ArticleCell death discovery2026
Novel imidazotetrazine derivatives overcome temozolomide resistance in glioblastoma by inducing ferroptosis and apoptosis.
Article in Cell death discovery, 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
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
1 citing paper in PubMed.
- Aurone analog LYK01 exerts oxidative stress-dependent antiproliferation, G2/M arrest, apoptosis, and DNA damage of oral cancer cells involving MAPK modulation.Molecular and cellular biochemistry · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastomas (GBM) is a highly malignant primary brain tumor with poor prognosis despite standard treatments of surgery, radiotherapy, and chemotherapy. Temozolomide (TMZ) is a key chemotherapeutic agent for GBM but is limited by resistance mechanisms. In this study, we developed a novel imidazotetrazine analogs to overcome TMZ resistance with enhanced therapeutic efficacy. CCK8 assays demonstrated that QX302 showed remarkable potency and effectively inhibited the viability of U251, U87, T98G, and HCT116 cells in a dose- and time-dependent manner. Proteomic analysis indicated that QX302 affected critical pathways, including nucleotide binding, chromatin organization, cell cycle regulation, and DNA repair processes. Further investigations revealed that QX302 effectively inhibits glioma spheroid growth and induces cell cycle arrest, ferroptosis, and apoptosis. Notably, QX302 induced DNA damage in cancer cells via the alkylation of DNA, leading to increased sensitivity to Olaparib via the base excision repair signaling pathway. Predictive modeling demonstrated QX302 has a favorable pharmacokinetic profile, including high blood-brain barrier permeability, highlighting its potential as a central nervous system-penetrating therapeutic agent. In conclusion, QX302 represents a promising therapeutic strategy for GBM, offering improved efficacy and the potential for use in combinatorial therapy with lower effective doses compared to TMZ.
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.