ArticleAngiogenesis2025
KC1036, a multi-kinase inhibitor with anti-angiogenic activity, can effectively suppress the tumor growth of Ewing sarcoma.
Article in Angiogenesis, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
4 citing papers in PubMed.
- Palliative Systemic Therapy in Advanced Thymic Epithelial Tumors in 2026-A Narrative Review.Cancers · 2026Review
- Precision oncology in the treatment of patients with bone sarcomas: an up-to-date narrative review.Exploration of targeted anti-tumor therapy · 2026Review
- Integrative biomarker and drug target discovery in osteosarcoma: traditional experimental approaches and AI-enabled insights.Frontiers in pharmacology · 2026Review
- KC1036 in ewing sarcoma: mechanistic insights and future directions for a multi-targeted therapeutic strategy.Angiogenesis · 2025Article
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
backgroundEwing sarcoma (ES) is a rare but extremely aggressive bone and soft-tissue tumor. Clinical outcomes for patients with metastatic or recurrent ES remain poor, particularly for patients who are resistant to chemotherapy. This underscores an urgent need for alternative treatment strategies for these patients. A deep and comprehensive understanding of the cell-cell communications in ES may help identify new therapeutic approaches.
methodsWe first applied single-cell RNA sequencing (scRNA-seq) data analysis to map the cell-cell communication network within the ES tumor microenvironment (TME). Then, based on the cell-cell communication map, we inferred that multi-kinase anti-angiogenic inhibitors might effectively treat ES. Therefore, we investigated the anti-tumor efficacy of a novel multi-kinase inhibitor, KC1036, which primarily targets VEGFR2, MET, and AXL in ES cancer cell lines. The efficacy of KC1036 in ES was further validated in cell line-derived xenograft (CDX) models and a treatment-naïve patient-derived xenograft (PDX) model.
resultsWe plotted a comprehensive cell-cell communication map of ES, where ES was characterized by highly immunosuppressive TME, strong autocrine signal NPY-NPY1R in tumor cells, wide activation of receptor kinase signaling pathways in cancer-associated fibroblasts (CAFs) (e.g., AXL, MET, FGFR, PDGFR, and KIT), and robust activation of tumor angiogenesis pathways (e.g., VEGFA/B-VEGFR1/2). Multi-kinase inhibitor KC1036 effectively inhibited ES tumor growth in both CDX and PDX models with superior efficacy compared to pazopanib, cabozantinib, and doxorubicin (DOX).
conclusionsThe novel anti-angiogenic inhibitor, KC1036, is effective in treating ES in the preclinical models.
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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.