ArticleACS omega2019
Glutathione-Depleting Pro-Oxidant as a Selective Anticancer Therapeutic Agent.
Article in ACS omega, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 49 citations in OpenAlex.
- Synthesis and Biological Evaluation of Thiophene-Bridged Indole-Artesunate Hybrids as Selective Anticancer Agents.ACS omega · 2026Article
- Reactive oxygen species (ROS) in cancer: from mechanism to therapeutic implications.Signal transduction and targeted therapy · 2026Review
- Self-synergizing mutual prodrug liposomes for targeted cancer therapyTheranostics · 2026Article
- Self-boosting targeted anticancer therapyTheranostics · 2026Article
- Reactive Oxygen Species: From Tumorigenesis to Therapeutic Strategies in Cancer.Cancer medicine · 2025Review
- Application of Redox-Responsive Cysteine-Based Organogels as a Drug Delivery System for Doxorubicin.ACS omega · 2025Article
- Flavonoids as modulators of metabolic reprogramming in renal cell carcinoma (Review).Oncology reports · 2024Review
- Form Equals Function: Influence of Coacervate Architecture on Drug Delivery Applications.ACS biomaterials science & engineering · 2024Review
- Photoactive nanocatalysts as DTT-assisted BSA-AuNCs with enhanced oxidase-mimicking ability for sensitive fluorometric detection of antioxidants.Journal of nanobiotechnology · 2024Article
- Critical learning from industrial catalysis for nanocatalytic medicine.Nature communications · 2024Review
- Exploring the Hypocholesterolemic Potential of aMarine drugs · 2024Article
- Naturally Derived Phenethyl Isothiocyanate Modulates Induction of Oxidative Stress via ItsAntioxidants (Basel, Switzerland) · 2024Article
- Harnessing small extracellular vesicles for pro-oxidant delivery: novel approach for drug-sensitive and resistant cancer therapy.Journal of controlled release : official journal of the Controlled Release Society · 2024Article
- Anticancer Potential of Flavonoids: An Overview with an Emphasis on Tangeretin.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Article
- Modeling Preclinical Cancer Studies under Physioxia to Enhance Clinical Translation.Cancer research · 2022Review
- Article
- Photocatalysis-mediated drug-free sustainable cancer therapy using nanocatalyst.Nature communications · 2021Article
- Unraveling Reversible DNA Cross-Links with a Biological Machine.Chemical research in toxicology · 2020Article
- Role of Glutathione in Cancer: From Mechanisms to Therapies.Biomolecules · 2020Review
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 at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A main challenge in the development of anticancer drugs that eradicate cancer cells specifically with minimal toxicity to normal cells is to identify the cancer-specific properties. Cancer cells sustain a higher level of reactive oxygen species, owing to metabolic and signaling aberrations and unrestrained growth. Cancer cells are also furnished with a powerful reducing environment, owing to the overproduction of antioxidants such as glutathione (GSH). Therefore, the altered redox balance is probably the most prevailing property of cancer cells distinct from normal cells, which could serve as a plausible therapeutic target. In this work, we developed a GSH-depleting pro-oxidant, benzoyloxy dibenzyl carbonate, termed B2C, which is capable of rapidly declining GSH and elevating oxidative stress to a threshold level above which cancer cells cannot survive. B2C was designed to release quinone methide (QM) that rapidly depletes GSH through esterase-mediated hydrolysis. B2C was able to rapidly deplete GSH and induce an overwhelming level of oxidative stress in cancer cells, leading to mitochondrial disruption, activation of procaspase-3 and PARP-1, and cleavage of Bcl-2. In the study of tumor xenograft models, intravenously injected B2C caused apoptotic cell death in tumors and significantly suppressed tumor growth. These findings provide a new insight into the design of more effective anticancer drugs, which exploit altered redox balance in cancer cells.
Identifiers
What OpenQuestion 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 OpenQuestion graph.