ArticleNature medicine2024
MYC targeting by OMO-103 in solid tumors: a phase 1 trial.
Article in Nature medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers.
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Who cites it
127 citing papers in PubMed.
- Host chromatin architecture in HPV-driven cervical cancer: molecular mechanisms and therapeutic resistance.Medical oncology (Northwood, London, England) · 2026Review
- Mapping the functional dark proteome in cancer.Nature reviews. Cancer · 2026Review
- RAD51AP1-MYC-Sam68 positive transcriptional feedback loop maintains lung cancer stemness.iScience · 2026Article
- Divergent c-MYC Expression Patterns in NET and NEC: Insights from a Multicentre Cohort of 1380 Neuroendocrine Neoplasms.Endocrine pathology · 2026Article
- A core transcriptional regulatory circuitry controls super-enhancer-driven activation of LGR5 in colorectal cancer.Nature communications · 2026Article
- Integrating molecular subtypes, genomics and functional dependencies to identify context-specific therapeutic vulnerabilities in small cell lung cancer.Biomarker research · 2026Review
- Aristolochic Acid and Alternative Lengthening of Telomeres Mechanisms Underlie Liver Angiosarcoma Pathogenesis.Liver cancer · 2026Article
- Targeting MYC-Driven Cancers: From Oncogenic Addiction to Therapeutic Vulnerability.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026Review
- Paediatric therapeutic development workshop on osteosarcoma.British journal of cancer · 2026Review
- Emerging Treatments in Bone Tumors: Lessons Learned from the ESMO Annual Meeting.Biomolecules · 2026Review
- Systematic multivariate analysis of chromatin complex dependencies reveals Set1C/COMPASS as a melanoma-enriched epigenetic vulnerability.PLoS computational biology · 2026Article
- MYC in Oncogenesis and Therapeutic Implications.MedComm · 2026Review
- Lethal clinical outcome and immuno-fibrotic contexture in refractory urothelial carcinoma harboring MYC amplification and overexpression.British journal of cancer · 2026Article
- The Pan-Tumor Landscape of Gene Amplifications and Copy Number Amplification Ratio for Established and Emerging Clinical Targets.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- Regulatory factor X 7 limits Myc activity during B cell activation and suppresses Myc-dependent lymphomagenesis.Nature immunology · 2026Article
- Multiple myeloma: A tale of deregulated transcription factors.HemaSphere · 2026Review
- Article
- Targeting the Undruggable: Deep Learning-Driven Design of Peptide Therapeutics in Cancer.Pharmaceuticals (Basel, Switzerland) · 2026Review
- RiboScreenBiomedicines · 2026Review
- Discovery of Macrocyclic Peptide Inhibitors Targeting MYC Oncoprotein via mRNA Display.Pharmaceuticals (Basel, Switzerland) · 2026Article
67 more citing papers are in PubMed but not listed here.
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21 authors.
Funding
Abstract
Among the 'most wanted' targets in cancer therapy is the oncogene MYC, which coordinates key transcriptional programs in tumor development and maintenance. It has, however, long been considered undruggable. OMO-103 is a MYC inhibitor consisting of a 91-amino acid miniprotein. Here we present results from a phase 1 study of OMO-103 in advanced solid tumors, established to examine safety and tolerability as primary outcomes and pharmacokinetics, recommended phase 2 dose and preliminary signs of activity as secondary ones. A classical 3 + 3 design was used for dose escalation of weekly intravenous, single-agent OMO-103 administration in 21-day cycles, encompassing six dose levels (DLs). A total of 22 patients were enrolled, with treatment maintained until disease progression. The most common adverse events were grade 1 infusion-related reactions, occurring in ten patients. One dose-limiting toxicity occurred at DL5. Pharmacokinetics showed nonlinearity, with tissue saturation signs at DL5 and a terminal half-life in serum of 40 h. Of the 19 patients evaluable for response, 12 reached the predefined 9-week time point for assessment of drug antitumor activity, eight of those showing stable disease by computed tomography. One patient defined as stable disease by response evaluation criteria in solid tumors showed a 49% reduction in total tumor volume at best response. Transcriptomic analysis supported target engagement in tumor biopsies. In addition, we identified soluble factors that are potential pharmacodynamic and predictive response markers. Based on all these data, the recommended phase 2 dose was determined as DL5 (6.48 mg kg
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