ArticleCell chemical biology2025
Targeting N-Myc in neuroblastoma with selective Aurora kinase A degraders.
Article in Cell chemical biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Photoproximity labeling of c-Myc reveals SLK as a cancer-specific co-regulator.Nature chemical biology · 2026Article
- Targeting MYCN Degradation by HLB-0532259 Induces Senescence in Retinoblastoma.Investigative ophthalmology & visual science · 2026Article
- AURORA A interacts with DICER and SETD2 to promote S-phase progression.EMBO reports · 2026Article
- MYC in Oncogenesis and Therapeutic Implications.MedComm · 2026Review
- The Role of Precision Medicine in Neuroblastoma: Targeted Therapies and Personalized Approaches-A Narrative Review.Health science reports · 2026Article
- MYCN-driven metabolic remodelling of the tumour microenvironment in neuroblastoma: implications for stromal biology and CAF heterogeneity.Cancer metastasis reviews · 2026Review
- Targeting the MYCN interaction network in neuroblastoma.Bioscience reports · 2026Review
- Comprehensive profiling of clinically approved kinase inhibitors reveals mutation-specific inhibitors and opportunities for drug repurposing.Nature biotechnology · 2026Article
- The protein phosphatase 2A-B56α complex regulates N-Myc degradation in neuroblastoma.The Journal of biological chemistry · 2026Article
- Covalent Peptide-Based N-Myc/Aurora-A Inhibitors Bearing Sulfonyl Fluoride Warheads.Journal of peptide science : an official publication of the European Peptide Society · 2026Article
- GSPT1-specific protein degradation is effective in preclinical models of chemoresistant MYCN-amplified neuroblastoma.Journal of experimental & clinical cancer research : CR · 2026Article
- A novel aurora kinase molecular glue-based degrader sp-2-067 inhibits prostate cancer cell growth and alters immune profile.Investigational new drugs · 2026Article
- Unhooking the Hook: Optimization of the Aurora A Targeting PROTACJournal of medicinal chemistry · 2026Article
- Discovery of a "First-in-Class" Selective Multikinase (CDK4/6/9-AURKA/B) Inhibitor, LCI133, for Neuroblastoma.Journal of medicinal chemistry · 2025Article
- Second-Generation AURKA-Targeting PROTACs: Structural Optimization toward in Vivo Degradation in Neuroblastoma.Journal of medicinal chemistry · 2025Article
- Discovery of the first-in-class Aurora B kinase selective degrader.European journal of medicinal chemistry · 2025Article
- Razing the scaffolding: the elimination of non-catalytic functions of kinases through targeted protein degradation.RSC medicinal chemistry · 2025Review
- Aurora A binds to the transactivation domain of c-Myc and recognizes the phosphorylated N-terminal degron motif.The Biochemical journal · 2025Article
- Targeting N-Myc in neuroblastoma with selective Aurora kinase A degraders.Cell chemical biology · 2025Article
- Molecular regulation and therapeutic targeting ofFrontiers in cell and developmental biology · 2025Review
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
The N-Myc transcription factor, encoded by MYCN, is a mechanistically validated, yet challenging, target for neuroblastoma (NB) therapy development. In normal neuronal progenitors, N-Myc undergoes rapid degradation, while, in MYCN-amplified NB cells, Aurora kinase A (Aurora-A) binds to and stabilizes N-Myc, resulting in elevated protein levels. Here, we demonstrate that targeted protein degradation of Aurora-A decreases N-Myc levels. A potent Aurora-A degrader, HLB-0532259 (compound 4), was developed from an Aurora-A-binding ligand that engages the Aurora-A/N-Myc complex. HLB-0532259 promotes the degradation of Aurora-A, which elicits concomitant N-Myc degradation, with nanomolar potency and excellent selectivity. HLB-0532259 surpasses the cellular efficacy of established allosteric Aurora-A inhibitors, exhibits favorable pharmacokinetic properties, and elicits tumor reduction in a murine xenograft NB model. This study broadly delineates a strategy for targeting "undruggable" proteins that are reliant on accessory proteins for cellular stabilization.
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Registered trials
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