identifiers
40515965What Socratic 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 Socratic graph.