ArticleNPJ precision oncology2024
BPI-28592 as a novel second generation inhibitor for NTRK fusion tumors.
Article in NPJ precision oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05302843 (A Phase 1，Open-label Study to Evaluate the Safety, Tolerability, Pharmacokinetics, and Efficacy of Ascendind Doses of BPI-28592 in Subjects With Advanced Solid Tumors), which is not on this map. Cited by 4 papers.
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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.
A Phase 1，Open-label Study to Evaluate the Safety, Tolerability, Pharmacokinetics, and Efficacy of Ascendind Doses of BPI-28592 in Subjects With Advanced Solid Tumors
Who cites it
4 citing papers in PubMed.
- Development of PROTACs for targeted degradation of oncogenic TRK fusions.RSC chemical biology · 2026Article
- The influence of neuro-tumor interactions on tumorigenesis and therapeutic response.Experimental hematology & oncology · 2026Review
- Development of PROTACs for targeted degradation of oncogenic TRK fusions.bioRxiv : the preprint server for biology · 2025Article
- Neurotrophic factors as double-edged swords in osteosarcoma: drivers of tumour growth and immune remodelling.Frontiers in immunology · 2025Review
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Authors and funding
6 authors.
Funding
Abstract
Aberrant activation of tropomyosin receptor kinases (TRKs) is a well-defined oncogenic driver for neurotrophic tropomyosin receptor kinase (NTRK)-fusion cancers, and acquired resistant mutations have emerged with clinical use of the first-generation TRK inhibitors. Here we present BPI-28592, a novel second-generation TRK inhibitor with efficacy against TRK fusion-positive cancers, including those with resistant mutations. Docking simulations indicated no steric hindrance between BPI-28592 and TRK mutants, suggesting its potential to overcome drug resistance. Biochemical assays showed strong inhibition and high selectivity against TRKA, TRKB, and TRKC. The inhibitor significantly reduced cell proliferation and blocked TRK signaling. In vivo studies demonstrated effective tumor suppression in xenograft models harboring TRK fusions with or without resistant mutations. Clinically, BPI-28592 achieved a complete response in a patient with malignant melanoma carrying an AP3S2-NTRK3 fusion (Clinicaltrials. gov identifier: NCT05302843).
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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.