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Receptor for advanced glycation end products (RAGE) antagonist. Blocks S100P, S100A4 and HMGB-1 mediated RAGE activation in vitro and in vivo. Inhibits growth and metastasis of rat glioma tumors. Reduces cell growth and RAGE-mediated NF-κB activity in human PDAC cell lines. Inhibits effects of TDI exposure in BALB/c mice.
(Modifications: Glu-1 = N-terminal Ac, Leu-10 = C-terminal amide)
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solubility||Soluble to 1 mg/ml in water|
References are publications that support the biological activity of the product.
Arumugam et al (2012) S100P-derived RAGE antagonistic peptide reduces tumor growth and metastasis. Clin.Cancer.Res. 18 4356 PMID: 22718861
Yao et al (2016) The receptor for advanced glycation end products is required for beta -catenin stabilization in a chemical-induced asthma model. Br.J.Pharmacol. 173 2600 PMID: 27332707
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Keywords: RAGE antagonist peptide, RAGE antagonist peptide supplier, Inhibitors, Inhibits, Antagonist, RAGE, Receptor, for, advanced, glycation, end, products, RAP, antagonist, peptide, NF-kB/IkB, 6259, Tocris Bioscience
1 Citation for RAGE antagonist peptide
Citations are publications that use Tocris products. Selected citations for RAGE antagonist peptide include:
Uderhardt et al (2019) Resident Macrophages Cloak Tissue Microlesions to Prevent Neutrophil-Driven Inflammatory Damage. Cell 177 541 PMID: 30955887
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Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* or download your copy today!
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Alzheimer's disease (AD) is a degenerative brain disease and the most common cause of dementia, affecting approximately 47 million people worldwide. Updated in 2015, this poster summarizes the structural and functional changes observed in the progression of this neurodegenerative disease, as well as classic AD drug targets.
Peripheral sensitization is the reduction in the threshold of excitability of sensory neurons that results in an augmented response to a given external stimulus. This poster outlines the excitatory and inhibitory signaling pathways involved in modulation of peripheral sensitization. The role of ion channels, GPCRs, neurotrophins, and cytokines in sensory neurons are also described.
Rheumatoid Arthritis Poster
Rheumatoid arthritis (RA) is a chronic destructive inflammatory autoimmune disease that results from a breakdown in immune tolerance, for reasons that are as yet unknown. This poster summarizes the pathology of RA and the inflammatory processes involved, as well as describing some of the epigenetic modifications associated with the disease and the potential for targeting these changes in the discovery of new treatments.