ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Dual-Targeting Cuproptosis and Mitophagy via a Flavopiridol-Copper Nanoplatform Potentiates Immunotherapy Against Uveal Melanoma.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Metal-dependent regulated cell death: Molecular architecture and translational frontiers.iMeta · 2026Review
- Dual-Targeting Cuproptosis and Mitophagy via a Flavopiridol-Copper Nanoplatform Potentiates Immunotherapy Against Uveal Melanoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mitophagy-driven immune evasion in skin cancer: multidimensional regulatory networks and context-dependent therapeutic strategies-a narrative review.Frontiers in immunology · 2026Review
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
Abstract
Uveal melanoma (UM) is a highly therapy-resistant ocular malignancy with an immunosuppressive tumor microenvironment (TME) and low tumor mutational burden. Here, we developed NP@Fla-Cu, a glutathione (GSH)-responsive nanoparticle designed to co-induce cuproptosis and mitophagy dysregulation. Cuproptosis, a copper-dependent mitochondrial cell death pathway, is amplified by NP@Fla-Cu's dual functionality: its GSH-degradable shell depletes copper-chelating GSH, while its core delivers a flavopiridol-copper complex (Fla-Cu). Flavopiridol acts as a copper ionophore, driving mitochondrial copper overload to trigger cuproptosis, while hyperactivating mitophagy, causing organelle depletion and metabolic collapse. In UM intraocular orthotopic xenograft models, NP@Fla-Cu exhibited tumor-specific accumulation and potent antitumor activity. Immunological evaluation in a B16F10 murine melanoma model further demonstrated that NP@Fla-Cu effectively remodeled the tumor immune microenvironment, as evidenced by enhanced CD8
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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 OpenQuestion graph.