ArticleACS chemical biology2026
Donor-PeT Control of Intersystem Crossing Enables ALDH1A1-Activated Photodynamic Therapy.
Article in ACS chemical biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Hydrogen sulfide in ocular physiology and pathology: molecular Mechanisms, therapeutic Paradoxes, and delivery challenges.Molecular biology reports · 2026Review
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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Aldehyde dehydrogenase 1A1 (ALDH1A1) is highly expressed in therapy-resistant and metastatic cancers and represents a clinically relevant biomarker for selective activation strategies. We report AAP, an OFF-ON photosensitizer activated through ALDH1A1-mediated oxidation that produces singlet oxygen upon light exposure. AAP uses a donor photoinduced electron transfer (d-PeT) mechanism to suppress intersystem crossing in its unreacted benzaldehyde form, which minimizes background activity. Oxidation by ALDH1A1 disrupts d-PeT and restores phototoxicity. AAP showed minimal off-target activation by other ALDH isoforms or oxidative stress.
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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.