ArticleCancer science2014
Flumatinib, a selective inhibitor of BCR-ABL/PDGFR/KIT, effectively overcomes drug resistance of certain KIT mutants.
Article in Cancer science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Effect of high-fat diet on the pharmacokinetics and safety of flumatinib in healthy Chinese subjects.Cancer chemotherapy and pharmacology · 2020Trial
- Optimizing Flumatinib Therapy in Chinese Chronic-Phase Chronic Myeloid Leukemia Based on Therapeutic Drug Monitoring.Drug design, development and therapy · 2026Article
- Safety and Efficacy of Flumatinib in Patients with Chronic Phase Chronic Myeloid Leukemia: A Real-Life Cohort Observational Study.Blood and lymphatic cancer : targets and therapy · 2026Article
- Evidential deep learning-based drug-target interaction prediction.Nature communications · 2025Article
- Safety and efficacy of flumatinib as later-line therapy in patients with chronic myeloid leukemia.Haematologica · 2024Article
- [Advances in basic and clinical research of flumatinib].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2024Review
- Gynecomastia in a Chronic Myeloid Leukemia Patient After Switching from Imatinib to Flumatinib.Patient preference and adherence · 2024Article
- RECOVER identifies synergistic drug combinations in vitro through sequential model optimization.Cell reports methods · 2023Article
- Studies on the inhibitory effect of isavuconazole on flumatinib metabolismFrontiers in pharmacology · 2023Article
- Case Report: A Missense Mutation ofFrontiers in medicine · 2022Article
- The V654A second-site KIT mutation increases tumor oncogenesis and STAT activation in a mouse model of gastrointestinal stromal tumor.Oncogene · 2020Article
- Review
- Pharmacologic characterization of CT-711, a novel dual inhibitor of ALK and c-Met.American journal of cancer research · 2018Article
- Detection ofOncotarget · 2017Article
- Y-632 inhibits heat shock protein 90 (Hsp90) function by disrupting the interaction between Hsp90 and Hsp70/Hsp90 organizing protein, and exerts antitumor activity in vitro and in vivo.Cancer science · 2016Article
- X66, a novel N-terminal heat shock protein 90 inhibitor, exerts antitumor effects without induction of heat shock response.Oncotarget · 2016Article
- Mechanisms, Clinical Phenotype and Potential Risk Prediction for Cardiovascular Toxicity Induced by Tyrosine Kinase Inhibitors In Chronic Myeloid Leukemia.Dose-response : a publication of International Hormesis SocietyReview
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activating mutations in KIT have been associated with gastrointestinal stromal tumors (GISTs). The tyrosine kinase inhibitor imatinib mesylate has revolutionized the treatment of GISTs. Unfortunately, primary or acquired resistance to imatinib does occur in GISTs and forms a major problem. Although sunitinib malate, a multi-kinase inhibitor, has shown effectiveness against imatinib-resistant GISTs, recent studies have indicated that some imatinib-resistant GISTs harboring secondary mutations in the KIT activation loop were also resistant to sunitinib. Therefore, new drugs capable of overcoming the dual drug resistance of GISTs probably have potential clinical utility. In this study, we investigated the efficacy of flumatinib, an inhibitor of BCR-ABL/PDGFR/KIT, against 32D cells transformed by various KIT mutants and evaluated its potency to overcome the drug resistance of certain mutants. Interestingly, our in vitro study revealed that flumatinib effectively overcame the drug resistance of certain KIT mutants with activation loop mutations (i.e., D820G, N822K, Y823D, and A829P). Our in vivo study consistently suggested that flumatinib had superior efficacy compared with imatinib or sunitinib against 32D cells with the secondary mutation Y823D. Molecular modeling of flumatinib docked to the KIT kinase domain suggested a special mechanism underlying the capability of flumatinib to overcome the drug-resistance conferred by activation loop mutations. These findings suggest that flumatinib could be a promising therapeutic agent against GISTs resistant to both imatinib and sunitinib because of secondary mutations in the activation loop.
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