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From molecular design to immune remodeling: Advances in perylene diimide-based multimodal cancer therapies.

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European journal of medicinal chemistry 2026 Vol.304() p. 118545
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Fu L, Liu C, Yue X, Xu T, Jia W, Jin X, Huo J

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Perylene diimide (PDI) is a programmable theranostic platform that combines high photostability with facile medicinal-chemistry modification at the imide and bay positions.

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APA Fu L, Liu C, et al. (2026). From molecular design to immune remodeling: Advances in perylene diimide-based multimodal cancer therapies.. European journal of medicinal chemistry, 304, 118545. https://doi.org/10.1016/j.ejmech.2025.118545
MLA Fu L, et al.. "From molecular design to immune remodeling: Advances in perylene diimide-based multimodal cancer therapies.." European journal of medicinal chemistry, vol. 304, 2026, pp. 118545.
PMID 41483508

Abstract

Perylene diimide (PDI) is a programmable theranostic platform that combines high photostability with facile medicinal-chemistry modification at the imide and bay positions. Recent advances in donor-acceptor tuning, π-conjugation extension/fusion, and aggregation control have pushed its absorption into the near-infrared II (NIR-II) window (1000-1700 nm), and enabled programmable partitioning between photothermal conversion and Type I/II photodynamic pathways under low irradiance. This review primarily surveys PDI derivatives reported from 2015 through 2025. We focus on mechanisms that move beyond conventional phototherapy: side-chain and topological designs enable precise localization to mitochondria, lysosomes, endoplasmic reticulum (ER), and nucleus, thereby coupling metabolic/oxidative-stress reprogramming, inducing ferroptosis, and potentially overcoming multidrug resistance; Nucleus-targeted PDI acts as a selective G-quadruplex (G4) stabilizer and dsDNA binder, stabilizing G4 structures in the c-MYC promoter and at telomeres/telomerase-associated sites to downregulate oncogenic transcription and provide light-independent chemotherapeutic potential. On the immunomodulation front, acute mitochondria-localized injury triggers immunogenic cell death (ICD) and releases mitochondrial DNA (mtDNA) to activate the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway; inhibiting ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1) to prolong cyclic GMP-AMP (cGAMP) persistence sustains pathway activation and converts "cold" tumors into "hot" phenotypes responsive to immune checkpoint blockade. Altogether, guided by structure-aggregation-spectrum-function relationships, we map programmable links between NIR responses, excited-state energy dissipation, and immune remodeling, and we outline design principles for evolving this molecular scaffold into a streamlined single-molecule platform that integrates chemotherapy, metabolic intervention, and immune activation.

MeSH Terms

Humans; Perylene; Imides; Neoplasms; Antineoplastic Agents; Drug Design; Molecular Structure; Animals; Combined Modality Therapy

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