ArticleJournal of the American Chemical Society2024
Mechanism of Action of KL-50, a Candidate Imidazotetrazine for the Treatment of Drug-Resistant Brain Cancers.
Article in Journal of the American Chemical Society, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Targeting O6-methylguanine-DNA Methyltransferase Deficiency in Preclinical Models of Extracranial Human Cancers with a Tumor-Selective DNA-Modifying Agent.Molecular cancer therapeutics · 2026Article
- Divergent Roles of Canonical and Non-Canonical Mismatch Repair in Regulating Temozolomide Sensitivity in Glioblastoma.International journal of molecular sciences · 2026Review
- Leveraging Homologous Recombination Deficiency via the Repositioned Prodrug CB1954.bioRxiv : the preprint server for biology · 2026Article
- CellPyAbility: automated image analysis for high-throughput dose-response screening.Bioinformatics (Oxford, England) · 2026Article
- Mismatch repair deficiency drives malignant progression and alters the tumor immune microenvironment in glioblastoma models.The Journal of clinical investigation · 2026Article
- Targeted CRISPR knockout screening identifies known and novel chemogenomic interactions between DNA damaging agents and DNA repair genes.NAR cancer · 2026Article
- Revisiting an old therapy for new, promising combinations: Biology and perspectives of lomustine in glioma treatment.Neuro-oncology · 2025Review
- Novel Strategies for Improved Treatment of O6-Methylguanine-DNA Methyltransferase Promoter-Methylated Glioma.Medical research archives · 2025Article
- Identifying active and inhibitor-resistant MGMT variants for gene therapy.American journal of human genetics · 2025Article
- Effects of Hydrogen Bonding Solvation by Diverse Fluorinated Bulky Alcohols on the Reaction Rate and Selectivity in Crown Ether Mediated Nucleophilic Fluorination in an Aprotic Solvent.ACS organic & inorganic Au · 2025Article
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Authors and funding
18 authors.
Funding
Abstract
Aberrant DNA repair is a hallmark of cancer, and many tumors display reduced DNA repair capacities that sensitize them to genotoxins. Here, we demonstrate that the differential DNA repair capacities of healthy and transformed tissue may be exploited to obtain highly selective chemotherapies. We show that the novel N3-(2-fluoroethyl)imidazotetrazine "KL-50" is a selective toxin toward tumors that lack the DNA repair protein O
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