ArticleNPJ breast cancer2023
RAGE inhibitor TTP488 (Azeliragon) suppresses metastasis in triple-negative breast cancer.
Article in NPJ breast cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 33 citations in OpenAlex.
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- Cancer-associated fibroblast-derived protein S100-A11 influences the response to anti-HER2 therapies in HER2-positive breast cancer.Neoplasia (New York, N.Y.) · 2026Article
- RAGE-Mediated Signalling in Gynaecological Disorders: Review of Molecular Mechanisms and Therapeutic Perspectives.Expert reviews in molecular medicine · 2026Review
- Aging promotes a RAGE-dependent increase in breast cancer metastasis.Communications biology · 2026Article
- Repurposing Azeliragon as a novel antibacterial agent against methicillin-resistant Staphylococcus aureus via combined membrane phospholipids and cell wall targeting.Communications biology · 2026Article
- Therapeutic targeting of RAGE/STAT3 signaling abrogates S100A7-driven breast tumorigenicity and immune suppression.Breast cancer research : BCR · 2026Article
- Multi-trait polygenic scores for COPD and COPD exacerbations implicate druggable proteins.JCI insight · 2026Article
- Deconstructing the RAGE signaling maze: the molecular key to opening a new dimension of ovarian anti-aging.Experimental & molecular medicine · 2026Review
- Cell-Free DNA-Based Theranostics for Inflammatory Disorders.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- JAK/STAT signaling pathway inhibitors in neurodegenerative diseases: current status and future perspectives.Frontiers in aging neuroscience · 2026Review
- Regulatory networks of post-translational modifications in diabetic kidney disease: from pathogenic mechanisms to therapeutic frontiers.Frontiers in endocrinology · 2026Review
- From Fork to Brain: The Role of AGE-RAGE Signaling and the Western Diet in Neurodegenerative Disease.NeuroSci · 2025Review
- Diabetic hyperglycemia-induced glycation regulates tumor vasculature integrity via NF-κB-mediated GM-CSF secretion by tumor cells.Cell biomaterials · 2025Article
- Direct interaction of HMGB1 with SARS-CoV-2 facilitates its infection via RAGE-dependent endocytosis.iScience · 2025Article
- Extracellular Matrix Signaling Cues: Biological Functions, Diseases, and Therapeutic Targets.MedComm · 2025Review
- Clinical Significance and Prognostic Value of TLR4 and AGER in Inflammatory Breast Cancer.Cancers · 2025Article
- Related Mechanism of Limonene Improves LPS-Induced Neuroinflammation.Journal of microbiology and biotechnology · 2025Article
- The Advanced Glycation End-Products (AGE)-Receptor for AGE System (RAGE): An Inflammatory Pathway Linking Obesity and Cardiovascular Diseases.International journal of molecular sciences · 2025Review
- Article
- Pathological role of RAGE underlying progression of various diseases: its potential as biomarker and therapeutic target.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple-negative breast cancer (TNBC) is a highly aggressive and metastatic cancer subtype, which is generally untreatable once it metastasizes. We hypothesized that interfering with the Receptor for Advanced Glycation End-products (RAGE) signaling with the small molecule RAGE inhibitors (TTP488/Azeliragon and FPS-ZM1) would impair TNBC metastasis and impair fundamental mechanisms underlying tumor progression and metastasis. Both TTP488 and FPS-ZM1 impaired spontaneous and experimental metastasis of TNBC models, with TTP488 reducing metastasis to a greater degree than FPS-ZM1. Transcriptomic analysis of primary xenograft tumor and metastatic tissue revealed high concordance in gene and protein changes with both drugs, with TTP488 showing greater potency against metastatic driver pathways. Phenotypic validation of transcriptomic analysis by functional cell assays revealed that RAGE inhibition impaired TNBC cell adhesion to multiple extracellular matrix proteins (including collagens, laminins, and fibronectin), migration, and invasion. Neither RAGE inhibitor impaired cellular viability, proliferation, or cell cycle in vitro. Proteomic analysis of serum from tumor-bearing mice revealed RAGE inhibition affected metastatic driver mechanisms, including multiple cytokines and growth factors. Further mechanistic studies by phospho-proteomic analysis of tumors revealed RAGE inhibition led to decreased signaling through critical BC metastatic driver mechanisms, including Pyk2, STAT3, and Akt. These results show that TTP488 impairs metastasis of TNBC and further clarifies the signaling and cellular mechanisms through which RAGE mediates metastasis. Importantly, as TTP488 displays a favorable safety profile in human studies, our study provides the rationale for evaluating TTP488 in clinical trials to treat or prevent metastatic TNBC.
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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.