ArticleAdvanced therapeutics2024
ROS-activatable Prodrug of Doxazolidine as Novel Cancer Therapy Paradigm.
Article in Advanced therapeutics, 2024. 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
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
2 citing papers in PubMed.
- Syntheses, Biological and Preclinical Evaluations, and Nanoparticle Formulations of the ROS-Activatable Prodrugs of Doxazolidine for Drug-Resistant Cancer Therapy.Molecular pharmaceutics · 2026Article
- SETD7 Dual Role in Disease and Opportunities for Therapeutic Intervention: Current Perspectives.Journal of inflammation research · 2025Review
Corrections and comments
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
Overcoming severe side effects from anticancer agents without decreasing their effects on tumor growth is a major challenge. We report on a prodrug technology using agents that are spatiotemporally activated primarily in tumors while the extratumoral toxicity to healthy cells is minimized. We developed ROS-activatable prodrugs of a strong anticancer agent, doxazolidine (doxaz). Doxaz is a DNA alkylating agent with a half-life of 3 min and significantly higher cytotoxicity than the clinically used parental compound doxorubicin (dox). Importantly, doxaz is not affected by p-glycoprotein expression since it irreversibly alkylates DNA while dox inhibits the topoisomerase II DNA complex. As drug activator, we use reactive oxygen species (ROS), already produced inside cancer cells in higher abundance than in normal cells but additionally generated by external stimuli such as radionuclides (via radiolysis of water) and/or ROS-inducing drugs. We synthesized the prodrug, Doxaz-BA, and evaluated its efficacy
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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.