ArticleActa pharmacologica Sinica2024
S670, an amide derivative of 3-O-acetyl-11-keto-β-boswellic acid, induces ferroptosis in human glioblastoma cells by generating ROS and inhibiting STX17-mediated fusion of autophagosome and lysosome.
Article in Acta pharmacologica Sinica, 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, 13 citations in OpenAlex.
- Targeting VAMP5 suppresses PLK1-driven growth of gliomas with high NDRG4 expression.Journal of neuro-oncology · 2026Article
- Ferroptosis in Glioblastoma and Neuroblastoma: Molecular Mechanisms and Novel Therapeutic Strategies.Current issues in molecular biology · 2026Review
- Article
- From mitochondrial dysregulation to ferroptosis: Exploring new strategies and challenges in radioimmunotherapy (Review).International journal of oncology · 2025Review
- Siramesine induced cell death of glioblastoma through inactivating the STAT3-MGMT signaling pathway.Journal of translational medicine · 2025Article
- Article
- Beta-boswellic acid facilitates diabetic wound healing by targeting STAT3 and inhibiting ferroptosis in fibroblasts.Frontiers in pharmacology · 2025Article
- 3-O-Acetyl-11-Keto-Oncology research · 2025Article
- [AKBA combined with doxorubicin inhibits proliferation and metastasis of triple-negative breast cancer MDA-MB-231 cells and xenograft growth in nude mice].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Research Progress on the Mechanism of Histone Deacetylases in Ferroptosis of Glioma.Oncology reviews · 2024Review
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) is the most common malignant tumor in the brain with temozolomide (TMZ) as the only approved chemotherapy agent. GBM is characterized by susceptibility to radiation and chemotherapy resistance and recurrence as well as low immunological response. There is an urgent need for new therapy to improve the outcome of GBM patients. We previously reported that 3-O-acetyl-11-keto-β-boswellic acid (AKBA) inhibited the growth of GBM. In this study we characterized the anti-GBM effect of S670, a synthesized amide derivative of AKBA, and investigated the underlying mechanisms. We showed that S670 dose-dependently inhibited the proliferation of human GBM cell lines U87 and U251 with IC
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